Medicine UWorld Flashcards
what is dx in pt: young - middle aged F chronic WIDESPREAD PAIN fatigue, impaired concentration tenderness at trigger points (ex mid trapezius, costochondral junction)
Fibromyalgia
how do you dx fibromyalgia
> = 3 months of symptoms with widespread pain index or symptom severity score
NORMAL lab studies
what is dx in pt with:
proximal muscle WEAKNESS (difficulty climbing stairs); usually symmetric
pain is mild/absent
polymyositis
how do you dx polymyositis
ELEVATED MUSCLE ENZYMES (ex Creatinine kinase, Aldolase, AST)
autoantibodies (ANA, anti-Jo-1)
Biopsy: Endomysial infiltrate, patchy necrosis
what is dx in pt:
>50yo
systemic signs and symptoms
STIFFNESS > pain in shoulders, hip girdle, neck
associated with giant cell temporal arteritis
polymyalgia rheumatica
how do you dx polymyalgia rheumatica
ELEVATED ESR
ELEVATED C-REACTIVE PROTEIN
rapid improvement with glucocorticoids
what is dx in pt with: systemic symptoms skin findings (lived reticularis, purport) kidney disease abdominal pain muscle aches or weakness
polyarteritis nodosa
which lab value is usually elevated in polyarteritis nodosa
CRP
what is dx in pt with:
pain and swelling in wrists and small joints of hands
morning stiffness
systemic symptoms
rheumatoid arthritis
which lab value correlates with rheumatoid arthritis disease activity
CRP
what is dx in pt:
Male 15-35yo
elevated ESR and CRP
back pain that worsens with rest and improves with activity
seronegative spondyloarthropathies (eg ankylosing spondylitis)
describe selection of asthma treatments based on asthma severity x4
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
what are steps 1-6 in asthma therapy
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
which asthma treatment has increased evidence of mortality when used as mono therapy, and how is that better managed
LABA mono therapy has evidence of increased mortality and treatment failure
the addition of LABA is indicated only in combination with an inhaled corticosteroid
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 daily controller medication, an inhaled corticosteroid in addition to the SABA
what is likely dx in immunocompromised pt with CT scan showing pulmonary nodules and surrounding ground-glass opacities (“halo sign”)
invasive aspergillosis
what is treatment for invasive aspergillosis
usually a combination of voriconazole and echinocandin (caspofungin)
what is dx in pt with no history of alcohol or gallstones presenting with acute pancreatitis, possibly with a recent vascular procedure
cholesterol emboli causing acute pancreatitis via vessel occlusion
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
cholesterol emboli
how do you manage acute pancreatitis from uncorrectable causes (ischemia, atheroembolism)
manage conservatively with analgesics and IV fluids
what is the dx in a pt with triad of nongonococcal urethritis, asymmetric oligoarthritis, and conjunctivitis
reactive arthritis
what are 2 common findings of reactive arthritis aside from its triad?
mucocutaneous lesions
enthesitis (Achilles tendon pain)
what does synovial fluid usually show in reactive arthritis
usually sterile
what is first line treatment for acute phase reactive arthritis
NSAIDs
what additional symptoms other than the triad would you look for in a pt where you suspect gonococcal septic arthritis from reactive arthritis
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
what is dx in triad of polyarthralgias, tenosynovitis, and vesiculopustular skin lesions
disseminated gonococcal infection
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
pulmonary contusion
may not be clinically evident immediately
what is management of pulmonary contusion
pain control
pulmonary hygiene (nebulizer treatment, chest PT)
supplemental oxygen and ventilatory support
(large doses of IV fluids may worsen pulmonary edema)
what is dx in pt with: blunt thoracic trauma hypotension, tachycardia, +/- arrhythmia \+/- signs of heart failure abnormal pulmonary capillary wedge pressure
myocardial contusion
may be asymptomatic in most cases
how does acute pancreatitis cause ARDS
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
what is the best way to improve mortality in pts with ARDS on mechanical ventilation
low tidal volume ventilation (LTVV)
this results in lower pulmonary pressures, which decreases the likelihood of over distending alveoli
what is the setting of a low tidal volume ventilation
LTVV = 6 mL/kg of ideal body weight
why are higher tidal volumes in ARDS harmful
may result in elevated pulmonary pressures due to work of forcing larger volumes into stiff lungs (decreased compliance), leading to increased alveolar distension
what is the oxygenation goal for mechanical ventilation in ARDS
SpO2 >88% (peripheral saturation)
PaO2 55-80mmHg (arterial partial pressure)
which acid/base abnormality will potentially develop (but permissive and not associated with increased mortality) in pts on LTVV
