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Step 1 12.12.12
Renal II
| Question | Answer |
|---|---|
| When is atrial naturetic peptide secreted? What does it do and what is the net effecT? | secreted when atrial P is high. incr GFR, and Na+ filtration = Na+ and volume loss |
| When is renin secreted? | in low blood volume |
| When is Parathyroid hormone (PTH) secreted? | when plasma Ca++ is low, or plasma PO4--- is high or vit D is low |
| What does PTH cause? | incr Ca++ reabsrobtion in DCt, decr PO4--- reabsorbtion in PCT, incr vit D production. also incr Ca++ and PO4 absorbtion from the gut |
| When is angiotensin II shynthesized? | in response to decr BP |
| What does Angiotensin II do? What is the net effect? | incr GFR but with compensatory Na+ reabsorbtion in PT, DCT. net effrect: preserves renal function in low volume state and reabsorbs Na+ to decr fluid loss |
| When is aldosterone secreted? | secreted in response to decr BV (AT II) and incr plasma K+ |
| What is the effect of aldosterone? | incr Na+ reabsorbtion, incr K+ secretion, incr h+ |
| When is ADH secreted? | secreted in response to incr plasma osmolarity and decr blood volume |
| What is the action of ADH (vasopressin)? | binds to receptors on principal c ells causing incr water channels and incr H20 reabsorbtioon |
| What are 6 causes of hyperkalemia by a shift of K+ from the ICF to the ECF? | 1insulin deficiency 2. Beta adrenergic antagonists 3. acidosis, exercise 4. hyper osmolarity 5. digitalis 6. cell lysis |
| How is hyperkalemia caused by insulin deficiency? | decr the Na+/K+ ATPase |
| How is hyperkalemia caused by beta adrenergic antagonists? | decr Na+/K+ ATPase |
| How is hyperkalemia caused by acidosis or severe exercise? | incr K+/H+ exchanger |
| How does digitalis cause hyperkalemia? | blocks Na/K+ ATPAse |
| What are 4 things that cause a hypokalemia by shifting K+ into the ICF? | 1. insulin 2. Beta adrenergic agonists 3. alkalosis 4. hypo osmolarity |
| How does inuslin, beta adrenergic agonists cause hypokalemia? | activate the Na+/K+ ATPase |
| How does alkalosis cause hypokalemia? | incr K+/H+ exchanger |
| What are the sx of hyponatremia? | disorientation ,stupor, coma |
| What are the sx of hypernatremia? | neurologic:irritability, delirium, coma |
| What causes hypochloridemia? | secondary to met alk., hypokalemia, hypovolumeia, incr aldosterone |
| What causes hyperchloridemia? | secondary to non-anion gap acidosis |
| What are the ECG sx of hypokalemia? | U waves on ECG, flattened T waves, arythmia, paralysis |
| What are the ECG sx of hyperkalemia? | peaked T waves, wide QRS, arrythmia |
| What are the sx of hypocalcemia? | tetany, NMJ irritability |
| What are the sx of hypercalcemia? | delerium, renal stones, abdominal pain, not necc. calciuria |
| What are the sx of hypomagnesia? | NMJ irritability, arrythmias |
| What are the sx of hypermagnesia? | delerium, decr DTRs, cardiopulmonary arrest |
| What are the sx of hypophosphatemia? | low mineral ion product causes bone loss, osteomalacia |
| What are the sx of hyperphosphatemia? | high mineral ion product causes renal stones, metastatic calcification |
| What happens to the pH, PCO2, and [HCO3-) in a metabolic acidosis? | decr pH, decr pCO2, decr HCO3- |
| What happens to the pH, PCO2, and [HCO3-) in a metabolic alkalosis? | incr pH, incr pCO2, incr HCO3- |
| What happens to the pH, PCO2, and [HCO3-) in a respiratory acidosis? | decr pH, incr pCO2, incr [HCO3-] |
| What happens to the pH, PCO2, and [HCO3-) in a respiratory alkalosis? | incr pH, decr PCO2, decr HCO3- |
| What is the compensatory response in a metabolic acidosis? | immediate hyperventialation |
| What is the compensatory response in a metabolic alkalosis? | immediate hypoventialtion |
| What is the compensatory response in a respiratory acidosis? | incr Renal HCO3- reabsorbtion (delayed) |
| What is the compensatory response in a respiratory alkalosis? | decr renal HCO3 reabsorbtion (delayed) |
| What is the henderson hasselbach equation for blood pH? | pH= pKa+ log [HCO3-]/0.03 PCO2 |
| What is Winter's formula for compensation in a metabolic acidosis? | PCO2 incr 0.7 for ever 1 HCO3- |
