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146 Cards in this Set
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prerenal azotemia etiology
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acute renal failure due to
hypovolemia (dehydration, burns, diuretic, vomitting, diarrhea, sweating, hemorrhage) hypotension (shock, anaphylaxis) third-spacing of fluids (peritonitis) osmotic diuresis low aldosterone (Addison) low cardiac output (CHF) low albumin (nephrotic syndrome) renal artery stenosis hepatorenal syndrome (hepatic failure, vasoconstriction of afferent) ACEi-induced (in susceptible patients, vasodilation of efferent) |
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prerenal azotemia diagnosis
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BUN/creatinine ratio 20:1
low urine sodium (<20) high urine osmolality (>500) low fractional Na (<1%) specific gravity >1.010 (RAA system retains water and concentrates urine) |
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postrenal azotemia etiology
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renal failure due to bilateral obstruction to urine flow
bladder stone or clot bladder cancer prostate hypertrophy or cancer bilateral ureteral disease (retroperitoneal fibrosis) neurogenic bladder |
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postrenal azotemia pathogenesis
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bilateral obstruction to urine outflow leads to postrenal azotemia
if obstruction takes a long time it can lead to tubular necrosis |
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postrenal azotemia diagnosis
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BUN/creatinine ratio can go as high as 20:1 but then starts to decrease
there's also concentrated urine and low fractional Na need to find distended bladder on physical OR bilateral hydronephrosis on renal sonogram or CT OR large volume of urine after Foley catheter |
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acute tubular necrosis etiology
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any cause of hypoperfusion or hypodrainage (pre or postrenal azotemia) can lead to tubular necrosis if prolonged;
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acute tubular necrosis phases
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prodromal (between injury and acute renal failure)
oliguric or anuric post oliguric (polyuria due to tubular death and lack of urine concentration function) |
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acute tubular necrosis diagnosis
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BUN/creatinine ration close to 10:1
low urine osmolarity (<350) high urine sodium (>40) high fractional Na (>1%) brown pigmented granular casts and epithelial casts |
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acute tubular necrosis management
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no effective medical therapy, just hydration and if life-threatening, dyalisis
dopamine or diuretics cannot reverse it |
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allergic interstitial nephritis etiology
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accounts for 10-15% of intrinsic renal failure
due to drug allergy in 70% penicillins, cephalosporins, sulfas, NSAIDs, allopurinol, rifampin, quinolones, CCBs, PPIs also caused by leptospira, legionella, CMV, ricketsia and strep |
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allergic interstitial nephritis presentation
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fever (90%)
rash (25-50%) hemolysis (95%, nonspecific) eosinophilia, eosinophiluria, proteinuria, increased IgE |
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allergic interstitial nephritis diagnosis
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initial test is urinalysis looking for WBCs then Hansel or Wright stain for eosinophils
also eosinophilia, eosinophiluria, proteinuria (<2g/24h), increased IgE |
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allergic interstitial nephritis management
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remove offending agent; if persistent failure then short course of steroids
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renal failure from pigments etiology
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hemoglobin and myoglobin are toxic to tubules and also precipitate
rhabdomyolisis can be caused by crush injury, seizures, severe exertion, statins, hypokalemia, hypophosphatemia, ABO incompatibility |
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renal failure from pigments diagnosis
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best intitial test --> urinalysis looking for positive blood dipstick but absence of red cells
confirm by extremenly high CPK levels also rapidly rising creatinine most important test is EKG or potassium level looking for peaked T waves which can lead to arrhythmia death |
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renal failure from pigments management
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if EKG abnormalities --> calcium chloride or gluconate is best initial therapy
hydration, manitol and urine alkalinization |
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acute renal failure from oxalate
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most commonly by ethylene glycol overdose in suicide attempt
intoxicated patient with anion gap metabolic acidosis and renal insuficiency confirm with oxalate crystals in urinalysis treat with ethanol or fomepizole, dyalisis and bicarbonate |
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acute renal failure from urate
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seen in tumor lysis syndrome of leukemia/lymphoma patients
