Patho Final Exam (Exams 1, 2, 3, 4)
Host Factors Influencing UTI
*Sterility of urine* -Maintained by "flushing" (frequent & complete emptying of bladder and constant inflow of newly formed urine), antibody, non-specific antibacterial substances in urogenital secretions, local defence mechanisms *Colonization of periurethral area with potential pathogens* -Usually prevented by bactericidal activity of urethral and vaginal secretions and presence of normal flora *Female gender* - short urethra *Sexual intercourse* (especially within previous 48 hours) *Residual urine* - enables bacteria to multiply *Incompetence of vesicoureteric valve* - due to congenital abnormality or inflammation of bladder wall, causes reflux of urine into kidney pelvis during micturition *Catheterization* - risk after single catheterization ~ 5 % -- almost all patients with indwelling catheter develop infection *Abnormalities of renal tract causing obstruction and stasis* ~Congenital structural abnormalities ~Urinary calculi ~Prostate enlargement
Signs and Symptoms of Lower UTI's
*Symptoms*: -Dysuria (burning pain on passing urine) -Urgency (urgent need to pass urine) -Frequency of micturition UTIs in elderly and those with indwelling catheters are often asymptomatic (may screen these folks) *Signs*: cloudy urine -Presence of pus (pyuria) - usually accompanies bacteriuria -Presence of bacteria (bacteriuria) -May contain blood (hematuria)
Complicated UTIs (pyelonephritis)
*Use intravenous antibacterial agent followed by oral therapy when signs and symptoms subside (14 days or longer)*
How is it usually acquired?
*acquired by ascending route from urethra to bladder* -May proceed to kidney and, occasionally, to bloodstream
Fibrinous exudate
++fibrinogen Sticky, thick meshwork
Fever in the elderly
- 1.1 degree over basal temperature (avg 36.4) - over 37.5
Physiology of Fever
- Exogenous pyrogen enters body->engulfed and digested by macrophages, monocytes, neutrophils, dendritic cells - Interleukins released and travel to hypothalamus - Cyclooxygenase 2 (COX-2) converts arachidonic acid in wall of brain to prostaglandin E2 (PGE2) ->PGE2 binds to hypothalamus which increases the "set-point" - Epi release->increases heart rate, initiates stress response
Prodromal Stage
- Mild headache, fatigue, aches, pains, mailaise - set point has changed
Treatment of fevers
- Modify external environment facilitate heat away from skin - Support hypermetabolic state - hydration - Protect vulnerable organs and systems - antipyretic - Treat primary cause
Sustained / continuous
- Never returns to normal - Varies minimally - +- .5
Remittent
- Never returns to normal, but varies up and down +/- 2
Intermittent
- Normal temperature reached once q24
Fever in Children
- Occurs frequiently - Immune system not as eveloped - Rectal temperature of 38 or higher requires monitoring and/or tx - Vacc have decreased occurence of some infection - Most sig in dev countries: haemophilus influenza and streptococcus pneumoniae
Conduction
- One surface to another - Cooling blankets
Four stages of fever
- Prodromal - Chill - Flush - Defervescence
Fever without source
- Rapid onset - No other signs or symptoms - Treated aggressively in young babes because incidence of serious infection higher ad immune system is not fully developed.
Flush
- Set point reached, no more shivering, vasodilation, av shunts opened. - Skin is red an warm
Defervescence
- Sweating provides heat loss
Chill
- Temperature is climbing, - Vasoconstriction, av shunts close, piloerection / cutis anseria, pale skin, shivering
Recurrent / Relapsing
- episodes of fever wit episodes of normal temperature, both lasting days at a time
Convection
- heat transfer through circ of air currents (wind chill)
Mechanisms for altered febrile response in elderly
- lower basal temperature (36.4) - disturbance in the ability of the hypothal to recognize altered body state - alterations in the release of endogenous pyrogens - inability to respond eg. Vasoconstrict, shiver, - inability to measure accurately (rectal and tympanic better)
Radiation
- opening of AV shunts - difference of temperature in environment than body - no contact, just air temperature
treatment IBS
- reduce emotional tension - improve intestinal motility
Evaporation
- water on skin turned to vapour by skin temperature
Neoplasia
-"New growth" -Overgrowth of a tissue -Neoplasm-Neoplastic mass (AKA-Tumor) -They proliferate to form new tissue (irreversible) -They don't wait for signals from the body that the new tissue is needed. -They ignore signals to stop dividing -They often do not mature normally to do the 'job" the tissue i supposed to do. -Apoptosis does not happen.
Erythrocytes
-"doughnut" shaped disc--shape increases surface area so it can carry more oxygen; very flexible, can flatten to squeeze through capillaries -lifespan: 3-4 months -function: transports oxygen via hemoglobin (molecule in cytoplasm of RBC) to the cell and carries CO2 to the lungs -normal level: 4.0-6.2 million/ul
Complete Blood Count
-# of WBCs -# of RBCs -Hemoglobin content -Hematocrit -Mean corpuscular volume -Mean corpuscular hemoglobin -Mean corpuscular hemoglobin concentration -Platelet count and volume
Diagnosis of UTIs
-*Dip test for preliminary diagnosis*: ~*Nitrites*: Bacteria that cause urinary tract infection produce an enzyme that converts urinary nitrates to nitrites -- presence of nitrites in urine indicates a UTI -*Leukocyte esterase (WBC esterase)*: Leukocyte esterase detects leukocytes (WBCs) in urine -- presence of WBCs in urine may indicate a UTI -*Microscopic examination* of urine allows a rapid *preliminary report* (look for bacterial cells, red and white blood cells) - not necessarily indicative of UTI (could be renal trauma, carcinoma etc) -*Culture and antibiotic susceptibility results* should be obtained
Who is more susceptible? (gender)
-*More common in women than men (10:1 ratio) -Shorter urethra -Sexual intercourse facilitates movement of microbes up urethra -Pregnancy -*In men*: -More common after 50 years of age -More common in uncircumcised male infants
Treatment of UTIs Uncomplicated Lower UTIs
-*Resolve spontaneously within 4 wks in < 40% of patients* -*Advise to drink large volumes of fluid and void frequently to aid normal flushing out process* -*Antibacterial agents reduce symptoms and ensure bacterial eradication* ~Oral antimicrobial chemotherapy (short course; 3 days usually adequate in normal, healthy patient) should be based on results of susceptibility tests ~Use "best guess" until lab results are available
Sample transport
-*Transport sample to lab with minimum delay* ~Urine is a good growth medium for many bacteria and *multiplication* of microbes between collection and culture will distort results -*Voided specimens of urine are rarely sterile (contamination is a problem), so use Quantitative Culture Methods to diagnose UTI* ~Differentiates between contamination and infection ~Bacteriuria is defined as significant when MSU specimen contains over *10^5 microbes/ml* (and usually contains only a single bacterial species) ~Contaminated urine usually has < 104 organisms/ml (and often >1 species)
Leukocytosis
-A 2-3 fold increase in circulation leukocytes. -Rapid change from release of neutrophils from bone marrow in response to cytokines and Colony Stimulating Factor released from macrophages T lymphocytes.
Gangrene
-A considerable mass of tissue undergoes necrosis.
Barrett's Esophagus
-A precancerous lesion that puts the patient at risk of developing esophageal cancer.
Cytoplasm
-A water solution containing minerals, gasses and organic molecules -Contains the cell organelles -Contains proteins and tubules that form a supportive framework
Carcinoma in situ (CIS)
-Abnormal growths in epithelial tissues that have atypical cells and increased proliferation rate compared with normal surrounding tissues. -These early growths are localized to the epithelium, but have not penetrated the local basement membrane or invaded the surrounding stroma. -These lesions can have 1 of the following 3 fates: 1) They can remain stable for a long time 2) They can progress to invasive and metastatic cancers 3) They can regress and disappear
Tumor
-Abnormal swelling
Chemical Mediators
-Activate both the vascular and cellular responses. -Cell derived mediators: Histamine & Prostaglandin, Cytokines & chemokines -Plasma derived mediators: Kinin, Complement, and Coagulation system
Ion Pumps
-Active transport systems that effect ion movement.
Organelle Changes
-Adaptation in order to inactivate, atrophy or detoxify materials more efficiently.
ATP
-Adenosine triphosphate. -The coenzyme used as an energy carrier in the cells of all known organisms; the process in which energy is moved throughout the cell.
Cellular Senescence
-All normal cells have a limited capacity for replication and after a fixed number of divisions, cells are unable to divide. -Telomere attrition
Coagulation Necrosis
-Architecture of dead tissues is preserved for days -Firm texture -Characteristic of hypoxic injury
Sarcomas
-Arise from the 3rd layer, the mesoderm -Arise from connective tissue and supporting tissue -ex. Chondrosarcoma, osteosarcoma, fibrosarcoma
Peripheral proteins
-Attached to the inner or outer surface of the membrane, do not extend through it
BRCA Gene
-BReast CAncer susceptibility gene. -BRCA1 and BRCA2 -They help protect from getting cancer. Changes or mutations on one or both of the genes makes cells more likely to divide and change rapidly, which can lead to cancer
Neutrophilia
-Bacterial infections and ischemic changes
Carrier Proteins
-Bind solutes and transport them across membrane
Fibrous Exudate
-Blood proteins in exudate (fibrinogen) -Fibrin strands are present
Necrosis & Tumor Growth
-Blood supply for tumor is from the invaded tissue -Able to induce new blood vessels to proliferate to meet the demand of the growing mass. -May outgrow blood supply -Results in necrosis of tissue that is deprived of the blood.
Patterns of of the Spread of malignant tumors
-By direct extension into surrounding tissues. -Through lymph channels to lymph nodes (lymphatic spread)--typical of carcinomas -Via the bloodstream (hematogenous spread)--typical of carinomas or sarcomas -Within body cavities (seeding)--by penetrating the wall of an organ, move into a body cavity and spread throughout the area
Cellular Accumulation
-Can be reversible if insult is controlled or stopped. -If it is progressive it can lead to cellular injury and death -Substance can be harmless or toxic
Enzymes
-Catalyze chemical reactions
Lead Toxicity
-Causes anemia (cardinal sign) by interfering with hemoglobin synthesis and decreases life span of RBC. -Demyelination of cerebral and cerbellar white matter and death to cortical cells
Pinocytosis
-Cell engulfs a small vesicle -mainly water
Phagocytosis
-Cell engulfs a solid substance -mainly larger vesicles -Steps: 1) Phagocyte is activated and moves to site of injury 2) It recognizes invader/insult 3) Engulf and destroy invader
Endocytosis
-Cell engulfs a substance by forming a vesicle around the substance
Alternative Metabolism
-Cell's ability to employ alternative metabolic pathways to adjust to certain conditions.
Dysplasia
-Cells are disorganized and variable in size and shape -Seen in sever, chronic irritation; usually epithelial -Is reversible, but less so than metaplasia -Can range from low grade to high grade. -High grade are considered to be in situ: cancers that are still in place. Has not penetrated through basement membrane.B
Invasion
-Cells have the ability to separate from amass and move into surrounding tissue -Low intercellularly adhesion property -Secrete enzymes that break own normal tissue barriers, which allows them to infiltrate tissues, lymphatic channels, and blood vessels.
Metastasis
-Cells in a primary tumor develop the ability to escape and travel in the blood or lymph. -Secondary site has the same tumor cells as primary site. These deposits are celled metastatic tumors.
Malignant tumors
-Classified according to the embryonic origin of tissue. -Contain cells that do not look like normal adult cells -Anaplasia: the loss of cellular differentiation -The cells are also pleomorphic, with marked variability of size and shape of cell and nuclei. -Increased nuclear size (increased nuclear/cytoplasmic ratio) -Prominent nucleoli or irregular chromatin distribution within nuclei -Especially irregular or bizarre mitoses -Atypia: a change for the worse form normal -Often have large darkly stained nuclei and mitotic cells -They divide rapidly and the tumors can grow quickly. -Does not have clear boundaries and sends "legs" out into surrounding tissue -Do no perform the normal functions of the organ and may secrete functions associated with other tissues -Can compress and/or destroy the surrounding tissues
Which are the two environments that it can be acquired?
-Community acquired -Hospital acquired (often associated with catheterization)
-itis
-Condition that is inflammatory
Lysosomes
-Consist of a membrane vesicle floating in the cytoplasm. -Digestive packets -Contain more than 30 different enzymes -Membrane resists degradation themselves by chemical properties. -Functions by aiding in foreign materials entering the cell.
Benign Tumors
-Contain cells that look like normal tissue cells (can be indistinguishable) -Slow growing -May perform the normal function of the tissue (like secreting of hormones) -Surround capsule of connective tissue -Generally are localized and remain in the tissue in which they originated. -These tumors are generally named according to the tissues from which they arise. -Glandular - adenoma -Fatty: Lipoma -Muscle: myoma -Vascular: Angioma -Brain: Meningioma -some grey area to this rule with epithelial tumors -some names are based on structure -Papilloma: warty type appearance
Purulent or Supportive Exudate
-Contains mainly inflammatory cells -Neutrohils present -appears as think yellow white (pus)
Cell Death
-Contents of cell are broken down by endogenous- lysosomal enzymes and by enzymes of cells that arrive at the scene -Debris is removed and healing begins
Cell Nucleus
-Control center of the cell
Metaplasia
-Conversion of one cell type to another type. -Adaptive response -Usually a reduced function of cell and an increased propensity to form neoplasia. (reversible)
Local Neoplasia
-Damage is confined to one area of the body
Nucleolus
-Dense collection of RNA and proteins -Site of ribosome production
Hypoxic Cell Injury
-Deprives cell of oxygen and interrupts oxidative metabolism and generation of ATP -The longer the tissue is hypoxic, the greater chance of irreversible cellular injury -Cells with higher metabolic demand are most susceptible (heart, brain, kidney) -Decrease oxygen results in decrease in cell's ability to synthesize ATP -4-6 minutes of oxygen deprivation to neurons causes permanent damage
Frustrated Phagocytosis
-Destructive capabilities of oxygen free radicals and the release of enzymes damage the host tissue by leucocyte. -This occurs when leukocytes are incapable of ingesting substance.
Recognition Proteins
-Detected by the cells of the immune system
Osmosis
-Diffusion of water through a selectively permeable membrane
Pigment molecules
-Endogenous or exogenous -Lipofuscin granules: pigment composed of lipid, carbohydrate, and protein and id the residue of lysomal digestion of cellular debris. -Found in neurons, liver, and myocardium. -Increase with age -Free radial injury -Cause no harm to the cell.
Bilirubin Retention
-Endogenous pigment from RBC destruction, liver disease, or biliary obstruction -Appears as a yellow discoloration of tissue.
Fat Accumulations
-Enzyme systems that metabolize fat are impaired can lead to accumulation of fat droplets within the cell or excessive fat uptake by cell -Progresses to cause swelling of cell and eventually organ -Kidney, liver, muscle, heart
Oxidative Stress
-Exposure to reactive oxygen species (ROS) and cell is not able to neutralize them.
Integral Proteins
-Extend into or through the lipid bilayer
Endoplasmic
-Extensive network of membranous SACS that extend from the nuclear membrane to the cell membrane
Genetic Derangements
-Extra Chromosome: Down syndrome, sickle cell anemia
Fatty Accumulation
-Fat droplets appear in parechymal cells (functioning cells of organ)
Pyrexia
-Fever -Non-specific response mediated by pyrogens released from cells in response to infectious or non infectious disorders -Pyrogens --> reset hypothalamic thermoregulatory center -Usually does not exceed 105 degrees
Chromatin
-Fibers of DNA and proteins -Stores info for synthesis of proteins
Granulomatous Inflammation
-Focal response leading to formation of a granuloma. -Grossly, seen as pale yellow nodules. -Caused in response to undigestible organisms and other foreign material -Tuberculosis -Fungal infections
Receptors
-For cellular recognition -They bind to ligands
Ribosomes
-Free floating or connected to ER. -Made of protein and rRNA. -Site of protein synthesis.
Cachexia
-Generalized muscle wasting -Cancer cachexia syndrome: Weight loss, muscle wasting, weakness, anorexia, anemia
Proliferation
-Generation of new cells from parent cells.
Glycogen Accumulation
-Genetic storage: rare genetic disease -Enzymes that breakdown glycogen are missing -Can lead to organ malfunction
Grading Tumors
-Grade I: Highly differentiated cells (resemble tissue of origin), well ordered, few if any mitotic figures -Grade IV: Poorly differentiated, pleomorphic, and increased mitosis
Blood Vessel Metastasis
-Hematogenous spread -Usually starts at thin wall capillaries/veins -Eventually leads to atrium -Then lungs, lodges in small vessels and the cells become actively invasive, secreting enzymes that promote passage into lung tissue -Lung is common site for metastasis -Liver is also common b/c of hepatoportal circulation-this is venous drainage of GI tract -Sinusoids of liver are common entrance point from tumors originating in intestines and stomach
Free Radicals and reactive oxygen Species (ROS) formation
-Highly reactive chemical species with an unpaired electron, which causes them to be unstable and highly reactive. -Seen in chemical and radiation injury, reperfusion, cellular aging, and microbial killing phagocytes. -Superoxide, H202, OH- are normal products of mitochondrial respiration and are normally removed by scavenger and detoxifying enzymes.
Collection of Specimens for Diagnosis of UTIs
-Ideally, collect sample *before* antimicrobial therapy is started *Collection of Sample*: -*Midstream urine sample (MSU) collection* ~Sterile wide-mouth container ~Careful cleansing of labia or glans with soap (not antiseptic) and water ~Void first part of urine stream to wash out contaminants, then collect MSU -*"Bag" collection, or suprapubic needle aspiration* of urine from full bladder of infants and young children -*Catheter specimen* from patients with catheter
Acute Lymphocytic Leukemia
-Immature cells with larger nuclei that contain nucleoli
Swelling
-Increase in flow of blood leads to increase in hydrostatic pressure. -Increases the force driving fluid out of the capillary, except now at an increased rate/time. -Loss of fluid and increase in vessel diameter leads to slowing of blood flow and an incease in viscosity of blood -As amount of fluid and rate of blood flow decreases, RBCs respond by aggregation and this leads to stasis. -Seen as vascular congestion and localized redness.
Adiposity
-Increase in storage of fat in fat cells
Vascular Response
-Increased blood flow to the injured area and the vasculature becomes more permeable -Involves arteriole, capillaries, and venules of micociculation. Facilitated by chemical mediators -Induces vasodilation and increased vascular permeability quickly follows -Objective is to get more blood flowing to the area.
Pain
-Inflammatory exudate increases the pressure and tension of free nerve endings in inflamed tissue -Chemical mediators trigger pain receptors (bradykinins) -Throbbing pain results from arterial pressure pulses that are transmitted to the swollen tissue, alternating increasing and decreasing the pain causing pressure.
Infection
-Inflammatory process caused by disease producing agent
Nutritional Imbalances
-Iron deficiency anemia -Obesity and insulin resistant diabetes
Tumor Immunity
-It is also possible that the lymphocytes below the epithelium are part of an immune response. -Neoplastic cells may be altered or express antigens to elicit an immune response.
Smooth (agranular) ER
-Lack ribosomes -Detoxification -Has enzymes that form major lipids -Steroid-secreting cells have a lot of SER.
Systemic Neoplasia
-Lesions are distributed throughout the body.
Free Radical Injury
-Lipid peroxidation: cell membrane damage -Oxidative modification of proteins: abnormal formation of proteins (enzyme damage) -DNA effects: mutations -Antioxidants, such as vitamin E, may reduce the damage caused by ROS.
Lymphatic Spread
-Lymphatic vessels similar to veins, easy to invade -Lumph nodes are easily invaded and become secondary sites (Sentinal node is the initial lymph node that is invaded). -Tumor can then enter into the blood.
Do not Follow Rules-Malignancy
-Lymphoma: Lymphoid tissue (Lymphosarcoma) -Melanoma: Melanin (Malingnant melanoma) -Glioma can be benign or malignant -Hepatoma: Hepatocellular carcinoma
Cancer
-Malignant neoplasm -does not always follows the rules
Liposarcoma
-Malignant tumor of fat cells.
Wilms
-Malignant tumor of the kidney occurring in childhood.
Adaptive Responses
-Mechanisms that enable the cell to cope with injury -Capable response: Alternative metabolism, organelle changes, altered size & number.
Serious Inflammation
-Mild Injury -Fluid with little protien -Blister
Transmembrane Proteins
-Most integral proteins, span the inter lipid
Cellular Response
-Movement of leukocytes, predominantly neutrophils and monocytes fromt he blood to the tissue. -These hemodynamic changes within the vessel also lead WBCs to move out of the mass of RBC aggregates in the center of the vessel closer to the vessel wall (margination) -allows them to attach to the wall and move out of the vessel. -Margination-->chemotaxis
Diffusion
-Movement of molecules from an area of higher concentration to an area of lower concentration.
Malignant Neoplasms
-Much more likely to spread to entirely different sites, or invade nearby structures. -Transplantation of cells to a different site. -Common sites: Lymphnodes, lungs, liver, and bone
Leukemia
-Neoplasms arising from blood forming tissues -Precursors of WBCs in bone marrow proliferate and crowd out normal blood forming cells. -Enter into the blood stream circulate in peripheral blood
Cytoskeleton
-Network of protein filaments throughout the cytosol -Provides structural support for the cell
Hyperplasia
-New cells formed by mitosis in response to stimulus -Can be physiologic or pathologic. -Can predispose to neoplasia.
Inflammation
-Non-specific response to any agent that causes injury to the cell. -Goals: Rid the host of initial cause, Remove consequence of injury, Prepare for tissue repair. -The degree and duration vary depending on the etiology and time course of injury. -3 Main components: Vascular response, cellular response, and chemical mediators.
What is angiognesis?
-Normal physiological process needed for growth, wound healing -New blood vessels form from pre-existing vessels -Also transition of benign state to malignant in tumor. (Process is triggered and regulated by tumor-secreted growth factors)
Apoptosis
-Normal type of cell death. -Acts as a protective and regulated mechanism -Is a continuous process -Operates in normal situations when excess cells need to be removed
Tumor Suppressor Genes
-Normally function to suppress cell proliferation -Loss of gene function by mutation can lead to unrestrained cell growth.
Resolution & tissue Repair
-Once Cause has been removed -Plasma protein systems and inflammatory mediators deactivate the response -Healing begins with either of the 2 events -Regeneration -Fibrous connective tissue repair (scar)
Exocytosis
-Opposite of endocytosis -substances in a vesicle fuse with cell membrane
Hypoxia
-Oxygen Deprivation -Results in decreased aerobic respiration and therefor ATP production. -Common cause of cell injury and death. -Causes include reduced blood flow (ischemia), decreased oxygen in blood, severe blood loss (hemorrhage). -Cell either adapts or dies depending on the severity.
Eosinophils
-Parasitic and allergic reactions
what are all tumors made up of?
-Parenchymal tissue = cells of tumors, determine growth -Supporting tissue = Connective tissue, extracellulare matrix and blood vessels, essential to tumor growth and carries blood supply and provides support for parachymal cells
Dystrophic Calcification
-Pathologic -Calcium deposits develop within the necrotic cells at site of injury because dying cells take in calcium.
Metastatic Calcification
-Pathologic -Calcium salt occurs in normal cells caused by excess blood calcium levels -Occurs in conditions that cause increased calcium levels. -Hyperparathyroidism -Certain neoplasia
Nuclear Envelope
-Porous double membrane -Separates nucleoplasm from cytoplasm
Malignancy
-Potential to spread quickly and throughout the body resulting in death.
Hypertrophy
-Process of cell enlargement that occurs in response to increased demands and/or hormone signaling -Happens for cells that have limited capacity to divide.
Cellular Respiration
-Process that releases energy by breaking down glucose and other food molecules in the presence of oxygen -Results in the synthesis of ATP.
Chronic Inflammation
-Prolonged and persistent inflammation marked chiefly by new connective tissue formation. -It may be a continuation of an acute form or a prolonged low-grade form. -Late in acute inflammation, macrophage predominates. these cells persist if the agent is not eliminated.
Liquefaction Necrosis
-Prompt breakdown of tissue without coagulation and tissue is transformed into liquid mass -Common in brain tissue post ischemic event -Some bacterial infections -Necrotic cells liquefy quickly because microbes stimulate leukocytes, which liberate enzymes -Forms pus: creamy yellow exudate from accumulated dead WBCs.
Hemorrhagic Exudate
-RBCs present from ruptured capillaries -Indicates more intense damage
Carcinogens
-Radiation -ROS -Hormones -Tobacco -Infectious microorganisms -Certain chemicals -Immune conditions -Diet -Inherited/genetic conditons
Pustule
-Raised spot on the skin containing pus
Ischemia
-Reduced or interrupted blood flow
Proto-oncogenes
-Regulate normal growth function in cells -Can mutate and can convert into an oncogene. -Oncogene stimulates excessive cell growth -Gene that causes cancer
DNA Repair Genes
-Regulate the processes that monior and repair DNA -Failure of DNA repair gene function increases the risks of DNA mutations which my cause unrestrained cell growth.
Active Transport
-Requires the energy from ATP to move molecules from an area of lesser concentration to an area of greater concentration -Movement against a concentration gradient
Cellular Aging
-Result of a progressive decline in cell function and viability caused by genetic abnormalities (intrinsic) and environmental stresses (extrinsic). -Aging is acomplex multifactorial process, whereny organisms undergo major cell degeneration and loss of function.
Adaptations
-Reversible responses which new steady states are achieved and allow the cell to continue to function
Cell Membrane
-Selectively permeable boundary of the cell
Hydropic degeneration
-Severe acute swelling where free water dilutes ctyoplasm -Grossly, pallor, increased turgor, and increase weight of organ
Atrophy
-Shrinking of the cell caused by factors that reduce the demand or adverse environmental conditions. -Cells adapt to reduce demand by gradually shutting down their specialized functions. -Decreased nervous input -Decreased hormonal stimulation. -Ischemia: Decreased blood supply. -Cachexia: Muscle wasting from loss of protein.
Calcification
-Sign of previous cell injury -Can cause organ damage -Serum calcium levels are normal -Can be useful diagnostically on radiographs to locate area of disease.
Rough ER
-Site of protein synthesis on surface of ribosomes. -Protein molecules may pass to the interior for storage or modification. -Proteins will be secreted by cell.
Granuloma
-Spherical mass formed by epithelioid cells (giant cells) (transformed macrophage). Fibroblast, lymphocytes are also present. -Typically develop necrotic center as it grows.
Golgi Apparatus
-Stack of membranous sacs -Modifies, packages and delivers proteins -Site of carb synth -To secrete a substance, small sacs of golgi membrane break off and fuse with the cell membrane, releasing the substance to the exterior of the cell
Staging of Tumor
-Stage I: growth is restricted to primary site -Stage IV: invaded extensively and shows wide metastatic spread
Oncology
-Study of tumors
Benign
-Suffix 'oma' is used with this tissue type.
Pediatric Neoplasms
-Suffix is 'blastoma- -Resemble primitive embryonic tissues. -Retinoblastoma Neuroblastoma Hepatoblastoma Medulloblastoma
Melanoma
-Superficial spreading melanoma is the leading cause of death from cancer in young adults. -Nodular melanoma can appear anywhere on the body and develop in an area that did not have a previous lesion.
what are s/s of liver failure?
-Sweet musty breath -Metabolic by-products of intestinal bacteria - Anemia, thrombocytopenia, coagulation defects, leukopenia -Fluid retention, hypokalemia, sexual dysfunction - Jaundice, red palms, spider nevi -Azotemia, increased plasma creatinine, oliguria - Asterixis, confusion, coma, convulsions -Lactulose
TNM Classification
-T indicates the size of the tumor. N stands for the involvement of regional lymph nodes and M refers to the presence of metastasis.
Wet Gangrene
-The affected area is cold, swollen, and pulseless. The skin is moist, black, and under tension. Blebs form on the surface. -Liquefaction from degrative bacterial enzymes occurs, and a foul odor is caused by bacterial action -The spread of tissue is rapid. -Putrefaction: anaerobic bacteria proliferate in the oxygen necrotic tissue.
Dry Gangrene
-The affected tissue becomes dry and shrinks, the skin wrinkles, and its color changes to dark brown or black. The spread of dry gangrene is slow. -A line of inflammatory reaction between the dead tissue and the tissue appears.
Genetic Involvement in Neoplastic Tissue
-The autonomous growth of neoplastic tissue is based in large part on defects in the genes that regulate the fine balance of cell production versus cell loss by apoptosis -3 Genes that regulte cells: 1) Proto-oncogenes 2) Tumor suppressor genes 3) DNA repair genes
Carcinogenesis
-The cell's transformation from normal to cancerous -Genetic alteration is the basis for the development of cancer. -Initiation: Initial mutation occurs -Promotion: Mutated cells are stimulated to divide. -Progression: Tumor cells compete with one another and develop more mutations which make them more aggressive. -TheseC factors may act together or in sequence to cause cancer -10 or more years often pass between exposure to external factors and detectable cancer
Intravasation
-The entrance of foreign matter into a vessel of the body.
Mitosis
-The process where a single cell divides resulting in generally 2 identical cells, each containing the same number of chromosomes.
Margination
-The rolling of WBCs along the endothelium.
