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IM Uworld > 15 > Flashcards

15 Flashcards

1
Q

What metabolic abnormality does diarrhea cause?

A

Non-anion gap metabolic acidosis due to bicarb loss in the intestine

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2
Q

Metabolic alkalosis with a low urine chloride (less than 20)

A

Typically due to ECF loss due to vomiting or NG suctioning which leads to increased renal chloride and sodium reabsorption and increased urinary H+ and K+ excretion
In contrast, current diuretic use will have high urine chloride
Both are saline – responsive

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3
Q

Metabolic alkalosis with high urine chloride that are saline – unresponsive

A

Bartter and Gitelman syndromes

If hypervolemic: access mineralocorticoid activity: primary hyperaldosteronism, Cushing disease, Ectopic ACTH production

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4
Q

How does obstructive uropathy present?

A

Flank pain, low volume void with or without occasional high-volume voids
If bilateral or if patient has one kidney can cause renal failure
In contrast interstitial nephritis presents with fever, rash, AKI, eosinophiluria with WBC casts

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5
Q

How to prevent uric acid stones

A

Hydration, alkalinize the urine with potassium citrate, allopurinol, low purine diet
In contrast, hydrochlorothiazide is used in calcium stones, decreases urinary calcium excretion

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6
Q

Renal changes in hypertension

A

Intimal thickening and luminal narrowing of renal arterioles with evidence of sclerosis, progressive decrease in renal blood flow and GFR

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7
Q

Renal changes in multiple myeloma

A

Obstruction of the distal and collecting tubules by large Laminated casts of Ben’s – Jones proteins, also, amyloid deposition and infiltration of kidneys by plasma cells

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8
Q

Renal changes in analgesic abuse

A

Typically tubulointerstitial disease: focal glomerulosclerosis

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9
Q

Winters formula and how to interpret

A

(1.5 x HCO3-) + 8 +/- 2 should equal PaCO2 if just compensating for metabolic acidosis
If lower than expected, there is a respiratory alkalosis as well, as seen in ASA toxicity

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10
Q

Appropriate compensation for metabolic alkalosis

A

Rise in PaCO2 by 0.7 mmHg for every 1 rise in serum HCO3-

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11
Q

acute respiratory acidosis and alkalosis compensation

A

Rise in HCO3 by 1 for every ^10 in PA CO2

Alkalosis: decrease in HCO3 by 2 for every 10 decrease in PaCO2

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12
Q

PH in aspirin toxicity

A

Typically within normal range, mixed respiratory alkalosis and metabolic acidosis
If it was a primary metabolic acidosis with respiratory compensation, pH would still be acidic, not in the normal range

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13
Q

Abnormal hemostasis in patient with chronic renal failure or is due to?

A

Platelet dysfunction: prolonged bleeding time but normal PT, PTT, platelet count
Treat with DDAVP: increases factor VIII: von Willebrand multimers
Others: cryoprecipitate, conjugated estrogens

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14
Q

Drugs associated with SIADH

What will you see on labs?

A

SSRIs, carbamazepine, NSAIDs
Low serum osmolality– less than 275, high urine osmolality – +100, elevated urine sodium concentration- +40
Dilute blood, inappropriately concentrated urine, patient should look euvolemic

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15
Q

nephrotic range proteinuria and hematuria with C3 deposits in GBM

A

membranoproliferative GN, type 2
persistent activation of alternative complement pathway
PSGN has C3 and IgG deposits

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16
Q

worsening renal function in chronic hepatitis pt, lack/minimal hematuria, RBC, protein, or granular casts, no improvement with fluids, think?

A

hepatorenal syndrome: cirrhotic pts develop splanchnic vasodilation and decreased SVR which activates RAAS and decreases renal perfusion
risk factors: GIB, SBP, vomiting, sepsis, diuretics, reduced GFR (NSAIDs)
tx: splanchnic constrictors: octreotide, NE, midodrine, albumin, liver transplant

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17
Q

Immobility, mutism, stupor, in a psych patient think?

