Exam 2
aortic dissection
"A tear in the media" ripping apart of the tunica media of the aorta by way of blood entering through a tear in the tunica media 2 types: Type A affects the ascending aorta Type B any dissection that does not affect the ascending aorta Treatment: Ultrasound, CT, MRI, angiography Lifestyle modification Surgery
Takotsubo Cardiomyopathy
"broken heart syndrome"; treatment is supportive---heart failure a person is in severe psychological and/or physiological stress and they develop stress-induced cardiomyopathy; release of catecholomines; causes an enlarged left area of ventricle mostly seen in women of post menopausal age symptoms: Chest pain (angina) Shortness of breath or difficulty breathing (dyspnea) Syncope, or fainting Presents with STEMI EKG changes Serum biomarkers increase No evidence of CAD
chronic blood loss related anemia
# 2 cause of iron deficiency anemia Cell morphology: Microcytic/hypochromic → b/c chronic blood loss Sources/Symptoms: Symptoms similar to iron deficiency anemia GI bleeding Hemorrhoids Menstrual blood loss Diagnostic Studies :Identifying source Treatment: Stopping bleeding Supplemental iron administration
ventricular remodeling
(1) Progressive myocyte (myocardial cell) contractile dysfunction over time; results from activation of the renin-angiotensin system caused by reduced blood flow to the kidneys, a common occurrence in low-output states; (2) after a myocardial infarction, permanent changes in the size and shape of the left ventricle due to scar tissue; such remodeling may decrease left ventricular function, cause heart failure, and increase morbidity and mortality.
3 layers of the heart
(outer) epicardium--start of coronary arteries, (middle) myocardium, (inner) endocardium
Clinical manifestations of sickle-cell anemia
*Typical patient is asymptomatic, except during sickling episodes *Back, chest, extremities (bone and joints), abdomen most common *Symptoms: Pain and swelling Fever, tenderness, tachypnea, HTN, n/v ,Pallor of mucous membranes, Shortness of breath, fatigue, dizziness jaundice (Jaundice occurs because the rapid breakdown of the red blood cells releases a byproduct called bilirubin and since the RBCs are breaking down quicker there is more bilirubin in the blood) Sickling episodes Sickle cell crisis (pain caused by inadequate blood flow) *Vaso-occlusive (occurs in any part of the body) pain Acute Tissue hypoxia Acute chest syndrome Atypical pneumonia d/t pulmonary infarction
Folate deficiency
*deficiency in folic acid *MCV >100 *Hb and Hct decreased *reticulocyte decreased (< 2.5) *macrocytic *pancytopenia *homocysteine decreased Causes: Malnutrition Dietary deficiency Alcoholism Malabsorption Pregnancy *Insidious onset: progress slowly Symptoms can take a few months to manifest *Daily requirements: 50 micrograms/day ↑ need during pregnancy & lactation Women planning to get pregnant and pregnant should supplement Treatment: folate replacement therapy Eat foods with large amounts of folic acid
causes of vitamin K deficiency
*take blood thinners, or anticoagulants, which prevent blood clots by inhibit vitamin K activation *take antibiotics that interfere with vitamin K production and absorption *do not get enough vitamin K from the foods they eat *take extremely high doses of vitamin A or E *celiac disease *cystic fibrosis *an intestinal or biliary tract (liver, gallbladder, and bile ducts) disorder *having had part of the intestine removed, such as during bariatric surgery
Heart Failure Compensatory Mechanisms
-Frank-Starling Mechanism - ↑ heart SV by ↑preload -SNS activation (release of catecholamines, which increase heart rate & contractility) -RAAS activation -cardiac hypertrophy Damaging effects over time >damage to endothelial >Increase risk for cardiac arrhythmias & sudden cardiac death >Increases workload of heart & myocardial O2 demand >Increases afterload and ventricular wall stress
stages of clotting
-Primary hemostasis -Secondary hemostasis -Final stage (fibrinolysis or thrombolysis)
complications of CAD
-formation of thrombosis -hypertension -myocardial infarction -heart failure
treatment of hydronephrosis
-removal of obstruction -stent insertion -nephrostomy tube -antibiotics
Key Properties of Myocardial Cells
1. Automaticity: Can produce electrical activity without outside nerve stimulation 2. Excitability: Ability to respond to an electrical stimulus 3. Conductivity: Ability to transmit an electrical stimulus from cell to cell throughout myocardium 4. Contractility: Ability of myocardial cell to contract when stimulated by an electrical impulse
Steps in the development of atherosclerosis
1. irritant damages the endothelium 2. LDL settles into the damaged endothelium forming a "fatty streak" 3. "fatty streak" oxidizes sending signals to the immune system to launch an inflammatory response 4. monocytes travel to plaque build-up, transforms into a macrophage that begins to eat the oxidized plaque 5. macrophage becomes engorged with plaque/cholesterol and dies (now known as a "foam cell"); when the macrophage dies, it sends out cytokines calling more macrophages and T-lymphocytes to the site of plaque 6. smooth muscle cells begin to release calcium into the plaque from below making it hard 7. Smooth muscle cells, ECM form fibrous cap over dead fatty core- atheroma (plaque) in an attempt to prevent thrombogenic materials from leaking
5 stages of chronic kidney disease
1. kidney damage with normal or increased GFR >90% 2. kidney damage with mild decrease in GFR 60-89% 3. moderate decrease in GFR 30-59% 4. severe decrease in GFR 15-29% 5. kidney failure < 15% of normal capacity (or dialysis) stages 1-3 PT are usually asymptomatic
Stages of hemostasis (blood clotting)
1. vasoconstriction 2. temporary platelet plug: primary homeostasis 3. coagulation-secondary homeostasis-clot contraction-serum formation 4. fibrinolysis: dissolves the clot, restores function 5. regeneration (repair)
urine specific gravity
1.010 - 1.025 a test that measures the concentration of solutes in the urine the darker the urine the higher the SG, because it is more concentrated with solutes elevated SG causes: dehydration, congestive heart failure, DM and SIADH decreased SG causes: DI, primary kidney disease (glomerulonephritis, pyelonephritis, and acute tubular necrosis). Ability of the kidneys to reabsorb water is disabled
blood pressure ratio
1/3 of 1 heart beat is systolic 2/3 of 1 heart beat is diastolic
Prothrombin normal range
11 to 13 seconds
ventricle
2 lower chambers responsible for pumping blood out of your heart; The right ventricle pumps blood to your lungs for oxygenation, while the left ventricle pumps blood to your entire body the left side of your heart is responsible for pumping that newly oxygenated blood all of the way down to your fingers and your toes; therefore, the myocardium is much thicker in the left ventricle than the right.
coagulation pathway
2 pathways: intrinsic and extrinsic
rheumatic heart disease
2 types: acute and chronic rheumatic fever; an inflammatory condition of the heart that occurs as a result of an autoimmune reaction to infection by streptococcal bacteria; The autoimmune response to rheumatic fever destroys myosin and endothelium, thinking that it is destroying M-proteins in streptococcal A. This causes rheumatic heart disease. a disease of the heart that is initially caused by strep throat. If the strep throat is left untreated it can progress to rheumatic fever and rheumatic heart disease
atrium
2 upper chambers of the heart; receiving chamber of the heart; walls are thinner; do not generate large contractions; left and right atrium are roughly the same size; no intake valves allowing blood to flow in continuously during contraction and relaxation
phases of MI repair
2-3 days - Acute inflammatory response Leukocytes infiltrate area & proteolytic enzymes degrade necrosis Macrophages remove necrotic tissue Granulation tissue begins forming 3-7 days - Infarcted center becomes soft & yellow Granulation tissue continues to form(less vascular & more fibrous) 10-14 days - Collagen matrix forms Stress can occur to area from increased patient activity 6-7 weeks - Scar tissue complete Lack ability to contract & relax like healthy tissue Unable to initiate or conduct action potentials
Hemolytic anemia
3rd major cause of anemia a condition in which the red blood cells are destroyed (intrinsic: due to defects in the cell) faster than they can be replaced; normocytic; hyperactive bone marrow; ↑ reticulocytes 2 types: inherited-sickle cell (RBCs only live 10-20 days) acquired-drug/medication induced; Treatment: Eliminating the causative agent Steroids, blood products
structural and functional changes in the heart due to MI
60 seconds - loss of contractile function 20 - 40 minutes of severe ischemia - necrosis occurs Zone of infarction-necrosis Zone of hypoxic injury (O2) Outer zone/Zone of ischemia (blood supply) Stunned myocardium Temporary loss of LV contractility Scar tissue Treatment
BUN (blood urea nitrogen)
8-20 mg/dL When proteins are digested by your body, a substance called ammonia is generated. Ammonia then goes to the liver, where it is converted into urea, and this travels via the blood to the kidneys, where it is excreted out in urine as a waste product---this is what is measured to determine liver and kidney health decreased levels indicate liver diseases or malnutrition increased levels indicate kidney disease or congestive heart failure
Causes of urethral stricture
>A medical procedure that involves inserting an instrument, such as an endoscope, into the urethra >Intermittent or long-term use of a tube inserted through the urethra to drain the bladder (catheter) >Trauma or injury to the urethra or pelvis >An enlarged prostate or previous surgery to remove or reduce an enlarged prostate gland >Cancer of the urethra or prostate >Sexually transmitted infections >Radiation therapy
causes/risk factors of aneurysms
>Atherosclerosis most common cause >Hypertension co-contributor in 50% individuals >Smoking >Infections (syphilis) >trauma >Collagen/connective tissue disorders (Marfan syndrome)
symptoms of DCM
>Dyspnea >Orthopnea >low ejection fraction (amount of blood pumped or ejected out of the heart's left ventricle with each contraction) >Thrombus formation, emboli >Arrhythmias, Sudden death >Cardiac output decreases, which triggers kidneys to activate RAAS
Polycythemia
>Excessive red blood cells present >Increased RBC count and hematocrit greater than 50% >2 types: relative and absolute *relative is "false"=plasma is decreased giving the impression RBCs are increased, but they really didn't; increased Hct *absolute has 2 types: primary and secondary secondary has 2 types: compensatory and abnormal
manifestations of aortic valve stenosis
>Systolic murmur ("ejection click") >Concentric left ventricular hypertrophy--Normal chamber size >Angina (1/4) >Dyspnea >Syncope (exertion) >Heart failure symptoms >Microangiopathic hemolytic anemia, which is essentially damage to red blood cells as they're forced through the smaller valve, splitting them into smaller fragments called schistocytes
Polycythemia Vera
>a blood cancer characterized by uncontrolled erythrocyte production. Virtually all patients with polycythemia have a mutation in JAK2, a cytoplasmic tyrosine kinase associated with EPO receptor. >mostly occurs in males average age of 62 >caused by a Myeloproliferative NEOPLASM or cancer of bone marrow >results in ↑ RBCs mass ↑ WBCs ↑ platelets >treatment: phlebotomy to reduce RBC volume; hydroxyurea to suppress bone marrow
Anemia of chronic disease
>an under production of RBC (iron is trapped), shortened RBC lifespan, decreased response to EPO >anemia of inflammation >most common anemia in RA, TB and Crohn's Disease patients, hospitalized and cancer patients, alcoholics and infection >2nd most common cause of any anemia >normocytic/normochromic >S/S=murmur, angina, weak, irritable, tired and pale, can't exercise
clinical manifestations of CKD
>azotemia >metabolic acidosis: kidneys cannot excrete H+ >hypertension >cannot activate vitamin D---thus calcium cannot be absorbed from the GI tract leading to HYPOCALCEMIA >renal osteodystrophy >decreased levels of EPO causing anemia >uremia >edema: unable to excrete Na+ and water >hyperkalemia >hyperphosphatemia
tPA (tissue plasminogen activator)
>converts plasminogen to plasmin >produced by the injured endothelium (takes 2-3 days)
anemia
>decrease in functional red blood cells >decreased oxygen carrying capacity of the blood >decreased total RBC mass >decreased Hgb, Hct, or RBC concentration
Folate vs. B12 deficiency
>increased MCV >100 = macrocytic >decreased Hb and Hct >decreased reticulocyte <2.5 >pancytopenia increased (increased in all megaloblastic anemias) >neurological impact in B12 ONLY >increased homocysteine >increase in methylmalonic acid in B12 only
purpura
>most common cause of thrombocytopenia >results from malfunction of primary hemostasis >it is a subcutaneous hematoma >3mm to 1 cm in size >due to extravasation of RBCs from the intravascular space to the dermis >does NOT blanch on pressure; RBCs are stuck in dermis
Plasminogen and Plasmin
>proteolytic enzyme that breaks down the clot in fibrinolysis by breaking down and inhibiting fibrinogen and fibrin (occurs during secondary hemostasis) >produced by the liver; a protein; floats in the plasma and then gets incorporated into the blood clot during it's formation (occurs during secondary hemostasis) >degradation products from the breakdown are cleared by the kidneys and liver
symptoms of aortic dissection
>severe "tearing" or "ripping >sharp, stabbing central chest pain that radiates to the upper back >N/V >sweating >lightheadedness >Cool, pulseless extremities >pulse differentials between UE and LE and right/left arms >BP differences due to impaired flow, ischemia leads to hypotension >Neurologic signs-paraplegia or hemiplegia >CNS changes >Decrease urine output (decreased flow)
symptoms of polycythemia vera
>↑ RBCs ↑ Hg ↑ Hct >↑ blood volume and ↑ blood viscosity Interferes with >cardiac output, blood flow resulting in dizziness, difficulty hearing and seeing d/t >↓ cerebral perfusion >Splenomegaly >Depletion of iron stores >Hypertension >Thromboembolism and hemorrhage >aquatic pruritis (hot showers release histamine causing itching)
rheumatic fever
A bacterial infection that can be carried in the blood to the joints symptoms: Fever, polyarthritis, erythema marginatum, chorea, pancarditis, murmur, Arrhythmias, pleural friction rub 2 types: acute recurrent group A strep Dx: Jone's Criteria
Causes of urinary stasis
A blockage (such as a kidney stone) that blocks the flow of urine out of the kidneys and/or through the ureters and urethra Dysfunction or weakening of the muscles around the bladder Urethral strictures (narrowing of the urethra) Damage to the nerves of the urinary system Enlarged prostate
Drug induced (heprin) 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 Heparin induced Associated with administration of heparin Can be triggered by any type, route or amount of heparin Pt develops heparin dependent anti-platelet antibody Clinical manifestations 5-10 days Possible thrombosis after heparin therapy (PE, DVT, MI, CVA) Thrombocytopenia symptoms Treatment d/c heparin, use alternative anticoagulant
anemia
A decrease in the oxygen-carrying ability of the blood causes: Altered RBC production in bone marrow Blood loss Increased destruction (hemolysis) Combination of factors
nephrotic syndrome
A glomerular disorder in which the pores in the glomerulus get bigger and results in hypoalbuminemia, proteinuria, and edema The glomerulus is the filter that is supposed to keep large things, such as proteins (albumin), inside of the blood while filtering out smaller toxins that get excreted in the urine. If the pores of the glomerulus, the little holes that allow for things to pass through the glomerulus and into the urine, are damaged, they get bigger. Bigger pores in any filter means that things that should've been kept out are now leaking into the urine and out of the blood.