Necrosis
-The structural changes that occur following cell death -Cell death in living tissue -Trigger WBCs to invade area and to digest the debris (phagocytosis). Result --> local inflammation and cell death
Cancer Diagnosis
-Tissue biopsy -Can also be from blood smears and cytology
Tumor Marker Test
-Tumor markers are chemicals made by tumor cells that can be detect in the blood. However, these are controversial because normal cells in the body also produce tumor markers which can give a false indication of noncancerous
Carcinomas
-Tumors of the skin and epithelial lining of the GI and respiratory tract and glandular tissue -Carcinomas arise from the Ectoderm and Endoderm. -Further designated by the type of epithelial tissue.
Acute Inflammation
-Usually a sudden onset (min/hours) -Short duration (hours-days) -Marked by the classical signs of heat, redness, swelling, pain, and loss of function -Neutrophils (Polymorphonuclear cells): 1st to arrive and most numerous in blood. Libr for up to 48 hrs and then die by apoptosis. -Monocytes (mononuclear cells): Called macrophages in tissues because of increase size and phagocytic ability. Later to arrive. Last longer and they clean up debris and dead neutrophils.
Mitochondria
-Variable numbers of mitochondria exist in cells depending on cell's requirements.
Phospholipid Bilayer
-Water-soluble "heads" form surfaces -Wter-insoluble "tails" form interior -Selectively permeable -Important because the cell depends on transmembrane movement for the uptake of nutrient and the out passage of cell products and waste.
Genetic Factors in Cancer Incidence
-Women from population groups with a higher frequencey of mutations in the creast caner susceptibility genes -Women of Ashkenazi Jewish descent, have an increased risk of breaks and ovarian cancer
Sickle-cell anemia
-abnormal shaped RBC's and abnormal hemoglobin synthesis -autosomal recessive disorders seen in persons from the equatorial countries -etiology: abnormal S (HB S ) hemoglobin which reacts to decreased oxygenation and dehydration; under normal conditions, no problem exists -conditions causing RBC sickling: hypoxia (infections), high altitudes, exercising, flying in unpressurized airplanes -when oxygen concentration decrease-the RBC's become "sickled", non-flexible, and stiff resulting in: 1. occluded blood vessels, 2. increased viscosity of blood, 3. further sickling of cells leading to increased deoxygenation of tissue and infarctions and pain, 4. most cells regain the normal shape when re-oxygenated and rehydrated
Macrophages
-agranulocyte -powerful phagocytes-monocyte is immature form -normal level: 2-8%
Lymphocyte
-agranulocyte -primary cells of immature response -normal level: 20-40%
Normocytic-Normochromic Anemias
-aplastic -post-hemorrhagic -hemolytic -anemia associated with chronic inflammation -sickle-cell anemai
Chronic Leukemias
-cells are well differentiated and can be identified -do not function as normal cells
what causes hepatocellualr cancer?
-chronic hepatitis B and C -chronic alcoholism -nonalcoholic fatty liver disease long-term exposure to environmental agents such as a aflatoxin
Respiratory system
-consists of passages that filter incoming air and transport it into the body, into the lungs, and to the many microscopic air sacs where gases are exchanged Ciliated columnar epithelial cells line the tracheobronchial tree and help move mucus and particles trapped in the mucus to the oropharynx to be expectorated • Cigarette smoking cause paralysis of the cilia breathing alveoli
Diagnosis, Treatment, and Prognosis for Leukemias
-diagnosis: bone marrow biopsy, blood tests -treatment: chemotherapy, anti-microbial therapy, blood transfusions, bone marrow transplants, supportive measures -prognosis: longer remission periods and increased survival rates with combined therapy (bone marrow transplants, chemotherapy, anti-microbial agents); ALL-5 year survival rate is 80%; 5 year survival rate for all leukemias is 38%; chronic leukemia have a longer life expectancy
DIC - Diagnosis, Clinical Manifestations, Treatment
-diagnosis: increased D-dimer-lysis of fibrin clot; measures the rate of fibrin -Clinical manifestations: 1. Microvascular (capillaries) clotting: CNS: decreased level of consciousness, Skin: ischemia leading to gangrene, Kidney: oliguria, renal failure, Lungs: SOB, pulmonary emboli, GI: acute ulcerations, necrosis 2. Hemorrhage: CNS: intracranial bleeding, Skin: petechiae, ecchymosis, Mucous membranes: gingival bleeding, Kidney: hematuria, GI: bleeding -Treatment: identify and treat cause; clotting: stop clotting, maybe administer anticoagulant; hemorrhage: replace platelets, red blood cells, and FFP; maintain organ viability **high mortality rate depending on the cause
Acute leukemias
-disorder of accumulation and proliferation of immature WBC's which do not function as normal cells; highly undifferentiated--blast cells -80% from B line cells -15-20% of all acute leukemias form T cells lines -crowds bone marrow--this causes a reduction in other cellular components of the blood (pancytopenia)
Pernicious anemia
-etiology: decreased gastric secretion of Intrinsic Factor (it is absent), leads to malabsorption of Vitamin B-12; then a decreased Vitamin B-12 leads to decreased erythrocyte production; the RBC's are abnormal and large, they die and this causes anemia; usually seen in late adult life, but also there is a congenital form (develops before 2 years of age) -treatment: Vitamin B-12 replacement, never cured, must have continuous treatment for life; may be given prophylactically in gastrectomy and ileal resection patients
Leukemia etiologies
-exact cause unknown -tends to recur in families (2-4 times greater chance if sibling has leukemia) -increased incidence in association with other genetic abnormalities such as Down's, Fanconi Syndrome -other risk factors include: acquired disorders such as myelofibrosis, Hodgkin's, multiple myeloma; CLL and CML may cause acute leukemias -large doses of ionizing radiation may cause myelogenous leukemia -drugs which cause bone marrow depression may predispose person to leukemia -high doses of chemotherapy for Hodgkin's, myeloma and ovarian cancer may cause acute myelogenous leukemia -viruses cause leukemia in animals, but not proven in humans yet
Thrombocytes
-function: blood coagulation and control of bleeding -lifespan: 5-9 days -normal level: 150,000-400,000/mm3
Hemophilia
-genetic disease caused by deficiency of blood clotting factors essential for forming a clot -factor deficiency: 1. Factor VIII-Hemophilia A, classic hemophilia, most common type 2. Factor IX-Hemophilia B, Christmas disease, X-linked recessive, less severe than Hemophilia A 3. Factor XI-Hemophilia C, autosomal recessive, least severe type -manifestations: symptoms infrequent in first years of life, start seeing at age 3-4, may notice excessive bruising and bleeding when starting to walk, running etc., hemoarthritis (hallmark of hemophilia) into elbows, knees, ankles causes pain and limits movement and predisposes to degenerative changes in joint, recurrent bleeding after injury or minor trauma -treatment: factor replacement (due to clotting of factor VIII gene and purification of the recombinant factor VIII, less of the plasma derived factors are being used); accident prevention, counseling, home care
Basophils
-granulocyte -anti-parasitic -normal level: 0.5-1.0%
Eosinophils
-granulocyte -controls inflammatory/allergic responses -normal level: 1-4%
Neutrophils
-granulocyte -function: first 2 days of inflammation -normal level=55-70% -segments are mature -bands are immature
what is major risk factors for being a hep. carrier?
-having HBV-infected mothers, may be as high as 90% to 95%,
Hyperchomic
-high concentration of hemoglobin
Anemia associated with chronic inflammation
-increased demand for erythrocytes -sometimes seen in HIV disease, and inflammatory diseases such as Lupus and Rheumatic fever -in chronic renal failure, the kidneys do not produce erythropoietin, so this can lead to chronic anemia
Aplastic anemia
-insufficient number of RBC's resulting from abnormal stem cell production, infiltrative disorders of bone marrow, or altered stem cell environment -etiologies: drugs-chloramphenical, benzene; toxins, radiation, immunologic injury to bone marrow
what is the cause of cholestasis?
-intrinsic liver disease affecting the intrahepatic canaliculi and bile ducts (intrahepatic cholestasis) -obstruction of the large bile ducts: strictures, gallstones, or neoplasms, a condition known as extrahepatic cholestasis - Genetic disorders involving the transport of bile into the canaliculi
Microcytic-hypochromic anemia
-iron-deficiency anemia is classified as microcytic-hypochromic anemia
Iron-deficiency anemia
-lack of iron for hemoglobin production; most common type of anemia -etiology: continual blood loss (menorrhagia, ulcers, ulcerative colitis, GI bleeds from medications); increased need-pregnancy; insufficient dietary intake-most common anemia 6 months to 2 years of age because increased iron needed for growth and cow's milk does not contain enough iron -pathophys: Stage 1. body's store of RBC's are depleted, Stage 2. insufficient iron, altered RBC's are produced, Stage 3. hypochromic RBC's put into circulation -manifestations: develop slowly-usually in Stage 3; common manifestation of anemia seen; children may show a pica, have decreased physical growth and/or developmental delays -treatment: iron replacement, treat of eliminate the cause
Macrocytic
-large RBC
Macrocytic-normochromic anemia
-large abnormal RBC's -normal hemoglobin -pernicious anemia
Leukocytes
-life span: 7-21 days -function: defend body against organisms and remove debris -normal level: 4,500-11,000/mm3 -granulocytes: phagocytes: neutrophils, basophils, eosinophils -agranulocytes: macrophages, lymphocytes
Post hemorrhagic anemia
-loss of RBC's -severe shock, lactic acidosis -death -if blood loss of 40-50%
Hypochromic
-low concentration of hemoglobin
Leukemia
-malignant disease of the blood and blood-forming organs causing an accumulation of dysfunctional cells and a loss of cell division regulation -classification: classified according to the cell involved and stage in the development in which maturation was stopped 1. Acute: cell immature (blast); onset is rapid and abrupt, survival time may be short; Acute lymphoblastic (ALL): 50% of childrens leukemia; Acute myelogenous (AML): common adult type 2. Chronic: cell mature but doesn't function normally; onset if gradual, longer survival; Chronic lymphocytic (CLL) common adult type
Lymphoma
-malignant disease of the lymphoid tissue (thymus, bone marrow, lymph nodes, spleen), 90% disease in lymph nodes -etiology: unknown-chromosome abnormality, virus, immunosuppression -incidence: Hodgkin's peaks 20-30 years of age; Non-Hodgkin's 50 years or older -pathophys: normal lymph node or tissue lymph structure is destroyed by excessive proliferation of lymphocytes -diagnosis: biopsy of lymph tissue -Hodgkin's: Reed-sternberg cells in lymph node -Non-Hodgkin's: bone marrow involvement, occurs more frequently than Hodgkin's -clinical manifestations: enlarged painless lymph nodes, night sweats, fever, weight loss -treatment: chemotherapy; radiation-may do combination chemo and radiation; stem cell transplants-bone marrow, peripheral blood, cord blood -cure rates: Hodgkin's: complete remission if treated in early stages (I and II); Non-Hodgkin's: varies, can be slow developing or aggressive and rapidly fatal
Multiple Myeloma
-malignant disorder characterized by proliferation or abnormal plasma (B-lymphocytes) cells in the bone marrow; peaks in the sixth decade of life -etiologies: unknown-genetics, viruses, bacteria, chemicals -pathophys: excess number of abnormal plasma cells (B lymphocytes) infiltrate the bone marrow, develop into tumors, destroy the bone, and invade lymph nodes, liver, spleen, and kidneys -abnormal plamsa cell produce: myeloma (m) protein -clinical manifestations: onset slow and insidious; frequent infections, anemia/bleeding; bone pain and pathological fractures; renal insufficiency/failure -diagnosis: bone marrow biopsy, bence jones protein in urine -treatment: chemotherapy/radiation, stem cell transplant, prevent dehydration/renal failure
Vasoocclusive crisis
-may occur if extensive sickling -begins in micro circulation-log jam occurs causing thrombosis and tissue infarction if not corrected--results in severe pain -manifestations of crisis: painful swelling of joints, hands, feet; abdominal pain; enlarged liver and spleen due to RBC breakdown -lasts 4-6 days -improves with rehydration and re-oxygenation
Normocytic
-normal RBC size
Normochromic
-normal hemoglobin
What are the five ways that cell injury can occur?
-physical agents -radiation -chemical injury -biologic agents -nutritional imbalances
Thrombocytopenia
-platelet count less than 100,000 -etiology: 1. autoimmune disorder-immune system destroys platelets 2. complication of heparin therapy-heparin induced thrombocytopenia (HIT) 3. Blood loss -clinical manifestations: decreased platelets; hemorrhage; epistaxis (nosebleed), petechiae, hematuria, bleeding gums, ecchymosis (bruising) -treatment: identify and treat cause; platelet transfusions
Hemolytic anemia
-premature destruction of RBC's can be acquired by infections, drugs, toxins, systemic diseases, liver or kidney diseases, can be hereditary -hemolytic disease of newborn: ABO incompatibility: mother type O and baby either A, B, or AB; Rh incompatibility: mother Rh negative and infant Rh positive
Amenia
-reduced circulating erythrocytes and/or decreased hemoglobin -etiologies: altered production, blood loss, increased destruction, combination of any of these -clinical manifestations: related to hypoxia: weakness, fatigue, increased respiratory rate, dizziness, fainting, lethargy, decreased hemoglobin, paleness of ear lobes, conjunctive, and palms; if allowed to continue, may have cardiac, renal, and other systemic results; classified according to causes or changes in erythrocytes
Manifestations for all Leukemias
-related to bone depression: anemia (decreased RBC), bleeding (decreased platelets), fever (decreased WBC) -other signs and symptoms: anorexia, weight loss, muscle wasting, abdominal pain and tenderness -neurological related to cerebral bleeding or neurological infiltrates: headache, vomiting, papilledema, blurred vision
Disseminated Intravenous Coagulation (DIC) - Etiologies and Patho
-sequence of events resulting from abnormal, diffuse activation of 1. coagulation (clot formation) 2. Firbinolysis (clot digestion) -etiologies: burns, trauma, shock, cancers (terminal), emboli, septicemia (sepsis)-overwhelming systemic blood infection (most common cause)--bacteria breaks down which releases endotoxins, and these act as a procoagulant -pathophys: procoagulants (substance stimulates clotting)-->overstimulation of coagulation system -->excess fibrin formation-->disseminated (systemic) intravascular clotting-->increased consumption of platelets and clotting factors-->decreased platelets-->hemorrhage OR disseminated intravascular clotting-->fibrin deposits in microcirculation-->ischemia and infarction-->clotting
Microcytic
-small RBC
Cells
-smallest living subunits of a multicellular organism .
what is Hepatic encephalopathy? s/s?
-totality of CNS manifestations of liver failure -accumulation of neurotoxins, which appear in the blood because the liver has lost its detoxifying capacity s/s -flapping tremor called asterixis -confusion -coma -convulsions
Sickle-cell anemia Clinical Manifestations, Treatment, and Prognosis
-usually do not appear until 6 months (because of decrease of Hg F at that time) -pallor, fatigue, jaundice, and irritability -treatment: supportive care, treat crisis with hydration, pain meds as needed in crisis, counseling, preventing crisis -prognosis: if the person is a carrier of the trait, then no symptoms, but can pass the trait on to offspring; if the person has the disease, life expectancy is completely unpredictable (may die early); infection is usually the cause of death
wheezing
-whistling sound; results from a narrowing of the airways and typically indicates some difficulty breathing.
five stages of hemostasis
1) Vessel Spasm 2) Platelet-plug formation 3) Coagulation (non-soluble fibrin clot formation) 4) clot retreival 5) clot disolution
State at least four ways that benign and malignant neoplasms differ in regards to their characteristics.
1. Benign - Well differentiated tumors that resemble the tissues of orgin but have lost the ability to control cell proliferation. 2. Malignant- are less well differentiated tumors that have lost the ability to control both cell proliferation and differentiation 3. Benign - They grow by expansion and are enclosed in a fibrous capsule, and do not cause death unless their location is such that it interrupts vital body functions 4. Malignant - Not well defined capsule or margin, They can break loose and invade surrounding tissue (crablike) and cause a release of toxins and enzymes. Solid tumors(confined to a specific organ/tissue) or hematologic cancers(in blood/lymph = disseminated from beginning)
Progression of cardiac ischemia
1. Caused by the partial or complete blockage of blood flow to the coronary arteries 2. The heart tissue fails to get necessary oxygen and nutrients 3. The tissue begins to starve and eventually dies
Congestive heart failure resulting from an AMI
1. Diseased heart valves or chronic hypertension cause an increased heart rate and enlargement of the left ventricle 2. Over times, these adaptations fail to make up for decreased heart function 3. The heart fails to pump effectively, causing lungs become congested with fluid (pulmonary edema) - Known as "congestive heart failure"
pathogen -- COPD
1. Inflammatory swelling of mucosa • Narrows bronchioles; increased resistance to expiration; causing air to be trapped in lung 2. Leukocytes accumulate in bronchioles and alveoli, releasing proteolytic enzymes that destroy elastic fibers • Loss of elastic recoil of alveoli and high residual volume of CO2 • Normally, that expiration is a passive process • Loss of this elasticity leads to 'force expiration' Bronchi and bronchioles have lost normal structural support and tend to collapse 3. Coughing and increased intrabronchial pressure convert alveoli into large, cystic air spaces, over-distended lung cannot expel air 4. Retention of secretions predisposes to pulmonary infection (pneumonia) 5. Bronchoconstriction form hyperactive airways to irritants
Coagulation cascade
1. Intrinsic pathway (blood vessel injury) 2. Extrinsic pathway (tissue injury) -->aggregation of platelets at site of injury -->prothrombin-->thrombin -->fibrinogen-->fibrin (Factor X stabilizes clot) -->fibrin clot -->breakdown of clots (FDPs)
Hemostasis normally occurs by...
1. Minor injuries: vasoconstriction (vasospasm) and formation of a platelet plug 2. Major injuries: clot formation (coagulation cascade)
Types of dysrhythmia
1. Premature ventricular contractions 2. Tachycardia 3. Bradycardia 4. Ventricular tachycardia 5. Ventricular fibrillation
3 steps of Phagocytosis
1. Recognition and adherence 2. Engulfment 3. Intracellular Killing
ascending infection from bladder (Upper UTI)
(ascending pyelonephritis) most common higher incidence in young women Older men with prostatitis obstructive uropathy --> predisposes to infec E coli most common
carried to kidneys from blood (UTI)
(hematogenous pyelonephritis) Less common Staphyloccocus aureaus is most common
Histamine from mast cells
**Cell Derived Mediators** -Mast cells are scattered throughout connective tissue Histamine Diffuses to injured site and causes vasodilation and increased permeability of adjacent small venules. -Venules leak plasma proteins (albumin) -Mast cells rapidly become depleted with histamine and histamine is diluted and inactivated by influx of water into the tissue
Prostaglandin
**Cell Derived Mediators** -Synthesis is initiated by injury to production is slower than histamine -All leukocytes, endothelial, and mast cells produce these -Produces vasodilation -Enhances the effect of other mediators -Mediates fever and pain indirectly -Controlling PGE is a way to control inflammation, fever, and pain.
Cytokines and Chemokines
**Cell derived mediators** -Serve to up and down regulate inflammation -Produced by many cell types
Kinin System
**Chemical Mediator in Plasma** -Causes increased vascular permeability and is a major factor in sustaining the flow of fluid and chemicals to site -Also directly acts on nerve endings causing pain -Is deactivated at some point via kininase and vascular response ceases
Coagulation system
**Chemical Mediator in Plasma** -Forms clot (fibrin)
Complement System
**Chemical Mediator in Plasma** -Punches holes in microorganism membranes causing lysis
Bacterial Factors Influencing UTI
*Adherence to uroepithelium* (ex. E. coli with specific fimbriae) *Capsular antigens* resist phagocytic mechanisms *Hemolysins* cause kidney damage *Urease* associated with ability to cause pyelonephritis and stones
Sites of Urinary Tract Infection
*Bladder* - cystitis (a "lower" UTI) *Urethra* - urethritis (a "lower" UTI) *Kidney* - pyelonephritis (an "upper" UTI) *In males, may get infection of prostate* - prostatitis
Signs and Symptoms of Upper UTI's
*Signs and Symptoms*: -As for lower UTIs -Loin pain and tenderness -Fever -Often renal abscesses -Recurrent episodes may result in loss of function of renal tissue (→ hypertension etc) -Symptoms in children may be non-specific (failure to thrive in infants, unexplained fever, febrile convulsions)
etiology pneumothorax
1. Trauma which lacerates the parietal pleural from the outside and air enters into the pleural space Puncture of chest wall leads to entrance of air This occurs because atmospheric pressure is higher than intrapleural pressure Stab wound or penetrating injury to chest wall: atmospheric air enters into pleural space Lung collapses because the subatmospheric pressure is lost (low pressure is necessary for lungs to maintain expanded position) 2. Rupture of the visceral pleura and air exits from the lungs into the pleural space Puncture of chest wall leads to entrance of air This occurs because atmospheric pressure is higher than intrapleural pressure Stab wound or penetrating injury to chest wall: atmospheric air enters into pleural space Lung collapses because the subatmospheric pressure is lost (low pressure is necessary for lungs to maintain expanded position) Escape of air into pleural space due to lung injury or disease From emphysema, when large bullae form creates increase risk of rupture air enters into the pleural space and lung collapse follows Interstitial lung disease or tumor invading the visceral pleura to produce a pneumothorax 3. spontaneous -- no apparent cause
State the importance of angiogenesis in cancer growth and metastasis
1. Tumors release chemicals like growth factor and interleukins to promote angiogenesis (creation of new blood vessel) 2. These chemicals reroute blood vessels to the tumour supplying it with the tools to grow and spread.
Name four negative characteristics of neoplasms
1. grow without sign that new tissue is needed 2. ignore signals to stop dividing 3. do not mature normally to do the "job" they were suppose to do. 4. do not die (apoptosis) to keep #'s of cells constant.
4 phases of kidney injury
1. initial= last hours to days and is time from insult to clinical signs 2. oliguria = associated with decrease GFR, retention of fluid, urea, creatinine, electrolytes Nephrons are filled with WBC and inflammation occurs 3. diuretic = kidneys are beginning to recover, urine output is high 4. recovery = time needed for final repair of renal damage; nephrons are compensating by becoming super nephrons- they hypertrophy and demonstrate hyperfiltration Urine becomes concentrated
Patient Evaluation
1.) History of current illness ◦Severity, time of onset, and character of patients symptoms 2.) Medical history ◦Details of general health and previous illnesses that may shed light on current problems 3.) Family history ◦Health of patients parents and family members; diseases that run in families 4.) Social history ◦Patients occupation, habits, alcohol and tobacco consumption, general health, current problemsVariation between cultures and perception of cause of the disease or if it is a disease 5.) Review of symptoms ◦Symptoms other than disclosed in history of present illness, suggesting other parts of the body affected by disease
Patient has abdominal pain: ________ Observer notes exaggerated response during abdominal palpation in upper right quadrant _________ X -ray reveals gallstones _______
1.) Symptom 2.) Sign 3.)Finding
State four differences between benign and malignant tumors
1.Characteristics of tumor cells 2. rate of growth 3. local invasion 4. ability to metastasize
Hypertensive emergencies occur when the systolic pressure is greater than _______________________
180 mm Hg
After about _________________ after blood flow is cut off, as many as half of the heart muscle cells in the area may be dead.
2 hours
About ___________________ after blood flow is cut off, some heart muscles begin to die.
30 minutes
Core Temperature
36-37.5 Reflects the balance between heat gain and heat loss
After about _________________ after blood flow is cut off, more than 90% of the heart muscle cells will be dead.
4 to 6 hours
what is the fish year survival rate of pancreatic cancer?
4-6%
what is liver failure?
80-90% loss of hepatic function capacity
1. A major complication of persistent gastroesophageal reflux is: A) strictures. B) heartburn. C) chest pain. D) hoarseness.
A
12. A 60-year-old male patient has presented to his primary care provider to follow up with his ongoing treatment for peptic ulcer disease. What is the most likely goal of this patient's pharmacologic treatment? A) Inhibiting gastric acid production B) Promoting hypertrophy of the gastric mucosa C) Increasing the rate of gastric emptying D) Increasing muscle tone of the cardiac sphincter
A
18. Which of the following meals is most likely to exacerbate an individual's celiac disease? A) Spaghetti with meatballs and garlic bread B) Stir-fried chicken and vegetables with rice C) Oatmeal with milk, brown sugar, and walnuts D) Barbecued steak and a baked potato with sour cream
A
2. The mechanisms of liver damage in viral hepatitis include: A) direct cellular injury. B) fatty liver changes. C) disrupted bile flow. D) bile duct inflammation.
A
3. Alcoholic liver disease manifests in three stages. The intermediate stage, alcoholic hepatitis, is characterized by liver cell: A) necrosis. B) nodules. C) atrophy. D) hypertrophy.
A
6. Crohn's type of inflammatory bowel disease is characterized by: A) granulomatous lesions. B) ulcerative erosions. C) fibrotic smooth muscle. D) necrotic crypt abscesses.
A
Thromboembolism
A blood clot that floats through blood vessels 1. The blood clot floats until it reaches an area too narrow for it to pass 2. The blood clot stops and block the blood flow at that point 3. Tissues beyond the blockage will become hypoxic - If the blood flow is not restored in a short time, the tissues will begin to die
TB (lower)
A chronic infectious disease characterized by necrosis of vital lung tissue Common in the respiratory system, but can affect other body systems as well Causative agent: acid-fast bacteria, Mycobacterium tuberculosis; aerobic bacterium The bacteria are most commonly transmitted in contaminated sputum expelled in the coughs of infected persons tuberculosis can also be caused by contaminated milk from infected cattle. Organism is inhaled in airborne droplets
Basophils
A circulating leukocyte that produces histamine. Account for 0%-1% of WBCs in the blood.
DNA
A complex molecule containing the genetic information that makes up the chromosomes.
Drug induced thrombocytopenia
A condition in which antibodies are produced against a medicine and the resulting immune complex binds to platelets, causing an immune response against the platelets is:
pacemaker
A device that delivers electrical impulses to the heart to regulate the heartbeat
Chronic Disease
A disease may begin insidiously and be long-lived Months to years Some chronic diseases have abrupt onset stealthily; or gradual and subtle development e.g., arthritis, hypertension
Polycythemia
A disorder characterized by an abnormal increase in the number of red blood cells in the blood
Congestive heart failure often occurs _______________ following AMI
A few days
adult resp. distress syndrome
A form of pulmonary edema that can quickly lead acute respiratory failure
Granulocytes
A group of leukocytes containing granules in their cytoplasm; neutrophils, eosinophils, basophils.
Acute coronary syndrome (ACS)
A group of symptoms caused by myocardial ischemia - Includes temporary myocardial ischemia and/or resulting angina pectoris or AMI
peptic ulcer
A group of ulcerative disorders that occur in areas of the upper gastrointestinal tract (esophagus, stomach, and duodenum) that are exposed to acid-pepsin secretions Most common forms are duodenal and gastric ulcers (approx. 10% of the population have or will develop one) Spontaneous remissions and exacerbations are common Can affect one or all layers of the g.i. tract Mucosa only or penetrate all the way to the outer wall
What is paraneoplastic syndrome?
A paraneoplastic syndrome is a disease or symptom that is the consequence of the presence of cancer in the body, but is not due to the cancer
ventricular tachycardia
A rapid heart rhythm in which the electrical impulse begins in the ventricle (instead of the atrium), which may result in inadequate blood flow and eventually deteriorate into cardiac arrest. Some cases of ventricular fibrillation begin as a rapid heartbeat called ventricular tachycardia (VT). This fast, regular beating of the heart is caused by abnormal electrical impulses that start in the ventricles.
TB 2ndary stage
A secondary infection occurs when the person is infected again or when the bacteria escape the walled-off lesions in the lungs (reactivation is most common) Persons in the secondary stage of the disease also lose weight and become cachectic; this is the basis for the classic name for tuberculosis, consumption. During the secondary infection, leukocytes now recognize the bacteria and mount an attack that leads to greater necrosis and destruction of lung tissue. Necrotic tissue, blood, and bacteria may be coughed up. The bacteria may spread to other organs like the brain, kidney, and bones.
Neutrophils
A type of white blood cell that engulfs invading microbes and contributes to the nonspecific defenses of the body against disease.
Monocytes
A type of white blood cell that transforms into macrophages, extends pseudopods, and engulfs huge numbers of microbes over a long period of time An agranular leukocyte that is able to migrate into tissues and transform into a macrophage.
Ventricular tachycardia
A very rapid heart rhythm - 150 to 200 beats/min
Which kind of electricity is the worst and why?
AC-alternating currents are the worst because they cause violent muscle contractions, preventing the person from releasing the electrical source and sometimes resulting in fractures and dislocation
disease of older adults but also seen in children and young adults.
AML: Acute myelocytic leukemia (AML)
clinical manifestations peptic ulcer
Abdominal pain ◦ Burning/cramplike that is rythmic and occurs when stomach is empty (usu. 1 - 2 a.m.) ◦ Evident in the epigastrium near the xiphoid and may radiate into the back or right shoulder ◦ Pain tends to recur at weekly or monthly intervals ◦ It can occur daily for a period of weeks then dissapears until the next recurrence ◦ Relieved by food or antacids Life threatening complications can occur without warning
Absence of B12 and Folic Acid
Abnormal red cell maturation or megaloblastic erythropoiesis with formation of large cells called megaloblasts Mature red cells formed are larger than normal or macrocytes; corresponding anemia is called macrocytic anemia The MCHC is normal or increased
Ectopic foci
Abnormally functioning tissue
Leukopenia
Abnormally low white blood cell count
What are some manifestations of paraneoplastic syndrome in the dematological system?
