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Pathophys-2 MT prep
Blood, Cardiovascular, Renal Systems
| Question | Answer |
|---|---|
| What are the five stages of hemostasis, in order? | spasm, plug, clot, clot retraction, clot "dissolution" (N.B. most sources include only the first 3) |
| What are the requirements for the clotting process? | platelets + Von Willebrand factor + clotting factors |
| What is the functions of the Von Willebrand factor in clotting? | promotes adhesion of platelets to subendothelial collagen |
| What is the functions of vitamin K in clotting? | LR needs vit K for synthesis of clotting factors (but factor VIII and vWF not made in LR) |
| What is the function of antithrombin III in the regulation of blood coagulation? | inactivates coagulation factors and neutralizes thrombin |
| What is the function of protein C in the regulation of blood coagulation? | inactivates the clotting factors Va and VIIIa |
| What is the function of protein S in the regulation of blood coagulation? | accelerates the action of protein C |
| What is the function of plasmin in the regulation of blood coagulation? | breaks down fibrin |
| How does atherosclerosis contribute to a hypercoaguability state? | Increases platelet function |
| How does smoking contribute to a hypercoaguability state? | Increases platelet function |
| How does DM contribute to a hypercoaguability state? | Increases platelet function |
| How do oral contraceptives contribute to a hypercoaguability state? | They increase clotting activity |
| How does immobility contribute to a hypercoaguability state? | Increases clotting activity |
| How do malignant states contribute to a hypercoaguability state? | They increase clotting activity |
| What is the mechanism of bleeding in liver disease? | lack of vitamine K --> deficient production of many clotting factors that are synthesized in LR |
| What is the mechanism of bleeding in vitamin C deficiency? | vitamin C deficiency --> collagen defects --> incompetence of endothelia cell walls |
| What is the mechanism of bleeding in Cushing's disease? | high serum cortisol levels --> protein wasting--> weak BV walls |
| What is the pathophysiology of hemophilia? | Hemophilia A is deficiency of (clotting) factor 8. Hemophilia B is deficiency of (clotting) factor 9. (Platelet plug forms okay, but b/c no clotting factors, stable clot cannot form.) |
| What are the clinical manifestations of hemophllia? | Uncontrollable bleeding following trauma, SQ hematomas or hemarthroses, GI bleeding, urinary tract bleeding |
| What is the pathophysiology of Von Willebrand disease? | decrease in platelet adhesion |
| How common is Von Willebrand disease? | most common hereditary bleeding disorder |
| Why is Disseminated Intravascular Coagulation (DIC) considered a "consumptive" coagulopathy? | massive activation of coagulation factors and platelets which leads to exhaustion of coagulation proteins and platelets-- and thus uncontrollable hemorrhage |
| What are the conditions associated with DIC? | obstetric conditions like abruptio placentae, dead fetus syndrome, and pre-eclampsia/eclampsia, cancers (metastatic cancer, leukemia). Infections, shock, trauma or surgery, blood transfusion reactions |
| What are the red blood cell morphologies in iron deficiency anemia? | RBCs are both smaller (microcytic) and also contain less Hgb (hypochromic) |
| What are the type of anemias due to intracorpuscular defects? | Hereditary spherocytosis, sIckle cell anemia, thalassemia, G6PD deficiency |
| What is the pathophysiology of sickle cell anemia? | abnormal conformation of RBCs elicits a tendency to clump together, obstructing capillary circulation and leading to ischemia and possible tissue infarction |
| What are the conditions which are likely to trigger a sickle-cell crisis? | hypoxia (including high altitude), low body (or environmental) temps, excessive exercise |
| What are the consequences of repeated sickle cell attacks? | Retarded intellectual developing (neurologic deficits), cardiopulmonary insufficiency, heart failure, recurrent infections |
| What is the pathophysiology of thalassemia? | Genetic defect that causes reduced rate of either alpha or beta globin chain synthesis (defect is quantitative, not qualitative) |
| What may be the X-ray finding of thalassemia in the calvarium? | crew cut appearance d/t compensatory bone hyperplasia ("spicules"), b/c thalassemia is a hypochromic anemia |
