Clinical Management FINAL EXAM

Antiemetic Drugs

-Histamine, Ach, dopamine, serotonin are the transmitters that frequently stimulate the vomiting center. -depress the CNS -decrease intracranial inflammation

Discuss the process of viral infection.

-Transmission and colonization Transmission from infected individual to uninfected individual -direct transmission -vector transmission Viruses evade the host immune response by -rapid division -intracellular survival -coat with self proteins -antigenic variation -neutralization of immune molecules -complement evasion -immune suppression 1. entry and uncoating 2. viral genome replication 3. viral protein synthesis -viral proteins 1. reduced host cell DNA, RNA, protein synthesis 2. metabolic derangements 3. cell lysis or fusion 4. neoplastic transformation 5. viral antigens (Host T cell come) 6. virus assembly to exit and infect more 7. viral inclusions

Sliding Scale: fast acting insulin

-determines the dodge of insulin based on patient's glucose reading, collected prior to meal -gives nurse flexibility without calling for provider order -above 400 could be ketoacidosis and call HO

Identify general considerations in dressing selection, as well as major categories of dressings

-eliminate dead space -control exudate -prevent bacterial overgrowth -ensure proper fluid balance -be cost-efficient -be manageable for the patient and nursing staff Ideal qualities for dressings -absorbs excessive wound fluid while maintaining a moist environment -protects the wound from further mechanical or caustic damage -prevets bacterial invasion or proliferation -conforms to the wound shape and eliminates dead space -does not macerate the surrounding viable tissue -does not shred fibers or compounds that could cause a foreign body or hypersensitivity reaction -eliminated pain during dressing and between dressing changes -minimizes dressing changes -inexpensive (long shelf life) -transparents in order to monitor wound appearance without disrupting dressing Primary -fills dead space -protects wound bed -prevents adhesion of dressing to wound Secondary -absorbs exudate -provides moisture barrier -protects wound from further trauma -classifies by their water-retaining abilities -open, gauze , semi-open, mesh gauze inpregnated with petroleum, paraffin wax, or other ointment -minimun expense and ease of application -do not maintain a moisture-rich environment of good exudate control , semi-occlusive, - films, foams, alginates, hydrocolloids, and hydrogel -Films allows for water evaporations but traps wound enzymes within dressing and prevents bacterial synthesis -tegaderm -Foams like films but with additional absorbency -Alginates are insoluble in water, but in Na+ rich wound fluid exchanges calcium for Na+ and forms a gel that covers wound -foams and alginates are from heavy to moderate exudate Hydrocolloids -traps educate and creates a most environment -gell and a film Hydrogels -synthetic polymers that are sandwiched between two shoes of removable film -useful with dry wounds, if its too dry it will keep it moist -lowers temperature and provides cooling pain relief for some patients Hydrogels for debridement stage Foam and low adherence dressings for the granulation stage Hydrocolloid (traps exudate and bacteria until yo and low adherence dressings for the epithelialization stage occlusive -occluded wounds heal up to 40 % more rapidly than non-occluded wounds

Infections Helminths

-parasitic worms -disease can be caused by inflammatory responses to the eggs or larvae

Energy Homeostasis

-some theories consider weight gain as a hormonal defect -insulin regulates fat accumulation Energy intake (food) matches energy expenditure (metabolism and exercise) and energy stores (fat mass) -signals from fast mass and GI system control every homeostatis (energy set-point) Energy intake will equal energy output pls energy stores Adipose tissues secretes adipokines which control a lot of hormone and processes. -food intake -bp -insulin sensitivity due to inflammation -inflammation -fat cells hyperplasia and hypertrophy hypothalamus is where appetite and metabolism are regulated

Innate Immunity Inflammatory Response

1. Fever -response to pyrogens that stimulates prostaglandin synthesis 2. Leukocytosis -accelerated release of leukocytes from bone marrow -"left shift" occurs when immature neutrophils (bands) are leased 3. Acute Phase Protein Synthesis -synthezized in the liver in increased numbers in response to inflammatory cytokines (C-reactive protein) (ESR) Chronic Inflammation -last longer than 2 weeks -unsuccessful acute inflammatory responses -failure to trigger, autoimmune response, oxidative stress from mediators -Macrophages accumulate and are responsible for tissue destruction seen in chronic inflammation Unchecked inflammation is an underlying component of many disease -Rheumatoid Arthritis, atherosclerosis, lung fibrosis Inflammation is terminated when mediators are dissipated

Large Intestine

1. concentrating waste -absorbtion of water and makes fecal matter 2. movement & defecation -ilececal valve controls chyme into colon -relaxes in sequence with intestinal peristalsis and gastric emptying (gastrocolic reflex) -Defecation reflex - increases abdominal pressure, relaxes sphincters. Feedback (further control of gastric emptying) and Feedforward -absorbes remaining Na+ and Cl- which drive water reabsorption (1-2 liters) -absorption of bacterials-derived vitamins -for every Cl- reabsorbed the body will excrete a bicarb in order to buffer the acidic environment of the absorption of the bacteria (flora) -babies dont have the natural flora to make helpful bacterial vitamins and need vitamin K shot -water and nutrients from the stomach, intestines, pancreas and spleen in the capillaries return to the hepatic portal vein, liver, hepatic vein, IVC, then RA.

Identify clinical manifestations of a fracture when assessing (You don't need to know the different types of fractures)

1. deformity 2. contraction of muscle around injury 3. loss of function 4. crepitation 5. non-specific : pain, tenderness, edema, swelling, ecchymosis

What are the major consequences of immobility?

1. oxygenation and hemostatsis -reduced lung expansion, atelectasis, reduced capacity for gas exchange -leads to hypoxemia- skin breakdown 2. perfusion -reduced cardiac return and reduces cardiac output and contraction 3. immunity, inflammation and infection -sustained pressure on skin/ reduced perfusion =breakdown 4. fluid & electrolyte balance -constipation -renal calculi, urinary stasis, infection 5. musculoskeletal -no contraction or weight barring will react by reducing mass -leads to contractures (muscle shortening) and demineralization and osteoporosis

Differentiate humoral and cell-mediated immune responses. What types of leukocytes are associated with each?

3rd line of defense is Specific response or adaptive response 1. Humoral immunity (antibody mediated) involves B lymphocytes that interact with pathogens found outside cells 2. Cell-mediated immunity involved T lymphocytes interact with intracellular pathogens B cells= humoral = attack outside cells T cells= cell mediated = attack inside cells

Jejunum and Ileum

Absorb digestive nutrients -mainly sugars and protein. Vitamins and minerals as well. -large amount of NA+ followed by water are absorbed with nutrients which enhance aldosterone secretion. -has deep circular folds and microvilli it increase surface area for absorption. =more surface area=more absorption -Aldosterone secretions will inhale NA+ secretion

Identify basic classifications of wounds

Acute or chronic acute means healing all anticipate to progress though the normal stages of wound healing -fluid rich in platelet-derived growth factor, basic fibroblast growth factor that interact with other cytokines to stimulate healing. Chronic - is defined as one that is physiologically impaired -elevation of inflammatory cytokines which may inhibit proliferation of fibroblasts Depth partial thickness -confined to the skin (dermis and epi) -heals by regeneration full thickness -involes dermis, epidermis, subcutaneous tissue and possibly muscle and bone -requires connective tissue repair Surgical Trauma Diabetic Venous - pooling of blood Arterial - ischemia blood can't get there Pressure

Describe nociceptive (acute) pain and how it is initiated.