Acanthosis nigricans
The pain of AMI signals the _______________________
Actual death of cells in the area of the heart where blood flow is obstructed - Once dead, the cells cannot be revived. - Dead cells turn to scar tissue and become a burden to the beating heart
Use the predominant white blood cell type and classification of acute or chronic to describe the four general types of leukemia.
Acute lymphocytic leukemia (ALL) - most common among children and adolescents Chronic lymphocytic leukemia (CLL): 1/3 of all Leukemias and is mainly a disorder of older persons, Malignancy of B lymphocytes. There are 2 types. 2 Types based on the aggressiveness of the disease and immunoglobulin variable (V) gene mutation Acute myelocytic leukemia (AML): Chronic myelocytic leukemia (CML): Excessive proliferation of marrow granulocytes, erythroid precursors, and megakaryocytes and Harbor the Philadelphia Chromosome abnormalit
This Leukemias most common form among children
Acute lymphocytic leukemia: ALL
Distinguish between acute renal failure and chronic kidney disease in terms of causes, treatment, and outcome
Acute renal failure can show up in a matter of hours or days and can be caused by a decrease in blood flow, ischemic, toxic, or obstructive tubular injury and obstruction of urinary tract flow. They can be categorized as prerenal, intrarenal, and postrenal. Usually AKI can be reversible if the right steps are taken, including diet changes. The best way to treat it is to find and correct the cause. Hemodialysis may by indicated if the water and electrolyte balance cannot be kept under control. Chronic kidney disease is irreversible and persists for months. It results in the loss of nephrons and a decline in function. It is determined by a decrease in the GFR. It results from hypertension, glomerulonephritis, systemic lupus erythematosus, and polycystic kidney disease. The signs and symptoms occur gradually and do not become evident until the disease is too far advanced. Treatment is kidney transplant or hemodialysis, as chronic renal failure is irreversible.
clinical manifestations acute tubular necrosis
Acute renal failure: oliguria, anuria Constriction of arterioles reduces blood flow, which ultimately reduces urine formation (decr. GFR) Physical blockage of tubules by necrotic debris - Decreased GFR leads to azotemia (high BUN), increased serum creatinine, and fluid retention - Decrease urine output (oliguria)
Cellular response to stress or injury
Adaptation: reversible Cellular injury: Reversible up to a point Cellular death: No hope!
What is an example of a non-physiological cause of Hypertrophy?
Adaptive hypertrophy - thickening of urinary bladder from obstructions, Myocardial hypertrophy from heart disease or hypertension compensatory hypertrophy - enlargement of a remaining organ after a portion has been removed.
treatment for neonate " "
Adrenal corticosteroids to mother before delivery to stimulate surfactant production; given 24 hours before delivery Oxygen + surfactant Instilled by inserting a endotracheal tube Several treatments daily
cystitis
Affects only the bladder More common in women than men; shorter female urethra, and, in young sexually active women, sexual intercourse promotes transfer of bacteria from urethra to bladder Common in older men, because enlarged prostate interferes with complete bladder emptying
what are risk factors of pancreatic cancer?
Age > 50 years old Cigarette Smoking Diabetes and Chronic pancreatitis
List the three types of white blood cells and briefly describe their function.
Agranulocytes are divided into 2 different parts: lymphocytes and monocytes/macrophages. Lymphocytes: make up 30% of leukocytes. They originate in bone marrow and migrate through peripheral lymphoid organs where they recognize antigens and participate in immune responses. Monocytes/macrophages: make up 3-8% of leukocytes. They travel from bone marrow to body tissue where they differentiate into various phagocytes.
Pneumothorax
Air entrance into the pleural cavity The air removes the normal pressure gradient that provides for the expansion of the lungs against the thoracic wall Leads to collapse of lungs Intrapleural pressure: pressure within pleural cavity Normally lesser than intrapulmonary pressure Referred as "negative pressure" or subatmospheric because it is lesser than atmospheric pressure The airtight intrapleural space between the lungs and the chest wall has a pressure slightly less than the pressure within the lungs ---This difference in pressure acts as a vacuum and prevents lung collapse Release of vacuum in pleural cavity leads to lung collapse
State the major determinant of airway resistance
Airway radius
What are the lab test for liver enzymes?
Alanine transaminase (ALT) Aspartate transaminase (AST) Gamma-glutamyl transferase (GGT) Alkaline Phosphatase (ALP) Bilirubin
Mast cells
Allergens
Eosinophils
Allergens, parasites, neoplasia
Basophils
Allergens, stress
iron deficiency adults
Almost always due to GI blood loss; could also be component of malabsorption or diet Iron stores in liver (ferritin) will be used before dropping Hb concentrations Chronic deficiency needed to become anemic
What drgus is use for Hyperuricemia?
Alopurinol
Describe the etiology, pathophysiology, clinical manifestations, and the specific role metabolic syndrome plays in the development of Type II diabetes mellitus: role of adipose tissue in the development of type II diabetes mellitus.
Although many details of the relationship between adipose tissue, insulin resistance, and increased glucose production in obese people with type 2 diabetes remain to be elucidated, several pathways have been proposed. Primary among these is the role of an increased concentration of free fatty acids (FFAs). Visceral obesity is accompanied by an increase in postprandial FFA concentrations and subsequent triglyceride storage, including in sites that do not normally store fat such as the liver, skeletal muscle, heart, and pancreatic beta cells. This has several consequences. First, excessive and chronic elevation of FFAs can directly cause pancreatic beta cell dysfunction (lipotoxicity). Second, at the level of the peripheral tissues, FFAs inhibit glucose uptake and glycogen storage. Third, the accumulation of FFAs and triglycerides reduces hepatic insulin sensitivity, leading to increased hepatic glucose production and hyperglycemia, especially in the fasting state. In the liver, the uptake of FFAs from the portal blood can lead to hepatic triglyceride accumulation and nonalcoholic fatty liver disease. In addition to the metabolic effects of visceral obesity, adipocytes are the source of a number of important factors (e.g., adiponectin, leptin, FFAs) involved in a wide range of other processes, including glucose and lipid metabolism, inflammation, and thrombosis. In obesity and type 2 diabetes, there is a reduction in the production of some factors that are normally synthesized by adipocytes (i.e., adiponectin), whereas there is an accelerated release of other factors such as angiotensinogen, plasminogen activator inhibitor-1, leptin, and proinflammatory cytokines (e.g., tumor necrosis factor-α). Adiponectin, which is secreted by adipocytes and circulates in the blood, is the only known adipocyte-secreted factor that increases tissue sensitivity to insulin. It has been shown that decreased levels of adiponectin coincide with insulin resistance in persons with obesity and type 2 diabetes. In skeletal muscle, adiponectin has been shown to decrease tissue triglyceride content by increasing the use of fatty acids as a fuel source. Adiponectin also appears to have antidiabetes, anti-inflammatory, and antiatherogenic effects.
Dysrhythmia
An abnormality of the heart rhythm
Arrhythmia
An absence of heart rhythm
If a thromboembolism causes a blockage in a coronary artery, it will cause _____________________
An acute myocardial infarction (AMI) - Classic heart attack - May occur at the site of other vital organs (ex: brain)
What are some typical manifestations of cancer?
Anorexia and cachexia (reduced food intake and wasting of body fats) -this causes a persistant inflammatory response. Fatigue and sleep disorders signs at the specific site Paraneoplastic syndrome - symptons at sites where cancer has not affected.
Immune Hemolytic Anemia
Antibodies "attack" normal rbcs resulting in a rapid clearance of them from the blood
What natural and synthetic molecule inhibits free radicals?
Antioxidents
State two conditions that contribute to increased clotting activity.
Antiphospholipid Syndrome Hyperviscosity syndrome: (eg. Polycythemia)
predisposing factors uti
Any condition that impairs free drainage of urine Stagnation of urine favors bacterial growth Injury to mucosa by kidney stone disrupts protective epithelium allowing bacteria to invade deeper tissue Introduction of catheter or instruments into bladder may carry bacteria Immunoglobulin A secreted by WBC's in urinary tract prevents adherence of bacteria to bladder wall Some women are non-secretors of IgA
Chronic diseases/conditions that are commonly associated with anemia.
Any type of infection. Cancer. Chronic kidney disease (Nearly every patient with this type of disease will be get anemia because kidneys make erythropoietin (EPO), a hormone that controls the production of red blood cells in the bone marrow.) Autoimmune diseases
Hemostasis
Arrest of bleeding; stopping blood flow
Response to Low Blood O2
Arteriole dilation-increased blood flow Increased cardiac output-increase blood flow Anaerobic metabolism-decreases O2 consumption and promotes dissociation of O2 from hemoglobin (remember how hemoglobin knows when to release O2 at the tissue level?)
Bohr Effect (Bohr Shift)
As acidity increases (pH decreases), affinty of Hb for O2 decreases -Increasing acidity enhances unloading -Shifts curve to right PCO2 -Also shifts curve to right -As PCO2 rises, Hb unloads oxygen more easily -Low blood pH can result from high PCO2
Reticulocyte count
Assessment of bone marrow function
complete heart block
Atria contract normally Impulses do not extend through the ventricles Results in the conduction system distal to the block to initiate impulse These impulses are generated at a slower rate Decreases cardiac output RESULTS IN DIZZINESS OR LOSS OF CONSCIOUSNESS results in the ventricles depolarizing independently from the atria
Describe cellular adaptations occurring in atrophy
Atrophy - decrease in size. uses less energy, r/t disuse, denervation, loss endocrine function, inadequate nutrition, ischemia
Immune Thrombocytopenic Purpura (ITP)
Autoimmune platelet destruction is a common cause of thrombocytopenia and should be suspected in patients with echymoses, petechiae, mucosal bleeding, and no other obvious causes of thrombocytopenia (ex- medications, bone marrow failure) . Occurs when circulating immunoglobulins react with platelets which are then destroyed by phagocytosis in spleen and to a lesser degree in the liver
3 major causes chronic gastritis
Autoimmune: associated with autoimmune disorders Chemical gastropathy reflux of alkaline duodenal contents or bile into the stomach Helicobacterpylori-mostcommon
BUN
Azotemia = increase BUN in blood Elevated BUN does not equal kidney dysfunction Can occur in dehydration High protein diets Extremely muscular individuals have higher nitrogen waste in blood because of high muscle breakdown Muscle cell proteins break down into amino acids, which are nitrogen compounds
10. Acute pancreatitis involves activated pancreatic enzymes that escape into surrounding tissues to cause _______. A) fatty deposits B) autodigestion C) bowel obstruction D) abscess formation
B
13. Which of the following individuals most likely faces the greatest risk of developing Clostridium difficile colitis? A) A 55-year-old man who takes proton pump inhibitors for the treatment of peptic ulcers B) A 79-year-old hospital patient who is being treated with broad-spectrum antibiotics C) A premature neonate who has developed hyperbilirubinemia and is receiving phototherapy D) A 30-year-old patient who has a history of Crohn disease and has been admitted to a hospital to treat a recent flare-up
B
3. The Helicobacter pylori protobacteria cause peptic ulceration by producing: A) acids B) toxins C) ischemia D) bleeding
B
Megaloblastic anemia is often caused by deficiency of one of these two vitamins:
B12 and Folate
Gastroesophogeal reflux
Backward movement of gastric contents into the esophagus Results in heartburn (pyrosis) Usually occurs soon after eating and short lived Rarely cause serious problem Transient relaxation of the LES after meals is common Increased occurrence after gastric distention and meals high in fat - Pressure is higher within the stomach and exceeds LES pressure Normally refluxed material is returned to the stomach by a 2nd peristaltic wave in the esophagus and saliva (bicarbonate) will neutralize the stomach acid
Neutrophils
Bacteria
Instead of the SA node (sinus node) directing the electrical rhythm, many different impulses rapidly fire at once, causing a very fast, chaotic rhythm in the atria.
Because the electrical impulses are so fast and chaotic, the atria cannot contract and/or squeeze blood effectively into the ventricle.
pathophysiology acute glomerulonephronitis
Begins with an antigen antibody reaction Immune-complex glomerulonephritis Usually follows a beta-streptococcal infection Circulating antigen and antibody complexes are filtered by glomeruli and incite inflammation The antigen (beta hemolytic strep) stimulates antibody formation The antibody - antigen complex becomes lodged in the glomerular capillaries Some are excreted in the urine Leads to an inflammatory response Leukocytes release lysosomal enzymes that cause injury to the glomeruli Results in damage to the epithelial membrane of the glomerulus The severity of the glomerular damage and renal insufficiency is related to the Size, number,location , & duration of exposure Most patients recover without incident
causes urinary obstruction
Bilateral: obstruction of bladder neck by enlarged prostate or urethral stricture Unilateral: ureteral stricture, calculus, tumor
what happens during cholestasis?
Bile flow in the liver slows down--> Bile accumulates and forms plugs in the ducts--> Ducts rupture and damage liver cells--> The liver is unable to continue processing materials--> materials normally transferred to the bile, including bilirubin, cholesterol, and bile acids, accumulate in the blood
what is the function of the liver?
Bile production Bilirubin excretion Drug and hormone metabolism -Biotransformation into water-soluble forms -Detoxification or inactivation Synthesize plasma proteins and blood clotting factors Store vitamins and minerals Maintain blood glucose Regulate VLDL
Blebs, Bulla
Bleb- air trapped in alveoli Bulla- air trapped more centrally
complications ulcerative colitis
Bleeding; bloody diarrhea Perforation: from extensive inflammation with leakage of intestinal contents into peritoneal cavity Long-standing disease may develop cancer of colon and/or rectum
urinary obstruction
Blockage of urine outflow leads to progressive dilatation of urinary tract proximal to obstruction, eventually causes compression atrophy of kidneys results in atrophy of the parenchyma caused by increased pressure exerted by the urine
Lab tests
Blood analysis, radiographs, exploratory surgery
hemmorrhagic anemia ACUTE
Blood loss is rapidly replaced by bone marrow with normal rbc's Normocytic anemia Loss of intravascular volume = shock
acute tubular necrosis
Blood supply to tubules is via the efferent artery Encountered in the absence of glomerular disease by: - Impaired renal blood flow causes tubular necrosis Shock and Marked drop in blood pressure impairs blood flow to kidneys = necrosis of tubules - Toxic drugs and chemicals Many drugs are excreted by kidneys = direct toxic injury
Clinical finding of multiple Myeloma
Bone marrow plasmacytosis → plasmacytomas (plasma cell tumors in soft tissue) and Lytic bone lesions Serum M-protein spike or the presence of Bence Jones proteins in the urine Other Laboratory features Hypercalcemia, elevated erythrocyte sediment rate (ESR), signs of kidney failure.
8. Factors that contribute to the formation of gallstones, or acute cholelithiasis, include: A) chronic pancreatitis. B) rapid elimination of bile. C) gallbladder inflammation. D) excessive alcohol intake.
C
List four types of normal body substances that cells may be filled up with.
CHO, proteins, lipids, bilirubin
State the definition, classifications, and diagnostic criteria for chronic kidney disease
CKD is a pathophysiologic process that results in the loss of nephrons and a decline in renal function as determined by a measured or estimated decrease in the GFR that has persisted for more than 3 months. It is characterized by a reduction in the GFR which reflects the reduction in the number of functioning nephrons. A GFR below 60 mL/min/1.73m2 represents a loss of half or more of normal adult kidney function. Serum creatinine levels and proteinuria help determine whether CKD is occurring and can measure nephron injury and repair.
As cholesterol deposits grow, _________ deposits can form as well
Calcium
Impaired calcium homeostasis
Calcium functions as an important second messenger and cytosolic signal for many cell responses Cytosolic calcium levels are kept low by energetic mechanisms Ischemia induced calcium disruption Inappropriate activation of enzymes Inability of the cell to regulate the balance of calcium within the cell. Can be caused by cytosolic calcium pump
etiology chronic renal failure
Can be the result of long-standing kidney disease (e.g. chronic glomerulonephritis, polycystic kidney disease) hypertension or diabetic nephropathy resulting from diabetes mellitus -most common
Characteristics of Malignant Neoplasm
Capable of invasion into surrounding tissue Capable of metastasis Bad clinical behavior/prognosis (death usually due to metastatic spread) Grow quickly Poor differentiation, does NOT resemble normal cell of origin Want to catch these BEFORE invasion or metastasis, these neoplasms will accumulate genetic defects that allow then to invade or metastasize
AMI usually result in __________________________ shock
Cardiogenic -Heart lacks power to force enough blood through circulatory system - Inadequate oxygen to body tissues causes organs to malfunction
Characteristics of Acute Inflammation
Cause: Injury, bacteria Foreign body, biological Duration: Short Onset: Often sudden Process: Leukocytes release interleukins and TNF This affects Thermoreg center causing fever. Affects CNS ->causes lethargy Liver makes fibrinogen and CRP which facilitate clotting, bind to pathogens and moderate response Exudation of fluid and plasma proteins Results in resolution, or progression to chronic inflamm or scarring and fibrosis.
Chronic inflammation
Cause: foreign body, biological cause (virus, bacteria, fungi parasite) Injured tissue, obesity Duration - greater than 3 months. Onset - begins insidiously patient often asymptomatic Process - Macrophages accumulate and release IM's. Fibroblasts proliferate->scar tissue Macrophages can also mass around Foreign bodies. Connective tissue forms to isolate mass
Interstitial or primary atypical pneumonia
Caused by a variety of microorganisms, including viruses and unusual bacteria called Mycoplasma pneumoniae. involves alveolar septa rather than alveoli; infiltrative cells are lymphocytes and plasma cell And monocytes rather than neutrophils
pre renal dysfxn
Caused by decreased blood flow and perfusion to kidneys Causes include decrease cardiac output or severe hypovolemia (decrease blood volume-hemorrhage e.g.), shock Large blood loss is a common cause of pre renal kidney injury caused by ischemia
Cite the two most common causes of acute tubular necrosis and describe the course of the disease in terms of the initiation, maintenance, and recovery phases
Causes are acute tubular damage due to ischemia, sepsis, nephrotoxic effects of drugs, tubular obstruction, and toxins from a massive infection. The initiating phase is the time from the onset of the precipitating event (toxin exposure or ischemic phase of prerenal failure) until tubular injury occurs. The maintenance phase involves either an oliguric or nonoliguric phase. Oliguria leads to fluid retention and gives rise to edema, water intoxication, and pulmonary congestion. If the period of oliguria is prolonged, hypertension can develop and signs of uremia occur. Untreated uremia manifestations can lead to seizures, somnolence, coma and death. The recovery phase is the period during which repair of renal tissue takes place. It usually occurs with a gradual increase of urine output and a fall in serum creatinine, which means that the nephrons have recovered to the point of urine excretion. BUN ans serum creatinine, potassium, and phosphate levels may remain elevated or rise continually but eventually the tubular function will be restored and concentration ability will improve.
State the causes and effects of increased platelet function.
Causes of increased platelet function: increase in platelet count and disturbances in blood flow, damage to the vascular endothelium, and increased sensitivity of platelets to factors that cause aggregation Effects of platelet function: predisposes to platelet adhesion, formation of clots, and the disruption of blood flow
Distinguish between cell proliferation and differentiation
Cell proliferation is the process where tissues acquire new or replacement cells through miotic cell division. Cell differentiation is the orderly process in which new cells acquire structure, function of the cells they replace. Cells that are well-differentiated are benign.
how do Hematologic disorders result from liver failure? what do these hematological disorders cause?
Changes in the lipid composition of the red blood cell membrane increase hemolysis. Because many clotting factors are synthesized by the liver, their decline in liver disease contributes to bleeding disorders. Malabsorption of the fat-soluble vitamin K contributes further to the impaired synthesis of these clotting factors. Thrombocytopenia often occurs as the result of splenomegaly. s/s: -easy bruising -abnormal menstrual bleeding -bleeding from the esophagus and other segments of the gastrointestinal tract.
Relate the effects of environmental factors such as chemical carcinogens, radiation, and oncogenic viruses to the risk for cancer development
Chemicals and radiation that are capable of triggering the development of cancer are called "carcinogens." Carcinogens act through a multistep process that initiates a series of genetic alterations("mutations") and stimulates cells to proliferate. Viruses- enter into living cells and cause the infected cell to produce more copies of the virus. Like cells, viruses store their genetic instructions in large molecules called nucleic acids. In the case of cancer viruses, some of the viral genetic information carried in these nucleic acids is inserted into the chromosomes of the infected cell, and this causes the cell to become malignant.
manifestations - pneumothorax
Chest pain Shortness of breath Reduced breath sounds on affected side Chest x-ray: lung collapse + air in pleural cavity In most cases, the defect that allows air to enter the pleural space usually closes as the lung collapses Healing leads to reexpansion of lung
Describe the effects of lead poisoning on children
Childrens absorption is greater. Mostly absorbed throught the lungs Causes demylenation of cebral and cerebellar white matter, resulting in development delay and lower IQ's. more permeable blood-brain barrier makes them more susceptible to brain damage.
Most gallstones are composed primarily of which of the following? cholesterol neutral fat bile pigment calcium oxalate
Cholesterol
what are Cholelithiasis (gallstones)?
Cholesterol, calcium salts, or mixed--> stones in the bile duct causes inflammation
Mechanisms of Anemia
Chronic bleeding resulting in iron deficiency Severe malnutrition Medical therapies Malignancy in blood-forming organs
etiology urolithiasis
Chronic dehydration Low fluid intake--> low volume of urine produced--> high concentrations of tone forming solutes in urine Urinary tract obstruction Diet High in animal protein, sodium, and calcium Recurrent UTI Genetic disorder Increase risk if family member with kidney stones
A patient have a Hallmark - presence of the BCR-ABL gene product detected in the peripheral blood. What disease does this patient have?
Chronic lymphocytic leukemia (CLL)
Excessive proliferation of marrow granulocytes, erythroid precursors, and megakaryocytes and Harbor the Philadelphia Chromosome abnormality.
Chronic myeloid leukemia (CML)
Harbor the Philadelphia Chromosome abnormality and Lymphadenopathy uncommon are the present of what disease?
Chronic myeloid leukemia (CML)
atelectasis
Collapse of parts of the lung - Obstructive atelectasis - Compression atelectasis
nephrotic syndrome
Combination of clinical finding that occur when the glomerulus is damaged Etiology Glomerulonephritis-chronic and progressive Diabetes (causing glomerular changes) Most common type Systemic lupus erythematosus, SLE-affect connective tissue Amyloidosis
chronic obstructive pulmonary disease (lower)
Combination of emphysema and chronic bronchitis and hyperactive airway disease • Pulmonary emphysema • Over distention of alveoli with trapped air creating obstruction of expiratory airflow • Chronic bronchitis: chronic inflammation of terminal bronchioles • Hypersecretion of mucous in large and small airways
State the basis for adverse drug reactions in patients with chronic kidney disease
Commonly among CKD patients is a loss of plasma proteins, especially albumin. With the loss of plasma proteins, the drugs entering the system have nothing to bond with, so they are free floating.
A 67-year man was admitted to the hospital after having sustained a severe myocardial infarction. Marked enlargement of both kidneys was detected on physical examination, and there was also clinical and laboratory evidence of severe renal insufficiency. The patient had seven brothers and sisters, four of whom had died between the ages of 40 and 60 of renal failure. Based on the information provided, which of the following would be the most likely diagnosis?
Congenital polycystic kidney disease
What does the Lymphoid Tissue Consist of?
Consist of lymphatic vessels, lymphoid tissue and lymph nodes, thymus, and spleen
Role of platelets
Constrict damaged blood vessels Form hemostatic plugs in injured blood vessels by becoming swollen and sticky Seal small breaks in capillaries Provide substances that accelerate blood clotting such as factors III and XIII and platelet factor 3
Describe factors associated with apoptosis
Controlled cell death • Removes cells that are being replaced or have "worn out" or unwanted tissue • Intact cell membrane • No inflammatory response
Brittle plaque will sometimes develop a ____________, exposing the inside of the atherosclerotic wall.
Crack 1. The crack acts like a torn blood vessel - Bleeding injury 2. The blood clotting system is activated 3. The resulting blood clot partially or completely blocks the lumen of the artery 4. If a partial blockage occurs, pieces of the blood clot may break off and start floating in the bloodstream (thromboembolism)
Causes protein wasting and loss of vessel tissue support because of excess cortisol
Cushing disease
What are some manifestations of paraneoplastic syndrome in the endocrine?
Cushings, hypercalemia, SIADH
treatment urolithiasis (x2)
Cystoscopy: snares and removes stones lodged in distal ureter Shock wave lithotripsy: stones lodged in proximal ureter are broken into fragments that are readily excreted
15. Which of the following patients likely faces the greatest risk of a gastrointestinal bleed? A) A man whose hypertension requires him to take a diuretic, an ACE inhibitor, and a -adrenergic blocker B) A patient who is taking a broad-spectrum antibiotic to treat a urinary tract infection C) A patient with a history of anxiety who takes benzodiazepines several times daily D) A patient who takes aspirin with each meal to control symptoms of osteoarthritis
D
19. A child who is experiencing the signs and symptoms of influenza has vomited frequently over the last 24 hours. Vomiting results from stimulation of what site in the neurologic system? A) Myenteric plexus B) Intramural plexus C) Vagus nerve D) Chemoreceptor trigger zone
D
2. Acute gastritis refers to a transient inflammation of the gastric mucosa that is most commonly associated with: A) diarrhea. B) food allergies. C) gastric reflux. D) alcohol intake.
D
7. Unlike the Crohn type of inflammatory bowel disease, the ulcerative colitis type is characterized by: A) skip lesions. B) steatorrhea. C) gastric ulcers. D) pseudopolyps.
D
diagnosis & treatment celiac disease
D: intestinal biopsy and anti-gluten antibodies in serum - Definitive diagnosis is by complete resolution of symptoms and resolution of intestinal changes after treatment T: avoid gluten
what is the difference Acute and chronic cholecystitis? what is similar?
DIFFERENT: acute is short and defined, chronic is consisent -acute: diffuse inflammation of the gallbladder, usually caused by presence of gallstones (calculous cholecystitis) -chronic: repeated episodes of acute cholecystitis or chronic irritation of the gallbladder by stones usually caused by acute exacerbations of gallbladder inflammation, common duct stones, and pancreatitis BOTH: Inflammation Obstruction of outlet
How do free radicals cause cell damage?
Damage cell membrane Inactivate enzymes damage nuclei acids in DNA
Hemorrhagic
Damage to blood vessels Blood (RBC's)
Infarction
Death of tissue
pathophysiology chronic renal failure
Decline in population of nephrons Normal renal function can be maintained with only 20 - 30 % of nephrons. Kidneys are resilient because huge number of nephrons (living with one kidney) These surviving nephrons receive a larger volume of blood to process at a higher pressure Compensate by hypertrophy and increasing their clearance capacity - Leads to thickening of glomerular arterioles and this leads to narrowing of their lumen along with glomerular capillary damage (sclerosis) Leads to glomerular destruction 1. Tubular damage results from the damage to these blood vessels 2. Ultimately results in more nephrons being damaged 3. Kidneys are smaller than normal because they begin to atrophy
clinical manifestations acute GLOMERULONEPHRITIS
Decrease urine output (oligouria) from blocked glomeruli by inflammation Leads to less blood filtered and therefore less urine formation Decreases Glomerular filtration rate Less urine formation leads to less waste product being excreted (accumulate in blood) Protein (albumin) and red cells leak through damaged glomerular membrane Leads to formation of casts-indicate glomerular damage Leads to low albumin (protein) Low albumin in blood (hypoalbuminemia) leads to diminished systemic colloid oncotic pressure (COP) Causes imbalance in hydrostatic and oncotic pressure Low COP is overcome by hydrostatic pressure and causes edema Low GFR leads to hypervolemia and increase in blood pressure
The nurse is caring for a client diagnosed with sickle cell disease. Select the most important factor for the nurse to be aware of that may cause the cells to sickle.
Decrease vascular volume Explanation: Diuretics, such as the thiazides, loop diuretics, and the aldosterone antagonist (potassium-sparing) diuretics, lower blood pressure initially by decreasing vascular volume (by suppressing renal reabsorption of sodium and increasing salt and water excretion) and cardiac output.
Etiology of Thrombocytopenia
Decreased production of platelets -Leukemia, drug induced, alcohol Decreased survival time -Immune mediated Sequestration -hypersplenism Dilution during transfusions-with prolonged blood storage the number of viable platelets decreases
heart block
Delay or interruption of impulse transmission from atria to ventricles, from arteriosclerosis of coronary arteries Results in inadequate blood supply 3 general forms: 1.)Mild form: delay in conduction of impulses 2.) Moderate block: when some impulses are able to reach AV node 3.)Severe block: no conduction exist through the AV node.
Describe the mechanism of symptom production in neutropenia.
Depends on the severity, Place patient at risk for infections and skin lesions and ulcerative necrotizing lesions of the mouth most common
hypoxic cell injury
Deprives cell of oxygen and interrupts oxidative metabolism and the generation of ATP The longer tissue is hypoxic, the greater chance of irreversible cellular injury. Cells with higher metabolic demand are most susceptible (heart, brain, kidney) Permanent damage of neurons in brain occurs with 4 to 6 minutes of oxygen deprivation hypoxia. Decrease in ATP results in failure of Na+-K+ pumpCell swells from
Cite two general causes of neutropenia.
Describe the mechanism of symptom production in neutropenia.
