UWorld 2

Question 1

Anion gap metabolic acidosis following a seizure

Answer 1

Usually from lactic acidosis. Seizures cause accelerated production of lactic acid in the muscle and reduced hepatic lactate uptake.

Post-ictal lactic acidosis is transient and usually resolves in 60-90min

Most appropriate treatment is observation and repeating the chemistry panel after 2 hours to see if the acidosis as resolved on its own. If not, it is best to look for other causes of metabolic acidosis.

Question 2

The use of bicarb in treatment of lactic acidosis or ketoacidosis

Answer 2

It’s controversial. It is recommended only in severe acute acidosis (pH below 7.2). Full correction with bicarb should not be sought. Only a sufficient amount of bicarb should be given to correct the pH to 7.2

In lactic acidosis, bicarb treatment may paradoxically depress cardiac performance and worsen the acidosis by enhancing lactate production.

Question 3

Common causes of ketosis

Answer 3

Diabetes, alcoholism, starvation

Question 4

Lipase level specificity

Answer 4

Elevations are not very specific to any one disease. They may be up in pancreatic processes but can also be elevated in DKA and other conditions

Question 5

Dopamine in the treatment of lactic acidosis.

Answer 5

Dopamine is a positive inotrope and a vasoconstrictor used in hypotension when IV fluids don’t work.

Hypotension with poor end organ perfusion may cause lactic acidosis. In this specific case, dopamine may be useful.

Question 6

Acute tubular necrosis following hypovolemic shock

Answer 6

Serum BUN/Cr less than 20. Also may see:

1) Urine osmalality of 300-350 mOsm/L (never below 300)
2) Urine Na of over 20
3) FENa over 2 percent

Prolonged hypotension from any cause can lead to ATN. Hallmark findings on UA are muddy brown granular casts consisting of renal tubular epithelial cells. This is nonspecific but very sensitive finding for ATN

Question 7

Broad casts

Answer 7

Seen in patients with chronic renal failure. The arise in the dilated tubules of enlarged nephrons that have undergone compensatory hypertrophy in response to the reduced renal mass.

Waxy casts (shiny and translucent) are also seen in chronic renal disease

Question 8

RBC casts

Answer 8

Indicative of glomerular disease or vasculitis

Question 9

WBC casts

Answer 9

Definitive evidence that urinary WBCs originate in the kidney. These are seen in cases of interstitial nephritis, pyelonephritis, etc

Question 10

Fatty casts

Answer 10

Seen in conditions causing nephrotic syndrome. Hyaline casts are composed almost entirely of protein and pass unchanged along the urinary tract; these may be seen in asymptomatic individuals and in patients with pre-renal azotemia.

Question 11

Findings seen in SIADH

Answer 11

Note - remember this could be from an underlying lung cancer

1) Serum osmolality less than 290 (water retention from high ADH)
2) Urine osmolality over 100 (inappropriately elevated)
3) Urine Na over 40
4) Normal serum creatinine, K, and acid base balance
5) Normal adrenal and thyroid function

Question 12

Patients with hyponatremia - signs and Tx

Answer 12

Patients with hyponatremia are usually ASx or have mild symptoms (forgetfulness, unstable gait) until serum sodium is below 120

ASx patients or those with mild symptoms usually respond to fluid restriction (less than 800mL per day) and/or salt tabs. Loop diuretics are also rec’d if urine osmolality is more than twice serum osmolality.

For moderate symptoms (confusion, lethargy), hypertonic saline in first 3-4h to raise Na above 120. The tx is then similar to that of mild hyponatremia

Severe symptoms (seizures, inability to communicate and/or coma) - Bolus of hypertonic saline until symptom resolution. Conivaptan is an IV renal ADH receptor antagonist that causes selective water diuresis and improves hyponatremia in SIADH. It can be given alone or in combo with hypertonic saline for moderate to severe hyponatremia

Note - D5W is hypotonic and is used for HYPERnatremia not hypo.

Question 13

Gradual correction of Na

Answer 13

Once it is above 120, gradually correct to avoid ODS. 0.5-1mEq/L/h or 10mEq/24h.

Question 14

Why is NS not adequate for effective management of SIADH?

