Step 1 - Renal 2rename
denniskwinn's version from 2015-04-25 16:17
|Kidney stones general||Can lead to severe complications, such a hydronephrois and pyelonephritls. Treat and prevent by encouraging fluid Intake|
|Ca kidney stones||Most common kldney stones (75-85%). Calcium oxalate (see Image 88), calcium phosphate, or both. 2. From conditions that cause hypercalcemia (cancer, ↑ PTH, ↑ vitamIn D, milk-alkali syndrome) can lead to hypercalciuria and stone. Tend to recur. 3. Radioopaque 4. Oxalate crystals can result from ethylene glycol or vitamin C abuse|
|Ammonium magnesium phosphate (struvite) kidney stones||2nd most common kidney stone. Caused by infection with urease-positive bugs (Proteus vulgaris, Staphylococcus, Klebsiella ). Can form staghorn calculi that can be a nidus for UTls). Radiopaque or radiolucent - worsened by alkaluria|
|Uric acid stones||Strong association with hyperuricemla (e .g., gout). Often seen as a result of diseases with ↑ cell turnover, such a leukemia and myeloproliferative disorders. RadiolUcent|
|Cystine kidney stones||Most often secondary to cystinuria 2. Hexagonal shape 3. Rarely may form cystine staghorn calculi 4. Faintly radiopaque 5. Treat with alkalinzation of urine|
|Immediately what happens?||aspirin STIM the medullary resp center= HYPEVENT= decrease CO2|
|What happens a few hours later||-AG metab acidosis|
-increase lipolysis, uncouple OX Phos
-inhib TCA=accum intermediates
-pH prob NL
|RCC||-MC renal malignancy.|
- Invades IVC and spreads hematogenously ; metastasizes to lung, bone.
-Most common in men ages 50-70. ↑ incidence with smoking and obesity.
-A/w with von Hippel-Lindau and gene deletion in chromosome 3.
-Originates in renal tubule cells → polygonal clear cells. -Manifests clinically with hematuria, palpable mass, 2° polycythemia, flank pain, fever, and welght loss.
- A/w with paraneoplastic syndrome (ectopic EPO, ACTH, PTHrP. and Prolactin)= PEAP the RCC's
|Wilm’s tumor (nephroblastoma)||-MC renal malignancy of early childhood (ages 2- 4). -Presents with huge, palpable flank mass and/or hematuria. -May be associated ted with hemihypertrophy syndromes(Big Will vs lil will). |
-Contains embryonic glomerular structures.
-Deletion of tumor suppressor gene WTI on chromosome 11.
-Can be part of WAGR complex: Wilms' tumor, Aniridia, Genitourinary malformation , and mental-motor Retardation.
|Transitional cell carcinoma||-MC tumor of urinary tract system (can occur In renal calyces, renal pelvis, ureters, and bladder). |
-Painless hematuria is suggestive of bladder cancer.
-A/w problems in your Pee SAC: Phenacetin, Smoking, Aniline dyes, and Cyclophosphamide
|Acute pyelonephritis||-Affects cortex with relative sparing of glomeruli/vessels. -White cell casts in urine are classic.|
- Presents with fever, CVA -tenderness, nausea, and vomiting
|Chronic pyelonephritis||Coarse, asymmetric corticomedullary scarring, blunted calyx, Tubules can contain eosinophilic casts (thyroidization of kidney)|
|Drug-induced interstitial nephritis||-Acute interstitial renal inflammation|
- Pyuria (typically eoslnophlls) and azotemia occuring 1- 2 weeks after admin.
-Associated with fever, rash, hematuria, and CVA tenderness. Drugs (e.g., diuretics, NSAIDs, penicillin derivatlves, sullfonamides, rifampin) act as haptens, Inducing hypersensitivity=ML type 3
|Diffuse cortical necrosis||-Likely due to a combination of vasospasm and DIC. |
-Associated with obstetric catastrophes (e.g., abruptio placentae) and septic shock.
-Acute generalized infarction of cortices of both kidneys.
|Acute tubular necrosis||-Most common cause of acute renal failure in hospItal. |
-Self-reverslble, but fatal if left untreated (provide supportive dialysis).
-A/w with renal ischemIa (e.g., shock, sepsis), crush injury (myoglobulinuria), toxins. Death most often occurs during initial oliguric phase
-Loss of cell polarity, epithelial cell detachment, necrosis, granular ("muddy brown") casts.