| What are some major causes of respiratory acidosis? | Hypoventialation: airway obstruction, acute lung disease, chronic lung disease, opioids, weakening of resp muscles |
| How do you calculate the anion gap? | Na+-(HcO3- + Cl-) normal is 8-12 |
| What is a mnemonic for the major causes of anion gap metabolic acidosis? | MUDPILES: Methanol (formic acid), uremia, DKA, paraldehyde or Phenoformin, Iron tablets, lactic acidosis, EtGly, Salicylates |
| What are the major causes of a normal anion gap metabolic acidosis? | diarrhea, glue sniffing, enal tubular acidosis, hyperchloremia |
| what is normal HCO3 and CO2 on ABG? | CO2=40, HCO3= 24 |
| What are some major causes of respiratory alkalosis? | hyperventialation: high altitude, aspirin injestion (early) |
| What are some major causes of metabolic alkalosis? | hypoventialtion with comp: diuretics, vomiting, anatacid use, hyperaldosteronism |
| What is Type 1 Renal tubular acidosis? What is it associated with? | defect in collecting tubules ability to excrete H+. assoc: hypokalemia and risk for calcium kidney stones |
| What is Type 2 renal tubular acidosis? What is it associated with? | defect in proximal tubule HCO3 reabsorbtion. associated wiht hypokalemia, and hypophosphatemic rickets |
| What is Type 4 renal tubular acidosis? What is it associated with? | hypoaldosteronism or lack of collecting tubule response to aldosterone. assoc: hyperkalemia, inhibitoon of ammonium excretion in PT. leads to decr urine pH due to decr buffering capacity |
| What 3 conditions are RBC casts seen? | glomerular nephritis, ischemia, malignant HTN |
| What 3 con ditions are WBC casts seen in the urine? | tubulointerstitial inflammation, acute pyelonephritis, transplant rejection |
| When are muddy brown granular casts seen in the urine? | acute tubular necrosis |
| When are waxy casts seen in the urine? | advanced renal disease/CRF |
| What do casts in general indicated? | that the hematuria or the pyuria is of renal origin |
| What will bladder cancer or kidney stones produce in the urine? | blood, no casts |
| What will acute cystitis produce in the urine? | pyuria, not casts |
| What does focal glomerular disease mean? | few glomeruli invovled as in FSGS |
| What does diffuse glomerular disease mean? | all glomeruli invovled as in diffuse proliferative GN |
| What does proliferative glomerular disease mean? | hypercellular glomeruli as in mesangial hypercellularity |
| What is a membranous glomerular injury? | thicking of GBM, as in membranous GN |
| What is a primary glomerular disease? | only the glomeruli are invovled as in minimal change disease |
| What is a seconday glomerular disease? | invovles glomeruli and other organs as in SLE, and nephropathy |
| What are 4 major GNs which produce nephritic syndrome? | 1. acute post strep GN 2. rapidly progressive GN 3. Berger's IgA glomerulopathy 4. Alport syndrome |
| What are 5 major GN producing nephrotic syndrome? | 1. focal segmental GN 2. membranous GN 3. minimal change disease 4. amyloidosis 5. diabetic glomerulopathy |
| What are 2 major GN which can cause both nephrotic and mephritic syndromes? | 1. diffuse proliferative GN 2. membranoproliferative GN |
| Is Nephritic or nephrotic syndrome inflammatory? | nephritic |
| What are some sx associated with nephritic syndrome ? | hematuria, RBC casts, azotemia, oliguria, HTN, proteinuria |
| What is the clinical picture and outcome of acute post streptococcal glomerulonephritis? | most frequently seen in children. peripheral and periorbital edema and dark urine. resolves spontaneously |
| What is seen on LM in acute post streptococcal glomerulonephritis? | glomeruli enlarged and hypercellular, neutrophils. lumpy bumpy appearance |
| What is seen on EM in acute post streptococcal glomerulonephritis? | subepithelial immune complex humps |
| What is seen on IF in acute post streptococcal glomerulonephritis? | granular appearance due to IgG, IgM, and C3 on GBM and mesangium |
| What are 3 major diseases that can lead to rapidly progressive ( crescentic) glomerularnephritis? | 1. Goodpasture's (type II hyper sens), Ab to GBM and alveolar BM 2. Wegener's granulomatosis 3. microscopic polyangitis |