Acute pain often originates from nociception -nervous systems way of detecting, transmitting and processing potential damage Nociceptors Found all through out tissue. Detecting, transmitting, and processing potential damage (brain is final say) -"free" nerve endings/dendrites of afferent nerves (mechanical, temp, chemical and damage) -require HIGHER threshold of activation than other recpetors, need a strong stimulus in order to signal the brain, not very mylenated Stimulation Mechanical -most common, mechanical pressure stretch of the membrane Temperature - hot cold Chemical/polymodal - chemical mediators due to inflammation and infection "Silent" - a stimulus created from inflammatory mediators (histamine, prostaglandin, bradykinin, arachidonic acid - converts into cox enzymes) Nocioception does paracrine signalling, so you can have a local response Corticosteroids (blocks the phospholipase making of aracondjonic acid) and NSAIDS (blacks making of prostaglandins) are effective in minimizing pain due to minimizing effects of chemical mediators especially prostaglandins Signals are sent by nocioceptors to brain through all of these phases everytime -travels down neuron with myelin sheeths for fast response/SALTATORY "jump" conduction (galial cells) and save energy bc the Na/K pump does not have to reset to RMP as often. Myelin also charges the ICF so when they feel negatively aggravated the can also feel positively attracted to the ECF 1. transduction - begining signal cell membrane is more permeable to Na+, causes a depol and repol cycle that convert noxious stimuli to impulse ANALGESICS - local anethesics wil decrease Na+/K+ transferes, slowing and stopping transmission 2. Transmission -action potential from site moves through spinal cord to brain. Primary Affernt Fibers AB fibers - large, highly myelinated, rapid, low activation threshold, light touch non-noxious, MECHANICAL Alpha Delta MECHANICAL CHEMICAL AND THERMAL smaller, light myelination, slow conduction than AB fibers, rapid sharp pain, initial reflex to acute pain. C fibers PAIN TEMP ITCH unmylenated, smallest afferent fiber, slowest, slow aching burning MECHANICAL CHEMICAL THERMAL -peripheral receptors of C fibers are activated by capsaicin, and local application can reduce pain -slow fibers are stimulated by bradykinin (normally inactive) and make the pain seem ongoing -all primary afferent fibers terminate in the dorsal horn and from there will go to a secondary fiber then go to the brain. Dorsal Horn Processing 1. NT released from primary afferent neuron 1. substance p-unique to send afferent signal to higher power in the brain 2. Glutamate- to increase the excitability of the dorsal horn Then signal goes to thalamus (spinothalamic) then third affereny sensory will go to somatosensory cortex which will help locate and intreptet pain. Spinoreticular -third order neurons in the thalamus can also send signals into other areas of the cortex (emotional aspects of pain) Drugs that block NT can impact pain transmission Local anesthetics and anti-inflammatory drugs block 3. perception - conscious experience (different for everyone) with 1. sensory - discriminative 2. affective -emotional 4. modulation - the act what are you going to do with pain. opioid receptors are located in the dorsal horn where pain signals are transmitted and in the brain 3 types of opioid receptors Mu -spinal cord, brain stem, and medial thalamus -analgesia, respiratory depression, sedation, decrease GI motility, euphoria Kappa - spinal cord, brain, limbic system (make you sad), -analgesia, sedation, dyspnea, dysphoria and respiratory depression Delta regulate transmission of pain signals in the dorsal horn and brain -synaptic knob is activated by opioid agonist which inhibits release of pain NT such as substance P (send to higher power)or glutamate (dorsal horn excitability) -opioids also activate GABA -intense euphoria on the MU receptors -brain generates 3 endogenous analgesics in response to pain -endorphins -binds to mu receptors to be happy -dynorphins - binds to kappa receptors that still have analgesic effect, make you sad -enkephalins - bind to delta opioid receptors. -exongenous opioids will lead to the same responses -all receptors causes respiratory depression, sedation, analgesia

What pathways of nerve conduction does the body use to carry pain signals?

Afferent (ascending sensory to spinal column) -sensroy neurons provide input by transmitting information from skin or skeletal muscles to the CNS through movement of action potentials Somatice sensor neurons transmit information from the skin or skeletal muscles (consciousness) Visceral sensory neurons transmit information from the internal organs to the CNS (generally doesn't reach our consciousness) Efferent (descending: innervate effector organs) ap tot he effectors causing some sort of reactions Somatic motor neuron s- innervate skeletal muscle and are under voluntary control Autonomic motor neurons - innervate smooth muscle and are involuntary

Pancreatic Islets of Langerhans

Alpha cells: secrete glucagon Beta cells : secrete insulin Delta cells: secrete somatostatin (inhibits parietal cell secretions, stops HCL and pepsin production) F cells: secrete pancreatic peptides PNS (stimulates secretions) & SNS (inhibits secretions) innervated As blood flows, insulin released from beta cells first effects the alpha cells because they are on the outside of the islet and inhibits glucagon.

The Lymphatic System

Arterial blood leave cap circulation and flow to tissues to deliver 02. Interstitial fluid picks up waste products and is 90% reabsorbed by venous return but the other 10% is known as lymph, flow upward towards neck in lymphatic vessels. -travels through lymph nodes (can be damaged and do not regenerate) to be filtered and lymphocytes attack debris. -the cleaned fluid enters venous circulation through subclavian veins

Differentiate aerobic and anaerobic bacteria. Describe the characteristics of gram negative versus gram positive bacteria.

BACTERIA Prokaryotes- have cell membranes but no nucleus or other membranes enclosed organelles -gram postive- THICK cell wall surrounding cell membrane -gram-negative - THIN cell wall btw eek two phospholipid bilayer membranes 2 types of bacteria 1. Aerobic - need 02 to survive (staph & strep) 2. Anaerobic - cannot grow in presence of 02 (deep wounds, abscess formation, foul-smelling puss and tissue destruction)

Labs for d

BMP -electrolytes and fluid status CBC- evaluate potential infection Stool sample - guiac (blood in stool) or pathogens (cultur Interventions -antidiarrhea -antibiotics if bacterial infection

What is BPH, and how does it influence micturition (action of urination)? What treatment options are available?

Benign Prostatic Hypertrophy hormonal changes that lead to enlargement of gland to cause compression of urethra leading to symptoms -alterantions in testosterone/estrogen balance -prostatic growth factors -increased stem cells/decreased stroll cell death -accumulation of dihydroxytestosterone Does NOT predispose to cancer Complications -urinary retention -UTI -sepsis secondary to UTI -residual urine -calculi -renal failure -hematuria -hernias,hemorrhoids (due to high pressure), bowel habit change CM -voiding symptoms -irritative symptoms Treatment -mild symtoms = watchful waiting bc the risk of therapy outweighs benefit of medical or surgical intervention -moderate to severe TURP -transurethral resection of the prostate

Review the function of organs involved in immunity (bone marrow, thymus, spleen and lymphoid tissue)

Bone Marrow -marrow stem cells can become any number of body cells types -myeloid stem cells can further bone marrow to form mast cells, basophils, neutrophils, eosinophils, macrophages monocytes, and erythrocytes -other cells migrate to and mature in the thymus to become lymphocytes Thymus -lies in the medisteinum of chest -produces mature T cells -hormones in thymus attract circulating stem-cells as precursors for T-cells and promote maturation -infant won't be able to fight infection if not present at birth Spleen -located in left upper abdominal quadrant both b and t cells are found -platlets are also stored -removed old, damaged, abnormal RBC and filters processes antigens -do not need to survive.

Discuss methods used to evaluate for infection: WBC, blood/wound cultures

CBC -4000-11000 (adds to 100%) -neutrophils, eosinophils, basophils, lymhopcytes, monocytes Neutrophils -bacteria, fungi (50-70%) Eosinophils- larger parasites, allergic response (1-4%) Basophils- release histamine for inflammatory response (0.1-2%) Lymphocytes - B cells -antibodies T cells- phagocytosis/NK cells (20-40%) Monocytes - migrate from bloodstream to other tissues and differentiate into tissue resident macrophages (2-8%) Blood Cultures -minimun of 2 specimens -use culture bottles to contain media for growing aerobic and anaerobic bacteria -clean tops of bottle prior ro obtains sample -postive results take 1-5 days Sputum, nasopharyngeal

Describe the cardinal features of adaptive immunity (specificity, memory and clonal diversity)

Cardinal signs of inflammation 1. redness 2. swelling 3. pain 4. heat Specificity -abiltiy to recognize and response to particular targets Memory -remembers distinct antigens and responds more rapidly and vigorously to subsequent exposures (secondary immune response) Clonal Diversity -lymphoid precursor cells can become B cells (humoral) lead to plasma cell or T cells (cell-mediated) Lymphoid organs & tissues -bone marrow, thymus gland, lymph nodes, spleen, tonsils, blood and lymphatic vessels -produce lymphocytes -B and t cells are produces from stem cells in the bone marrow -B cell remain in bone marrow to mature -T cell travels to thymus gland to mature

How are T cells activated? What types of T cells are the major influences of immune response? How are they different? What is the action of CD4 vs. CD8 and CD25 cells?

Cell-Mediated Immunity T-cells defend against pathogens that lodge inside cells, where humoral (only outside cell )responses are not effective MHC 1 - identity self and danger signals Cells that are invade by virus will generate MCH 1 marker that include antigen from invading pathogen and create cytotoxic T cells APC with MHC 2 protein that are invaded will travel to lymphoid tissue and create Helper T cells T cells have TCR t cell receptors that are similar to antibodies found on B cells 1. Helper T cells with CD4+ markers -modualte activity of other immune cells by augmentation activity of activated lymphocyte and macrophages -most numerous -changes shape to activate B cells need to be activated by helper T cells 2. Cytotoxic T cells with CD8+ markers -destroy abnormal cells -lysis of the target cell -Natural killer cells don't need MCH 1 protein, will attack anyways. 3. Regulatory (suppressor) T cells with CD4+CD25+ markers -control immune system when antigen/pathogen has been destroyed 4. memory T cells -can give life long immunity to particular infections -stimulate memory b cell to produce antibodies -can trigger production of killer T cells

Phases of Digestion

Cephalic Phase -physical digestion via mastication -secretion of saliva -chemcial digestion via salivary amylase and lingual lipase (Von Ebner's Glands) -preparation for swallowing DEGLUTITION reflex- swallowing, bolus on soft palet, sphincter UES releaxes, larynxs elevated, epiglottis covers trachea, peristalsis and gravity move food down Gastic Phase -Deglutition reflex (swallowing) moves food to the stomach (3.5 liters of content /day enters fundus) MAIN FUNCTIONS of the STOMACH 1. Store ingested food until it can emptied into the small intestine 2. secreted HCL acid and enzymes to begin protein digestion. 3. Convert stomach contents into chyme through salivary amylase degeneration and secretions -no significant absorption takes place except for lipid soluble substances (because of mucuous)like aspirin, alcohol, and caffeine which are directly absorbed through the stomach lining. Intentional Phase - by the time cephalic and gastric phases are complete 1. initial digestion of proteins 2. formation of chyme 3. controlled entry of chyme should be established this phase: 1. ongoing forward movement of chyme 2. buffers via pancreatic enzyme secretion 3. Digestion by pancreatic exocrine secretion, bile from gall bladder, and intentional mucosal enzymes 4. Absorption of most nutrients and water Enteric nervous system triggers secretion of secretin (BICARB), CCK (hypothalamus), incretin (insulin release from panaceas) all slow gastric emptying and gastric secretions -feedback loop that will control the empty of the stomach -feed forward loop withh promote digestion of rest of substance

Differentiate acute and chronic constipation. What are some of the causes of each? Why should they be treated differently? How does constipation lead to fecal impaction?