| What is the pathophysiology of hereditary spherocytosis? | RBCs are spherical rather than donut shaped (“bi-concave”) |
| What is its treatment of choice for hereditary spherocytosis? | splenectomy |
| What is the pathophysiology of anemia in G6PD deficiency? | G6PDH is required to produce NADPH which, in turn, is required for production of GLUTATHIONE. WITH NO GLUTATHIONE, Hgb gets oxidized and “denatured” by H2O2 → damage to RBCs → anemia |
| What are the causes of secondary aplastic anemia? | cytotoxic medications, radiation therapy (rarely viral infection) |
| What is the most common form of anemia? | iron deficiency anemia |
| What are the lab findings in iron deficiency anemia? | both Hgb AND Hct (as well as serum iron and ferritin) will be low. But.. total plasma iron-binding capacity will be HIGH! |
| What are the functions of vitamin B12 and folic acid? | cofactors for DNA synthesis and alo for RBC maturation |
| What are the neurologic symptoms in vitamin B12 deficiency anemia? | Destruction of posterior and lateral columns of spinal cord result in loss of sense of vibration and proprioception, as well as lost of DTR in lower extremities |
| What is the morphology of neutrophils in megaloblastic anemia? | HYPERSEGMENTED |
| What are the red blood cell morphologies in both vitamin B12 and folic acid deficiency anemia? | LARGER than normal RBCs (macrocytic), normal Hgb (normochromic) |
| What are the causes and characteristics of infectious mononucleosis? | Epstein-Barr virus is cause. Sx can include fever, fatigue, swollen LN, maybe sore throat |
| What are the characteristic pathologic findings for the diagnosis of Hodgkin’s lymphoma? | Reed Sternberg cell |
| What are the features of 3 symptom-related stages of Hodgkin’s lymphoma? | Stage A: Asymptomatic; Stage B: Weight loss, fever, pruritus or night sweats; Advanced Stage: Fatigue, anemia. LV, LU, GI, CNS involvement |
| What are the features of 4 lymphadenopathy-related stages of Hodgkin’s lymphoma? | Stage I: single lymph node involvement (or group of contiguous nodes at one site); Stage II: 2 or more sites on same side; Stage III: Disease on both sides; Stage IV: Widespread extralymphatic involvement (LV, Marrow, LU) |
| How common is non-Hodgkin’s lymphoma? | "3x more common than Hodgkin's" |
| What are the differences between the sites of involvement of the endemic and sporadic variants of Burkitt’s lymphoma? | Endemic affects children infected with EBV: Mandible, maxilla, facial soft tissue, Sporadic type (seen in children and young adults) presents as abdominal mass (ovarian or intestinal) mass). |
| What are the characteristics of leukemia cells? | Acute leukemia= a rapid increase in the numbers of IMMATURE blood cells. Chronic leukemia= the excessive build up of relatively MATURE, but still abnormal WBCs. |
| What are the complications of leukemias? | Crowds out normal cells in BM, damages BM (which then affects all blood cell lineages), could spread to other organs |
| What is the most common leukemia in children? | ALL |
| What is the most common leukemia in adults? | AML |
| What is the most common leukemia in the elderly? | CLL |
| What is the bone marrow feature needed to establish the diagnosis of acute leukemias? | For dx of ACUTE (either lymphoblastic or myeloid/myeloblastic) >20% of blasts need to be abnormal |
| What is Philadelphia chromosome? | a specific chromosomal abnormality associated with chronic myelogenous leukemia (CML). 95% of people with CML have it. First described in 1960 by Peter Nowell from Univ of Pennsylvania SOM (and David Hungerford from Fox Chase Cancer Center) |
| What is the relationship of prognosis with the presence of Philadelphia chromosome in chronic myelogenous leukemia? | Good prognosis |
| What is the pathophysiology of multiple myeloma? | It is a cancer of plasma cells |
| What are the pathological changes that occur in the bones in multiple myeloma? | Proliferation of malignant plasma cell destroys bone marrow and surrounding bone (causes fractures (and release of Ca+ into blood --> hypercalcemia) |
| What are the complications in multiple myeloma, other than in the bones? | Damage to KD (b/c light chain IgG muck up filters) and then reduced RBC (and WBC!) counts. Also hyperviscosity syndrome. (Not sure why...) |
| What are the diagnostic tests in multiple myeloma? | X-rays for LYTIC LESIONS on bones. BENCE JONES protein in urine. Biopsy. |