3 stages: inciting event→ maintenance (low urine) → recovery (2-3 weeks).
|Renal papillary necrosis||-Sloughing of renal papillae → gross hematuria, proteinuria|
-May be triggered by recent infection or immune stimulus. Associated with :
1. Disease: Diabetes mellitus, or Sickle cell anemia
2. Infection: Acute pyelonephritis
3. Hardcore: Chronic phenacetin use (acetaminophen is phenacetin derivative)
|Acute renal failure||an abrupt decline in renal function with ↑ creatinine and ↑ BUN over a period of several days.|
|Prerenal azotemia||↓ RBF (e.g., hypotension) →↓, GFR. Na+/H2O and urea retained by kidney, so BUN/creatinine ratio ↑ in attempt to conserve volume|
|Intrinsic renal failure||generally due to acute tubular necrosis or ischemia/toxins; less commonly due to acute glomerulonephritis (e.g., RPGN). Patchy necrosis leads to debris obstructing tubule and fluid backflow across necrotic tubule →↓ GFR. Urine has epithelial/granular casts. BUN reabsorption is impaired → ↓BUN/creatinine ratio|
|Postrenal failure||outflow obstruction (stones, BPH, neoplasia, congenital anomalies). Develops only with bilateral obstruction.|
|Prerenal azotemia labs||Urine osmolality (>500), Urine Na (<10), FeNa(<1%), Serum BUN/Cr(>20)|
|Intrinsic renal failure labs||Urine osmolality (<350), Urine Na(>20), Fe(>2%), Serum BUN/Cr(<15)|
|Postrenal failure||Urine osmolality (<350), Urine Na (>40), Fe(>4%), Serum BUN/Cr (>15)|
|Consequences of renal failure||1. Na+/H2O retention (CHF, pulmonary edema, hypertension) 2. Hyperkalemia 3. Metabolic acidosis 4. Uremia-clinical syndrome 5. Anemia (failure of erythropoietin production) 6. Renal osteodystrophy (failure of vitamin D hydroxylation) 7. Dyslipidemia (especially ↑ triglycerides) 8. Growth retardation and developmental delay (in children)|
|Uremia-clinical syndrome||↑ BUN and ↑ creatinine, Nausea and anorexia, Pericarditis, Asterixis, Encephalopathy, Platelet dysfunction|
|Fanconi’s syndrome||↓ proximal tubule transport of amino acids, glucose, phosphate, uric acid, protein, and electrolytes. Can be congenital or acquired. Causes include Wilson's disease, glycogen storage diseases, and drugs (e.g., cisplatin, expired tetracycline). 2. Defects - ↓phosphate reabsorption,↓HCO3 reabsorption, ↓early Na+ reabsorption 3. Complication - Rickets, Metabolic acidosis (type II RTA), ↑ distal Na+ reabsorption→hypokalemia|
|ADPKD||Multiple, large, bilateral cysts that ultimately destroy the parenchyma. Enlarged kidneys. Presents with flank pain, hematuria, hypertension, urinary infection, progressive renal failure. Autosomal-dominant mutation in APKDl or APKD2. Death from complication of chronic kidney disease or hypertension (due to i renin production). Associated with polycystic liver disease, berry aneurysms, mitral valve prolapse|
|ARPKD||Infantile presentation in parenchyma. Autosomal recessive. Associated with congenital hepatic fi brosis. Significant renal failure in utero can lead to Potter's; concerns beyond neonatal period are hypertension, portal hypertension, and progressive renal insufficiency|
|Dialysis cysts||Cortical and medullary cysts resulting from long-standing dialysis.|
|Simple cysts||Benign, incidental finding. Cortex only.|
|Medullary cystic disease||These cysts sometimes lead to fibrosis and progressive renal insufficiency with urinary concentra ting defects. Ultrasound shows small kidney. Poor prognosis|
|Low Na+ symptoms||Disorientation, stupor, coma|
|Low Cl- symptoms||2° to metabolic alkalosis, hypokalemia, hypovolemia, ↑ aldosterone|
|Low K+ symptoms||U waves on ECG, flattened T waves, arrhythmias, paralysis|
|Low Ca+2 symptoms||Tetany, neuromuscular irritability|
|Low Mg+2 symptoms||Neuromuscular irritability, arrhythmias|
|Low PO4 symptoms||Low-mineral ion product causes bone loss, osteomalacia|
|High Na+ serum||Neurologic: irritability, delirium, coma|
|High Cl- serum||secondary to non-anion gap acidosis|
|High K+ serum||Peaked T waves, wide QRS, arrhythmias|
|High Ca2+ serum||Delirium, ↓ DTRs, cardiopulmonary arrest|
|High PO4 serum||High mineral ion product causes renal stones, metastatic calcifications|
|Mannitol mechanism||Osmotic diuretic, ↑tubular fluid osmolarity. producing ↑urine flow|
|Mannitol clinical use||Shock, drug overdose, increased ICP/Intraocular pressure |
- used to ↓ extracellular fluid volume
|Mannitol toxicity||Pulmonary edema, dehydration |
. Contraindicated in anuria, CHF
- Causes self-limited NaHCO3 diuresis and reduction in total-body HCO3 stores.
|Acetazolamide clinical use||Glaucoma, urinary alkalinization, metabolic alkalosis, altitude sickness(fix resp alk)|
|Acetazolamide toxicity||-Hyperchloremic metabolic acidosis=|
leads to increase K+ =NH3 toxicity
-Neuropathy, sulfa allergy
|Furosemide Mechanism||-Sulfonamide loop diuretic.|
-Inhibits cotransport system (Na+, K+, 2 CI-) of TAL of loop of Henle.