Inflamm bowel disease
Designates 2 types of related disorders Crohn's disease Chronic ulcerative colitis
ECG (electrocardiogram)
Detects disturbances in rate, rhythm, conduction, muscle injury, extent of muscle damage Measures electrical activity of heart; diagnostic tool Recording of electrical changes that occur in the myocardium Used to assess heart's ability to conduct impulses
Describe the etiologies, pathophysiology, and acute complications of diabetic mellitus: diabetic ketoacidosis (DKA).
Diabetic ketoacidosis is a serious complication of diabetes that occurs when your body produces high levels of blood acids called ketones. The condition develops when your body can't produce enough insulin. Insulin normally plays a key role in helping sugar (glucose) enter your cells. Without enough insulin, your body begins to break down fat as fuel. This process produces a buildup of acids in the bloodstream called ketones, eventually leading to diabetic ketoacidosis if untreated. The development of DKA is commonly preceded by a day or more of polyuria, polydipsia, nausea, vomiting, and marked fatigue, with eventual stupor that can progress to coma. Abdominal pain and tenderness may be experienced without abdominal disease. The breath has a characteristic fruity smell because of the presence of volatile ketoacids. Hypotension and tachycardia may be present because of a decrease in blood volume. A number of the signs and symptoms that occur in DKA are related to compensatory mechanisms. The heart rate increases as the body compensates for a decrease in blood volume, and the rate and depth of respiration increase (i.e., Kussmaul respiration) as the body attempts to prevent further decreases in pH. [A DIABETIC COMPLICATION WHERE TO BODY PRODUCES EXCESS BLOOD ACIDS (KETONES).]
Describe methods used in the diagnosis and treatment of kidney stones
Diagnosis is usually based on symptoms, urinalysis and x-rays. Intravenous pyelography and abdominal ultrasonography can also be used. Urinalysis can show info about hematuria, infection, presence of stone-forming crystals and the pH of the urine. Most stones show up clearly on an x-ray IVP uses a contrast medium that is filtered in the glomeruli to visualize the collecting system of the kidneys and ureters. Ultrasonography is sensitive to hydronephrosis, which can allude to a ureteral obstruction. To treat kidney stones it is usually supportive. Pain relief can help during acute phases, and if a UTI develops antibiotics should be given. Once the stone has passed and analyzed, prevention is the best treatment.
Describe the scientific principles underlying dialysis treatment and compare hemodialysis with peritoneal dialysis
Dialysis is needed when advanced uremia or serious electrolyte imbalances are present. Dialysis is life sustaining for those not on a transplant list or awaiting a transplant. Hemodialysis makes use of an artificial kidney consisting of a blood delivery system, a dialyzer, and a dialysis fluid delivery system. The dialyzer is where the blood circulated and dialysate travels outside the tubules. All molecules except blood cells and plasma proteins are able to move freely in and out of the semipermeable membrane material in the dialysis chamber. Peritoneal dialysis is a procedure facilitated by the surgical implantation of a silastic catheter in the peritoneal cavity below the umbilicus. A dialyzing solution is instilled through the catheter and dwells in the cavity where metabolic end products and extracellular fluid diffuse into the dialysis solution.
clinical manifestations antibiotic assoc.
Diarrhea, abdominal pain, fever Clinical manifestations can be mild with diarrhea Symptoms usually subside after antibiotics are dicontinued severe with ulcerative lesions can form - life threatening; fever, tachycardia, abdominal distention , dehydration
Stem cells
Differentiate into mature hemopoietic cells Also form new stem cells-self renewal
intrarenal dysfxn
Direct damage to nephrons from trauma or toxins Most common cause is nephrotoxic drugs (aminoglycosides, NSAIDS), renal infections (post streptococcal glomerulonephritis), systemic illness
Ischemic heart disease
Disease involving decrease in blood flow to one or more portions of the heart muscle
Atherosclerosis
Disorder in which calcium and a fatty material called cholesterol build up and form a plaque inside the walls of blood vessels, obstructing flow and interfering with their ability to dilate or contract - The inner wall of the artery is normally smooth and elastic, but becomes rough and brittle from the plaque - Over time may cause complete occlusion (blockage) or a coronary artery
Describe the physiologic basis of acute disseminated intravascular coagulation.
Disseminated intravascular coagulation: DIC is the abnormal formation of blood clots throughout the body due to the tissue factor generated by monocytes and endothelial cells during a life threatening situation which in turn overwhelms the fibrinolytic system and it gets out of control.
diverticula
Diverticulosis: pouch like sacs of mucosa that protrude through the wall of the large intestine ◦ Usually sigmoid colon ◦ Many are asymptomatic, but can have abdominal pain, less intense discomfort, and constipation ◦ Related to low fiber diet, which produces a dryer smaller stool that requires more forceful colonic contractions. This increase in colonic intraluminal pressure promotes diverticula formation
State the mechanisms of drug-induced thrombocytopenia, immune thrombocytopenia purpura, and thrombotic microangiopathies and the differing features in terms of onset and resolution.
Drug induced: induce antigen-antibody response and formation of immune complexes that cause platelet destruction Immune: autoimmune disorder that increases the formation of platelet antibody that increases the destruction of platelets Thrombotic microangiopathies: combination of clinical syndromes and manifestations including fever, thrombocytopenia, microangiopathic hemolytic anemia, renal failure and transient neurologic abnormalities
What can cause chemical injury?
Drugs (alcohol, prescriptions, OTC) Lead (paint, dust, soil, pottery glaze) Mercury (Fish, amalgams, vaccines)
Describe factors associated with wet gangrene
Due to decreased venous drainage • Fast spreading • May be internal as well as in extremities • No line demarcating normal from diseased tissue • Involves bacterial invasion with foul odour
Cellular Stage of Inflammation
During cellular stage, leukocytes emigrate from circ to site of infection 1. Margination - Leukocytes migrate to site of injury and accumulate in vessel 2. Adhesion - Leukocytes migrate to site of injury and stick to vessel walls 3. Transmigration - Adhesion causes endothelial (vessel)cells to separate so that leukocytes can "climb" through. 4. Chemotaxis - Leukocytes follow chemical trail left by chemokines to site of infection 5. Leukocytes engulf and degrade bacteria and cellular debris by phagocytosis
What causes the Cardinal signs of inflammation
During the vascular stage of inflammation, bv at sight of injury constrict momentarily and then dilate. Blood rushes into capillaries (redness and heat. 2. Vascular permeability increases and exudate (protein) pours into intracellular spaces pulling water with it.(swelling, pain and impaired function)
clinical manifestations pleural effusion
Dypnea, tachypnea, sharp chest pain, decreases breath sounds on affected side
what is to measure hepatic excretory function?
Dysfunction of liver -increase Serum bilirubin= decreased conj. of bilirubin--> cannot excrete--> increase serum levels -increase γ-glutamyltransferase (GGT): sensitive indicator of hepatobiliary disease but not used much clinically as it has limited use in specific disease diagnosis -increase alkaline phosphatase (ALP): this is in membranes btw liver cells and the bile duct and is released by disorders affecting the bile duct. -decrease albumin: decreased production and reduced serum levels
clinical manifestations COPD
Dyspnea, cough, wheezes, prolonged exhalations, barrel shaped chest and cyanosis Right ventricular failure-distention of jugular veins, ascites, ankle edema hepatosplenemagaly
What is Used to diagnosed Infectious Mononucleosis?
EBV genome enters circulation and produce hetrophil antibodies
Monocytes / Macrophages
Eat
what is the difference btw endocrine and exocrine pancreas?
Endocrine pancreas Releases hormones into the blood Exocrine pancreas -Acinar Cells - Secrete digestive enzymes -Releases digestive juices through the common bile duct to the duodenum -Proteases (trypsin), amylase, lipases -Secreted as inactive form; becomes activated in the intestines
Mechanism of heat production
Epi and norepi are increased Increase in metabolism Shivering and chattering Hypothal impulse-> incrase in muscle tone-> oscillating rhythmic tremor->heat Physical exertion
what happens if there is excessive unconj. bilirubin?
Excess unconjugated bilirubin in blood -> bilirubinemia -> jaundice(high bilirubin in blood)--> -yellowish discoloration to the skin and deep tissues (sclera of the eye) OVERALL: janunice turns everything yellow
what is the cause of jaundice ?
Excessive destruction of RBC: Impaired uptake of bilirubin by liver cells/ dysfunction of the liver Decreased conjugation of bilirubin/ dysfunction of the liver Obstruction of bile flow
What is a physiological cause of Hypertrophy?
Exercise - increases in muscle mass,
1Which of the following does NOT occur in Addison's disease? Increased skin pigmentation Exophthalmos High levels of ACTH in blood Low levels of cortisol in blood
Exophthalmos
A 25-five-year-old woman is hypothyroid caused by chronic thyroiditis. Which of the following does NOT normally occur in this condition? A slightly enlarged thyroid gland Lymphocytic infiltration of the gland as demonstrated by fine-needle aspiration of thyroid gland or biopsy of the gland A high level of thyroid-stimulating hormone (TSH) in the blood Exophthalmos
Exophthalmos
Premature ventricular contractions
Extra beats in a damaged ventricle. - Harmless - Common among healthy as well as sick people
symptoms of arrhythmias
Fast or slow heart beat, Skipping beats, Lightheadedness, dizziness, Chest pain, Shortness of breath, Paleness, and Sweating
Symptoms of lead poisoning?
Fatigue, abdominal pain --> anemia
Example of Auto immune diseases
Felty syndrome a variant of rheumatoid arthritis
what happens during liver failure?
Fetor hepaticus: from decrease metabolism Hematologic disorders Endocrine disorders Skin disorders Hepatorenal syndrome Hepatic encephalopathy Symptomatic Treatment OVERALL: liver functions failure--> -decrease metabolism -decrease kidney function
Exudate
Fibrinous - Hemorrhagic Membranous Purulent Serous
Structure of red bone marrow
Fibroblasts macrophages fat cells and blood vessels Thin walled marrow sinusoids-allows cells to enter blood
List the common problems associated with chronic kidney disease, including alterations in fluid and electrolyte balance and disorders of skeletal, hematologic, cardiovascular, immune, neurologic, skin, and sexual function, and explain their physiologic significance
Fluid and electrolyte imbalance: in CKD, the kidneys have a diminished ability to concentrate the urine, and can either produce dehydration or fluid overload. Normal kidneys can tolerate large variations in sodium intake and still manage a normal sodium level, but in CKD they can not regulate sodium excretion. Potassium excretion increases as the kidneys adapt to a decreased GFR in CKD. The kidneys also regulate the acid base balance of the blood and in CKD metabolic acidosis can occur. Acidosis can stabilize as the kidney failure progresses but it can contribute to skeletal disorders. Cardiovascular complications: People with CKD are more likely to die of cardiovascular disease than kidney failure. CKD can produce hypertension and heart disease. Hypertension is caused by increased vascular volume, elevation of peripheral vascular resistance, decreased levels of renal vasodilator prostaglandins, and increased activity of the renin-angiotensin-aldosterone system. Heart disease can be caused by an increased prevalence of left ventricular dysfunction because of extracellular fluid overload, shunting of blood through an arteriovenous fistula for dialysis, and anemia. Anemia is developed early in CKD and is due to chronic blood loss, hemolysis, bone marrow suppression, and decreased RBC production due to impaired production of erythropoietin and iron deficiency. It can also cause coagulation disorders because of platelet dysfunction. The platelet count may be decreased and bleeding time is prolonged because of abnormal adhesiveness and aggregation. Immunologic disorders: High levels of urea and metabolic wastes can adversely affect immune function. Typical responses to CKD are decreased granulocyte count, defective phagocyte function, impaired acute inflammatory and impaired humoral and cell-mediated immunity. Neuromuscular: The lower limbs are more frequently affected than upper limbs, but if affects both motor and sensory function and is symmetric. It is usually associated with the atrophy and demyelination of nerve fibers. Restless leg syndrome is often a manifestation. Sexual dysfunction: Impotence occurs in 56% of male patients on dialysis. Testosterone levels decrease and prolactin and LH increases. Skin disorders: The skin and mucous membranes are often dry, and subcutaneous bruising is common. Sweat glands decrease in size and oil glands diminish in activity.
What are B-cell zones?
Follicles
Based on the pathophysiology of diabetes mellitus explain why foot ulcers and infection are so common and can lead to extremely devastating effects in patients.
Foot problems are common among people with diabetes and may become severe enough to cause ulceration, infection, and, eventually, the need for amputation. Foot problems have been reported as the most common complication leading to hospitalization among people with diabetes. They represent the effects of neuropathy and vascular insufficiency. Distal symmetric neuropathy is a major risk factor for foot ulcers. People with sensory neuropathies have impaired pain sensation and often are unaware of the constant trauma to the feet caused by poorly fitting shoes, improper weight bearing, hard objects or pebbles in the shoes, or infections such as athlete's foot. Neuropathy may prevent people from detecting pain; they are unable to adjust their gait to avoid walking on an area of the foot where pressure is causing trauma and necrosis. Motor neuropathy with weakness of the intrinsic muscles of the foot may result in foot deformities, which lead to focal areas of high pressure. When the abnormal focus of pressure is coupled with loss of sensation, a foot ulcer can occur. Common sites of trauma are the back of the heel, the plantar metatarsal area, or the great toe, where weight is borne during walking.
Formation of bilirubin
Formed from the breakdown of RBCs in the spleen Fe released from heme is recycled by transferrin tetrapyrole ring of heme is converted to bilirubin
Three major mechanisms whereby most injurious agents exert their effects
Free radical damage Hypoxic cell injury Impaired calcium homeostasis
What are three mechanisms of cell death?
Free radical formation Hypoxia & ATP depletion Increased intracellular calcium
What is non-ionizing radiation?
Frequencies below those of visible light ex: infra red light, ultrasound, microwaves, and laser energy
compression atelectasis
From external compression of lung by: Fluid Air Blood I Accumulations in pleural cavity Reduced lung volume and expansion
Parenchyma
Fundamental tissue composed of thin-walled living cells that function in photosynthesis and storage.
how do you treat portal hypertension?
GOAL: prevention of initial hemorrhage management of acute hemorrhage, and prevention of recurrent hemorrhage. Pharmacologic therapy: -lower portal venous pressure and prevent initial hemorrhage: Nonselective β-adrenergic blocking drugs (propranolol, nadolol) acute hemo: -pharmacologic therapy: administration of octreotide, a long- acting synthetic analog of somatostatin--> reduces splanchnic and hepatic blood ow and portal pressures -balloon tamponade -emergent endoscopic therapy lowering portal venous pressure and diverting blood flow away from the easily ruptured collateral channels -the surgical creation of a portosystemic shunt -transjugular intrahepatic portosystemic shunt (TIPS)
what are the s/s of gallstones?
Gallstones cause symptoms when they obstruct bile flow -jaundice -pain of URQ or epigastric area and may be referred to the upper back, right shoulder, or midscapular region
List two types of abnormal body substances that cells may be filled up with.
Glycogen, pigments (bilirubin, lipofuscin)
Binds fibrinogen (factor I) and acts to connect platelets together to form large aggregates.
Glycoprotein IIb/IIIa (gpIIb/IIIa)
What is grading of a tumour?
Grading - level of differentiation
Compare methods used in grading and staging of tumor cells.
Grading is microscopic examination and staging is CT and MRI.
What are the steps of grading a tumor cell?
Grading: Microscopic examination of cancer cell Grade I: well differentiated Grade IV: poorly differentiated with marked anaplasia (loss of differentiation)
A 25-year-old woman has acromegaly. Which of the following does NOT occur in this condition? Coarsening of the facial features resulting from overgrowth of facial bones Elevated level of growth hormone in the blood Growth in height Adenoma of pituitary gland
Growth in height
causes peptic ulcer
H. pylori-80% Aspirin Most ulcerogenic as compared to others NSAIDS Higher risks in those who smoke and are older
what can hep B lead to?
HBV infection can produce -acute hepatitis -chronic hepatitis -hepatocellular carcinoma -fulminant hepatic failure: -participates in the development of hepatitis D (delta hepatitis)
what is chronic viral hepatitis caused by?
HBV, HCV, HDV
Sickling in Sickle Cell
HbA & HbF ↓sickling; HbC ↑sickling Dehydration ↑ sickling Coexisting α-thalassemia ↓sickling (less globin, therefore less Hemoglobin present). lower pH and low O2 tension ↑sickling. Hyperbilirubinemia (jaundice), *gallstones*
Angina pectoris (AKA "angina") occurs when the ________________________
Heart's need for oxygen exceeds the available supply - Usually occurs during physical or emotional stress - When the increased oxygen demand goes away, the pain typically goes away - Can result from a spasm of an artery, but is most often a symptom of atherosclerotic coronary artery disease
What is unconjugated bilirubin?
Hemoglobin from old red blood cells becomes unconjugated bilirubin.
Factors that may contribute to hemolysis
Hemolysis inside the body can be caused by a large number of medical conditions, including many Gram-positive bacteria (e.g., Streptococcus, Enterococcus, and Staphylococcus), some parasites (e.g., Plasmodium), some autoimmune disorders (e.g., drug-induced hemolytic anemia), some genetic disorders (e.g., Sickle-cell
Differentiate between the mechanisms of bleeding in hemophilia A and von Willebrand disease.
Hemophilia A and von Willebrand disease are two of the most common inherited disorders of bleeding. Hemophilia A is an X-linked recessive disorder that primarily affects males. Is a Factor VIII deficiency. Bleeding occurs in soft tissues, the GI tract, and the hip, knee, elbow, and ankle joints. Spontaneous joint bleeding usually begins when a child begins to walk - prone to recurrent incidences. Von Willebrand disease affects both men and women and is typically diagnosed in adulthood Has a compound defect involving platelet function and the coagulation pathway.
complications peptic ulcer
Hemorrhage Bleeding from erosion of ulcer into artery or vein Hematemesis or melena May be sudden , severe, and without warning (no prior pain) Weakness, dizziness, thirst, cold, melena or hematochezzia, coffee ground emesis Circulatory shock Perforation ◦ Peritonitis ◦ Present with severe back pain, night distress, that is not allleviated with food or antacids
Uncommon autosomal dominant disorder that is characterized by thin-walled, dilated capillaries and arterioles
Hemorrhagic Telangiectasia
Some types of hepatitis are transmitted by the fecal-oral route, and others are transmitted by contact with infectious blood or body fluids. Below is a list of various types of hepatitis. From this list, select the types of viral hepatitis that have a similar means of transmission. Hepatitis A, hepatitis B, and hepatitis C all have a similar means of transmission. Hepatitis A and hepatitis B have a similar means of transmission. Hepatitis A and hepatitis C have a similar means of transmission. Hepatitis B and hepatitis C have a similar means of transmission.
Hepatitis B and hepatitis C have a similar means of transmission.
Name some factors linked to cancer
Heredity (breast, prostate, ovarian, pancreatic) Radiation Viral/microbial (HPV, HHV etc) Obesity Immunological mechanisms Chemical carcinogens
Explain how host factors such as heredity increase the risk of cancer?
Heredity -Persons who inheret the mutant gene are born with one normal and one mutant copy of the gene.
hepatic necrosis
High O2 demand
predisposing factors: urolithiasis
High concentration of salts in urine saturates urine causing salts to precipitate and form calculi Urinary tract infections reduce solubility of salts in urine; clusters of bacteria are sites where urinary salts may crystallize to form stone Urinary tract obstruction causes urine stagnation, promotes stasis and infection, further increasing stone formation
ionizing radiation
High energy radiation associated with X-rays, nuclear radioactivity Can kill or damage cell by production of free radicals
1. A middle-aged woman has CushingÕs disease associated with hyperplasia of both adrenal glands. Which of the following does NOT normally occur in this condition? Microadenoma of the pituitary gland High levels of ACTH in the blood High level of cortisol in the blood High level of catecholamines (epinephrine-norepinephrine) in the blood
High level of catecholamines (epinephrine-norepinephrine) in the blood
An 18- year-old woman has hyperthyroidism caused by diffuse hyperplasia of the thyroid gland. Which of the following does NOT occur in this condition? Exophthalmos High level of thyroid-stimulating hormone (TSH) in the blood due to hyperfunctioning pituitary gland Slight enlargement of thyroid gland High level of thyroid hormones (T3 and T4) in the blood
High level of thyroid-stimulating hormone (TSH) in the blood due to hyperfunctioning pituitary gland
Diagnostic test
Histological lesions-kidney is infiltrated with leukocytes and bacterial Many tubules filled with leukocytes urinalysis: hematuria , bacteria, wbc's (pyuria) wbc casts Culture and sensitivity for definitive diagnosis Imaging studies
diagnosis peptic ulcer
History of NSAID ingestion Laboratory test: hypochromic anemia and occult blood in stools Endoscopy-visualize ulcer and biopsy to test for H.Pylori and r/o malignancy Contrast radiographs to detect ulcer crater
Describe the manifestations of thrombocytopenia.
History of easy bruising, bleeding from gums, epistaxis, melena, and abnormal menstrual bleeding in those with moderately reduced platelet counts. Splenic enlargement (site of platelet destruction). Purpura and Petechiae
Is a multi-step process that maintains the integrity of a closed high-pressure circulatory system after vessel injury
Homeostasis
What is an example of a physiological stimuli causing hyperplasia?
Hormonal - breast and uterine enlargement during pregnancy Compensatory -regeneration of liver after partial removal
how do hormones increase the risk of cancer?
Hormones - possible ability of hormones to drive the cell division of a malignant phenotype.
Physiology of fever
Hydrogen activates the hypothalamus to induce changes in its set point via the second messenger cyclic adenosine monophosphate (cAMP). Initiation through shivering , vasoconstriction equals fever is established.
manifestations urinary obstruction
Hydroureter: dilatation of ureter Hydronephrosis: dilatation of pelvis and calyces Result of obstruction of outflow of urine distal to renal pelvis Leads to tissue damage in chronic cases
Prophylactic therapy with allopurinol is used for?
Hyperuricemia
Increased proliferation or increased breakdown of purine secondary to leukemic cell death from chemotherapy.
Hyperuricemia.
Inability to produce specific antibodies and Abnormal activation of complement.
Hypogammaglobulinemia
Describe the etiologies, pathophysiology, and acute complications of diabetic mellitus: hypoglycemia.
Hypoglycemia, or an insulin reaction, occurs from a relative excess of insulin in the blood and is characterized by below-normal blood glucose levels. It occurs most commonly in people treated with insulin injections, but prolonged hypoglycemia also can result from some oral hypoglycemic agents (i.e., sulfonylurea). There are many factors that can precipitate an insulin reaction in a person with type 1 or type 2 diabetes, including error in insulin dose, failure to eat, increased exercise, decreased insulin need after removal of a stress situation, medication changes, and a change in insulin injection site. Hypoglycemia usually has a rapid onset and progression of symptoms. The signs and symptoms of hypoglycemia can be divided into two categories: (1) those caused by altered cerebral function and (2) those related to activation of the autonomic nervous system. Because the brain relies on blood glucose as its main energy source, hypoglycemia produces behaviors related to altered cerebral function. Headache, difficulty in problem solving, disturbed or altered behavior, coma, and seizures may occur. At the onset of the hypoglycemic episode, activation of the parasympathetic nervous system often causes hunger. The initial parasympathetic response is followed by activation of the sympathetic nervous system; which causes anxiety, tachycardia, sweating, and a cool and clammy skin due to constriction of the skin vessels. The signs and symptoms of hypoglycemia are highly variable, especially in children and the elderly, and not everyone manifests all or even most of the symptoms. Elderly people may not display the typical autonomic responses, but typically do display signs of altered cerebral function, including mental confusion. Also, some medications, such as β-adrenergic blocking drugs, interfere with the autonomic response normally seen in hypoglycemia. Some people develop hypoglycemic unawareness. [LOW BLOOD SUGAR LEVELS.]
Compare the manifestations of hypoxia and hypercapnia
Hypoxia: Pulmonary vasoconstriction, Increased production of RBCs, shift to the right in the oxygen dissociation curve (releases more O2 to the tissues) • Hypercapnia: Respiratory acidosis, increased bicarbonate retention, other manifestations accompanying hypoxia.
Describe the effects of urinary tract obstruction on renal structure and function
If an obstructed kidney goes untreated, the kidney can atrophy and cause kidney disease. The destructive effects usually depend on the degree of obstruction and how long it is obstructed. Stasis of urine predisposes you for infection and stone formation and progressive dilation of the collecting ducts and tubules which leads to atrophy. Infection is a common complication in obstruction and is difficult to treat. Even with obstruction, glomerular filtration continues but it can lead to backups in the tubules. Eventually the GFR will diminish.
resp. infections (low vs upper)
Illnesses range from trivial to fatal --Divided into infections of upper respiratory system (head and neck) and lower respiratory system (chest) Upper respiratory infections very common and uncomfortable, but not life-threatening, clear without treatment in about a week Lower respiratory infections (e.g., pneumonia, tuberculosis) often serious, may be fatal
How can immune system functions increase the risk of cancer
Immune system - the immune system plays a central role in resistance against the development of tumors. It has been suggested that the development of cancer might be associated with impairment or decline in the surveillance capacity of the immune system. For example, increases in cancer incidence have been observed in people with immunodeficiency diseases and in those with organ transplants taking immunosuppresant drugs
Megaloblastic anemia
Impaired DNA synthesis that causes ineffective hematopoiesis and abnormally large Red blood cells Etiology: -B12 deficiency =Decreased intake -Impaired absorption -Pernicious anemia Folate deficiency -Decrease intake -increased requirement (pregnancy) -impaired utilization
Manifestations of anemia
Impaired oxygen transport with the resulting compensatory mechanisms Reduction in red cell indices and hemoglobin levels Signs and symptoms associated with the pathologic process that is causing the anemia
treatment and prevention
In U.S., skin tests, lung X-rays used to identify cases; both ATBD and LTBI treated, especially in high-risk individuals Antimicrobials medication; long term New vaccines being developed
diagnosis acute glomerulonephronitis
Increase in blood creatinine and BUN levels Low creatinine clearance because of inability to excrete creatinine (low GFR) Amount of total creatinine filtered at glomerulus Low specific gravity of dilute urine caused by inability of kidneys to concentrate urine presence of blood, albumin, and casts in the urine Urine is dark in color because of RBC's (cola colored) Patients usually recover without residual damage to kidneys may have recurrent episodes
What is Hematopoietic Growth Factors (recombinant human G-CSF) use for?
Increase white blood cells production
Polycythemia clinical manifestations
Increased viscosity leads to interference with cardiac output and blood flow and hypertension Venous stasis appears as a bluish discoloration to skin Cyanosis (bluish color) caused by lack of O2 in the blood Most evident in fingernails, lips, and mucous membranes
Describe the pathogenesis, clinical manifestations of infectious mononucleosis.
Incubation period from exposure to onset of symptoms - 4 to 8 weeks. Prodromal period - last several days - malaise, anorexia, and chills May have abrupt high fever Day 5 to 7 - pharyngitis and lymph node enlargement
chronic bronchitis (lower)
Indicated by repeated attacks of acute bronchitis and coughing with sputum production, lasting for at least 3 months for 2 consecutive years. Symptoms are persistent. Chronic bronchitis may be a complication of another respiratory infection, or can result from long-term environmental exposure
TB (cont) -- Infection arrested and granulomas heal with scarring
Infection may be asymptomatic, detected only by chest x-ray and/or Mantoux test Infection reactivated: healed granulomas contain viable organisms reactivated with reduced immunity leading to progressive pulmonary TB The bacteria may spread this way when the person's resistance is reduced because of stress, infection, malnutrition, or immuno-deficiency.
What hep. is a carrier?
Infections of: -Hep B -Hep C -Hep D *when babe carries a dogs, it is infectiously cute*
Define infectious mononucleosis and describe the pathogenesis, clinical manifestations, and treatment.
Infectious mononucleosis (AKA; Kissing disease) is a Self-limiting lymphoproliferative disorder caused by the Epstein Barr virus (EBV) - a member of the herpesvirus family. Can occur at all ages - more in adolescents and young adults and Spread person to person through contact with infected oral secretions Proliferation of EBV is controlled by CD8 cytotoxic T cells and NK cells and T-cells appear large - increase node size.
what is Cholangitis?
Inflammation of the common bile duct
acute glomerulonephronitis
Inflammation of the glomeruli that leads to damage to the membrane Caused by antigen-antibody reaction 1-4 weeks after skin or throat infection with group A beta hemolytic streptococci (GABHS) -- most common Glomerulonephritis may follow "strep" cases of pharyngitis, tonsillitis or impetigo -skin infection from GABHS Can also arise from other bacterial, fungal , viral, or parasitic infections and Autoimmune disease (SLE) Primarily affects children and young adults
Pneumonia (lower)
Inflammation of the lung = pneumonia The inflammatory process is the same as in other tissues
rhinitis (upper)
Inflammation of the nasal mucosa: -Bacterial, fungal, viral, allergies -Common cold-most common ~100 or more types of human rhinoviruses cause ~30-50% Symptoms/signs: -Malaise (vague feeling of discomfort), sore throat, nasal dischare, cough, hoarseness -Nasal secretions initially watery, then thicken, finally become cloudy and greenish -No fever unless secondary bacterial infection
Describe two types of immune mechanism involved in glomerular disorders
Injury resulting from antibodies reacting with fixed glomerular antigens or antigens planted within the glomerulus and injury resulting from circulating antigen-antibody complexes that become trapped in the glomerular membrane.
nutritional imbalances cell injury
Iron deficiency anemia Obesity and insulin resistant diabetes Anorexia
Iron-deficiency in infancy
Iron deficiency anemia most commonly affects babies 9 through 24 months old. Breastfed babies need less iron because iron is absorbed better when it is in breast milk. ... Infants younger than 12 months who drink cow's milk rather than breast milk or iron-fortified formula are more likely to have anemia.
