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249 Cards in this Set
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Proximal convoluted tubule (cortex) |
- all glucose, bicarbonate (HCO3-), amino acids, and metabolites are reabsorbed |
Organic acids (e.g., uric acid, etc.) and bases are secreted into tubules |
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Descending loop of Henle (medulla)
Fxn: Absrpt&Secrete |
- water reabsorption and concentration of tubule fluid
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only segment of the loop that is permeable to H2O
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Ascending loop of Henle (medulla) |
Active reabsorption of Na+, Cl-, and potassium (K+) by Na+/K+/Cl-cotransporter
Reabsorption of Mg2+, Ca2+, and K+ through paracellular diffusion |
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Distal convoluted tubule (cortex)
Fxn: Absrpt&Secrete |
Na+ and Cl- reabsorbed by Na+/Cl- transporter
Ca+ reabsorbed via parathyroid hormone activity impermeable to water |
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Collecting tubule (cortex) and duct (medulla)
Fxn: Absrpt&Secrete&Hormone |
Principal cells drive Na+ reabsorption and K+ secretion when stimulated by aldosterone |
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H/P=Flank paiN, chills, nausea, vomiting, urinary frequency, dysuria, urgency; fever (>101.5°F/38°C), Costovertebral tendernesS
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Pyelonephritis
Infection of renal parenchyma most commonly caused by Escherichia coli; Staphylococcus saprophyticus, Klebsiella, and Proteus are less common pathogens; Candida is a potential cause in immunocompromised patients Most commonly occurs as sequelae of ascending urinary tract infection (UTI) Risk factors = urinary obstruction, immunocompromise, history of previous pyelonephritis, diabetes mellitus (DM), sexual intercourse >3 times/week, new sexual partner, spermicide use Complications = + risk of preterm labor and low birth weight in pregnant women |
Labs = + white blood cell count (WBC), erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP); white blood cell casts in urine; +urine cultures with >105 bacteria/mL urine (possibly- when due to hematogenous spread)
Treatment = intravenous (IV) fluoroquinolones, aminoglycosides, or cephalosporins (third generation) for 1–2 days IV antibiotics followed by outpatient oral antibiotics; severe or complicated cases may require 14–21 days of IV antibiotics; early mild cases in reliable patients may be amenable to oral antibiotics alone |
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H/P = Acute severe colicky flank paiN that may extend to inner thigh or genitals, nausea, vomiting, dysuria; possible gross hematuria
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Nephrolithiasis
Formation of “kidney” stones; stone formation can also occur elsewhere in the urinary tract; symptoms arise when stones become stuck in the urinary tract and cause obstruction Risk factors = family history, prior nephrolithiasis, low fluid intake, frequent UTIs, hypertension (HTN), DM, gout, renal tubular acidosis, hypercalcemia, hyperparathyroidism, certain drugs (e.g., acetazolamide, allopurinol, loop diuretics); males > females Complications = hydronephrosis, recurrent stones |
Labs = urinalysis shows hematuria
Radiology = abdominal x-ray shows stones in most cases (except uric acid stones); computed tomography (CT) or ultrasound (US) may locate stones; intravenous pyelogram (IVP) shows filling defect, but is used less frequently Treatment = hydration and pain control (possibly, narcotics and/or ketorolac); shockwave lithotripsy can break up stones <3 cm diameter so that they pass through the ureters; surgery may be required for larger stones |
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Nephrolithiasis, Radiopaque
+Idiopathic hypercalciuria, small bowel diseases |
Calcium oxalate
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Most patients have no identifiable cause
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Nephrolithiasis, Radiopaque
+Urinary tract infection |
Struvite (Mg-NH4-PO4)
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More common in women; may form staghorn calculi
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Nephrolithiasis, Radiopaque |
Calcium phosphate
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Nephrolithiasis, Radiolucent |
Uric acid
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Treat by alkalinizing urine
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Nephrolithiasis, Radiopaque
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Cystine
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May form staghorn calculi
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H/P = possibly asymptomatic; dull or intermittent flank pain with history of UTI; anuria suggests significant bilateral ureteral obstruction
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Hydronephrosis
Dilation of renal calyces as a result of increased pressure in the distal urinary tract Caused by increased intrarenal pressure from urinary tract obstruction (e.g., stones, anatomic defects, extra-/intra-urinary mass) Can lead to permanent damage of renal parenchyma Complications = renal failure |
Radiology = US or IVP detects dilation
Treatment = drainage via nephrostomy tube; treat underlying obstruction (balloon dilation of ureter and placement of double-J stent in ureter may allow urine flow) |
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H/P = asymptomatic until adulthood (dominant form); flank pain, chronic UTI, gross hematuria; large, palpable kidneys; possible hypertension; symptoms exacerbated by cyst rupture |
Polycystic kidney disease
Hereditary syndrome characterized by the formation of cysts in one or both kidneys leading to eventual kidney functional impairment and failure (see Color Figure 4-1) Types Autosomal dominant: most common form; affects adults; large multicystic kidneys that function poorly Autosomal recessive: rare form; presents in children; fatal in initial years of life (without transplant) Complications = end-stage renal disease, hepatic cysts, intracranial aneurysms, subarachnoid hemorrhage, mitral valve prolapse; more severe symptoms and quicker deterioration occur in the recessive form |
Labs = + blood urea nitrogen (BUN), + creatinine (Cr), anemia; urinalysis shows hematuria and proteinuria
Radiology = US or CT will show large multicystic kidneys; stones may be a comorbid finding Treatment = vasopressin receptor antagonists and amiloride can help prevent collection of fluid in cysts; preserve kidney function by treating UTI and HTN; drainage of large cysts helps with pain control; dialysis or transplant may be required if function deteriorates into renal failure |
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H/P = flank pain, weight loss; abdominal mass, HTN, fever, hematuria
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Renal cell carcinoma
Most common primary malignant neoplasm of renal parenchyma Risk factor = tobacco smoking, exposure to cadmium and asbestos Complications = poor prognosis if not caught in early stages; early recognition significantly improves prognosis |
Labs = polycythemia (secondary to increased erythropoietin activity); urinalysis shows hematuria; biopsy can be performed, but is usually foregone in favor of immediate surgical resection
Radiology = US, magnetic resonance imaging (MRI), or CT with contrast may show renal mass Treatment = nephrectomy or renal-sparing resection with lymph node dissection (typically performed without biopsy for solid mass with adequate radiographic imaging); immunotherapy, radiation therapy, and chemotherapy used for metastatic or unresectable disease, but infrequently improve survival |
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H/P = symptoms of acute renal failure, nausea, vomiting, malaise, rash; fever
Medication causes include β-lactam antibiotics, sulfonamides, aminoglycosides, nonsteroidal anti-inflammatory drugs (NSAIDs), allopurinol, proton pump inhibitors (PPIs), and diuretics (in addition to several other drugs) Toxic causes include cadmium, lead, copper, mercury, and some poisonous mushrooms Other causes include infection, sarcoidosis, amyloidosis, myohemoglobinuria (from muscle injury or excessive exercise) and high uric acid levels |
Interstitial nephropathy