| What are the major risk factors for coronary heart disease (CHD)? | Age (men >45, women >55), male gender, family history (“genes”), high LDL/low HDL, high homocysteine levels, obesity, hypertension, DM, smoking, inactivity, “clotting factors” |
| What are the four important localized forms of atherosclerosis? | (HT, HT brain, extremities): Coronary arteries, cerebral vascular disease, atherosclerosis of AORTA, peripheral vascular disease |
| What is the pathophysiology of atherosclerosis? | Endothelial injury → deposition of monocytes, platelets, serum lipoproteins → “proliferation of smooth muscle cells of arterial wall” → OXIDATION of lipids → smooth muscle cells & macrophages “eat the oxidized LDL” and turn into FOAM CELLS → … ? |
| What are the major complications of atherosclerosis? | Ischemic heart disease, stroke, peripheral vascular disease, hypertension (resulting from RENAL ARTERY hypertension, causing release of renin), aortic aneurysm, ischemic BOWEL disease (resulting from atherosclerosis of intestinal arteries), gangrene! |
| Define aneurysm | an abnormal localized dilation of an artery or vein |
| What is the most common location of atherosclerotic aneurysm? | the abdominal aorta |
| What may be the presentation and complication of atherosclerotic aneurysm? | They are often SILENT. Aortic dissection= ACUTE, LIFE-THREATENING CONDITION |
| What is the pathogenesis of intermittent claudication of lower limbs? | Chronic, obstructive arterial occlusion (d/t atherosclerosis) |
| What is the pathogenesis of familiar hypercholesterolemia? | also known as Type IIa hyperlipidemia, familial hypercholesterolemia is caused by LDL receptor defect/deficiency (in LR) which limits/inhibits its uptake/processing in LR |
| What is the pathogenesis of Raynaud’s disease? | “functional d/o caused by intense vasospasm of the arteries and arterioles in the fingers and, less often, toes. Seen in otherwise healthy young women. Precipitated by cold—or by strong emotions” |
| What are the risk factors and complications of deep vein thrombosis (DVT)? | “Virchow’s Triad” of risk factors: 1. Stasis of blood (immobility, SPI, MI, CHD, shock, venous obstruction); 2. Increased coagulability (stress, trauma, preg, oc use, dehydration, cancer); 3. Vessel wall injury (indwelling cath, surgery, trauma) |
| What are the risk factors for pressure ulcers? | Diminished sensory perception, Increased skin moisture, Dirty bed (urinary, fecal contamination), Bedridden, “Altered nutritional and hydration status," Compromised circulation |
| What are the causes of secondary hypertension? | 1) KD disease, 2) adrenal (cortical) disorders (e.g., Cushing’s, or primary hyperaldosteronism), 3) pheochromoocytoma (tumor of the adrenal medulla), 4) coarctation of aorta, 5) sleep apnea |
| What is the pathogenesis of hypertension? | Not sure if this is the answer he wants, but there are 3 factors: 1) Increase in blood volume, 2) increase in cardiac output, 3) increase in peripheral resistance (e.g., constricted arterioles) |
| What are the risk factors for hypertension? | Family history, (advanced) age, (AA) race, insulin resistance (“metabolic abnormalities”), circadian rhythm (“non-dippers”), lifestyle factors (salt, fat, ETOH, oral contraceptives, poorly managed stress) |
| What are the possible complications of hypertension? | (HT, HT, KD, brain, eye): Cardiac hypertrophy, CHD, renal insufficiency, hypertensive encephalopathy, hypertensive retinopathy |
| What are the causes of orthostatic hypotension? | 1) Decrease in vascular volume (e.g., dehydration), 2) impaired muscle function (e.g., spinal cord injury, confined to bed), 3) impaired (baroreceptor) reflexes (disorder of autonomic nervous system (ANS) or side-effect of some medications) |
| What is the pathogenesis of constrictive pericarditis? | Scar tissue develops between the parietal and visceral layers of the serous pericardium |
| What are the consequences of sudden occlusion of a coronary artery? | Acute, rapid onset, crushing chest pain and MI |
| What are the consequences of gradual occlusion of a coronary artery? | Congestive heart disease (CHD) and recurring AP (angina pectoris) |
| What are the two types of atherosclerotic lesions in respect of stability? | fixed (stable) vs. vulnerable (unstable) |
| What are the complications of an unstable plaque? | Risk of RUPTURE (which might be followed by platelet adhesion and thrombus formation); implicated in “unstable angina” and MI |
