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MS3 > Internal Med 6 > Flashcards

Internal Med 6 Flashcards

1
Q

What type of infection causes skin ulcerations that travel up the lymphatic chain

A
  • Sporotrichosis from Sporothrix schenckii
  • Fungus
  • From decaying plant matter/soil (rose bush)
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2
Q

Describe timeline of common complications associated with MI

A
  • Reinfarction (hours - 2 days)
  • Ventricular septal rupture (hours - 1 week)
  • Free wall rupture (hours - 2 weeks)
  • Postinfarction angina (hours - 1 month)
  • Papillary muscle rupture (2 days - 1 week)
  • Pericarditis (1 day - 3 months)
  • LV aneurysm (5 days = 3 months)
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3
Q

What will you see on EKG in a ventricular aneurysm

A

Persistent ST-elevation after a recent MI and deep Q waves in the same leads

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4
Q

Describe thyroid adenoma

A

• Almost always a “cold” nodule

Does not overproduce thyroid hormone

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5
Q

Describe Papillary thyroid carcinoma

A 
•	Most common type of thyroid cancer
•	Histology:
o	Orphan Annie eye nuclei
o	Nuclear grooves 
o	Psammoma bodies
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6
Q

Describe Follicular thyroid carcinoma

A

• Second most common type of thyroid cancer
• Histologically the same as follicular adenoma but invade the tumor capsule
o This finding is made on exam of a surgically excised nodule
o Cannot differentiate based on histology)
• Histology:
o Uniform follicles

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7
Q

Describe Medullary thyroid carcinoma

A
  • From parafollicular “C cells”

* Will have increased calcitonin (hypocalcemia)

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8
Q

How long after liver transplant will you likely see bacterial vs. viral infection

A

Bacterial < 1 month

Viral 1-6 months

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9
Q

What are the 2 renal diseases associated with SLE

A

Diffuse proliferative glomerulonephritis or membranous glomerulonephritis

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10
Q

Diagnose: Unexplained, painless, episodic GI bleeding (hematochezia) and anemia

A

Angiodysplasia

♣ Tortuous dilation of vessels within the bowel, leading to hematochezia

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11
Q

Tx of angiodysplasia

A
  • None for asymptomatic patients

* Endoscopic cautery for patients with anemia or gross/occult bleeding

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12
Q

What are the tumors of MEN 1

A

♣ Pituitary tumors (prolactin or GH)
♣ Pancreatic endocrine tumors (Zollinger-Ellison syndrome, insulinomas, VIPomas, glucagonomas)
♣ Parathyroid adenomas

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13
Q

What are the tumors of MEN2A

A

♣ Medullary thyroid carcinoma (neoplasm of parafollicular C cells which secrete calcitonin)
♣ Pheochromocytoma
♣ Parathyroid hyperplasia

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14
Q

What are the tumors of MEN2B

A

♣ Medullary thyroid carcinoma
♣ Pheochromocytoma
♣ Mucosal neuromas (oral/intestinal ganglioneuromatosis) / Marfanoid habitus

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15
Q

Where is calcitonin produced and what is its function

A
  • Produced by Parafollicular cells of thyroid

- “Tones” down calcium - inhibits osteoclasts, leading to decreased bone resorption

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16
Q

What can calcitonin be used to treat

A
  • Osteoporosis
  • Hypercalcemia of malignancy
  • Paget disease
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17
Q

What is the effect of parathyroid hormone

A
  • Increases bone resorption (increasing Ca2+)
  • Increases calcium reabsorption at the kidney
  • Decreases phosphate reabsorption
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18
Q

Tx of hypercalcemia of malignancy

A

Bisphosphonates + Calcitonin

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19
Q

Describe ankylosing spondylitis

A

o Involves sacroiliac joint and spine
o Fusion of vertebrae (ankyloses) bamboo spine
♣ Reduced spine mobility
♣ Improves with exercise
o Uveitis
o Aortitis (weakened walls may lead to dilation and aortic regurgitation)
o Think: Pandas:
♣ They eat bamboo bamboo spine
♣ Raccoon eyes uveitis
♣ Clumsy climbing up trees causes branches to bend aortitis

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20
Q

How do you decide if you should anticoagulate a patient with A-fib

A

CHADSVASc score

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21
Q

What are the components of CHADSVASc

A 
C = CHF
H = HTN
A = age >75
D = DM
S = Stroke/TIA/Thromboembolism
V = Vascular disease (MI, PAD)
A = Age 65-74
S = Sex (female)
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22
Q

What CHADSVASc score do you need before anitcoagulation is indicated

A

Score = 1 (Rivaroxaban or ASA)

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23
Q

What lab values will you see in sarcoidosis

A

Elevated Ca2+ and ACE

24
Q

Tx of sarcoidosis

A

Steroids

25
Q

Diagnose: Hypopigmented lesion with no sensation as well as nodular, painful nearby nerves