Damage of renal tubules or parenchyma caused by drugs, toxins, infection, or autoimmune processes Complications = acute tubular necrosis (ATN) (i.e., progressive damage of renal tubules), acute or chronic renal failure, renal papillary necrosis (ischemic necrosis of renal parenchyma), end-stage renal disease |
Labs = increased Cr, eosinophilia; urinalysis may show granular or epithelia casts; toxin screens may detect offending agents; renal biopsy shows infiltration of inflammatory cells and renal tubular necrosis
Treatment = stop offending agent; supportive care until renal recovery; corticosteroids may be beneficial in refractory cases |
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H/P = varies with pathology; oliguria and gross hematuria (evidenced by brown urine) are common
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Nephritic syndromes
Acute hematuria and proteinuria that result secondary to glomerular inflammation PIG WAIL: Postinfectious glomerulonephritis, IgA nephropathy, Goodpasture's syndrome, Wegener's granulomatosis, Alport's syndrome, Idiopathic crescentic glomerulonephritis, Lupus nephritis. |
Labs = vary with pathology; generally + BUN, + Cr; hematuria and proteinuria seen on urinalysis; 24-hr urine collection measures protein as <3 g/day
Treatment = varies with pathology; dialysis or renal transplantation may be required in cases of renal failure |
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H/P=Recent infection, oliguria, edema, brown urine, hypertension; more common in children
lab=Hematuria and proteinuria in urinalysis, high antistreptolysin O titer, bumpy deposits of IgG and C3 on renal base-ment membrane on elec-tron microscopy |
Postinfectious glomerulonephritis
Sequelae of systemic infection (most commonly streptococcus) |
treatment=Self-limited, supportive treatment (- edema & hypertension)
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H/P=Hematuria, flank pain; low-grade fever
Lab=Increased serum IgA, mesangial cell proliferation on electron microscopy; histology indistinguishable from Henoch-Schonlein purpura renal disease |
IgA nephropathy (Berger's disease)
may be related to infection; deposition of IgA antibodies in mesangial cells |
treatment=Occasionally self-limited; give ACE-I and statins for persistent proteinuria; give corticosteroids if nephrotic syndrome develops
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H/P=Dyspnea, hemoptysis, myalgias, hematuria
Lab=Serum IgG antiglomerular basement membrane antibodies, anemia, pulmonary infiltrates on CXR, linear pattern of IgG antibody deposition on fluorescence microscopy of glomeruli |
Goodpasture's syndrome
Deposition of antiglomerular and antialveolar basement membrane antibodies |
treatment=Plasmapheresis, corticosteroids, immunosuppressive agents; can progress to renal failure
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H/P=Hematuria, symptoms of renal failure, High-frequency hearing losS
Lab=Red cell casts, hematuria, proteinuria, and pyuria on urinalysis; Glomerular basement membrane inconsistency on electron microscopY |
Alport's syndrome
Hereditary defect in collagen IV in basement membrane |
Variable prognosis with no therapy identified to halt cases of renal failure; ACE-I may reduce proteinuria; renal transplant may be complicated by Alport-related development of Goodpasture's syndrome
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H/P=Sudden renal failure, weakness, nausea, weight loss, dyspnea, hemoptysis, myalgias, fever, oliguria
Lab=Positive ANCA; inflammatory cell deposition in Bowman's capsule and crescent formation (basement membrane wrinkling) on electron microscopy |
Idiopathic crescentic glomerulonephritis
Rapidly progressive renal failure from idiopathic causes or associated with other glomerular diseases or systemic infection |
Poor prognosis with rapid progression to renal failure; corticosteroids, plasmapheresis, and immunosuppressive agents may be helpful; renal transplant frequently required
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H/P=Possibly asymptomatic, possible hypertension or renal failure; may develop nephrotic syndrome
lab=ANA, anti-DNA antibodies; hematuria, and possible proteinuria on urinalysis |
Lupus nephritis (mesangial, membranous, focal proliferative, and diffuse proliferative types)
Complication of systemic lupus erythematosus involving proliferation of endothelial and mesangial cells |
Treatment=Corticosteroids or immunosuppressive agents can delay renal failure; ACE-I and statins help reduce proteinuria
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H/P=Weight loss, respiratory symptoms, hematuria, fever
lab=c-ANCA; deposition of immune complexes in renal vessels seen on electron microscopy; pulmonary biopsy helpful in diagnosis |
Wegener's granulomatosis
Similar to crescentic disease with addition of pulmonary involvement; granulomatous inflammation of airways and renal vasculature |
treament=Corticosteroids, cytotoxic agents; variable prognosis
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H/P = varies with pathology; generally edema, foamy urine, dyspnea; hypertension, ascites
Labs = vary with pathology; generally decreased albumin and hyperlipidemia; proteinuria >3 g/day seen on 24-hr urine collection |
Nephrotic syndromes
Significant proteinuria (>3 g/day) associated with hypoalbuminemia and hyperlipidemia Frequently subsequent to glomerulonephritis Most Dogs Find Meat Mesmerizing: Minimal change disease, Diabetic nephropathy, Focal segmental glomerular sclerosis, Membranous glomerulonephritis, Membranoproliferative glomerulonephritis |
Treatment = varies with pathology; frequently includes diuretics and dietary salt and protein restriction
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H/P=Possible hypertension, increased frequency of infections; more common in young children
Labs=Hyperlipidemia, hypoalbuminemia; proteinuria on urinalysis; flattening of basement membrane foot processes seen on electron microscopy |
Minimal change disease
Idiopathic; may involve flattening of foot processes on basement membrane |
Treatment=Corticosteroids, cytotoxic agents
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H/P=Possible hypertension; more common in adults
lab=Hyperlipidemia, hypoalbuminemia; hematuria and high proteinuria on urinalysis; sclerotic changes seen in some glomeruli on electron microscopy |
Focal segmental glomerular sclerosis
Frequently idiopathic or associated with drug use or HIV; segmental sclerosis of glomeruli |
Treatment=Corticosteroids, cytotoxic agents, ACE-I, statins; progressive cases that require renal transplant (uncommon) frequently have recurrence
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H/P=Edema, dyspnea; history of infection or medication use may lead to diagnosis
Lab=Hyperlipidemia, hypoalbuminemia; proteinuria on urinalysis; “spike and dome” basement membrane thickening on electron microscopy |
Membranous glomerulonephritis
Idiopathic or associated with infection, systemic lupus erythematosus, neoplasm, or drugs; thickening of basement membrane |
treatment=Corticosteroids, cytotoxic agents, ACE-I, statins; variable rates of renal failure and renal vein thrombosis (requires anticoagulation)
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H/P=Edema, HTN; history of systemic infection or autoimmune condition; gradual progression to renal failure
lab=Hyperlipidemia, hypoalbuminemia, possible hypocomplementemia; proteinuria and possible hematuria on urinalysis; IgG deposits may be seen on basement membrane on fluorescence microscopy; BM thickening with double-layer “train track” appearancE on electron microscopy |
Membranoproliferative glomerulonephritis
Idiopathic or associated with infection or autoimmune disease; thickening of basement membrane |
treatment=Corticosteroids combined With either aspirin or dipyridamole may delay progression to renal failure
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H/P=History of DM, hypertension, progressive renal failure
Lab=Hyperlipidemia, hypoalbuminemia; proteinuria on urinalysis; basement membrane thickening on electron microscopy seen in both types; round nodules (Kimmelstiel-Wilson nodules) seen within glomeruli in nodular type |
Diabetic nephropathy (diffuse, nodular)
Basement membrane and mesangial thickening related to diabetic vascular changes |
treatment=Treat underlying DM, dietary protein restriction, ACE-I, tight blood pressure control