treat with allopurinol and alkalinization of urine before chemo confirm with uric acid crystals in urinalysis |
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renal failure from calcium
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hypercalcemia is most common in hyperparathyroidism
surgical resection of parathyroids indicated if renal impairment |
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aminoglycoside renal toxicity
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10-20% of drug-induced nephrotoxocity and usually reversible; due to high trough levels, not peak levels therefore give once a day to allow same bactericidal effect (peak level) and low trough levels (less toxicity)
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amphotericin B renal toxicity
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leads to renal insufficiency and distal tubular acidosis after several days from cumulative dosing; find high creatinine; stop medication
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atheroembolic renal failure
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usually angioplasty patient after several days
presents with eosinophilia, low complement, bluish discoloration of fingers and toes, livedo reticularis |
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contrast agent renal failure
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onset is faster than other toxics (12-24 hours)
rise in creatinine in 3-5 days BUN/creatinine ratio may be as high as 20:1 diabetics, hypertensives and myeloma patients are predisposed |
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nephrotoxic drugs
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aminoglycosides
contrast agents pentamidine vancomycin cyclosporine lithium indinavir ampB NSAIDs cysplatine |
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NSAID nephropathy
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mechanisms: interstitial nephritis, direct toxic, papillary necrosis, membranous GN, inhibition of vasodilatory prostaglandins
risk factors are elderly, hypertension, diabetes or other renal impairment diagnose with history of NSAIDs + rise in BUN/creatinine and sterile pyuria |
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papillary necrosis
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risk factors are sickle cell, diabetes, urinary obstruction, chronic pyelonephritis and acutely precipitated by NSAIDs
flank pain, hematuria, pyuria, fever and necrotic cells in urinalysis most accurate diagnosis is bumpy countours of renal pelvis on CT |
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prevention of contrast-induced renal failure
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most importantly is hydration; then bicarbonate and N-acetyl cysteine have been shown to decrease it
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glomerulonephritis general presentation
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hematuria with dysmorphic red cells, edema, hypertension, proteinuria <2gm/24h
biopsy is extremely important for specific Rx |
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glomerulonephritis from vascular causes
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Wegener
Churg-Strauss Henoch-Schonlein PAN TTP HUS cryoglobulinemia |
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glomerulonephritis from glomerular disease
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Goodpasture
postinfectious GN IgA nephropathy RPGN Alport SLE hypertension amyloid diabetes (nodular or diffuse glomerulosclerosis) |
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Wegener glomerulonephritis presentation
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glomerulonephritis associated with rhinitis, sinusitis, nasal ulcers, cough and hemoptysis
it's systemic and also affects skin, joints, eyes nonspecific: ↑ESR, anemia, leukocytosis best initial test: c-ANCA (anti-proteinase-3) most accurate: biopsy of kidney or lung looking for granulomas treat with cyclophosphamide + steroids |
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Churg-Strauss glomerulonephritis
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glomerulonephritis with respiratory symptoms similar to Wegener
eosinophilia and adult-onset asthma are characteristic best initial tests are ↑eosinophils and p-ANCA (antimyeloperoxidase) definitive is lung biopsy showing granulomas treat with cyclo + steroids |
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Goodpasture syndrome
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glomerulonephritis + hemoptysis, cough and shortness of breath
no other organs are affected best intial test: anti-basement membrane Abs to type IV colagen confirm with biopsy showing hemosiderin-ladden macrophages (in lungs) and linear Ig deposits (kidneys) treat with plasmapheresis and steroids |
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polyartheritis nodosa
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involves every organ except lungs
kidney involvement presents as GN and renal insufficiency there are systemic nonspecific signs abdominal and joint pain are prominent best initial tet is p-ANCA (present only in minority) biopsy is confirmatory (usually sural nerve) treat with cyclo + steroids |
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Henoch-Schonlein purpura
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palpable purpura, arthralgias, abdominal pain and GN/renal insufficiency due to systemic IgA deposition
biopsy is confirmatory but not performed in majority of patients because it's self-limited treatment is supportive, steroids if severe |
