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MS3 > Internal Med 5 > Flashcards

Internal Med 5 Flashcards

1
Q

Ddx of macrocytic anemia

A
  • B12 deficiency

- Folate deficiency

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2
Q

Ddx of of microcytic anemia

A
  • Iron deficiency
  • Lead poisoning
  • Thalassemia
  • Sideroblastic anemia
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3
Q

What is the next thing you should look at if you have a normocytic anemia

A

Reticulocyte count

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4
Q

Ddx of normocytic anemia with high reticulocyte count

A
  • Hemorrhage

- Hemolysis

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5
Q

Ddx of normocytic anemia with low reticulocyte count (deficiency dye to underproduction)

A
  • Leukemia
  • Aplastic anemia
  • Infection
  • Medication side effect
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6
Q

Causes of B12 deficiency

A
  • Pernicious anemia (autoimmune destruction of gastric mucosa - recall that parietal cells make intrinsic factor, necessary for B12 absorption)
  • Pancreatic insufficiency pancreas creates enzymes that cleave B12 from R-binder)
  • Damage to terminal ileum (e.g. Crohn’s) - site of B12 absorption
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7
Q

Lab value to differentiate B12 from folate deficiency

A

Methylmalonic acid - will be normal in Folate deficiency but increased in B12 deficiency

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8
Q

Difference in clinical picture between folate and B12 deficiency

A

B12 can lead to neuro defects (methylmalonic acid builds up in myelin of spinal cord)

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9
Q

What is the cause of anemia in anemia of chronic disease

A

♣ Hepcidin sequesters iron into storage sites

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10
Q

How do you differentiate between iron deficiency anemia and anemia of chronic disease

A

In anemia of chronic disease ferritin will be high (iron is being stored), and TIBC will be low because liver is pumping out less transferrin molecules because it wants to hide the iron

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11
Q

Describe defect in sideroblastic anemia

A

♣ Defect in heme synthesis
• Defect in protoporphyrin synthesis leads to iron buildup in the mitochondria =iron-laden mitochondria form a ring around nucleus of erythroid precursors

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12
Q

Causes of sideroblastic anemia

A
  • Congenital = ALA synthetase deficiency

- Acquired = lead poisoning, alcohol

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13
Q

Describe hereditary spherocytosis

A

o Defect of RBC cytoskeleton proteins
o Membranes are formed and lost over time
♣ Loss of membrane = spherocytes
♣ Spherocytes cannot maneuver through splenic sinusoids so are consumed by macrophages

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14
Q

Describe findings in hereditary spherocytosis

A

♣ Spherocytes with loss of central pallor
♣ Increased RDW – cells of all different sizes
♣ Increased MCHC (mean corpuscular hemoglobin concentration) – cell shrinks but Hb remains the same
♣ Splenomegaly and jaundice – short lifespan of spherocytes and chronic hemolysis causes high hemoglobin turnover
♣ Pigmented gallstones and dark urine due to hyperbilirubiniemia
♣ Aplastic crisis

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15
Q

Diagnosis of hereditary spherocytosis

A

♣ Osmotic fragility test – High percentage of lysis of RBCs in hypotonic solution

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16
Q

Treatment of hereditary spherocytosis

A

♣ Splenectomy

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17
Q

What type of anemia will you see in sickle cell

A

Normocytic anemia with high reticulocyte count

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18
Q

Describe paroxysmal nocturnal hemoglobinuria

A

o Deficiency of GPI, which usually anchors DAF (CD55) to RBC membrane to protect from complement destruction
♣ Complement is activated in acidic situations
♣ Lysis occurs at night due mild respiratory acidosis

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19
Q

What does S3 heart sound indicate and what are causes

A

• S3 = rapid flow of blood from the atria to the ventricles
o Presence of S3 in adults indicates volume overload (e.g. congestive heart failure, advanced mitral or tricuspid regurgitation) or dilated ventricles
o Causes of S3 heart sound:
♣ Dilated cardiomyopathy, congestive heart failure, mitral regurgitation, L-to-R shunting

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20
Q

What are the symptoms of carcinoid syndrome

A
  • Bronchospasm and wheezing
  • Flushing
  • Diarrhea
  • R-sided heart lesions (e.g. valvular disease with tricuspid regurg)
21
Q

What vitamin deficiency might you see in carcinoid syndrome

A

o Niacin deficiency (dermatitis, diarrhea, dementia)
♣ Serotonin is synthesized in carcinoid cells from tryptophan, which is also used in the production of Niacin or Nicotinic acid
♣ Increased tryptophan conversion to serotonin and its metabolites may result in tryptophan and niacin deficiency

22
Q

Diagnosis of carcinoid syndrome

A
  • Elevated 24-hour urinary excretion of 5-HIAA
  • CT/MRI of abdomena and pelvis to localize tumor
  • OctreoScan to detect metastases
  • Echocardiogram (if sx of carcinoid heart disease are present)
23
Q

Treatment of carcinoid syndrome

A
  • Octreotide for symptomatic patients and prior to surgery/anesthesia
  • Surgery for liver metastases
24
Q

What are the 5 classes of pulmonary HTN

A

♣ . Pulmonary arterial HTN (PAH)
• Idiopathic, drugs/toxins, connective tissue disease, HIV, portal HTN
♣ 2. PH due to L heart disease
♣ 3. PH due to chronic lung disease and/or hypoxemia
♣ 4. PH due to chronic thromboembolic pulmonary HTN
♣ 5. PH due to unclear multifactorial mechanisms