Chronic Constipation 1. slow transit -prolonged delay of stool movement 2. dyssynergistic defecation -difficulty evacuating stool from the rectum 3.irritable bowel syndrome Treatment -education, dietary changes (increase in fiber & fluids) and bulk forming laxatives 1. psyllium and methylcellulse 2. cereals that resist digestion and retain water 3. citrus/legumes that stimulate colic flora 4. prunes Acute and Chronic -diet -drugs -behavioral -lifestyle -endocrine -metabolic -neurologic -psychiatric Children struggle due to playing, fear or distress Elderly struggle due to natural defecation impaired from laxatives. Constipation leads to fecal impaction due to build up of fecal mater that becomes solid and immobile to pass. Acute Constipation Treatment -osmotic agents -diarrhea (polyethylene glycol) -stimulant laxative or dis-impaction (cannot designate to aid because you are putting pressure to vegas nerve and can go into cardiac arrest) -suppositories -enemas -digital stimulation to trigger stretch receptors

How does compartment syndrome develop after a fracture? What are the cardinal signs of compartment syndrome?

Compartment syndrome -elevated intra-compartmental pressure within a confined compartment that compromises neuro function\ -lost within 6 hours Cause- restrictive dressings, splints, casts, premature closure of fascia -increased compartment content -deep, throbbing increasing pain unresponsive to opioid administration 6 p's 1. paresthesia - pins and needles 2. paralysis -loss ability to moe 3. pain distal to injury that intensifies with passive ROM 4. pallor -pale 5. pulseless-ness 6. pressure -frequent assessments -elevate extremity to heart level (release of pooling of blood) and release restrictive devices -fasciotomy-open it up

Cellular products of inflammation

Cytokines -polypeptides produced in response to microbes that mediate and regular immune responses Interleukins -proinflammatroy versus anto inflammatory -endogenous pyrogens Interferons -protect against viral infections -modify inflammation 1. cell infected wth virus produced interferon 2. release interferon and binds to unaffected cell and induced synthesis of antiviral protein 3. antiviral protein block viral DN synthesis Tumor Necrosis Factor- Alpha -secreted by macrophages in response to pathogen -induces fever -increases synthesis of inflammatory serum proteins -causes muscle wasting (cachexia) and intravascular thrombosis Platelet Activating Factor -circulating platelets are activated by products of the innate and adaptive immune systems after an injury occurs -activation results in interaction with the clotting system to stop bleeding and in degranulation Nitric Oxide -causes local arterial vasodilation

What are detrusor muscles, and how do they impact micturition? What stimulates these muscles to contract?

Detrusor muscles surround the bladder and sphincters. They are stimulated through stretch receptors in the bladder wall which encourage the internal sphincter to relax and urge brain to void. Conscious brain then relaxes external urethral sphincter

Nutritional Disorders Insufficient Oral Intake

Diets Regular -no restriction Liquid -clear: water, broth, clear juice, gelatin -Full: milk, pudding, vegetable juice -Pureed: any food in liquid form Soft -cooked fruits, veggies, bananas, soft eggs -Mechanical soft: all foods that can be chopped, mashed or pureed Enteral Feedings -maintains our mucosal physiology -preserves gut barrier function -may modulate immune response -inexpensive compared with PN Options Polymeric formulas -protein, carbs, lipid -fully function GI Elemental -lactose free (small fat %) -proteins are broken down, malabsorption disorders Semi-elemental -larger molecules that are easily digested and absorbed -malabsorption syndromes, bowls obstructions, IBD, fistula Modular or Disease-specific -contains single nutrient the can be combined -burns to replace nitrogen

Intestinal Phase : Absorption

Duodenum (first 6 inches) Jejunum & Ileum (remaining 18 feet that has not physical division but has structural differences in tunica mucosa) Tunica Mucosa - simple columnar epithelium specialized for secretion and absorption. Constantly being replaced. Loose connective tissue is underneath, very vascular so nutrient are absorbed into capillaries. Tunica Submucosa - another layer of Loose Connective Tissue that contains larger blood vessels and nerve plexes. Tunica Muscularis - two layers of smooth muscle 1. circular layer 2. longitudinal layer Tunica Serosa - outsider wall of the digestive tract is a layer of simple squamous epithelium that makes a slippery outside and allow friction against other organs.

What is the action of antibodies in elimination of pathogens?

Enhance innate immune response to promote antigen destruction -antibodies do not directly destroy pathogen but enhance phagocytosis 1. Neutralization (opsinization) 2. Agglutination (deform antigen shape, clumping makes it easier to find it ) 3. Precipitate (dissolved antigen) theses 3 enhance phagocytosis by macrophage Antigen-antibody complexes stimulate complement proteins that activate inflammation and bacterial lysis

Intestinal Phase : Secretion & Digestion

Entrance of chyme into duodenum stimulates the enteric nervous system neural signals) and trigger 1. Secretin - slows gastric emptying, gastric production, stimulates bicarbonate production from pancreas to buffer acidic chyme 2. Cholecystokinin - responds to lipid presence and slows gastric motility and gastric acid secretion, acts hormonally on hypothalamus 3. Incretin hormones - slows gastric acid and emptying, stimulate insulin release from pancreas. -all three slow gastric emptying and decrease gastric acid

Fungus Infections

Eukaryotes -grow wither as budding yeast cells or as hyphae Dermatophytes -fungal species confined to skin, hair, nails, -tinea Deep fungal Infections -spead systemically and invaded tissues in immunocompromised hosts but usually heal or remain latent in normal hosts -Opportunistic fungi -colonize normal human skin or gut without causing illness Rare infections but highest rates are in 1. immunocompromised patients 2. bone marrow suppression 3. preterm infants Most common organisms 1. asperigillus (mold) 2. Candida albicans (normal flora in GI tract, yeast)

Identify sources and risk factors of hospital acquired infection

Exogenous - infections originate from outside sources Endogenous - GI floor can cause infection in immunocompromised patients Prokaryotes- have cell membranes but no nucleus or other membranes enclosed organelles -gram postive- THICK cell wall surrounding cell membrane -gram-negative - THIN cell wall btw eek two phospholipid bilayer membranes 2 types of bacteria 1. Aerobic - need 02 to survive (staph & strep) 2. Anaerobic - cannot grow in presence of 02 (deep wounds, abscess formation, foul-smelling puss and tissue destruction) Damage to the host can happen BACTERIA 1. Directly - toxins break down tissue, inhibit mRNA translation, alter permeability or intentional cells -clostridia produce neurotoxins 2. Indirectly - damage from inflammation -supper antigens -septic shock Risk Factors 1. surgical or invasive procedures 2. central venous catheters 3. peripheral IV lines Any device that enters the body or a body cavity is a source of infection -Urinary catheters -mechanically ventilated patients (pneumonia due to inability to clear secretions) 1. malnurtion- ;ears to cachexia in cancer patients decreases bone marrow and liver ability to mount an immune response and inflammatory response 2. Immunosuppression -cancer, aplastic anemia, liver disease -corticosteroids -cognital immunodeficiencies General Guidelines Medical vs Asepsis - hand hygiene between patient contact -wear gloves with body secretions -change gloves -dont recap needles

Complications of fracture

Fat embolism syndrome -diffusion of fat globules release from fracture into vascular compartment which can result in occlusion Deep Vein thrombosis -clot Compartment syndrome -elevated intra-compartmental pressure within a confined compartment that compromises neuro function\ -lost within 6 hours Cast care fracture healing - hematoma formation, soft callus formation, hard callus, cone remodeling

Identify basic complications of wound healing

Fistula -abnormal passage between organ or vessel and another organ or vessel or layers of skin -dead space infection Sinus tract/tunneling and undermining Periwound Changes 1. Macerations - white around wound edges -too much moisture 2. Denouement -loss of epidermis 3. Excoriation - abrasion of the skin like scratching, trauma, infection, or the healing process. 4. Adhesive skin stripping -mechanical disruption and reduction of the outermost layer 5. Erythema - is an abnormal redness of the skin caused by irrigation, inflammation, and dilation of blood vessels Calus -thickening of the epidermis Lymphangitis -inflammation of the lymph channel that occurs as a result of infection at the site distal to the channel Wet Gangrene -leads to sepsis and death -untrreated infection where loal blood supply has been reduced or stopped by tissue swelling and bacterial toxins are being produced

Identify the major neurotransmitters involved in pain signaling.