| What is seen on IF and what are the common sx of Goodpasture's syndrome? | linear IF on GBM, see hematuria coupled with hemoptysis |
| What Ab is seen in microscopic polyangitis vs. Wegener's granulomatosis? | MP:pANCA WG: cANCA |
| What is seen on LM anf IF in rapidly progressive ( crescentic) glomerularnephritis? | crescent moon shaped consisting of fibrin and plasma proteins (C3b) with glomerular parietal cells, monocytes, macrophabges |
| What is the prognosis in rapidly progressive ( crescentic) glomerularnephritis? | poor. rapidly deteriorating renal function |
| What are 2 processes causing diffuse proliferative glomerular nephritis? | SLE or MPGN |
| What is seen on LM in diffuse proliferative glomerular nephritis? | wire looping of capillaries |
| what is seen on EM in diffuse proliferative glomerular nephritis? | subendothelial and sometimes intramembranous IgG ICs often with C3 |
| What is seen on IF in diffuse proliferative glomerular nephritis?? | granular |
| How do SLE and MPGN present? | can present as nephrotic and nephritic together. diffuse proliferative glomerular nephritis is the most common cause of death in SLE |
| Henloch Schonlein purpura is related to what GN? | Berger's disease (IgA nephropathy) |
| How does Berger's disease (IgA nephropathy)present? | flares of URI and acute gastroenteritis. intermittent hematuria |
| What is seen on LM in Berger's disease (IgA nephropathy)? | mesangial proliferation |
| qWhat is seen on EM in Berger's disease (IgA nephropathy)? | mesangial IC depositis |
| What is seen on IF in Berger's disease (IgA nephropathy)? | IgA ICs in mesangium |
| What is the pathophysiology of Alport Syndrome? | mutation in type IV collagen-->split basement membrane |
| What sx is Alport syndrome associated with? | nerve disroders, orcular defects, deafness, X-linked |
| How does nephrotic syndrome present? What is it associated with? | massive proteinuria (>3.5 g/day), hyperlipidemia, fatty casts, edema. Associated wiht thromboembolism (hypercoagulable state due to ATIII loss in urine) and incr infection |
| What is seen on LM in focal segmental glomerularnephritis? Who is most likely to get? | most common GN in HIV pt. see segmental sclerosis and hyalinosis |
| What causes membranous glomerularnephritis (diffuse mebranous glomerulopathy)? When is it most commonly seen? | caused by drugs, infection, SLE, solid tumors. most common cause of adutls with nephrotic syndrome |
| What is seen on LM in membranous glomerularnephritis (diffuse mebranous glomerulopathy)? | diffuse capillary and GBM thickening |
| What is seen on EM in membranous glomerularnephritis (diffuse mebranous glomerulopathy)? | spike and dome with subepithelial deposits |
| What is seen on IF in membranous glomerularnephritis (diffuse mebranous glomerulopathy)? | granular. SLE's nephrotic presentation |
| What causes minimal change disease? who gets it? How is it tx? | can be triggered by infection or immune stimulus. most common in children. responds to corticosteroids |
| What is seen on LM in minimal change disease? | normal |
| What is seen on EM in minimal change disease? | foot process effacement. slective loss of albumin due to GBM polyanion loss |
| What is amyloidosis associated with in the kidney? | chronic conditions like multiple myeloma, Tb, RA |
| What is seen on LM in amyloidosis? | congo red stain, apple green birefringence |
| what is seen generally in membranoproliferative glomerular nephritis? | subendothelial ICs with granular IF |
| What is seen in type I membranoproliferative glomerular nephritis LM? | tram track appearance due to GBM splitting caused by mesangial in growth |
| What is seen on EM in type II membranoproliferative glomerular nephritis? | dense deposits |
| How can membranoproliferative glomerular nephritis present? | either as nephrtic or nephrotic |
| What is Type I MPGN associated with? | HBV, HBC |
| What is Type II MPGN associated with? | C3 nephritic factor |
| What is the pathophysiology of diabetic glomerulo-nephropathy? | nonenzymatic glycosylation of GBM--> incr permeability, thickening |
| What is seen on LM of diabetic glomerulo-nephropathy? | mesangial expansion, GBM thickening, eosinophilic nodular glomerularsclerosis (Kkimmelstiel-Wilson lesion) |