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IgA nephropathy (Berger)
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most common glomerulopathy worldwide
IgA deposition that affects only kidney causing GN presents as hematuria 1-2 days following viral illness or pharyngeal infection 40-50% progress to end-stage renal disease initial test --> IgA (↑ in 50%) confirm with kidney biopsy showing IgA deposits no proven effective therapy |
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postinfectious glomerulpnephritis
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due to any organism but mostly from throat or skin infection with group A strep
hematuria, red cell casts, proteinuria, edema, hypertension initial test: ASO and anti-hyaluronic acid test biopsy --> humps on electron micro and granular IgG/C3 deposits on IF treat hypertension and proteinuria with ACEi or ARBs and penicillin for infection |
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thrombotic thrombocytopenic purpura
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pentad for clinical diagnosis
hemolytic anemia, uremia, thrombocytopenia, fever, neurologic findings intravascular hemolysis with schistocytes and fragmented RBCs, ↑LDH, ↑reticulocytes, ↓haptoglobin mild disease resolves, if severe --> plasmapheresis don't transfuse platelets or give antibiotics |
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hemolytic uremic syndrome
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E. coli 0157:H7
triad for clinical diagnosis --> hemolytic anemia, uremia, thrombocytopenia intravascular hemolysis with schistocytes and fragmented RBCs, ↑LDH, ↑reticulocytes, ↓haptoglobin mild disease resolves, if severe --> plasmapheresis don't transfuse platelets or give antibiotics |
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cryoglobulinemia
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renal diasease associated with hep B or C, joint pain, neuropathy and purpura; no GI involvement (different from HSP); ↑ESR, ↓complement and confirmation with cryoglobulins; treat underlying hepatitis with interferon and ribavirin; if severe --> pulse steroids and plasmapheresis
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diabetic nephropathy
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directly proportional to duration of diabetes
nodular (Kimmelstein-Wilson) or diffuse glomerulosclerosis screen for microalbuminuria and creatinine level treat with ACEi or ARB |
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lupus nephritis
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asymptomatic proteinuria or hematuria or severe renal disease requiring dialysis
initial test is dsDNA confirm and determine treatment with kidney biopsy if sclerosis --> no therapy needed if proliferative --> steroids with mycophenolate |
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Alport syndrome
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glomerular disease + congenital eye problems and sensorineural hearing loss
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rapidly progressive glomerulonephritis
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can be due to other glomerular diseases or idiopathic in which there's crescent formation
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amyloidosis etiology
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AL type is from Ig light chains in multiple myeloma
AA is from rheumatoid arthritis, IBD, myeloma |
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amyloidosis presentation
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glomerulonephritis
restrictive cardiomyopathy, arrhythmias, heart blocks macroglosia carpal tunnel syndrome malabsorption |
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amyloidosis diagnosis
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biopsy of involved organ such as kidney shows green birefringence in Congo red stain
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amyloidosis treatment
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control underlying disease; melphalan and prednisone can control protein production
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nephrotic syndrome etiology
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primary: membranous GN, Nil, membranoproliferative, focal-segmental GN
1/3 associated with diabetes, hypertension or myeloma any glomerulonephritis can convert to nephrotic syndrome if severe enough |
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nephrotic syndrome presentation
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proteinuria >3.5g/24h, edema, hyperlipidemia, hypoalbuminemia
can have hyperlipiduria (maltese cross) and hypercoagulable states (arterial or venous thrombosis from loss of antithrombin, proteins C and S) |
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nephrotic syndrome diagnosis
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initial test is proteinuria >3.5g/24h or albumin/creatinine ratio >3.5 on urinalysis
renal biopsy is most accurate |
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nephrotic syndrome management
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treat underlying disease
if primary --> steroids if unresponsive --> cyclo or mycophenolate ACEIs for all with proteinuria |
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membranous glomerulonephritis
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most common nephrotic syndrome in adults
associated with lymphoma, breast cancer, endocarditis, chronic hepatitis, lupus treat with steroids |
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Nil lesion
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minimal change disease most common in children, 15% adults