Function of iron in the formation of hemoglobin
Iron is an essential element for blood production Hemoglobin is essential for transferring oxygen in your blood from the lungs to the tissues. Myoglobin, in muscle cells, accepts, stores, transports and releases oxygen
Chest pain/discomfort is usually related to ______________
Ischemia - Decreased blood flow
kidneys vulnerable to injury
Ischemic injury can occur if not provided with high blood flow Important that all tubule fluid from nephrons travel to ureters, which requires a high pressure to prevent stasis or back flow of urine Many drug metabolites are nephrotoxic
State the function of clot retraction
It squeezing serum from the clot and joining the edges of the broken vessel. Retraction failure indicative of a low platelet count
early symptoms of ventricular fibrillation
It's possible to see signs and symptoms that start about an hour before your heart goes into ventricular fibrillation and fainting. These include: Chest pain, Rapid heartbeat (tachycardia), Dizziness, Nausea, and Shortness of breath
what are s/s of alcoholic hep?
JANDICE!!! other s/s: fever, hepatic tenderness, pain, anorexia, nausea, ascites, and liver failure. -severe alcoholic hepatitis may have encephalopathy
List common causes of urinary tract obstruction
Kidney stones are the most common cause of urinary tract obstruction. Other causes are congenital anomalies, pregnancy, benign prostatic hyperplasia, scar tissue resulting from infection and inflammation, tumors and neurologic disorders such as spinal cord injury.
What are some manifestations of paraneoplastic syndrome in the neurological system?
Lambert-Eaton myasthenic syndrome (LEMS) Myastenia gravis
AMI is more likely to occur in the _________________________
Left ventricle
Decrease in the absolute number of leukocytes in the blood Can affect any of the WBCs
Leukopenia
Free radical damage
Lipid peroxidation-cell membrane damage. Oxidative modification of proteins-abnormal formation of proteins (enzyme damage). DNA effects-mutations Contribute to cell damage, disease progression and aging Most studies have linked ROS to disease states such as cancer, insulin resistance, diabetes mellitus, cardiovascular diseases, atherosclerosis, and aging.
what is the stage of fatty liver?
Liver cells contain fat deposits; the liver is enlarged
Characteristics of Benign Neoplasm
Localized CANNOT invade surrounding tissue CANNOT undergo metastasis Grow slowly Good differentiation, resembles normal cell of origin Good clinical behavior or prognosis
clinical manifestations (Upper UTI)
Localized pain and tenderness over affected kidney Back pain that spreads over the abdomen fever, chills Nausea and vomiting +/- gross hematuria **Responds well to antibiotics Cystitis and pyelonephritis are frequently associated Signs will include those of lower UTI Chronic pyelonephritis may have more subtle signs/symptoms Some cases become chronic and lead to kidney failure Kidneys will become shrunken and contain Increase scar tissue Renal functions declines
As more fatty materials are deposited, the __________ narrows
Lumen - Inside diameter of the artery
Trace the pathway for hematologic spread of a metastatic cancer cell.
Lungs and liver are the most frequent metastatic sites for hematologic spread since venous blood from the gastrointestinal tract, pancreas, and spleen is routed through the portal vein to the liver, and all vena caval blood flows to the lungs. To metastasize, a cancer cell must be able to break loose from the primary tumor, invade the surrounding extracellular matrix, gain access to a blood vessel, survive its passage in the blood stream, emerge from the blood stream at a favorable location, invade the surrounding tissue, begin to grow, and establish a blood supply
Explain the manifestations of leukemia in terms of altered cell differentiation.
Lymphocytic leukemia affects your lymph cells which includes, NK cells, T-cells, B-cells and plasma cells. Myelogenous leukemias which includes, Monocyte, Granulocyte: Neutrophil, Eosinophil, and Basophil, Platelets
Use the concepts regarding the central and peripheral lymphoid tissues to describe the site of origin of the malignant lymphomas, leukemias, and plasma cell dyscrasias.
Lymphocytic leukemias: Immature lymphocytes and their progenitors that infiltrate the spleen, lymph nodes, CNS, and other tissues. Myelogenous leukemias Involve the pluripotent myeloid stem cells in bone marrow- interfere with the maturation of all blood cells, including the granulocytes, erythrocytes, and thrombocytes. Plasma cell dyscrasias:
Lymphocytic versus myelogenous
Lymphocytic: Nuetophil, eosinophil,
Manifestations of multiple Myeloma
Main sites of involvement - bones and bone marrow Bone pain - one of the first symptoms
Explain the pathogenosis of Paraneoplastic syndrome
Manifestations can be caused by increased hormones and cytokines and immune response against the tumor. The manifestations usually arise before the cancer diagnoses.
Diagnostics TB
Mantoux test (TST= tuberculin skin test) - Inject small amount of purified protein derivative from M. tuberculosis Does not distinguish between active and latent disease - Redness and firm swelling at injection site peaks at 48 - 72 hours after injection is a positive test Positive reaction = LTBI , ATBD or a TB immunization Xrays: screening for those with a positive TB test Culture and DNA test: definitive tests
clinical manifestations nephrotic syn
Marked leg edema Facial edema ; especially periorbital Ascites and pleural effusion Hematuria and hypertension are often seen Increased susceptibility to infefection
other causes of kidney disease
Marked loss of protein in the urine Urinary excretion of protein > protein production Protein level (albumin) in blood falls Albumin is the most numerous of proteins in blood and are the major determinant of plasma osmotic pressure Immunoglobulins and other large molecules are also lost Causes edema due to low plasma osmotic pressure The cause is injury to the glomerulus that allow proteins to leak through the damaged membrane
Morbidity
Measure of disability
Physical Cellular injury
Mechanical trauma temperature extremes Atmospheric pressure changes Electrical shock
Chemical mediators of inflammation
Mediators of increased vascular permeability in inflammatory edema: cell derived vasoactive mediators and plasma derived vasoactive mediators; Mediators involved in cell recruitment (chemotactic factors)
is in the bone marrow stimulated and by Thrombopoietin, which is the production of platelet
Megakaryocytes
hemorrhagic anemia Chronic
Microcytic hypochromic anemia because of depleted iron stores Anemia occurs also if rate of loss > the regenerative capacity of marrow
actin filaments, myosin, and actin-binding proteins maintain the platelet's disk shape
Microtubules,
Agranulocytes
Monocytes / Macrophages Lymphocytes, plasma cells
Bleeding resulting from vascular disorders, sometimes called?
Monthrombocytopnic purpura
A Fib
Most common arrythmia Older individuals with history of cardiovascular disease. chronic pulmonary disease, hyperthyroidism, and no history of illness
Congenital polycystic kidney disease
Most common cause of multiple cysts; bilateral fluid filled cysts Epithelial cycle becomes dysfunctional leading to hyperplasia Hyperplastic cells cause outpocketing of the tubule wall that fill will fluid from glomerular filtrate Mendelian dominant transmission Cysts enlarge and destroy renal tissue and function Impairment of renal function Onset of renal failure by late middle age
Describe the following complications of acute leukemia and its treatment
Most common form among children. Abrupt onset of symptoms Fatigue resulting from anemia Low-grade fever, night sweats, and weight loss due to the rapid proliferation and hypermetabolism of the leukemic cells Bleeding due to a decreased platelet count Bone pain and tenderness due to bone marrow expansion. Infection results from neutropenia - risk of infection Treatments options are: Chemotherapy Bone marrow and stem cell transplantation Not recommended in patients older than 50 to 55 years of age
serum creatinine
Muscle breakdown product that is practically filtered at the glomerulus and is not reabsorbed by the tubules Increase serum creatinine indicates decreased filtering of creatinine at the glomerulus Exceptions to rule Persons with increased daily muscle breakdown may have abnormally high creatinine A frail person will have low amount of serum creatinine daily
causes hiatal hernia
Muscle weakness common with increase age, trauma, congenital
what are s/s of hepatitis?
N/V: anorexia and weight loss Fever chills jaundice dark urine hx of potential exposure
Granulocytes
NEB for M Neutrophils Eosinophils Basophils Mast cells
Describe the etiologies and pathophysiology of the following common chronic complications of diabetes mellitus: -Neuropathies -Nephropathies -Retinopathies -Macrovascular complications -Diabetic foot ulcers -Infections
NEUROPATHIES Diabetic neuropathy is a type of nerve damage that can occur if you have diabetes. Depending on the affected nerves, symptoms of diabetic neuropathy can range from pain and numbness in your legs and feet to problems with your digestive system, urinary tract, blood vessels and heart. NEPHROPATHIES Diabetic nephropathy is a serious kidney-related complication of type 1 diabetes and type 2 diabetes. It is also called diabetic kidney disease. Up to 40 percent of people with diabetes eventually develop kidney disease. RETINOPATHIES Retinopathy is any damage to the retina of the eyes die to diabetes, which may cause vision impairment. Retinopathy often refers to retinal vascular disease, or damage to the retina caused by abnormal blood flow. MACROVASCULAR COMPLICATIONS Diabetes causes things like coronary artery disease, peripheral arterial disease, and stroke. DIABETIC FOOT ULCERS A diabetic foot ulcer is an open sore or wound and is commonly located on the bottom of the foot. INFECTIONS Although not specifically an acute or a chronic complication, infections are a common concern of people with diabetes. Certain types of infections occur with increased frequency in people with diabetes: soft tissue infections of the extremities, osteomyelitis, urinary tract infections and pyelonephritis, candidal infections of the skin and mucous surfaces, dental caries and periodontal disease, and tuberculosis. Moreover, infections often are more serious in people with diabetes. Suboptimal response to infection in a person with diabetes is caused by the presence of chronic complications, such as vascular disease and neuropathies, and by the presence of hyperglycemia and altered neutrophil function. Sensory deficits may cause a person with diabetes to ignore minor trauma and infection, and vascular disease may impair circulation and delivery of blood cells and other substances needed to produce an adequate inflammatory response and effect healing. Pyelonephritis and urinary tract infections are relatively common in persons with diabetes, and it has been suggested that these infections may bear some relation to the presence of a neurogenic bladder or nephrosclerotic changes in the kidneys. Hyperglycemia and glycosuria may influence the growth of microorganisms and increase the severity of the infection. Diabetes and elevated blood glucose levels also may impair host defenses such as the function of neutrophils and immune cells. Polymorphonuclear leukocyte function, particularly adherence, chemotaxis, and phagocytosis, is depressed in persons with diabetes, particularly those with poor glycemic control.
Membranous
Necrotic cells in fibromembranous exudate Develop on mucous membrane. Dead cells in mesh sticky stuff. (canker sore?)
Define neoplasm and explain how neoplastic growth differs from the normal adaptive changes seen in atrophy, hypertrophy, and hyperplasia
Neoplasm is a abnormal tissue mass with uncontrolled proliferation of cells not coordinated with normal cells.They serve no useful purpose and continue to grow at the expense of the host. Normal adaptive changes (atrophy, hypertrophy, hyperplasia) occur to permit cell survival and maintenance.
Differentiate the pathology and manifestations of the nephrotic syndrome from those of the nephritic syndrome
Nephritic syndrome is due to glomerular disease that is usually of acute onset and is accompanied by grossly visible hematuria, mild to moderate proteinuria, and hypertension. Nephrotic syndrome is characterized by heavy proteinuria, hypoalbuminemia, and severe edema.
Subtypes of granulocytes
Neutrophils. Eosinophils. Basophils.
List the three subtypes of granulocytes and briefly describe their role.
Neutrophils: make up 60-65% of leukocytes. They maintain normal host defenses against invading bacteria nad fungi cell debris, and a variety of foreign substances. Eosinophils: make up 1-3% of leukocytes. They are a part of 2 reactions. Allergic reactions: they release enzymes or chemical mediators that detoxify agents associated with the reaction. Parasitic infections: Basophils: make up .3-.5% of leukocytes. They contain heparin, an anticoagulant; and histamine, a vasodilator, and other mediators of inflammation.
benign neoplasm
Non-cancerous new growths
Cause - structurally weak vessel walls or damage to vessels by inflammation or immune responses. Is also Characterized by easy bruising and the spontaneous appearance of petechiae and purpura of the skin and mucous mem-branes.
Nonthrombocytopenic purpura
Compare normal and abnormal clotting.
Normal clotting successfully goes through those five steps each time there is a vessel injury. Abnormal clotting means that something is going wrong during the clotting process
Incidence
Number of new diagnoses in a set time frame (usually 1 yr). Incidence is more useful for the impact of an acute illness, rather than chronic.
what is the patho for cirrhosis?
OVERALL: fibrous tissue that replaces normally functioning liver tissue forms constrictive bands that disrupt flow in the vascular channels and biliary duct systems of the liver. detailed: fibrous septa extend through the sinusoids from the central to the portal regions and the entrapped hepatocytes --> fine, uniform nodules on its surface(micronodular or Laennec cirrhosis).--> With more advanced cirrhosis, regenerative processes cause the nodules to become larger and more irregular in size and shape--> liver becomes relobulized through the formation of new portal tracts and venous out flow channels--> The nodules may compress the hepatic veins, curtailing blood flow out of the liver--> -vascular channels predisposes to portal hypertension and its complications -obstruction of biliary channels and exposure to the destructive effects of bile stasis(extrahepatic portosystemic shunts) -loss of liver cells, leading to liver failure.(cholestasis)
what are the metabolic functions of the liver?
OVERALL: Carbohydrate, protein, and lipid metabolism -Glucose-->glycogen--> used to make fats, formed from amino acids and other substrates -Lipids--> oxidized for energy, synthesized, packaged into lipoproteins -Proteins are synthesized from amino acids, transamination, and deamination--> ammonia(byproduct)--> urea--> circulation--> filtered through kidneys
what are s/s of cholestasis?
OVERALL: features of cholestasis depend on the underlying cause. Accumulation of bile pigment in the liver Skin xanthomas: focal accumulations of cholesterol from hyperlipidemia and impaired excretion of cholesterol reduced bile flow relate to intestinal absorption: nutritional deficiencies of the fat-soluble vitamins A, D, E, and K. Pruritus (itching): Increased bile acids in blood and skin
How does obesity increase the risk of cancer?
Obesity - associated with insulin resistance and increased production of pancreatic insulin, both of which have a carcinogenic effect. increased production of androgens and estrogens, which can act as mitogens that stimulate cell proliferation, inhibit apoptosis, and therefore increase the chance of malignant cell transformation particularly of endometrial and breast tissue.
signs
Objective evidence of disease observed on physical examination, such as abnormal pulse or respiratory rate, fever, sweating
acute appendicitis
Occur at any age, but most common abdominal surgery in children Pathogenesis: obstruction of narrow lumen, establishes conditions favoring resident bacterial growth Mucous secretions continues behind obstruction causing increase pressure Mucosal veins collapse leading to blockage of inflow of blood-->mucosal damage and inflammation As inflammation develops, further collapse of larger vessels leads to decrease oxygen supply and favors growth of anaerobic bacteria - Gangrenous necrosis resultS
signs of anemia
Palpitations, , weakness, pale, dizziness, angina, pallor, weakness
What are T-cell zones?
Paracortex - contain most of the T-cells
Biologic cell injury
Parasites, fungi, bacteria , viruses, prions
celiac disease
Patients are unable to have gluten as it triggers injury to the mucosa of the small intestine - Autoimmune disease which antibodies to a component of gluten resulting in damage to the intestinal epithelium Results in malabsorption o Failure to digest and absorb food
GERD
Persistent reflux of gastric contents o signs and symptoms occur at least twice a week interfere with daily life A chronic digestive disease
Provide critical binding sites for calcium and coagulation factors in the intrinsic coagulation pathway.
Phospholipids
Mechanisms of heat retention
Piloerection - decreases SA for heat loss AV shunts close, Traps air and decreases blood flow to superficial tissues. Vasoconstriction - decreases blood flow to surface
Also called "thrombocytes", are large fragments from the cytoplasm of bone marrow cells called "Megakaryocytes"
Platelets
What are the components of Homeostasis
Platelets plasma clotting factors Naturally occurring anticoagulants the inherent properties of endothelial lining of the blood vessels
List the three types of cells of the hematopoietic system.
Pluripotent stem cells Multipotent stem cells Committed progenitor cells
tension pneumothorax and treatment
Positive pressure develops in pleural cavity Air flows through perforation into pleural cavity on inspiration but cannot escape on expiration Pressure builds up in pleural cavity displacing heart and mediastinal structures away from affected side this impairs expansion of opposite lung: Treatment = Chest tube inserted into pleural cavity; left in place until tear in lung heals Prevents accumulation of air in pleural cavity Aids re-expansion of lung
Discuss the risk factors for gestational diabetes mellitus.
Pregnant women who are: -overweight -related to someone who has diabetes -are Hispanic/Latina, African American, American India, Alaska Native, Asian American, or a Pacific Islander -older than 25
at risk groups for neonate" "
Premature infants Infants delivered by cesarean section Infants born to diabetic mothers
Differentiate the prerenal, intrinsic, and postrenal forms of acute renal failure in terms of the mechanisms of development and manifestations
Prerenal AKI effects the blood flow into the kidney and glomerulus. It is the most common cause of AKI and is characterized by a decrease in renal blood flow. Causes include depletion of vascular volume, impaired perfusion due to heart failure, and decreased vascular filling due to vascular capacity. Vasoconstriction can cause hypoperfusion and prerenal injury. Several drugs can impair renal adaptive mechanisms. It is manifested by a sharp decrease in urine output and a disproportionate BUN and serum creatinine level. Postrenal injury results from obstruction of urine outflow from the kidneys. It can occur in the ureter, bladder, or urethra. Both ureters must be occluded to cause AKI. The treatment consists of finding the cause of the obstruction and reestablishing urine flow. Intrarenal results from damage within the kidney. It is usually caused by ischemia associated with prerenal injury, injury to the nephron tubules, and intratubular obstruction. Acute tubular necrosis can also be a cause.
Primary disease prevention
Prevent disease occurrence - IMMUNIZATIONS (e.g., HPV vaccination)
Hematopoesis
Production of blood cells in bone marrow
neonate respiratory distress syndrome
Progressive respiratory distress soon after birth Hyaline membrane disease after red-staining membranes lining alveoli
Use the terms proliferation, sclerosis, membranous, diffuse, focal, segmental, and mesangial to explain changes in glomerular structure that occur with glomerulonephritis
Proliferation is used to describe a hypercellular inflammatory process with proliferation of glomerular cells Sclerosis is an increase in the amount of extracellular material in the mesangial, subendothelial, or subepithelial tissue of the glomerulus Membranous is an abnormal thickening of the glomerular basement membrane Focal: only some of the glomeruli are affected and others are normal Segmental: certain segments of each glomerulus Mesangial: affecting only mesangial cells.
Relate the clonal expansion of immunoglobulin-producing plasma cells and accompanying destructive skeletal changes that occur with multiple myeloma.
Proliferation of malignant plasma cells in the bone marrow and osteolytic bone lesions throughout the skeletal system. Induces angiogenesis - Proteins increase blood viscosity Suppresses cell-mediated immunity - Immune depression Develops paracrine signaling loops - Infiltrate organs Unregulated production of abnormal monoclonal paraprotein - M protein - secreted in the urine - Bence Jones Protein Produce abnormal antibodies Proliferation of osteoclasts
Free radicals react with
Proteins, lipids, CHO (Carbohydrates)
Relate the proteinuria, hematuria, pyuria, oliguria, edema, hypertension, and azotemia that occur with glomerulonephritis to changes in glomerular structure
Proteinuria: in glomerulonephritis the glomerulus becomes more permeable and allows proteins to filter into the urine. Hematuria: The increased permeability also allows for RBC's to filter out of the glomerulus and into the urine. Pyuria: the presence of pus in the urine, typically from bacterial infection Oliguria: a decreased urine output and occurs because of the decreased GFR Edema occurs because of the retention of water and salts Hypertension occurs because there is water and salt retention. Azotemia: is an elevation of blood urea nitrogen (BUN) and serum creatinine levels. The reference range for BUN is 8-20 mg/dL, and the normal range for serum creatinine is 0.7-1.4 mg/dL.
Increase viscosity causes?
Pulmonary vessel occlusion - shortness of breath and dyspnea Cerebral leukostasis - diffuse headache and lethargy that progresses to confusion and coma
The death of heart muscle can severely diminish the heart's ability to ______________________
Pump - Leads to cardiac arrest
Purulent
Pus Degraded wbc's, protein, tissue debris Can be various colors and smelly
Acute Disease
Quick onset, short duration (< Few weeks), e.g., influenza, measles, and the common cold
What are the major targets of lead toxicity?
RBC's (effects enzymes that form hemoglobin) GI tract kidneys (renal failure) nervous system
Tachycardia
Rapid beating of the heart - 100 beats/min or more
Ventricular fibrillation (V-fib)
Rapid, uncoordinated depolarization of ventricular contraction. Results in severe decrease in blood delivery to lungs and tissues
Where is core temperature measured
Rectal, oral, tympanic, esophageal, pulm artery, urinary cath
5 Cardinal Signs of Inflammation
Redness Heath Swelling Pain Loss of Function
post renal dysfxn
Related to obstruction of urine outflow from the kidneys Urine backs up within the ureter and kidneys resulting in a fluid filled kidney (hydronephrosis) -Urine is toxic to cells -Urine stagnation predisposes to secondary infection Etiology: obstructive uropathy Examples: uroliths, prostatic enlargement
A patient is prescribed an angiotensin converting enzyme inhibitor (ACEI) for hypertension. The nurse knows that ACEIs are contraindicated by which clinical condition?
Renal artery stenosis Explanation: ACEI are contraindicated in renal artery stenosis, a condition that relies on the renin-angiotensis system to maintain adequate renal perfusion. ACEI are used clinically in the management of heart failure. Coronary artery disease and diabetes do not contraindicate ACEI.
manifestations urolithiasis
Renal colic associated with passage of stone Obstruction of urinary tract causes hydronephrosis-hydroureter proximal to obstruction
Describe the genetic basis for renal cystic disease, the pathology of the disorder, and its signs and symptoms
Renal kidney disease can be an autosomal dominant or autosomal recessive disease and may involve one or both kidneys. It is more prevalent in males than in females and have been reported in more than 50% of patients over 50.
Chronic obstructive pulmonary disease
Restrictive: (can't breath in) pulmonary fibrosis (scar tissue over lungs) / inhalation disorder / ARDS (viral infection-lung inflammation) Obstructive: (can't breath out) COPD- emphysema, bronchitis / asthma
complications GERD
Result from persistent reflux Hyperemia ( excess blood ), edema, and erosion of the mucosal surface of the esophagus Can lead to strictures of the esophagus, edema, spasms, scar tissue formation during healing Narrowing of the esophagusdysphagia Barrett's** esophagus Normal Squamous mucosa is replaced by columnar epithelium (metaplasia-conversion of cell type) Prolonged gastroesophageal refluxinflammationulceration healing occurs in low pH environmentgastric/intestinal epithelium, which is more resistant to acid Predisposes to adenocarcinoma
Describe factors associated with gas gangrene
Results from infection - cell death plus bacteria, likely from trauma and compound fractures where dirt and debris enter wound.
Clinical Manifestations of sickle cell anemia
Results in hemolytic anemia, severe pain, and organ failure. Pain and organ failure result from blood vessel obstruction, sluggish blood flow, and poor oxygen delivery from the abnormally shaped RBCs.
pathophysiology pleural effusion
Results when hydrostatic pressure in the lung tissue greatly exceeds oncotic pressure, fluid leaks out of the pulmonary capillaries and cells into the pleural space
Cellular Response - Adaptations
Reversible responses which new steady states are achieved and allow the cell to continue to function. Occur in response to normal physiologic stimuli (pregnancy) or pathologic stimuli Adaptations are functional and structural changes that the cell undergoes allowing it to survive and function
Goals of inflammation
Rid the host of initial cause Remove consequence of injury (necrotic and injured cells) Prepare for tissue repair Provides nutrients
iron deficiency adolescent
Risk factors include primarily blood losses with menstruation, followed by low dietary intake and increased demand due to growth.
Explain how diseases such as SLE, diabetes mellitus, and hypertension result in glomerular injury
SLE: glomerular injury is caused by the deposition of immune complexes within the glomerular wall. They also cause tubulointerstitial inflammation because the immune complexes localize in the renal interstitium, walls of interstitial vessels, and basement membranes. Diabetes causes widespread thickening of the glomerular capillary basement membrane and cause lesions to the kidneys. The thickening of the basement membrane is followed by mesangial cell proliferation and impingement on the capillary lumen, which reduces the surface area for filtration. Diabetes can also lead to glomerulosclerosis Hypertenstion causes hyaline to accumulate in the walls of small arterioles and thicken the wall as well as narrow the lumen. It makes the glomerulus smaller and can cause hyaline in the lumen of the nephron.
Secondary Disease Prevention
Screening early for disease (e.g., Pap smear)
Caused by impaired collagen synthesis due to the aging process.
Senile purpura (i.e. Bruising in elderly persons)
Syndrome
Sets of signs and symptoms occur concurrently in some diseases
Cite a definition of tubulointerstitial kidney disease
Several disorders that cause a histologic and functional alteration affecting renal tubular structures and affect the interstitial tissue surrounding the tubules.
pathogen of adult resp distress syndrome
Shock, sepsis, or trauma Shock is the major manifestation Conditions that cause shock lead to Decrease blood pressure Reduced blood flow to the lungs Impaired lung perfusion Damaged alveolar capillaries and lining cells leak fluid and protein into alveolar interstitium leading to alveolar collapse, narrowing of small airways and lung compliance decreases Impairs ventilation and reduces gas exchange
hemolytic anemia features
Shortened RBC life span (<120days) Elevated erythropoietin levels and a compensatory increase in erythropoiesis (increase reticulocytes) Accumulation of hemoglobin degradation products that are created as part of the process of hemolysis
crohns disease
Slowly progressive Recurrent Granulomatous inflammation that can affect any area of the GI tract Most common locale is ileum and cecum Granulomatous lesions may be scattered with normal intervening areas or "skip areas" Submucosal layer is mostly involved Over time the bowel wall becomes thickened and inflexible
renal cyst
Solitary cysts common; not associated with impairment of renal function Multiple cysts
Which of the following statements regarding hepatitis B is INCORRECT? Transmission is primarily by means of blood and body fluids Some infections are acquired by eating incompletely cooked meat from animals infected with the virus. Immunization with hepatitis B surface antigen vaccine confers active immunity against the virus. chronic hepatitis B infections may lead to the development of cirrhosis
Some infections are acquired by eating incompletely cooked meat from animals infected with the virus.
Endothelial Injury causes local and humoral release from platelets and injured tissue. Release of the Vasoconstrictor TXA
Stage 1 - Vessel Spasm
Hemostasis, which refers to the stoppage of blood flow, is divided into five stages. What are the five stages of hemostasis
Stage 1: Vessel Spasm Stage 2: Formation of the Platelet Plug Stage 3: Blood coagulation Stage 4: Clot Retraction Stage 5: Clot dissolution or Lysis Is a multi
What is staging of a tumor cell?
Staging: extent and spread
What are the steps of staging a tumour cell?
Staging: varies with organ, size of primary tumour, lymph node involvement, and metastists?
what is Choledocholithiasis? how do you Dx it?
Stones in the common bile duct -usually originate in the gallbladder but can form spontaneously in the common duct. Dx:it causes Bilirubinuria and an elevated serum bilirubin(jaundice) *Chole don't like this(choledocholithiasis) common stuff(common duct)*
urolithiasis
Stones or calculi may form anywhere in the urinary tract Nephrolithiasis: renal calculus
diagnosis helicobacter pylori
Stool antigen test Endoscopic biopsy for urease testing Serologic test o H. pylori antibodies titers Carbon urea breath test
If untreated, hypertensive emergenciescan lead to _____________________
Stroke or dissecting aortic aneurysm
Disease
Structural or functional change in the body that is harmful to the organism. Specifically, disease occurs when the cellular environment changes to a degree that tissues are no longer able to perform their function optimally-out of homeostasis.
Pathophysiology
Study of abnormal functioning of diseased organs
Cite three theories that are used to explain the formation of kidney stones
Supersaturated urine, an environment that allows the stone to grow, and a nucleus that facilitates crystal aggregation. Supersaturated urine has stone components such as calcium salts, uric acid, and magnesium and it increases that risk for stone formation. The supersaturated urine depends on the pH, solute concentration, ionic strength, and complexation. The greater the concentration, the more likely they are to form stones. In supersaturated urine, stones begin forming with small clusters of crystals and then larger ion clusters from nuclei and can grow at supersaturation levels below their need for creation.
Upper UTI
Suppurative inflammation of the kidney and renal pelvis, caused by Escherichia coli found in the colon; streptococci, and staphylococci are examples of such bacteria -Acute or chronic -Involvement of upper urinary tract from
Composed of Glycoproteins, Glycosaminoglycans and Coagulation factors adsorbed from plasma
Surface Coat - Glycocalyx
What are the treatments of cancer?