| What are the severe complications of kidney stones? Hoe to you tx and prevent? | can lead to severe complications like hydropnephrosis and pyelonephritis. tx and prevent by encouraging fluid intake |
| What is the x ray and what pH precipitates calcium kidney stones? What are the 2 types? | acidic or neutral pH. radiopaque on XR. either Ca oxalate or Ca phosphate |
| What conditions can lead to calcium kidney stone? | hypercalcemia conditions like cancer, PTH. |
| What conditions could lead to a Calcium oxalate stone? | ethylene glycol or vitamin C abuse |
| What is the x ray and what pH precipitates ammonium magnesium phosphate (struvite) stones? | alkaline pH, radiopaque |
| What causes ammonium magnesium phosphate (struvite) stones? what can they lead to? | infection with urease positive magnesium and radiolucent buds like Proteus, Staphylococcus, Klebsiella. can form stagcorn stones which predispose to UTI |
| What conditions can worsen ammonium magnesium phosphate crystals? | alkaluria |
| What is the x ray and what pH precipitates of uric acid stones? | acidic pH, radiolucent |
| What conditions can predispose to uric acid stones? | gout, leukemia |
| What is the x ray and what pH precipitates cysteine stones? | acidic pH, radiopaque |
| What do cysteine stones look like? how do you treat them? | hexagonal. tx with alkalinization of urine |
| What is hydronephrosis? What does it cause? | results from urinary tract obstruction. causes dilation up to obstruction and parenchymal thickening chronically |
| What is the origin or renal cell carcinoma? What does it look like on histology? | originates from renal tubular cells. see polygonal clear cells filled with lipids and carbohydrates |
| Who gets renal cell carcinoma? What are the major RF? | most commonly in men 50-70 y/o. incidence incr with smoking and obesity |
| How does renal cell carcinoma present clinically? | hematuria, palpable mass, secondary polycythemia, flank pain, fever, weight loss. |
| What does a renal cell carcinoma invade and where does it spread? | invades IVC and spreads hematogenously to lung and bone |
| What is a key genetic association of renal cell carcinoma? | von-Hippel Lindau syndrome and gene deletion at 3p |
| What paraneoplatic syndromes is renal cell carcinoma associated with? | ectopic EPI, ACTH, PTHrP, prolactin |
| Who gets Wilm's tumor? What will it contain? | most common renal malignancy in age 2-4. contains embryonic glomerular structures |
| How does Wilm's tumor present? | huge, palpable flank mass and or hematuria |
| What is the genetic component of Wilm's tumor, What syndrome can it be a part of? | deletion of WT1 tumor surpressor on Chr 11. can be part of WAGR complex: Wilm's tumor, aniridia, genitourinary malformation, mental motor Retardation |
| Where can transitional cell carcinoma occur? What is a key finding on urinalysis? | can occur in renal calyces, pelvis, ureters, bladder. painless hematuria with no casts suggests bladder cancer |
| What are the major RF for transitional cell carcinoma? Mnemonic? | problems in the Pee SAC: phenacetin, smokings, aniline dyes, cyclophosphamide |
| How does acute pyelonephritis present? What does it affect? | fever, CVA tnederness, n/v. affects cortex with sparing of glomeruli |
| What is seen on histology in chronic pyelonephritis? | coarse, assymetric corticomedullary scarring. tubuloes can contain eosinophilic casts (thyroidization of kidney) |
| What is a classic urinalysis findings for chronic pyelonephritis? What is required for the development? | white cell casts are classic. need vesicouteral reflux to develop chronic pyelopnephritis |
| What causes drug induced interstitial nephritis? What is seen? | diruetics, NSAIDs, penicillin derivatives, sulfonamides, rifampin causing pyuria and azotemia. acute interstitial inflammationm |
| How does induced interstital nephritis present? | fever, rash, hematuria, CVA tenderness. azotemia 1-2 weeks after drug admistration |
| What is diffuse cortical necrosis? | acute generalized cortical infarction of both kidneys. like due to vasospasm and DIC |
| What is diffuse cortical necrosis associated with? | obstetric catastrophes and septic shock |