GABA= opioids activare = intense euphoria Substance P - pain fibers activates afferent signals for transmission to higher level neurons Glutamate- excitiatory binding =pain singnals to higher level neurons and increased excitabiltiy fo the dorsal horn =sensitivity to injury area.

Inflammatory Disorders

Gout - uric acid formation -hyperuricemia -attacks of acute arthritis -tohpi around joints -joint destruction Rheumatoid Arthritis -chronic autoimmune disorder characterized by inflammation of the synovial lining of the joints -more common in women -intermittent flare-ups

H-2 Receptor Blockers

H1- inflammation H2- increased acid secretion in stomach H2RB decrease volume and acidity of parietal cell secretions (short term treatment for GERD) Histamine also triggers parietal cells to release HCL acid.

H-2 Atagonists Antacids Bismuth Salts Sucralfate treating PUD caused by H.pylori 1. H-2 Blocker or PPI and 2 Anti-infectives -amoxicillin, clarithromycin, metronidazole, tetracycline -pepto-bismol

IV for NPO patients -do not decrease acid production, just neutralization, with calcium added -inhibits bacterial adhesion and growth -coats ulcer and binds to fibrin

What are the processes that move chyme through the large intestine? What is meant by gastrocolic reflex? What triggers the internal and external sphincters during defecation?

Ileum to ileocecal valve to cecum 1. propulsive (chopping and mixing of a gush of clearing one area of colon) or peristalsis due to enteric nervous system gastrocolic (when the stomach begin tot start emptying contents into duodenum) and duodenocolic reflexes increase colonic activity -signal seems to be stimulated by fat in proximal small intestine Stretch receptors in the rectal walls trigger contraction of rectal muscles, relaxation of the internal anal sphincter (causes signal to be sent to brain signaling urge to defecate) and initial contraction of external sphincter. PNS motor fibers encourage contraction of rectum, relaxation of internal anal sphincter, smooth muscle. If convient to defecate, country motor neurons are inhibited allowing the external anal sphincter to relax. Through reverse peristalsis can return feces into rectum, but if not released it can harden and result in constipation.

Identify common skin disorders

Inflammatory disorders Dermatitis -eczema -lesions with indistinct borders Allergic Contact dermatitis -hypersensitivity type iV reaction -erythema, swelling, pruritus, vesicular lesions Papolosquamous Disorders -Psoriasis - t cell immune mediated disease -papules, scales, plaques and erythema -chronic, relapsing skin disorder Skin infections - Bacterial -Cellulitis, infection of the dermis and subcutaneous tissues usually by staphylococcus or group B strep -Erysipelas -acute superficial infection of the upper dermis (surperifcal form of cellulitis) -most often group A strep -Impetigo - superficial lesion of the skin caused by staphylococcus or alpha hemolytic streptococci Viral Infections -Herpes simplex virus H1 is cold sores h2 genital warts -Herpes zoster (shingles)/varicella (chickenpox) caused by herpes varicella-zoster virus Benign tumors Skin Cancer Frost bite -burning reaction from cycles of vasoconstriction and dilation Burns -loss of body fluid -dehydration and fatal shock 1,2,3

Describe general process of wound healing stages

Inflammatory phase/hemostasis Epithelization Phase - temporary protection, cytokines stimulate proliferation Proliferation Phase -restores skin integrity by filling in wound with new tissue -stimulated by cytokines Remodeling phase -completes wound healing -can take several years

Antihistamine and Anticholinergic

Inhibit the action of histamine on H1 receptors or ACH on muscarine receptors. -both limit vestibular system on afferent visceral stimulation -dry mouth, urinary retention, potential blurred vision

Infections Ectoparasites

Insects or arachnids -attach to and live in or on the skin -produce disease by damaging host and serving as vectors for transmission of infectious agents into the host

Review how glucagon & insulin work in the body

Insulin -anabolic hormone (inhibits catabolic processes) responsible for limiting blood glucose and fatty acid levels. -short 1/2 life of 15 minutes -increases in response to increase in glucose or PNS stimulation of B-cells. -decreases w low serum glucose levels, high insulin levels or SNS stimulation of alpha cells. A large % of glucose is absorbed from the small intestine is immediately taken up by hepatocytes (insulin promoted conversion of glucose to glycogen and main storage of glycogen is in the liver) -excess glucose is used for synthesis of tryiglycerides (3 FFA)and be exported from liver to lipoproteins which are reduced to FFA in circulation. (insulin facilitates entry of glucose into adipocytes, which uses it to synthesize glycerol) -FFA + Glyceol = triglyceride Insulin also drives cells to use carbs first and accumulate fat in adipose tissue. Insulin influences glycogen storage in the liver and in skeletal muscle because of the vast quantities of glucose needed to make ATP for muscle contraction. -insulin facilitates diffusion of glucose into skeletal muscle -the receptor for insulin is embedded in the plasma membrane, and is composed of two alpha subunits (hormone-binding domain) and two beta (ATP-binding and tyrosine kinase domain) subunits -GLUT 4 transporters in the cytoplasm rapidly fuse to the plasma membrane and make a pathway for glucose to be up-taken by the cell once insulin binds to insulin receptors on the cel membrane. -once it enters the cell it can be used for metabolism by increasing enzyme activity in metabolic pathways -Insulin lowers amino acid levels and enhances protein synthesis by promoting active transport of AA into muscles. -Facilitates intracellular transport of K+, elevated insulin increases affinity for sodium in the Na+/K+ pump and increases turn over rate. Na+ goes out and K+ goes in. A sustained elevation of insulin causes up-regulation of the pump. -high insulin low k+ (Na going out and K going in) Glucagon -promotes the breakdown of glycogen (stored in the liver) into glucose and into the blood stream. -preproglucogon circulates in its unbound form (6-min 1/2 life) -increase in ketogenesis -comes from pancreas and goes to the liver first by (1) acting on hepatocytes to activate enzymes that depolymerize glycogen and release glucose or (2) activate hepatic gluconeogenesis by which AA are converted to glucose, providing a second source of glucose.

What are the differences in composition of the major types of vaccines? What is cold chain?

Live Vaccine -are made from live infectious agents without augmentation -only live vaccine is "variola" small pox vaccine, made from live vaccine cow-pox virus which is not pathogenic but antigenic, giving cross immunity. Live Attenuated Vaccine -virulent pathogenic organisms are treated to become attenuated and avirulent, but antigenic. They have lost their capacity to induce full-blown disease but retain their immunogenicity. -should not be administered to persons with suppressed immune response -oral polio, measels/mumps/rubella/intranasal influenza/varicella/shingles Inactive (killed) Vaccines -organisms are killed or inactivated by heat or chemicals but remain antigenic -they are usually safe but less effective than live attenuated vaccines -the only absolute contraindication to their administration is a severe local or general relations to a previous dose. -rabies, polio, IM influenza Toxoids -use exotoxins from the pathogen that cause disease instead of germ itself -the antibodies produced due to toxoid administration neutralize the toxic chemicals produced during infection rather than act upon the organism itself. -highly efficacious and safe immunizing agents -diptheria -tetanus Cellular Fraction Vaccines -prepared from extracted cellular fractions (antigen of the cell wall, proteins) -pneumococccal pneumonia -hep B -HPV -menigococcal The cold chain is a system of storage and transport of vaccines at low temperature from the manufacture to the actual vaccination site. This is necessary because vaccine failure may occur due to failure to store and transport under strict temp controls.

What are MHC antigens? What are the two classes of MHC proteins? How are they different?

MHC They identify "self" cells through MHC Major Histocompatibility Proteins on the surface of all cells except RBC. Class 1 and Class 2 Class 1 - on all nucleated cells, self antigens Class 2- only on APC, B-cells, macrophages and dendritic cells

Duodenum

Many function of the duodenum relate to the liver and pancreatic ducts that drain into it 1. specific absorption site for lipids, iron, and calcium LIC the DUOD 2. sugars and protein also get absorbed here & along the length of the small intestine

GI Basic Function

Motility - movement, peristalsis, segmentation (chopping and mixing) Secretion - release of substance to inhale digestion Digestion - physical & chemical breakdown of food Absorption - transfer of materials to internal enviorment

Discuss the central sensitization that can lead to chronic pain, including the influences of allodynia and hyperalgesia.

Moving from acute pain to chronic pain is sensitization stating with peripheral sensitizations (site of injury, pathogen release, inflammation) to central (CNS) -can the reversible and quickly permanent Central (Sensitization) - nerves have a reduced threshold for firing as a result of noxious stimuli. Aka easily fired. Due to increase NMDA and glutamate. Allodynia -pain from typically non-noxious stimuli Hyperalgesia - extreme sensitivity to painful stimuli; this conditions of neuronal hyperexcitiabiltiy at the injury site may extend into surrounding uninjured tissue.