-Abolishes hypertonicity of medulla= preventing concentration of urine.
-↑Ca2+ excretion. Loops lose calcium.
|Furosemide clinical use||Edematous states (CHF, cirrhosis, nephrotic syndrome, pulmonary edema), HTN, hypercalcemia|
|Furosemide Toxicity||Ototoxicity, Hypokalemia, Dehydration, Allergy (sullfa), Nephritis (interstitial), Gout - OH DANG|
|Ethacrynic acid mechanism||Phenoxyacetlc acid derivative (NOT a sulfonamide). Essentially same action as furosemide.|
|Ethacrynic acid clinical use||Diuresis in patients allergic to sulfa drugs|
|Ethacrynic toxicity||Similar to furosemide, can cause hyperuricemia & acute gout (never used to treat gout)|
|HCTZ mechanism||Inhibits NaCI reabsorption in early distal tubule, reducing diluting capacity of the nephron . ↓ Ca2+ excretion.|
|HCTZ clinical use||Hypertension, CHF, idiopathic hypercalciuria, nephrogenic diabetes Insipidus|
|HCTZ toxicity||-Hypokalemic metabolic alkalosis, hypponatremla, hyperGlycemia, hyperLipidemla, hyperUricemia, and HyperCalcemia.|
|K+ sparing diuretics||Spironolactone, Triamterene, Amdoride, eplerenone|
|Spironolactone mechanism||a competitive aldosterone receptor antagonist in the CORTICAL collecting tubule.|
|Triamterene and amiloride mechanism||act at CCT by blocking Na+ channels in the CCT.|
|K+ sparing diuretics clinical use||Hyperaldosteronism, K+ depletion, CHF [use this class drug]|
|K+ sparing diuretics toxicity||-Hyperkalemia (can lead to arrhythmias)|
-Endocrine effects with aldosterone antagonists (e.g.,spironolactone causes gynecomastia, antiandrogen effects).
|Diuretic effects on Urine NaCl||↑(all diuretics-carbonic anhydrase inhIbitors, loop diuretics, thiazides, K+-sparing diuretics). Serum NaCI may ↓ as a result.|
|Diuretic effects on Urine K+||↑ (all except K+ sparing) - serum K+ may decrease as a result|
|Diuretic that cause acidemia||Carbonic anhydrase inhibitors, ↓HC03- reabsorption. K+ sparing aldosterone blockade prevents K+ secretion and H+ secretion. Additionally. hyperkalemia leads to K+ entering all cells (via H+/K+ exchanger) in exchange for H+ exiting cells.|
|Diuretics that cause alkalemia||Loop diuretics and thiazides cause alkalemia through several mechanisms:|
1. Volume contraction → ↑AT II → ↑ Na+/H+ exchange in proximal tubule → ↑ HCO3 ("contraction alkalosis")
2. K+ loss leads to K+ exiting all cells (via H+/K+ exchanger) in exchange for H+ entering cells
3. In low K+ state, H+ (rather than K+) is exchanged for Na+ in cortical collecting tubule, leading to alkalosis and "paradoxical aciduria”
|Diuretics that increase urine Ca||loop diuretics: Abolish lumen-positive potential in thick ascending Iimb of loop of Henle →↓ paracellular Ca+ reabsorption → hypocalcemIa, ↑ urinary Ca|
|Diuretics that decrease urine Ca||thiazides: Volume depletion → upregulation of sodium reabsorption→ enhanced paracellular Ca reabsorption in proximal tubule and loop of Henle. Thiazide also block luminal Na+/CI- co transport in distal convoluted tubule → ↑NA+ gradient →↑ interstitial Na+/Ca exchange → hypercalcemia.|
|ACE inhibitors||Captopril, enalapril, lisinopril|
|ACE inhibitor mechanism||-Inhibit angiotensin -converting enzyme, reducing levels of angiotensin II and preventing inactivation of bradykinin, a potent vasodilator.|
-Renin release is ↑ due to loss of feedback inhibition
|Losartan mechanism||-[ARB] angiotensin II receptor antagonist - is not an ACE inhibitor |
- does not cause cough
|ACE inhibitor clinical use||HTN, CHF, diabetic renal disease|
|ACE inhibitor Toxicity||-Cough, Angioedema, Proteinuria, Taste changes, hypOtension, Pregnancy prob lems (fetal renal damage), Rash, Increased renin, Lower angiotensin II . |
-Also hyperkalemia[B/c no Aldosterone is being made]
-Avoid with bilateral renal artery stenosis because ACE Inhibitors significantly ↓ GFR by preventing constriction of different arterioles. [CAPTOPRIL]