electron micro shows fusion of foot processes responds to steroids |
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membranoproliferative glomerulonephritis
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nephrotic syndrome associated with chronic hepatitis and hypocomplement
immunofluorescensce detects mesangial IgM deposits steroid-resistant, dipyridamole and aspirin are useful |
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focal segmental glomerulonephritis
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nephrotic syndrome associated with heroin use and HIV; limited response to steroids; ESRD over 5-10 years
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things to check for in urinalysis
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proteinuria, hematuria, nitrites, bacteriuria, casts
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proteinuria
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urine dipstick detects only albumin not Ig light chains
found in glomerular or tubular disease, glomerulonephritis, diabetes, fever, CHF, severe exercise, orthostatic microalbuminuria is 30-300g/24h in diabetic nephropathy |
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hematuria
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found in diseases of bladder or kidney; stones, cancer, bleeding disorders, trauma, cyclo, glomerulonephritis, cystitis, prostatitis
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nitrites
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gram negative bacteria reduce nitrate to nitrite and is marker for infection
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bacteriuria
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if isolated, has limited significance unless pregnant since they can develop pyelonephritis; >100,000 colonies indicates urinary infection
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hyaline casts
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dehydration; not necessarily disease
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red cell casts
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glomerulonephritis
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broad, waxy casts
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chronic renal failure
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granular/muddy casts
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acute tubular necrosis
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white cells in urinalysis
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pyelonephritis, interstitial nephritis
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indications for dyalisis
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life-threatening abnormalities such as refractory fluid overload, acidosis, pericarditis, encephalopathy, other neuropathies, hyperkalemia, uremia (nausea, vomitting, bleeding diathesis)
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end-stage renal disease etiology
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diabetic nephropathy
hypertension glomerulonephritis (15%) cystic disease (5%) interstitial nephritis (5%) requires dialysis |
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anemia as ESRD complication
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normo normo anemia from decreased production of erythropoietin; replace EPO
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hypocalcemia as ESRD complication
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from decreased production of 1,25 dihydroxy vitamin D (1-hydroxylase); vitamin D replacement
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hyperphosphatemia as ESRD complication
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from decreased ability to excrete
treat with calcium carbonate or calcium acetate cinacalcet in refractory cases aluminum-containing binders should not be used due to dementia and bone abnormalities risk |
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osteodystrophy as ESRD complication
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osteitis fibrosa cystica
bone cysts due to ↓vitamin D --> secondary hyperparathyroidism manage by improving calcium and treating hyperPTH |
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hypertension and atherosclerosis as ESRD complication
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acceleratd atherosclerosis not known why
most common COD for dialysis patients hypertension goal is 130/80 |
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infection as ESRD complication
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second most common COD
white cells don't function well under uremia staph is most common due to catheters |
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bleeding as ESRD complication
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uremia-induced platelet dysfunction increases bleeding time
treated with desmopressin to increase vWB and factor VIII |
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minor signs present in ESRD
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pruritus
hyperuricemia decreased libido weakness fatigue glucose intolerance not indications for dialysis |
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dietary treatment in ESRD
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restricted Na, K, protein, magnesium, phosphate
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renal transplant
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survival
live related donor 95%/1 year, 72%/5years cadaver donor 88%/1 year, 58%/5 years dialysis alone 30-40%/5 years average wait for transplant is 2-4 years graft rejection prevention with cyclosporine, tacrolimus, mycophenolate |