Intestinal Phase : Motility

Muscle contraction of the digestive tract, initiated by interstitial cells of Cajal 1. propels food through GI 2. mixes food w digestive juices -facilitate digestion and absorption through peristalsis (depends on ANS, paracrine signals and hormones) & segmentation (mixing in intestine) -peristalsis and segmentation

GI Regulation

Neural - nervous system Hormonal -blod Paracine - local Controls through : -long & short reflexes -autonomic function of the enteric nervous system -GI peptide reflexes 1. Long Reflexes - initiated within the CNS. Feedforward & emotional reflexes are initiated and integrated entirely outside the GI tract (called CEPHALIC REFLEXES) -sensation goes to spinal cord and sensory cell synapses in spinal cord or brain then sends efferent information to peripheral ganglion (synapse outside of spinal cord) then to muscle. 2. Short Reflexes - initiated by the enteric nervous system through changes in pH, dissension, osmolarity, products of digestion. submucosal plexus contain sensory neurons that send afferent information to peripheral ganglia and efferent information back to submucosal & myenteric plexuses for control of secretion, motility, and growth. -sensory cell synapses only in peripheral ganglion 3. Enteric Nervous System - PNS & SNS do not directly innervate the digestive tract. Extrinsic neurons originating in the CNS innervate the enteric neurons meaning without enteric neurons, digestive activities that rely on neural stimulation (peristalsis and secretion) cannot occur, even if the PNS & SNS are intact. 4. GI peptide Reflexes - peptides released from the Gi tract can act as HORMONES (secreted into he blood and act on other accessory organs, other parts of GI, or brain) as PARACRINE signals (secreted into the lumen ((lumens signals bind to epithelial receptors)) or ECF ((ECF signals act in the immediate vicinity of secretion) -these alter behavior related to eating -alter secretion -alter motility.

Bacterial Exemplar

Otitis media -inflammation of the middle ear -common in toddlers -strep pneumonia, H influenza, moraxella catarryalis -tubes, feeding positions, immature immune defense mechanisms Risk Factors -male -young -sibling history -formula feeding in infancy -day care attendance -ethniticty -expose to cig smoke -pacifier use -underlying pathology (allergies, cleft palate, downs) -fall or winter season -previous antibiotic use

Differentiate acquired and passive immunity.

Passive Immunity is antibodies acquired through mother's placenta or breastmilk. Acquired immunity is active acquired immunity though vaccinations. -antigens are deliberately introduced to the immune system to produce immunity, minimal symptoms occur because the virus has been killed or weakened, vaccines have eradicated or severely limited diseases.

Discuss pain management strategies, including pharmacologic and non-pharmacologic.

Pharmacologic Non-opioid analgesic agents -efficacious as mono-therapy for mild pain or as polypharmacy for chronic pain. Ceiling doses. -not recommended form chronic pain Opioids -mild -severe. Most have NO ceiling doses. Causes dependence. Most block at MU or Kappa receptors block release of substance P(sending to a higher power). Antidepressants -inhibit NE and serotonin reuptake Antiepileptic/anticonvulsant drugs -decrease excitability of neurons by modulating sodium channels (decreasing AP) -gabapentin, nerve pain and chronic pain Muscle relaxants Antimigraine agents Topical analgesic agents Serotonin Agonists Terminate migrant attacks -vasoconstriction -Triptans - increase intracranial pressure e -Ergotamine - more systemic effects Non-pharmacologic -hot and cold therapy -distraction -acupunture -essential oils -breathing techniques -positiong/slpinting

Identify characteristics of primary, secondary and tertiary healing

Primary -wound dos not involve tissue loss -heal by re-epitheliaization -4-14 days -minimal scarring EX// surgical wounds, superficial wounds, first degree sunburn Secondary -has some degree of tissue loss -longer healing times, leave open -reult sin scarring -partial and full thickness wounds EX// pressure ulcers, burns, dehisced surgical wounds, traumatic injuries Tertiary -wounds remind open fro an extended period of time -may be closed when ready -more scarring than primary but less than secondary because you are going to close it up eventually EX// deep wounds,

Review Gluconeogenisis

Process of synthesizing glucose from non-carbohydrate sources are limited by the increased presence of insulin. and Glycogenolysis (breakdown of glycogen into glucose) ^ this is the primary pathway the liver uses when glucagon is present. gluconeogenesis is the secondary pathway by using AA to convert into glucose

GI Secondary Function

Protection - huge external surface for pathogens to gain entrance into the internal enviornment -tight junctions -mucous production -all regulated

Discuss identification of infection in a wound

Redness and warmth swelling pain pus/increased exudate foul odor discoloration or granulation tissue infectious agent must be present inflammation with documented presence of bacteria overwhelming the body's normal response s systemic infection should be identified through systemic symptoms before antibiotics -all wounds have bacteria and microbes but that doesn't mean they are infected.

What are some of the ways the first line of defense protects against pathogen invasion?

Skin! -forms a shield against invaders and secretes chemicals that pill potential invaders -shed between 40-50 thousand cells every day -most bacteria are incapable of penetrating intact skin due to dryness, temperature, low pH, bactericidal secretion by sebaceous glands, desquamation (sloughing), perspiration (sweat contains lysosomes) -eyes blink and have lysosomes in tears -ear wax contains antibacterial components -salivia contains chemicals the can break down bacteria -the lining of the airway and GI tract trap and expel pathogens

Review basics of the musculoskeletal system (anatomy, physiology, muscle contraction)

Risk -older adults and children -chronic conditions -orothopedic injuries -medications -prolonged inactivity Older adults -loss of bone mass in older women -joint and disk cartilage dehydrates -fall risk -muscle tone decreases Children -ossification begins during embryonic development and undines until 18-21 -growth plate severed to absorb shock and protect joint -bones are more pliable and more vulnerable to greenstick fractures (incomplete)

" Identify risk factors and types of pressure ulcers as well as staging

Risk Factors -immobility -advanced age -fragile skin -decreased subcutaneous fat -incontinence -infection -low blood pressure - -decreased protein levels are directly correlated to development of pressure ulcers -friction, shear, moisture -muscle is more sensitive to pressure than skin Stage 1 -intact skin with non-blanchable redness of a localized area usually over a bony prominence Stage 2 -partial thickness loss of dermis presenting as a shallow open ulcer with a red pink wound bed without slough Stage 3 -full thickness tissue loss -subcutaneous fat may be viable but bone tendon and muscles are not exposed -slough may be present Stage 4 -ful thickness tissue loss with exposed bone, tendon, or muscle -slough to eschar may be present on some parts of the wound bed -often include undermining and tunneling Unstageable -full thickness tissue loss in which the base of th ulcer is covered y slight and eschar in the wound bed. base of wound cannot be visualized Pressure reduction -continuous repositioning -use beds to support the weight -fully inspect skin folds -avoid pressure from tubes and medical devices -use transfer aides to limit friction and shear -dont leave bed pans or commode longer than necessary.

Why is the inflammatory response called a non-specific response? How is inflammation triggered? What is the role of mast cells in inflammation? What are the vascular, cellular and plasma protein responses to inflammatory mediators? What is the role of the three major plasma proteins?

Second line of defense = non-specific response -the non-specific response is called the inflammatory response because it brings potential response mechanisms to the site of stimuli (acute inflammation) before the 3rd line of defense which is specific immune response. Mast cells are granule-filled cells located in loose connective tissues close to blood vessels that are alerted for noxious stimuli (pathogens, temp changes, chemicals, hypersensitivity in asthma, or injury) Mast cells when triggered 1. degranulation (release histamine) 2. synthesis of lipid-derived chemical mediators -leukotrines (signal immune system and histamine effects) -prostaglandins (increase vascular permeability, neutrophil chemotaxis and pain, suppress histamine) -cytokines (TNF-alpha and IL-13) increase vascular permeability, B-cell proliferation and antibody production Vascular Response to Inflammation 1. histamine release triggers a temporary vasoconstriction and then vasodilation to increase cap permeability 2. blood becomes more viscous and flows more slows -this allows flow of plasma into the surrounding tissue Cellular Response in inflammatory Response -the release of histamine also triggers the release of chemotactic factors 1. leukocytes (beginning w neutrophils) begins to arrive at the site and begin to emigrate into the tissue -selectins protruding from the vessel lining catch integrins (ligand) and cause the leukocyte to anchor. 2. binding with selectins alters the plasma membrane of the leukocytes and allows it to move out of the vasculature and into the tissue (diapedesis) 3. the leukocytes are attracted to chemotaxis (chemical mediators released at the site on damage) 4. binding of chemotaxis activates a mechanism that allows for amoeba-like crawling, a concentration gradient of chemotaxis draws the cell towards the site of injury 5. phagocytosis occurs -cels ingest and dispose of foreign material Phagocytes 1. neutrophils - first responders to inflammation, short lived, and become component of the purulent exudate 2. Monocytes & macrophages - produced in bone marrow, enter circulation and migrate to the inflammatory site where they develop into macrophages -3-7 days after neutrophils -secrete cytokines/stim inflammation -initiation of healing 3. Natural Killer T cells -recognize and eliminate viruses, cells infected with viruses and some cancer cells Plasma Protein System Response 1. Complement System -perpetuates inflammation -causes bacterial cell lysis (pokes holes in cell membrane) Classical Pathway : activated by antibody/antigen complexes Lectin Pathway: activated by bacterial carbs Alternative Pathway: activated by gram-negative bacterial and fungal wall polysaccharides 2. Clotting System -Primary : vasoconstriction and platelet plug formation -Secondary - formation of stable clot, generation of fibrinogen (soluble), to fibrin (non-solvable) which forms clot. Extrinsic Pathway -external trauma -involves factor VII Intrinsic Pathway -activated by vasculature trauma -slower but more important 3. Kinin System -activated by collagen -final product is bradykinin (vasodilation, vascular permeability, pain signals)