Surgery chemotherapy hormone therapy biotherapy targeted therapy Radiation
diagnosis polycystic disease
Suspected by physical examination that reveals greatly enlarged kidneys u/s or CT scans and intravenous pyelogram (IVP) Some form cysts in liver or cerebral aneurysm
Describe the pathogenesis, treatment nfectious mononucleosis
Symptomatic and supportive. Bed rest, analgesics (acetaminophen, NSAIDS) to relieve pain, fever, headache and sore throat. Also, most people recover without incidence.
Symptoms
Symptoms are subjective indications of disease reported by the patient, such as pain, dizziness, and itching
iron deficiency anemia
THE MOST COMMON CAUSE OF ANEMIA Iron in diet replaces these losses- women need more Sources: meat, legumes, liver, eggs, nuts, and beans Animal source is more readily absorbed (heme) Plant sources must be processed by gastric acid - promotes soluble complexes of iron Iron is absorbed in the duodenum ,primarily -Also in stomach, jejunum, ileum, and colon to lesser extent
List three types of exogenous products that cells may be filled up with.
Tattoos product, lead, coal dust
Trace the development of the different blood cells from their origin in the pluripotent bone marrow stem cell to their circulation in the bloodstream.
The Pluripotent stem cell gives rise to the lymphoid stem cell and the myeloid stem cell. These both differentiate into different cells. The Lymphoid stem cell differentiates into T cells, B cells, and natural killer (NK) cells. B cells turn into plasma cells. Meanwhile, myeloid stem cells differentiate into monocytes, granulocytes, megakaryocytes, and erythrocytes. Monocytes turn into monoblasts. Granulocytes turn into eosinophils, neutrophils, and basophils. Megakaryocytes turn into platelets. Erythrocytes turn into reticulocytes. This is what circulates in the blood stream.
Compare the Somogyi Effect to the Dawn Phenomenon.
The Somogyi effect describes a cycle of insulin-induced posthypoglycemic episodes. In people with diabetes, insulin-induced hypoglycemia produces a compensatory increase in blood levels of catecholamines, glucagon, cortisol, and growth hormone. These counterregulatory hormones cause blood glucose to become elevated and produce some degree of insulin resistance. The cycle begins when the increase in blood glucose and insulin resistance is treated with larger insulin doses. The hypoglycemic episode often occurs during the night or at a time when it is not recognized, rendering the diagnosis of the phenomenon more difficult. Research suggests that even mild insulin-associated hypoglycemia, which may be asymptomatic, can cause hyperglycemia in people with type 1 diabetes through the recruitment of counterregulatory mechanisms, although the insulin action does not wane. A waning of insulin's effects when it occurs (i.e., end of the duration of action) causes an exacerbation of the posthypoglycemic hyperglycemia that occurs and accelerates its development. These findings may explain the labile nature of the disease in some people with diabetes. Measures to prevent hypoglycemia and the subsequent activation of counterregulatory mechanisms include a redistribution of dietary carbohydrates and an alteration in insulin dose or time of administration. The dawn phenomenon is characterized by increased levels of fasting blood glucose, or insulin requirements, or both, between 5 am and 9 am without antecedent hypoglycemia. It occurs in people with type 1 or type 2 diabetes. It has been suggested that a change in the normal circadian rhythm for glucose tolerance, which usually is higher during the latter part of the morning, is altered in people with diabetes. Growth hormone has been suggested as a possible factor. When the dawn phenomenon occurs alone, it may produce only mild hyperglycemia, but when it is combined with the Somogyi effect, it may produce profound hyperglycemia. [SOMOGYI EFFECT: HYPOGLYCEMIA IN THE LATE EVENING CAUSES HYPERGLYCEMIA IN THE EARLY MORNING.] [DAWN PHENOMENON: JUST HYPERGLYCEMIA IN THE MORNING.]
Asystole
The absence of all heart electrical activity - Usually reflects a long period of ischemia
Identify the age-related factors that predispose children and elderly persons to chronic kidney disease
The causes in children include congenital malformations, inherited disorders, acquired diseases, and metabolic syndromes. In the elderly, structural and functional changes predispose the aging kidney to CKD. The changes that occur in the elderly including decreased renal mass and volume, a decrease in renal blood flow, decreased ability to concentrate urine and a decrease in the GFR all predispose to CKD.
State the purpose of coagulation
The coagulation process is use to remove clots that are no longer needed. it results in the fibrinogen to be converted to fibrin, creating a meshwork to catch platelets in order to form a clot
Ventricular fibrillation
The disorganized, ineffective quivering of ventricles - No blood is pumped through the body - Unconsciousness occurs within seconds
Contrast and compare the signs and symptoms of Hodgkin lymphoma and non-Hodgkin lymphoma.
The first sign of the disease is often the appearance of enlarged lymph nodes. The two forms of lymphoma are marked by a painless swelling of the lymph nodes. Weight loss Fatigue and anemia - indicative of spread Hodgkin lymphomas are more likely to arise in the upper portion of the body (the neck, underarms, or chest). Non-Hodgkin lymphoma can arise in lymph nodes throughout the body, but can also arise in normal organs. Arise in T and B cells Non-Hodgkin lymphoma, by contrast, can be derived from B cells or T cells. And Hodgkin lymphoma can be derived from the B cells. None-Hodgkin Lymphoma: Spreads unpredictable fashion and None-Hodgkin Lymphoma Hodgkin Lymphoma: Reed Sternberg cell tumor marker Hodgkin Lymphoma: Arise in a single node or chain of nodes and spreads to the next node in a fashionable manner
State the goals for dietary management of persons with chronic kidney disease
The goal of dietary management is to provide optimum nutrition while maintaining tolerable levels of metabolic wastes.
A fib treatment
The goals of treatment for atrial fibrillation include regaining a normal heart rhythm (sinus rhythm), controlling the heart rate, preventing blood clots and reducing the risk of stroke. Electrical shock Medication: -Rhythm Control drugs: help return the heart to normal sinus rhythm -Anticoagulant Medications: Anticoagulant or antiplatelet therapy medications reduce the risk of blood clots and stroke, but they do not eliminate the risk. Pooling of blood in the atria = clots Lifestyle Changes: diet, exercise, smoking
Describe the etiologies, pathophysiology, and acute complications of diabetic mellitus: hyperglycemic hyperosmolar state.
The hyperglycemic hyperosmolar state (HHS) is characterized by hyperglycemi , hyperosmolarity, and dehydration, the absence of ketoacidosis, and depression of the sensorium. Hyperglycemic hyperosmolar state may occur in various conditions, including type 2 diabetes, acute pancreatitis, severe infection, myocardial infarction, and treatment with oral or parenteral nutrition solutions. It is seen most frequently in people with type 2 diabetes. A partial or relative insulin deficiency may initiate the syndrome by reducing glucose utilization while inducing a glucagon-stimulated increase in hepatic glucose output. With massive glycosuria, obligatory water loss occurs. If the person is unable to maintain adequate fluid intake because of associated acute or chronic illness or has excessive fluid loss, dehydration develops. As the plasma volume contracts, renal insufficiency develops and the resultant limitation of renal glucose losses leads to increasingly higher blood glucose levels and an increase in severity of the hyperosmolar state. In hyperosmolar states, the increased serum osmolarity has the effect of pulling water out of body cells, including brain cells. The condition may be complicated by thromboembolic events arising because of the high serum osmolality. The most prominent manifestations are weakness, dehydration, polyuria, neurologic signs and symptoms, and excessive thirst. The neurologic signs include hemiparesis, Babinski reflex, aphasia, muscle fasciculations, hyperthermia, hemianopia, nystagmus, visual hallucinations, seizures, and coma. The onset of HHS often is insidious, and because it occurs most frequently in older people, it may be mistaken for a stroke. [A COMPLICATION OF DIABETES MELLITUS IN WHICH HIGH BLOOD SGUAR RESULTS IN HIGH OSMOLARITY WITHOUT SIGNIFICANT KETOACIDOSIS.]
what is the stage of Alcoholic hepatitis? s/s?
The immediate prognosis correlates with severity of liver cell injury other s/s: fever, hepatic tenderness, pain, anorexia, nausea, ascites, and liver failure. -severe alcoholic hepatitis may have encephalopathy
Explain the vulnerability of the kidneys to injury caused by drugs and toxins
The kidneys are exposed to everything that enters the bloodstream. They are exposed to toxic metabolies because they are involved in metabolic transformations of the drugs. The tubular cells are especially at risk because of their role in concentrating and reabsorbing filtrate. Drugs can cause a decrease in renal blood flow and others form crystals that can obstruct urinary flow in the tubules.
what does the liver do with unconj. bilirubin?
The liver links unconjugated bilirubin in blood (to glucuronide)--> conjugated bilirubin--> bile
role of lymphoid tissue
The lymphatic system has multiple interrelated functions: It is responsible for the removal of interstitial fluid from tissues. It absorbs and transports fatty acids and fats as chyle from the digestive system. It transports white blood cells to and from the lymph nodes into the bones
Describe the etiology, pathophysiology, clinical manifestations, and the specific role metabolic syndrome plays in the development of Type II diabetes mellitus: metabolic abnormalities.
The metabolic abnormalities involved in type 2 diabetes include (1) insulin resistance, (2) increased glucose production by the liver, and (3) impaired secretion of insulin by the pancreatic beta cells. Insulin resistance, which can be defined as the failure of target tissues to respond to insulin, predates the development of hyperglycemia. That is, in the early stages of the evolution of type 2 diabetes, insulin resistance is usually accompanied by compensatory beta cell hyperfunction and hyperinsulinemia. In skeletal muscle, insulin resistance prompts decreased uptake of glucose. Although muscle glucose uptake is slightly increased after a meal, the efficiency with which it is taken up (glucose clearance) is diminished, resulting in an increase in postprandial (following a meal) blood glucose levels. In contrast, in the liver, insulin resistance leads to impaired suppression of glucose production with an overproduction of glucose despite a fasting hyperinsulinemia. In fact, the excessive rate of hepatic glucose production is the primary determinant of elevated FPG in persons with type 2 diabetes. Several mechanisms can lead to impaired secretion of insulin by the pancreatic beta cells. These include an initial decrease in beta cell mass related to genetic or epigenetic factors, increased apoptosis or decreased regeneration of beta cells, or beta cell exhaustion due to long-standing insulin resistance. According to one study, beta cell function was reduced by an average of 50% at the time of diagnosis in type 2 diabetes, and progressively decreased resulting in worsening hyperglycemia even when the degree of insulin resistance remained stable.
Trace the process of fibrinolysis.
The process in which the strands of the clot are dissolved. Which involves the action of plasmin to dissolve the clot and allow blood flow to be reestablished and tissue healing to take place. Plasmin digests the fibrin strands and certain clotting factors, such as fibrinogen (I), factor V, factor VIII, prothrombin (II), and factor XII
Defibrillation
The process of shocking the heart with a specialized electrical current to restore normal cardiac rhythms
Lymphocytes
The two types of white blood cells that are part of the body's immune system: B lymphocytes form in the bone marrow and release antibodies that fight bacterial infections; T lymphocytes form in the thymus and other lymphatic tissue and attack cancer cells, viruses, and foreign substances.
If the heart beats to slowly, ________________________.
The volume of blood circulated per minute decreases due to the slow pulse rate
Cite the risk factors and manifestations of renal cell carcinoma.
There has shown to be a correlation between heavy smoking and kidney cancer. Obesity is a risk factor primarily in women, other risk factors are occupational exposure to petroleum products, heavy metals, and asbestos. The risk is increased for those with acquired cystic kidney disease. Manifestations are usually hematuria, flank pain, and a presence of a palpable flank mass. The tumor may reach considerable size before being detected.
Describe the etiology, pathophysiology, clinical manifestations, and the specific role metabolic syndrome plays in the development of Type II diabetes mellitus: insulin resistance.
There is increasing evidence to suggest that when people with type 2 diabetes present predominantly with insulin resistance, the diabetes may represent only one aspect of a syndrome of metabolic disorders. Hyperglycemia in these people is frequently associated with intra-abdominal obesity, high levels of plasma triglycerides and low levels of high-density lipoproteins (HDLs), hypertension, systemic inflammation (as detected by C-reactive protein [CRP] and other mediators), abnormal fibrinolysis, abnormal function of the vascular endothelium, and macrovascular disease (coronary artery, cerebrovascular, and peripheral arterial disease). This constellation of abnormalities often is referred to as the insulin resistance syndrome, syndrome X, or, the preferred term, metabolic syndrome.
If the heart beats too fast, ___________________.
There's not enough time between contractions for the heart to refill completely
How can nutritional imbalances cause cell injury and what are two examples of this?
They predispose cells to injury. predispose to atherosclerosis Iron deficient anemia
causes and effects of increased platelet function
Thrombocythemia and thrombocytosis Reactive thrombocytosis is platelet overproduction in response to another disorder. There are many causes, including acute infection, chronic inflammatory disorders (eg, rheumatoid arthritis, inflammatory bowel disease, tuberculosis, sarcoidosis), iron deficiency, and certain cancers.
Manifestation of thrombocytopenia
Thrombocytopenia signs and symptoms may include: Easy or excessive bruising (purpura) Superficial bleeding into the skin that appears as a rash of pinpoint-sized reddish-purple spots (petechiae), usually on the lower legs. Prolonged bleeding from cuts.
What is used to describe elevations in the platelet count
Thrombocytosis Elevation in the platelet count is above 1,000,000
TB (cont) -- inhaled airborne droplets
Tissue inflammation occurs as bacteria multiply and pulmonary macrophages and WBC's migrate to area WBC can not kill microbes, an immune response occurs which walls off infection and forms a tubercle (granulomatous accumulation of WBC, bacterium and fibrous tissue) Scar tissue forms and bacterium becomes inactive
Prevalence
Total number of individuals with the disease at any given time. Prevalence is more useful for the impact of a chronic illness.
Heat loss
Transferance of blood to surface via circ - radiation - opening of AV shunts - Convection - air currents - Evaporation - sweat, insensible perspiration - Exhalation - Urine/feces - Heat edema - Increased heart rate
treatment peptic ulcers
Treat H. pylori and treat symptomatically Discontinue NSAID use H2 anatagonist, proton pump inhibitors, mucosal protects
What are treatments for multiple Myeloma
Treatment (rapidly changing) Front line therapy - High-dose chemotherapy with autologous stem cell transplantation
Tertiary Disease Prevention
Treatment to reduce disability from disease - ANTIBIOTICS (e.g., chemotherapy)
Describe the treatment measures used in Hodgkin disease and non-Hodgkin lymphoma.
Treatments:Localized radiation Combination - radiation and chemotherapy
True or false: a thromboembolism may cause a blockage at the site of other vital organs
True - Ex: the brain
True or false: angina pectoris does not usually lead to death or permanent heart damage
True - Still a serious warning sign
Which of the following blood vessel layers is composed primarily of smooth muscle cells?
Tunica media Explanation: The tunica media consists primarily of circumferentially arranged layers of smooth muscle cells. The tunica externa is composed of loose connective tissue and the tunica intima of endothelial cells. The endothelium is the lining of the vascular system and is composed of endothelial cells.
Describe the etiology, pathophysiology, and clinical manifestations of Type I diabetes mellitus.
Type 1 diabetes mellitus, which is characterized by destruction of the pancreatic beta cells and accounts for 5% to 10% of those with diabetes, is subdivided into type 1A immune-mediated diabetes and type 1B idiopathic (non-immune-related) diabetes. In the United States and Europe, approximately 90% to 95% of people with type 1 diabetes mellitus have type 1A immune-mediated diabetes. The rate of beta cell destruction is quite variable, being rapid in some individuals (mainly infants and children) and slow in others (mainly adults). Some individuals, particularly children and adolescents, may present with diabetic ketoacidosis (DKA) as the first manifestation of the disease. Others may have modest elevations in FPG that can rapidly change to severe hyperglycemia and DKA in the presence of stress and infection. Still others, particularly adults, may retain sufficient beta cell function to delay onset of clinical diabetes for many years. The destruction of beta cells and absolute lack of insulin in people with type 1 diabetes mellitus mean that they are particularly prone to the development of DKA. One of the actions of insulin is the inhibition of lipolysis (i.e., fat breakdown) and release of free fatty acids (FFAs) from fat cells. In the absence of insulin, ketosis develops when these fatty acids are released from fat cells and converted to ketones in the liver. Because of the loss of insulin response, all people with type 1A diabetes require exogenous insulin replacement to reverse the catabolic state, control blood glucose levels, and prevent ketosis. Diabetes mellitus may have a rapid or an insidious onset. In type 1 diabetes, signs and symptoms often arise suddenly. The most commonly identified signs and symptoms of diabetes are often referred to as the three polys: (1) polyuria (i.e., excessive urination), (2) polydipsia (i.e., excessive thirst), and (3) polyphagia (i.e., excessive hunger). These three symptoms are closely related to the hyperglycemia and glycosuria of diabetes. Weight loss despite normal or increased appetite is a common occurrence in people with uncontrolled type 1 diabetes. Other signs and symptoms of hyperglycemia include recurrent blurred vision, fatigue, paresthesias, and skin infections. [A CHRONIC CONDITION IN WHICH THE PANCREAS PRODUCES LITTLE OR NO INSULIN RESULTING IN HIGH BLOOD SUGAR LEVELS IN THE BODY.]
PEEP
Type of lung therapy for inhalation disorder
imaging studies
Ultrasound, Intravenous pyelography, Radiographs, Computed tomography scans, MRI renal biopsy
Describe factors associated with necrosis
Uncontrolled cell death • Occurs in injured cells • Loss of membrane integrity: cells swell & rupture with release of products • Causes inflammatory response
Bradycardia
Unusually slow beating of the heart - 60 beats/min or less
diagnosis urolithiasis
Urinalysis, blood analysis Radiographs, IVP, or ultrasound Stone analsysis
hemmorrhoids
Varicose veins of hemorrhoidal venous plexus that drains rectum and anus Constipation and straining predispose to development Hemorrhoids can itch and bleed (usually bright red blood, during defacation). Relieved by high-fiber diet rich in fruits and vegetablesresults in large bulky stool that can pass w/o straining
general signs and symptoms of dysfxn
Variety of multisystemic presentation as a result of reduced secretory and excretory functions of the kidney Fatigue, weakness, nausea, constipation, abdominal pain, and confusion Costovertebral angle tenderness is a classic sign of kidney disorder
Compare and constrast vascular stage vs. cellular stage
Vascular - increased blood flow and structural changes Cellular - emigration of leukocytes to site of infection Vascular begins immediately Cellullar - neutrophils don't arrive within 90 minutes
Describe the effect of vascular disorders on hemostasis.
Vascular disorders can lead to weakened and damaged vessel walls due to immune responses or inflammation. It can also cause petechial and purpura of the skin.
3 main components of inflammation
Vascular response: Increased blood flow to the injured area, and the vasculature becomes more permeable Involves arteriole, capillaries, and venules of microcirculation. Cellular response: Movement of leukocytes, predominantly neutrophils and monocytes from the blood into the tissue. Chemical mediators: Activate both the vascular and cellular responses
ventricular fibrillation
Ventricles unable to contract normally, incompatible with life Sometimes occurs after a heart attack Emergency treatment for ventricular fibrillation includes cardiopulmonary resuscitation (CPR) and shocks to the heart with a device called a defibrillator.
Defibrillation may convert arrhythmia caused by _______________
Ventricular fibrillation
__________________ may deteriorate into ventricular fibrillation
Ventricular tachycardia
Lymphocytes, plasma cells
Viral / fungal infection
What are the different types of Hepatitis?
Viral hepatitis Hepatitis A virus (HAV) Hepatitis B virus (HBV) Hepatitis B-associated delta virus (HDV) Hepatitis C virus (HCV) Hepatitis E virus (HEV)
What are three biological agents that cause cell injury?
Viruses Bacteria Parasites
Results in poor collagen synthesis and failure of capillary cells to be cemented together properly, which in turn causes a fragile vascular wall
Vitamin C deficiency
hypocalcemia
Vitamin D is not able to be activated results in decrease absorption of calcium Leads to neuromuscular irritability and seizures PTH is secreted and results in demineralization of bone Increase susceptibility of fractures
Describe the role of vitamin K in coagulation.
Vitamin K is essential for coagulation, because it must be present in order for factors II, VII, IX, and X to function properly. Without it, the clotting factor will be made, but it will be inactive. Therefore the Vitamin K is required.
What Clinical Manifestations is the following? Spontaneous bleeding from the nose, mouth, and gastrointestinal tract; excessive menstrual flow; and a prolonged bleeding time in the presence of a normal platelet count. Severe cases - GI bleeding and joint hemorrhage
Von Willebrand disease: (vWF)
Serous
Watery clear Fluid with a few proteins pushed out of tissue because of plasma going into injury site
Characterize Wilms tumor in terms of age of onset, possible oncogenic origin, manifestations, and treatment
Wilms tumor is a nephroblastoma common in younger children. It usually occurs between 3-5 years and is the second most common malignant abdominal tumor in children. The elements of the tumor resemble normal fetal tissue (blastemic, stromal, and epithelial). It is usually a solitary mass that can occur in any part of the kidney, and is usually sharply demarcated. It usually presents as an abdominal mass and accompanies hypertension. Some children may experience abdominal pain, and/or vomiting. It can be treated by surgery, chemotherapy, and possibly radiation.
Explain the mechanisms of pain and infection that occur with kidney stones
You can develop colicky or noncolicky pain due to kidney stones. Renal colic pain describes pain that accompanies stretching of the collecting system of the ureter. It is manifested by acute, intermittent, and excruciating pain in the flank or upper outer quadrant of the abdomen on the affected side. Noncolicky pain is caused by stones that produce distention of the renal calyces or renal pelvis. It is usually a dull, deep ache in the flank or back that can be mild or intense. It is often made worse by drinking large amounts of fluid. Acute renal colic can lead to urinary tract infections, and needs to be treated with antibiotics if it does.
sickle cell anemia
a genetic disorder (autosomal recessive disease) that causes abnormal hemoglobin, resulting in some red blood cells assuming an abnormal sickle shape Mutation in Beta-globin that leads to red cell distortion, hemolytic anemia and organ damage
prognosis
a prediction of the course of a disease
CBC (complete blood count)
a set of tests that include all WBC, RBC and platelet measurements.
cardiac conduction system
a system of specialized muscle tissues that conducts electrical impulses that stimulate the heart to beat
Eosinophils
a white blood cell containing granules that are readily stained by eosin.
A patient has a large colon carcinoma with a hypochromic (iron-deficiency) anemia. The anemia is probably due to which of the following? a. Chronic blood loss from the ulcerated surface of the tumor b. poor appetite c. Impaired absorption of nutrients caused by the tumor d. Metastases to the liver
a. Chronic blood loss from the ulcerated surface of the tumor
Helicobacter pylori have been implicated as a cause of which of the following gastrointestinal diseases? a. Chronic gastritis b. Barrett's esophagus c. Meckel's diverticulitis d.Regional enteritis (Crohn disease)
a. Chronic gastritis
Which of the following does not predispose to kidney stone formation? a.) Increased concentration of protein in the urine b.)Increased concentration of salts in the urine c.)Urinary tract obstruction d.)Infection of the urinary tract
a.) Increased concentration of protein in the urine
symptoms celiac disease
abdominal pain, diarrhea, flatulence, and fatty, foul smelling stool, weight loss, vitamin and mineral deficiency Linked to development of lymphoma and adenocarcinoma
Neoplasms
abnormal growths of new tissue that are classified as benign or malignant
pulmonary edema
accumulation of fluid around the alveoli that inhibit oxygen transfer Occurs when there is an increase in hydrostatic pressure in the capillary bed of the lungs Most common cause is LVH Presents as respiratory distress, dyspnea, pink frothy sputum Hypoxia leads to stupor and confusion Crackles
formation of platelet plug
activated platelets become sticky and adhere to the defect form a temporary plug
what is the difference Acute and chronic cholecystitis in s/s?
acute: onset of upper right quadrant or epigastric pain -mild fever -anorexia -n/v chronic: vague than those of acute cholecystitis -intolerance to fatty foods -belching -other indications of discomfort. -episodes of colicky pain with obstruction of biliary flow caused by gallstones.
what happens during pancreatitis? acute vs. chronic?
acute: inflammatory condition of the pancreas due to inappropriate activation of pancreatic enzymes causes autodigestion of pancreatic tissue by inappropriately activated pancreatic enzymes. -reversible - caused by viral infections. chronic: progressive destruction of the endocrine and exocrine pancreas -irreversibility of pancreatic function
clot retraction
after coagulation, platelets contract pulling torn blood vessel together, stabilization
IBS
aka spastic colitis or mucous colitis Episodes of cramping abdominal discomfort, loud gurgling bowel sounds, and disturbed bowel function without structural or biochemical abnormalities ◦ Hallmark is abdominal pain that is relieved by defecation Alternating diarrhea and constipation Excessive mucus secreted by colonic mucosal glands Thought to be a result of dysregulation of intestinal motor and sensory function ◦ Associated with psychological and physiological stress
albuminuria
albumin in urine
What happens in Sinusoids?
all the exchange btw Blood from the hepatic portal vein and hepatic artery take place
what are the function of kupffer cells?
also called reticuloendothelial cells -large resident macrophages that are capable of removing and phagocytizing old and defective blood cells, bacteria, and other foreign material from the portal blood as it flows through the sinusoid
perfusion
amount of blood through the pulmonary circulation, eventually providing oxygen to the system while capillaries supply blood to alveoli at a rated of 5L/min
Arachidonic acid
an omega-6 fatty acid derived from linoleic acid
bowel inflammation
any part of intestinal tract Small, large, or both
All myeloid cells affected resulting in anemia, thrombocytopenia, and agranulocytosis
aplastic anemia
clinical manifestations helicobacter pylori
are dependent on both host factors and virulence of microbe o Acute infection Nausea and abdominal pain -may last for days; Usually progresses to asymptomatic chronic mucosal inflammation o Chronic infection Leads to gastric atrophy and peptic ulcers associated with increased risk of adenocarcinoma and low grade gastric lymphoma
signs and symptoms hiatal hernia
asymptomatic heartburn related to gastroesophageal reflux Dull burning ache that may radiate to neck Large paraesophageal hernias can result in difficult, painful swallowing, chest pain, and vomiting.
atrial fibrillation begins in
atria with abnormal focus of electrical activity = atrial myocardial fibers contact haphazardly at a rapid rate The ventricles contract irregularly, leading to a rapid and irregular heartbeat.
P Wave
atrial depolarization spread of impulses from SA node
A 60-year-old male patient has presented to his primary care provider to follow up with his ongoing treatment for peptic ulcer disease. What is the most likely goal of this patient's pharmacologic treatment? a. Promoting hypertrophy of the gastric mucosa b. Inhibiting gastric acid production c. Increasing the rate of gastric emptying d. increasing muscle tone of the cardiac sphincter
b. Inhibiting gastric acid production
All of the following protect against cystitis and pyelonephritis EXCEPT: a. large urine volume b. infrequent urination c. an acid urine d. complete emptying of the bladder
b. infrequent urination
what is hepatitis A virus (HAV) caused and transmitted by? is prevention available ?
benign and self- limited disease caused by a small, nonenveloped, single- stranded ribonucleic acid (RNA) picornavirus. tranmission: fecal-oral route prevention: vaccine A *Hep A and E are vowels that comes from the bowel*
what is the pathway of bile?
bile canaliculi--> common duct--> gallbladder
Lower UTI
bladder and urethra Very common; maybe acute or chronic Most infections are caused by gram-negative bacteria E. coli most common Organisms contaminate perianal and genital areas and ascend urethra
Immature cells
blast crisis
For nephrons to filter blood ...
blood entering into glomerulus need to have high hydrostatic pressure
Hemorrhagic anemias result from
blood loss
antibiotic assoc. colitis
broad-spectrum antibiotics destroy normal intestinal flora C. difficile is non-invavasive and requires disruption of normal flora Allows growth of anaerobic spore-forming bacteria, Clostridium difficile not inhibited by antibiotic taken Colonization occurs by fecal oral route commonly acquired in hospitals,nursing homes ◦ Organisms produce toxins causing inflammation and necrosis of colonic mucosa
treatment asthma
bronchodilators,corticosteroidsinhalers Epinephrine and oral corticosteroids in severe cases
diagnosis IBS
by exclusion ◦ Rule out pathogenic infections, food intolerance, and inflammatory conditions ◦ Thorough history of recurrence of symptoms 12 week duration
A 6-year old boy complained of abdominal discomfort. His mother noted that his face, abdomen, scrotum and legs were very edematous. His urine contained large amount of protein and a few casts. His serum protein and serum albumin were both much lower than normal. Based on the information given above, which of the following is the most likely disorder in this patient? a. pyelonephritis b. obstructive uropathy c. nephrotic syndrome d. nephrolithiasis
c. nephrotic syndrome
primary polycythemia
cancer of erythropoietic cell line in red bone marrow or mutations can be an overproduction of red, white, and platelets
hyperkalemia (K+)
cardiac dysrhythmias and muscle weakness
what is hepatitis B virus (HBV) caused by?
caused by a hepatotropic deoxyribonucleic acid (DNA)-containing Hepadnavirus: -outer envelope -an inner nucleocapsid that contains the viral DNA -viral polymerase that exhibits both DNA polymerase and reverse transcriptase activity
obstructive atelectasis
caused by bronchial obstruction from: - Mucous secretions, tumor, foreign object - Part of lung supplied by obstructed bronchus collapses as air absorbed - Reduced volume of affected pleural cavity Mediastinal structures shift toward side of atelectasis Diaphragm elevates on affected side - May develop as a postoperative complication From decrease of deep breathing and decrease cough due to pain mucous accumulates in bronchi
neurogenic fever
caused by disease or trauma to hypothalamus
Apoptosis differs from necrosis in that necrosis
causes cells to swell and burst, whereas apoptotic cells shrink and condense.
