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

25
Diagnose: Hypopigmented lesion with no sensation as well as nodular, painful nearby nerves
Leprosy
26
Tx of Mycobacterium leprae
- Tuberculoid form = Dapsone + Rifampin | - Lepromatous form = Dapsone + Rifampin + Clofazimine
27
Describe lab findings seen in intravascular hemolyisis
• Hemoglobinemia, hemoglobinuria, hemosiderinuria (due to iron taken up by renal tubular cells, which later shed), decreased serum haptoglobin, corrected reticulocyte count > 3%
28
Why is there elevated haptoglobin in intravascular hemolysis
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
Which classes of antiarrythmics control rhythm vs. rate
Rhythm control = Class I and III Rate control = Class II and IV
30
MOA of each class of anti-arrythmic
- Class I = Na channel blocker - Class II = beta blocker - Class III = K+ channel blocker - Class IV = CCB
31
What are the Class IA antiarrhythmicc
Procainamide, Quinidine, and Disopyramide
32
Uses of Class IA
supraventricular and ventricular arrhythmias, WPW
33
What are the Class IB
Lidocaine, Phenytoin, Mexiletine
34
Uses of Class IB
Ventricular arrhythmias (especially in ischemic tissue)
35
Names of Class IC
Flecanide, Propafenone
36
Uses of Class IC
Supraventricular arrhythmias, A-fib
37
Uses of beta blockers in arrhythmias
Causes prolongation of AV conduction - Supraventricular arhythmias (e.g. A-fib with RVR) - Rate control in A-fib / A-flutter
38
Names of Class III antiarrhythmics
- Amiodarone (properties of Class I, II, III, and IV) - Sotalol (Class III and II) - Dofetilide and Ibutilide ("til I die")
39
Uses of Class IV antiarrythmics
Non-dihydropyridine CCB - Supraventricular arrythmias (e.g. A-fib with RVR) - Rate control in A-fib
40
Describe MOA of Digoxin in arrhythmias
* 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
Uses of Digoxin in arrhythmias
Atrial arrthythimias (e.g. A-fib)
42
Describe use of Magnesium in arrhythmias
Treatment of torsades de pointes
43
Describe MOA of Adenosine in arrhythmias
• 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
Uses of adenosine in arrhythmias
* First line agent for acute treatment of supraventricular arrhythmias * Coronary dilation (mediated by A2 receptors)
45
Describe how each will appear on EKG: - Ischemia - Injury - Infarct
- Ischemia = ST depression or T wave inversion - Injury = ST elevation - Infarct = pathologic Q waves
46
What are the lateral leads
I, aVL, V5-V6
47
What are the inferior leads
II, III, aVF
48
What are the anterior leads
V1-V4
49
What vessel provides the lateral leads
LCX (or LAD)
50
What vessel provides the inferior leads
RCA
51
What vessel provides the anterior leads
LAD
52
Serious 6 of chest pain
- ACS - PE - PTX - Dissection - Tamponade - Esophageal rupture
53
Medical tx for acute MI
MONA BASH C Morphine, O2, Nitro, ASA, BB, ACEi, Statin, Heparin, Clopidogrel Things to ALWAYS give: ASA and high dose Statin
54
Most common EKG findings in PE
1) tachycardia 2) R axis deviation 3) S1Q3T3 (rare)
55
When do you use tPA in PE
Refractory hypotension (pt with massive PE given O2 and Heparin and fluids and still remains hypotensive)
56
Tx of PE
1. LMWH 2. DOAC (higher risk of cranial bleed) 3. Warfarin (higher risk of GI bleed)