Pancreatic Duct and Secretions

Secretion (proteases, amylases, lipase) are produced in the Acini flow uno the central conduit called the PD which are then delivered tot he duodenum. -this is the last glans to secrete digestive enzymes so it is responsible for that final enzymatic breakdown into absorbable molecules. -also secretes an aqueous fluid as a medium for enzyme transport. Protease - breaks down polypeptides in duodenum. Mucous secretion from the duodenal cells protect intestinal wall. -secreted as proenzymes and pancreatic proenzymes are activated in the duodenum (this is a protective measure) 1. Trypsinogen is a proenzyme that is activated into a protease called trypsin in the duodenum cells. Cascade effect of activating other trypsinogen molecules. -can turn on other proenzymes -for this reason, pancreas produces a trypsin inhibitor that prevents accidental activation of trypsinogen while still in the pancreas. Lipases - secreted by acinar cells responsible for fat digestion (breaks down triglycerides into absorbable fatty acids) and can be secreted as its active from straight into the duodenum. -pancreas is the only gland who produces lipase and can't perform fat digestion without it. Amylase - breaks down polysacarides into disaccharide that can be absorbed in the intestines. Can be secreted in its active form straight into the duodenum.

Hormones

Somatostatin - produced by Delta cells & is essential in nutrient substrate metabolism (protein, fats, carbs) -may be involved in hi biting glucagon and insulin secretion -limits parietal cell secretions Gastrin- poorly understood, likely controls secretion of glucagon -promotes stomach digestion Gherlin - stimulates appetites, promotes satiety and plays a role in insulin sensitivity regulation Pancreatic Polypeptide - released by F cells in response to hypoglycemia and protein-rich meats promotes gastric secretions

What are the two classes of anti-inflammatory drugs? Where is their mechanism of action?

Steroidal -cortisone -hydrocortisone -glucocorticoids are hormones produced by the adrenal cortex that have anti-inflammatory effects due to inhibition of phospholipase -increase liver glycogen -increase blood glucose levels -affect metabolism -block the action of phospholipase Non-steroidal -aspirin -ibuprofen (motrin) -naproxen sodium (aleve) -celecoxib (celebrex) -indomethacin (ihdocin) -ketorolac (toreador) -block the action of cyclooxyrgenase (COX) enzymes, COX make prostaglandins COX 1 - nonselective , aspirin COX 2 - selective just for pain , celebrex -NSAIDS are also prostaglandin inhibitors and have fewer side effects of glucocorticoids -GI ulceration, bleeding, bone marrow suppression

Histology of stomach

Stomach lumen is made up of folded gastric epithelium into gastric puts that make the lamina propia 1. Parietal Cells -secrete HCL (pepsinogen to pepsin due to low pH 1-3, break down of large protein fibers, and kill microorganisms) and intrinsic factor (binds to b12 for absorption) into the gastric pits 2. Chief Cells - secrete pepsinogen (this is a proenzyme meaning it is secreted into gastric pits, makes its way tot he gastric lumen and once it is exposed to the acidic pH of the stomach (activated by HCL) it converts into the active enzyme pepsin) Pepsin is a protease that digests protein into small chain fatty acids -gastric lipase (does not need a proenzyme) 3. Surface Epithelial Cells/ Mucus - secrete mucous that coats the inner lining of the stomach which is a protective, alkaline barrier against HCL & pepsin. -any irrigation or direct stimulation of gastric lining by ingested food will stimulate mucous production -release of prostaglandins is another factor that stimulates gastric mucous production -physical barrier -neutralize H acid by lining. 3. Enterochromaffin-like Cells - secretes histamine in response to PNS activity (gastrin - stimulates gastric acid and mucous production) from parietal cell secretion HIS MUFFIN-histamine H2 blockers don't work the best because other things can directly stimulate HCL secretions 4. D-cells - secretes somatostatin when pH stops to inhibit further parietal cell secretions (enterochromaffin-like cells are opposite) D DECREASE -stops parietal cell secretions, also found in the pancreas G Cells- gastrin secretion promoted

Define types of debridement

Surgical Debridement -uses a scalpel or other sharp instruments to remove devitalized tissue Enzymatic Debridement -applying exogenous enzymatic agents to the wound Biological debridement -maggot therapy

Why is traction used? What are the common types of traction? How is Buck's traction different from manual traction? From skeletal traction? What is a halo?

TRACTION - devices can exert a pulling force, weights that provide a constant isotonic force -these forces must remain constant until fracture edges untie 1. is to prevent muscle spasm 2. immobilize joint or part of body 3. reduce fracture or dislocation 4. treat joint pathology 3 types 1. manual -exerts pulling force on bone, reserved for stable fractures or dislocation prior to immobilization 2. Skin (buck's) -used for fractures requiring moderate pulling for a short period of time (pediatric) should not be used if more than 5-7 lbs of land os required 3. skeletal - force directly to bone, using pins of halos, 20-30 lbs, control rotation Halos- device around the head, allows patient out of bed, combined with body jackets,

Identify the spectrum, MOA, and teaching priorities for anti-infective drugs

Vanco - allergic to penicillin -cidal (kill it) and static (prevent it from spreading and diving)- plasma concentration of the drug or the bacterial species. -administer on a regular interval Narrow spectrum (selective) - early penicillin Broad spectrum (non selective) - meropenem Adverse Side Effects -Nephrontoxocity - kidney damage -Gastointestional Toxicity -Ototoxity -ears -Hypersenstivitiy Supra infection- C DIF Peak (highest concentration of drug present in the blood) and Tough (lowest level of drug before giving another dose of antiinfectives) - clearing Interferes Cell Wall Synthesis B lactams -penicillin (bacterial -cidal), vanco if allergic OR aztreonam (ring structure is slightly different) , most common Monobactams Glycopeptides/lipoglycopeptides Penicillin - therapeutic and prophylactic -diarrhea (orally) -urticaria (rash) -Steven's Johns Syndrome SJS -a t-cell mediated cytotoxic reaction to drug antigens in keratinocytes -can get into bodily fluids Ampicillin - synthetic pen, lessen contraceptives, little broader spectrum Amoxicillin - oral ampicillin equivalent, drug of choice for endocarditis, amoxicillin. Cephalosporins - beta lactic from fungus 5 generations if allergic to pen pros allergic to this as well. 2ns gen- gets into spinal fluid and can treat meningitis (inflammation of the brain and spinal cord) Carbapenems -vacomycin inhibits cell wall synthesis and given when allergic to pen -oral prep can be used from bowel infections particularly C diff -Red Man Syndrome (harsh flossing of the skin) slow the IV infusion rate and treat with antihistamines Daptomycin - binds and depolarizes cell membranes leading to cell lysis from electrolyte disturbances -use for vanco gallery or resistant Tetracycline - mess up teeth by binding to calcium -milk, antacids, or iron -broad spectrum Macrolides - erythromycin are strong inhibitors of CYP enzymes (metabolize and eliminate drugs) Aminoglycosides - alter protein synthesis Sulfonamides - inhibits growth of bacteria by inhibits the growth of bacterial. Fluroquinolones metronidazole

Define visceral pain, and discuss why it is often referred pain.

Viceral pain is pain from your internal organs that are mostly innervated by your C-fibers, dull/deep/nausea pain triggered by 1. smooth muscle distension 2. stretching of capsule surrounding organ 3. ischemia 4. necrosis or irritation by chem. inflammatory mediators. Visceral pain is where your referred pain comes from. due to the convergence of afferent to same dorsal horn Gallbladder is the shoulder.

Nutrition Part 2 N/V

Vomiting Center -lies in the medulla oblongata -direct stimulation or increased inter cranial pressure due to head trauma can lead to projectile vomiting -indirect stimulation can be from back of throat stimulation, dissension of stomach, intestinal, vagal or sympathetic input based on presence of certain substance in duodenum, vestibular response to motion, medications, trauma of pelvic organs, emotional factors Can lead to -hypovolemia -hyponatremia -cerebral edema due to pulling water into cells -metabolic alkalosis -elevated blood pH Critical areas of the brain cause nausea from emotion

Nutrition

The science of optimal cellular metabolism and its impact on health and disease Optimal - all nutrients are available in balanced amounts Sub-optimal (mal nourished) - insufficient to excessive nutrients avaliable Poor - negative impacts on health, imbalnace cant support you anymore Poor health can cause poor nutrition and poor nutriton can cause poor health Macronutrients Carbs prtoteins fats Micro vitamins minerals photochemcials (immune boositng, antioxidant, antimicrobial)

How do phagocytic cells recognize pathogens and differentiate inflammatory stimulus related to tissue trauma?