Define hypoxia
cells become deprived of oxygen causing their metabolism and their production of ATP to be interrupted
where do the sinusoids empty into?
central veins--> hepatic vein--> IVC
what is Fetor hepaticus?
characteristic musty, sweetish odor of the breath in the person in advanced liver failure, resulting from the metabolic by-products of the intestinal bacteria.
Vascular response of acute inflammation
characterized by increased blood flow followed by increased vascular permeability and leakage of protein-rich fluid into extravascular tissues
chemical response of acute inflammation
chemotaxis monocytes, neutrophils
diagnostics pleural effusion & thoracentesis
chest rads, CT scan Thoracentesis: relieves pressure and provides fluid for analysis
signs and symptoms of acute gomerulonephronitis
chills and fever, loss of appetite, and a general feeling of weakness, edema, particularly in the face and ankles. +/- costovertebral tenderness
what is chronic viral hepatitis lead to?
chronic liver disease, cirrhosis, and hepatocellular cancer
Chronic ITP
chronic usually arises in women of childbearing age. Can cause thrombocytopenia in infants because ITP is IgG mediated
what is Pancreatic Cancer usually caused by?
cigarette smoking
B12 and Folate are
coenzymes for DNA synthesis Lack of either results in defective nuclear maturation and delay or block in cell division
pleural effusion
collection of fluid within the pleural cavity that compresses lungs and inhibits inflation Fluid may be a transudate, exudate, purulent, lymph, or sanguinous (bloody)
umbilical hernia
common in both sexes loop of bowel protrudes into umbilicus through defect in the abdominal wall
inguinal hernia
common in men; loop of small bowel protrudes through a weak area in inguinal ring and descends downward into scrotum
what are risk factors to Cholelithiasis (gallstones)?
common: -preg. -starvation -rapid weight loss -obesity -Drugs that lower serum cholesterol levels -Native Americans OVERALL:All of these factors cause the liver to excrete more cholesterol into the bile
Morphologic changes
concerned with both the gross anatomic and microscopic changes that are characteristic of a disease
clinical manifestations cystitis
congestion inflammation of bladder mucosa Burning pain on urination- Dysuria= painful or difficulty urinating Desire to urinate frequently Urine contains many bacteria and leukocytes Responds well to antibiotics May spread upward into renal pelvis and kidneys Upper urinary tract infection
treatment adult resp distress syndrome
correct shock Treat underlying condition Improve oxygenation by posit
symptoms urolithiasis
costovertebral angle pain (flank pain) or abdominal pain when stone is high in tract Distinctive pain = renal colic pain when lodged in the ureter, pain radiates to the groin, hematuria, nausea, vomiting, diarrhea
Which of the following statements regarding diverticulosis of the colon is INCORRECT? a. Diverticulum may become infected, causing diverticulitis. b. Ulceration of lining of diverticula caused by fecal material in the diverticula may cause bleeding from the ulcerated diverticulum. c. Low-residue (fiber) diet predisposes to colon diverticula d. Diverticula predispose to colon carcinoma.
d. Diverticula predispose to colon carcinoma.
If a patient complains of burning pain on urination and a desire to urinate frequently, this person should be checked for which of the following conditions? a. pyelonephritis b. cystitis c. hydronephrosis d. both cystitis and pyelonephritis
d. both cystitis and pyelonephritis
All of the following are complications of peptic ulcers EXCEPT: a. anemia b. hemorrhage c. perforation. d. scarring.
d. scarring
sickle cell anemia leads to
damaged organs (heart kidneys, spleen) bone marrow increases erthropoeisis obstruction of blood flow through clumping RBC
Mortality
death rate
Anemia
decrease in O2 carrying capacity of RBC's nReduction in red cell mass
increase ventricular contraction leads to irregularities in ventricular filling time which leads to
decrease in cardiac output This results in a discrepancy between the radial pulse (fewer beats detected) than the number of ventricular contractions heard during auscultation-'pulse deficit'
granuloctyopenia
decrease of peripheral blood granulocytes below lower limit of normal range
Neutropenia
deficiency of neutrophils
Caseous Necrosis
degeneration and death of tissue with a cheese-like appearance
Pathogenesis
development of disease
subacute disease (and example)
disease that is intermediate between acute and chronic EX: subacute sclerosing panencephalitis: a rare brain disease characterized by diminished intellectual function and loss of nervous function
The process of fibrinolysis
dissolves clots
Chemical cell injury
drugs, lead toxicity, mercury toxicity
Describe factors associated with dry gangrene
due to lack of arterial blood supply • Slow spreading • Confined to extremities • Line demarcates normal from diseased tissue • Tissue tends to coagulate.
Reproduction
duplication of cells (normal)
Describe cellular adaptations occurring in dysplasia.
dysplasia - deranged cell growth - r/t cancer (d=deranged=bad), r/t chronic inflammarion and irritation, MAY be reversible.
How does ionizing radiation effect cells?
effects the cell by causing ionization of molecules and atoms By directly hitting the target molecules in the cell, or by producing free radicals that interact with critical cell components It can kill cells, interrupt cell replication, or cause mutations
clinical manifestations chronic renal failure
electrolyte abnormalities (Na+, K+, Ca2+) metabolic acidosis from acid retention hypoalbuminemia glomerular damage proteinuria
vommiting
emesis Sudden and forceful oral expulsion of contents (vomitus) of the stomach ◦ Rids GI tract from noxious agents ◦ Pallor (paleness) and increased salivation precede vomiting
what is the stage of Cirrhosis?
end result of repeated bouts of drinking-related hepatocyte injury and regeneration. Intrahepatic cholestasis--> Scar tissue partially blocks sinusoids and bile canaliculi-->primary biliary cirrhosis and impaired liver
pathophys asthma
episodes of spastic reactivity in bronchioles Allergen trigger immune system causing brochial constriction, inflammation, and increase in size and number of goblet cells Allergens interact with mast cells coated with IgE antibody causes release of histamine and leukotrienes that induce bronchospasm and inflammation Eosinophils are attracted to area Bronchoconstriction + bronchial edema + viscous mucus with thickening of the basement membrane Multiple episodes promote airway remodeling causing proliferation of respiratory epithelium and hypertrophy of respiratory smooth muscle Leads to fixed airway obstruction Epithelial cell injury exposes the airway to triggers for hyperreactivity resulting in more frequent episodes Clinical presentation: wheezes, prolonged exhalations, dyspnea, cough, accessory muscles used during breathing The wheezing sound results from air passing through the narrowed tubes.
what is the brief patho for Alcoholic hepatitis?
excessive alcohol intake--> inflammation and necrosis of liver cells--> liver cell failure--> Jaundice
Describe the mechanisms whereby physical agents such as extremes of temperature produce cell injury.
exposure to low intensity heat causes cell injury by inducing vascular injury,accelerating cell metabolism, inactivating temperature-sensitive enzymes, and disrupting cell membrane. Exposure to cold increases blood viscosity and vasoconstriction and may lead to hypoxic tissue injury
Describe the mechanisms whereby physical agents such as electrical forces produce cell injury.
extensive tissue injury and disruption of neural and cardiac impulses
what are s/s of chronic viral hep?
extremely variable and not predictive of outcome. -some ppl only have persistent elevation of serum aminotransferases -frequently reported s/s: fatigue, abdominal discomfort, and joint or muscle ache -However, even asymptomatic persons with normal serum aminotransferase levels are at risk for developing liver damages
aplastic anemia
failure of blood cell production in the bone marrow Etiology: specific marrow suppressants associated with infections, chemotherapy, radiation, or drug reactions, but can be idiopathic or autoimmune.
techycardia
fast heart rate
clinical presentation : pneumonia
fever, tachypnea, use of accessory muscles with breathing, tachycardia, possible cyanosis, cough - a productive cough accompany this disease. - Oxygen exchange is impaired, causing difficulty breathing. - Diagnostic test - Physical exam-auscultation-crackles and abnormal breath sounds CBC = elevated WBC's - chest radiographs - pulse oximetry and ABGs - Culture and Sensitivity on sputum sample
hypervolemia
fluid imbalance BP regulation
Hematopoiesis
formation of blood cells takes place in red bone marrow in axial skeleton, femoral, humeral proximal head, flat bones
what is Hepatorenal syndrome?
functional renal failure -progressive azotemia -increased serum creatinine levels -oliguria contribute to hepatic encephalopathy and coma
What are the lobules of the liver?
functional units of the liver
Clinical Manifestations of Thrombocytopenia
generally asymptomatic bleeding (mucosal or cutaneous) first symptom epistaxis (nose bleed), petechiae, purpura, ecchymoses hemorrhage: major complication DIAGNOSTICS -Platelet counts less than 20,000/mm3 -Abnormal platelet size and appearance -Anemia from hemorrhage Treatment -corticosteroids to suppress immune system Splenectomy-site of antibody coated platelet destruction
In hypoxic situations, cell adapts by switching to
glycolysis (anaerobic respiration) to make ATP Or breaking down proteins and fats if glucose levels are low
A marked decrease in the number of granulocytes cells
granulocytopenia
Folic Acid
green leafy vegetables and animal protein foods
etiology pleural effusion & pleuritis
heart failure, severe pulmonary infection, or neoplasm pleuritis = inflam of pleura
what is viral hepatitis?
hepatic infections due to a group of viruses known as hepatotropic viruses that have a particular affinity for the liver -hepatitis A: HAV -hepatitis B: HBV -hepatitis C: HCV -hepatitis D: HDV -hepatitis E: HEV
All of the following conditions may lead to hepatic cirrhosis, EXCEPT: excessive alcohol intake hemochromatosis hepatitis A viral infection chronic hepatitis caused by hepatitis C virus
hepatitis A viral infection
What are free radicals?
highly reactive chemical species with an unpaired electron in the outer orbit of the molecule
inflammatory mediators
histamine, prostaglandins, and bradykinin
asthma (lower)
hyperactive airway disease Chronic inflammatory disorder that causes reversible bronchial constriction
Describe cellular adaptations occurring in hyperplasia.
hyperplasia - # cells in organ increase, process reversible when stimulus stops - ex. endometriosis, warts
Describe cellular adaptations occurring in hypertrophy
hypertrophy - increase cell size, increase in functional components of cell, r/t hormonal stimulation, increased use, compensation for organ loss.
diagnosis
identification of a disease
pathogenesis MWS
inadequate relaxation of the esophageal sphincter during vomiting resulting in stretching and tearing of the esophageal junction during expulsion of gastric contents Can lead to upper gastrointestinal bleeding 10% of cases presenting with hematemesis Usually heal on own
path gen neonate resp. distress syn
inadequate surfactant in lungs Alveoli do not expand normally during inspiration Tends to collapse during expiration Increased permeability of pulmonary capillaries Fluid rich fibrinogen leaks out from pulmonary capillaries causing clotting and adhesion of membranes; cover alveolar septa impeding gas exchange
diarrhea
increased fluidity of fecal matter ◦ Caused by increased colonic fluid volume, which increases distention and activates the defecation reflex
what is Portal hypertension?
increased resistance to flow in the portal venous system and sustained increase in portal venous pressure-->body builds collate circulation bc liver cannot filter and it starts to build inflammation.. salt and water retention by the kidney and increase in capillary pressure--> fluid acummulation -->increased pressure in peritoneal capillaries--> ascites(amount of fluid in the peritoneal cavity is increased) gradual obstruction of venous blood flow in liver: the pressure in the portal vein increases-->Portosystemic shunting of blood--> -> Development of collateral channels/circulation-->esophageal varices, gastric varices, and caput medusa ->shunting of ammonia and toxins from the intestine into the general circulation->Hepatic encephalopathy Splenomegaly: shunting of blood into the splenic vein--> Spleen enlarges progressively -->enlarged spleen= increase blood elements and development (hypersplenism)--> decrease in the life span of all the formed elements of the blood and a subsequent decrease in their numbers-->anemia, thrombocytopenia, and leukopenia--> bleeding OVERALL: portal hypertension causes -ascites from fluid acumm, -Portosystemic shunts from obstruction -bleeding from enlarged spleen *When I bleeding(SE), I see(spleen) the fluid accumulate(SE) and I have the obstruct(SE) the bleeding by shuting the wound from application(ascites)*
complications of pancreatitis
infection cities
diverticulitis & complications
inflammation incited by bits of fecal material trapped within outpouchings Complications: inflammation, perforation, bleeding (ulcer formation), scarring, abscess in pelvis
enteritis
inflammation of any part of the intestinal tract
Acute bronchitis (lower)
inflammation of bronchi and bronchioles Etiology: bacteria, viruses, inhalation of chemicals or gases Pathophysiology: bronchial tissue cells are irritated and mucous membrane become edematous leading to decrease function of mucociliary apparatus Air passages become obstructed with mucus and WBCs ----leads to productive cough Clinical presentation: sore throat nasal discharge, productive cough, +/- fever, muscle ache -->Wheezing
sinusitis (upper)
inflammation of paranasal sinuses infection (bacteria, virus, fungi) or allergy obstructs sinus drainage from accumulated fluid and edema caused by the inflammatory process fluid accumulation predisposes to bacterial growth symptoms: headache, facial pain or pressure over sinus area, purulent nasal discharge, fever, ear pain, decreased sense of smell, sore throat Bending forward causes increase in head ache pain
pathophys: pneumonia
inhalation of droplets containing pathogen enter in upper airway and gain entry into lungs Pathogens adhere to epithelium and stimulate inflammatory reaction Vasodilation with attraction of neutrophils out of capillaries and into air spaces. Excessive stimulation of goblet cells increase mucous Chronic bronchitis may be a complication of another respiratory infection, or can result from long-term environmental exposure -----Neutrophils phagocytize microbes ----Crackles are heard during auscultation; result from alveoli opening against exudative fluid -----Layer of edema and exudate at the capillary alveoli interface hinders gas exchange leads to hypercapnea, hypoxemia Affected lung portion becomes relatively solid (consolidation) Exudate may reach pleural surface causing irritation and inflammation
what are s/s of hepatocellular cancer?
insidious in onset and masked by those related to cirrhosis or chronic hepatitis initial symptoms include weakness, anorexia, weight loss, fatigue, bloat- ing, a sensation of abdominal fullness, and a dull, aching abdominal pain. -often far advanced at the time of diagnosis bc of similar initial s/s
micro analysis
inspection for white blood cells, bacteria, red blood cells, or collections of cellular debris, crystals, and cast Red blood cells and WBC's up to 5/HPF can be normal Increased RBC = hematuria Increased WBC = pyuria Crystals can be associated with renal calculi Casts are substances secreted in the tubules and retain the shape of the tubule Can be benign or associated with kidney disease
Define intracellular accumulations and cite four sources
intracellular accumulations represent the buildup of substances that cells can not immediately use or eliminate.
cardiac arrhythmia
irregular heartbeat
Arrythmias are
irregular heartbeats caused by damage to part of the conduction pathway, or by an ectopic focus
chronic renal failure
irreversible progressive disease, generally ending in death Kidney is unable to excrete waste products or control blood volume Kidneys can maintain normal function until about 75 % become nonfunctional Few symptoms appear until >75% damage Disease develops over months to years 90 - 95% of nephrons affected
where is the pancreatic duct?
it joins with the bile duct and empties into the duodenum
pernicious anemia
lack of mature erythrocytes caused by inability to absorb vitamin B12 into the bloodstream
Ulcerative colitis
large intestines and rectum Inflammation is limited to mucosa, bowel not thickened unlike in Crohn's Inflammatory process tends to be continuous Leads to pinpoint mucosal hemorrhages, which may become necrotic and ulcerate Frequently begins in rectal mucosa and spreads until entire colon is involved
Elevated circulating blast count (usually 100,000 cells/μL) Increases blood viscosity
leukostasis
what do the hepatic cells do?
lie along the sinusoids -pick up chemicals from blood -modify blood's composition (Kupffer cells).
Platelet are made in the
liver kidney smooth muscle bone marrow
what is Alcoholic Liver Disease?
liver and kidney failure Alcohol Metabolism -Two Pathways (ADH & MEOS) -Production of Acetaldehyde toxic effects Fatty liver (steatosis)-this stage is reversible-->Alcoholic hepatitis -->Cirrhosis(end result)
what is the treatment of chronic viral hepatitis?
liver transplantation in adults
what do serum protein levels(albumin) and prothrombin time (i.e., synthesis of coagulation factors) indicate about the liver?
liver's synthetic capacity is reflected in measures protein levels(albumin) and prothrombin time USUALLY Liver injury -decreased production and reduced serum levels of albumin -decrease prothrombin time=Deficiencies of fibrinogen and coagulation factors (II, VII, IX, and X) may occur
anorexia
loss of appetite precedes nausea
pulmonary embolism
lot that has traveled to the pulmonary arterial circulation and caused obstruction of arterial blood flow through the lungs Most do not demonstrate symptoms; common cause of death
A 33-year old man had been drinking heavily for many years and was in the habit of consuming about 1 qt. of liquor per day. Recently, he had noticed weakness and a loss of appetite. The physical examination revealed that he was slightly jaundiced. His liver was enlarged. Which of the following laboratory findings would be expected in this case? low serum albumin levels low bilirubin levels low serum ALT low serum AST
low serum albumin levels
Describe the role of the lymphoid tissues.
lymphocyte production for immune response. Lymphoid tissue makes up the lymph nodes, thymus, spleen, and bone marrow. In the lymph nodes, lymphoid tissue makes up fibrous capsules and radiating trabeculae which provides a supporting structure, and a delicate reticular network contributes to internal support.
B12
meat, liver, and foods rich in animal protein Used for structural and functional integrity of nervous system (myelin breakdown); deficiency may lead to neurologic disturbances Vitamin B12 in food combines with intrinsic factor in HCL and enzymes Intrinsic factor is secreted by gastric mucosal cells Vitamin B12 intrinsic factor complex absorbed in ileum Stored in the liver and used in the bone marrow and other tissues for cell growth and maturation
What are the physical agents responsible for cell and tissue injury?
mechanical forces extremes of temperature electrical forces.
treatment of gallstone
meds that break it down removal of gallbladder
Describe cellular adaptations occurring in metaplasia
metaplasia - adult cell replaced by another type of adult cell, ex. chronic inflammation from smoking changes cell types in airways.
what are the s/s of pancreatitis?
mild with minimal organ dysfunction to severe and life-threatening: - fever -tachycardia -hypotension -severe abdominal tenderness respiratory distress -abdominal distention -s/s of diabetes mellitus and the malabsorption syndrome (e.g., weight loss, fatty stools steatorrhea) become apparent -gallstones -hyperlipidaldemia -fluid accumulation(swelling) -elevate enzymes levels(amlase and lipase)
types of white blood cells
monocytes, lymphocytes, and granulocytes
how long is the viral serology of chronic viral hep?
more than 6 months duration
what is hepatocellular cancer?
most common form of liver cancer
etiology of pneumonia
most important, serves as a guide for treatment - Bacteria, viruses, fungi, Chlamydia, Mycoplasma, Rickettsia - Pneumonias are often qualified using the specific organism that is causing the disease Example: staphlococcus pneumonia - Pneumonia can be caused by a variety of microorganisms, and it may affect different areas of the lungs.
etiology asthma
multifactorial; gene mutation and environmental factors Allergies are most common cause -allergens like dust, mold, pollen, animal dander, and various foods Viral infections are common triggers in children Gastroesophageal reflux increases susceptibility NSAIDs have been shown to trigger attacks Occupational exposure Farming, painting construction , landscaping Exercise induced bronchospasms occur during vigorous activity in some Psychogenic factors such as anxiety are frequently associated with an asthma attack. A tense situation or an emotional experience can trigger attack
Differentiation Neoplasia
neoplastic cells resemble their normal counterparts
Abnormally low number of neutrophils - less that 1500/μL Benign ethnic neutropenia. Seen in African descent and other Middle East ethnics - without predisposition to infections And Role of gene encoding the Duffy antigen receptor for chemokines - Provides protection from malaria.
neutropenia
colitis
nflammation of colon
functional disease
no morphological abnormalities yet body functions are profoundly disturbed ex.) Hypertension: Increased blood pressure noted on P.E. Over time, structural changes occur in blood vessels and then in the form of end-organ damage, such as necrosis of renal tissue. Long-standing hypertension causes arteriosclerosis of the renal artery, which reduces blood flow to the kidneys and damages them.
mortality rate
number of deaths from a disease in relation to the population in a given time
pharmacological treatment GERD
o Antacids o Histamine-2-receptor antogonist Inhibit gastric acid secretion o Proton pump inhibitors inhibit the gastric proton pump
clinical manifestations acute gastritis
o Asymptomatic o C/O Heartburn or 'sour' stomach o Vomiting o Abrupt violent gastric distress with vomiting 1 - 6 hours after ingestion of contaminated food with enterotoxins (e.g. staphylococcal enterotoxins) o May present with massive hematemesis ("coffee grounds"), melena, and fatal blood loss
treatment GERD
o Avoidance of predisposing factors o Decrease size of meals o Eat sitting up instead of lying down o Avoid lying down for several hours after a meal o Bending should also be avoided (increases intra-abdominal pressure) o Avoid ingestion of foods that reduce LES tone Caffeine, chocolate, fats, alcohol, and smoking o Sleep with head elevated o Weight loss
chronic gastritis
o Characterized presence of chronic inflammatory changes and occurs slowly over time o Leads to atrophy of glandular epithelium of stomach and metaplasia
diagnostic testing acute gastritis
o Endoscopy o Contrast radiographs o Helicobacter pylori test o Self limiting with complete healing in several days of removal of inciting agent-most common scenario
pathogenesis helicobacterpylori
o Grow within layer of mucus covering epithelial cells o Able to move through the mucosa because of their multiple flagella o Produce urease that decomposes urea, a product of protein metabolism, into ammonia o Ammonia neutralizes gastric acid allowing organisms to flourish o Produce enzymes and toxins that break down mucus layer o Interferes with local protection of the mucosa and produces an inflammatory response
signs / symptoms of GERD
o Heartburn o Severe and occurs 30 - 60 minutes after a meal o Is worsened with bending at waist or when lying down o Usually relieved by sitting up o Antacids give prompt relief (transient) o Usually at night o Chest pain Epigastric region or retrosternal area that may radiate to throat, shoulder, or back Confused with Angina
predisposing factors of GERD
o Hiatal hernia o Weakened lower esophageal sphincter o Food or alcohol ingestion, cigarette smoking that lower LES pressure o Increased abdominal pressure (obesity or pregnancy) o Delayed gastric emptying
diagnosis GERD
o History of symptoms of reflux o Selective use of the following tests o Radiographic studies o Contrast medium (e.g. barium) o Endoscopy o Ambulatory esophageal pH monitoring
etiology acute gastritis
o Idiopathic o Commonly associated with local irritants: o Alcohol: a gastric irritant o Bacterial toxins o Non-steroidal anti-inflammatory drugs (NSAID) aspirin**, ibuprofen, naproxen **most common**
acute gastritis
o Inflammation of the gastric lining o Results from sudden disruption of the normal barrier o Can be from increased acid secretion, decrease bicarbonate buffer, decreased bloodflow, disruption of mucous lining, direct damage to epithelium
helicobacterpylori
o Small, curved, gram-negative organisms that colonize surface of gastric mucosa o Spreads via person-to-person through close contact (mouth - mouth) and fecal-oral route o Possible environmental reservoirs
Describe the mechanisms whereby physical agents such as mechanical forces produce cell injury.
occurs as a result of body impact with another object (fractured bones, injured blood vessels, teared tissue, etc..)
what age is usually pt. with pancreatic cancer?
ovre 50
reagent strips(dipsticks)
pH should be close to neutral -Vary from acid to basic -Diet can change pH -Specific gravity should be between 1.001 (dilute) and 1.030 (concentrated Measurement of the dissolved materials in urine --distilled water=1.000 --indicator of concentrating ability of the kidneys All other tests should be negative
Treatment of Heart Block
pacemaker
what are the s/s of Pancreatic Cancer?
pain:dull epigastric pain often accompanied by back pain, often worse in the supine position, and relieved by sitting forward. jaundice: causes pruritus(iching) weight loss Later more serous: Migratory thrombophlebitis (deep vein thrombosis)
what is the Fourth leading cause of death in the United States?
pancreatic cancer
non axial
paraesophogeal Portion of the stomach enters through a widened opening Hernia Progressively enlarges and can lead to the entire stomach within the thoracic cavity ; require surgery
expiration
passive process
what is cholestasis?
pathologic condition of impaired bile formation and bile flow, leading to accumulation of bile pigment in the parenchymal tissues of the liver.
Hematocrit
percentage of blood volume occupied by red blood cells
status asthmatics
persistent bronchoconstriction that endures despite attempts to treat with medication Pulmonary gas exchange is dimished by the uneven distribution of ventilation resulting from generalized bronchoconstriction Leads to dramatic decrease in arterial oxygenation Total aveolar ventilation fails, cyanosis, and CO2 retention Can be fatal
what is a hep carrier?
person does not have symptoms but harbors the virus and can therefore transmit the disease 2 types of carriers: -there are healthy carriers who have few or no ill effects -there are those with chronic disease who may or may not have symptoms.
urinalysis
physical description of urine (i.e. color, clarity, smell), biochemical, and microscopic analysis Normal physical description Odorless Foul smell from infections Sweet smell from diabetes mellitus clear to slightly hazy, yellow to amber color
Three types of cells of the hematopoietic system
platelets, red blood cells, and white blood cells.
Thrombocyte (basic)
platelets; coagulation (clotting); if lower than normal=thrombocytopenia; if low problems=bleeding (poor clotting)
kidney dysfxn
pre renal, intrarenal, post renal
what is Dx of hepatitis?
presence of antibody/antigen in serum
Coagulation
process of blood clotting
ventilation
process of inspiration and expiration of air through the pulmonary airways In normal lung function, the alveoli receeive air at rate of 4L/min
Substances necessary for hematopoiesis
protein, vitamin B12, folic acid, iron
hiatal hernia
protrusion or herniation of the stomach through the esophageal hiatus of the diaphragm 1.axial 2.nonaxial
diagnosis/treatment urinary obstruction
pyelogram, CT san relieve obstruction
Causes of aplastic anemia.
radiation, drugs, hepatitis, neoplastic infiltration of bone marrow
what are the s/s of cirrhosis?
ranging from asymptomatic hepatomegaly to hepatic failure portal hypertension: increase pressure in the liver causes splenomegaly, ascites, and portosystemic shunts (esophageal varices, gastric varices, and caput medusae) splenomegaly: decreased clotting factors and thrombocytopenia
Atrial Flutter
rapid rate of atrial depolarization
Proliferation
rapid reproduction of cells (abnormal)
atrial fibrillation
rapid, random, ineffective contractions of the atrium
Ventilation-perfusion ratio (V-Q ratio)
ratio of the amount of air reaching the alveoli to the amount of blood reaching the alveoli Ideal ratio occurs when ventilation and perfusion are equal or matching V/Q ratio of 4:5 or 0.8 Ventilation - perfusion mismatching occurs when air cannot flow into alveolus or when blood flow around alveolus is altered - Common cause is pulmonary embolus-clot prevents blood flow to the alveolus and gas exchange cannot occur -Dead space refers to an area with no perfusion -Shunt refers to an area with not ventilation
Erythrocyte (basic)
red blood cell; transport O2; if lower than normal=anemia (erythrocytopenia); if low problems=hypoxia, fatigue, activity intolerance
how does Excessive destruction of RBC cause jaundice?
red blood cells are destroyed at a rate in excess of the liver's ability to remove the bilirubin from the blood
Five cardinal signs of acute inflammation
redness, heat, swelling, pain, loss of function
hemolytic anemia
reduction in red cells due to excessive destruction Hereditary (sickle cell anemia) Acquired (autoimmune)
What is ultraviolet radiation?
represents the portion of the spectrum of electromagnetic radiation just above the visible range
what is the Tx of hepatitis?
rest activity as tolerated nutrition hydration
clinical manifestations IBD
result of activation of inflammatory response that causes nonspecific tissue damage Symptoms are periodic with diarrhea and cramping, weight loss, and fecal urgency May develop intestinal blockage May have joint, eye, and skin inflammation during periods of activity
Acute ITP
rises in children with a viral infection. usually resolves in weeks
The Bohr effect describes
shift to the right in the oxygen-hemoglobin dissociation curve
Asymptomatic
showing no symptoms of disease
Clinical manifestation
signs and symptoms or evidence of disease Diagnosis: Patient evaluation and Laboratory test Clinical course and outcome: treatment and prognosis
what is the issue with pancreatic cancer?
silent-->don't regnoize it to its too late Usually metastasized by the time of diagnosis
axial hernia
sliding Characterized by a bell shaped protrusion of the stomach above the diaphragm Common and of no significance in asymptomatic individuals
etiology -- COPD
smoking is the major cause, environmental exposures to chemicals, dusts, and secondhand smoke • Combination of genetic susceptibility and environmental factors
types urolithiasis
staghorn calculus Most are Small stones Some can cause damage to ureter mucousa and cause hematuria Some become impacted in the ureter and need to be removed- Many can be passed and excreted in urine Bladder stones Usually secondary to infection and urine stasis
Progenitor cells form
stem cells and become committed to a given cell line
release of erythropoietin
stimulates bone marrow to synthesize RBC
normal anatomy of stomach
stomach lining prevents against injury from acid secretion ◦ Gastric mucosal barrier: mucous layer, HCO3- secretion (alkaline microenvironment), tight junctions
diagnosis and treatment
stool culture, toxin in stool stop antibiotic treatment; give vancomycin or metronidazole (inhibits growth of organism)
treatment
stop NSAIDS Acid reduction (H2 blockers, proton pump inhibitors) Used as first line medication in trauma pts Antacids that neutralize stomach acid.
what is the function of the gall bladder?
store bile
complications urinary obstruction
structural damage , stone formation; infections from stagnation of urine, This can lead to increase in the degree of obstruction
Pathology
study of disease
acute renal failure (pre renal, intra, post)
sudden pre renal: *impaired blood flow to kidneys (most common cause) CAUSES SHOCK* Pre - renal and is reversible with prompt treatment Hypovolemic, cardiogenic, septic shock will result in decrease perfusion Leads to acute tubular necrosis (ATN) Intrinsic nephrotoxic drugs (NSAIDS, aminoglycosides) or poisons (ethylene glycol) Leads to ATN trauma Infections (pyelonephritis) post renal??