Answer 14

Treatment requires infused fluid to have a higher electrolyte concentration than the urine (not just the plasma). NS has electrolyte concentration of nearly 300 mOsm/kg. This is only slightly higher than the serum osmolality and leads to NaCl excretion. However, the extra ADH causes more water retention, further concentrates the urine, dilutes the serum and worsens hyponatremia.

Hypertonic saline (3%) has a concentration of nearly 1025 and minimizes this effect.

Question 15

Classic signs of dehydration - special consideration for elderly patients

Answer 15

AMS, dry oral mucosa, marginally high serum lytes and hematocrit, and BUN/Cr over 20.

Elderly patients are especially prone to dehydration after various or even minor insults (minor febrile illness). The predisposing factors of elderly patients to dehydration include

1) Decreased thirst response to dehydration
2) Impaired renal Na conservation
3) Impaired renal concentration ability.

Mainstay of treatment is administration of IV sodium-containing crystalloid solutions (usually NS). Rehydration therapy in elderly patients should be undertaken with caution bc Na loading can unmask subclinical heart failure

Question 16

What causes urge incontinence?

Answer 16

Detrusor overactivity.

Sudden overwhelming or frequent need to empty bladder

Treat with lifestyle mods and bladder training (first line). Nonresponders can get antimuscarinic agents (oxybutynin) that increase bladder capacity and decrease detrusor contractions by reducing ACh activity (side effects are dry mouth, constipation and blurry vision)

Question 17

Bethanechol

Answer 17

A cholinergic agonist used for urinary retention due to neurogenic bladder. Can be used with intermittent urinary cath.

Normal PVR is less than 150 in women and less than 50 in men.

Question 18

Nephrolithiasis and Crohn Disease

Answer 18

Nephrolithiasis - flank pain and hematuria frequently with nausea and vomiting

Patients with Crohn or any other SI disorder resulting in fat malabsorption are predisposed to hyperoxaluria.

Oxalate is obtained from the diet and is a normal product of human metabolism. Symptomatic hyperoxaluria is classically the result of increased oxalate absorption in the gut.

Normally, calcium binds oxalate in the gut and prevents its absorption. In patients with fat malabsorption, calcium is preferentially bound by fat leaving oxalate unbound and free to be absorbed into the bloodstream.

Failure to adequately absorb bile salts in states of fat malabsorption also cause decreased bile salt reabsorption in the small intestine. Excess bile salts may damage the colonic mucosa and contribute to increased oxalate absorption

Increased absorption is the most common cause of symptomatic hyperoxaluria and oxalate stone formation!

Question 19

Causes of hyponatremia

Answer 19

Hypovolemic hyponatremia (this class has appropriately increased ADH)

1) Volume depletion (acute blood loss) - look for subtle ways of stating this, like recent antiplatelet or anticoagulation therapies
2) Primary adrenal insufficiency
3) GI losses (diarrhea, vomit)
4) Renal losses (diuretics)

Euvolemic (inappropriately high ADH)

1) SIADH (drugs, malignancy)
2) Primary (psychogenic) polydypsia
3) Secondary adrenal insufficiency
4) Hypothyroidism

Hypervolemic (inappropriately high ADH)

1) CHF
2) Cirrhosis
3) CKD or nephrotic syndrome

Question 20

ADH secretion regulation

Answer 20

Mainly by plasma osmolarity. However, significant hypovolemia is also a potent stimulator of ADH release from the pituitary to conserve water

Increased ADH stimulates renal water reabsorption leading to hypoNa.

The hypoNa would normally suppress further ADH release, but persistent hypovolemia overrides this suppression. Hypovolemic patients may also drink excessive water without replacing Na losses which further worsens the hypoNa.

Hypovolemia decreases effective arterial volume to the kidney which activates RAAS leading to high levels of renin, angiotensin and aldosterone

Question 21

What is the most common cause of death in dialysis patients?

Answer 21

Cardiovascular disease. It accounts for half of all deaths in this population. Infection accounts for 15-20%. Withdrawal from dialysis is 20%.

Cardiovascular disease is also number 1 cause of death in renal transplant patients.

Question 22

What are the million risk factors for cardiovascular disease in dialysis patients?