| What are the 3 stages of acute tubular necrosis? | 1. inciting event, 2. maintenance phase : oliguric lasts 1-3 weeks with risk of hyperkalemia 3. recovery:= polyuric, BUN and SeCr fall, risk of hypokalemia |
| What are some key assocations of acute tubular necrosis? | renal iscehmia, crush injury, toxin |
| Muddy brown granular casts are a key finding in? | acute tubular necrosis |
| What is the pathophysiology and etiology of renal papillary necrosis? | sloughing of renal papillae-->gross hematuria, proteinuria. may be triggered by recent infection or immune stimulus. |
| What are 4 key associated conditions with renal papillary necrosis? | 1. DM 2. acute pyelonephritis 3. chronic phenacetin use 4. SCA and trait |
| How do you define acute renal failure? | abrupt decline in renal fx with incr Creatinine and incr BUN over several days |
| What causes prerenal azotemia? What is seen? What happens to BUN/Cr? | due to decr renal blood flow. see decr GFR, Na+ and H2O retained by kidney and an attempt to conserve volume so BUN/Cr ration incr |
| What causes intrinsic renal failure? What is seen? What happens to BUN/Cr? | ATN or ischemia or toxins or rarely RPGN. patchy necrosis leading to debris blocking the kidney and fluid backflow. see decr GFR, epithelial/granular casts, decr BUN/Cr ration due to decr BUN reabsorbtion |
| What causes postrenal failure? What is seen? What happens to BUN/Cr? | sue to outflow obstruction like stones, BPH, neoplasia. only develops if obstruction is bilateral |
| What urine osm is seen in prerenal vs. renal vs postrenal failure? | Pre: >500. Renal: <350 Post: less than 350 |
| What urine Na+ is seen in prerenal vs. renal vs postrenal failure? | Pre: <10 Renal: >20. Post: >40 |
| What FeNa is seen in prerenal vs. renal vs postrenal failure? | Pre: <1% Renal: >2% Post: >4% |
| What Serum BUN/Cr is seen in prerenal vs. renal vs postrenal failure? | PRe:>20. Renal: <15. Post: >15 |
| What are the consequences of Na/H2O retention in renal failure? | CHf, pulmonary edema, HTN |
| What are the major consequences of renal failure? | 1. Na/H2oO retetnion 2. hyperkalemia 3. Metabolic acidosis 4. uremia 5. anemia, 6. renal osteodystrophy 7. dyslipidemia (esp TGs) 8. growth reatrdation and developmental delay |
| What marks the clinical syndrome of uremia? | incr BUn , Cr, nausea and annorexia, pericarditis, asterixis, encephalopathy, platelet dysfx |
| What is renal osteodystrophy? | failure to hydroxylate vit D-->Ca++ wasting and Po4 retention-->secondary hyperPTH. decr intestinal absrobtion along wiht decr Ca++ due to hyper PO4. causes subperiosteal thinning of bones |
| What is seen grossly in ADPKD? | multiple, large, bilateral cysts that destroy the kidney parenchyma |
| How does ADPKD present? | flank pain, hematuria, HTN, urinary infection, progressive renal failure |
| What is the genetic issue in ADPKD? What are some key associated problems of ADPKD? | auto D mutation in PKD1 or PKD2. death from CKD or HTN due to incr renin. Associated wiht: polycystic liver, berry aneurysm, mitral valve prolapse |
| What are some key associated conditions with ADPKD? | congenital hepatic fibrosis. Potters, after neonatal period: HTN, portal HTN renal insufficency |
| What are dialysis cysts? | cortical and medullary cysts resulting from long term dialysis |
| What are simple cysts? | beingn, commion, incidental finding. non enhancing and cortical and fluid filled |
| What is medullay cystic disease? | medullary cysts can sometimes lead to fibrosis and progressive insufficiency. ultrasound shows small kidney. 70% develop kidney stones. poo prognosis |
| What diuretic acts primarily at the PCT? | acetazolamide |
| What diuretic acts primarily at the proximal striaght tubule? | mannitol |
| Where do loop diuretics primarily work? | thick ascending limb |
| Where do thizaide diuretics primarily work? | DCT |
| Where do K+ sparing diuretics primarily work? | collecting tubule |
| Where doe ADH antagonists primairly work? | collecting duct |
| What is the mech of mannitol? | osmotic diuretic, incr tubular fluid osm, incr urine flow |
| What is the use of mannitol? | shock, drug OD, incr intracranial and intraocular P |
