00 Renal&genitourinary Disorders Chp 04. Usmle Step 2 Step Up

Front 1

Proximal convoluted tubule (cortex)
Fxn: Absrpt&Secrete

Back 1

- all glucose, bicarbonate (HCO3-), amino acids, and metabolites are reabsorbed
- 2/3 Na+ is reabsorbed; Cl- and H2O are reabsorbed passively along osmotic gradient

Hint 1

Organic acids (e.g., uric acid, etc.) and bases are secreted into tubules

Front 2

Descending loop of Henle (medulla)
Fxn: Absrpt&Secrete

Back 2

- water reabsorption and concentration of tubule fluid

Hint 2

only segment of the loop that is permeable to H2O

Front 3

Ascending loop of Henle (medulla)
Fxn: Absrpt&Secrete

Back 3

Active reabsorption of Na+, Cl-, and potassium (K+) by Na+/K+/Cl-cotransporter
Reabsorption of Mg2+, Ca2+, and K+ through paracellular diffusion

Front 4

Distal convoluted tubule (cortex)
Fxn: Absrpt&Secrete

Back 4

Na+ and Cl- reabsorbed by Na+/Cl- transporter
Ca+ reabsorbed via parathyroid hormone activity
impermeable to water

Front 5

Collecting tubule (cortex) and duct (medulla)
Fxn: Absrpt&Secrete&Hormone

Back 5

Principal cells drive Na+ reabsorption and K+ secretion when stimulated by aldosterone
Intercalated cells secrete H+ and reabsorb K+
Antidiuretic hormone (ADH) drives H2O reabsorption

Front 6

H/P=Flank paiN, chills, nausea, vomiting, urinary frequency, dysuria, urgency; fever (>101.5°F/38°C), Costovertebral tendernesS

Back 6

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

Hint 6

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

Front 7

H/P = Acute severe colicky flank paiN that may extend to inner thigh or genitals, nausea, vomiting, dysuria; possible gross hematuria

Back 7

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

Hint 7

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

Front 8

Nephrolithiasis, Radiopaque
+Idiopathic hypercalciuria, small bowel diseases

Back 8

Calcium oxalate

Hint 8

Most patients have no identifiable cause

Front 9

Nephrolithiasis, Radiopaque
+Urinary tract infection

Back 9

Struvite (Mg-NH4-PO4)

Hint 9

More common in women; may form staghorn calculi

Front 10

Nephrolithiasis, Radiopaque
+Hyperparathyroidism, renal tubular acidosis

Back 10

Calcium phosphate

Front 11

Nephrolithiasis, Radiolucent
+Chronic acidic/concentrated urine, chemotherapeutic drugs, gout

Back 11

Uric acid

Hint 11

Treat by alkalinizing urine

Front 12

Nephrolithiasis, Radiopaque

Back 12

Cystine

Hint 12

May form staghorn calculi

Front 13

H/P = possibly asymptomatic; dull or intermittent flank pain with history of UTI; anuria suggests significant bilateral ureteral obstruction

Back 13

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

Hint 13

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)

Front 14

H/P = asymptomatic until adulthood (dominant form); flank pain, chronic UTI, gross hematuria; large, palpable kidneys; possible hypertension; symptoms exacerbated by cyst rupture

Back 14

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

Hint 14

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

Front 15

H/P = flank pain, weight loss; abdominal mass, HTN, fever, hematuria

Back 15

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

Hint 15

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

Front 16

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

Back 16

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

Hint 16

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

Front 17

H/P = varies with pathology; oliguria and gross hematuria (evidenced by brown urine) are common

Back 17

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.

Hint 17

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

Front 18

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

Back 18

Postinfectious glomerulonephritis
Sequelae of systemic infection (most commonly streptococcus)

Hint 18

treatment=Self-limited, supportive treatment (- edema & hypertension)

Front 19

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

Back 19

IgA nephropathy (Berger's disease)
may be related to infection; deposition of IgA antibodies in mesangial cells

Hint 19

treatment=Occasionally self-limited; give ACE-I and statins for persistent proteinuria; give corticosteroids if nephrotic syndrome develops

Front 20

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

Back 20

Goodpasture's syndrome
Deposition of antiglomerular and antialveolar basement membrane antibodies

Hint 20

treatment=Plasmapheresis, corticosteroids, immunosuppressive agents; can progress to renal failure