Answer 22

Risk factors not related to dialysis - A large number of patients on dialysis already have multiple risk factors

1) HTN (90%)
2) Diabetes (54%)
3) Low serum HDL (33%)
4) LVH by ECG criteria (22%)
5) CAD - about 75% of patients with total ESRD have at least a 50% narrowing of at least one coronary artery
6) Increased age - avg age of patients at start of dialysis is about 60

Additional risk factors due to ESRD and dialysis

1) ESRD - This, by itself, is an independent risk factor for cardiovascular disease
2) Anemia
3) Metabolic abnormality, particular hyperP and increased PTH
4) Increased homocysteine levels - due to impaired metabolism and decreased removal
5) Accelerated atherogenesis in dialysis patients - due to enhanced oxidant stress due to uremia and bioincompatible renal replacement therapies
6) Increased Ca intake (ca is given to correct hyperP in dialysis patients). This enhances coronary artery calcification
7) Inhibition of NO - This is a common finding in dialysis patients and can cause vasoconstriction and HTN

Question 23

Prerenal azotemia

Answer 23

This is essentially reduced renal perfusion

Decreased renal blood flow activates the RAAS. Initially, angiotensin constricts the glomerular arterioles. The efferent arteriole constricts significantly more than the afferent arteriole, which maintains intraglomerular pressure and GFR despite reduced RBF

Low RBF also causes release of prostaglandins that dilate the afferent arteriole to maintain GFR.

Continued volume depletion (diuretics) overwhelms this adaptive response, and intraglomerular pressure falls, reducing GFR despite maximal efferent arterioler constriction. Factors that may aggravate prerenal azotemia include decreased fluid intake (elderly), ACEIs (prevent action of AT on arterioles), and ASA (inhibits the effects of prostaglandins)

In prerenal azotemia, the renal tubules avidly reabsorb Na and H2O in response to a high ADH level. Urea reabsorption also increases, causing a high BUN/Cr over 20. Persistent untreated renal hypoperfusion leads to intrinsic renal failure due to ischemia. Tubules undergo acute ischemic necrosis and reabsorption of solutes is impaired. The blood urea level and BUN/Cr then decreases below 20. Other causes of intrinsic renal failure also reduce BUN/Cr. Mechanism is disease dependent

1) Age related renal functional decline (progressive loss of renal mass and thickening of GBM) causes a gradual decline in renal function
2) Hypertensive arteriolosclerosis from uncontrolled HTN
3) Nodular glomerulosclerosis in diabetic nephropathy

Question 24

Kidney stone makeup

Answer 24

75-90% are calcium oxalate stones. The crystals are envelope shaped. Small bowel disease, surgical resection or chronic diarrhea can lead to malabsorption of fatty acids and bile salts and predispose to these stones.

Calcium phosphate stones - Primary hyperparathyroidism and renal tubular acidosis

Uric acid stones - when urine is acidic or when there is increased cell turnover, thereby resulting in hyperuricemia and hyperuricosuria. dehydration is an important risk factor

Cysteine - When there is increased excretion of cysteine which is an inborn error of metabolism. Positive family history may be found

Struvite - when urine is alkaline bc of infection with urease producing bacteria (Proteus). History of recurrent UTIs may be seen

Question 25

What kind of acid-base abnormality is caused by AKI?

Answer 25

non-anion gap metabolic acidosis due to impaired H excretion, ammonia generation or bicarb reabsorption

Normal anion gap is 10-14

Can cause cause an anion gap metabolic acidosis due to retention of unmeasured uremic toxins which can also cause encephalopathy.

Question 26

What acid-base issue can lead to CNS depression?

Answer 26

Acidemia itself does not do it but the underlying cause of the acidemia can, such as hypoventilation

In a CO2 retainer (COPD), CO2 narcosis (usually seen at PaCO2 above 60) can occur

Question 27

CO2 retainer (chronic) vs acute hypercarbia

Answer 27

Acute hypercarbia has associated acidosis and low bicarb levels

Chronic CO2 retainers have normal pH and high bicarb

Question 28

Diagnosis of orthostatic hypotension

Answer 28

Within 2-5minutes of standing from supine position

1) Drop in SBP of at least 20 OR
2) Drop in DBP of at least 10

Question 29

Diuretic abuse

Answer 29

Orthostatic hypotension, abnormal serum and urine lytes (HypoNa, HypoK, HypoCl, increased urinary Na and K)