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/P = may initially be asymptomatic; possible fatigue, anorexia, nausea, oliguria, gross hematuria, flank pain, or mental status changes; possible pericardial friction rub, hypertension, fever, diffuse rash, edema
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Acute renal failure
Sudden decrease in renal function (e.g., glomerular filtering, urine production, or chemical excretion abnormalities with BUN and Cr retention) resulting from prerenal, intrarenal, or postrenal causes Prerenal causes include hypovolemia, sepsis, renal artery stenosis, drug toxicity Intrarenal causes include ATN (drugs, toxins), glomerular disease, renal vascular disease Postrenal disease is caused by obstruction of renal calyces, ureters, or the bladder (e.g., stones, tumor, adhesions) Patients with ARF can't VOID RIGHT: Vasculitis, Obstruction (calyces, bladder, or ureters), Infection, Drugs (ATN), Renal artery stenosis, Interstitial nephropathy, Glomerular disease, Hypovolemia, Thromboembolism. |
Labs =
+ BUN, + Cr Urinalysis may show hematuria and red cell casts (glomerular or vasculitic disease), granular casts (ATN), pyuria with waxy casts (interstitial disease or obstruction), pyuria alone (infection) Fractional excretion of Na+ (FeNa) <1% suggests a prerenal cause, >2% suggests ATN Findings consistent with nephritic or nephritic syndromes should prompt renal biopsy Radiology = US, CT, IVP, or renal angiography may be useful to detect masses, hydronephrosis, abnormal blood flow, obstruction, or vasculitis Treatment = prevent fluid overload, stop drugs causing ATN; dietary protein restriction, corticosteroids, dialysis |
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H/P = gradual development of uremic syndrome (i.e., changes in mental status, decreased consciousness, HTN, pericarditis, anorexia, nausea, vomiting, gastrointestinal (GI) bleeding, peripheral neuropathy, brownish coloration of skin)
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Chronic kidney disease (CKD)
Progressive damage of renal parenchyma that can take several years to develop HTN and DM are the most common causes Complications = end-stage renal disease (i.e., chronic kidney disease with severe symptoms and electrolyte abnormalities requiring dialysis for survival), renal osteodystrophy (i.e., bone degeneration secondary to low serum Ca-), encephalopathy, severe anemia (caused by decreased erythropoietin) |
Labs = + K+, - Na+, + phosphate, - Ca+, anemia, metabolic acidosis, + BUN, + Cr; urine osmolality is similar to serum osmolality
Radiology = US may show hydronephrosis or shrunken kidneys Treatment = restrict dietary salt and protein, correct electrolyte abnormalities, treat underlying condition; dialysis or renal transplant may be needed in progressive cases |
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nonanion gap metabolic acidosis
urine>5.3, low K+ radiology=possible stones cause=Idiopathic, autoimmune diseases, drugs, chronic infection, nephrocalcinosis, cirrhosis, SLE, obstructive nephropathy |
Renal Tubular Acidosis, Distal (Type 1)
Impaired H+ secretion leading to secondary hyperaldosteronism |
Treatment=Oral HCO3-, K+, thiazide diuretic |
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nonanion gap metabolic acidosis
urine<5.3, low K+, HCO3- radiology=bone lesions cause=Idiopathic, multiple myeloma, Fanconi syndrome, Wilson's disease, amyloidosis, vitamin D deficiency, autoimmune diseases |
Renal Tubular Acidosis,
Proximal (Type 2) HCO3- reabsorption |
Treatment=Oral HCO3-, K+; thiazide or loop diuretic
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nonanion gap metabolic acidosis
urine<5.3, High K+, Cl- cause=Primary renin or aldosterone deficiency, DM, Addison's disease, sickle cell disease, interstitial disease |
Renal Tubular Acidosis,Low Renin/Aldosterone (Type 4) |
Treatment=Fludrocortisone, K+ restriction
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acid-base disturbances |
normal anion gap Metabolic acidosis |
PCO2 = 1.5 [HCO3-] + (8 ± 2) |
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acid-base disturbances |
anion-gap Metabolic acidosis |
PCO2 = 1.5 [HCO3-] + (8 ± 2) |
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acid-base disturbances
Vomiting, diuretics, Cushing's syndrome, hyperaldosteronism, adrenal hyperplasia |
Metabolic alkalosis
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If PCO2 >50, then additional respiratory acidosis |
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acid-base disturbances
COPD, respiratory depression, neuromuscular diseases |
Respiratory acidosis
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acute: |
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acid-base disturbances
Hyperventilation, high altitude, asthma, aspirin toxicity, pulmonary embolism |
Respiratory alkalosis
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acute:
pH ^ = 1/10x0.08x(PCO2-40) chornic: pH^=1/10x0.03x(PCO2-40) |
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corrected, HCO3- is different from measured value
normal: + : - : |
Mixed disorder
normal: solitary high anion-gap acidosis + : metabolic alkalosis with high anion-gap acidosis - : nonanion-gap acidosis with high anion-gap acidosis |
Corrected HCO3- = measured anion gap - normal anion gap + measured HCO3-(for which 12 = value of normal anion gap) |
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H/P = oliguria, thirst, weakness, lethargy, decreased consciousness, mental status changes, seizures
6 Ds: Diuretics, Dehydration, Diabetes insipidus, Docs (iatrogenic), Diarrhea (and vomiting), Disease of kidney (hyperaldosteronism). |
Hypernatremia
Serum Na+ >155 mEq/L Complications = seizures, CNS damage; too rapid hydration can cause cerebral edema |
Treatment =
Gradual hydration with hypotonic saline for inadequate fluid intake or excess fluid loss (maximal Na1 reduction = 12 mEq/day) Approximate required correction in a patient with purely fluid losses as a cause of hypernatremia can be determined through calculation of the water deficit: .6xmass in kgx([Na]/140-1) Half of deficit is given in 24 hrs in addition to maintenance fluids, remainder is given over following 24–48 hrs; close monitoring of Na+ required to avoid excessive correction Because total body water will be slightly greater than patient's body water content at time of hypernatremia (because of fluid loss), calculated water deficit may be artificially high |
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H/P = polydipsia, polyuria, signs of dehydration
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Diabetes insipidus (DI) |
Labs = |
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H/P = confusion, nausea, weakness, decreased consciousness |
Hyponatremia |
Treatment = treat underlying condition (stop offending agent, correct hyperglycemia or hyperlipidemia, etc.); salt administration and H2O restriction unless hypovolemic and serum osmolality <280 mOsm/kg (rehydrate with saline no faster than 12 mEq/day); give loop diuretics or hypertonic saline for severe cases (Na+ <120 mEq/L) |
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H/P = chronic symptoms of hyponatremia |
Syndrome of inappropriate ADH secretion (SIADH) |
Treatment = fluid restriction; loop diuretics and hypertonic saline if symptomatic; demeclocycline may help maintain normal Na+ levels |
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H/P = weakness, nausea, vomiting; arrhythmias; paralysis or paresthesia in severe cases
CRAMP KIT: Catabolism of tissues (e.g., trauma, chemotherapy, radiation), Renal failure, Aldosterone deficiency, Metabolic acidosis, Pseudohyperkalemia, K+-sparing diuretics, Insulin deficiency, Tubular (renal) acidosis type 4. |
Hyperkalemia
Serum K+ >5.0 mEq/L Pseudohyperkalemia occurs from red blood cell hemolysis following blood collection, so K+ should be measured immediately in drawn blood and increased serum K+ should be confirmed with a repeat blood sample using a large-gauge needle. |
(ECG) = tall, peaked T waves |
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H/P = fatigue, weakness, possible paralysis; GRAPHIC IDEA: GI losses (vomiting, diarrhea), Renal tubular acidosis (types I and II), Aldosterone (high), Periodic paralysis, Hypothermia, Insulin excess, Cushing's syndrome, Insufficient intake, Diuretics (loop, thiazide), Elevated β-adrenergic activity, Alkalosis (metabolic, respiratory).