| What are the major Se of mannitol? | pulmonery edema, dehydration,. CONTRAI in anuria, CHF |
| What is the mech of acetazolamide? | carbonic anhydrase inhibitor. causes self limited NaHCO3 diuresis and reduction of body stores of HCO3 |
| What is the clinical use of acetazolamide? | glaucoma, urinary alkalinization, metabolic alkalinosis, altitude sickness |
| What are the major SE of acetazolamide? | hyperchloremic metabolic acidosis, neuropathy, NH3 toxicity, sulfa allergy |
| What is the mech of furosemide? | sulfonamide loop diuretic. inhibits the Na/K/Cl cotransporter of thick ascending limb of loop of henle. abolishes the hypertonicity of the medulla preventing concentration. incr Ca++ excretion |
| What is the effect of furosemide on PGE? What can inhibit it? | stimulates PGE release (vasodilates afferent arteriole), inhibited by NSAIDs |
| What is the clinical use of loop diuretics? | edematous states (CHF, cirrosis, nephrotic syndrome, pulm. edema), HTN, hypercalcemia |
| What are the major SE of furosemide? Mnemonic? | OH DANG! Ototoxicity, hypokalemia, dehydration, allergy (sulfa), Nephritis (interstitial), Gout |
| What is the mech of ethacrynic acid? | phenoxyacetic acid derivative which inhibits Na/K/CL in thick ascending limb of LoH. |
| What is the clinical use of ethacrynic acid? | diuresis in pt with allergies to sulfa drugs |
| What are the major SE of ethacrynic acid? | similar to furosemide (OH DANG), can be use in hyperuricemia and acute gout |
| What is the mech of hydrochlorothiazide? | thiazide diuretic. inhibits NaCl reabsorbtion in early distal tubule. reducing diluting ability of nephron, decr Ca++ excretion |
| What is the clinical use of hydrochlorothiazide? | HTN, CHF, idiopathic hypercalciuria, nephrogenic DI |
| What is are the major SE of hydrochlorothiazide? | hypokalemic metabolic alkalosis, hyponatermia, hyper glycemia, hyperlipidemia, hyperuricemia, hypercalcemia. sulfa allergy. hyperGLUC |
| What is the class of Spironolactone, triameterne, amiloride? | K+ sparing diuretics |
| What is the mech of spironolactone? | competitive aldosterone receptor antagonist in cortical collecting tubule |
| What is the mech of amiloride and triamterene? | act at cortical collecting tubule by ccblocking Na+ channels |
| What is the clinical use of spironolactone, triameterene, amiloride? | hyperaldosteronism, K+ depletion, CHF |
| What are the major SE of spironlactone? | hyperkalemia, gynecomastia |
| What are the SE of amiloride and triamterine? | hyperkalemia |
| What happens to urine Na and serum Na+ in diuretic use? | urine incr, serum decr |
| What happens to urine K+ in diuretic use? | incr in all except K+ sparing diuretics |
| What diuretics could cause an acidemia? | Carbonic anhydrase inhibitors ( decr HCO3 reabs), K+ sparing (aldosterone blockade prevents H+ secretion), hyperkalmeia causes K+ to enter cells in exchange for H+ |
| How can loop and thiazide diuretics cause an alkalemia? | 1. volume contraction-->incr AT II--> incr Na/H exchange in PT= incr HCO3 2. K+ loss leads to K+ exiting cells for H+ entering cells 3. in low K+, H rather than K is exchanged for Na+ in CCT leading to alkalosis and paradoxical aciduria |
| How does urine Ca+ vary with loop vs thiazide diuretics? | incr in loop diuretics, dec in thiazides. thiazides incr reabsorbtion in PT and LoH |
| What is the mech of lisinopril, enalapril, captopril? | inhibit ACE, reducing levels of Ang II and preventing bradykinin inactivation. renin release is incr due to loss of feedback inhbitiosn |
| what is the mech of the -sartans? What is a key diff between them and the prils? | angiotensin II receptor blockers. do NOT incr kallikrein= NO cough |
| What is the clinical use of the -prils? | HTN, CHF, diabetic renal disease. prevent heart remodeling in chronic HTN |
| What are the major SE of the prils? Mnemonic? | CAPTOPRIL: Cough, angioedema, proteinuria, tasts changes, hypOtension, Pregnancy damage, Rash, incr renin, Lower angII. also hyperkalemia |
| What condtion besides pregnancy should -prils be avoided? | bilateral renal artery stenosis b/c ACeI decr GFR causing incr in SeCr |
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tjs2123
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