1) Normally, dehydrated patients with hypoNa are expected to have low urine Na. Elevated urine sodium suggests salt wasting (diuretic use, cerebral salt wasting, adrenal insufficiency)
2) Normally, patients with hypoK respond by reducing urine K, except in cases of renal K wasting (diuretic use, hyperaldosteronism, RTA)
3) Hypochloremia is likely a result of diuresis and contraction alkalosis

Diuretic use is sometimes abused to lose weight. Patients may gain access from family members with prescriptions

NOTE!!! Lax abuse will also cause hypotension and hypovolemia. BUT elevated urine Na means that sodium loss is through urinary tract (diuretics) and not GI tract (lax)

Question 30

Cerebral salt wasting

Answer 30

Always occurs due to neurologic insult like injury or surgery

High urine sodium (above 20) and hyponatremia

Question 31

Uncomplicated cystitis

Answer 31

Dysuria, urinary frequency, suprapubic tenderness

Commonly occurs in otherwise healthy patients and has a low risk of treatment failure. In patients with suggestive findings (dysuria, urgency), UA will confirm and patients can be treated WITHOUT a UCx. Culture is reserved for those who fail initial therapy.

Preferred treatment options include TMP-SMX (3d), Nitrofurantoin (5d), and fosfomycin (single dose).

Fluoroquinolones only if above cannot be used (sulfa allergy) or for settings with high local resistance rates

Question 32

Complicated cystitis

Answer 32

Infections associated with factors that increase risk of ABx resistance or treatment failure. Such factors include diabetes, CKD, pregnancy, immunocompromised state, or urinary tract obstruction; hospital-acquired infection; or infection associated with a procedure (cystoscopy) or indwelling foreign body (catheter or stent)

These patients should have UCx prior to therapy.

Complicated cystitis in otherwise stable patients may be managed with oral fluoroquinolones (5-14d), but more severe cases may require IV broad spectrum tx (ceftriaxone) while awaiting culture results

Do not use fluoro in pregnancy

Question 33

Pyelonephritis

Answer 33

UTI with fever and flank pain/tenderness also requires UCx prior to starting tx.

Stable patients with uncomplicated pyelo can be treated with oral ABx (usually fluoro) but unstable patients and those with complicated infection require IV ceftriaxone

Question 34

Hypochloremic metabolic alkalosis and hypokalemia

Answer 34

Vomiting

Gastric contents are rich in H, Cl, and K

Bicarb rises as result of H loss and activation of RAAS.

Giving isotonic saline and K is used to reverse these lyte abnormalities

Question 35

Acute Interstitial Nephritis

Answer 35

Causes - Drugs (penicillins, TMP-SMX, cephalosporins, rifampin, diuretics, NSAIDS). Less commonly, infectious like Legionella, Mycobacerium TB, Strep.

Clinical features

1) Maculopapular rash
2) Fever
3) New drug exposure
4) May have arthralgias

Labs

1) AKI
2) Pyuria, hematuria, WBC casts
3) Eosinophilia, urinary eosinophils***
4) Renal bx - inflammatory infiltrate, edema

Management

1) D/C offending drug
2) May or may not use systemic steroids

Symptoms usually 5d to several weeks after use of an offending agent. Drugs cause most AIN cases

Question 36

Characteristics of renal cysts

Answer 36

When a renal cyst is found on imaging, it is often possible to differentiate between a simple cyst and a malignant cystic mass based on radiological features. Incidentally discovered cysts with benign features require no additional follow-up evaluation or imaging, and the patient may be reassured.

Simple

1) Thin, smooth, regular wall
2) Unilocular
3) No septae
4) Homogenous content
5) Absence of contrast enhancement on CT/MRI
6) Usually ASx
7) No f/u needed

Malignant

1) Thick, irregular wall
2) Multilocular
3) Multiple septae, occasionally thick and calcified
4) Heterogenous content (solid and cystic)
5) Presence of contrast enhancement
6) May cause pain, hematuria, or HTN
7) Requires f/u imaging and urological evaluation for malignancy

Question 37

Uric acid stones

Answer 37

Radiolucent. Must be evaluated by CT, US, or IV pyelography

Can cause an ileus due to a vagal reaction caused by ureteral colic. Needle-shaped crystals(!!!!) on UA indicate uric acid stones.

Ileus will resolve when ureterolithiasis is treated. Stones less than 1cm may pass on own with hydration and analgesia; otherwise surgical intervention is needed.

