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00Step 2 > Medicine UWorld > Flashcards

Medicine UWorld Flashcards

1
Q 
what is dx in pt:
young - middle aged F
chronic WIDESPREAD PAIN
fatigue, impaired concentration
tenderness at trigger points (ex mid trapezius, costochondral junction)
A

Fibromyalgia

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2
Q

how do you dx fibromyalgia

A

> = 3 months of symptoms with widespread pain index or symptom severity score

NORMAL lab studies

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3
Q

what is dx in pt with:
proximal muscle WEAKNESS (difficulty climbing stairs); usually symmetric
pain is mild/absent

A

polymyositis

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4
Q

how do you dx polymyositis

A

ELEVATED MUSCLE ENZYMES (ex Creatinine kinase, Aldolase, AST)

autoantibodies (ANA, anti-Jo-1)

Biopsy: Endomysial infiltrate, patchy necrosis

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5
Q

what is dx in pt:
>50yo
systemic signs and symptoms
STIFFNESS > pain in shoulders, hip girdle, neck
associated with giant cell temporal arteritis

A

polymyalgia rheumatica

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6
Q

how do you dx polymyalgia rheumatica

A

ELEVATED ESR
ELEVATED C-REACTIVE PROTEIN

rapid improvement with glucocorticoids

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7
Q 
what is dx in pt with:
systemic symptoms
skin findings (lived reticularis, purport)
kidney disease
abdominal pain
muscle aches or weakness
A

polyarteritis nodosa

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8
Q

which lab value is usually elevated in polyarteritis nodosa

A

CRP

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9
Q

what is dx in pt with:
pain and swelling in wrists and small joints of hands
morning stiffness
systemic symptoms

A

rheumatoid arthritis

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10
Q

which lab value correlates with rheumatoid arthritis disease activity

A

CRP

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11
Q

what is dx in pt:
Male 15-35yo
elevated ESR and CRP
back pain that worsens with rest and improves with activity

A

seronegative spondyloarthropathies (eg ankylosing spondylitis)

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12
Q

describe selection of asthma treatments based on asthma severity x4

A

Intermittent:
SABA use <=2 days/week
Night <=2 times/month
Step 1 therapy

Mild persistent:
SABA > 2 days/week
Night 3-4 times/month
Step 2 therapy

Moderate persistent:
SABA use daily
Night >1 time/week but not nightly
Step 3 therapy

Severe persistent:
SABA use throughout the day
Night 4-7 times/week
Step 4 or 5 therapy

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13
Q

what are steps 1-6 in asthma therapy

A

Step 1:
SABA PRN

Step 2:
low-dose inhaled corticosteroid

Step 3:
low-dose inhaled corticosteroid + LABA
OR
medium-dose inhaled corticosteroid

Step 4:
medium-dose inhaled corticosteroid + LABA

Step 5:
High-dose inhaled corticosteroid + LABA
AND
consider Omalizumab for pts w/ allergies

Step 6:
High-dose inhaled corticosteroid + LABA + oral corticosteroid
AND
consider Omalizumab for pts w/ allergies

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14
Q

which asthma treatment has increased evidence of mortality when used as mono therapy, and how is that better managed

A

LABA mono therapy has evidence of increased mortality and treatment failure

the addition of LABA is indicated only in combination with an inhaled corticosteroid

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15
Q

if a short-acting beta-2 agonist (SABA) is not adequately controlling asthma symptoms, what is the next most likely addition to the pt’s treatment regimen

A

a daily controller medication, an inhaled corticosteroid in addition to the SABA

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16
Q

what is likely dx in immunocompromised pt with CT scan showing pulmonary nodules and surrounding ground-glass opacities (“halo sign”)

A

invasive aspergillosis

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17
Q

what is treatment for invasive aspergillosis

A

usually a combination of voriconazole and echinocandin (caspofungin)

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18
Q

what is dx in pt with no history of alcohol or gallstones presenting with acute pancreatitis, possibly with a recent vascular procedure

A

cholesterol emboli causing acute pancreatitis via vessel occlusion

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19
Q

what is dx in pt with skin, kidney, and GI manifestations of:
livedo reticularis (reticulated, mottled, discolored skin), blue toe syndrome
AKI
pancreatitis, mesenteric ischemia

A

cholesterol emboli

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20
Q

how do you manage acute pancreatitis from uncorrectable causes (ischemia, atheroembolism)

A

manage conservatively with analgesics and IV fluids

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21
Q

what is the dx in a pt with triad of nongonococcal urethritis, asymmetric oligoarthritis, and conjunctivitis

A

reactive arthritis

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22
Q

what are 2 common findings of reactive arthritis aside from its triad?