How to treat?

A

Catatonia, treat with benzo’s – lorazepam, if refractory, ECT

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18
Q

Cauda equina versus conus medullaris syndrome

A

Cauda equina: LMN, saddle anesthesia, asymmetric motor weakness, hyporeflexia, LATE onset bowel/bladder dysfunction
conus medullaris: LMN/UMN (still part of the spinal cord) perianal anesthesia, symmetric motor weakness, hyperreflexia, EARLY bowel/bladder dysfunction

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19
Q

FAT RN, Think? How to treat?

A

TTP, treat with plasma exchange

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20
Q

Pheochromocytoma versusthyroid storm in surgical patient receiving anesthesia

A

Pheo: severe hypertension, tachycardia, pallor (catecho-vasoconstriction)
Thyroid storm: less acute, almost all patients will have pyrexia

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21
Q

Difficulty initiating swallowing, feeling of something stuck in throat, right lower lobe pneumonia, think? How to work up?

A

Oropharyngeal dysplasia – in contrast to esophageal dysphasia
Videofluoroscopic modified barium swallow: evaluate swelling mechanics, degree of dysfunction, severity of aspiration
If esophageal: should not cause difficulty initiating swallowing, would do motility studies and endoscopy

22
Q

Characteristics of uremia

A

Metabolic acidosis, fluid overload, encephalopathy, hyperkalemia, pericarditis

23
Q

Manifestations of renal failure besides uremia

A

Anemia: loss of EPO
Low calcium: kidney converts 25 to 1, 25 vit D
Osteodystrophy, secondary hyperparathyroidism, Hyperphosphatemia, hypermagnesiumia
Bleeding, infection, itching
Atherosclerosis and hypertension: MCC of death in dialysis patients is cardiac
Endocrinopathy: anovulation, low testosterone, ED

24
Q

Treatment of hyperphosphatemia in ESRD

A

Correct calcium – corrects PTH, So less phis released from bones: calcium acetate, calcium carbonate
Phosphate binders: Sevelamer, Lanthanum

25
Q

What lab values in TTP/HUS? How to treat?

A

Thrombocytopenia, PT and PTT are normal
Most cases of HUS will resolve, plasmapheresis if severe
plasmapheresis for TTP, it’s not a choice use FFP, steroids and platelet transfusions do not help

26
Q

Polycystic kidney disease presentation and associations

MCC?

A

Pain, hematuria, stones, infection, hypertension
Liver cysts, ovarian cysts, MVP, diverticulosis, cerebral aneurysms
MCC of death: renal failure from recurrent episodes of pyelonephritis and nephrolithiasis

27
Q

How do high glucose levels change sodium levels?

A

For every 100 mg/dL or a glucose above normal, there is a 1.6 mEq/L decrease in sodium
So a glucose of 500 will have a sodium that is about 8 below normal, i.e. 127 when it’s actually 135

28
Q

What can cause SIADH?

A

Any lung or brain disease: small cell cancer

SSRIs,sulfonylureas, vincristine, cyclophosphamide, TCAs

29
Q

Moderate versus severe hyponatremia presentation and treatment

A

Moderate: minimal confusion, NS and loop diuretic
Severe: lethargy, seizures, coma; hypertonic sailing, vaptans -ADH antagonist
Demeclocycline for chronic SIADH
In SIADH, NS without a diuretic makes it worse

30
Q

What conditions have a normal anion gap metabolic acidosis? Why is the gap normal?