They identify "self" cells through MHC Major Histocompatibility Proteins on the surface of all cells except RBC. They recognize "non-self" through 1. Exogenous pathogen-associated molecular patterns (PAMPs) -proteins (antigens) found on pathogen walls 2. response to PAMP's initiates adaptive immune response -self recognition is an autoimmune disorder TRL's (toll-like receptors) are recognition receptors on neutrophils and macrophages that recognize PAMP's (foreign antigens) and trigger phagocytic destruction and secretion of prolonged inflammation -the adaptive immune response must be triggered, requires the generation of antigen presenting cells that can travel from the site of inflammatory response to lymphatic organs and stimulate WBC response -TRL have specific recognitions for pathogens PAMP and tissue injury DAMP Trauma Related -injured or necrotic cells release DAMP's that send signals and bind to TRL on neutrophils and macrophages -DAMPS endogenous associated molecular patterns are recognized through ATP released from trauma-damaged cells -TRL recognition of DAMP initials secretion of chemicals that prolong inflammation

Population Coverage

To be significantly effective in prevention of disease at community level a satisfactory proportion (75% or more) of the at risk population must be immunized.

Viral Infections

Transient infections -by viruses that elicit an effective immune response that eliminates the virus -may or may not have life-long protections ex. wast nile, viral hemmorhagic fevers, influenza Chronic Latent Infections -immune system cannot eliminate virus and individual has persistent viremia ex. hep B. herpes virus, periodic reactivation and shredding of virus (herpes simplex virus, cytomegalovirus, varicella-zoster virus) Transforming Infections -implicated in human cancer -Epstein-Barr Viruss (EBV) -HPV

UTI

Upper is pyelonephritis (kidney) Lower cyctisis urethritis (STI) prostatitis More common in females and kids (shorter LOH, immature tubular function, nephrons are less efficient, kidneys are still growing) Dysuria increased frequency hematuria fever n/v flank pain Urinalysis cyctisis, prostatitis, pyelonephritis e coli, strap. saptophyticus, proteus mirabilis, klebsiella, enterococcus Urethritis chlamydia gonorrhea Teaching -front to back -avoid tight clothes -cotton underware -avoid holding -freqeunt urination -empty bladder completely -avoid straining with stool -encourage fluid intake

Differentiate urge, stress and overflow incontinence. What treatment options, including pharmacological, are available?

Urge incontinence -detrusore muscles are contracting -involuntary leakage accompanied by immediate urgency -associated with detrusor over-activity (involuntary contraction of detrusor) that may be age-related, idiopathic, secondary to lesions in central inhibitory pathway or local bladder irritation (infection, bladder stones, inflammation, tumors) -neurologic disorders -600 mms capacity -300 mms is a normal void -relaxes normally and only contracts when voiding Stress incontinence -leakage with effort to exertion on sneezing or coughing -coincident with increased intra-abdominal pressure in absence of bladder contraction -leakage due to impaired pelvic support or less commonly failure to close urethra. -pressure -some kind of motion that is putting stress on pressure. -detrusor muscle is not contacting Mixed Incontinence -leakage with urgency and increased pressure Overflow -urethral blockage and prevents normal emptying -catheterization Treatment 1. behavioral -times voiding -fluid restriction 2. pharm -alpha-adrenergic agonists (increasing urethral tone) -tricyclic antidepressants (anticholinergic effects -cant pee) -anticholinergic agents (reducing urge) -muscarinic agonists (increase smooth muscle tone and stimulate bladder to contract making emptying easier, not used in BPH) 3. functional electrical stimulation 4. surgery

What are the stages of infection?

Vaccine-Preventable Pertussis Cathedral Stage : most contagious, cough is dry, hacking, lasts 1-2 weeks Paroxysmal Stage : whoop, high pitched crowing sound, often cheeks flushed eyes bulge and lounge protrudes, lasts 4-6 weeks Convalescent Stage: cough is dissipating, cough can return with subsequent respiratory infections, lasts 7-10 days 1. Colonization 2. Invasion 3. Multiplication 4. Spread Clinical Infectious Disease 1. incubation - initial entry of the pathogen to the host 2. prodromal - organism continues to multiply and host will experience s/s but will be non specific 3. invasion ILLNESS - s/s of ideas are severe and usually type of disease is evident by s/s 4. Decline - period of decline 4.Convalescense- no signs or symptoms

What is the role of antigen-presenting cells in the immune response?

When TRL encounters PAMP, this pathogen presence requires the triggering of the adaptive immune response. Adaptive immunity requires the generation of antigen presenting cells -APC travel from the site of inflammatory response to lymphatic organs and stimulate leukocyte response "Self-antigens" and "danger signals" are a type of MHC-1 major histocompatibitly protein and can be one of 3 HLA proteins -HLA mark self identification -all nucleated cells have MHC 1 -cytotoxic T-cells have new type of MHC 1 marker that include piece of invading antigen from pathogen Phagocytic cells can become APC through processing pathogens and creating a new antigen 1. intake enemy 2. break it down inside 3. enzymes degrade enemy cell 4. small enemy fragments of antigen present on APC surface 5. leftovers are released through exocytosis Antigen Presenting Cells with MCH 2 proteins 1. dendritic cells, t-cell areas (viral antigen) 2. B cells, follicle (microbial toxin) 3. Macrophages (bacterium) -MCH 2 are only on APC -Helper T cells have this bc APC will come to lymphoid tissue

What is reduction? What are the types of reduction? What is fixation?

aligns fracture fragments to correct anatomic alignment and rotation -this minimizes soft tissue complications Closed reduction -aligns bone fragments through manipulation or manual contact Common Joint reductions -elbow dislocation -shoulder dislocation -hip dislocation TRACTION - devices can exert a pulling force, weights that provide a constant isotonic force 1. is to prevent muscle spasm 2. immobilize joint or part of body 3. reduce fracture or dislocation 4. treat joint pathology Open Reduction -aligns bone fragments through a surgical incision utilizing internal fixation device Fixation is Immobilization Internal fixation -utilizes wires, screws, pins, plates intra-meduallry rods or nails to immobilize the fracture External fixation -utilizes bandages, casts, splints, continuous traction or external fixators to immobilize the fracture

Define neuropathic pain.

type of chronic pain w exacerbation stemming from dysfunction of nerves -neuropathy (loss of sensory) secondary to conditions like diabetes, spinal injury, stroke, cause is unknown.

What is the origin of B cells? How are they activated? What happens when a B cell is activated? What two types of cells are produced, and what is their function?

b cells are produced from stem cells in the bone marrow and remain there to complete maturation Stem cell to lymphoid precursor to B cell to plasma cell B cells = humoral = external cel attack of pathogens B cells have membrane-bound antibodies (immunoglobulins) that differs from TRL's (identify major classes of pathogens) Immunoglobulin allow for binding of one particular type of pathogen APC come to B cell with MCH 2 complex and interacts with immunoglobulin on B cel surface and activate differentiate. Differentiation causes the Native B cell to 1. proliferate (clonal expansion) 2. design some new cells plasma and memory cells - this is slow bc limited native b cells are sitting around Plasma cells produce antibodies specific to the antigen -antibodies are proteins that enhance innate immune response to promote antigen destruction -enhance phagocytosis through neutralization (opsonization), agglutination(deformation), precipate dissolved antigen particle Antibody-antigen complexes stimulate complement proteins (bacterial lysis and inflammation) -2000 per second -5-7 days Memory B cells "withdraw from the cell cycle" -larger immunoglobulin cells before clonal expansion, so if pathogen comes again more cells will see it -much quicker response to proliferate and differentiate when memory cell binds to antigen

Nutritional Disorders PUD Peptic Ulcer Disease

condition that result in a break in the mucosal lining of the digestive tract - 5 million in US have this. -75% of PUD are caused by H. Pylori infection -organism burrows into mucus and converts urea into ammonia & Co2 and neutralizes HCL acid in the stomach which allows the bacteria to survive in the upper digestive tract. -tunnels created by bacteria also waken the mucus layer and HCL, pepsin, cause direct inflammation. Early stages are gastritis and chronic inflammation. Also, H.Pylori is thought to stimulate gastrin (makes more HCL) and turns pepsinogen to pepsin which breaks down the stomach lining. Can induce carcinogenic changes in the epithelial cells. -NSAIDS increase the risk of peptic ulcer disease (lowers prostaglandins, lowers mucous secretion, and increases ulceration risk) -20% of people have family history w duodenal ulcers -Nicotine stimulates stomach acid secretion and enhances pepsinogen to pepsin -Alcohol can erode mucosal layer and irritate stomach lining which increase HCL secretion. Patho -acid can cause cell injury and pepsin will begin to auto digest the tunica mucosa leading from lesion to erosion. -once its past the tunica mucosa into the sub, its an ulcer and since the submucosa is vascular the lesion will often bleed. -erosin can occur down to tunica muscular and eventually lead to perforation of the digestive tract wall LABS 1. Gastri mucosal biopsy -rapid urease test -histopathology -culture 2. Fecal antigen testing 3. Blood test -antibodies to H. Pylori

Cancer pain

considered chronic acute pain resulting from chemical mediators secreted by tumor cells that stimulate acute nociceptive pain -nerve pain can also simulate neuopthic pain

Diarrhea

dehydration hypokalemia (majority of dietary K+ is reabsorbed in large intestine) metabolic acidosis 9significant bicarb loss) Osmotic : have matter that is poorly absorbed or unabsorabale so as it goes thorough GI it pulls water Secretory: over excrete Cl- or bicarb or Na+ is not absorbed correctly, Entertoxins by bacteria which will causes water to go into feces. Can get acidotic. Base out the butt. Motility : shorting of the bowel, short bowel syndrome, occurs due to resection of some portion of the bowel.