Front 21

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

Back 21

Alport's syndrome
Hereditary defect in collagen IV in basement membrane

Hint 21

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

Front 22

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

Back 22

Idiopathic crescentic glomerulonephritis
Rapidly progressive renal failure from idiopathic causes or associated with other glomerular diseases or systemic infection

Hint 22

Poor prognosis with rapid progression to renal failure; corticosteroids, plasmapheresis, and immunosuppressive agents may be helpful; renal transplant frequently required

Front 23

H/P=Possibly asymptomatic, possible hypertension or renal failure; may develop nephrotic syndrome
lab=ANA, anti-DNA antibodies; hematuria, and possible proteinuria on urinalysis

Back 23

Lupus nephritis (mesangial, membranous, focal proliferative, and diffuse proliferative types)
Complication of systemic lupus erythematosus involving proliferation of endothelial and mesangial cells

Hint 23

Treatment=Corticosteroids or immunosuppressive agents can delay renal failure; ACE-I and statins help reduce proteinuria

Front 24

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

Back 24

Wegener's granulomatosis
Similar to crescentic disease with addition of pulmonary involvement; granulomatous inflammation of airways and renal vasculature

Hint 24

treament=Corticosteroids, cytotoxic agents; variable prognosis

Front 25

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

Back 25

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

Hint 25

Treatment = varies with pathology; frequently includes diuretics and dietary salt and protein restriction

Front 26

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

Back 26

Minimal change disease
Idiopathic; may involve flattening of foot processes on basement membrane

Hint 26

Treatment=Corticosteroids, cytotoxic agents

Front 27

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

Back 27

Focal segmental glomerular sclerosis
Frequently idiopathic or associated with drug use or HIV; segmental sclerosis of glomeruli

Hint 27

Treatment=Corticosteroids, cytotoxic agents, ACE-I, statins; progressive cases that require renal transplant (uncommon) frequently have recurrence

Front 28

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

Back 28

Membranous glomerulonephritis
Idiopathic or associated with infection, systemic lupus erythematosus, neoplasm, or drugs; thickening of basement membrane

Hint 28

treatment=Corticosteroids, cytotoxic agents, ACE-I, statins; variable rates of renal failure and renal vein thrombosis (requires anticoagulation)

Front 29

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

Back 29

Membranoproliferative glomerulonephritis
Idiopathic or associated with infection or autoimmune disease; thickening of basement membrane

Hint 29

treatment=Corticosteroids combined With either aspirin or dipyridamole may delay progression to renal failure

Front 30

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

Back 30

Diabetic nephropathy (diffuse, nodular)
Basement membrane and mesangial thickening related to diabetic vascular changes

Hint 30

treatment=Treat underlying DM, dietary protein restriction, ACE-I, tight blood pressure control

Front 31

/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

Back 31

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.

Hint 31

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

Front 32

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)

Back 32

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)

Hint 32

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

Front 33

nonanion gap metabolic acidosis
urine>5.3, low K+
radiology=possible stones
cause=Idiopathic, autoimmune diseases, drugs, chronic infection, nephrocalcinosis, cirrhosis, SLE, obstructive nephropathy

Back 33

Renal Tubular Acidosis, Distal (Type 1)
Impaired H+ secretion leading to secondary hyperaldosteronism

Hint 33

Treatment=Oral HCO3-, K+, thiazide diuretic

Front 34

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

Back 34

Renal Tubular Acidosis,
Proximal (Type 2)
HCO3- reabsorption

Hint 34

Treatment=Oral HCO3-, K+; thiazide or loop diuretic

Front 35

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

Back 35

Renal Tubular Acidosis,Low Renin/Aldosterone (Type 4)
1st or 2nd aldosterone deficiency

Hint 35

Treatment=Fludrocortisone, K+ restriction

Front 36

acid-base disturbances
Diarrhea, diabetic ketoacidosis, lactic acidosis, renal tubular acidosis

Back 36

normal anion gap Metabolic acidosis

Hint 36

PCO2 = 1.5 [HCO3-] + (8 ± 2)
If PCO2 <expected, then additional respiratory alkalosis
If PCO2 >expected, then additional respiratory acidosis

Front 37

acid-base disturbances
MUD PILES: Methanol, Uremia, Diabetic ketoacidosis, Paraldehyde, Isoniazid (INH), Lactic acidosis, Ethanol, Salicylates

Back 37

anion-gap Metabolic acidosis

Hint 37

PCO2 = 1.5 [HCO3-] + (8 ± 2)

Front 38

acid-base disturbances
Vomiting, diuretics, Cushing's syndrome, hyperaldosteronism, adrenal hyperplasia