hydroxyurea
A medication used in patients with sickle cell disease to prevent sickle cell crises (episodes of severe pain).
bile
A substance produced by the liver that breaks up fat particles.
blood loss and acute anemia
ACUTE: >Result of sudden hemorrhage: Trauma Surgery Vascular disruption >Interventions: Stop blood loss ID source Replace blood volume >Cell morphology: Normocytic/normochromic → b/c acute blood loss
characteristics of a MI
Abrupt severe, crushing chest pain (sudden, substernal, tightness) dyspnea syncope N/V Fatigue & weakness Sympathetic stimulation Skin - diaphoretic (diaphoresis) increased heart rate Restless/anxious SOB Radiation arms, back, neck, jaw Not relieved by nitro >15 minutes Severe cardiac dysfunction Ventricular fibrillation Silent MI - DM, older adults
complications of shock
Acute lung injury/respiratory distress syndrome Acute kidney injury Gastrointestinal complications Disseminated intravascular coagulation Multiple organ dysfunction syndrome
acute kidney injury
Acute renal failure, aka acute kidney injury, refers to a sudden and rapid decrease in the ability of the kidneys to filter the blood that develops in less than two days' time. 3 types: prerenal intrarenal postrenal
spectrin and ankyrin
As key components of the erythrocyte membrane skeleton, spectrin and ankyrin specifically interact to tether the spectrin cytoskeleton to the cell membrane
manifestations of heart failure
Atrial fibrillation. Sudden cardiac death Why? Nocturia (early) Why? Oliguria (late) Dyspnea on exertion Paroxysmal nocturnal dyspnea (PND) Fatigue Cardiac asthma Cachexia, malnutrition, and tissue wasting fatigue, depression, feeling of fullness from congestion Cyanosis How is this different for people of color? Pulmonary edema - Air hunger, pink frothy sputum, confusion, cackles Edema- Extremities, ascites, pleural effusions
types of aneurysms
Berry Fusiform Saccular Dissecting
left sided heart failure
Blood backs up: Left heart lungs right heart body Caused by diastolic and systolic dysfunction
Neural Mechanisms for controlling blood pressure
Cardiovascular center is located in the medulla oblongata The vagus nerve is stimulated during a parasympathetic response causing HR to decrease. Simultaneously, the vasomotor center is inhibited causing vasodilation and bronchoconstriction to occur. When the sympathetic nervous system is activated heart rate increases along with the force of ventricle contraction. During a sympathetic response the vasomotor center is stimulated causing vasoconstriction and bronchodilation to occur.
humoral mechanism for blood pressure control
Catecholamines (epinephrine and neoepinephrine)
risk factors of renal calculi
Caucasians experience them more than African Americans A personal or family history of kidney stones - once you have had them, you are more likely to have them again Obesity Gastric bypass surgery Immobilization Metabolic disorders Anatomic kidney or urinary tract abnormalities High blood pressure Diet: high levels of protein, salt, or sugar can cause stones to form, as can dehydration because less urine is produced
osmoreceptors
Cells in the HYPOTHALAMUS that monitor the concentration of solutes in the blood. An abnormal increase, as occurs in dehydration, stimulates the release of VASOPRESSIN from the PITUITARY gland. This acts on the kidney to reduce water loss.
baroreceptors
Cells that are sensitive to blood pressure changes.
Complications of acute pericarditis
Complications Pericardial effusion/restriction Cardiac tamponade Decreased CO → hypotension Pulsus paradoxus
Causes of aortic regurgitation
Congenital: Marfan syndrome Acquired: Infective Endocarditis, Rheumatic Fever, hypertension, trauma, valve failure, aortic dissection, syphilis Manifestations: Acute - Sudden large volume to LV Increase LV end-diastolic pressure Culminates in pulmonary edema Diastolic murmur Increased systolic pressure, decreased diastolic pressure Increased Stroke Volume LV eccentrically hypertrophies Heart Failure symptoms (dyspnea, orthopnea, PND) Widened pulse pressure (systolic-diastolic) Corrigan (water-hammer pulses) Quincke's pulse (capillary beds in the fingernails to pulsate) Decrease CO, sympathetic response Head pounding, palpitations, PVC
Signs and symptoms of urethral stricture
Decreased urine stream Incomplete bladder emptying Spraying of the urine stream Difficulty, straining or pain when urinating Increased urge to urinate or more-frequent urination Urinary tract infection
Diagnosis of Ischemic Heart Disease
Diagnosis Non invasive testing ECG ECHO Exercise stress testing Nuclear imaging studies Cardiac catheterization and coronary arteriogram
DX and TX of cobalamin deficiency
Diagnosis: CBC MCV>100fL MCHC WNL (macrocytic anemia) RBCs appear large Abnormal shapes Oval Shilling Test Treatment: injections of vitamin B12
Diagnosis and treatment of aplastic anemia
Diagnosis: Blood tests, CBC, Bone marrow biopsy Treatment: Identify and treat cause, Prevent complications
diagnosis and treatment of iron deficient anemia
Diagnostic Studies: CBC, Iron levels, Colonoscopy Treatment: Treat underlying disease/problem (blood loss, diet) Replacing iron
What does plasmin do?
Digests fibrin, fibrinogen, & clotting factors II (prothrombin), V, VIII, XII to break up the clots and prevent clot formation resulting in hypocoagulability
treatment of DCM
Diuretics, beta blockers, ACE inhibitors Cardioverters/defibs Heart Transplant
signs/symptoms of left-sided heart failure
Dyspnea orthopnea paroxysmal nocturnal dyspnea, or severe shortness of breath while sleeping Crackles in the lungs Fatigue paleness, or cyanosis Frothy pink sputum
acute coronary syndrome complications
Dysrhythmias Most common V-Fib->death Heart failure Cardiogenic Shock Stroke Thromboemboli Mechanical Defects Pericarditis
causes of mitral valve prolapse
Familial trait- lean, tall women Marfan syndrome Autonomic dysregulation Mucinous degeneration of valve
Symptoms of infective endocarditis
Fever, murmur change, emboli, bacteremia Petichiae (pinpoint red dots), cough, dyspnea, arthralgia (joint pain)
constrictive pericarditis
Fibrous scar tissue making the pericardium stick to the heart
heart anatomy
Four chambers: 2 upper atrium, 2 lower ventricles Four one-way valves: AV valves (tricuspid and mitral) close during ventricle contraction (lub sound); semi-lunar valve separate the ventricles from the blood vessels leaving the heart (pulmonary and aortic) closed during relaxation (dub sound)
clinical manifestations of cobalamin deficiency
General symptoms of anemia Sore, beefy, red tongue (glossitis) Diarrhea Hepato/splenomegaly Neurologic issues- can be irreversible Altered thought processes paresthesia-the sensation of pins and needles as a result of nerve dysfunction
types of primary cardiomyopathy
Genetic 1. Hypertrophic 2. Arrhythmogenic Right Ventricular Dysplasia Mixed: 1. Dilated
Clinical manifestations of PAD
Gradual 6Ps Dependent rubor Intermittent claudication
Complications of sickle cell anemia
Gradual involvement of all body systems Pulmonary infarctions - lead to MI, HF Stroke Prone to infection Why? Sickle-cell crisis Acute chest syndrome
risk factors of atherosclerosis (irritants to the endothelium)
High "bad" cholesterol (LDL) (hyperlipidemia) Low "good" cholesterol (HDL) Smoking High blood pressure Diabetes Autoimmune disease Elevated C-reactive protein Increased serum fibrinogen level Oxidative stress Infection Periodontal disease
tubuloglomerular feedback
If there is too much sodium in the filtrate, macula densa cells cause the increase of a substance called adenosine, which constricts the afferent arteriole. Since the afferent arteriole constricts, little blood can enter the glomerulus. This then decreases the pressure inside of the glomerulus and therefore decreases the glomerular filtration rate back to normal in order to try and preserve fluid in your body. if not enough sodium is sensed by the macula densa cells, signal the juxtaglomerular cells to release renin to cause aldosterone to constrict the EFFERENT arterioles causing a backup of blood in the glomerulus, thus increasing pressure and filtration
Causes of glomerulonephritis
Immunologic, hemodynamic, DM, toxic drugs may develop a week or two after recovery from a strep throat infection or, rarely, a skin infection (impetigo); to fight the infection, your body produces extra antibodies that can eventually settle in the glomeruli, causing inflammation Bacterial endocarditis viral infection
causes of anemia of chronic disease
Impaired renal function (erythropoietin deficiency) Chronic, inflammatory or infectious disease (AIDS, osteomyelitis) Blood loss from platelet disorders Cancer Autoimmune (RA, lupus) Chronic liver disease Inflammatory bowel disease
clinical manifestations of mitral valve regurgitation
Increased preload L atrial dilation left ventricular hypertrophy (eccentric) Pansystolic murmur (mid-systolic click) Atrial fibrillation Pulmonary congestion Heart failure Shortness of breath, especially following exercise OR when laying down flat Heart palpitations, it feels as the heart is pumping extra hard and/or missing a beat Lightheadedness and/or fatigue Swelling of the lower legs, ankles and feet Coughing
Frank-Sterling Mechanism
Increased stretch of myocardial fibers causes increased force of contraction
atypical MI signs in women
Indigestion Nausea/vomiting Dizziness Fatigue Shoulder blade pain Weakness Sense of impending doom
Aschoff bodies
Inflamed areas in the myocardial tissue; They result from inflammation in the heart muscle and are characteristic of rheumatic heart disease
Acute Pericarditis
Inflammation of the pericardium caused by infection, uremia, neoplasm, MI, surgery, trauma, connective tissue disorders, radiation Inflammation of the pericardium may restrict the heart's movement due to: Serous exudate filling the pericardial cavity (pericardial effusion) Fibrous scar tissue making the pericardium stick to the heart (constrictive pericarditis) Can be recurrent
arrhythmias
Irregular heartbeats; deviation from normal sinus rhythm
Complications of atherosclerosis
Ischemia Partial occlusion Complicated lesion w/obstruction Myocardial infarction Thrombus & emboli Aneurysm 1. If thrombogenic material leaks out of the plaque build up, a blood clot forms; causing an obstruction to the flow of blood---leads to myocardial infarction (death of heart muscle below the blockage due to lack of oxygen)
clinical manifestations of iron deficient anemia
Koilonychia (spoon shaped nail) Glossitis (red, swollen, painful tongue) Pica (craves ice) Cheilitis (inflammation of the lips) Cold sensitivity Weakness and fatigue Classic anemia manifestations
symptoms of mitral valve stenosis
L atrial dilation Diastolic murmur Pulmonary congestion/pulmonary hypertension PND (paroxysmal nocturnal dyspnea---sleep apnea) orthopnea Atrial arrhythmias- 40% Fatigue, weakness Chest pain or palpitations Mural thrombi (formation of thrombus in an artery)
causes of right sided heart failure
Left Ventricular HF RV infarct Intrinsic lung disease or Pulmonary HTN (Cor Pulmonale)
Treatment of Hypertension
Lifestyle Modification! Pharmacologic treatment ACE Inhibitors Calcium Channel Blockers Diuretics
labs and morphology of iron deficient anemia
Low hemoglobin (iron levels) Low serum iron and ferritin Hypochromic and microcytic erythrocytes Poikilocytosis Anisocytosis
Causes of infective endocarditis
Major causes: Staph infection dental infection IV drug use Immunodeficiency DM alcoholism
Non-modifiable risk factors for CAD
Major/Non-modifiable Advanced age Male & postmenopausal Family history/Genetics Hyperlipidemia Social Determinants of Health
clinical manifestations of nephrotic syndrome
Massive proteinuria Lipiduria Hypoalbuminemia (<3 g/dL) Generalized edema Hyperlipidemia Dyspnea (pulmonary edema) puffy face weight gain ascites
acute coronary syndrome treatment
Medication utilized (MONA) Morphine Oxygen Nitrates Aspirin Anti-platelets Anticoagulants Beta blockers ACE inhibitors Reperfusion Therapy Fibrinolytics (TPA) PCI - placement of stents CABG
Causes of nephrotic syndrome
Minimal change disease Focal segmental glomerulosclerosis Membranous nephropathy Diabetic nephropathy infection autoimmune disease
complications from rhumatic heart disease
Mitral stenosis: narrowing of the mitral valve, which blocks blood flow in the heart (other heart valves such as the aortic, bicuspid, and pulmonary can be damaged as well, but the mitral valve is the most prominently seen) Bacterial endocarditis: infection of the membrane that lines the inside of the heart chambers Verrucus endocarditis: abnormal growth of blood clot vegetation that stops the heart from functioning properly
left sided valve disorders
Mitral valve stenosis Mitral valve regurgitation Mitral valve prolapse Aortic valve stenosis Aortic valve regurgitation
Modifiable risk factors for CAD
Modifiable Hyperlipidemia HTN Smoking Type II Diabetes & insulin resistance Obesity Sedentary life style Stress Diet
types of acquired cardiomyopathy
Myocarditis Takotsubo cardiomyopathy
Kidney Damage from hypertension
Nephrosclerosis Progressive damage to vessel & arterioles leading to ischemic death of nephrons Accelerates other types of kidney disease Diabetic nephropathy
Preventative care of sickle cell anemia
Newborn screening Vaccinations Prophylactic antibiotic therapy (2 mos.-5 years)
Causes of acquired hemolytic anemia
Normal RBCs produced RBCs damaged by external factors Toxins/drugs/chemicals Mechanical injury (heart valves) DIC Renal disease Immuno-hemolytic disease
Treatment of sickle cell anemia
O2 for hypoxia and to control sickling Rest, fluid Pain management Acute chest syndrome Antibiotics added to care plan Hydroxyurea: anti-sickling agent Hematopoietic stem cell transplant
clinical manifestations of acute tubular necrosis
Oliguria Edema Pulmonary congestion HTN Uremia Coma Death
pulsus paradoxus
On inhaling, the right ventricle fills with extra blood. Because the heart cannot expand fully when the right ventricle is overfilled, the left ventricle is compressed and cannot accept much blood. On the next heartbeat, the left ventricle does not send out much blood: systolic BP drops-> cardiac output drops->obstructive shock
glomerulus
Once blood enters the kidneys, it enters the first part of each nephron; a network of capillaries responsible for the filtration of blood; surrounded by the Bowman's Capsule does not filter cells, albumin or hemoglobin--only small ions and molecules can pass through to the Bowmen's space
Clinical Manifestations of Aplastic Anemia
Onset Insidious Acute and severe S&S associated with low WBCs and platelets usually appear first Petechiae Ecchymoses Bleeding (nose, gums, GI) Infections Weakness Fatigue Pallor
Intrinsic reflexes for BP
Osmoreceptors Baroreceptors Chemoreceptors
6 P's for PAD (O2 assessment)
PAIN PARATHESIA PULSELESSNESS PALLOR POLAR (POIKILOTHERMIA) PARALYSIS
Pathophysiology of Aplastic anemia