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Hypokalemia
Serum K+ <3.5 mEq/L Complications = overly rapid replacement can lead to arrhythmias |
ECG = T-wave flattening, ST depression, U waves |
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H/P = deep pain, easy fractures, possible nephrolithiasis, nausea, vomiting, constipation, weakness, mental status changes, polyuria |
Hypercalcemia |
Labs = increased parathyroid hormone in hyperparathyroidism; very high Ca2+ and normal or low parathyroid hormone frequently seen with neoplasm; increased vitamins A or D seen in hypervitaminoses |
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family history of hypercalcemia, low urine Ca2+, and absence of osteopenia, nephrolithiasis, and mental status changes
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familial hypocalciuric hypercalcemia
genetic disorder of Ca2+-sensing receptors |
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H/P = abdominal pain, dyspnea; tetany, Chvostek's sign (i.e., tapping facial nerve causes spasm), carpal spasm when blood pressure cuff inflated (i.e., Trousseau's sign)
hypoparathyroidism, hyperphosphatemia, vitamin D deficiency, loop diuretics, pancreatitis, or alcoholism |
Hypocalcemia |
Labs = Ca2+ should be adjusted for hypoalbuminemia (lower limit of normal Ca2+ decreases 0.8 mg/dL for each 1 g/dL albumin <4); decreased corrected Ca2+; increased phosphate seen with hypoparathyroidism and renal failure |
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H/P = urinary frequency, dysuria (i.e., painful urination), suprapubic pain, urgency
Labs = urinalysis shows increased nitrates, increased leukocyte esterase and white blood cells in urine; urine culture will show >105 pathogen colonies/mL; blood tests usually not helpful unless due to hematogenous spread |
Urinary tract infection (UTI)
Ascending infection of urethra, bladder, and ureters resulting from inoculation of lower urinary tract (rarely hematogenous spread) Most commonly due to E. coli, S. saprophyticus, Proteus, Klebsiella, Enterobacter, Pseudomonas, and enterococcus Risk factors = obstruction, Foley catheter, vesicoureteral reflux, pregnancy, DM, sexual intercourse, immunocompromise; female > male Complications = abscess formation, pyelonephritis, renal failure, prostatitis |
Treatment = amoxicillin, trimethoprim-sulfamethoxazole (TMP-SMX), or fluoroquinolones for 3 days; relapsing infection should be treated for 14 days |
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H/P = painless gross hematuria; suprapubic pain, frequency, dysuria, and urgency occur later in disease; palpable suprapubic mass
Labs = urinalysis shows hematuria; urine cytology shows malignant cells; biopsy confirms diagnosis |
Bladder cancer
Transitional cell carcinoma (common), squamous cell cancer (uncommon), or adenocarcinoma of the bladder (uncommon) Risk factors = tobacco, schistosomiasis, aniline dye, petroleum byproducts, recurrent UTI; male 3 × > female Complications = frequent recurrence |
Radiology = cystoscopy is important for visualization of lesions, urine specimen collection, and lesion biopsy; pelvic CT, MRI, or IVP may detect mass |
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H/P = dysuria, frequency, urgency, Burning urination; purulent urethral discharge seen with N. gonorrhoeaE
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Urethritis
Infection of urethra caused by sexually transmitted Neisseria gonorrhoeae or Chlamydia trachomatis Complications = urethral strictures, frequent reinfection when sexual partners not treated |
Labs = Gram stain shows Gram-negative diplococci for N. gonorrhoeae; Thayer-Martin culture will detect N. gonorrhoeae; negative Gram stain suggests C. trachomatis; diagnosis of Chlamydia may be confirmed with nucleic acid amplification testing |
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H/P = perineal pain, dysuria, frequency, urgency; fever, tender prostate on digital rectal examination |
Prostatitis
Inflammation of prostate from unknown cause or as complication of UTI |
Labs = may be suggestive of UTI; possible hematuria; white blood cells seen in prostatic secretions |
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H/P = urinary hesitancy, straining, weak or intermittent stream, dribbling; frequency, urgency, nocturia, and urge incontinence develop secondary to incomplete emptying or UTI; digital examination detects uniformly enlarged, rubbery prostate |
Benign prostatic hyperplasia (BPH)
Benign enlargement of prostate seen with increasing frequency as men age beyond 40 yrs BPH develops in the central zone of the prostate adjacent to the urethra, and does not predispose patients to prostate cancer. |
Labs = possible mild increase in prostate-specific antigen (PSA); rule out infection (urinalysis), cancer (biopsy), and renal failure (serum electrolytes, BUN, Cr) |
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H/P = frequently asymptomatic; weakened urinary stream, urinary retention, weight loss, back pain in later disease; Nodular or irregular prostate on digital examinatioN, lymphedema
Labs = urinalysis may show hematuria and pyuria; increased PSA, increased alkaline phosphatase; biopsy provides diagnosis |
Prostate cancer |
Radiology = transrectal US shows irregular prostate; bone scan, chest x-ray (CXR), and CT may detect metastases |
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H/P = epididymal pain relieved by Supporting scrotuM, dysuria; scrotal tenderness, and induration
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Epididymitis
Inflammation of epididymis associated with testicular inflammation Caused by prostatitis, STDs (especially Chlamydia), urinary reflux |
Labs = urinalysis shows white blood cells; urine culture with specialized culture media may help diagnose STDs |
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H/P = very painful and swollen testes, nausea, vomiting; fever, Testes displaced superiorlY, mass in spermatic cord may be felt, absent cremasteric reflex
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Testicular torsion
Twisting of spermatic cord leading to vascular insufficiency of testes Complications = testicular ischemia or infarction without prompt treatment |
Radiology = US may show torsion |
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H/P = painless testicular mass, possible gynecomastia or lower abdominal pain; GI or pulmonary symptoms can result from metastases
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Testicular cancer
Germ cell (seminomatous, nonseminomatous) or stromal cell (Leydig, Sertoli, or granulosa cell) tumors of testicles Risk factors = prior history of testicular cancer, undescended testes, family history Complications = prognosis is very good, but nonseminomas have lower cure rates and increased risk of recurrence |
Labs = biopsy provides diagnosis; increased β-human chorionic gonadotropin (β-hCG) and increased α-fetoprotein in germ cell tumors; increased estrogen in stromal cell tumors |
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H/P = history of testicular trauma, surgery, chemotherapy, or infection can be contributory; varicocele (collection of veins in scrotum), undescended testes, or penile defects may be seen on examination
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Infertility (male)
Inability of couple to achieve pregnancy following 1 yr of normal sexual activity without use of contraception |
Labs = hormone analysis, complete blood count (CBC), and urinalysis may be useful for diagnosis; semen analysis for sperm motility, morphology, volume, and concentration may be useful |
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H/P = history of trauma, surgery, or infection can be contributory; examination should consider vascular (decreased pulses and perfusion), hormonal (testicular atrophy or gynecomastia), and neurologic (decrease anal wink reflex and paresthesias) etiologies
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Impotence |
Labs = possible decreased testosterone, decreased luteinizing hormone (LH), or increased prolactin |
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H/P = weight loss, nausea, vomiting, dysuria, polyuria; palpable abdominal or flank mass, hypertension, fever
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Wilms tumor
Malignant tumor of renal origin presenting in children <4 yr of age Risk factors = family history, neurofibromatosis, other genitourinary abnormalities |
Labs = measure BUN, Cr, and CBC to assess kidney function |
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H/P = defect apparent on examination and during urination
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Urethral displacement |
Treatment = surgical correction (ideally during infancy), do not circumcise before surgical correction |
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H/P = almost always nonpathologic; unusual findings in history and examination should prompt further workup
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Enuresis
Nocturnal bedwetting seen in young children Seen in all children; most cases resolve by age 4 yr; rare cases associated with disease |
Treatment = education, enuresis alarms, dietary modifications (no fluids near bedtime); desmopressin or imipramine used in refractory cases |
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H/P = empty scrotal sac, testes inconsistently found in scrotum |
Undescended testes (cryptorchidism) |
Treatment = exogenous hCG administration or orchiopexy before age 5 yr to reduce risk of cancer and allow testicular development |
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metformin discontinued in what conditions?