Back 38

Metabolic alkalosis

Hint 38

If PCO2 >50, then additional respiratory acidosis
If PCO2 <40, then additional respiratory alkalosis

Front 39

acid-base disturbances
COPD, respiratory depression, neuromuscular diseases

Back 39

Respiratory acidosis

Hint 39

acute:
pH ^ = 1/10x0.08x(PCO2-40)
chornic:
pH^=1/10x0.03x(PCO2-40)

Front 40

acid-base disturbances
Hyperventilation, high altitude, asthma, aspirin toxicity, pulmonary embolism

Back 40

Respiratory alkalosis

Hint 40

acute:
pH ^ = 1/10x0.08x(PCO2-40)
chornic:
pH^=1/10x0.03x(PCO2-40)

Front 41

corrected, HCO3- is different from measured value
normal:
+ :
- :

Back 41

Mixed disorder
normal: solitary high anion-gap acidosis
+ : metabolic alkalosis with high anion-gap acidosis
- : nonanion-gap acidosis with high anion-gap acidosis

Hint 41

Corrected HCO3- = measured anion gap - normal anion gap + measured HCO3-(for which 12 = value of normal anion gap)

Front 42

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).

Back 42

Hypernatremia
Serum Na+ >155 mEq/L
Complications = seizures, CNS damage; too rapid hydration can cause cerebral edema

Hint 42

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

Front 43

H/P = polydipsia, polyuria, signs of dehydration

Back 43

Diabetes insipidus (DI)
Disorders of ADH-directed water reabsorption leading to dehydration and hypernatremia
Central: failure of posterior pituitary to secrete ADH; can result from idiopathic causes, cerebral trauma, pituitary tumors, hypoxic encephalopathy, or anorexia nervosa
Nephrogenic: kidneys do not respond to ADH; can result from hereditary renal disease, lithium toxicity, hypercalcemia, or hypokalemia

Hint 43

Labs =
Increased Na+
Low urine osmolality with large urine volume
Water deprivation test
2- to 3-hr water deprivation followed by ADH administration
Normal response is no change in urine osmolality
Shows normal result in nephrogenic type
Increased urine osmolality after ADH administration in central type
Radiology = CT with contrast or MRI may show pituitary tumor
Treatment =
Treat underlying condition
Central DI: desmopressin (DDAVP) given as ADH analogues
Nephrogenic DI: salt restriction, increased H2O intake; thiazide diuretics may reduce fluid loss (cause mild hypovolemia through activity at distal convoluted tubule to induce increased water absorption at proximal tubule); treat underlying condition (stop medications, treat tumor or renal disease)

Front 44

H/P = confusion, nausea, weakness, decreased consciousness
renal H2O retention (e.g., congestive heart failure, syndrome of inappropriate ADH secretion [SIADH]), thiazide diuretics (i.e., salt wasting), hyperglycemia (i.e., osmotic hyponatremia), or high fluid intake

Back 44

Hyponatremia
Serum Na+ <135 mEq/L
To calculate [Na1] that will result from correction of hyperglycemia, add 1.6 mEq/L Na+ for every 100 mg/dL glucose >100 mg/dL.
Complications = CNS damage; overly rapid correction with hypertonic saline can cause central pontine myelinolysis

Hint 44

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)

Front 45

H/P = chronic symptoms of hyponatremia
Labs = serum hypo-osmolality (<280 mOsm/kg) with urine osmolality >100 mOsm/kg; urine Na+ >20 mEq/L

Back 45

Syndrome of inappropriate ADH secretion (SIADH)
Nonphysiologic release of ADH, resulting in hyponatremia
Caused by CNS pathology, sarcoidosis, paraneoplastic syndromes, psychiatric drugs, major surgery, pneumonia, or human immunodeficiency virus (HIV

Hint 45

Treatment = fluid restriction; loop diuretics and hypertonic saline if symptomatic; demeclocycline may help maintain normal Na+ levels

Front 46

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.

Back 46

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.

Hint 46

(ECG) = tall, peaked T waves
Treatment = calcium gluconate (treats cardiac effects but does not change K+ level), NaHCO3, or glucose with insulin to encourage K+ uptake by cells; sodium polystyrene sulfonate binds K+ and removes it through the GI tract; dialysis may be required in severe cases

Front 47

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).