Question 38

Gross painless hematuria

Answer 38

Common causes of hematuria in the USA include neoplasms, infections, trauma, nephrolithiasis, glomerulonephritis, and prostatic disease (BPH).

Initial assessment includes UA to r/o UTI and confirm microhematuria (at least 3 RBCs per hpf) since other things can cause red urine (myoglobinuria, beet ingestion, rifampin).

Renal disease (glomerulonephritis) is usually associated with RBC casts, proteinuria, HTN, peripheral edema, or elevated creatinine.

Nearly 80% of malignancies of the kidney, ureter, and bladder in adults presents with gross hematuria. Risk factors include age over 35, smoking history, occupational history (chemicals, dyes), and drug exposure (cyclophosphamide). These patients should have imaging (contrast CT) and cystoscopy to evaluate the bladder and urethra. Of these malignancies, bladder cancer is the most common cause of gross hematuria in patients over 35 with a smoking history

Question 39

Primary renal causes of nephrotic syndrome

Answer 39

1) Focal segmental glomerulosclerosis - African Americans and Hispanics, obesity, HIV, heroin
2) Membranous nephropathy (most common form of nephrotic syndrome associated with malignancies - usually solid tumors tho) - Adenocarcinoma (breast, lung), NSAIDs, Hep B, SLE
3) Membranoproliferative glomerulonephritis - Hep B, Hep C, lipodystrophy
4) Minimal Change Disease - NSAIDs, lymphoma (Hodgkin)
5) IgA nephropathy - URIs

Question 40

Dietary recs for patients with renal calculi

Answer 40

1) Increased fluid intake
2) Decreased sodium intake
3) Normal dietary calcium intake

Question 41

ASA intox

Answer 41

Should be suspected in patient with triad of fever, tinnitus and tachypnea

Acute salicylate toxicity leads to respiratory alkalosis by stimulating the respiratory center in the medulla and causing tachypnea (resultant low PaCO2 as CO2 is blown off). It then causes an anion gap metabolic acidosis by uncoupling oxidative phosphorylation in the mitochondria leading to anaerobic metabolism (with resultant low HCO3 from acid buildup)

Adults develop a mixed respiratory alkalosis and anion gap metabolic acidosis. A normal pH in an acid-base disturbance typically signifies mixed respiratory and metabolic disorder

Question 42

What is a common mistake in management of ASA intox?

Answer 42

People see pH close to 7.4 and do not recognize a mixed acid-base disorder. Treatment (alkalinization or dialysis) is delayed as it may seem that the patient is compensating adequately for the acidosis

Question 43

Papillary necrosis

Answer 43

Refers to ischemic necrosis of renal papillae.

Analgesic overuse is the most common cause, but diabetes, infections, urinary tract obstruction, hemoglobinopathies, cirrhosis, CHF, shock, and hemophilia can also be associated.

Question 44

Post-strep glomerulonephritis

Answer 44

Seen 10-20 days after strep throat or skin infections.

Presenting features may include periorbital swelling, hematuria, and oliguria. Patient may be hypertensive and UA shows hematuria with RBC casts and proteinuria.

Serum C3 complement levels are low

Question 45

IgA nephropathy

Answer 45

Patients typically present with hematuria after a URI and a latent period between infection and the actual onset of disease.

Development of features of glomerular disease is less than 5d. Serum complement is normal.

Question 46

What 4 conditions should you suspect in a patient with hypoK, alkalosis, and normotension?

Answer 46

1) Surreptitious vomiting - scars/calluses on dorsum of hands and dental erosions
2) Diuretic abuse - high urine Cl
3) Bartter - high urine Cl
4) Gitelman’s - high urine Cl

Question 47

Diabetic nephropathy

Answer 47

Typically occurs 10-15y after onset of type 1 and 2 diabetes. Hyperglycemia leads to microvascular damage (microangiopathy). The advanced glycation end products and other inflammatory mediators damage the glomerulus, resulting in proteinuria, overt glomerular nephropathy and ESRD.

Up to half of type 1 and 2 diabetic patients can develop initial mild proteinuria (microalbuminuria) which is 30-300mg/day. The degree of albuminuria doesnt always correlate with the severity of disease progression.

Histo changes: Mesangial expansion, GBM thickening, glomerular sclerosis

Question 48

How can you tell if proteinuria in a diabetic is due to DN or some other origin?