| What are the complications of a stable plaque? | Chronic obstruction of blood flow + “stable angina” |
| What are the characteristics of unstable angina? | AP of 1) increasing frequency, 2) increasing duration, and 3) precipitated by progressively lower levels of (physical) activity |
| What are the causes of unstable angina? | sequence of events= plaque disruption, platelet adhesion/aggregation, “secondary” hemostasis → thrombosis |
| What are the manifestations of myocardial infarction? | Abrupt onset of severe and crushing (chest) pain, usually substernal and radiating to the left arm, neck or jaw, lasting >30 minutes; a rapid & weak pulse, profuse sweating (diaphoresis), SOB (dyspnea) d/t pulmonary congestion; pale, cool, moist skin. |
| What are the two types of infarcts with respect to extent of involvement of heart muscle? | transmural and subendocardial |
| What is the cause of dilated cardiomyopathy? | (affects ejection/systole): virus, ETOH, cardiotoxic drugs |
| What is the cause of hypertrophic cardiomyopathy? | (affects filling/diasystole): usually genetic (chromosomal abnormality) |
| What is the cause of restrictive cardiomyopathy? | (affects filling/ diasystole): sarcoidosis, amyloidosis, fibrosis (including damage from radiation therapy) |
| What is the pathogenesis of infectious endocarditis? | “Colonization or invasion of the heart valves OR the mural endocardium by a microbe (endocarditis of ‘previously damaged´ valves most commonly caused by Strep viridians (or, in IDUs, Staph aureus) infection) |
| What are the complications of infectious endocarditis? | Heart murmur (fibrosis of valve, preventing it from closing properly); more serious complication is spread (“embolization”) of infection into systemic circulation → bacteremia with shaking chills |
| What is the pathogenesis of rheumatic fever? | Sequelae of “Group A strep” (GAS) sore throat. (Abs cross-react w/ Ags (similar to those of GAS) of heart, joints, connective tissue |
| What are the probable causes of congenital heart disease? | “Idiopathic” (most cases), viral infections (TORCH: Toxo, Other, Rubella, CMV, HBV), fetal alcohol syndrome, chromosomal (i.e., Turner’s, Down) |
| What are the causes of heart failure? | He dividedinto 2 categories: decreased function (myocardial disease, valve, constrictive periocarditis) & increased work demand (subdivided into pressure work (HBP & coarct), volume work (shunting, excess IV fluid), perfusion work (thyrotoxicosis, anemia) |
| What are the compensatory mechanisms adapted by the body in heart failure? | 1. Frank Starling mechanism, 2. activation of SNS (sympathetic nervous system), 3. renin-angiotensin-aldosterone mechanism, 4. natriuretic peptides (e.g., ANP), 5. (locally produced) vasoactive substances (e.g., prostaglandins), 6. myocardial hypertrophy |
| What is high output HT failure? | excessive need for cardiac output (e.g., Paget’s or anemia) |
| What is low output HT failure? | pump insufficiency (ischemic HD, cardiomyopathies) |
| What is systolic HT faiilure? | Ejection problem |
| What is diasystolic HT failure? | Filling problem |
| Possible causes of right-sided HT failure? | constriction of vessels into lung, stenosis or regurgitation of tricuspid or “pulmonic” (aka pulmonary aka semilunar) valves, R ventricular infarc, persistent L side failure, cor pulmonale, cardiomyopathy |
| Possible causes of left-sided HT failure? | Acute MI or cardiomyopathy |
| Symptoms of right-sided HT failure? | systemic edema (especially lower legs but also liver) |
| Symptoms of left-sided HT failure? | Mostly pulmonary edema (main sx= SOB/dyspnea) |
| Define edema | “increased interstitial fluid volume” |
| What are the physiologic mechanisms that contribute to edema formation? | 1) increased capillary pressure (HT failure), 2) decreased colloid osmotic pressure (LR disease), 3) increased capillary permeability (severe burns and hives), 4) lymph node obstruction (b/c of tumor or consequence of (cancer) surgery) |
| What is the pathogenesis of central diabetes insipidus? | problem with the synthesis or release of ADH d/t any number of brain problems: brain tumor, meningitis, intracranial hemorrhage, trauma to bones @ base of skull |
| What is the pathogenesis of nephrogenic diabetes insipidus? | a problem with the KD itself (failure to respond to ADH). This may be due to 1) chromosomal abnormalities (genetic), 2) K+ depletion, 3) hyper Ca+, or 4) LITHIUM |