A

mucocutaneous lesions

enthesitis (Achilles tendon pain)

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23
Q

what does synovial fluid usually show in reactive arthritis

A

usually sterile

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24
Q

what is first line treatment for acute phase reactive arthritis

A

NSAIDs

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25
Q

what additional symptoms other than the triad would you look for in a pt where you suspect gonococcal septic arthritis from reactive arthritis

A

fever
lack of mouth ulcers and enthesitis (achilles)

synovial fluid futures are negative in 50% of pts, so you can’t always rely on that

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26
Q

what is dx in triad of polyarthralgias, tenosynovitis, and vesiculopustular skin lesions

A

disseminated gonococcal infection

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27
Q

what is dx in pt presenting <24 hrs after blunt thoracic trauma with:
tachypnea, tachycardia, HYPOXIA
RALES or decreased breath sounds
normal pulmonary capillary wedge pressure
CT or CXR showing patchy alveolar infiltrate NOT RESTRICTED BY ANATOMICAL BORDERS

A

pulmonary contusion

may not be clinically evident immediately

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28
Q

what is management of pulmonary contusion

A

pain control

pulmonary hygiene (nebulizer treatment, chest PT)

supplemental oxygen and ventilatory support

(large doses of IV fluids may worsen pulmonary edema)

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29
Q 
what is dx in pt with:
blunt thoracic trauma
hypotension, tachycardia, +/- arrhythmia
\+/- signs of heart failure
abnormal pulmonary capillary wedge pressure
A

myocardial contusion

may be asymptomatic in most cases

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30
Q

how does acute pancreatitis cause ARDS

A

increased serum concentrations of pancreatic enzymes (ex phospholipase A2) can cross the pulmonary capillaries,
damage lungs
activate inflammatory cascade

ultimately leads to:
leakage of bloody and proteinaceous fluid into alveoli
alveolar collapse 2/2 loss of surfactant
diffuse alveolar damage

31
Q

what is the best way to improve mortality in pts with ARDS on mechanical ventilation

A

low tidal volume ventilation (LTVV)

this results in lower pulmonary pressures, which decreases the likelihood of over distending alveoli

32
Q

what is the setting of a low tidal volume ventilation

A

LTVV = 6 mL/kg of ideal body weight

33
Q

why are higher tidal volumes in ARDS harmful

A

may result in elevated pulmonary pressures due to work of forcing larger volumes into stiff lungs (decreased compliance), leading to increased alveolar distension

34
Q

what is the oxygenation goal for mechanical ventilation in ARDS

A

SpO2 >88% (peripheral saturation)

PaO2 55-80mmHg (arterial partial pressure)

35
Q

which acid/base abnormality will potentially develop (but permissive and not associated with increased mortality) in pts on LTVV

A

LTVV strategies are associated with hypercapnia, and therefore
respiratory acidosis

36
Q

what drug usage commonly causes injury that mimics viral hepatitis

A

isoniazid

37
Q

what is the most common composition of kidney stone

A

calcium oxalate

38
Q

why might small bowel disease, surgical resection, or chronic diarrhea lead to formation of calcium oxalate stones

A

malabsorption of fatty acids and bile salts

fat malabsorption leads to increased absorption of oxalic acid because the unabsorbed fatty acids chelate calcium, making oxalic acid free for absorption

39
Q

which kidney stone is common in primary hyperparathyroidism and renal tubular acidosis

A

calcium phosphate

40
Q

which kidney stone is common in increased cell turnover and dehydration

A

uric acid stones

increased cell turnover causes hyperuricemia and hyperuricosuria

41
Q

which kidney stone is common in alkaline urine from urease-producing bacterial infection

A

struvite stones

42
Q

what is dx in pt with:
elevated aminotransferases (often >1000)
encephalopathy
INR >= 1.5 (synthetic liver dysfunction)

A

acute liver failure

43
Q

which drug is a common cause of acute liver failure, that may be potentiated by chronic alcohol use

A

acetaminophen

44
Q

how does liver toxicity 2/2 acetaminophen overdose occur

A

toxicity results from overproduction of the toxic metabolite N-acetyl-p-benzoquinone imine (NAPQI),
which leads to hepatic necrosis

NAPQI is normally safely detoxified through glucuronidation in the liver, but this pathway becomes overwhelmed in overdose

chronic alcohol use is thought to potentiate this toxicity by depleting glutathione lives and impairing glucuronidation process