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renal tubular acidosis type I etiology
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problem in distal tubules
usually sporadic or secondary to autoimmune disease, ampB, lithium, NSAIDs, nephrocalcinosis, sickle cell, familial, chronic hepatitis |
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renal tubular acidosis type I presentation
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inability to develop ↑[H+] in urine
urine pH >5.4 secondary hyperaldosteronism nephrocalcinosis nephrolithiasis hypokalemia |
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renal tubular acidosis type I diagnosis
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Acid load test: give amonium chloride which should lower urine pH, with disease urine pH remains high; serum bicarbonate ~10; hypokalemia
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differentiate RTA from diarrhea acidos
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urine anion gap = (Na + K) - Cl
both have normal serum anion gap metabolic acidosis but diarrhea has negative urine anion gap (↑ urine Cl-) and RTA type I cannot excrete H+ so Cl- will be low and urine anion gap is positive |
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renal tubular acidosis type I treatment
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oral bicarbonate because proximal tubule reabsoprtion is intact and potassium replacement
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renal tubular acidosis type II etiology
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inability to absorb bicarbonate in proximal tubules
Fanconi, Wilson, amyloidosis, myeloma, acetazolamide, vitD deficiency, secondary hyperPTH, chronic hypocalcemia |
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renal tubular acidosis type II presentation
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initial urine pH is basic but then becomes <5.4
hypokalemia serum bicarbonate 18-20 malabsorption of glucose, amino acids, urate, phosphate osteomalacia/rickets |
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renal tubular acidosis type II diagnosis
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sodium bicarbonate IV is not reabsorbed; basic urine in presence of acidemia; bicarbonate in urine
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renal tubular acidosis type II treatment
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potassium, thiazides and large amounts of HCO3
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difference between type I and type II RTA
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type I is inability to excrete H+ and has nephrolithiasis
type II inability to reabsorb HCO3 and has osteomalacia/rickets |
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renal tubular acidosis type IV etiology
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aldosterone deficiency or adrenal insensitivity to angiotensin II
diabetes (50%) Addison sickle cell renal failure |
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renal tubular acidosis type IV presentation
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asymptomatic hyperkalemia
mild to moderate renal failure hyperchloremic (nonanion gap) metabolic acidosis |
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renal tubular acidosis type IV diagnosis
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high urine sodium with oral salt restriction is diagnostic
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renal tubular acidosis type IV treatment
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fludrocortisone has mineralocorticoid effect
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types of kidney stones
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calcium oxalate (70%)
calcium phosphate (10%) Mg/aluminum/phosphate (struvite) uric acid cysteine indinavir |
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causes of hypercalciuria
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increased absorption: vitamin D intoxication, ↑vitamin D from sarcoidosis or granulomatous diseases; familial, idiopathic; resorptive: hyperPTH, multiple myeloma
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causes of hyperoxaluria
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primary familial, enteric; fat malabsorption binds calcium and leaves oxalate to be reabsorbed
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causes of uric acid stones
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acid tubules and high uric acid from gout, hematologic malignancies, Crohn
radiolucent on x-rays |
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causes of struvite stones
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infections with urease-producing proteus, pseudomonas, klebsiella; highly alkaline urine
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nephrolithiasis presentation
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constant flank pain, hematuria, pain radiating to groin
stones < 5mm should pass spontaneously |
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nephrolithiasis diagnosis
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plain x-ray is rarely used
ultrasound, spiral CT strain the urine check serum and urine calcium never do intravenous pyelogram |
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nephrolithiasis treatment
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analgesia, hydration, bed rest
shockwave lithotripsy for stones <2cm but fragments may obstruct ureteroscopy percutaneous removal (anesthesia and hospital stay) |
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adult polycystic kidney disease presentation