Pancytopenia (decreased red and white blood cells and platelets) Thrombocytes Old RBCs are not replaced by new ones Normocytic/normochromic
Diagnosing Sickle cell anemia
Peripheral blood smear Sickling test Electrophoresis of hemoglobin Skeletal x-rays Magnetic resonance imaging (MRI)
Atherosclerosis
Plaque buildup in our cardiovascular system that builds up underneath the inner lining, the endothelium, of an artery; intra-arterial deposits of fat (lipids) and fibrin that harden over time in vessel wall and narrow or block vessel wall, reducing blood flow
age related changes that cause an increase in blood pressure
Prevalence increases with age ½ of people age 60-69 have HTN ¾ of people 70 and older have HTN Myocardial and blood vessel stiffening Contributor to systolic HTN, Risks for CV events (strokes), dementia Changes in neurogenic control over vascular tone Catecholamine receptor sensitivity Baroreceptor activity decreases with age Antihypertensive medication in smaller doses Increased peripheral vascular resistance & decreased renal blood flow Left ventricular hypertrophy & fibrosis Disruption of growth factor Imbalance in collagen synthesis & degradation
proteinuria
Protein in the urine; indication of kidney disease
Clinical Manifestations of Acquired Hemolytic Anemia
Rapid onset Anemia S/S: tired dizziness shortness of breath racing heartbeat paleness cold hands and feet complication: kidney failure
Blood labs
Red Blood Cell Count Total number of RBCs/microliter Mean Corpuscular Volume (MCV) Reflects volume/size of RBCs Mean Corpuscular Hemoglobin Concentration (MCHC) Concentration of hemoglobin in each cell Hematocrit % of blood by volume that is made up of RBCs Hemoglobin Measures the hemoglobin content of the blood Percentage of Reticulocytes (immature red blood cells) Index of the rate of red cell production
causes of angina
Reduced supply: hypotension hemorrhage decreased diastolic filling time anemia hypoxia valve incompetence shock states Increased demand: hypertension tachycardia increased ventricular volume increased blood viscosity increased contractility
Consequences of pericardial effusion
Restricts heart expansion The left ventricle cannot accept enough blood Decreased cardiac output Decreased blood pressure and shock The right ventricle cannot accept enough blood Increased venous pressure Jugular distension
STEMI
ST segment elevation myocardial infarction The ST segment on an EKG is elevated with this heart attack since the heart attack is caused by a complete blockage of the blood supply to more of the heart muscle causing more of the muscle to be damaged. Common causes are thrombosis (blood clots) or embolytic diseases (blood clots break loose and travel through the body) and hypertension. heart attack that is often referred to as the 'widow maker': The reason for this is that the blockage occurs near the beginning portion of the main branch of the coronary artery that supplies the left side of the heart, which is the largest part of the heart that does the most of the work. When the blood supply is cut off to the left side of the heart, a very large amount of the heart tissue dies.
pericardial effusion
Serous exudate filling the pericardial cavity; Compresses heart chambers; Rapidity of accumulation; Elasticity of pericardium
Acute Pericarditis Clinical manifestations
Sharp, stabbing pleuritic pain Retrosternal chest pain- worse with deep breath, cough, position change, may radiate to back Dysphagia, restlessness, irritability, anxiety, weakness, malaise low-grade fever Pericardial friction rub ECG changes (ST elevation, PR-segment depression)
Diastolic Dysfunction
Stiffening or poor relaxation of the left ventricle which causes inefficient fillings; s4 sound; normal/preserved ejection fraction ↓Compliance & ventricular stiffness → ↑ intraventricular pressures Pressures are transmitted backwards → congestion Cardiac output decreases because of ↓ ventricular filling but preserved EF d/t ↑ contractility
Brain damage from hypertension
Stroke ↑ BP causes dilation of small nonelastic vessels leading to hemorrhagic stroke Ischemic stroke - occlusion Hypertensive Encephalopathy Vascular spasm, HA, confusion Cerebral edema, papilledema, visual deficits Dementia Narrowing & sclerosis leads to hypoperfusion → probable cause of white matter demyelination Vascular dementia
clinical manifestations of agina
Substernal pain/pressure/tightness/ heaviness Indigestion/epigastric pain Poorly localized Radiation to neck, jaw, shoulder, arms Weakness/numbness in arms, wrist, hands Shortness of breath Pallor Diaphoresis Dizziness, lightheadedness Nausea & vomiting Unease, anxiety Fatigue Palpitations
Treatment and Symptoms of Diastolic Dysfunction
Symptoms: Dyspnea on exertion Fatigue Pulmonary symptoms Treatment: Medications that promote ventricular relaxation & filling time
hypertension
Systolic and diastolic readings diagnosing hypertension *Has rested for at least 5 minutes *Has not smoked or ingested caffeine within 30 minutes *Diagnosed on a series of measurements
Micturition (urination)
The act of releasing urine from the urinary tract to outside of the body
end-systolic volume
The amount of blood remaining in the ventricles after contraction
Process of phelonephritis
The bacteria reach the kidneys in one of three major ways: Via the bloodstream Via the urethra (an ascending infection) Surgical contamination
renal interstitium
The connective tissue surrounding and enclosing the nephrons of the kidney
tunica externa
The outer layer of the artery; primarily composed of elastic fibers and collagen, a protein that makes up all of the connective tissue in your body
adrenal cortex
The outer portion of the adrenal gland that secretes 3 steroid hormones known as corticosteroids
baroreceptor reflex
The primary reflex pathway for homeostatic control of blood pressure
function of the tubule cells of the kidney
The tubule cells help filter the blood as it flows through the kidney. As the kidneys filter the blood, they remove waste products and excrete these waste products in the urine.
urinary sphincter
The valve that controls the release of urine from the bladder. It has an internal part made of smooth muscle (thus involuntary) and an external part made of skeletal muscle (thus voluntary).
end-diastolic volume
The volume of blood in the ventricles at the end of diastole
stroke volume
The volume of blood pumped from the left ventricle per beat The lower the afterload the more blood the heart will eject with each contraction; reduced afterload = greater contraction
arterial structure
The walls of all arteries are composed of three layers: the tunica intima, tunica media and tunica adventitia, which are arranged one on top of the other like the layers of an onion. 'Tunica' simply means 'coat.'
arcuate arteries
These arteries are located right at the border of the outer and inner portion of the kidney - the renal cortex and medulla..."the arch"
Treatment of anemia of chronic disease
Treat underlying disease Erythropoietin administration Blood transfusion
treatment of ischemic heart disease
Treatment Symptom Reduction Smoking cessation Stress reduction Exercise program Dietary modifications Weight reduction Avoidance of cold Pharmacology Nitrates Beta blockers Calcium channel blockers PCI or CABG
Unstable angina in acute coronary symdrome
Unstable angina-reversible myocardial ischemia Small fissure or superficial erosion of plaque Perfusion returns with out necrosis No ST elevation on EKG Pain without evidence of serum biomarkers Occurs at rest More than 20 minutes if untreated Severe, new onset, more prolonged Lesion is complicated Infarction may follow
role of vitamin K in clotting
Vitamin K is required for the synthesis of clotting factors; necessary for the liver to produce prothrombin, which is one of five clotting proteins
trigone
Within the base of the bladder; triangular area made up of the openings from the ureters and the opening into the urethra
pheochromocytoma
a benign tumor of the adrenal medulla that causes the gland to produce excess epinephrine and norepinephrine resulting in increased blood pressure (the sympathetic nervous system is always on)
neurogenic bladder
a bladder dysfunction stemming from neurological damage that causes flaccid or spastic bladder dysfunction; the detrusor muscle in the bladder or the urethral sphincter malfunctions; detrusor muscle overstretches causes: stroke, diabetes, herniated disk, MS, Parkinson's Disease, alcohol abuse, ALS hypotonic or underactive: PT cannot sense full bladder because of sensory nerve damage to the detrusor muscles---results in constant dribbling of urine; incontinence spastic or overactive: nerves single the detrusor muscle to contract involuntarily and unpredictably; volume of urine in bladder is normal or low; treatment: catheter, meds and surgery
POLYCYTHEMIA
a blood disorder in which there are too many red blood cells; Increased RBC count and hematocrit greater than 50% 2 types: polycythemia vera and secondary polycythemia
renal artery
a blood vessel, coming off of the surface of the abdominal aorta, which supplies a kidney with blood, there are 2
Bundle of His
a collection of cardiac muscle fibers that transmit the electrical impulse from the AV node after a 0.04 second delay; branches into the right and left bundle branches that continue the conduction fibers that transmit the electrical impulse down the ventricles
Juxtaglomerular apparatus
a collection of cells responsible for the hormonal regulation of the body's blood pressure, the kidney's blood flow, and the glomerular filtration rate a control center that allows a certain amount of blood to flow through the glomerulus and hence influence the glomerular filtration rate contains 3 cells: juxtaglomerular/granular cell, macula densa cells, Mesangial Cells
Beck's Triad
a collection of three classic clinical signs associated with cardiac tamponade
Disseminated Intravascular Coagulation (DIC)
a condition in which clotting becomes overactive; scattered blood clots within the vessels leading to too few platelets in the blood causing clotting deficiency when an injury to the tissue or blood vessel occurs Etiology: Malignancy, Sepsis, Trauma ,Transfusion reaction, Burns, Shock, Liver disease Pathophysiology: problems at steps 2, 3, and 4 of homeostasis Manifestations- Thrombotic Symptoms; Microemboli; Bleeding Symptoms; Pallor; Petechiae; Oozing blood through venipuncture sites; Acrocyanosis (blue feet and hands) *First symptom post-surgery can be hemorrhage from surgical site Diagnosis Labs- D-dimer: increased PT: increased PTT: increased LDH: increased Platelet count: decreased Fibrinogen: decreased Treatment- Stabilize patient and treat cause! Transfusion of blood products
urinary stasis
a condition in which the bladder is not able to completely empty
intrinsic renal failure
a condition in which the kidneys stop functioning due to internal kidney disease the nephron or renal interstitum stops functioning causes: >Ischemic damage from pre-renal injury >Acute tubular necrosis >Intratubular obstruction >toxins (chemotherapy) >Glomerulonephritis (burns holes in the glomerulus, the filter, as a result of the inflammatory process and therefore causes kidney dysfunction) >pyelonephritis (infection of the kidneys) >inadequate oxygen delivery (cells suffocate) >autoimmune diseases
acute tubular necrosis
a condition in which the tubule cells of the kidney become damaged and then die two primary causes: lack of blood flow to the kidneys due to ischemia, nephrotoxic drugs, or tubular obstruction Destruction of tubular epithelial cells (obstruction of tubule and ↑ intraluminal pressure → ↓ GFR and fluid movement from tubule to interstitium (back leak)) There are three main phases of acute tubular necrosis: Initiation: kidney function decreases; last from a few hours to a few days; the ability of the kidneys to filter the blood drastically decreases due to low blood flow. Because the kidneys cannot filter the blood effectively, waste products begin to build-up in the blood Maintenance: waste products build up in the blood; lasts a couple of weeks to months; kidneys continue to have decreased filtering capability. Waste products continue to accumulate in the blood, and urine production decreases; ↑Bun/Cr, oliguria, electrolyte disturbances; can be oliguric or non oliguric. Recovery: regeneration of cells and improved kidney function; lasts 3-12 months; cells become healthier, the kidney begins to regain its filtering capabilities, which results in decreased waste products in the blood, and increased production of urine; BUN/Cr levels decrease
chronic venous insufficiency
a condition in which venous circulation is inadequate due to partial vein blockage or leakage of venous valves causes: Outflow obstruction valve incompetence Skeletal muscle pumps Signs: impaired blood flow Edema (weeping) Hyperpigmentation (hemosiderin) Necrosis of SQ fat deposits Advanced disease - impaired tissue nutrition (Stasis Dermatitis- dry flaky, reddened skin; Venous ulcer- medial, distal lower leg, large; Ulcers are typically painless)
mitral valve stenosis
a condition that results in narrowed and hardened mitral valve; can lead to right sided heart failure because the right ventricle is working too hard trying to push blood through the pulmonary valve that is backed-up from the mitral valve stenosis and eventually cause tricuspid regurgitation causes: rheumatic fever congenital treatment; Blood thinners Valve replacement
deep vein thrombosis (DVT)
a condition where blood clots form in the deep veins of the extremities Symptoms Swelling of foot, ankle, or calf Tenderness Pain Do not dorsiflex!! Complications Pulmonary embolus Treatment IVC filters, anticoagulant Bedrest Prevention is key Mobility, pressure boots
Systolic Dysfunction
a decrease in the force of ventricular contraction (impaired contractability) caused by weakened heart muscles due to decreased cardiomyocytes results in an increased ventricular size and thinner heart muscle walls; S3 gallop causes: 1. cardiomyopathies (dilated cardiomyopathy) 2. reduced blood volume (coronary artery disease, MI, chronic hypertension) 3. valve diseases (regurgitation-volume overload; stenosis-pressure overload) 4. arrhythmias (decreased pumping efficiency) measured according to ejection fraction, which is the % of blood ejected with each beat (volume ejected/total volume filled x 100 = ejection fraction) normal range is 55-70% heart failure is when EF is < 40% decreased cardiac output results in the activation of RAAS & baroreceptors stimulation
Cardiomyopathies
a disease of the heart muscle that makes it harder for your heart to pump blood to the rest of your body; can lead to heart failure. 2 types: primary acquired
Pernicious anemia
a disorder in which the body cannot make enough red blood cells because the intestines cannot properly absorb vitamin B12 due to a lack of intrinsic factor. Your body needs vitamin B12 to make red blood cells.