A

RTA, diarrhea, think hard ass
Gap is normal because the chloride level rises: hyperchloremic metabolic acidosis
In contrast, increase gap in ethylene glycol or methanol poisoning or lactic acidosis as these conditions are anionic and drive down the chloride level

31
Q

RTA 1

A

Distal tubule, bicarb cannot be generated, so acid is not secreted into the tubule urine pH is above 5.5,calcium phosphate kidney stones
Amphotericin, SLE, Sjogren’s
Diagnosed with acid administration, urine will stay basic
Treat with bicarb

32
Q

RTA 2

A

Proximal, decreased ability to reabsorbed bicarb, eventually becomes so depleted urine pH will become less then 5.5, is higher at first (variable)
Amyloidosis,MM, Fanconi syndrome, acetazolamide, heavy metals
Diagnosed with giving bicarb, kidneys can’t reabsorb and urine will get more basic
Treat with thiazide diuretics which caused volume depletion which enhances bicarb re-absorbtion
Both type 1 and 2 are hypokalemic

33
Q

RTA 4

A

Diabetes, decreased amount/affect of Aldo, high urine sodium
Urine pH less than 5.5, hyperkalemia
Diagnosed with urinary salt loss, treat with fludrocortisone which is a steroid with mineral corticoid effects

34
Q

How to distinguish between diarrhea and RTA as a cause of normal anion gap metabolic acidosis

A

Calculate the urine anion gap:
UAG = Na+ minus Cl-
And RTA, less Cl- is excreted as less H+ is excreted, so +UAG
And diarrhea, kidneys compensate by excreting more H+ and Cl- (Hypochloremic metabolic acidosis) so UAG is negative

35
Q

Meds to help pass kidney stones

A

Nifedipine and tamsulosin

36
Q

Kidney stone treatment bigger than 5mm

A

Lithotripsy less than 2-3 cm if halfway up ureter, if halfway down, basket removal
Bigger than 2 cm: surgery with stent placement

37
Q

Treatment for urge incontinence

A

Anticholinergics: oxybutynin, tolterodine, solfenacin, dariferancin

38
Q

Best initial therapy for HTN

A

Thiazides, CCBs, ACEs/ARBs

39
Q

Best initial therapy for HTN crisis

A

Labetolol, nitroprusside

Then: enalapril, CCBs (diltiazem, verapamil), esmolol, hydralazine

40
Q

65-year-old with pneumonia, dramatic leukocytosis, hepatosplenomegaly, cervical lymphadenopathy, think? How to diagnose?

A

CLL
diagnosed with flow cytometry – showing a clonality of mature B cells
Do not need LN biopsy

41
Q

Acting out dreams, remember dreams think

A

REM sleep behavior disorder

42
Q

lupus anticoagulant is paradoxical how

A

is actually PRO-thrombotic (misnomer)

BUT causes a paradoxically prolonged PTT +/- PT ex vivo

43
Q

preferred treatment for specific phobias

A

behavior therapy
benzos appropriate only once in a while
eye movement desensitization and reprocessing therapy for PTSD

44
Q

MCC of congenital hypothyroidism

A

thyroid dygenesis: aplasia, hypoplasia, ectopic gland
in contrast, defective synthesis is more rare (AR)
transplacental TSH-receptor Abs (mom has Graves) leads to hyperthyroidism

45
Q

ARDS vs fluid overload/CHF

A

ARDS: bilateral pulmonary infiltrates with increased FiO2 requirement (<300 ratio)
fluid overload CHF will have JVD, cardiomegaly or S3

46
Q

exposure and outcome measured at same time (“snapshot study”) think?

A

cross-sectional study

47
Q

pathophys of digital clubbing

A

megakaryocytic skip normal fragmentation process in lung and get trapped in fingertips and release PDGF and VEGF that cause tissue hypertrophy and cap perm and vascularity

48
Q

how is bronchiectasis different from bronchitis? how to dx?

A

recurrent infections, more sputum, bacterial (instead of viral) infection, requires abx
dx: high resolution CT

49
Q

carbohydrate (lactulose, glucose) breath test used for?

A 
bacterial overgrowth (i.e. small intestine)
measures production of H+ by intestinal flora
50
Q

liver vs RH failure

A

RHF: murmur, ^JVP, b/l peripheral edema, hepatojugular reflux
liver: ascites, splenomegaly (liver may be any size) +/- asterixis, spider agiomas, etc., +/- pleural effusion

IM Uworld (16 decks)

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