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flank pain, hematuria, palpable mass, UTIs, calculi
hypertension hepatic cysts (40%) colonic diverticula intracraneal aneurysm mitral valve prolapse |
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adult polycystic kidney disease diagnosis and treatment
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ultrasound and CT; treatment is nonspecific with management of hypertension, UTIs and calculi
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simple cysts
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cysts with irregular walls or debris should be aspirated to exclude malignancy
dialysis can cause cysts |
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serum osmolality formula
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(2 x sodiun) + (BUN / 2.8) + (glucose / 18); if glucose and BUN are normal then ~ 2 x Na + 10
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hyponatremia specific etiologies
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pseudohyponatremia, hypervolemic state, hypovolemic state, euvolemic states, SIADH
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hypovolemic hyponatremia causes
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dehydration (with free water replacement)
vomitting diarrhea sweating (with free water replacement) diuretics ACEIs renal salt waste Addison cerebral sodium waste |
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hypervolemic hyponatremia causes
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CHF, nephrotic syndrome, cirrhosis, renal insufficiency
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hyponatremia general presentation
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Na < 135mEq; symptoms depend on how fast it drops
neurologic in nature forgetfulness --> disorientation --> obtundation --> seizure --> coma |
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hyponatremia management
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if asymptomatic --> fluid restriction
mild symptoms --> normal saline + furosemide seizure or coma --> 3% hypertonic saline avoid central pontine myelinolysis by correcting Na at 0.5-1mEq/hour or 2mEq if seizure or coma |
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pseudohyponatremia
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total Na is normal, serum Na is low
for every 100mg/dL of hyperglycemia there's 1.6mEq/L decrease in Na hyperlipidemia causes Na lab artifact |
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euvolemic hyponatremia
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psychogenic polydipsisa, hypothyroidism, diuretics, ACEIs, endurance exercise, SIADH
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SIADH etiology
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small cell lung CA, pancreas CA, ectopic ADH secretion
TB, lung abscess head injury, CVA, encephalitis chlorpropamide, clofibrate, vincristine, vinblastine, cyclophosphamide, carbamazepine |
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SIADH presentation
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water retention
ECF expansion without edema or hypertension (natriuresis) hyponatremia concentrated urine signs of cerebral edema when hyponatremia is severe (irritability, confusion, seizures, coma) |
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SIADH diagnosis
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hyponatremia <130mEq/L
urine sodium > 20mEq/L maintained hypervolemia ↓RAA low electrolytes in blood (BUN, creatinine, uric acid) low albumin |
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SIADH management
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treat underlying cause
fluid restriction to 800-1000mL/d demeclocycline (AVP inhibitor) in case of cerebral edema: hypertonic 3% saline 200-300mL IV in 3-4h |
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insensible water losses and hypernatremia
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↑skin loss (sweating, burns, fever, exercise), respiratory infections
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gastrointestinal water losses and hypernatremia
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osmotic diarrhea from gluten or lactose intolerance, some infectious diarrhea
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transcellular water shift and hypernatremia
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rhabdomyolysis or seizures cause muscle to take up lots of water
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renal disease and hypernatremia
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diabetes insipidus or osmotic diuresis (diabetic KA, nonketotic hyperosmolar coma, mannitol, diuretics
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central diabetes insipidus etiology
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neoplastic/infiltrative lessions in hypothalamus or pituitary adenomas, craniopharyngiomas, leukemia, sarcoid histocytosis
surgery, radiotherapy, trauma, anoxia, hypertension, meningitis, encephalitis, TB, syphillis could also be idiopathic |
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nephrogenic diabetes insipidus etiology
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idiopathic or secondary to
hypercalcemia hypokalemia sickle cell amyloidosis myeloma pyelonephritis sarcoidosis Sjogren lithium demeclocycline colchicine |
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diabetes insipidus presentation
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polyuria, polydipsia
hypernatremia, urine specific gravity <1,010 severe dehydration, weakness fever, altered mental state prostration, nocturia |