Answer 48

Albuminuria due to nondiabetic renal disease:
1) Onset of proteinuria less than 5 years after disease onset

2) Active urine sediment (red cells, cellular casts)
3) More than 30% reduction of GFR within 2-3mo of starting ACEI or ARB

Question 49

What is the major extracellular buffer in human blood?

Answer 49

CO2-Bicarb buffer pair. Its pK is 6.1

pH is 6.1 plus log ((HCO3)/(0.3xPaCO2)). The acid is CO2 and conj base is HCO3.

We have 3 variables. pH, HCO3, PaCO2. If given any 2, the third can be found. This is how acid-base status is determined.

Question 50

Interstitial cystitis

Answer 50

AKA painful bladder syndrome

Epi

1) More in women
2) Associated with psychiatric disorders (anxiety) and pain syndromes (fibromyalgia)

Clinical presentation

1) Bladder pain with filling, relief with voiding
2) Increased frequency and urgency
3) Dyspareunia

Dx

1) Bladder pain with no other attributable cause for at least 6 weeks
2) Normal UA

Tx

1) Not curative; focus on quality of life
2) Behavioral modification and trigger avoidance
3) Amitriptyline
4) Analgesics for exacerbations

Pain can be exacerbated by exercise, sex, and alcohol consumption

UA is obtained to exclude other causes of bladder pain (UTI, STD, cancer). Results are normal in interstitial cystitis.

Question 51

cystocele

Answer 51

Refers to bladder prolapse into anterior vaginal wall, which can cause vaginal pressure, dyspareunia, urinary frequency and urgency, and incontinence

Question 52

Renal artery stenosis

Answer 52

Common finding in older patients, with high prevalence in those with severe HTN or peripheral artery disease.

Most patients with HTN have essential HTN. However, renovascular HTN is the most common correctable cause of secondary HTN and should be suspected in all patients with resistant HTN and diffuse atherosclerosis

Patients with RAS and renovascular HTN should be managed with aggressive risk factor reduction (ASA, optimal diabetes and hyperlipid control, smoking cessation) to prevent cardiovascular disease. Patients with HTN should be managed initially with ACE or ARB.

RAS causes decreased renal blood flow and activation of the renin-angiotensin system, resulting in HTN. ACEIs reduce AT2 levels and dilate glomerular efferent arterioles
With unilateral RAS, the stenotic kidney experiences reduced RBF and a resultant fall in GFR. However, the unaffected kidney compensates for this fall in GFR as it is no longer subject to angiotensin II-induced renal vasoconstriction. With bilateral RAS, the fall in GFR generally leads to a rise in serum Cr (acceptable rise is less than 30 percent); in this setting, ACEIs are sometimes contraindicated but can still be used with close renal function monitoring due to their longterm nephroprotective effects.

Question 53

Revascularization (surgical or percutaneous angioplasty with stenting) for RAS

Answer 53

Not been proven to be better than medical therapy. It is reserved for selected patients who are intolerant or fail to achieve adequate blood pressure control with optimal medical therapy and for those with recurrent flash pulmonary edema and/or refractory heart failure due to severe HTN

Question 54

Acyclovir toxicity

Answer 54

Occurs in 5-10% of patients who receive the drug intravenously.

Acyclovir is excreted in urine mainly via glomerular filtration and tubular secretion. When the acyclovir concentration in the collecting duct exceeds its solubility, crystallization, crystalluria, and renal tubular damage may result

In most cases, this toxic complication is transient and can be prevented (as well as treated) with adequate hydration and dosage adjustment, which includes slowing the rate of IV infusion

Look for acute elevation in serum creatinine

Measuring blood levels of acyclovir is not reliable in preventing nephrotoxicity. It can still develop secondary to drug crystallization within collecting duct even when blood levels are not within established toxic range (esp during states of low intravascular volume - dehydration)

Question 55

Allopurinol pre-treatment - when?

Answer 55

May be used in lymphoma and leukemia to prevent tumor lysis-associated urate crystal nephropathy

Question 56

Pre-treatment with prednisone during what?

Answer 56

Sometimes used to minimize radiocontrast-induced allergic reactions

Question 57

When should you suspect myoglobinuria?