distal convuluted tubule (DCT)
a duct of the renal tubule located in the kidney's cortex that reabsorbs calcium, sodium, and chloride and regulates the pH of urine by secreting protons and absorbing bicarbonate. connects to the connecting tubule
supraventricular tachycardia (SVT)
a faster than normal heart rate above the ventricles. For example, the atria of the heart can beat between 100 - 300 beats per minute during a SVT episode as opposed to the normal 60 - 100 beats per minute.
distributive shock
a form of shock in which severe vasodilation despite normal blood volume results in improper distribution of blood flow; not enough blood to fill the circulatory system---less blood is returned to the heart, less blood is circulated to the body any factor that stimulates parasympathetic activity or inhibits sympathetic activity of vascular smooth muscles can cause neurogenic shock, which results in widespread and massive vasodilation
prothrombin
a glycoprotein present in the plasma that is converted into thrombin by extrinsic thromboplastin during the second stage of blood clotting
primary hyperaldosteronism
a hormonal disorder that leads to high blood pressure; occurs when your adrenal glands produce too much aldosterone
Anti-diuretic hormone (ADH, vasopressin)
a hormone released from the posterior pituitary gland that causes an increase in blood pressure; vasoconstricts our blood vessels, which causes increased blood pressure. It also increases water absorption from the distal tubule and collecting ducts
BNP
a hormone secreted by cardiomyocytes in the heart ventricles in response to stretching caused by increased ventricular blood volume; causes a decrease in systemic vascular resistance and central venous pressure as well as an increase in natriuresis
epinephrine
a hormone secreted by the adrenal medulla in response to short-term stress; increases heart rate, blood pressure, cardiac output and blood glucose levels
Ventricular fibrillation
a life-threatening arrhythmia; ventricles are quivering similar to how you might tremble when you're cold; chaos being conducted throughout the ventricles; no organized contraction, so blood is not being pumped anywhere.
urine
a liquid mixture of excess water and electrolytes as well as wastes that were filtered from the blood
Loop of Henle
a long duct mainly located in the kidney's medulla that creates a concentration gradient, called a countercurrent exchange system, that allows for the reabsorption of water in order to create concentrated urine 3 parts: thin, descending limb of henle: permeable to water allowing for reabsorption back into the blood thin, ascending limb of henle: not permeable to water, reabsorb sodium, chloride, calcium and potassium thick, ascending limb of henle: not permeable to water, reabsorb sodium, chloride, calcium and potassium
renal tubule
a long series of ducts in the nephron
SA Node
a mass of cells that set the pace of the heart; the pacemaker of your heart; cells of the SA node can depolarize on their own without any external influence; sends electrical impulses to AV node with a 0.09 second delay
Prothrombin time (PT)
a measurement that assesses the extrinsic and common pathways of the coagulation cascade; measures how long it takes for the blood to clot longer PT indicates: cirrhosis of the liver, liver disease or vitamin K deficiency
Partial thromboplastin time (PTT)
a measurement that assesses the intrinsic and common pathways of the coagulation cascade
Obstructive shock
a medical emergency; there is a decrease in diastolic filling of the heart, which then decreases cardiac output; The decreased amount of blood getting to the heart is caused by an obstruction. Shock then occurs due to the lack of blood getting to the organs and decreasing their functioning capacity. causes: Obstruction to heart or great vessels Cardiac tamponade Pulmonary emboli Aortic occlusion, dissecting aortic aneurysms Tension Pneumothorax Tumor hypertension
Iron deficient anemia
a microcytic, hypochromic anemia that results from low iron stores in the body, which in turn causes improper red blood cell production Develops in 3 stages Stores depleted Deficient cells produced Deficient cells released most common form of anemia worldwide women and children increased risk causes: >decreased supply (malnutrition, poverty, malabsorption, GI surgery, Ulcers, cirrhosis, hemorrhoids, ulcerative colitis, cancer) >increased demand (pregnancy, growth, menorrhagia) >blood loss (2 mL blood contain 1mg iron GI, GU losses, hemolysis)
hypertension (HTN)
a multifactorial condition when your systolic blood pressure is higher than 120 mmHg and your diastolic blood pressure is above 80 mmHg, averaged over time***2 classifications: primary and secondary 4 stages: >Normotensive blood pressure: No risk for hypertension (measured as less than 120 mmHg systolic or less than 80 mmHg diastolic) >Prehypertensive blood pressure: At risk for developing hypertension (measured as 120-139 mmHg systolic or 80-89 mmHg diastolic) >Stage 1 hypertension: High blood pressure that may be treated with lifestyle changes or medication (measured as 140-159 mmHg systolic or 90-99 mmHg diastolic) >Stage 2 hypertension: High blood pressure that may require one or two medications (measured as greater than 160 mmHg systolic or higher than 100 mmHg diastolic). This is the most severe form of hypertension.
factor V leiden
a mutation of factor V, one of the clotting factors in the blood, and causes the development of abnormal blood clots
plasma
a non-living component or the fluid that blood cells float in composed of water, proteins, and electrolytes
thromboxane A2
a product of activated platelets that promotes the collection of more platelets and vasoconstriction
acute coronary syndrome
a range of conditions associated with sudden, reduced blood flow to the heart. One such condition is a heart attack (myocardial infarction)
Hemophilia A
a rare x-linked recessive genetic bleeding disorders in which the blood does not clot properly; affects males more than females; no cure caused by a deficiency in clotting factor VIII Manifestations- (d/t trauma or local lesion) Ecchymoses (bruising) Subdural hematomas Hemarthrosis (bleeding into a joint) prolonged nosebleeds bruises easily warm, painful, swollen joints with decreased movement GI hemorrhage tarry stools cola-colored urine Treatment- Stop bleeding Clotting factors, immobilize joint Manage life threatening complications (avoid injury and meds that promote bleeding, good nutrition, good dental hygiene, IV administration of deficient clotting factor)
ECG or EKG (electrocardiogram)
a recording of the flow of the electrical current through the heart
Norepinephrine
a second hormone secreted by the adrenal medulla that increases heart rate, blood pressure, respiratory rate, cardiac output and blood glucose levels
efferent arteriole
a small artery carrying filtered blood away from the glomerulus; lumen has a smaller diameter
afferent arteriole
a small artery supplying the glomerulus with unfiltered blood; lumen has a larger diameter creating greater pressure through the glomerulus to "ultrafilter" the blood
fibrinogen
a soluble protein that is produced by the liver and found in blood plasma. When tissue damage results in bleeding, it is converted at the wound into fibrin by the action of thrombin, a clotting enzyme an inactive clotting factor that helps bind the platelets to form a clot
heart failure
a state in which the heart has malfunctioned to the point of being unable to pump blood adequately enough to meet the energetic demands of body tissues and organs
erythema marginatum
a type of erythema (redness of the skin or mucous membranes) involving pink rings
Dressler Syndrome
a type of inflammation of the sac surrounding the heart (pericarditis); believed to be an immune system response after damage to heart tissue or to the sac surrounding the heart (pericardium). Such damage may occur from events such as a heart attack, surgery or traumatic injury. Symptoms include chest pain, which may be similar to chest pain experienced during a heart attack.
angiotensin II
a vasoconstrictive hormone that increases systemic blood pressure, renal perfusion pressure and the glomerular filtration rate constricts both efferent and afferent arterioles, but with greater emphasis on the efferent arteriole increases the absorption of Na+ and water into the blood from the renal tubules stimulates the release of aldosterone from the adrenal glands
renal vein
a vein that carries the blood purified by the kidney back into general circulation
cardiac tamponade
acute compression of the heart caused by fluid accumulation in the pericardial cavity; assessed using Beck's Triad; obstructive shock
hydronephrosis
affects 1/500 people in the US slowly progresses, not overnight occurs when one kidney becomes swollen due to the buildup of urine (urine flow obstruction → urine backs up into kidneys → increased pressure → dilation of renal pelvis and calyces) usually caused by a blockage in the ureter---this type of blockage is most often the result of an acute unilateral obstructive uropathy, which is a sudden blockage in the ureter---such as blood clot, kidney stone, tumor or scar tissue
epicardium
also known as the visceral pericardium, is the inner most layer of the pericardium and directly adheres to the heart tissue; serous-producing
septic shock
an abnormal body-wide inflammatory response to an infection that can result in death (40% mortality); the heart fails to pump blood adequately; blood clots begin to form all over the body in accordance with the body's inflammatory response preventing blood flow and tissue perfusion the inflammatory mediators (tumor necrosis factor-alpha and interleukin-1) cause the blood to be shunted and distributed away from the capillaries responsible for delivering oxygen and taking away waste products produced by the organ Decreased cardiac output lowers BP The sympathetic system responds Vasoconstriction increases resistance to blood flow Increased workload on the heart worsens heart failure causes systemic signs of inflammation: fever and increased respiration, metabolic acidosis, vasodilation, warm flushed skin
macrocytic, normochromic, megaloblastic anemia
an abnormally large red blood cell with increased RDW causes: Pernicious (B12) anemia Folate deficiency
Cobalamin Deficiency (Pernicious Anemia)
an autoimmune disease that attacks parietal cells and intrinsic factor, causing cobalamin malabsorption and subsequent anemia; macrocytic (improper DNA synthesis that also causes leukopenia); B12 is absorbed in the jujenum of the small intestines
Von Willebrand Disease
an autosomal dominant bleeding disorder that affects the blood's ability to clot due to a deficiency of von Willebrands factor (Von Willebrand Factor is a blood protein that acts as the glue that holds the platelets together in the blood clotting process.) 3 types: type 1 involves not enough VWF type 2 involves a defect in VWF function or structure type 3 involves no VWF Manifestations- Spontaneous bleeding from nose, mouth, and GI Menorrhagia ; prolonged bleeding time - normal platelet count easy bruising Treatment- Avoid aspirin DDAVP (clotting promoter)
angiotensin-converting enzyme (ACE)
an enzyme located mainly in the lungs that converts angiotensin I into angiotensin II
renin
an enzyme released by the juxtaglomerular cells of the kidneys in response to low blood pressure, travels to the liver and catalyzes the transformation of angiotensinogen to angiotensin I
renal osteodystrophy
an increase in the levels of parathyroid hormone (PTH) due to renal failure, results in PTH trying to increase blood calcium levels by mining and breaking apart your bones (which store the calcium). This leads to renal osteodystrophy, a condition resulting in the weakening, deformation, and fracturing of bone as a result of chronic kidney disease
Creatinuria
an increased concentration of creatinine in the urine; indicates loss of muscle mass
Polycystic Kidney Disease
an inherited autosomal dominant disorder characterized by the formation of cysts within the kidneys. A cyst is a fluid, semi-solid, or air-filled membranous sac---the kidneys look like bubble wrap
MEGALOBLASTIC ANEMIAS
anemia caused by impaired DNA synthesis due to lack of B12 vitamin and folic acid; characterized by the presence of large red blood cells (macrocytic) erythrocytes die prematurely MCV >100 Hgb concentration WNL
clinical manifestations/assessment of atherosclerosis
angina pectoris Pain- ischemia Arterial bruits -turbulence
consequences of post-renal failure
anuria, the absence of urination Hyperkalemia - increased levels of potassium, an electrolyte, in the blood. Hyperphosphatemia - increased levels of phosphorus, another electrolyte, in the blood. Metabolic acidosis increased BUN and creatinine decreased GFR
renal pyramids
any of the triangular sections of tissue that constitute the medulla of the kidney. The pyramids consist mainly of tubules that transport urine from the cortical, or outer, part of the kidney, where urine is produced, to the calyces, or cup-shaped cavities in which urine collects before it passes through the ureter to the bladder.