45
Q

what is an effective antidote for acetaminophen overdose, and what is its MOA

A

N-acetylcysteine

it increases glutathione levels and binds to NAPQI, the toxic metabolite of acetaminophen (normally detoxified by glucuronidation in liver)

46
Q

what are aminotransferase levels in cirrhosis

A

normal to moderately elevated aminotransferase levels

47
Q

what causes right-to-left intrapulmonary shunting and an extreme V/Q mismatch, where hypoxemia does not correct increased concentrations of inspired oxygen

A

pneumonia

48
Q

what is pathogenesis of pneumonia causing lung problems

A

in consolidative pneumonia, the alveoli become filled with inflammatory exudate
marked impairment of alveolar ventilation in that portion of the lung
results in R–> L intrapulmonary shunting, which describes perfusion of lung tissue in absence of alveolar ventilation (V/Q mismatch)
unable to correct the hypoxemia even if you increase the concentration of inspired oxygen (FiO2) because V = 0

49
Q

what does R–> L intrapulmonary shunting mean

A

perfusion of lung tissue in absence of alveolar ventilation

V/Q mismatch

50
Q

diffuse alveolar hypoventilation can be caused from what 2 physiologic alterations

A

decrease in either tidal volume or respiratory rate

51
Q

what is increased pulmonary capillary wedge pressure indicative of

A

increased LA pressure,

a sign of L heart failure

52
Q

what is dx in pt with painful, visible tophi +/- chalky white drainage and a history of episodic mono arthritis in fingers and feet

A

tophaceous gout

53
Q

what is pathognomonic for gout

A

uric acid tophi

54
Q

what is dx in pt with deposition of calcium and phosphorus in skin presenting as scattered whitish papules, plaques, or nodules

A

calcinosis cutis

55
Q

Which disease produces Heberden and Bouchard nodes

A

osteoarthritis

56
Q

what is dx in pt with firm, flesh-colored, nontender nodules occurring over pressure points like the elbow and extensor surface of proximal ulna

A

rheumatoid nodules

57
Q

what 3 broad categories encompass the signs of liver cirrhosis

A

portal hypertension

hyperestrenism

hepatic synthetic dysfunction

58
Q

what signs are a result of portal hypertension in a cirrhotic pt

A 
esophageal varices
splenomegaly
ascites
caput medusae
anorectal varices
59
Q

what signs are a result of hyperestrenism in a cirrhotic pt

A 
spider angiomata
gynecomastia
loss of sexual hair
testicular atrophy
palmar erythema

circulating estrogens affect vascular wall dilation

60
Q

what signs are a result of hepatic synthetic dysfunction in a cirrhotic pt

A

ecchymosis
edema

decreased coagulation factor synthesis

low protein synthesis = hypoalbuminemia
hypoalbuminemia = decrease in intravascular oncotic pressure and fluid shifts to the extravascular space

61
Q

what dx is the defective mineralization of the bone matrix

A

osteomalacia

62
Q

what is osteomalacia commonly due to

A

severe vitamin D deficiency,
which leads to decreased intestinal Ca and Phosphorus absorption,
resulting in secondary hyperparathyroidism

Ca and P are needed for mineralization the bone matrix

63
Q

what is dx in pt with decreased bone density, thinning of cortex, and pseudo fractures (Looser zones)

A

osteomalacia

64
Q

what is dx in pt with accelerated focal bone remodeling

A

Paget’s disease of bone

65
Q

what is pathogenesis of Paget’s disease of bone

A

first, increased osteoclastic activity

then rapid and disorganized new bone formation by osteoblasts

66
Q

what are lab values in Paget’s disease of bone

A

normal serum Ca, P, and PTH

markers of bone resorption (C-telopeptide, n-telopeptide) and bone formation (Alk phos, osteocalcin) are significantly elevated

67
Q

what is dx in pt with defective type 1 collagen formation

A

osteogenesis imperfecta

68
Q

what is dx in pt with low bone mass but adequate bone mineralization

A

osteoporosis

69
Q

what are lab values in osteoporosis

A

normal serum Ca, P, PTH, and Alk Phos

70
Q

what is dx in pt with lytic bone lesions

A

activation of osteoclasts,
from solid tumors (breast, renal cell)
or multiple myeloma

71
Q

what is ESR a marker for

A

inflammation

72
Q

what is initial evaluation step in pt with h/o difficulty initiating swallowing with cough, choking, or nasal regurgitation

A

pt likely has oropharyngeal dysphagia,

so first step is video fluoroscopic modified barium swallow test

73
Q

what presents as dysphagia with solids and liquids at onset

A

motility disorder

74
Q

what presents as dysphagia with solids progressing to liquids

A

mechanic obstruction

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