Step 1 - Renal 2

denniskwinn's version from 2015-04-25 16:17

Kidney stones

Question Answer
Kidney stones generalCan lead to severe complications, such a hydronephrois and pyelonephritls. Treat and prevent by encouraging fluid Intake
Ca kidney stonesMost 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 stones2nd 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 stonesStrong 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 stonesMost often secondary to cystinuria 2. Hexagonal shape 3. Rarely may form cystine staghorn calculi 4. Faintly radiopaque 5. Treat with alkalinzation of urine

aspirin OD

Question Answer
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

Kidney Malignancies

Question Answer
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 cellspolygonal 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

Damaged kidney

Question Answer
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 pyelonephritisCoarse, 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)

Renal failure

Question Answer
Acute renal failurean 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 failuregenerally 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 labsUrine osmolality (>500), Urine Na (<10), FeNa(<1%), Serum BUN/Cr(>20)
Intrinsic renal failure labsUrine osmolality (<350), Urine Na(>20), Fe(>2%), Serum BUN/Cr(<15)
Postrenal failureUrine osmolality (<350), Urine Na (>40), Fe(>4%), Serum BUN/Cr (>15)
Consequences of renal failure1. 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


Question Answer
ADPKDMultiple, 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
ARPKDInfantile 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 cystsCortical and medullary cysts resulting from long-standing dialysis.
Simple cysts Benign, incidental finding. Cortex only.
Medullary cystic diseaseThese cysts sometimes lead to fibrosis and progressive renal insufficiency with urinary concentra ting defects. Ultrasound shows small kidney. Poor prognosis


Question Answer
Low Na+ symptomsDisorientation, stupor, coma
Low Cl- symptoms2° to metabolic alkalosis, hypokalemia, hypovolemia, ↑ aldosterone
Low K+ symptomsU waves on ECG, flattened T waves, arrhythmias, paralysis
Low Ca+2 symptomsTetany, neuromuscular irritability
Low Mg+2 symptomsNeuromuscular irritability, arrhythmias
Low PO4 symptomsLow-mineral ion product causes bone loss, osteomalacia
High Na+ serumNeurologic: irritability, delirium, coma
High Cl- serumsecondary to non-anion gap acidosis
High K+ serumPeaked T waves, wide QRS, arrhythmias
High Ca2+ serumDelirium, ↓ DTRs, cardiopulmonary arrest
High PO4 serum High mineral ion product causes renal stones, metastatic calcifications


Question Answer
Mannitol mechanismOsmotic diuretic, ↑tubular fluid osmolarity. producing ↑urine flow
Mannitol clinical useShock, drug overdose, increased ICP/Intraocular pressure
- used to ↓ extracellular fluid volume
Mannitol toxicityPulmonary edema, dehydration
. Contraindicated in anuria, CHF
Acetazolamide mechanism-CAI.
- Causes self-limited NaHCO3 diuresis and reduction in total-body HCO3 stores.
Acetazolamide clinical useGlaucoma, 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 useEdematous states (CHF, cirrhosis, nephrotic syndrome, pulmonary edema), HTN, hypercalcemia
Furosemide ToxicityOtotoxicity, Hypokalemia, Dehydration, Allergy (sullfa), Nephritis (interstitial), Gout - OH DANG
Ethacrynic acid mechanismPhenoxyacetlc acid derivative (NOT a sulfonamide). Essentially same action as furosemide.
Ethacrynic acid clinical useDiuresis in patients allergic to sulfa drugs
Ethacrynic toxicitySimilar to furosemide, can cause hyperuricemia & acute gout (never used to treat gout)
HCTZ mechanismInhibits NaCI reabsorption in early distal tubule, reducing diluting capacity of the nephron . ↓ Ca2+ excretion.
HCTZ clinical useHypertension, CHF, idiopathic hypercalciuria, nephrogenic diabetes Insipidus
HCTZ toxicity-Hypokalemic metabolic alkalosis, hypponatremla, hyperGlycemia, hyperLipidemla, hyperUricemia, and HyperCalcemia.
-Sulfa allergy
- HyperGLUC
K+ sparing diureticsSpironolactone, Triamterene, Amdoride, eplerenone
Spironolactone mechanisma competitive aldosterone receptor antagonist in the CORTICAL collecting tubule.
Triamterene and amiloride mechanismact at CCT by blocking Na+ channels in the CCT.


Question Answer
K+ sparing diuretics clinical useHyperaldosteronism, 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 alkalemiaLoop 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 Caloop diuretics: Abolish lumen-positive potential in thick ascending Iimb of loop of Henle →↓ paracellular Ca+ reabsorption → hypocalcemIa, ↑ urinary Ca
Diuretics that decrease urine Cathiazides: 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 inhibitorsCaptopril, 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 useHTN, 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]