| What is the cause of SIADH? | “Failure of negative feedback system that regulates release and inhibition of ADH." Causes (think "Cancer, cancer drugs, Lung, Lithium"): neoplasm (lung, prostate, pancreas), neurologic disease, lung disease, certain meds (antipsychotics, chemo, LITHIUM) |
| What are the causes of hyperkalemia? | Dietary excess, release from intracellular compartment (d/t burns or other tissue trauma), renal insufficiency/failure, some medications (ACE inhibitors and potassium-sparing diuretics) |
| What are the cardiovascular manifestations of hyperkalemia? | “Risk of cardiac arrest if ‘severe’ excess” |
| How licorice can cause HYPOkalemia? | licorice increases cortisol levels (which apparently “looks like” aldosterone to your KD), triggering the same effects as aldosterone; potassium wasting through the urine, sodium retention, water retention, and HYPERTENSION!! |
| What are the causes of hypocalcaemia? | HypoPARAthyroidism, vitamin D deficiency, renal failure, ACUTE PANCREATITIS |
| What are the manifestations of hypocalcaemia? | Muscle cramps, parethesias (numbness, tingling), carpopedal spasm, TETANY, +Trousseau signs (a test of “latent” tetany), osteomalacia |
| What are the causes of hypercalcemia? | HyperPARAthyroidism, neoplasm, milk-alkali syndrome, too much vitamin D (or Ca+) in diet, prolonged immobilization, some medications (thiazide diuretics, LITHIUM) |
| What are the manifestations of hypercalcaemia? | Stones (kidney stones), Bones (brown tumors d/t decalcification), Moans (personality & behavioral changes + depression), Groans (stomach ulcers), fatigue OVERTONES (lethargy, muscle weakness) |
| In which disease states was LITHIUM implicated? | SIADH, HYPER-Ca+ (via hypothyroidism). And NEPHROgenic diabetes insipidus. |
| In which disease states was ACUTE PANCREATITIS implicated? | hypocalcemia (fatty acids released from pancreatic inflammation (or rupture!) have AN EXPOSED CARBOXYL GROUP! (-1 charge!!) and, for whatever reason, strongly bind to serum calcium (+2), "precipitating" it out of circulation |
| What are the hematologic manifestations of chronic renal failure? | anemia and coagulation disorders |
| What are the cardiovascular manifestations of chronic renal failure? | HTN, pericarditis, HT disease |
| What are the four stages of chronic renal failure? | Diminished renal reserve, renal insufficiency, renal failure, ESRD |
| What are the GFRs in each of the 4 stages of renal failure? | 50% (diminished), 20-50% (insufficiency), less than 20% (fafilure), LESS THAN 5%!!=ESRD |
| What are the prerenal causes of renal failure? | hypovolemia, decreased vascular filling, HT failure, shock, decreased renal perfusion |
| What are the renal causes of renal (aka intrinsic) failure? | Acute tubular necrosis, renal ischemia, nephrotoxin exposure, intratubular obstruction, acute renal disease |
| What are the postrenal causes of renal failure? | bilateral ureter obstruction, bladder outlet obstruction |
| What are the differences between acute and chronic renal failures? | Acute renal failure has sudden onset and is often reversible if treated promptly. Chronic renal failure develops over years and is likely to end in a dialysis (or transplant) situation. |
| What are the age groups and clinical presentations of renal cell carcinoma? | 50 years and older. Often with paraneoplastic events: hypercalcemia, erythrocytosis (too many RBCs) |
| Why is renal cell carcinoma referred to as "internist's tumor?" | b/c, even though it is the most common KD cancer, it is often asymptomatic ("silent") and discovered accidentally on physical exam (or routine radiologic testing, according to eMedicine) that only your internist/primary care physician is likely to perform |
| What is the clinical presentation of renal cell carcinoma? | Renal cell carcinoma (RCC) may remain clinically occult for most of its course. The classic triad of flank pain, hematuria, and flank mass is uncommon (10%) until more advanced disease. |
| What is the age group for Wilm’s tumor? | infants and young children |
| How bad is a Wilm's tumor? | most are benign |
| What is the typical clinical presenation of a Wilm's tumor? | large abdominal mass, HTN |