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discontinue in acute renal failure, hepatic failure, or sepsis --> develop lactic acidosis |
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nephrotic condition: hypercoagulability
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manifests as venous or arterial thrombosis, and even pulmonary embolism. renal vein thrombosis it he most frequent manifestation. complications of nephrotic syndrome include: protein malnutrition, iron-resistant microcytic hypochromic anemia, increased susceptibility to infxn, and vitD deficiency
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drug-induced interstitial nephritis
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fever, rash, and arthralgiasother features are peripheral eosinophilia, hematuia, sterile pyuria, and eosinophiluria. WBC casts may be present in the urine, but red cell casts are rare. discontinue offending agent
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indications for cystoscopy
|
gross hematuria or with microscopic hematuria and other risk factors for bladder cancer. Risk factors include: cigarette smoking, certain occupational exposures (painters, metal workers), chronic cystitis, iatrogenic causes (eg cyclophosphamide), and pelvic radiation exposure
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causes of microscopic hematuria
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renal (renal cell canger, IgA nephropathy), ureteral (stricture, stone), bladder (CA, cystitis), and prostate/urethral (BPH, prostate CA, urethritis) abnormalities
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colloids vs crystalloids in rehydration
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colloid solutions (albumin) usually used in burns or conditions accompanied by hypoproteinemiacrystalloid solutions: usually 0.9% NaCl = normal salinerehydration therapy with elderly patients should be undertaken with caution bc sodium loading can unmask subclinical heart failure
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membranous nephropathy vs minimal change disease in cancer
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generally, membranous nephropathy is the most common nephropathy a/w carcinomahowever, nephrotic syndrome is a well-known complication of Hodgkin's lymphoma, and is usually caused by minimal change dz
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HIV kidney dz
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collapsing focal and segmental glomerulosclerosis is the most common form of glomerulopathy in HIVtypical presentaiton of focal segmental glomerulosclerosis includes nephrotic range proteinuria, azotemia, and nl sized kidneys
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renal vein thrombosis a/w what nephrotic/nephritic syndrome
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most common in membranous glomerulonephritis --> look for pt with sudden onset abdominal pain, fever, and hematuriaantithrombin III is lost in the urine and puts pts at an increase risk of venous and arterial thrombosis
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acyclovir causes nephropathy. what can be done to prevent this?
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can cause crystalline nephropathy is adequate hydration not provided
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earliest renal abnormality in diabetic nephropathy
|
glomerular hyperfiltration -> also the major pathophysiologic mechanism of glomerular injury in these patientsthickening of the glomerular basement membrane is the first change that can be quantitated. This is followed by mesangial expansion. nodular sclerosis is superimposed later and is specific for diabetic nephropathy.
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most common cause of painless hematuria in adults
|
kidney, ureter, or bladder malignancy appropriate assesment with contrast ct scan or IV pyelogram was well as endoscopic assessment of hte bladder and urethra. most common causes of hematuria in the US are neoplasms, infxn, trauma, nephrolithiasis, glomerulonephritis and prostatic dz.
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removal of K+ achieved with what agents
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dialysis, cation exchange resins (kayexalate) or diuretics
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acute epididymitis
|
characterized by fever, painful enlargement of the testes, and irritative voiding sx. can be either sexually transmitted or non-sexually transmitted. sexually transmitted acute epidiymitis is more common in adults and is a/w urethritis, which causes pain at the tip of the penis and urethral dischargenonsexually transmitted acute epididymitis occurs in older persons and is usually a/w UTI. younger: chlamydia and gonorrheaolder: GNR such as E.coli
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most common kidney stones
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calcium oxalate = 75-90% of stones. calcium phosphate stones common in primary hyperparathyroidism and RTAuric acid stones -> increased cell turnovercysteine stone: inborn error of metabolism. positive family history may be found in such casesstruvite stones: alkaline urine bc of infection wit urease producing bacteria (proteus!!!) IN such cases, a h/o recurrent UTI may be present
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ADPKD can cause what?
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potential cause of hypertensionhepatic cysts are the most common extrarenal manifestationintracranial berry aneurysms in 5-10%!!characterized by multiple renal cysts, intermittent flank pain, hematuria, UTI, and nephrolithiasis
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paraproteinemia
|
multiple myeloma -> characterized by clonal proliferation of plasma cells, resulting in excessive production of a single Ig (monoclonal paraproteins). characterized by normochromic, normocytic anemia, fatigue, and bone pain (especially in back and chest). labs show anemia, hypercalceia, bence jones proteins in the urine, and a monoclonal protein peak on electrophoresis. xrays may reveal punched out lesions, osteoporosis, or pathologic fx
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oliguria and acute renal failure due to suspected bladder outlet obstruction in postop setting. next step?
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urgent bladder scan and cath!
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recurrent hypercalciuric renal stones treated with?
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increased fluid intake, sodium restriction, and thiazide diureticcalcium restriction not advised.
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nephrotic syndrome in relation with accelerated atherosclerosis
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nephrotic syndrome can result in alterations in lipid metabolism. Dyslipidemia puts affected patients at increased risk for accelerated atherosclerosis. This atherosclerotic tendency, along with intrinsic hypercoagulability, paces pts with nephrotic syndrome at risk for complications such as stroke and MI
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obstructive uropathy sx
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unilateral likely d/t renal calculi -> flank pain, suggeting renal capsular distension; poor UOP, suggesting mechanical obstruction to urine outflow; intermittent episodes of high volume urination, which can occur when an obstruction is overcome by a large volume of retained urine. In this condition, UA may show occasional RBCs and WBCs but no casts
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unilateral varicoceles that fail to empty when a pt is recumbent
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raises suspicion for an underlying mass pathology, such as RCC, that obstructs venous flow. CT scan of the abdomen is the most sensitive and specific test!
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renal cyst
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simple renal cysts are almost always BENIGN and do not require further evaluation!!! Features concerning for malignant renal mass include a multilocular mass, irregular walls, thickened septae, and contrast enhancement.
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dietary recommendations for patients with renal calculi
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1) decreased dietary protein and oxalate2) decreased sodium intake3) increased fluid intake4) increased dietary calciummost common renal stones are calcium stones. CT scan of the abdomen w/o contrast is the diagnostic procedure of choice because it can detect radioopaque (eg Ca2+_ as well as radiolucent (uric acid) stones.
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most common associations with priapism
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Prazosin! also trazodoneother common causes include:1) sickle cell dz and leukemia2) perineal or genital trauma such as laceration of the cavernous artery3) neurogenic lesions such as spinal cord injury, cauda equina compression, etc4) medications: such as trazodone and prazosin
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pt with pyelonephritis does not respond to appropriate antibiotics after 48-72 hours of appropriate antibiotic therapy. next step in mgmt?
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renal US to look for underlying pathologies such as obstructions or complications such as renal abscess
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patient started on EPO for end stage renal dz
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major cause of anemia in pts with ESRD is deficiency of EPO. Anemia is normocytic and normochromic. Tx of choice is recombinant EPO, which is started if Hb is < 10. Most common side effects are worsening of HTN!!!, headaches, and flu-like sxextremely high yield!!