Back 47

Hypokalemia
Serum K+ <3.5 mEq/L
Complications = overly rapid replacement can lead to arrhythmias

Hint 47

ECG = T-wave flattening, ST depression, U waves
Treatment = treat underlying disorder; give oral or IV KCl (10–20 mEq/hr)

Front 48

H/P = deep pain, easy fractures, possible nephrolithiasis, nausea, vomiting, constipation, weakness, mental status changes, polyuria
CHIMPANZEES: Calcium supplementation; Hyperparathyroidism; Immobility; Milk-alkali syndrome; Paget's disease; Addison's disease; Neoplasms; Zollinger-Ellison syndrome; Excess vitamin A; Excess vitamin D; Sarcoidosis.

Back 48

Hypercalcemia
Serum Ca2+ >10.5 mg/dL
“bones” (fractures), “stones” (nephrolithiasis), “groans” (GI symptoms), and “psychiatric overtones” (changes in mental status).

Hint 48

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
Treatment = treat underlying disorder; hydration; calcitonin and bisphosphonates in cases of excess bone reabsorption; glucocorticoids decrease intestinal absorption in severe cases; surgery indicated for hyperparathyroidism

Front 49

family history of hypercalcemia, low urine Ca2+, and absence of osteopenia, nephrolithiasis, and mental status changes

Back 49

familial hypocalciuric hypercalcemia
genetic disorder of Ca2+-sensing receptors

Front 50

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

Back 50

Hypocalcemia
Serum Ca2+ <8.5 mg/dL

Hint 50

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
Treatment = treat underlying disorder; oral Ca2+ or IV Ca2+ for severe symptoms; vitamin D supplementation, if necessary

Front 51

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

Back 51

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

Hint 51

Treatment = amoxicillin, trimethoprim-sulfamethoxazole (TMP-SMX), or fluoroquinolones for 3 days; relapsing infection should be treated for 14 days
Perform a workup for sexually transmitted urethritis in any man with a suspected UTI because the symptoms may appear similar.

Front 52

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

Back 52

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

Hint 52

Radiology = cystoscopy is important for visualization of lesions, urine specimen collection, and lesion biopsy; pelvic CT, MRI, or IVP may detect mass
Treatment = transurethral cystoscopic resection for superficial tumors; partial or total cystectomy for more invasive tumors; adjuvant intravesical chemotherapy and radiation therapy commonly utilized; regional radiation therapy and systemic chemotherapy for large tumors and metastatic disease

Front 53

H/P = dysuria, frequency, urgency, Burning urination; purulent urethral discharge seen with N. gonorrhoeaE

Back 53

Urethritis
Infection of urethra caused by sexually transmitted Neisseria gonorrhoeae or Chlamydia trachomatis
Complications = urethral strictures, frequent reinfection when sexual partners not treated

Hint 53

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
Treatment = single dose ceftriaxone with doxycycline or azithromycin used to treat both possible infections simultaneously; treat sexual partners; report of cases to public health office may be required

Front 54

H/P = perineal pain, dysuria, frequency, urgency; fever, tender prostate on digital rectal examination

Back 54

Prostatitis
Inflammation of prostate from unknown cause or as complication of UTI

Hint 54

Labs = may be suggestive of UTI; possible hematuria; white blood cells seen in prostatic secretions
Treatment = TMP-SMX (frequently for 4–6 wks); treat for sexually transmitted diseases (STDs) in sexually active males

Front 55

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

Back 55

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.

Hint 55

Labs = possible mild increase in prostate-specific antigen (PSA); rule out infection (urinalysis), cancer (biopsy), and renal failure (serum electrolytes, BUN, Cr)
Radiology = transrectal US shows enlarged prostate
Treatment = α1-receptor blockers (e.g., terazosin, etc.) and 5 α-reductase inhibitors (e.g., finasteride, etc.) improve symptoms; surgery needed for refractory cases (i.e., transurethral resection of prostate [TURP]); transurethral needle ablation may be performed in men who are poor surgical candidates

Front 56

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

Back 56

Prostate cancer
Adenocarcinoma occurring in peripheral zone of prostate
Risk factors = increased age, family history, high-fat diet, prostatitis
Complications = incontinence and impotence are common with radical prostatectomy

Hint 56

Radiology = transrectal US shows irregular prostate; bone scan, chest x-ray (CXR), and CT may detect metastases
Treatment =
Good prognosis with early treatment
Radical retropubic, perineal, laparoscopic, or robotic prostatectomy; retropubic approach used for more extensive tumors
Radiation therapy via external beam radiation or brachytherapy (i.e., implantation of radioactive seeds in prostate) may be used in early tumors in place of surgery
Follow up with PSA posttreatment to monitor for metastases and recurrence
Antiandrogen therapy (i.e., hormone therapy or orchiectomy) with chemotherapy can be used to improve symptoms in high-grade or metastatic disease
Older men may not be treated because tumors are frequently slow-growing