What can UV radiation cause?
sun burn and increase the risk of skin cancers.
treatment cysts
supportive and delay progression;kidney transplant
nausea
symptom The awareness of an unpleasant sensation referred to the epigastrium and abdomen ◦ Usually precedes vomiting
what is chronic viral hepatitis?
symptomatic, biochemical, or serological evidence of continuing or relapsing disease that has persisted for more than 6 months
act of vommiting
taking a deep breath, closing airways, contraction of abdominal muscles and diaphragm along with opening of the lower esophageal sphincter The vomiting center in the medulla oblongata initiates the vomiting reflex reflex in response to sensory input from the walls of the GI tract, abdominal viscera, cerebral cortex, and vestibular apparatus
Common causative organisms of urinary tract infection
the percentages of infections caused by different bacteria in outpatients and hospital inpatients are shown below *Escherichia coli* is by far the most common isolate in both groups of patients
Respiration
the process of exchanging gases between the atmosphere and the body cells -inspiration and expiration
what are s/s of viral hep?
the prodromal: abrupt to insidious, with general malaise, myalgia, arthralgia, easy fatigability, and severe anorexia out of proportion to the degree of illness -Gastrointestinal symptoms: N/V, diarriah, consipiation. -right side abd pain - Chills and fever preicterus period - Serum levels of AST and ALT show variable increases during the preicterus phase icterus period(within 5 to 10 days) - rise in bilirubin that accompanies the onset of the icterus or jaundice phase of infection -become worse with the onset of jaundice, followed by progressive clinical improvement. - Severe pruritus and liver tenderness convalescent period. - increased sense of well-being, return of appetite, and disappearance of jaundice
hemodynamics
the science of the blood flow through the circulation
etiology of disease
the study of the causation of disease 1.)Genetic etiology-genes are responsible for some structural or functional defectInherited from parents/grandparents◦ 2.) Developmental (CONGENITAL) Etiology-born with disease Example-fetal alcohol syndrome 3.)Acquired -other factors encountered later in life
if your pt has elevated Alanine transaminase (ALT) and Aspartate transaminase (AST), what does that mean?
there are parallel rises in ALT and AST - indicate liver injury -The most dramatic rise is seen in cases of acute hepatocellular injury, as occurs with viral hepatitis, autoimmune hepatitis, hypoxic or ischemic injury, acute toxic injury, or Reye syndrome.
Severe COPD...
there is poor ventilation and hypoxia: In areas of poor ventilation, hypoxia stimulates pulmonary arterial vasoconstriction called pulmonary hypertension Leads to increase pulmonary arterial resistances against R ventricle right ventricular hypertrophy and eventual failure This is called "cor pulmonale"
arrythmias are not big deal unless what
they affect cardiac output
How do biologic agents differ from other injurious agents?
they are able to replicate and can continue to produce their injurious effects
what causes Cholelithiasis (gallstones)
thickened gallbladder mucoprotein with tiny trapped cholesterol crystals(slugde): -abnormalities in the composition of bile -stasis of bile -inflammation of the gallbladder.
complications crohn disease
thickening can lead to blockage Fistula (tube like passages) form connections between different sites of intestinal tract or other organs Abscess formation
How does radiation exert its beneficial effects on cancer?
thorugh ionizing radiation to the affected cells. This causes cellular damage when the rays are absorbed into the tissue. It produced fast acting electrons interact with free or loosly bonded electrons and produce free radicals that interact with critical cell componets. It can immediatly kill cells, delay or halt cell cycles and or damage the nucleus resulting in cell death.
S-T segment
time at which ventricles are fully depolarized
PR interval
time for depolarization to pass from atria to ventricles via AV bundle
what is the process of the liver to degrade protein and eliminate ammonia?
transamination: an amino group (NH2) is transferred to an acceptor substance--> amino acids can participate in the intermediary metabolism of carbohydrates and lipids-->r emoval of the amino group and a hydrogen atom from an amino acid. This yields ammonia (NH3)--> removed from the blood by the liver and combined with carbon dioxide to form urea-->excreted by the kidneys. OVERALL: dietary protein gets broken down to amino acids and ammonia--> ammonia gets turned into urea--> kidneys
what is hepatitis B virus (HBV) transmitted by? is prevention available ?
transmitted through: -inoculation with infected blood or serum: transfusion or administration of blood products(IV, IM) -by oral or sexual contact(body secretions): unprotected sexual intercourse Prevention: -routine screening methods -vaccination OVERALL: transmitted through blood, saliva and serum. Prevented by vaccine and screening
malignant neoplasm
tumor that invades surrounding tissue and is usually capable of metastasizing; can be located in any organ or tissue in the body
stress ulcers
ulcers that develop in relation to major physiologic stress risk factors: Trauma, sepsis, Acute respiratory distress syndrome, large surface area burns, cardiovascular shock ◦ Typically they are multiple and smaller than peptic ulcers ◦ Mucosal disruption is linked to mucosal ischemia that develps secondary to widespread vasoconstriction response or hypotension related to circulatory shock Decrease mucosal blood flow leads to damage to the mucosa and gastric acid is able to produce widespread surface erosions
nonionizing radiation
ultrasound, microwave UV -sunburns, increase risk of skin cancer (damages DNA) ROS are formed
etiology IBD
unknown; multifactorial- evidence of genetic predisposition, autoimmune, microorganisms
diagnostics cystitis
urinalysis; dipstick, cytology, and C & S -increase WBC, RBCs
staghorn calculus
urinary stones that increase in size to form large branching structures that adopt to the contour of the pelvis and calyces
uremia
urine in blood
Common Lab Tests
urine, pap, blood tests, radiography Diagnostic: cat scan, MRI PCR, biopsy
What are some manifestations of paraneoplastic syndrome in the hematologic system?
venous thrombosis nonbacterial thrombolytic endocarditis
QRS wave
ventricular depolarization Impulses travel through the ventricles Ventricles contract after QRS
T Wave
ventricular repolarization
Fibrillation
very rapid and uncoordinated contractions
Describe the formation of the platelet plug
when a vessel is injured, a clotting factor binds to the platelet receptors, which cause the adhesion of the platelets to the exposed collagen fibers. As they adhere they are activated and release ADP which attract additional platelets, leading to aggregation
secondary polycythemia
when less O2 is available (high altitude) or when EPO production increases increased Erythropoietin production Etiology-- •Emphysema, • pulmonary fibrosis, • congenital heart disease; •increased erythropoietin production by renal tumor •High altitude
end result kidney failure
when renal excretion drops to about 10% of normal Waste products (urea and creatinine) accumulate to a poisonous level in the blood Urea is a small molecule and can enter into RBCs and causes hemolysis leads to anemia (also from failure of EPO production) Urea is converted to ammonia, which acts as an irritant in the gastrointestinal tract to produce nausea, vomiting, and diarrhea. The nervous system is affected; vision becomes dim, mental ability is decreased, and convulsions or coma may ensue. Low protein diets are recommended because remaining healthy nephrons have difficulty removing nitrogenous wasted from blood
Leukocyte (basic)
white blood cell; defend against and fight infection; if lower than normal=leukopenia; if low problems=increased risk of infection
Contain fibrinogen, coagulation factors, plasminogen, plasminogen activator inhibitor, and platelet-derived growth factors
α-granules
Important role in platelet aggregation, blood coagulation and initial phase of vessel repair
α-granules
The Central Part of the platelets contain of the Mitochondria, what are the 2 types of Mitochondria
α-granules and δ-granules (dense granules)
Contain adenosine diphosphate (ADP), ATP, ionized calcium, serotonin, and histamine
δ-granules (dense granules)
Facilitate platelet adhesion and vasoconstriction at the site of vessel injury
δ-granules (dense granules)
5. Differentiate between the causes and manifestations of acute and chronic gastritis
• Acute o Acute mucosal inflammatory process- hemorrhage into mucosa of stomach o Local irritants- aspirin, alcohol, bacterial toxins o Heartburn or sour stomach, vomiting o Self-limiting disorder • Chronic o Absence of grossly visible erosions and the presence of chronic inflammatory changes o Leads to atrophy of glandular epithelium of stomach
2. Relate the pathophysiology of gastroesophageal reflux to measures used in diagnosis and treatment of the disorder in children and adults
• Adult o Heartburn occurring 30-60 min after eating o Weak or incompetent lower esophageal sphincter that allows reflux to occur o Pain radiates to throat, shoulder, back o Treatment is conservative measure- avoid positions and conditions that increase gastric reflux. • Children o Small reservoir capacity of stomach for frequent spontaneous reductions in sphincter pressure contribute to reflux o Evidence of pain when swallowing o Feeding problems reported o Treatment is small frequent feedings recommended, thickening of feedings position on left side.
15. Describe the rationale for the symptoms associated with appendicitis
• Appendix becomes inflamed, swollen, gangrenes • Pain caused by stretching of appendix during early inflammatory process • Pain gradually increases and leads to nausea
Describe the causes and manifestations of atelectasis
• Atelectasis is incomplete expansion of a lung or portion of a lung o Causes: airway obstruction, lung compression, increased recoil of the lung due to loss of surfactant o Manifestations: tachypnea, tachycardia, dyspnea, cyanosis, signs of hypoxemia, diminished chest expansion, absence of breath sounds, intercostal retractions (pulling in of the intercostal spaces) If the collapsed area is large, the mediastinum and tracheal shift to the affected side, in compression atelectasis, the mediastinum shifts away from the affected lung.
17. Explain why a failure to respond to the defecation urge may result in constipation
• Because fecal matter will get hard and will be harder to pass over time
State the chief manifestations of bronchiectasis
• Bronchiectasis: permanent dilation of bronchi caused by destruction of the bronchial muscle wall and elastic supporting tissue. • Chronic productive cough, foul-smelling sputum up to hundreds of ml a day, hemoptysis, dyspnea, wheezing, weight loss, anemia, clubbing of the fingers, hypoxemia
State the difference between chronic obstructive pulmonary diseases and interstitial lung diseases
• COPD is a group of respiratory disorders characterized by chronic and recurrent obstruction of airflow in the pulmonary airways. • Interstitial Lung Diseases are a group of lung disorders that produce similar and fibrotic changes in the interstitium or interalveolar septa of the lung and are a set of restrictive disorders.
13. Describe the common causes of infectious enterocolitis
• Contaminated food or water • Viruses, bacteria, protozoa- infect GI tract
12. Compare the characteristics of Crohn disease and ulcerative colitis
• Crohns o Sharply demarcated, granulomatous lesions surrounding by normal appearing mucosal tissue o All layers of bowel involved o Periods of exacerbations and remissions • Ulcerative colitis o Nonspecific inflammatory condition of colon o Confined to rectum and colon o Relapsing disorder marked by attacks of diarrhea
Describe the genetic abnormality responsible for cystic fibrosis and state the disorder's effect on lung function
• Cystic Fibrosis: an inherited disorder involving fluid secretion by the exocrine glands in the epithelial lining of the respiratory, GI, and reproductive tracts. • It is an autosomal recessive trait caused by a mutation in a single gene on the long arm of chromosome 7. • It severely decreases the lung function and causes chronic airway obstruction, chronic infection and impairs mucociliary clearance.
1. Define dysphagia and achalasia
• Dysphagia: difficulty swallowing • Achalasia: pain quickly following swallowing
Characterize the early-phase and late-phase responses in the pathogenesis of bronchial asthma and relate them to the current methods of treatment of this disorder
• Early-phase: develops within 10-20 minutes of exposure to the allergen, and it is caused by a release of chemical mediators from IgE-coated mast cells. The reaction occurs when antigen binds to previously sensitized mast cells on the mucosal surface of the airways. The release of the mediator causes the infiltration of inflammatory cells which allows for an increased access of the antigen to mast cells. Bronchospasms occur by the stimulation of parasympathetic receptors and mucosal edema is caused by increased vascular permeability. • Late-phase: 4-8 hours after exposure involving inflammation and increased airway responsiveness that prolong the attack and put in motion exacerbations. This may persist for 12-24 hours but usually only lasts for a few hours. The initial release of inflammatory cells causes the migration and activation of other inflammatory cells cuasing epithelial injury and edema.
Explain the distinction between chronic bronchitis and emphysema in terms of pathology and clinical manifestations
• Emphysema: loss of lung elasticity and abnormal enlargement of the air spaces distal to the terminal bronchioles, with the destruction of the alveolar walls and capillary beds. o Pathology: results from the breakdown of elastin and other alveolar wall components by enzymes o Manifestations: lack of cyanosis, use accessory muscles, pursed-lip breathing, barrel-chest, decrease in breath sounds • Chronic Bronchitis: represents airway obstruction of the major and small airways. Requires a history of a productive cough for more than three months out of the year for two consecutive years, long term from cigarette smoke o Pathology: hypersecretion of mucus in the large airways causing sputum overproduction, and effect the small airways by changing them which is important in the obstruction that develops. o Manifestations: cyanotic, right-sided heart failure
Compare and contrast extrinsic (atopic) asthma and intrinsic (nonatopic) asthma
• Extrinsic, or atopic, asthma is the type that is imitated by a type I hypersensitivity reaction induced by exposure to an extrinsic antigen or allergen. It usually begins during childhood or adolescence and they also have other allergic disorders as well. • Intrinsic, or nonatopic, asthma is triggered by respiratory infections, exercise, hyperventilation, cold air, drugs, and chemicals. Other things like inhaled irritants can also trigger an intrinsic response
8. Describe the goals for pharmacologic treatment of peptic ulcer disease
• Focuses on eradicating H. pylori, relieving ulcer symptoms, healing the ulcer crater
10. List risk factors associated with gastric cancer
• Genetic predisposition, carcinogenic factors in diet, N-nitrous compounds and benzo pyrene found in smoked or preserved foods, autoimmune gastritis, gastric adenomas or polyps
6. Characterize the proposed role of Helicobacter pylori in the development of chronic gastritis and peptic ulcer and cite the methods for diagnosing the infection
• H. Pylori is a bacterium that colonizes and burrows into the walls of the stomach. It can not be submersed in the stomach acid but thrives on the environment created by the acid. The burrowing increases the production of stomach acid and can create a hole in the wall, also known as an ulcer. The presence of an accumulation of H. Pylori causes the chronic gastritis.
Describe the interaction between heredity, alterations in the immune response, and environmental agents in the pathogenesis of bronchial asthma
• Heredity: often seen among families • Immune response: inflammatory mediators are released by mast cells and the basophils induce bronchoconstriction through the release of chemicals including histamine and nitric oxide. T-helper cells differentiate in the ways they respond to microbes and stimulate the differentiation of B cells into immunoglobulin M and IgG producing plasma cells. • Environmental agents: usually part of the triggering of an allergic reaction. There are many allergens in the air that the body sees as harmful and fights off. They are categorized differently based on where the allergen is found, or when it is found/when the allergic reaction occurs in its presence (seasonal allergies)
Characterize the mechanisms whereby respiratory disorders cause hypoxemia and hypercapnia
• Hypoxemia: Hypoventilation, impaired diffusion of gases, inadequate circulation of blood through the pulmonary capillaries, and mismatching of ventilation and perfusion • Hypercapnia: Hypercapnia is inversely related to alveolar ventilation. Decreased respiratory function leads to increased carbon dioxide levels (PCO2)
Define the terms hypoxia, hypoxemia, and hypercapnia
• Hypoxemia: reduction in the PO2 of the arterial blood. • Hypoxia: deficiency in the amount of oxygen reaching the tissues • Hypercapnia: Increase in the carbon dioxide content of the arterial blood
4. Describe the factors that contribute to the gastric mucosal barrier
• Impermeable epithelial cell surface • Coupled secretion of H+ and HCO3- • Characteristics of gastric mucous
7. Describe the predisposing factors in the development of peptic ulcer and cite the three complications of peptic ulcer
• Infection with bacteria H. pylori and use of aspirin • Advancing age, prior history of peptic ulcers, NSAID use and current use of corticosteroid drugs • Complication- hemorrhage , perforation, gastric outlet obstruction
Define inspiratory reserve, expiratory reserve, vital capacity, and residual volume, total lung capacity, Tidal volume
• Inspiratory reserve: maximum amount of air that can be inhaled from the point of maximal expiration (tv + irv= inspiratory capacity) • Expiratory reserve: Maximum volume of air that can be exhaled from the resting end-expiratory level (tv + erv= exploratory capacity) • Vital capacity: Maximal amount of air that can be forcibly exhaled from the point of maximal inspiration (irv + erv + tidal volume) • Residual volume: Volume of air remaining in the lungs after maximal expiration - Tidal volume: the amount of air you breath in and out - Forced vital capacity: the amount of air you breath in and then breath out forcefully - Total lung capacity: sum of all volume in the lungs
inspiration
• Intra-alveolar pressure decreases to about 758mm Hg as the thoracic cavity enlarges due to diaphragm downward movement caused by impulses carried by the phrenic nerves • Atmospheric pressure then forces air into the airways
State the definition of intrathoracic, intrapleural, and intra-alveolar pressures, and state how each of these pressures change in relation to atmospheric pressure during inspiration and expiration
• Intrathoracic: the pressure in the thoracic cavity o Expiration causes the intrathoracic pressure to increase, inspiration causes a decrease in intrathoracic pressure. • Intrapleural: the pressure in the pleural cavity o Inflation causes the intrapleural pressure to decrease, causing the expansion of the chest wall and expiration causes intrapleural pressure to increase, causing the deflation of the chest wall • Intra-alveolar: the pressure inside the airways and alveoli. The pressure is equal to atmospheric pressure just before inspiration and expiration, when the glottis is open but no air is moving in or out.
Use Laplace law to explain the need for surfactant in maintaining the inflation of small alveoli
• Laplace law: pressure = 2 x surface tension/radius • If the surface tension were equal throughout the lungs, the smallest alveoli would have the greatest pressure which would cause them to empty into larger alveoli. But this does not occur because surfactant lowers the surface tension on the inner surface of the alveoli. This increases the lung compliance.
19. Describe the characteristics of the peritoneum that increase its vulnerability to and protect it against the effects of peritonitis.
• Large, unbroken space that favors the dissemination of contaminants, has large surface that permits absorption of bacterial toxins in blood • Controls infections • Exude thick sticky fibrous structures that adhere to other structures to seal off perforation and localized process
State a definition of lung compliance
• Lung compliance: the ease with which the lungs can be inflated and is determined by the elastic properties of the lung and alveolar surface tension, as well as the compliance of the chest cage.
18. Differentiate between mechanical and paralytic intestinal obstruction in terms of cause and manifestations
• Mechanical- intrinsic or extrinsic factors that encroach on patency or bowel lumen o Intussusception o External hernia and postoperative adhesions • Paralytic o Neurogenic or muscular impairment of parastalsis o After abdominal surgery o Result from chemical irritation, bacterial toxins, electrolyte imbalances and vascular insufficiency
State the most common cause of pulmonary embolism and the clinical manifestations of the disorder
• Most arise from a DVT in the large veins of the lower legs, typically in the popliteal vein or those above it. These thrombosis' are often not known about until an embolus occurs. • Manifestations depend on the size and location. Small ones may go unrecognized, but moderate-sized ones are often breathless, have pleuritic pain, apprehension, a slight fever, and a blood-streaked productive cough. Tachycardia often occurs and breathing is shallow and rapid. Patients with large emboli usually collapse suddenly, have crushing substernal chest pain, shock, and loss of consciousness. Pulse is rapid and weak, BP is low, neck veins are distended and skin is cyanotic and diaphoretic. They often result in death.
Trace the movement of air through the airways, beginning in the nose and oropharynx and moving into the respiratory tissues of the lungs
• Nasopharynx oropharynx larynx trachea R/L primary bronchi Secondary bronchi tertiary bronchi terminal bronchiole respiratory bronchiole alveolar ducts and sacs alveoli
16. Compare the causes and manifestations of inflammatory and noninflammatory diarrhea
• Noninflammatory o Large ordure, watery and non-bloody stools, periumbilical cramps, bloating, nausea and vomiting o Caused by toxin producing bacteria • Inflammatory o Presence of fever and bloody diarrhea o Bacterial invasion of intestinal cells o Small in volume
Describe the basic properties of gases in relation to their partial pressures and their pressures in relation to volume
• Partial pressure: The pressure exerted by a single gas in a mixture. The law of partial pressure states that the total pressure of a mixture of gases is equal to the sum of the partial pressures of the different gases in the mixture. • Lung volume: the amount of air exchanged during ventilation. During breathing, the volume of air that moves in and out of the lungs is directly related to the pressure difference between the lungs and the atmosphere and inversely related to the resistance that the air encounters as it moves through the conducting airways
11. State the diagnostic criteria for irritable bowel syndrome
• Persistent or recurrent symptoms of abdominal pain, altered bowel function and varying complaints of flatulence, bloating, nausea and anorexia, constipation or diarrhea, anxiety or depression • Abdominal pain relieved by defecation and change in frequency and consistency of stools • Symptoms with 12 weeks duration or pain preceding 12 months
Characterize the pathogenesis and manifestations of pleural effusion
• Pleural effusion: abnormal collection of fluid in the pleural cavity o Pathogenesis: occurs when the rate of fluid formation exceeds the rate of fluid removal, congestive heart failure, renal failure, liver failure, malignancy. Transudate: clear fluid Hydrothorax: the accumulation of serous transudate in the pleural cavity Purulent: containing pus Chyle: milky, including lymph and emulsified fats Sanguineous: bloody Exudate: pleural fluid that has a specific gravity greater than 1.020 and often contains inflammatory cells Chylothorax: effusion of lymph in the thoracic cavity o Manifestations: vary with the cause Dullness to percussion Diminished breath sounds Hypoxemia Dyspnea-the most common symptom Pleuritic pain (only when inflammation is present) Constant discomfort may be felt
State the characteristics of pleural pain and differentiate it from other types of chest pain
• Pleural pain results from somatic pain fibers that innervate the parietal pleura. The pain is usually unilateral and abrupt in onset, and is usually made worse with chest movements such as deep breathing and coughing. Those movements exaggerate the the change in pressure in the pleural cavity and the increased movement inflamed or injured surfaces. Tidal volumes are usually small, and breathing becomes rapid. • Other pain is usually bilateral or located at specific parts of the rib cage. Different things happening causes different types of pain, and there is usually a felt difference like dull versus sharp.
Differentiate between pulmonary and alveolar ventilation
• Pulmonary: the total exchange of gases between the atmosphere and the lungs • Alveolar: the transfer of gases within the gas exchange portion of the lungs
Differentiate the function of the respiratory and pulmonary circulations that supply the lungs
• Respiratory circulation: also known as bronchial circulation; provides the blood supply for the conducting airways and the supporting structures of the lung. It has a secondary function of humidifying and warming incoming air as it moves through the conducting airways. • Pulmonary circulation: arises from the pulmonary artery and provides for the gas exchange function of the lungs. It removes thrombo-emboli from the circulation, functions as a metabolic organ, and serves as a blood reservoir for the left side of the heart
Differentiate among the causes and manifestations of spontaneous pneumothorax, secondary pneumothorax, traumatic pneumothorax, and tension pneumothorax
• Spontaneous pneumothorax: thought to occur due to the rupture of an air-filled bleb on the surface of the lung o Bleb: blister on the edge of the lung o Causes: When the blebs rupture it allows atmospheric pressure to flow from the airways into the pleural cavity. Since the alveolar pressure is greater than pleural pressure, the air flows out of the alveoli and into the pleural space which causes the lung to collapse o Manifestations: the manifestations of all pneumothorax include ipsilateral chest pain, increased respiratory rate, dyspnea, chest asymmetry, hyperresonant sound during percussion, decreased or absence breath sounds over area of pneumothorax. • Secondary pneumothorax: spontaneous pneumothorax occurring in people with lung disease. o Causes: lung conditions cause the trapping of gases and the destruction of lung tissue, but the most common cause is emphysema. Other diseases causing secondary are Tb, CF, sarcoidosis, bronchogenic carcinoma, and metastatic pleural diseases o Manifestations: same as spontaneous pneumothorax • Traumatic pneumothorax: chest injury causing pneumothorax o Cause: penetrating or nonpenetrating chest injuries, most commonly fractured or dislocated ribs that penetrate the pleura o Manifestations: same as spontaneous, with the addition of a deviated trachea toward the opposite side of the pneumothorax, decreased cardiac output, increase in heart rate, distension of neck veins, subcutaneous emphysema and clinical signs of shock due to impaired cardiac function
Describe the physiology of bronchial smooth muscle as it relates to airway disease
• The bronchial smooth muscle controls the diameter of the airway. Parasympathetic stimulation leads to bronchoconstriction, and sympathetic stimulation leads to bronchodilation. • Bronchial asthma is a form of asthma that causes the bronchiole smooth muscle to constrict, narrowing the airways
State the difference between the conducting and the respiratory airways
• The conducting airways: the passageway air moves through as it passes through the atmosphere and the lungs • Respiratory airway: where gas exchange takes place
3. State the reason for the poor prognosis associated with esophageal cancer
• The disease has already metastasized by the time the diagnosis is made.
alveoli
• The functional gas exchange unit of the lung • Also have pneumocytes ( cells responsible for surfactant secretion) • And alveolar macrophages (immune function)
Explain why increasing lung volume (e.g., taking a deep breath) reduces airway resistance
• The outside of the airways are connected to the surrounding lung tissues by elastic-type fibers, causing the airways to be pulled open as the lungs expand during inspiration and they become more narrow as the lungs expire.
Describe the method for measuring FEV1.0
• The percentage of the FVC. It is the volume of air expired in the first second of FVC.
14. Relate the use of a high-fiber diet in the treatment of diverticular disease to the etiologic factors for the condition
• Try to promote at least one bowl movement a day • Increased bulk promotes regular defecation and increased colon contents and colon diameter -> decrease intraluminal pressure
State the function of the two types of alveolar cells
• Type I: involved in the gas exchange process. They are very thin and occupy 95% of the surface area of the alveoli. • Type II: produce surfactant, a surface-active agent.
Thrombotic Microangiopathies
• WIDESPREAD FORMATION OF THROMBI IN MICROCIRCULATION**** PLATELETS AND FIBRIN THROMBOCYTOPENIA- platelet thrombi- lacking ADAN TS13 MICROANGIOPATHIC HEMOLYSIS- comes from mechanical damage. Normal PT and PTT. END ORGAN DYSFUNCTION RENAL FAILURE MENTAL STATUS CHANGES Intravascular hemolysis
Define the term water vapor pressure and cite the source of water for humidification of air as it moves through the airways
• Water vapor pressure: the pressure at which water vapor is in thermodynamic equilibrium with its condensed state. The relative humidity refers to the % of moisture in the air compared to the amount of water air can hold without producing condensation. Warm air is able to hold more than cool air. • Water is humidified in the conducting airways via the respiratory circulation.
9. Cite the etiologic factors in ulcer formation related to Zollinger-Ellison syndrome and stress ulcer
• Zollinger-Ellison- caused by gastric secreting tumors found in pancreas or small intestine • Stress ulcer- gastrointestinal ulcerations that develop in relation to major physiologic stress
Test conducted to determine the underlying cause of GI bleeding.
• fecal occult blood test in which stool samples are examined for blood • colonoscopy in which the colon is carefully inspected for polyps or other sources of bleeding. Bone marrow evaluation
Describe the function of the mucociliary blanket
• protects the respiratory tract by trapping dust, bacteria and other foreign particles that enter the airways
Mallory-weiss syndrome
◦ Non-penetrating mucosal tears at the gastroesophageal junction Longitudinal lacerations cause: severe bouts of retching and vomiting Most often seen in chronic alcoholism May also be seen during acute illness with severe vomiting
Hernia
◦ Protrusion of loop of bowel through a small opening, usually in abdominal wall ◦ Herniated loop pushes through peritoneum to form hernial sac
general signs/symptoms of esophageal disorders
◦ Substernal discomfort or pain ◦ Difficulty swallowing (dysphagia) ◦ Inability to swallow (complete obstruction) ◦ Regurgitation of food into trachea A backward flow of undigested food Choking and coughing
intestinal obstructions (volvulus & Intussusception)
◦ Volvulus: rotary twisting of bowel impairing blood supply common site: sigmoid colon ◦ Intussusception: telescoping of a segment of bowel into adjacent segment; from vigorous peristalsis or tumor