Macula Densa Cells
are cells of the juxtaglomerular apparatus that monitor changes in sodium concentration in the kidney's distal convoluted tubules in order to regulate glomerular filtration rate and signal the juxtaglomerular cells to release renin or they increase adenosine
juxtaglomerular cells
are cells of the juxtaglomerular apparatus that secrete renin, an enzyme that helps to increase your body's blood pressure once it is released mainly part of the afferent arteriole, they sense decreased blood pressure
sex hormones
are steroid hormones produced by the adrenal cortex that influence male and female sexual characteristics.
proper hepatic artery
arterial blood that supplies oxygen to the liver
interlobar arteries
arteries between the renal lobes; arteries that supply the renal lobes with blood
coronary arteries
arteries that supply blood to the heart muscle
Coronary artery disease
atherosclerosis of the heart; narrowing of the coronary arteries due to a buildup of plaque
sickle-cell disease (anemia)
autosomal recessive disorder that causes a form of anemia in which the red blood cells take on a crescent or sickle shape. These sickle-shaped cells are sticky and stiff and create a traffic jam within the bloodstream Affected gene produces abnormal hemoglobin Hemoglobin S (HbS): This atypical hemoglobin is what distorts the shape of the red blood cell into the characteristic sickle shape HbS causes the RBC to stiffen and elongate forming sickled cells
Causes of inherited hemolytic anemia (sickle cell disease)
autosomal recessive disorders *Heterozygote - sickle cell trait *Homozygote - sickle cell disease *Affects 50,000 Americans African Americans, Mediterranean, S. and Central America, Middle East, East Indian *In areas of Africa with endemic malaria - gene prevalence is 30% Why? *ID during infancy and childhood *Incurable disease, can be fatal
morphological classification
based on the size or volume of the red blood cell and may also be classified by the hemoglobin content of the red blood cell
primary hemostasis
begins immediately after injury; involves the formation of the platelet plug endothelial cells secrete proteins, which sends signals to the blood an injury has occurred; platelets are the first responders platelets store proteins necessary for hemostasis step 1: vasoconstriction >caused by a nerve reflex and endothelian secretion by endothelial cells step 2: platelet adhesion >platelets have surface receptors made of glycoproteins (1b, 2b, 3a) >Von Willebrand Factor (glue) is secreted by endothelial cells at the site of injury and binds to the subendothelial collagen and the G1b receptors on the platelets >platelet is activated once it binds to VWF and then changes shape allowing 2b and 3a receptors on the platelet to change shape and bind step 3: activation and degranulation >activated platelets release fibrinogen, VWF and thromboxane A2 during degranulation step 4: >mediated by 2b and 3a platelet receptors that allow the platelet to bind fibrinogen forming platelet plug
Peripheral Arterial Disease (PAD)
blockage of arteries carrying blood to the legs, arms, kidneys and other organs causes peripheral limbs (especially legs) to become pale, cold, blue because there is no warm, oxygenated blood flowing to the extremities DX: ankle-brachial index Absence of pulse and hair Round, red sores (rubor) Toes/feet pale or black (Eschar/gangrene) Sharp pain in calf, intermittent claudication
thrombosis
blood clot
Thrombocytopenia
blood does not have enough platelets and may cause trouble controlling bleeding; normal range 150,000-300,000 causes: the body does not produce enough platelets: any condition that negatively affects the bone marrow (cancer, alcoholism, HIV, toxic chemicals, chemo/radiation) the body destroys the platelets: pregnancy, medications, bacterial infections, cardiac or vascular surgery the platelets get trapped in the spleen: cancer of the spleen S/S: ecchymosis (bruising) prolonged bleeding petechiae (pinpoint microhemorrhages) hematochezia melena hematuria hematemesis menorrhagia bleeding gums purpura (purple spots) epistaxis (nosebleed) intracranial bleeding Platelet count <150,000/microLiter; Spontaneous bleeding occurs <20,000/microLiter Tx: steroids blood transfusions splenectomy
aortic regurgitation
blood flows back from the aorta into the left ventricle during diastole, or during ventricular filling 50% caused by aortic root dilation---This is when the root dilates, or gets bigger, and in doing so pulls apart the leaflets, making it harder for the valves to fit snugly together and close all the way, letting some blood flow backward valvular damage caused by chronic inflammation leads to fibrosis that prevents the valves from sealing closed
how do you control blood pressure?
blood pressure is controlled by regulating cardiac output and pulmonary vascular resistance
Hypertensive emergency
blood pressure is so high that organ damage can occur; 180/120
Renal artery
blood vessel that carriers blood to kidney containing body's waste from cellular metabolism and food after nutrients have been extracted
thrombus (coagulation)
bodies natural hemostatic ability to form blood clots
Bundle Branches
branches of the AV bundle that divide to the right and left sides of the interventricular septum; if injured they might slow down or block the conduction of the electrical impulse to the ventricles, making it harder for the heart to pump blood efficiently through the body.
interlobular arteries
branches of the arcuate arteries that supply the renal cortex with blood; will eventually give off a branch called the afferent arteriole that will supply the functional unit of the kidney, the nephron, with blood
causes of hypovolemic shock
burns hemorrhage vomiting/diarrhea diabetes insipidus diuresis
vasospastic angina
can happen at anytime may or may not have atherosclerosis ischemia from coronary artery vasospasms transmural ischemia reversible ST-segment elevation treated with nitroglycerin and calcium-channel blockers
Right Heart Failure
can occur alone or as a consequence of left-sided heart failure (due to something like hypertension). If the lung vessels are overfilled with blood during left-sided heart failure, it means that there's barely any room left for the right ventricle to pump blood into the lungs. Increased blood pressure leads to jugular venous pressure; jugular venous distension; Hepatic congestion; Ascites; Peripheral edema - usually in the ankles and legs; pitting edema
bladder cancer
cancerous tumor arising from cells lining bladder; symptom is hematuria most common is transitional cell carcinoma causes: smoking (#1 cause) parasitic infection diagnosis: cystoscopy treatment: surgery radiation therapy chemotherapy
myocardial cells
cardiac muscle cells themselves
thrombin
catalyzes the conversion of fibrinogen to fibrin
ADH
cause the collecting duct and the distal convoluted tubule to become permeable to water, leading to the absorption of more water in times of need.
polycythemia vera
caused by a problem with the bone marrow, resulting in an overproduction of cells RBCs and platelets the overproduction of cells appears to be due to a gene mutation involving the JAK2 gene
secondary polycythemia
caused by an increased production of erythropoietin, resulting in an overproduction of red blood cells 2 types: compensatory and abnormal *compensatory is in response to hypoxia as a result of COPD, sleep apnea; smoking, high altitudes, carbon monoxide poisoning, Rt-Lt. cardiac shunt; renal stenosis; *abnormal is in response to a tumor secreting EPO
myocardial infarction (heart attack)
caused when a blood clot blocks the flow of blood to the heart, causing cardiac muscle to die due to lack of oxygen most common cause is atherosclerosis in coronary arteries, which compromises blood flow and oxygenation of the heart muscle cardiomyocytes slow down as oxygen decreases, when oxygen is absent membranes break down and cells rupture releasing toxic cell waste containing troponins (cardiac proteins) into the blood brain signals release of adrenaline causing heart to beat faster once the heart muscle dies, blood starts to back up and flows into the lungs causing shortness of breath
subendocardium ischemia
causes the release of adenosine (causes vasodilation) and bradykinin (causes pain)
adrenal medulla
central region of the adrenal gland develops from nervous tissue, and it is stimulated to release its hormones by impulses from the sympathetic nervous system secrete catecholamines
chemoreceptors
chemical sensors in the brain and blood vessels that identify changing levels of oxygen and carbon dioxide; monitor pH in the blood
Clinical manifestations of myocardial infarction
chest pain, tightness and pressure in the chest shortness of breath discomfort in the neck, jaw and arms nausea and vomiting fainting (syncope)
Risk factors for PAD
cigaretts, DM
CBC
complete blood count RBC 4.5 - 5.5 million/mm3 (4.0 - 5.0 females) Hgb 14 - 17 g/dL males (12 - 16 g/dl females) Hct 42 - 52% males (36 - 48% females) MCV 84 - 96 fL (femtoliters) MCHC 32 - 36 g/dL RET 0.5-1.5% Platelets 150,000-400,000/mm3 (150-400) WBC 4000-11,000 cells/microliter (4-11)
Purkinje fibers
conducting fibers that relay the electrical impulse throughout the ventricles
coarctation of aorta
congenital cardiac condition characterized by a narrowing of the aorta
Nephrotic syndrome
consequence of glomerular inflammation causing scarring (known as glomerulonephritis) that results in hematuria, proteinuria, and hypertension. The glomerulus is damaged due to an inflammatory process
pericardial cavity
contains the heart, the muscular pump that drives the blood around the cardiovascular system
chronic pyelonephritis
continuing pyogenic infection of the kidney that occurs in patients with a history of frequent UTIs and acute pyelonephritis; can lead to chronic kidney disease Symptoms consist of fever, malaise, and flank pain, Polyuria, Nocturia, Proteinuria Medical diagnosis is with urinalysis, culture, and imaging tests. Treatment is with antibiotics and correction of any structural disorders. Reflux of infected urine into the kidney pelvis is the typical cause; other causes include: obstructive uropathy, struvite calculi, and vesicoureteral reflux (VUR).
systole
contraction of the heart ventricles; AV valves shut, semi-lunar valves open; when PT is relaxed systole is shorter than diastole
normocytic normochromic anemia
decreased in amount of red blood cells of hemoglobin, but red blood cells are of a normal size and color MCV is normal causes: under production, over destruction or acute blood loss (>20%) Aplastic Anemia of chronic disease
Treatment of renal calculi
depends on the type of kidney stone >supportive: 90% pass on their own >pain medications >Alpha blockers: helps muscles relax making it easier to pass stones >Ureteroscopy: a small wire with a camera on the end may be inserted through the urethra to the bladder so that the stone can be found and captured >lithotripsy: external sound waves are directed at the stone to try to break it up into smaller pieces that are easier to pass. This procedure can be painful and can produce bleeding in the abdomen or kidneys.
QRS wave
depolarization of the ventricles; associated with the contraction of the ventricles and beginning of systole; lub sound
clinical manifestations of intrinsic renal failure
diluted urine high sodium in urine azotemia
hydroureter
distention of the ureter with fluid, due to obstruction slowly progresses, not overnight urine flow obstruction in distal ureter → urine backs up into ureter → increased pressure → dilation of ureter
primary hypertension
does not have a clearly identifiable cause; rarely has any accompanying symptoms and tends to creep up over the years, which is why it has been deemed a silent killer; multifactorial with association to modifiable risks and lifestyle; 92-95% of people with hypertension
Hemodyalysis
done by using a machine to filter the circulating blood in the vessels through an artificial membrane. Metabolites and excess fluid are removed from the blood
ECHO
echocardiogram; sound waves to create pictures of heart
ECG changes in coronary artery disease
electrocardiogram T wave inversion ST - segment elevation (ACS) Development of Q wave (ACS)
azotemia
elevation of blood urea nitrogen (BUN) and creatinine in the blood
Dilated cardiomyopathies
enlargement of the heart muscle by expanding out just like a balloon to the point of its dysfunction irreversible, progressive heart condition that results in ventricular chamber enlargement, potentially diminished ventricular thickness, and subsequent systolic dysfunction. flabby heart chambers (2-3X) normal size
layers of the heart wall
epicardium, myocardium, endocardium
clinical manifestations of folate deficiency
fatigue gray hair mouth sores swollen tongue forgetfulness depression anorexia trouble concentrating birth defects poor growth
symptoms of hydronephrosis
feeling of micturition, abdominal pain, nausea, vomiting, painful urination, UTI and fever
Function of Kidney
filter and remove waste from the blood (blood is filtered through kidneys 288x/day; 200 mL/minute) balances fluid levels in the body through the release of hormones regulate blood pressure help to make RBCs activates vitamin D
Proximal convoluted tubule
first duct in the renal tubule after Bowman's space section of the renal tubule located in the kidney's cortex that is responsible for the reabsorption of the majority of ultrafiltrate the majority of water (H2O), sodium (Na +), chloride (Cl-), calcium (Ca 2+), potassium (K +), phosphate (PO4 3-), bicarbonate (HCO3 -), and urea, as well as all of the glucose and amino acids, are reabsorbed from the ultrafiltrate made by the glomerulus back into the bloodstream thanks to the proximal tubule.
fatty streak
first signs of atherosclerosis that are visible without magnification
Thrombus formation
first the smooth muscles of your damaged blood vessels begin to spasm to constrict or reduce blood flow to the area. Concurrently, the platelets in your blood begin to gather in the damaged area. The damaged skin cells begin to secrete a substance called von Willebrand factor, making the accumulating platelets stick to the wounded skin. Lastly, your blood undergoes something called a coagulation cascade, where a series of different proteins, known as clotting factors, cascade through a series of interactions that result in the conversion of a particular protein called fibrinogen. Fibrinogen is converted into fibrous strands, called fibrin. The fibrin begins forming chains and collecting in and around the platelets, forming a mesh-like structure that traps larger blood cells and aids in completing the clot formation.