| What is the pathogenesis of acute tubular necrosis? | sudden DECREASE in arterial pressure leading to major DECREASE in KD perfusion causing destruction (ischemia -> necrosis) of TUBULAR EPITHELIAL CELLS. Most common cause= MI, drug sfx, shock, massive blood loss. |
| What is the pathogenesis of hypertensive nephropathy? | thickening and fibrosis of renal ARTERIOLES leading to ischemia and decreased renal function |
| Explain proteinuria and microalbuminuria in the context of diabetes mellitus | BOTH are measures of albumin in urine. Microalbuminuria (>30mg albumin/24hr urine) is used to monitor the progression of DM- but can also signal HT or other KD disease. Proteinuria >300mg albumin/24hr urine) typically doesn't develop until much later. |
| What measures can be taken to slow down the progression to ESRD in diabetes mellitus? | treat the hyperinsulinemia and the hypertension (someone suggests ACE inhibitors and angiotensin receptor blockers (ARBs)) |
| What is the most common KD neoplasm in adults? | renal cell carcinoma (RCC) |
| What is the pathogenesis of diabetic nephropathy? | Chronic hyperglycemia causes changes in the glomeruli, arterioles and interstitium. |
| (What is the pathogenesis of diabetic nephropathy?) | (very similar to the pathogenesis in hypertensive nephropathy: fibrosis which leads, over time, to decreased renal function) |
| How common is diabetic nephropathy? | said to affect 30% of DM patients (or "persons living with DM") |
| What is the most common cause of end-stage renal disease (ESRD) in DM persons/patients? | diabetic nephropathy |
| Trick question: Is diabetic nephropathy seen more in Type I or Type 2 diabetes folks? | The risk (and prevalance) is greater in Type I, but since there are many more people with Type II DM, it is seen more often in Type II. |
| What is the gross appearances of kidneys in end-stage renal disease? | shrunken with GRANULAR texture |
| What is the cause of Goodpasture’s syndrome? | antibody in the glomerular "basement membrane" |
| What is the presentation of Goodpasture’s syndrome? | usually MALE patient (6:1), w/ (Paul Harvey out in the field harvesting prairie oysters (gonads)?: gnidaph) TRIAD of 1) pulmonary hemorrhage, 2) iron deficiency anemia, and 3) glomerulonephritits |
| What is the pathogenesis of IgA nephropathy? | deposition of (IgA) Ab-Ag immune complexes in the MESANGIUM/MESANGIA of the glomerulus |
| What are the presenting features of IgA nephropathy? | flu-like illness, upper respiratory infection or GI distress followed by GROSS HEMATURIA |
| What are fish oil benefits for IgA nephropathy? | used to slow the progress of the disease "but is not proven effective" |
| Most common form of acute glomerulonephritis? | IgA nephropathy |
| another name for Berger's disease? (hint: it is the common form of acute glomerulonephritis) | IgA nephropathy |
| What are the manifestations of Henoch-Schonlein purpura? | who the f%&# cares |
| What are the manifestations of Henoch-Schonlein purpura? | Palpable purpura (basically raisde purple blotches-- like that Dr Seuss "Put Me In The Zoo" spots book) on lower limbs w/ arthrosis, abd pain and hematuria. Usually self-limiting lasting 1-6 wks. Most common in children. |
| What is the most common cause of nephrotic syndrome in children? | LIPOID NEPHROSIS aka "minimal change disease" (b/c the damage to the glomeruli "can only be seen under an ELECTRON microscope"!!) |
| What are the glomerular features of nephrotic syndrome in children? | Fusion of the FOOT PROCESSES (i know this is lame, but i am going to think about how cute babies' feet are, maybe how the dimples look like kidneys?) |
| What is the most common cause of primary nephrotic syndrome in adults? | "membranous nephropathy" (good luck with that) |
| What is the pathogenesis of primary nephrotic syndrome in adults? | massive deposition of immune complexes in the glomerular capillary walls leading to THICKENING of the glomerular BASEMENT membrane |
| So what are the THREE immune complex mediated KD diseases we discussed. What are they? | Primary nephrotic syndrome (adults), acute proliferative glomerulonephritis (children), and IgA nephropathy (the last one is easy. but how to remember the other 2??) |
| What is the pathogenesis of acute proliferative glomerulonephritis? | immune response occurring 7-10 days after strep infection (impetigo). AGAIN... Deposition of immune complexes in the glomerular basement membrane -> occlusion or compression of the renal capillaries -> release of renin -> increase in BP |