Wound dressings

gauze -allows moisture in wound bed to evaporate, lowering temperature, causing vasoconstriction and hypoxia Hydrofiber -transforms soft gel form after absorbing liquids creating most wound environment -wound packing silver (antimicrobial activity) -used to fill wound cavities -permits gas exchange -wound fillers help collagen play a critical role in all phase of wound healing Negative Pressure Wound Therapy -reduces edema and increases the rate of granulation tissue formation\ -stimulates circulation

Lorazepam

help with emotion factors as well as nausea.

Serotonin Antagonists

inhibit the action of serotonin on the 5-HT3 receptor in the small intestine, vagus nerve and CTZ. -decreases afferent visceral and CTZ stimulation of the vomiting center -minimal side effects

" What is the role of pain in the body?

it is a protective mechanism. You will get a signal (a produce from the nervous system) but your brain is the final say. Pain is subjective to the person and is emotional due to traveling in the limbic system.

Review basic structure and function of skin

it is the largest organ -first line of defense -receptors for pain, pressure, heat and cold -regulates body temperature through vasoconstriction and dilation of vessels in the dermis -involved in the production of vitamin D 1. epidermis -outermost layer -keratinocytes -continuously generated and migrate from the dermis 2. dermis -inner layer -composed of collagen to perform elastin and flexibility -contain hair follicules 3. hypodermis -submucosa tissue -contains major blood vessels, lymph, and nerves Skin color Melanin Carotene Hemoglobin

Describe some of the problems with unresolved pain.

leads to emotional distress, suffering, to lack of control, anxiety, spiritual distress that can lead to CHRONIC PAIN In periphery -reduce inflammation -limit additional tissue damage In spinal cord -NMDA antagonists (ketamine, methadone) -opioids -adjuvant therapies (anti-inflammatories, non-pharmacologic methods)

Understand what influences blood sugar in the body

low blood glucose is going to trigger alpha cells of pancreas to release glucagon and the liver will release glucsoe into the blood to achieve normal blood levels High glucose will trigger beta cells to release insulin and fat cells take in glucose from blood

What is pain

unpleasant sensory and emotional experience associated with actual or potential tissue damage pain is always the product of the nervous system sending signals, with the brain having the final say

Describe gate control theory.

neural gate can open and close thereby modulating pain closed- small diameter pain fibers dont excite dorsal horn transmission when the gate is closed , AB fibers Physical - medications, counter stimulus, heat massage, Mental - concentration, distraction, involvement in life activities, Emotional - positive emotion, rest, relaxation Turn off pain signals Open - signals excite dorsal horn transmission cells -AD and C fibers -physical (injury extent, inappropriate level of activity) -mental (focusing on pain, boredom) -emotional conditions (anxiety worry tension depression)

Identify mechanism of action for opioids and non-opioid analgesics.

nociceptive pain NSAID and acetaminophen //tylenol Analgesia Opioid Gabapentin -neuropathetic pain, anticonvolusant NSAIDS- decrease inflammation decrease pain -non selective or non selective -asprin is non-selective (RAYS syndrome, don't use aspirin before 18 years old, ringing in the ear is a sign of toxicity. ) -celebrex is selective for COX 2 Acetaminophen - antipyretic but not antiimflammatory, NSAID is stronger and have ceiling dose MU receptors are the primary targets for opioates Codine and hydrocodone are pro drugs, and effect CYP deficiencies. Fentanyl -mcg not ml and is strong than morphine

Define equilanalgesia

non-noxious (no damage) can start to stimuli are able to produce a pain signal.

Phenothiazines

reducing intensity of nausea signals (dopamine) to the brain 1. alpha blockade (hypotension) 2. histamine blockade (sedation) 3. muscarinic blockade (anticholinergic effects) 4. dopamine blockade (EPS -typically post op or drug induced nausea and vomitting -known to treat psychosis at a much larger dose

Nutritional Disorders GERD

reflux of HCL and gastric enzymes through LES and into esophagus Risk factors - hiatal hernia -pyloric sphincter stenosis Patho -decreased LES tone &/or increased intra-abdominal pressure results in refuels of HCL and pepsin into lower esophagus. -erosion and ulcerations -epithelial injury stimulated inflammatory response and edema H2RB are short term treatment for GERD

Transmission (ascending)

site of stimulus will travel thorough the first afferent fiber (primary fibers) to the dorsal horn and release a NT (substance P, glutamate) then secondary fiber (opioid receptors MU, K, D) will travel to the thalamus (spinothalamic) then third fiber will travel to somatosensory cortex (spinoreticular) and other cortexes to locate and interpet pain.

Diabetes Mellitus

syndrome characterized by chronic hyperglycemia and other disturbances of carb, fat, and protein metabolism. DM Type 1 A- b cell destruction usually leading to absolute insulin deficiency -autoimmune destruction of pancreas -HLA complex, which helps the immune system distinguish the body's own proteins from foreign invaders is not present. -10% higher is of getting DM1 if parent or sibling has it. -viral infections can cause autoimmune disease (rubella, and cytomegalovirus) -dietary triggers (cow's milk and nitrosamines and stressful factors have also been linked. -cytotoxic T cells and antibodies will do the killing -alpha cells will continually release glucagon thinking cells are starving and increase glucose in blood steam. Results -DKA fruity breath DM Type 1B - less common autoimmune and is secondary to other diseases like chronic pancreatitis and cystic fibrosis. -asain or african decent Destruction of Pancreatic B Cells -alpha cells are not triggered by insulin release (insulin inhibits glucagon release) therefore an increase of glucagon causes imbalance and leads to hepatic glucose & fat metabolism which both contribute to hyperglycemia. Consequences of DM 1 -cell starvation bc glucose can't enter cells -AA uptake and protein synthesis can't happen due to lack of insulin (loose weight) -fatty acids become primary fuel source (DKA) -hyperkalemia Osmotic Diuresis -hyperglycemic conditions often make carrier molecules in PCT reach full saturation (Tm) for glucose reabsorption in the kidneys. -glucose then is excreted in the unrine and water follow due to osmosis, preventing reabsorption and causing diuresis. -Decreased K+ uptake into the cells, can cause hyperkalemia and can cause fatal arrhythmia -lack of insulin promotes lipolysis so the new FA can be used as a fuel source. These liberate ketones, and if kidney can not rapidly secrete them then acidosis occurs. DKA CM -Hyperglycemia causes 1. polyuria - due to osmotic diuresis and urine will be glycosuria 2.Polydipsia - THIRST due to increase glucose serum and dehydration from osmotic diuresis 3. Polyphagia & weight loss - constant unger and eating will still loos weight since cells metabolize AA since they are starving from no glucose uptake. DM Type 2 -results from progressive insulin secretory defect on the background of insulin resistance (down regulation of receptors and hormone) Risk Factors -obesisty (especially truncal) and inactivity leads to release of adipokines -over age of 40 -ethnicity (NA and AfA) -family history -development of insulin resistance -hyperinsulinemia (down regulation of insulin receptors) leading to insulin resistance Insulin resistance 1. hyperinsulinmia -down regulation of receptors 2. abnormalities in membrane transport mechanisms of glucose 3. post-receptor defects where signaling pathways in insulin-dependent cells are impaired 4. release of adipokines by adipose cells (obesity) stimulate insulin resistance due to inflammation of the beta cells which can lead to type 1 DM. Path 1. could have genetic defect that prevents the ability to secrete more insulin in ratio to glucose intake. Consequences of DM2 -decrease glucose uptake -osmotic diuresis -development of dyslipidemia - low HDL and high triglycerides (fat mass releases lipids into plasma in order to give starving cells food long before type 2 is diagnosed) -beta cell destruction and decrease insulin secretion (adipokines and anyloids from protein strains infiltrate pancreas, type 2 can lead to type 1) CM 1. hyperglycemia 2.polydispia -frequent thirst 3. polyphagia and weight loss (uses AA and FA as fuel source instead of glucose) 4. Fatigue Regular insulin - cant eat right after but eat withint 30 mins

Respiratory Pertussis

the bacteria deforms the cilla in the respiratory tract and makes the toxin less likely one cleared out and more likely to diffuse into the system.

PPI Proton Pump Inhibitors

the proton pump in parietal cells is activated by input from gastrin, histamine and Ach receptors. -disabling the pump will cause great decrease in acid production (90%) -take 30 mins before meal bc PP is activate by food.

Define types of musculoskeletal trauma: fractures, strains, sprains, etc.

tissue that is subjected to more force than it can absorb -depends on amount of force and location Types 1. soft tissue trauma -contusion : bleeding into soft tissue the can cause hematoma, swelling and discoloration -sprain : ligament injury due to twisting motion. Grade 1 = swelling and stiffness Grade 2 = tearing and bruising Grade 3= ligament fully torn Strain :microscopic tear in the muscle 2. fractures - resistance of bone against stress is overcome by stress force resulting in discontinuity in structure 3. complete amputation