Answer 57

Whenever test results show large amount of blood on UA with a relative absence of RBCs on urine microscopy. Myoglobinuria is usually caused by rhabdo, which frequently leads to acute renal failure

Remember for rhabdo - it could just be a recent tonic-clonic seizure

Large amounts of myoglobin in urinary system can result in tubular injury and acute renal failure

Question 58

Manifestations of cyanide accumulation and toxicity

Answer 58

1) Skin - flushing (cherry red color), cyanosis (occurs later)
2) CNS - HA, AMS, seizures, coma
3) CV - arrhythmias
4) Resp - Tachypnea followed by respiratory depression, pulmonary edema
5) GI - abdominal pain, nausea, vomiting
6) Renal - metabolic acidosis (from lactic acidosis), renal failure

Common etiologies include combustion of carbon- and nitrogen containing compounds (wool, silk), industrial exposure (metal extraction in mining), and meds (sodium nitroprusside). CN binds to cytochrome oxidase and inhibits mitochondrial oxidative phosphorylation. cells shift to anaerobic metabolism with decreased ATP production and eventual lactic acidosis

Sodium nitroprusside is potent arterial and venous vasodilator often used for hypertensive emergencies. The drug contains 5 CN groups and undergoes rapid conversion to CN and eventually thiocyanate, which is eliminated by the kidneys. Prolonged infusion (more than 24h) at high rates (5-10 mcg/kg/min) can lead to CN toxicity, esp in patients with CKD. As a result, low infusion rates (less than 2), short term use, and close monitoring are recommended. Treatment includes sodium thiosulfate.

Question 59

Lacunar infarct

Answer 59

Small stroke from occluded penetrating arteries, usually located in deep brain structures. Usually present with sensory or motor deficits, impaired cognition, or dysarthria.

Question 60

Aminoglycoside toxicity (renal)

Answer 60

Amikacin is a common offender. Can cause acute renal failure. ESP in patient with CKD. Look for these clues:

1) Patient had pyelonephritis with a multidrug resistant organism which was prob a gram neg rod. Aminoglycosides are commonly used in this setting.
2) Urine sediment does not contain WBCs. If patient had acute interstitial nephritis (like from penicillins), eosinophils and white blood cell casts would be present in the urine.
3) Elevated FENa is not consistent with pre-renal origin of ARF

Aminoglycosides may be used in patients with renal dysfunction, but their serum levels and the patient’s renal function must be followed closely. Bc of their adverse effects and need to monitor, aminoglycosides are being used less and less, esp in elderly

Question 61

Lithium - renal issues

Answer 61

Can cause nephrogenic DI. Treat with salt restriction and D/C lithium

Question 62

Familial hypocalciuric hypercalcemia

Answer 62

Patient with mild, asymptomatic hypercalcemia and normal renal function. In light of a high-normal PTH level and low urinary calcium excretion, this presentation is consistent with FHH.

FHH is a benign autosomal DOMINANT disorder caused by a mutation of the calcium-sensing receptor. Normally, high-normal calcium levels suppress PTH by the parathyroid glands, but in FHH higher Ca concentrations are required to suppress PTH release. Also, the defective calcium sensing receptor leads to increased reabsorption of calcium in renal tubules

In the evaluation of hyperCa, an elevated (or inappropriately normal) PTH level suggests either primary hyperparathyroid or FHH. However, patients with primary hyperparathyroid have increased urinary calcium excretion due to excessive mobilization of calcium from bones, whereas patients with FHH usually have very low urinary calcium levels (less than 100mg in 24h). Urinary calcium/creatine clearance ratio…

UCCR is (CaUrine/CaSerum)/(CrUrine/CrSerum). UCCR is usually less than 0.01 in FHH compared to over 0.02 in primary hyperparathyroidism

Most patients with FHH are asymptomatic, although potential complications include pancreatitis and chondrocalcinosis. In the absence of complications, no specific tx is required.

Question 63

Renal Cell Carcinoma

Answer 63

1) Flank pain, hematuria, and a palpable abdominal renal mass
2) Scrotal varicocele (L sided)
3) Paraneoplastic symptoms - anemia, erythrocytosis, thrombocytosis, fever, hypercalcemia, cachexia

Unilateral varicocele that fail to empty when a patient is recumbent raise suspicion for an underlying mass pathology such as RCC that obstructs venous flow. CT of abdomen is the most sensitive and specific test for diagnosis RCC.