Clinical manifestations of post-infectious glomerulonephritis
fluid retention with generalized swelling swelling of the abdomen swelling of the face or eyes swelling of the feet, ankles, and arms and legs high blood pressure Coca-Cola colored urine, blood in the urine (hematuria) decreased amount of urine (oliguria), decreased GFR joint stiffness and joint pain proteinuria
2 types of MI
full thickness infarct/transmural---STEMI partial thickness infarct/subendocardial---NSTEMI
nephron
functional unit of the kidney---filters the waste combining it with water to form urine produces urine in the process of removing waste and excess substances from the blood. There are about 1,000,000 nephrons in each human kidney composed of 2 main parts: renal corpuscle renal tubule
Hypertensive encephalopathy
general brain dysfunction due to significantly high blood pressure; blood pressure is greater than 200/130 Clinical Manifestations: Headache, Confusion Restlessness Motor & sensory deficits Visual disturbances from pressure on optic nerve CVA, Coma, death
Nephrosclerosis
hardening of the walls of the small arteries and arterioles of the kidney; caused by hypertension
Hypertrophic Cardiomyopathy
heart muscle is too big and stiff; LV chamber size (lumen) is much smaller; thickened septum blocks LV outflow; 2 types: primary and secondary; Need more oxygen and perform less efficiently, so the person is prone to heart failure and may suffer sudden death during exertion; diastolic dysfunction because the LV cannot fill primary: Most common; Autosomal dominant disorder due to a missense mutation that codes for proteins in the sarcomeres of the heart muslce (B-myosin, myosin binding protein C and troponin T); a genetic heart condition that results in increased ventricular wall thickness, diastolic dysfunction, heart failure, and sudden death secondary: If the left ventricle has to work hard against increased blood pressure or aortic stenosis, then the left ventricular wall thickens in order to become stronger to overcome the pressure to eject the blood into the aorta leads to ischemia resulting in fast arrhythmias that lead to sudden death, especially in young athletes
catecholamines
help you deal with short-term stress. We know that the sympathetic nervous system fires when you feel threatened or under stress. This then stimulates the adrenal medulla to release catecholamines. These hormones then enter your bloodstream and essentially prolong the fight-or-flight response initiated by the sympathetic nervous system.
Triad of Virchow
helps to identify the 3 main risk factors for when a blood clot forms in the veins; tend to occur in the lower extremities increasing risk for pulmonary embolism clots begin to form in the cusp of the vein valve 1. Stasis of venous circulation -immobilized -varicose veins -surgery -sitting for a long-time while traveling -obstruction -heart failure -Atrial fibrilation 2. Hypercoagulability -factor V Leiden -HIT -cancer -sepsis -pregnancy 3. Endothelial damage -plaques -turbulent flow -trauma -toxins, IV drug use -medications
causes of hemolysis
hepatitis, Epstein-Barr virus, typhoid fever, sickle cell anemia, E. coli or streptococcus bacteria, leukemia, lymphoma, tumors, penicillin, pain medication, lupus, or Wiskott-Aldrich syndrome
Blood damage from hypertension
high blood glucose levels
secondary hypertension
high blood pressure caused by the effects of another disease; accompanies severe kidney disease or can occur as a side effect of certain medications; causes an increase in blood volume and viscosity---thus increasing pressure in the vessels (i.e. blood pressure and heart rate); 5-8% of people with hypertension
Hyperlipidemia
high cholesterol
Initial lesion stage of atherosclerosis
histologically normal, macrophage infiltration, isolated foam cells
bladder
holding reservoir for urine
Thrombopoietin
hormone released by the liver that signals the bone marrow to produce platelets
ANP
hormone secreted by the atria of the heart when the atria begin to overstretch due to increased blood volume; promotes the excretion of salt (and thereby water) out of the body via the urine; decreases the intestinal absorption of sodium and water into the body; promote blood vessel dilation- thus reducing BP (hypotensive); lowers blood pressure, and inhibition of aldosterone secretion stopping the RAAS cascade and ADH secretion
adrenal gland
hormone-producing glands located on top of the kidney 2 parts: cortex and medulla
Risk factors for aortic dissection
hypertension Male Age (40-60) Degeneration of medial layer of vessel connective tissue diseases: Marfan's
causes of diastolic dysfunction
hypertension with LV hypertrophy cardiomyopathy fibrosis amyloidosis sarcoidosis pericarditis hemochrmatosis valvular disease age
retinal damage from hypertension
hypertensive retinopathy
Types of shock
hypovolemic cardiogenic obstructive distributive neurogenic anaphylactic septic
immune thrombocytopenic purpura
immune disorder that causes an unusually low level of platelets in the blood 2 types: Child-acute onset, usually after a viral infection Sudden onset of petechiae and purpura Self limiting Adult-chronic, insidious onset after infection Manifestations - hx of bruising and bleeding Splenomegaly Causes: HIV hepatitis H. pylor S/S: Easy or excessive bruising Superficial bleeding into the skin that appears as pinpoint-sized reddish-purple spots (petechiae) that look like a rash, usually on the lower legs Bleeding from the gums or nose Blood in urine or stools Unusually heavy menstrual flow Tx: If asymptomatic, do not treat unless platelet count is below 20,000-30,000 Steroids splenectomy immunosuppression
symptoms of anemia
impaired healing paresthesia N/V jaundice headache anorexia pallor (decreased hemoglobin) ↑ heart rate chest pain (angina) ↑ RR and depth hypoxia SOB/dyspnea dizziness/weakness syncope (fainting) red eyes (in severe cases) heart attack
Vitamin K deficiency
important for blood clotting clinical manifestations: experience increased bleeding and easy bruising; main symptom of a vitamin K deficiency is excessive bleeding caused by an inability to form blood clots; bleeds in mucous membranes that line areas inside the body; stool that is dark black, tar-like, or contains blood Good sources of vitamin K include kiwi and green vegetables, such as kale, spinach, Brussels sprouts and turnip greens. Vitamin K is also produced by your body thanks to bacteria in your large intestine that make vitamin K.
Hypovolemic (hemorrhagic) shock
improper tissue perfusion as a result of severe blood loss, other fluid loss from the body, or inadequate fluid intake, any of which end up decreasing intravascular fluid volume; results in hypotension Acute loss of over 15% of circulating blood volume Blood loss, dehydration, third spacing sympathetic nervous system and RAAS activated
post renal failure
in cases where everything is fine except for the fact that the outflow of urine is blocked somewhere in the ureters, bladder, or urethra due to things like stones or cancer increased BUN levels BUN:creatinine will decrease to < 20:1
pressure natriuresis
increase in sodium excretion from increased blood pressure
pressure diuresis
increase in urinary volume from increased blood pressure
acute pyelonephritis
infection of the kidney and renal pelvis caused by bacteria; the most common of which is E. coli---leads to scarring, inflammation, atrophy of the cortex and pus in the kidneys; Bacteria enters your urinary tract through the urethra that can multiply and travel to your kidneys. Clinical Manifestations: Nausea and/or vomiting Fever Flank or back pain Chills Frequent urination and/or a strong urge to urinate Painful urination or a sensation of burning when urinating Abdominal or groin pain Pus or blood in the urine, which will tinge the urine white or red treatment: (antibiotics) Ciprofloxacin Ceftazidime Vancomycin diagnosis: positive urinalysis confirms the diagnosis risk factors: being female having a urinary tract blockage immunocompromised damage to nerves around the bladder using a catheter urine backflow
inflammatory disorders of the heart
infective endocarditis pericarditis
polyarthritis
inflammation of many joints
infective endocarditis
inflammation of the endocardium (inner lining of the heart) 2 types: Acute- High Fever, chills Subacute/Chronic- Low fever, systemic signs Risk factors: history of heart disease, especially valve (mitral) disorders rheumatic heart disease Complications: vegetative lesions or vegetations due to blood clot formation that is the result of the inflammatory process (Bulky lesion, Release bacteria into bloodstream, Destroy valve--valve prolapse)
pericarditis
inflammation of the pericardium 2 types: acute-sudden and severe Dressler Syndrome chronic important sign is a pericardial friction rub; caused by: infection, autoimmune disease such as lupus
glomerulonephritis
inflammation of the tiny filters in your kidneys (glomeruli); occurs on its own or as part of another disease, such as lupus (autoimmune diseases) or diabetes mellitus, nephrotoxic drugs (vancomycin), hypertension; can cause kidney damage if left untreated Acute glomerulonephritis is when the inflammation of the glomeruli occurs suddenly due to an infection in the kidneys or in the bloodstream Chronic glomerulonephritis is when the inflammation develops over time due to a disease that is present in the body diagnose with kidney function tests and blood cultures
epicardium
innermost layer of the pericardium
fibrin
insoluble protein that is produced in response to bleeding and is the major component of the blood clot; a tough protein substance that is arranged in long fibrous chains; it is formed from fibrinogen Fibrin molecules combine to form long fibrin threads that entangle platelets, building up a spongy mass that gradually hardens and contracts to form the blood clot. This hardening process is stabilized by a substance known as fibrin-stabilizing factor, or factor XIII. biological glue that seals the damaged vessel and ensures hemostasis; forms long strands of fibrin threads that crisscross heavily and form a fibrin mesh over the original wound site.
stage atheroma of atherosclerosis
intracellular lipid accumulation, core of extracellular lipid
intermediate lesion stage of atherosclerosis
intracellular lipid accumulation, small extracellular lipid pools
collecting duct
involved in regulating the urine's pH, water, and electrolyte balance as well as the channeling of urine out of the kidneys; not part of the renal tubule;
types of anemia
iron deficient folate deficient megaloblastic aplastic chronic disease pernicious
Platelets
irregular-shaped bodies that help the clotting process by sticking to the lining of the blood vessels; they release chemicals that cause the platelets to kick into action and become sticky; first responder to an injury
renal hypertension
is high blood pressure caused by the narrowing of your arteries that carry blood to your kidneys. It is also sometimes called renal artery stenosis. Because your kidneys are not getting enough blood, they react by releasing renin and activating the RAAS cascade that makes your blood pressure rise; caused by a part or total bock of the arteries that supply blood to your kidneys or narrowing of the arteries to the kidneys
Renal Calculi (Nephrolithiasis)
kidney stones; are small, hard deposits that form in the urine that are made up of mineral and acid salts; transported throughout the urinary tract; commonly found in ages 20-40 years old cause obstruction of urinary flow and pain form when there are more solid waste particles filtered by the kidneys than there is urine to dissolve them; increase fluid to prevent the formation of stones types: >calcium (most common): (70-80%) -composed of calcium oxalate and/or calcium phosphate; Usually associated with ↑ Ca levels in blood and urine Immobility contributes to ↑ bone resorption → ↑ Ca in blood >uric acid: found in men, chemotherapy PT and PT with gout--metabolic waste product of purine breakdown--result of low fluid volume/dehydration >struvite: substance formed from Magnesium ammonium phosphate; Form only in alkaline environment; forms due to infection, most commonly in women >cystine: rare form; occurs in people with the genetic disorder cystinuria, where their kidneys excrete too much of certain amino acids
common hepatic duct
large bile duct leading from liver; joins with the cystic duct to form the common bile duct
transitional epithelium
layer of cells found lining the inside of the bladder that can contract and expand as necessary
parietal pericardium
lies just underneath the fibrous pericardium, and is one of two layers responsible for producing serous fluid, which helps lubricate your heart and decrease friction against other organs as it pumps
Ventricular tachycardia
life-threatening; ventricles contract wildly and taking over conduction of the heart
endothelial cells
line the blood vessels; help the blood to flow smoothly and sends out signals when hemostasis needs to begin
sinoatrial nodes
located in the right atria; contain pacemaker cells to stimulate contraction
ureters
long tubes that connect the kidneys to the bladder located in the renal hilum, which is a groove in the kidney where the ureter, renal artery, vein, and nerves are located use peristalsis to move the urine down the tube in addition to the helps of gravity
Sinus Tachycardia
looks like a normal rhythm, but it is fast. It's also considered an arrhythmia because it is faster than normal for the SA node, or greater than 100.