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membranoproliferative glomerulonephritis, type 2
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unique glomerulopathy caused by persistent activation of the alternative complement pathwaydense itramembranous deposits that stain for C3 is a characteristic microscopic finding for membranoproliferative glomerulonephritis, type 2 (also called dense deposit dz)
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headache, elevated BP, and renal bruit
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highly suggestive of renovascular HTN 2/2 renal artery stenosis -> usual cause is fibromuscular dysplasia in young adults and atheromatous plaque in older patients. goals of tx: decrease blood pressure and restore perfusion to ischemic kidney. Interventional therapy is more effective! than medical mgmt alone; hence, ANGIOPLASTY WITH STENT PLACEMENT is the best tx option |
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analgesic nephropathy
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most common form of drug-induced chronic renal failure. Papillary necrosis and chronic tubulointerstitial nephritis are the most common pathologies seen. pts with chronic analgesic abuse are also more likely to develop premature aging, atherosclerotic vascular dz, and urinary tract CA
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indications for hemodialysis
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refractory hyperkalemiavolume overload or pulmonary edema not responding to diureticsrefractory metabolic acidosisuremic pericarditisuremic encephalopathy or neuropathycoagulopathy due to renal failure
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most common cause of death in dialysis pts
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cardiovascular dz -> approx 50% of deathsmost common cause of death in renal transplant pts too
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amyloidosis classic findings
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apple-green birefringence under polarized light after staining with congo redlook for h/o RA (predisposes to amyloidosis), enlarged kidneys, and hepatomegaly.
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size of stone in regards to mgmt
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size < 5mm diameter typically pass spontaneously with conservative mgmt. This includes fluid intake of greater than 2L daily. increased hydration increases UOP and lowers the urinary solute concentration, thus preventing stone formation. |
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most common cause of bleeding in renal failure and tx?
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platelet dysfunction. nl PT, PPT, and plt count. BT prolongedDDAVP treatment of choice, which increases release of factor VIII: von Willebrand factor multimers from endothelial storage sites. Plt transfusion not indicated bc transfused platelets quickly become inactiveEXTREMELY HIGH YIELD!
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renal transplant dysfunction
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can be caused by ureteral obstruction, acute rejection, cyclosporine toxicity, vascular obstruction, and ATNradioisotope scanning, renal US, MRI, and renal bx can be employed in conducting a differential dxacute rejection best treated with IV steroids!Extremely high yield!
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common causes of hyperkalemia
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acute or chronic kidney dz, meds, or disorders impairing the renin angiotensin axiscommon offending meds: nonselective beta blockers, K sparing diuretics, ACE/ARB, and NSAIDs
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young black male with painless hematuria
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suspect sickle cell traitcause is suspected to be papillary ischemia, which is d/t the relatively low local O2 partial pressure, and which predisposes the diseased RBCs to sickling. Papillary necrosis can occur with massive hematuria, but the episodes are usually mild and resolve spontaneously
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mgmt of goodpasture's syndrome and wegener's
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goodpasture's: plasmapharesiswegener's: combo of cyclophosphamide and steroids
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acute bacterial prostatitis
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presents in a manner similar to other UTI, but with addition of PERINEAL PAIN, pronounced systemic sx (fever, chills, acute ilness), and a tender, boggy prostate on exam.urine cx should be obtained to direct antibiotic therapy
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acyclovir can cause what kind of renal damage?
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crystalluria with renal tubular obstruciton during high dose parenteral therapy, especially in inadequately hydrated patients.
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mixed esential cryoglobinemia
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palpable purpura, glomerulonephritis, nonspecific systemic sx, arthralgias, hsm, peripheral neuropathy, and hypocomplementemia.most pts have hep C
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side effects of cyclosporine and tacrolimus
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nephrotoxicity, hyperK, HTN, gum hypertrophy, hirsutism, and tremortacrolimus has similar toxicities, except for hirsutism and gum hypertrophy
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toxicity of azathioprine and mycophenolate
|
azathioprine: dose-related diarrhea, leukopenia, and hepatotoxicity mycophenolate: bone marrow suppression |
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focal segmental glomerulosclerosis
|
more common in AA patients and in patients with obesity, heroin use and HIV
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cystinuria
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inherited dz causing recurrent renal stone formationlook for personal h/o recurrent kidney stones from childhood and a positive family hx. characteristic stones are hard and radioopaque. U/A shows typical HEXAGONAL crystalsurinary cyanide nitroprusside test is widely used as a qualitative screening proceduredue to AMINO ACID TRANSPORT ABNORMALITY -> cystine is porly soluble in water leading to formation of hard, radioopaque renal stones3949
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initial vs terminal vs total hematuria
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initial: urethral damageterminal: bladder or prostatic damagetotal hematuria: damage in kidney or uretersclots not usually seen with renal causes of hematuria
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how disc herniation can cause incontinence
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large midline disk herniation can cause nerve root injury known as cauda equina syndrome, a condition characterized by bladder atony with overflow incontinence, bilateral sciatica, saddle anesthesia, and loss of anal sphincter tone
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chlamydia vs gonorrhea physical exam and lab findings
|
chlamydia: presence of MUCOPURULENT urethral d/c. UA reveals absent bacteriuria. urine cx shows less than 100 colonies/mLgonococcal: less common than chlamydia. urethral d/c is PURULENT (rather than mucopurulent), and gram stain usually reveals the causative organisms
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prevention of uric acid stones
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radiolucent but may be seen on US or CT scan. they are highly soluble in alkaline urinethus, alkalinzation of hte urine to pH 6 -6.5 with ORAL POTASSIUM CITRATE i the treatment of choice
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woman with chronic headaches presenting with painless hematuria |
very typical for ANALGESIC NEPHROPATHY -> PAPILLARY NECROSISbelieved that several years of analgesic abuse is required to induce this condition characterized by chronic tubulointerstitial damage.
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Wright Hansel stain
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stains eosinophils in urine. tests for allergic interstitial nephritis.
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Tamm-Horsfall protein
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normal protein in urine
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what diagnosis is suggested by waxy casts in urine?
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chronic renal disease
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NSAID and ACEi activities on renal vasculature
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NSAID: vasoconstriction of afferent arterioleACEi: vasodilation of efferent arteriole
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differentiate renal failure precipitated by contrast media from that precipitated by other drugs
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contrast media has immeidate reaction. other drugs require build up (5-10 days)
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pre-renal azotemia affect on urinary sodium and fraction of excreted sodium
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pre-renal azotemia causes decreased renal perfusion, which causes increased release of aldosterone, causing decreased urinary sodium and decreased fraction of excreted sodium
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define isosthenuria
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urine osmolality = blood osmolality
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management for contrast media renotoxicity
|
fluid (not N-acetylcystine and bicarbonate)
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mechanism of acute tubular necrosis from contrast media, and how does it differ from other causes of acute tubular necrosis
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contrast media causes afferent ateriole spasm, which leads to decreased urinary sodium and FeNa. Other causes of acute tubular necrosis all cause incrased urinary sodium and FeNa (due to inability of tubules to reabsorb sodium)
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treatment for rhabdomyolysis
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1. hydration2. mannitol3. bicarbonate
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management for hypocalcemia in rhabdomyolysis
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leave it alone. should correct itself in recovery
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type of renal failure in hepatorenal syndrome
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pre-renal azotemia
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what is livedo reticularis? and how should it be investigated?