A

Leprosy

26
Q

Tx of Mycobacterium leprae

A
  • Tuberculoid form = Dapsone + Rifampin

- Lepromatous form = Dapsone + Rifampin + Clofazimine

27
Q

Describe lab findings seen in intravascular hemolyisis

A

• Hemoglobinemia, hemoglobinuria, hemosiderinuria (due to iron taken up by renal tubular cells, which later shed),decreased serum haptoglobin, corrected reticulocyte count > 3%

28
Q

Why is there elevated haptoglobin in intravascular hemolysis

A

o Haptogloblin is the protein that will carry Hb to spleen
o In intravascular hemolysis, the amount of free Hgb exceeds the binding capacity of haptoglobin, thereby decreasing the level of haptoglobin

29
Q

Which classes of antiarrythmics control rhythm vs. rate

A

Rhythm control = Class I and III

Rate control = Class II and IV

30
Q

MOA of each class of anti-arrythmic

A
  • Class I = Na channel blocker
  • Class II = beta blocker
  • Class III = K+ channel blocker
  • Class IV = CCB
31
Q

What are the Class IA antiarrhythmicc

A

Procainamide, Quinidine, and Disopyramide

32
Q

Uses of Class IA

A

supraventricular and ventricular arrhythmias, WPW

33
Q

What are the Class IB

A

Lidocaine, Phenytoin, Mexiletine

34
Q

Uses of Class IB

A

Ventricular arrhythmias (especially in ischemic tissue)

35
Q

Names of Class IC

A

Flecanide, Propafenone

36
Q

Uses of Class IC

A

Supraventricular arrhythmias, A-fib

37
Q

Uses of beta blockers in arrhythmias

A

Causes prolongation of AV conduction

  • Supraventricular arhythmias (e.g. A-fib with RVR)
  • Rate control in A-fib / A-flutter
38
Q

Names of Class III antiarrhythmics

A
  • Amiodarone (properties of Class I, II, III, and IV)
  • Sotalol (Class III and II)
  • Dofetilide and Ibutilide (“til I die”)
39
Q

Uses of Class IV antiarrythmics

A

Non-dihydropyridine CCB

  • Supraventricular arrythmias (e.g. A-fib with RVR)
  • Rate control in A-fib
40
Q

Describe MOA of Digoxin in arrhythmias

A
  • Exerts direct parasympathomimetic effects via direct stimulation of the vagus nerve, leading to AV inhibition
  • Similar effect of beta-blockers (Class II) and Ca2+ blockers (Class IV)
41
Q

Uses of Digoxin in arrhythmias

A

Atrial arrthythimias (e.g. A-fib)

42
Q

Describe use of Magnesium in arrhythmias

A

Treatment of torsades de pointes

43
Q

Describe MOA of Adenosine in arrhythmias

A

• Activates inhibitor A1 receptors on the myocardium and at the SA and AV nodes
• Activation of A1 receptors increases potassium outward conduction and suppresses calcium inward current
o This causes membrane potential to remain negative for a longer period and calcium-dependent action potentials (at nodes) are suppressed
o This decreases AV conduction, leading to prolonged AV refractory period

44
Q

Uses of adenosine in arrhythmias

A
  • First line agent for acute treatment of supraventricular arrhythmias
  • Coronary dilation (mediated by A2 receptors)
45
Q

Describe how each will appear on EKG:

  • Ischemia
  • Injury
  • Infarct
A
  • Ischemia = ST depression or T wave inversion
  • Injury = ST elevation
  • Infarct = pathologic Q waves
46
Q

What are the lateral leads

A

I, aVL, V5-V6

47
Q

What are the inferior leads

A

II, III, aVF

48
Q

What are the anterior leads

A

V1-V4

49
Q

What vessel provides the lateral leads

A

LCX (or LAD)

50
Q

What vessel provides the inferior leads

A

RCA

51
Q

What vessel provides the anterior leads

A

LAD

52
Q

Serious 6 of chest pain

A
  • ACS
  • PE
  • PTX
  • Dissection
  • Tamponade
  • Esophageal rupture
53
Q

Medical tx for acute MI

A

MONA BASH C

Morphine, O2, Nitro, ASA, BB, ACEi, Statin, Heparin, Clopidogrel

Things to ALWAYS give: ASA and high dose Statin

54
Q

Most common EKG findings in PE

A

1) tachycardia
2) R axis deviation
3) S1Q3T3 (rare)

55
Q

When do you use tPA in PE

A

Refractory hypotension (pt with massive PE given O2 and Heparin and fluids and still remains hypotensive)

56
Q

Tx of PE

A
  1. LMWH
  2. DOAC (higher risk of cranial bleed)
  3. Warfarin (higher risk of GI bleed)

MS3 (88 decks)

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