Sinus bradycardia
looks like a normal rhythm, but it is slow. It is considered an arrhythmia because of this slower than normal rate for the SA node. The conduction is normal for this rhythm
orthostatic hypotension
low blood pressure that occurs upon standing up Causes: Reduced blood volume Drug induced Aging Bed rest & immobility ANS dysfunction Symptoms: Dizziness syncope
pacemaker cells
made up of specialized heart muscles that are self-excitatory and controlled by the autonomic nervous system -160mV
Fatty streak stage of atherosclerosis
mainly intracellular lipid accumulation
secondary hemostasis
makes the platelet plug (formed during primary hemostasis) stronger when fibrin is laid down and adheres to the "unstable" plug fibrin is converted from fibrinogen by thrombin via the coagulation cascade
tunica media
middle coat of the artery; composed of elastic fibers and muscle, is the thickest layer of an artery's wall; allows your arteries to expand with each heartbeat and to contract when the heart rests; helps to control blood pressure through dilation and constriction
causes of DCM
mitral and aortic valve regurgitation drugs endocrine diseases alcohol viral infection
stable angina
most common 70% due to stenosis (blocked by plaque) occurs during stress or exercise when the heart muscle requires more oxygen, but cannot receive it because of the blockage no pain at rest caused by atherosclerosis of 1 or more coronary arteries OR thickened heart muscle wall due to hypertrophic cardiomyopathy, aortic stenosis or hypertension ST-segment depression treating with nitroglycerin reversible
heart damage from hypertension
myocardial infarction hypertensive cardiomyopathy (heart failure)
2 short term mechanisms for controlling blood pressure
neural mechanism: *Intrinsic reflexes for BP (baroreceptors, osmoreceptors and chemoreceptors) *parasympathetic *sympathetic humoral mechanism: *RAAS *release of ADH *release of Catecholamines: epinephrine and norepinephrine
Reticulocytes
new red blood cells
NSTEMI
non ST segment elevation myocardial infarction This heart attack happens when the blood supply to the heart is partially blocked or only blocked for a short period of time. Common causes are heart disease, coronary artery spasms, or demand ischemia (temporary imbalance between the supply of oxygen to the heart muscle and the oxygen needed by the heart muscle) The amount of damage to the heart muscle is not very severe.
BPH (benign prostatic hyperplasia)
non-cancerous enlargement of the prostate gland typically seen in older males - it occurs in high numbers among men over the age of 75 but is rare among those under the age of 50 diagnosis: Physical examination is conducted to assess the patient's overall health. Urinalysis is done to check the overall health of the urinary system. Rectal examination allows the physician to feel the prostate, which will help determine if it is enlarged or not. Prostate specific antigen (PSA) blood testing is ordered to determine the presence of prostate cancer. clinical manifestations: Difficulty voiding Weak urine stream Dribbling urine once you have stopped urinating Having the constant feeling of having to urinate Voiding several times during the night An increase in urinary tract infections (UTIs) Bladder or kidney stones treatment: (prescription medicine) 5-alpha reductase inhibitors reduce the size of the prostate gland by blocking hormones from getting to the gland. Alpha blockers relax the bladder, making it easier to void. (surgery) Transurethral needle ablation involves sending high-frequency radio waves through a needle and into the prostate. This breaks down the enlarged portions of the gland. Transurethral microwave therapy is a procedure in which microwaves are delivered into the prostate and break down the enlarged portions. Transurethral resection of the prostate is a surgical procedure in which a scope is inserted into the penis and, with a cutting tool, the surgeon removes portions of the enlarged prostate. Prostatectomy requires an incision into either the abdomen or between the base of the penis and the rectum to remove the prostate gland. This is only done when other treatments have proven ineffective and the patient's gland is severely enlarged.
Creatinine
normal by product of muscle metabolism that is excreted by the kidneys 0.6 - 1.2 mg/dL cannot be reabsorbed by the kidneys; measures GFR---which indicates how well the blood is being filtered and thus how healthy the kidneys are decreased GFR results in increased levels of creatinine in the blood, because it gets "backed-up" in the blood when the kidneys can't filter it out decreased in PT with low muscle mass---like older adults increased levels in pre-renal failure, renal failure and post-renal failure
hepatic vein
nutrient and oxygen poor blood that the vein that collects from the liver and returns it to the heart
aneurysm
occurs when an artery bulges or balloons out in a particular area of the body usually occur in the aorta (3/4 of all aneurysms), but can occur in the brain, heart, or anywhere else in the body if an artery stretches too much it will eventually burst leading to hemorrhage and death Cardiac chamber aneurysm common after MI (stretching of necrotic cardiac muscle)
Hypertensive crisis
occurs when blood pressure spikes -- blood pressure readings are 180/120 or higher -- but there is no damage to the body's organs Associated with secondary hypertension and medication non-compliance
Structure of the Kidney
outer portion: renal cortex inner portion: renal medulla, contains several cone-shaped tissue masses called renal pyramids thin outer layer: renal capsule renal papilla
renal colic
pain caused by a kidney stone in ureter that leads to stretching Cool and clammy skin nausea and vomiting
unstable angina
pain during exercise/stress OR at rest doesn't go away/can happen at anytime occurs when a thrombosis forms on the plaque causing more narrowing of the artery, decreasing oxygen perfusion to the muscle EMERGENCY!!! high-risk of myocardial infarction reversible ST-segment depression treated with nitroglycerin
symptoms of hemolysis
pale skin, feel tired, experience weakness, have a fever, and show signs of confusion, dizziness, or lightheadedness
causes of cobalamin deficiency
pernicious anemia Loss of parietal cells and intrinsic factor GI surgery Long-term use of H2-histamine receptor blockers Nutritional deficiency Strict vegans Malabsorption syndromes
hematopoietic
pertaining to the formation of blood cells
thrombocytes
platelets; cells ('cytes') whose main function is the formation of blood clots ('thrombo'); formed from megakaryocytes, the largest cell in the bone marrow, when stimulated by thrombopoietin a glycoprotein hormone released by the liver and kidneys thrombocytopenia--low levels of thrombocytes thrombocytosis--high levels of thrombocytes
Albuminuria
presence of a protein called albumin in the urine
bacteriuria
presence of bacteria in the urine; indicates UTI
hematuria
presence of blood in the urine, caused by kidney stones, infection, kidney damage, or bladder cancer
calciuria
presence of calcium in the urine; indicate that the kidneys cannot properly reabsorb calcium or that there is an endocrine condition where there's too much calcium in the blood
glycouria
presence of sugar in the urine; indication of DM
homeostasis
prevention of blood loss; the process in which the body repairs a damaged blood vessel to prevent the further loss of blood 1. tissue/vessel injury 2. vascular spasm 3. platelet plug formation 4. coagulation
Temporary platelet plug
primary homeostasis; platelets
hemoglobin
primary iron-containing protein found in red blood cells
GFR (glomerular filtration rate)
process of pressurized filtration of blood by the glomerulus per unit of time (>90 ml/min/1.73m2)
VLDL
produced in the liver and released into the bloodstream to supply body tissues with a type of fat (triglycerides); High levels of VLDL cholesterol have been associated with the development of plaque deposits on artery walls, which narrow the passage and restrict blood flow
Liver function
produces a hormone, called thrombopoietin that tells the bone marrow to make platelets responsible for producing enzymes and solutions necessary for digestion; catabolism and anabolism responsible for the storage of carbs and fats for energy use detoxify and remove harmful substances in the bloodstream (cytochrome P450) Production of cholesterol, which is a lipid necessary for hormone production Vitamin storage, such as vitamins A and K Digestion and recycling of red blood cells and components when they become old produces all 5 clotting factors (clotting factors are proteins or globulins)
EPO (erythropoietin)
protein hormone synthesized in the kidneys that stimulates the production of new RBCs; this is why renal failure is related to anemia and a decrease in RBCs
glycoproteins
proteins with a sugar attached to them
two arterial divisions within your body
pulmonary and systemic The pulmonary division, which contains only the pulmonary arteries, is much shorter than the systemic division. The pulmonary arteries carry blood away from your heart and deliver it to your lungs, where the blood becomes oxygenated. This oxygenated blood then returns to your heart through your pulmonary veins. The systemic division contains the aorta and all of its branches
symptoms of anaphylactic shock
rapid onset dyspnea (tight throat, bronchospasm, laryngeal edema) feelings of apprehension tingling and swelling in mouth, face, throat and tongue itching decreased blood pressure tachycardia loss of consciousness
blood composition
red blood cells (erythrocytes), white blood cells (leukocytes), platelets (thrombocytes) and plasma
Intrinsic Hemolytic Anemia
red blood cells produced by the body are defective
dependent rubor
redness that develops in an extremity that is dependent, especially as a sign of inflammation; classic symptom of PAD
Symptoms of acute glomerulonephritis
reduction in urine (Oliguria) bloody urine, often pink or cola-colored from red blood cells in your urine (hematuria) Foamy urine due to excess protein (proteinuria) azotemia (increased BUN) renal insufficiency (decreased GFR) hypertension edema
Anemia of chronic disease
refers to anemia as a result of long-standing medical conditions, such as cancer and autoimmune diseases or alcoholism---inflammation destroys the precursors of red blood cells
diastole
relaxation of the heart ventricles; pressure within the heart is low; AV valves are open; semi-lunar valves are closed; when PT is relaxed diastole is longer than systole---becomes shorter during tachycardia
Glucocorticoids
released by the adrenal cortex and help regulate carbohydrate, fat and protein metabolism and have an anti-inflammatory effect on the body; increase glucose
mineralocorticoids
released by the adrenal cortex and help regulate the water and electrolyte balance in the body, particularly sodium and potassium
Von Willebrand Factor
released by the damaged endothelial cells and platelets; glycoprotein that plays an important role in stopping the escape of blood from vessels (hemostasis) following vascular injury; works by mediating the adherence of platelets to one another and to sites of vascular damage---helps the platelets stick to the injured skin
T wave
repolarization of ventricles; ventricles are relaxed and under less pressure; beginning of diastole; semilunar valves close; dub sound
Why is folate and B12 important?
required for RBC synthesis and red blood cell maturation
Symptoms of renal calculi
restlessness, blood in the urine, nausea, vomiting, discolored urine, bad-smelling urine, chills, fever, difficulty urinating, or frequently feeling the urge to urinate but only producing a small amount.
prerenal kidney failure
result of a decrease in the blood supply to the kidneys resulting in decreased oxygenation and a decreased GFR, which leads to an increase in waste products and toxins in the blood and the activation of RAAS, all of which ultimately leads to kidney failure causes: dehydration hemorrhage (hypovolemia) Heart failure: can't pump blood to the kidneys Decreased renal perfusion (drugs, vasoactive mediators) Decreased vascular filling (certain shocks) obstruction
pre-renal failure
result of low blood volume; problem occurs before the kidneys (kidneys are not the problem) ratio of BUN:creatinine will be > 20:1
uretheral stricture
scarring that narrows the tube that carries urine out of your body (urethra); restricts the flow of urine from the bladder and can cause a variety of medical problems in the urinary tract, including inflammation or infection
diabetic glomerulonephritis
scarring/inflammation in the tiny blood vessels in the kidneys called the glomeruli Occurs in type 1 and 2 diabetes mellitus #1 cause of chronic kidney disease #1 cause of kidney failure DM → thickening of glomeruli capillary basement membrane Proliferation of mesangial cells → ↓ capillary lumen → ↓ surface area for GFR symptoms: proteinuria (Microalbuminuria) edema ESRD
coagulation
secondary hemostasis; clotting factors
aldosterone
secreted by the adrenal cortex; causes the reabsorption of sodium, and therefore water, in the distal tubule and collecting ducts. This hormone will also cause these two segments to secrete potassium and acid, in the form of hydrogen ions, into the urine and out of the body helps to regulate low blood pressure
cardiac cycle
sequence of events in a single heartbeat
urinary tract
set of structures that make up the urinary system
bowman's capsule
single layer of epithelium surrounding the glomerulus;
fibroatheroma state of atherosclerosis
single/multiple lipid cores, fibrotic/calcific layers
microcytic hypochromic anemia
small red blood cell causing a decrease in red blood cell number or function; measured by MCV; most common form is iron deficient anemia hypochromic=decreased color; red blood cells are pale; measured with MCHC causes: inadequate intake of iron improper absorption (celiac) increased loss increased need (pregnancy) Thalassemia
P wave
small wave; represents the depolarization of the atria---contraction of the atria
prerenal kidney failure clinical manifestations
sodium levels in the plasma increase (hypernatremia) ↓↓ urine output (oliguria) ↑ BUN/Creatinine (azotemia) metabolic acidosis hyperkalemia anorexia changes in level consciousness vomitting neurological problems (seizures, coma)
causes of neurogenic shock
spinal cord injury above T5 spinal anesthesia vasomotor center depression: severe pain, drugs, hypocomia insulin shock emotion type 1 hypersensitivity (anaphylactic shock) inflammatory response to infection (septic shock)
Types of angina
stable, unstable, variant
Noncolicky renal pain
stones produce distention of renal calyces/pelvis = dull ache in flank (mild to severe) & worsens w/ fluid intake
hemostasis
stoppage of bleeding; clotting; 2 stages: primary and secondary
PTH (parathyroid hormone)
stops the proximal convoluted tubule from reabsorbing calcium and phosphate; Instead, the majority of calcium will be reabsorbed actively in the distal convoluted tubule and connecting segment as well as part of the loop of Henle, whereas, phosphate will be excreted out of the body as urine via the collecting ducts release is triggered by low calcium levels in the blood activate in the kidneys a prehormone produced in the liver called calcifediol into the active form of vitamin D, called calcitriol. This will lead to further reabsorption of calcium from the glomerular ultrafiltrate passing through the renal tubule.