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venous swelling from capillary occlusion. investigate with biopsy, which should show cholesterol crystals |
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presentation of papillary necrosis
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rapid onset flank pain after ingesting NSAID, with background of renal insufficiency
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differentiate btw symptoms of Goodpasture and Wegener
|
Goodpasture: no URT involvement
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differentiate btw timelines of PSGN and IgA nephropathy
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PSGN: glomerulonephritis 1-2 weeks after infectionIgA nephropathy; glomerulonephritis 1-2 days after infection
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management for severe proteinuria
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ACEi and steroids
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Alport syndrome clinical presentation
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glomerular disease, visual disturbance, and sensorineural deafness. all due to collagen defect
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most and least affected organ in polyarteritis nodosa
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most affected: kidneysleast affected: lungs
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infection to screen for in polyarteritis nodosa
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Hepatitis B
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treatment for polyarteritis nodosa
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prednisone and cyclophosphamide
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urine microscopy finding in nephrotic syndrome
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maltese cross (lipid and cells in urine)
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management for nephrotic syndrome
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edema: diureticsproteinuria: ACEi / ARBhyperlipidemia: statin
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define end stage renal disease
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uremia, requires dialysis
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management for hyperphosphatemia in ESRD
|
chelate with Ca. in case of hypercalcemia, use non Ca chelators such as sevelamer and lanthanum
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|
5 clinical characteristics of TTP
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1. intravascular hemolysis2. thrombocytopenia3. renal insufficiency4. fever5. neurological disturbance
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most common COD in polycystic kidney disease
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renal failure
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early sign and best initial test for DI
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early sign: high volume nocturiabest initial test: water deprivation test
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what is the effect of hyperglycemia on serum sodium?
|
hyperglycemia draws ICF out into ECF and causes pseudohyponatremia by dilution
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|
effect of hypothyroidism on free water excretion
|
hypothyroidism decreases free water excretion (therefore, hypothyroidism can cause euvolemic hyponatraemia)
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|
3 types of hyponatraemia
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hypervolemic: CHF/cirrhosis/renal nephrotic syndromehypovolemic: chronic free water replacement in hypernatraemiaeuvolemic: hyperglycemia, hypothyroidism, psychogenic polydipsia (check bipolar disorder), SIADH
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management for acute and chronic SIADH
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acute: tolvaptan/ conivaptan (vasopressin receptor antagonists)chronic: demeclocycline
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triamterene and amiloride
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K sparing diuretics
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main systems affected by Na and K imbalance
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Na: CNS (seizures, confusion, etc)K: muscle/ heart (weakness, arrhythmia)
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EKG findings for hyperkalaemia
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1. peaked T wave2. widened QRS3. prolonged PR interval
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management for hyperkalaemia
|
1. calcium chloride/ gluconate (cardioprotective)2. insulin/glucose 3. bicarbonate (especially in hyperkalaemia due to acidosis)4. kayexelate (GI K chelator)
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|
Bartter syndrome
|
loop of Henle salt wasting. causes hyponatraemia and hypokalaemia
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|
electrolyte disturbances that lead to hypokalaemia
|
1. alkalosis2. hypomagnesaemia
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4 types of renal tubular acidosis
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RTA1: distal segment cannot excret H+RTA2: proximal segment cannot reabsorb HCO3-RTA3: mix of 1 & 2RTA4: hypoaldosteronism
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EKG findings for hypokaelaemia
|
1. u wave2. flat T wave3. ST depression4. ventricular ectopy
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2 causes for metabolic acidosis with normal anion gap and how to differentiate them
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diarrhoea and RTA. differentiate with urine anion gap. positive urine anion gap suggests RTA (reduced H+ excretion in urine causes reduced chloride in urine)
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management for distal vs. proximal RTA
|
use HCO3- for distal (proximal tubule can reabsorb HCO3). add in diuretic for proximal RTA, since volume depletion enhances bicarbonate reabsorption
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analysis for proximal and distal RTA
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distal: check urine pH after giving H+proximal: check urine pH after giving HCO3-
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management for RTA4
|
fludrocortisone (steroid with highest mineralcorticoid activity)
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milk alkali syndrome and its associated acid base disturbance
|
increased ingestion of absorbable calcium salt (commonly milk and antacids in patients with gastritis) causes hypercalcaemia, which then leads to nephrogenic DI and hypoparathyroidism, both of which can cause metabolic alkalosis
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|
how does Crohn's disease predispose patient to kidney stones
|
fat malabsorption chelates Ca in GIT, which allows for increased oxalate absorption, which increases risk of kidney stones (calcium oxalate is most common source of kidney stones)
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management for kidney stones btw 5mm and 7mm |
nifedipine (CCB) and tamsulosin (alpha blocker) |
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how does metabolic acidosis predispose to kidney stones
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causes increased serum calcium (leached from bones) as well as decreased citrate (normal chelates calcium)
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initial treatment for essential hypertension without comorbidities
|
thiazide diuretic
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initial treatment for essential hypertension with hyperthyroidism
|
beta blocker
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with what comorbidities should beta blocker be avoided in treatment of hypertension
|
asthma and depression
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management for hypertensive crisis
|
labetolol (alpha and beta blocker)nitroprusside (not commonly used due to need for arterial line monitoring)do not drop BP too quick, may precipitate stroke
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management for hypercalcemia
|
hydration and loop diuretic (increased renal clearance)
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histological finding for membranous nephropathy
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IgG and C3 in spike and dome pattern
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management for GI hematoma
|
conservative management (nasogastric tube to clear GI contents and parenteral nutrition). should resolve in 1-2 weeks |
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differentiate btw management of anterior and posterior uethral injur |
anterior: surgical correction posterior: divert urine with suprapubic catheter, and allow to heal spontaneously. fix any residual damage with surgery. |
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Renal tubular acidosis (RTA) associated with abnormal H+ secretion and nephrolithiasis.
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Type I (distal) RTA.RTA = Renal Tubular Acidosis |
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Renal tubular acidosis (RTA) associated with abnormal HCO3– and rickets.
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Type II (proximal) RTA.RTA = Renal Tubular Acidosis
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Renal tubular acidosis (RTA) associated with aldosterone defect.
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Type IV (distal) RTA.RTA = Renal Tubular Acidosis
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“Doughy” skin
|
Hypernatremia.
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Differential of hypervolemic hyponatremia.
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Cirrhosis, CHF, nephritic syndrome.
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Chvostek’s and Trousseau’s signs.
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Hypocalcemia.
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The most common causes of hypercalcemia.
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Malignancy and hyperparathyroidism.
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T-wave flattening and U waves.
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Hypokalemia.
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Peaked T waves and widened QRS.
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Hyperkalemia.
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|
First-line treatment for moderate hypercalcemia.
|
IV hydration and loop diuretics (furosemide).
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|
Type of ARF in a patient with FeNa < 1%.
|
Prerenal.
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|
A 49-year-old man presents with acute-onset flank pain and hematuria.
|
Nephrolithiasis.Nephrolithiasis - Kamienie nerkowe
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|
The most common type of nephrolithiasis.
|
Calcium oxalate.
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A 20-year-old man presents with a palpable flank mass and hematuria. Ultrasound shows bilateral enlarged kidneys with cysts. Associated brain anomaly?
|
Cerebral berry aneurysms (autosomal-dominant PCKD).
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Hematuria, hypertension, and oliguria.
|
Nephritic syndrome.
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Proteinuria, hypoalbuminemia, hyperlipidemia, hyperlipiduria, and edema.
|
Nephrotic syndrome.
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|
The most common form of nephrotic syndrome.
|
Membranous glomerulonephritis.
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The most common form of glomerulonephritis.
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IgA nephropathy (Berger’s disease).
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Glomerulonephritis with deafness.
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Alport’s syndrome.
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Glomerulonephritis with hemoptysis.
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Wegener’s granulomatosis and Goodpasture’s syndrome.
