AAC 2 Flashcards

1
Q

Tx of acute gout attack

A

o NSAIDs (indomethacin)
o Glucocorticoids
o Colchicine – stabilizes tubulin to impair leukocyte chemotaxis

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2
Q

Tx of chronic gout

A

o Probenecid – inhibits reabsorption of uric acid in PCT
o Allopurinol – inhibits xanthine oxidase, thus inhibiting uric acid synthesis
o Febuxostat – also xanthine oxidase inhibitor

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3
Q

What will you see in x-ray of osteoarthritis

A

Joint space narrowing, osteophytes, and polishing of the bone

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4
Q

What will you see on x-ray os pseudo gout

A

Chondrocalcinosis - Calcification of joint cartilage

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5
Q

What will you see on x-ray of RA

A

Periarticular osteopenia with erosion of the joint margin

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6
Q

Describe skin/MSK findings in Marfan syndrome

A

Tall, long limbs, arachnodactyly, hyperflexible joints (not skin)

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7
Q

Describe cardio findings of Marfan

A

Aortic dilation, aortic regurg (diastolic murmur), acute aortic dissection

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8
Q

Describe pulm findings of Marfan

A

Spontaneous pneumothorax from apical blebs

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9
Q

Describe common findings in Ehlers danlos

A

♣ Elastic skin
♣ Hypermobility of joints
♣ Increased bleeding tendency
♣ May also be associated with joint dislocation, berry and aortic aneurysm, organ rupture

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10
Q

Describe De Quervain tenosynovitis

A
  • Caused by inflammation of the abductor pollicis longus and extensor pollicis brevis as they pass through a fibrous sheath at the radial styloid process
  • Tenderness can be elicited with direct palpation of the radial side of the wrist at the base of the hand
  • The Finkelstein test, which is conducted by passively stretching the affected tendons by grasping the flexed thumb into the palm with the fingers, elicits pain
  • Often affects new mothers who hold their infants with the thumb outstretched (abducted/extended)
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11
Q

Describe MEN 1

A
  • Pituitary tumors (prolactin or GH)
  • Pancreatic endocrine tumors (Zollinger-Ellison, insulinoma, glucagonoma)
  • Parathyroid adenoma
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12
Q

Describe MEN 2A

A
  • Medullary thyroid carcinoma (secrete calcitonin - hypocalcemia)
  • Pheochromocytoma
  • Parathyroid hyperplasia
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13
Q

Describe MEN 2B

A
  • Medullary thyroid carcinoma
  • Pheochromocytoma
  • Mucosal neuromas
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14
Q

Tx of seborrheic dermatitis

A

Topical antifungals or anti-inflammatory (topical steroids)

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15
Q

When do you use octreotide in cirrhosis

A

During active variceal bleeding

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16
Q

What are the most common bugs in secondary bacterial pneumonia

A

Staph aureus, Strep pneumo

  • Strep is most common (age >65)
  • Secondary bacterial pneumonia is less likely in younger people and more likely to be staph in the young
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17
Q

Describe pathogenesis of bronchiectasis

A
  • Chronic infection of the bronchi causes permanent dilation of airways
  • Cronchial wall damage and airway dilation due to recurrent cycle of infection, inflammation, and tissue damage
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18
Q

Presentation of bronchiectasis

A
  • Cough, dyspnea, foul-smelling sputum
  • Rhinosinusitis, hemoptysis
  • Crackles, wheezing
  • Clinical presentation is similar to that of chronic bronchitis, however sputum production is more prominent in bronchiectasis and exacerbation are typically bacterial and require antibiotics
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19
Q

Most common cause of bacterial meningitis

A

Strep pneumo

20
Q

What might be produced by squamous cell lung cancer

A

May produce PTH = hypercalcemia

REMEMBER: sCa++mous

21
Q

What might be produced by small cell lung cancer

A
  • ADH = SIADH
  • ACTH = Cushings
  • Antibodies against pre-synaptic Ca2+ channels = Lambert Eaton
22
Q

Presentation of mycobacterium avium complex (MAC)

A
  • Nonspecific sx (fever, cough, abd pain, diarrhea, night sweats, weight loss)
  • splenomegaly
  • elevated alk phos
23
Q

Tx of MAC

A

Azithromycin

24
Q

What are the cut-offs for positive tuberculin PPD skin test

A

♣ >/5 mm
• HIV+ patients
• Recent contacts of known TB cases
• Nodular or fibrotic changes on CXR consistent with previously healed TB
• Organ transplant recipients or other immunosuppressed

♣ >/= 10 mm
• Recent immigrants (<5 years) from TB-endemic areas
• Injection drug users
• Residents and emplyees of high-risk settings (e.g. prisons, nursing homes, hospitals, homeless shelters)
• Mycobacteriology lab personnel
• Higher risk for TB reactivation (e.g. DM, leukemia, ESRD, chronic malabsorption syndromes)
• Children age <4, or those exposed to adults in high-risk categories

♣ >/= 15 mm
• All of the above plus healthy individuals

25
Q

When with Hep B core antibody be positive

A

• IgM = acute/recurrent infection
• IgG = prior exposure or chronic infection
o Will NOT be positive if immunized
o Think of HBcAB as a marker of positive history of disease
• Positive in window period (when antibodies are binding antigens and neither antigens or antibodies are detectable)

26
Q

what is the triad seen in Felty syndrome

A
  • RA
  • Neutropenia
  • Splenomegaly
27
Q

What age group and how often should mammograms happen?