LTVV strategies are associated with hypercapnia, and therefore
respiratory acidosis
what drug usage commonly causes injury that mimics viral hepatitis
isoniazid
what is the most common composition of kidney stone
calcium oxalate
why might small bowel disease, surgical resection, or chronic diarrhea lead to formation of calcium oxalate stones
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
which kidney stone is common in primary hyperparathyroidism and renal tubular acidosis
calcium phosphate
which kidney stone is common in increased cell turnover and dehydration
uric acid stones
increased cell turnover causes hyperuricemia and hyperuricosuria
which kidney stone is common in alkaline urine from urease-producing bacterial infection
struvite stones
what is dx in pt with:
elevated aminotransferases (often >1000)
encephalopathy
INR >= 1.5 (synthetic liver dysfunction)
acute liver failure
which drug is a common cause of acute liver failure, that may be potentiated by chronic alcohol use
acetaminophen
how does liver toxicity 2/2 acetaminophen overdose occur
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
what is an effective antidote for acetaminophen overdose, and what is its MOA
N-acetylcysteine
it increases glutathione levels and binds to NAPQI, the toxic metabolite of acetaminophen (normally detoxified by glucuronidation in liver)
what are aminotransferase levels in cirrhosis
normal to moderately elevated aminotransferase levels
what causes right-to-left intrapulmonary shunting and an extreme V/Q mismatch, where hypoxemia does not correct increased concentrations of inspired oxygen
pneumonia
what is pathogenesis of pneumonia causing lung problems
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
what does R–> L intrapulmonary shunting mean
perfusion of lung tissue in absence of alveolar ventilation
V/Q mismatch
diffuse alveolar hypoventilation can be caused from what 2 physiologic alterations
decrease in either tidal volume or respiratory rate
what is increased pulmonary capillary wedge pressure indicative of
increased LA pressure,
a sign of L heart failure
what is dx in pt with painful, visible tophi +/- chalky white drainage and a history of episodic mono arthritis in fingers and feet
tophaceous gout
what is pathognomonic for gout
uric acid tophi
what is dx in pt with deposition of calcium and phosphorus in skin presenting as scattered whitish papules, plaques, or nodules
calcinosis cutis
Which disease produces Heberden and Bouchard nodes
osteoarthritis
what is dx in pt with firm, flesh-colored, nontender nodules occurring over pressure points like the elbow and extensor surface of proximal ulna
rheumatoid nodules
what 3 broad categories encompass the signs of liver cirrhosis
portal hypertension
hyperestrenism
hepatic synthetic dysfunction
what signs are a result of portal hypertension in a cirrhotic pt
esophageal varices splenomegaly ascites caput medusae anorectal varices
what signs are a result of hyperestrenism in a cirrhotic pt
spider angiomata gynecomastia loss of sexual hair testicular atrophy palmar erythema
circulating estrogens affect vascular wall dilation
what signs are a result of hepatic synthetic dysfunction in a cirrhotic pt
ecchymosis
edema
decreased coagulation factor synthesis
low protein synthesis = hypoalbuminemia
hypoalbuminemia = decrease in intravascular oncotic pressure and fluid shifts to the extravascular space
what dx is the defective mineralization of the bone matrix
osteomalacia
what is osteomalacia commonly due to
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
what is dx in pt with decreased bone density, thinning of cortex, and pseudo fractures (Looser zones)
osteomalacia
what is dx in pt with accelerated focal bone remodeling
Paget’s disease of bone
what is pathogenesis of Paget’s disease of bone
first, increased osteoclastic activity
then rapid and disorganized new bone formation by osteoblasts
what are lab values in Paget’s disease of bone
normal serum Ca, P, and PTH
markers of bone resorption (C-telopeptide, n-telopeptide) and bone formation (Alk phos, osteocalcin) are significantly elevated
what is dx in pt with defective type 1 collagen formation
osteogenesis imperfecta
what is dx in pt with low bone mass but adequate bone mineralization
osteoporosis
what are lab values in osteoporosis
normal serum Ca, P, PTH, and Alk Phos
what is dx in pt with lytic bone lesions
activation of osteoclasts,
from solid tumors (breast, renal cell)
or multiple myeloma
what is ESR a marker for
inflammation
what is initial evaluation step in pt with h/o difficulty initiating swallowing with cough, choking, or nasal regurgitation
pt likely has oropharyngeal dysphagia,
so first step is video fluoroscopic modified barium swallow test
what presents as dysphagia with solids and liquids at onset
motility disorder
what presents as dysphagia with solids progressing to liquids
mechanic obstruction