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|
Presence of red cell casts in urine sediment.
|
Glomerulonephritis/nephritic syndrome.
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Eosinophils in urine sediment.
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Allergic interstitial nephritis.
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Waxy casts in urine sediment and Maltese crosses (seen with lipiduria).
|
Nephrotic syndrome.
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Drowsiness, asterixis, nausea, and a pericardial friction rub.
|
Uremic syndrome seen in patients with renal failure.
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|
A 55-year-old man is diagnosed with prostate cancer. Treatment options?
|
Wait, surgical resection, radiation and/or androgen suppression.
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Low urine specific gravity in the presence of high serum osmolality.
|
Diabetes insipidus.
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|
Treatment of SIADH?
|
Fluid restriction, demeclocycline.
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|
Hematuria, flank pain, and palpable flank mass. |
Renal cell carcinoma (RCC). |
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The most common type of testicular cancer. |
Seminoma, a type of germ cell tumor.
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The most common histology of bladder cancer. |
Transitional cell carcinoma.
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Complication of overly rapid correction of hyponatremia.
|
Central pontine myelinolysis. |
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|
Salicylate ingestion occurs in what type of acid-base disorder? |
Anion gap acidosis and 1° respiratory alkalosis due to central respiratory stimulation. |
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|
Acid-base disturbance commonly seen in pregnant women. |
Respiratory alkalosis.
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|
systemic diseases that lead to nephrotic syndrome. |
DM, HTN, SLE, and amyloidosis. |
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|
Elevated erythropoietin level, elevated hematocrit, and normal O2 saturation suggest? |
RCC or other erythropoietin-producing tumor; evaluate with CT scan. |
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|
A 55-year-old male presents with irritative and obstructive urinary symptoms. Treatment options? |
Likely BPH. Options include no treatment, terazosin, finasteride, or surgical intervention (TURP). |
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|
best test to dx post-renal azotemia |
ULTRASOUND |
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|
decreased bun/crt ratio, high urine na, low osmolarity and casts, which type of azotemia? |
intra-renal azotemia
|
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|
most common drug that causes allergic nephritis
|
cephalosporins
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tx for myoglobinuria
|
high flow iv fluids to prevent crystalization
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pt at risk of oxalate crystalization
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anti-freeze ingestionvitamin C vitaminosis
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mcc of end stage renal failure |
diabetes and HTN |
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acute manifestations of end stage renal dz requiring emergency dialysis (5) |
hyperkalemiametabolic acidosisfluid overloadpericarditisencephalopathy |
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most likely cause of hyponatremia w/ high osmolality
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hyperglycemia |
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most likely cause of hyponatremia w/ normal osmolality
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high trigs
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formula to calculate osmolality
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2 x na + 10
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drug that mimics ADH fnx
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oxytocin
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most likely cause of hyponatremia w/ low osmolality in a euvolemic pt
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SIADH
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low blood osmolality and high urine osmolality. DX?
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SIADH
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tx for nephrogenic diabetes insipidus
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thiazides: na loss increases h2o reabsorptionnsaids: prostagladin inhibition impairs urine concentration ability
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electrolyte imbalance due to beta-agonist tx |
hypokalemia (more k into the cells) |
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drugs that cause hypokalemia (3)
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diuretics beta-agonists insulin |
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What is going on in HIV patient receiving tx that develops heamturia and needle-shaped crystal sediment?
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Crystal induced nephropathy2/2 Indinavir (protease inhibitor)
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What ion shifts does aldosterone cause in kidneys?
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acts on distal tubules to increase Na reabsorption, and secrete K and H ions
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What is the most common form of glomerulopathy associated with HIV?
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collapsing focal and segmental glomerulosclerosis
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What renal disease is characterized by dense deposits w/in glomerular basement membrane w/immunofluorescence positive for C3, not immunoglobulins? What is mechanism?
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Membranoproliferative glomerulonephritis, type 2persistent activation of alternative complement pathwaycaused by IgG antibodies (termed C3 nephritic factor) directed against C3 convertase of alternative complement pathway, leading to persistent complement activation & kidney damage
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How do ACE inhibitors and NSAIDs affect kidney blood flow specifically?
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Normally, angiotensin constricts glomerular efferent arteriolesprostaglandins dilate glomerular afferent arteriolethis maintains GFRthese meds blunt this
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What is Bartter's and Gitelman's syndrome? What distinguishes them from other conditions with similar presentation?
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Defective sodium and chloride reabsorption in thick ascending limb (Bartter) or distal convoluted tubule (Gitelman)presents as polyuria, polydipsia, growth & mental retardationsimilar to diuretic use and surreptitious vomiting, all have elevated plasma and renin levels, hypokalemia, and metabolic alkalosisBartter and Gitelman syndrome have elevated URINE CHLORIDE, where the others do not
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What kind of renal disease is associated with Hepatitis C?
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Membranoproliferative glomerulonephritisless freq membranous nephropathy
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What is the management of Goodpastures syndrome?
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Early / immediate plasmapheresispulmorenal dz caused by circulating anti-glomerular basement membrane antibodies, early removal of abs by emergency plasmapheresis minimizes extent of kidney injury, improves prognosis
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What is the treatment for fibromuscular dysplasia?
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percutaneous angioplasty w/stent placement
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What are the 4 main side effects of erythropoietin?
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Worsening hypertension (~30%)Headaches (~15%)Flu-like syndrome (~5%)Red cell aplasia - rare
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Muddy brown casts?
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Acute tubular necrosis
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RBC casts?
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Glomerulonephritis
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WBC casts?
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Interstitial nephritis and pyelonephritis
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Fatty casts?
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Nephrotic syndrome
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Broad and waxy casts?
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chronic renal failure
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What is MCC of nephrotic syndrome in patients with hepatitis B?
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Membranous glomerulonephritisalso associated w/membranoproliferative glomerulonephritis
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What patients typically have Focal segmental glomerulosclerosis?
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African americansHIV infection
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What condition causes hypocalcemia, hyperphosphatemia, and increased PTH?
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2ndary hyperPTH in chronic renal failure
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What is the most common nephropathy associated with carcinomas? What is a cancer that is an exception to this?
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Membranous glomerulonephritisHodgkin's lymphoma has association with minimal change dz
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What is a radiolucent kidney stone made of? What is treatment?
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Uric acid stones (10-15% of total cases)seen in low urine pH levels and hyperuricosuriatx - alkalinize urine, hydration, low-purine dietalkalinize urine to pH > 6.5 w/oral KHCO3 or K-citrate
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What is the MCC of nephrotic syndrome in adults? What is a vascular complication?
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Membranous glomerulonephritisloss of Antithrombin III increases risk of venous and arterial thrombosis, including Renval vein thrombosis (abdominal pain, fever, hematuria)
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What is the MCC of nephrotic syndrome in children? Tx?
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Minimal change disease (80%)empiric steroids (prednisone), no renal biopsy required
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What are the 3 types of renal tubular acidosis?
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Type 1 (distal RTA) - defect in hydrogen ion secretion, genetic disorder, paretns w/nephrolithiasisType 2 - decreased bicarb reabsorption in proximal tubule (Fanconi syndrome is common cause)Type 4 - defect in Na/K exchange in distal tubule, hyperkalemia, hyperchloremic acidosis (obstructive uropathy(
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15 yo w/hematuria episodes over last 2 years, electrton microscopy shows alternating areas of thinned and thickened capillary loops w/splitting of glomerular basement membranes? |
Alport syndrome also has sensorineural deafness |
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Up to what age do all children with first febrile UTI receive renal & bladder ultrasound? |
Up to 24 months
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