Function of the Spleen
stores white blood cells; converts old red blood cells into bilirubin that attaches to bile for excretion from the body; where lymphocytes mature
Laminar
streamline movement of blood; blood flows in layers which move parallel to the long axis of the blood vessel
renal pelvis
structure that collects urine formed in the kidney and channels it into the ureter
serum (cardiac) biomarkers
substances that are released into the blood when the heart is damaged or stressed. Measurements of these biomarkers are used to help diagnose acute coronary syndrome (ACS) and cardiac ischemia
chorea
sudden, rapid, jerky, purposeless movement involving limbs, trunk, or face
portal vein
supplies the liver with nutrient rich blood
sympathetic vs parasympathetic
sympathetic (fight or flight) >increased heart rate >increased force of contraction and stroke volume >vasoconstriction >increased cardiac output >increased blood pressure parasympathetic (rest and digest) >decreased heart rate >increased force of contraction and stroke volume >vasodilation >decreased cardiac output >decreased blood pressure
anaphylactic shock
systemic response to the inflammatory mediators released in type 1 hypersensitivity histamine, kinins, leukotrienes and prostaglandins all cause vasodilation and bronchoconstriction causes: insect stings medication rxn food allergy
causes of cardiogenic shock
systolic dysfunction diastolic dysfunction arrhythmias structural problems
clinical manifestations of cardiogenic shock
tachycardia anxiety and delirium increased preload pulmonary congestion decreased cardiac output dusky skin color decreased blood pressure narrow pulse pressure oliguria dyspnea cyanotic respiratory acidosis hyperventilation
third-spacing
the accumulation of fluid from the blood within body cavities, intestinal areas, or areas of the body that normally contain little fluid
myocardium
the actual muscular layer of the heart responsible for contracting and pumping blood throughout your body; contracts and relaxes to pump blood; varies in thickness
cardiac output
the amount of blood ejected from the heart per minute; the product of two variables, stroke volume and heart rate
Cushing's Syndrome
the body experiences the effects of too much cortisol for too long of a period of time; causes high blood pressure and high blood sugar, lowers inflammation
aplastic anemia
the bone marrow doesn't make enough red blood cells
uremia
the condition of having high levels of urea in the blood leads to: Fatigue Peripheral neuropathy Restless leg syndrome Sleep disturbances Uremic encephalopathy Anorexia Nausea Pruritis
coronary artery disease (CAD)
the coronary arteries that deliver oxygen to the heart muscle begin to develop fatty plaques caused by atherosclerosis, which leads to restriction of blood flow to the heart
hemolysis
the destruction of red blood cells before their normal life span is up (destruction > production); When red blood cells burst, hemoglobin, (the part that carries oxygen), is released into the rest of the blood. This can decrease the amount of oxygen the body gets. RBC metabolic activity decreases with age → brittle cell membrane Eventually RBCs break as they squeeze through tight spaces such as the spleen capillaries 2 types: intrinsic and extrinsic Treat the underlying cause!
urinalysis
the diagnostic physical, chemical, and microscopic examination and testing of urine for abnormalities measures: pH, specific gravity,
cardiac reserve
the difference between the rate at which the heart pumps blood and its maximum capacity for pumping blood at any given time
aortic aneurysm
the dilation of the aorta greater than 50% of it's normal diameter; "balloons" out and can burst, leading to death
Urinary meatus/urinary orifice
the exit from the urinary system
turbulant
the flow can be described as being chaotic; noisy and can be heard by using a stethoscope placed over the artery at or distal to the point of constriction or obstruction occurs in large arteries at branch points, in diseased and narrowed (stenotic or partially obstructed) arteries, and across stenotic heart valves.
renal corpuscle
the glomerulus and its surrounding Bowman's capsule; located in the renal cortex; first structure involved in the nephron's formation of urine; ultrafiltration of blood filters: water, glucose, amino acids, bicarbonate, urea, and creatinine as well as ions such as potassium, sodium, chloride, calcium, and phosphate
Chronic kidney disease
the gradual loss of kidney function over many months or years causes: Diabetes Hypertension Glomerulonephritis Pyelonephritis, or kidney infection Obstruction of the urinary tract due to a stone Genetic defects, leading to conditions such as polycystic kidney disease Autoimmune diseases (lupus, IgA nephropathy) Polycystic Kidney Disease
renovascular disease
the impairment of renal perfusion caused by disease affecting the arterial supply of the kidney; Renal hypoperfusion leads to hyperactivation of the renin-angiotensin-aldosterone axis, causing hypertension; important cause of secondary hypertension and chronic kidney disease
cardiogenic shock
the inability of the heart to maintain cardiac output necessary to meet body needs; extra strain on the heart causes decreased tissue perfusion resulting in hypoxia and hypoperfusion results in decreased cardiac output lowering BP The sympathetic system responds and RAAS (compensatory neurohumoral responses) Vasoconstriction increases resistance to blood flow Increased workload on the heart worsens heart failure
Cystitis (UTI)
the inflammation of the bladder, usually as a result of infection, most commonly due to bacteria (E. coli) that enter through the urethra more common in women because the urethra is shorter, and the location of the urethra opening is closer to the vagina and anus treated with antibiotics Predisposing factors Obstruction, Urinary reflux, Urine stasis, Sexually active ♀ Protective factors Washout phenomenon Mucin Bacteria Lower UTIs can cause a frequent, urgent need to urinate, pain or burning while urinating, urine that is cloudy in appearance (normal urine is usually straw colored and clear), blood in the urine, and urine with a strong odor. Upper UTIs can have all of those same symptoms but may also include chills, fever, vomiting, and pain in the upper back area
tunica intima
the innermost layer of the arterial wall and the layer that is most intimate with your blood composed of 3 layers: A thin, inner layer of endothelial cells provides a smooth, almost frictionless surface that allows your blood to flow freely through the artery. Surrounding the endothelial cells is a thin layer of connective tissue, which is then coated by a fine network of elastic fibers that help support the tunica intima and attach it to the next layer, which is the tunica media.
intrinsic conduction system
the internal regulating system that causes the heart to contract rhythmically
aorta
the largest artery and carries blood from the heart to the body ascending aorta: first section of the aorta and contains blood from the left ventricle of the heart. baroreceptors are special receptors that detect how much the aorta is stretching; helps regulate blood pressure
mitral valve prolapse
the mitral valve does not close properly; "floppy valve". When the left ventricle contracts, blood flows both backwards toward the left atrium and forward through the aorta, called mitral valve regurgitation Symptoms: Usually asymptomatic If Symptomatic: SNS symptoms- palpitations, anxiety CP w/ dyspnea, fatigue & lightheaded Diagnosis and Treatments: Echocardiogram No caffeine, smoking, stimulants Beta blockers surgery
Mitral valve regurgitation
the mitral valve fails to completely close the door so to speak, allowing blood to flow BACK into the atrium The leading cause and the most common of all valvular conditions, is mitral valve prolapse; Infective endocarditis, rheumatic heart disease; Damage to cardiac structures such as myocardial inarction
red blood cells (erythrocytes)
the most abundant cell type in the human body carry oxygen around the body and remove the carbon dioxide from the body with the help of hemoglobin; hemoglobin lives inside of red blood cells and likes to hold and carry the oxygen to other cells that need it The shape of a red blood cell is a flat circle, or disk. Normal lifespan of RBC = 120 days
renin-angiotensin-aldosterone system
the most important system involved in the regulation of systemic blood pressure, renal blood flow and glomerular filtration rate regulates HYPOTENSION
myocardial infarction
the occlusion of one or more coronary arteries caused by plaque buildup (heart attack)
cardiac preload
the pressure of the blood on the muscle fibers in the ventricles of the heart at the end of diastole; if the blood returned to the atria from the body has more volume than normal, the result is increased preload; when there is less volume of blood returned to the atria from the body it is decreased preload increased in: hypervolemia regurgitation of heart valves cardiac failure
erythropoiesis
the process of producing red blood cells. Red blood cell formation is signaled by the release of a hormone known as erythropoietin, or EPO. Erythropoietin is released by the kidneys in response to several conditions, including decreased blood flow to the kidneys, low atmospheric or blood oxygen levels, and low blood pressure (hypotension). When erythropoietin is released, it will migrate to the red bone marrow and bind to receptors that stimulate the maturation of red blood cells. Stem cells, which are cells that have not been differentiated into specified cell types, are converted into reticulocytes, which contain a nucleus. Upon maturation, the nucleus is ejected from the cell, and a mature red blood cell is formed.
cardiac afterload
the resistance that the ventricle of the heart has to overcome to eject the blood from the ventricle chamber during systole increased in: hypertension vasoconstriction age increased afterload = increased cardiac workload/decreased contraction
Post-Infectious Glomerulonephritis (GN)
the result of an infection of a completely different area, such as the skin or throat. The infection causes filters in the kidneys to become swollen. This makes the kidneys less able to filter and remove wastes. This disorder may begin to develop 7-12 days after an untreated throat infection, and three to four weeks after an untreated skin infection. This condition can occur at any age. However, it is mostly common in children ages six to ten. This condition is also known to affect twice as many males than females. most commonly caused by Group A β-hemolytic streptococci infection
pericardium
the sac around the heart that encases, protects and secures the heart; composed of 3 layers--- the outer fibrous pericardium, the middle parietal pericardium, and the inner epicardium (also referred to as the visceral pericardium
ureterovesical junction
the site of entry of the ureter into the bladder
Extrinsic Hemolytic Anemia
the spleen, due to various reasons, destroys red blood cells faster than they can be made destruction > production
endocardium
the thin innermost layer of tissue that makes direct contact with the blood pumping through the heart chambers; very thin layer of cells that line the interior chambers of your heart; provides a smooth surface for the blood to glide against (acts as Pam does on a baking dish)
Total peripheral resistance
the total resistance to flow of blood in the systemic circulation
urethra
the tube from the bladder to the outside of the body; males: 6-7" long; females" 1-2" long
intrinsic renal failure
the urea is unable to be filtered out of the blood properly because the kidneys are very sick, resulting in increased levels of urea in the blood increased BUN levels; decreased GFR; increased waste retention BUN:creatinine will decrease to < 20:1
Chronic rheumatic heart disease
the valves, typically the mitral valve, develop scar tissue from repeated inflammation. The leaflets of the valves become thicker and can actually fuse together, called commissural fusion. the chordae tendinae which are attached to the valves can become thickened as well; These changes can cause complications with the valves, most commonly regurgitation, meaning that they don't close all the way. This can progress to stenosis, or narrowing of the opening, sometimes called "fish-mouth" stenosis or "buttonhole" stenosis.
fibrous pericardium
thick, fibrous outer layer of the pericardium; anchors your heart in place at the sternum and diaphragm
cardiac catheterization
thin, flexible tube is guided into the heart via a vein or an artery
Mesangial Cells
this cell is sometimes referred to as the 'Lacis cell.' These cells are juxtaglomerular apparatus cells that may secrete a hormone called erythropoietin, which is critical for the production of red blood cells.
complications of hemolysis
thrombosis, chronic kidney disease, pulmonary hypertension, organ damage, anemia, and a decreased quality of life
renal papilla
tip of the renal pyramid helps excrete urine formed in the cortex and medulla of the kidney into the renal pelvis
clinical manifestations of polycythemia vera
tissue ischemia shortness of breath dyspnea h/a fatigue dizziness weight loss/night sweats joint pain CVA (thromboembolism) painful, intense itching venous stasis dusky red/blue fingers, lips, mucous membranes
AV node
transmit the electrical impulse from the atria to the ventricles
treatment of diabetic glomerulosclerosis
treatment: Immune system medicines. Medicines used to block the body's immune system. This prevents the body from making antibodies that may attack the glomerulus. Dialysis. A treatment to remove wastes and excess fluid from the blood after the kidneys have stopped working. Kidney transplant. This procedure replaces your diseased kidney with a healthy one from a donor. Blood pressure lowering medicines Diet changes: control blood glucose stop smoking
coagulation cascade
triggered by factor III a series of reactions involving clotting factors that stop bleeding by forming a clot 2 pathways that form into the common pathway intrinsic: triggered when there is INTERNAL damage to a blood vessel; involves factor VIII, IX, XI, XII extrinsic: triggered when there is EXTERNAL damage to a tissue; involves factor VII common pathway involves factors I, II, V, X
urethral sphincters
two muscles that control the emptying of the bladder into the urethra
Post-renal Failure
type of acute renal failure that occurs as a result of obstruction to urine outflow; GFR decreases due to the back up of fluid; azotemia occurs This obstruction to urine outflow can occur anywhere after, or 'post-,' the kidneys. This means that if a ureter, bladder, or urethra is obstructed due to: Stones A tumor MOST COMMON CAUSE: An enlarged prostate Strictures Neurogenic bladder
complicated lesion of atherosclerosis
unstable with a surface defect leads to hematoma/hemorrhage, thrombosis
Washout phenomenon
urine from bladder washes bacteria out urethra to prevent infections
stunned myocardium
viable myocardium salvaged by coronary reperfusion that exhibits prolonged postischemic dysfunction after reperfusion
treatment of vitamin K deficiency
vitamin K supplement called phytonadione
anisocytosis
when red blood cells are of varying and unequal sizes as opposed to being uniform throughout
aortic valve stenosis
when the aortic valve doesn't open all the way, and it gets harder to pump blood out to the body resulting in less blood to the body, which leads to less perfusion causes: *Congenital *Damage to endothelial cells over time causing fibrosis and Calcification Plaques *Chronic Rheumatic Fever that causes repeated inflammation and repair Diagnosis & Treatment Echocardiogram medication Surgery
Atrial fibrillation
when the atria of the heart flutter or shiver rather than fully contract, moving blood to the ventricles to be pumped out to the body. Blood may collect and pool during atrial fibrillation, resulting in ineffective blood flow through the heart and body.
vesicoureteral reflux
when urine gets forced back up to the kidney due to a blockage resulting in swelling of the kidney or hydronephrosis
molecular mimicry
where antibodies accidentally target proteins on our own cells because they look like the proteins on foreign cells; occurs in rheumatic fever causing rheumatic heart disease