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diabetes insipidus diagnosis
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plasma/urine osmolarity ratio falls to the right of shaded area; then if vasopressin response is normal --> central diabetes insipidus, else nephrogenic
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diabetes insipidus differential
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primary polydipsia
drug-induced polydipsia from chlorpromazine, anticholinergics, thioridazine hypothalamic disease |
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diabetes insipidus management
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CDI: ADH hormone replacement or ADH secretion stimulators (chlorpropamide, clofibrate, carbamazepine); NDI: HCTZ or amiloride or chlortalidone as well as correction of calcium balance
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hypokalemia from GI losses
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vomitting, diarrhea, tube drainage
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hypokalemia from transcellular shift
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alkalosis, ↑insulin, B12 replacement, ↑beta-adrenergeic activity (trauma)
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hypokalemia from urinary losses
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diuretics, ↑aldosterone states (Conn, licorice, Barter, Cushing, renal artery stenosis), ↓magnesium, type I and II RTA
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hypokalemia presentation
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muscular weakness to paralysis; arrhythmias; rhabdomyolisis
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hypokalemia diagnosis
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normal levels is 3.7-5.2mEq/L; in emergencies do EKG looking for T-wave flattening and U-waves
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hypokalemia treatment
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treat underlying cause
give 4-5mEq/Kg/point; IV max 10-20mEq/h don't use dextrose containning fluids complication is fatal arrhythmia |
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hyperkalemia from transcellular shift
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pseudohyperkalemia (secondary hemolysis, mechanical trauma from venipuncture, platelets >1,000,000, WBCs >100,000)
acidosis insulin deficiency tissue breakdown (rhabdomyolisis, tumor lysis, seizures) |
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hyperkalemia in acidosis
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for every 0.1 in pH potassium increases 0.7 points
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hyperkalemia from renal causes
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renal failure, hypoaldosteronism (ACEIs, type IV RTA, adrenal enzyme deficiency, heparin), Addison, amiloride, spironolactone
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hyperkalemia presentation
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muscular weakness when K > 6.5
abnormal cardiac conduction hypoventilation |
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hyperkalemia diagnosis
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normal levels 3.7-5.2mEq/L; ECG: peaked T waves, wide QRS, short QT or prolonged PR
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hyperkalemia management
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if ECG abnormalities -->
calcium chloride (membrane stabilizer) sodium bicarbonate (alkalosis, not in same IV line as calcium) glucose/insulin (30-60 minutes to work) cation exchange resin (absorbs 1mEq og K/gram) dialysis |
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anion gap formula
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(Na + K) - (HCO + Cl); normal = 8-14
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low anion gap metabolic acidosis
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myeloma (myeloma proteins are cations, HCO and Cl go up)
↓albumin (for every 1 point, 2 point decrease in anion gap) lithium (decreases Na level) "MAL" |
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normal anion gap metabolic acidosis
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diarrhea, renal tubular acidosis, uretero sigmoidoscopy "DiREct (ureter sigmo)"
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increased anion gap metabolic acidosis
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lactate
aspirin methanol uremia diabetic ketoacidosis paraldehyde propylene glycol ethylene glycol |
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respiratory acidosis
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hypoventilation of any cause
COPD pickwickian obesity suffocation opiates sleep apnea kyphoscoliosis myopathies neuropathy effusion aspiration |
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metabolic alkalosis from H+ loss
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steroids
GI loss (vomitting, nasgastric suction) renal loss (Conn, Cushing, ↑ACTH, licorice) ↓Cl intake, diuretics |
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metabolic alkalosis from HCO3 retention
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bicarbonate administration, contraction alkalosis, milk-alkali syndrome
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metabolic alkalosis from transcellular shift
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hypokalemia
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respiratory alkalosis
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hyperventilation of any cause
anemia pulmonary embolus sarcoid anxiety pain "SAAPP" |