| What are the presenting features of acute proliferative glomerulonephritis? | generalized edema, proteinuria, hematuria, oliguria and HTN. (children will have SWOLLEN FACE and hypertension after an empetigo infection) |
| What is the pathology of autosomal dominant polycystic kidney disease (ADPKD)? | Appears after age 40. Hereditary disorder resulting from mutant genes PKD1 and PKD2 leading to fluid fiilled cysts on both kidneys that ultimately destroys the parenchema and leads to renal failure. |
| What are the,manifestations of autosomal dominant polycystic kidney disease (ADPKD)? | Abd or flank pain, microscopic hematuria, history of KD stones or UTI’s, HTN |
| What is the prognosis for autosomal dominant polycystic kidney disease (ADPKD)? | supportive treatment, slow progression of disease, 50% will have ESRD by age 60 |
| What are the proteins which prevent urinary stone formation? | There are 3: Tamm-Horsfall protein, nephrocalcin, urpontin |
| What are the (4) types of kidney stones? | Calcium struvites, cystine, uric acid |
| What are the characteristics of a calcium stone? | most common, made of calcium oxalate and calcium phrosphate. Can occur w/ hyperparathyroidism, sarcoidoisis, (w/ or w/o)hypercalcemia, hypercalcuria |
| What are the characteristics of struvite stones? | large branched stones, difficult to remove. Associated w/ women who have frequent UTI’s. Occur in alkaline urine and in the presence of proteus bacteria |
| What are the characteristics of cystine stones? | rare. Smooth polished glass appearance. associated w/ patients w/ inborn errors of amino acid metabolism (excess cystone in the urine) |
| What are the characteristics of uric acid stones? | These stones are RADIOLUCENT (meaning X-rays pass through them)!!! Associated with patients w/ gout and high uric acid content on the urine. |
| What are causes of functional obstruction to the urine flow? | There are FOUR: neurogenic (aka "nervous") bladder, infrequent voiding, detrussor (the bladder muscle) instability, constipation |
| What are the usual causes of cystitis in elderly men and in women? | (Most common cause is E. coli infection.) In elderly men can be secondary to nodular prostatic hyperplasia. In women it is associated with sexual intercourse and pregnancy. |
| What are the pathological features of acute cystitis? | irritation and hemorrhage of UB mucosa |
| What are the pathological features of chronic cystitis? | leading d to thickening of the UB wall and ulceration |
| What are the clinical manifestions of acute cystitis? | fever, pain, hematuria and pyuria |
| What are the clinical manifestions of acute cystitis? | "chronic irritation of UB mucosa"? |
| What is the pathogenesis of acute pyelonephritis? | bacterial KD infection (most commonly E coli) |
| kWhat is the pathogenesis of chronic pyelonephritis? | multiple episodes of pyleonephritis leading to scarring and destruction of the renal parenchema |
| What are the potential complications of asymptomatic bacteriuria in pregnancy? | can cause low birth weight, premature delivery and pregnancy toxemia (eclampsia or preeclampsia) |
| What are the manifestations of asymptomatic bacteriuria in pregnancy? | (kind of sounds like an oxymoron: asymptomatic manifestations??) but I think he wants: "persistent bacteruria" slash pyelonephritis |
| What is the pathogenesis of nephritic syndrome? | an inflammatory response in the glomerulis that damages the capillary wall and allows RBCs to spill into the urine |
| What is the pathogenesisof nephrotic syndromes? | decreased integritiy of the glomerular capillary membrane allowing plasma proteins to ESCAPE into the glomerular filtrate |
| What are the characteristics features of nephritic syndrome? | levels), generalized edema, hematuria w/ RBC’s in the urine, oliguria, proteinuria, hypoalbuminemia. |
| What are the characteristics features of nephrotic syndrome? | MASSIVE PROTEINURIA, hypoalbunemia, peripheral EDEMA, lipiduria w/ lipid casts in urine, hyperlipidemia. NO HEMATURIA!! |
| Why renal vein thrombosis (and other thromboembolic complications) common in nephrotic syndrome? | d/t the loss (in the urine-- from the MASSIVE PROTEINURIA!) of the anticoagulant factors, antithrombin 3, protein C and protein S. (there is also increased hypercoagulability because of the loss of antithrombin.) |
Created by:
mrbarr
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