A
  • Women age 50-75

- Every 2 years

28
Q

Describe pathophysiology of CO poisoning

A

♣ The affinity of CO for binding hgb is >200x that of O2

♣ Once bound to Hb, CO forms carboxyhemoglobin, which impairs O2 delivery to tissue

29
Q

Tx of CO poisoning

A

♣ High flow 100% oxygen

♣ Intubation/hypercarbic oxygen therapy

30
Q

What is haptoglobin and what do decreased levels indicate

A
  • Haptoglobin is the protein used to carry free Hgb to the spleen
  • Haptoglobin will be low in intravascular hemolysis because it will all be bound up to Hgb
31
Q

What acid-base disorder would you expect in Primary adrenal insufficiency

A

Metabolic acidosis

32
Q

Diagnostic imaging for kidney stones

A

US or NON-contrast CT

33
Q

What 4 groups of patients would benefit from statin therapy

A
  1. Pts with clinical ASCVD (ACS, h/o MI, stable or unstable angina, stroke, TIA, or PAD)
  2. Pts with LDL >190
  3. Pts with DM, age 40-75 with LDL of 70-189
  4. Pts w/o DM, age 40-75, with ASCVD >/= 7.5%
34
Q

Whats the difference between Cushing Syndrome and Cushing Disease

A
  • Cushing syndrome = cortisol

- Cushing disease = ACTH-secreting pituitary adnoma

35
Q

What is the cause of pancytopenia in lupus

A

Auto-immune destruction (e.g. peripheral destruction)

36
Q

Next step in management of pt with suspected giant cell arteritis and vision loss

A

High-dose IV corticosteriods (even before biopsy to make official diagnosis - blindness can be permanent!)

37
Q

Presentation of glucagonoma

A
  • Mild hyperglycemia
  • Necrolytic migratory erythema
  • Diarrhea
  • Weight loss
38
Q

Best method for diagnosis of aortic dissection

A

♣ Transesophageal echo (TEE) – preferred method in patients with renal insufficiency of hemodynamic instability
♣ CT angiography with contrast – preferred in hemodynamically stable patients; requires contrast so avoid in renal insufficiency
♣ MR angiography – time consuming; avoid in patients with kidney disease

39
Q

What are Wells criteria

A

♣ Wells Scoring Criteria:
• Clinical symptoms of DVT (leg swelling, pain with palpation) = 3
• Other diagnosis less likely than PE = 3
• Heart rate > 100 = 1.5
• Immobilization (>/= 3 days) or surgery in the previous 4 weeks = 1.5
• Previous DVT/PE = 1.5
• Hemoptysis = 1
• Malignancy = 1

Scoring
• Wells <2 = low probability = Get D-dimer
• Wells >4-6 = high probability = CTA angio

40
Q

Tx of hypertrophic cardiomyopathy

A

• Beta blockers
o Negative inotropes prolong diastole and decrease myocardial contractility, which in turn decreases LVOT obstruction and improves symptoms of angina

• Non-dihydropyridine CCBs (e.g. Verapamil)
o Used when symptoms persist despite beta blocker therapy

41
Q

Symptoms of lupus

A
R - rash
A - arthritis
S - serositis (e.g. pleuritic, pericarditis)
H - hematologic disorders (anemia, leukopenia, lymphopenia, thrombocytopenia)
O - oral ulcers 
R - renal disease
P - photosensitivity
A - antinuclear antibody
I - immunologic disorder
N - neurologic disorders
42
Q

Meds used to treat BPH

A
  • Alpha-1 antagonists
  • 5a-reductase inhibitors
  • Antimuscarinics (to treat symptoms)
43
Q

How do alpha-1 antagonists work to treat BPH

A

♣ Relax smooth muscle in bladder neck, prostate capsule and prostatic urethra

44
Q

How do 5a-reductase inhibitors work to treat BPH

A

♣ Inhibit conversion of testosterone to dihysrotestosterone

♣ Reduce prostate gland size

45
Q

When do you see bite cells?

A

o Due to Glucose-6-phosphate dehydrogenase (G6PD) Deficiency
♣ No NADPH created in order to reduce glutathione, which is needed to protect RBCs from oxidative damage
o Heinz bodies are precipitated hemoglobin within the RBC
o Bite cells are due to the phagocytic removal of bite cells

46
Q

What is the difference between Steven Johnson Syndrome and Toxic Epidermal Necrolysis

A

SJS involves <10% of skin

TEN involves >30% of skin