25
Q

What are the drugs used to treat hypertensive emergency

A

♣ Beta-1 antagonists (e.g. Esmolol and Metoprolol)
♣ Alpha- and beta-antagonist (e.g. Labetalol)
♣ Calcium channel blockers (e.g. Nicardipine and Cleviidipine)
♣ Hydralazine
♣ Nitroprusside (nitrate)
♣ Fenoldopam (D1 receptor agonist)

26
Q

What’s the next step when you suspect a PE

A

o Determing pretest probability Wells Score
♣ 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

27
Q

Next step in PE evaluation if you have a low Wells score

A
  • Wells < 2 = low probability = get D-dimer, if low, likely not a PE
28
Q

Next step in PE eval if you have a high Wells score

A 
•	Wells >4-6 = high probability
o	CTA with IV contrast 
♣	Best test 
♣	Must have normal kidney
o	V/Q scan
♣	Can perform with abnormal kidneys
♣	Must have a normal CXR
29
Q

What PFT will you see in COPD?

  • FEV1/FVC
  • Residual volume
  • Total lung capacity
A
  • Decreased FEV1/FVC ratio (< 80%)
  • Increased residual volume (RV) and functional residual capacity (FRC)
  • Increased total lung capacity (TLC) due to air trapping
30
Q

What are the two types of emphysema

A
  • Centriacinar

- Panacinar

31
Q

Describe centriacinar emphysema and its associations

A

o Associated with smoking
♣ Pollutants in smoke = excessive inflammation = protease-mediated damage
o Worse in upper lobes

32
Q

Describe panacinar emphysema and its associations

A

o Associated with alpha-1-antitrypsin (A1AT) deficiency
♣ No A1AT to neutralize proteases (elastase) = elastase destroys elastic tissue of alveoli
o Worse in lower lobes
o Also associated with liver cirrhosis
♣ A1ATD due to misfolding of mutated proteins
♣ Misfolded proteins accumulate in the endoplasmic reticulum of hepatocytes

33
Q

Will the pulmonary capillary wedge pressure be high or low in ARDS?

A

Low

Vs. cardiopulmonary disease (CHF) where it will be high

34
Q

What will you seen on PFTs in restrictive lung disease

A
  • Decreased TLC
  • Decreased FEV1 and FVC, but FVC is decreased more
  • FEV1:FVC ratio is increased (> 80%)
35
Q

Tx of restrictive lung disease

A

• Steroids

36
Q

What will you see on XR in Sarcoidosis

A

Granulomas most commonly involve the hilar lymph nodes and lung

37
Q

Other findings of sarcoidosis other than lung

A

♣ Erythema nodosum (nodules on shins), uveitis, salivary and lacrimal glands (mimics Sjogren)
♣ Can have cardiac involvement via cardiac noncaseating granulomas
• Infilatration of granulomas leads to surrounding inflammation which can cause
o Conduction defects (complete AV block most common)
o Restrictive cardiomyopathy (early manifestation)
o Dilated cardiomyopathy (late manifestation)
o Valvular dysfunction
o Heart failure

38
Q

Exposures associated with asbestos

A

Shipbuilidng, roofing, plumbing

39
Q

Important complication of asbestosis

A

Leads to cancer, both lung and pleural (mesothelioma)

40
Q

describe how you dose insulin

A
  • Total daily dose: Want 0.5-1 x weight in kg
  • Divide total daily dose into two halves
    o Give half as basal, long acting dose (e.g. Glargine Q24H or NPH Q12H)
    o Give other half as meal time / SSI (e.g. Lispro)
41
Q

What are the precipitants of A-fib

A
  • HF
  • ACS
  • Hyper/hypothyroidism
  • PE
  • Physiologic stress
  • Pheochromocytoma
  • Alcohol
  • Drugs/Toxins
  • Infection
42
Q

What drug would you use to treat if the pt was stable but symptomatic with the following rhythms

  • Fast with wide QRS
  • Fast with narrow QRS
  • Slow
A
  • Fast with wide QRS = V-tach = Amiodorone
  • Fast with narrow QRS = SVT = Adenosine
  • Slow = Atropine
43
Q

What is the MOA of nitrates in angina

A

Cause veno-dilation, which decreases preload, resulting in a decrease in LV wall stress

44
Q

Tx of severe hypercalcemia

A
  • *IVF

- Bisphosphonates

45
Q

Diagnose: hypercalcemia, bone pain, renal failure, anemia

A

Multiple myeloma

46
Q

What is vitiligo

A

♣ Localized loss of skin pigment due to autoimmune destruction of melanocytes
• Most cases progress gradually
• Repigmentation is spontaneous in 10-20% of cases

47
Q

Tx of vitiligo

A
  • Limited disease: Topical corticosteroids

* Extensive/unresponsive disease: oral corticosteroids, topical calcineurin inhibitors, PUVA

48
Q

What drug treats exophthalmos of Graves

A

glucocorticoids

49
Q

Diagnosis of IBS

A

♣ Recurrent abdominal pain associated with > 2 of the following occurring for >/= 3 days/month for the past 3 months:
• Pain improves with defecation
• Change in stool frequency
• Change in stool appearance

MS3 (88 decks)

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