Front 57

H/P = epididymal pain relieved by Supporting scrotuM, dysuria; scrotal tenderness, and induration

Back 57

Epididymitis
Inflammation of epididymis associated with testicular inflammation
Caused by prostatitis, STDs (especially Chlamydia), urinary reflux

Hint 57

Labs = urinalysis shows white blood cells; urine culture with specialized culture media may help diagnose STDs
Treatment = ceftriaxone and doxycycline or fluoroquinolone; NSAIDs and scrotal support for noninfectious causes

Front 58

H/P = very painful and swollen testes, nausea, vomiting; fever, Testes displaced superiorlY, mass in spermatic cord may be felt, absent cremasteric reflex

Back 58

Testicular torsion
Twisting of spermatic cord leading to vascular insufficiency of testes
Complications = testicular ischemia or infarction without prompt treatment

Hint 58

Radiology = US may show torsion
Treatment = emergent surgical reduction of torsion within several hours of onset; manual detorsion can be attempted before surgery (may be difficult to determine correct direction to rotate); testes attached to scrotal wall (i.e., orchiopexy) to prevent recurrence

Front 59

H/P = painless testicular mass, possible gynecomastia or lower abdominal pain; GI or pulmonary symptoms can result from metastases

Back 59

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

Hint 59

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
Radiology = US may detect dense testicular mass; CXR or CT can detect extent of tumor and metastases
Treatment = radical orchiectomy with/without chemotherapy and radiation therapy for early stage seminomas; radical orchiectomy with/without retroperitoneal lymph node dissection or chemotherapy for early stage nonseminomas; chemotherapy and possible postchemotherapy debulking performed for more extensive disease

Front 60

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

Back 60

Infertility (male)
Inability of couple to achieve pregnancy following 1 yr of normal sexual activity without use of contraception

Hint 60

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
Treatment = treat underlying condition; surgical correction of anatomic defects, hormone therapy, education in sexual technique, or in vitro fertilization may help in achieving pregnancy

Front 61

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

Back 61

Impotence
Inability to obtain or maintain erection during sexual activity
Caused by deinnervation, vascular insufficiency, endocrine abnormalities, psychological concerns, drugs, or alcoholism

Hint 61

Labs = possible decreased testosterone, decreased luteinizing hormone (LH), or increased prolactin
Treatment = treat underlying condition; stop offending agents; psychological counseling and sexual education; papaverine injection or oral phosphodiesterase-5 inhibitors may help maintain penile vascular engorgement

Front 62

H/P = weight loss, nausea, vomiting, dysuria, polyuria; palpable abdominal or flank mass, hypertension, fever

Back 62

Wilms tumor
Malignant tumor of renal origin presenting in children <4 yr of age
Risk factors = family history, neurofibromatosis, other genitourinary abnormalities

Hint 62

Labs = measure BUN, Cr, and CBC to assess kidney function
Radiology = CT or US shows renal mass; CXR and CT can show metastases
Treatment = surgical resection or nephrectomy, chemotherapy, and possible radiation; good prognosis without extensive involvement

Front 63

H/P = defect apparent on examination and during urination

Back 63

Urethral displacement
Urethral opening on top (i.e., epispadias) or underside (i.e., hypospadias) of penis associated with other penile anatomic abnormalities
Complications = may contribute to infertility

Hint 63

Treatment = surgical correction (ideally during infancy), do not circumcise before surgical correction

Front 64

H/P = almost always nonpathologic; unusual findings in history and examination should prompt further workup

Back 64

Enuresis
Nocturnal bedwetting seen in young children
Seen in all children; most cases resolve by age 4 yr; rare cases associated with disease

Hint 64

Treatment = education, enuresis alarms, dietary modifications (no fluids near bedtime); desmopressin or imipramine used in refractory cases

Front 65

H/P = empty scrotal sac, testes inconsistently found in scrotum

Back 65

Undescended testes (cryptorchidism)
Testes lying in abdominal cavity and not consistently located within scrotum
Complications = testicular cancer (risk reduced but not eliminated by surgical correction), infertility

Hint 65

Treatment = exogenous hCG administration or orchiopexy before age 5 yr to reduce risk of cancer and allow testicular development