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HMS Homeostasis I > Final Review > Flashcards

Final Review Flashcards

1
Q

Myocardial oxygen supply and demand

A
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2
Q

How do nitrates work as an anti-anginal therapy?

A

To reduce preload and thereby reduce myocardial wall stress.

They do also increase coronary dilation, however most patients with atherosclerotic disease have maximally dilated coronaries at baseline. For a patient with angina due to vasospasm, these effects are more significant.

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3
Q

The ONLY two NDHP CCBs

A

verapamil and diltiazem

Act like beta blockers

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4
Q

Evolution of STEMI and NSTEMI on ECG

A
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5
Q

Anatomic localization of infarct by ECG

A
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6
Q

58 year old man develops sharp left anterior pleuritic chest pain and has a cardiac rub on auscultation 1 week after MI.

What is the likely cause?

A

Pericarditis

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7
Q

58 year old man develops sharp left anterior pleuritic chest pain and has a cardiac rub on auscultation 3 weeks after MI.

What is the likely cause?

A

Dressler syndrome (Type III Hypersensitivity)

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8
Q

Aortic dissection may lead to ___

A

Aortic dissection may lead to aortic regurgitation

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9
Q

Model for myelopoietic disorders

A
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10
Q

In a patient with a healthy heart, if you push on the liver. . .

A

. . . the JVD won’t go up. Because, the right atrium and ventricle will just accept more blood.

It is really when the right heart is struggling against high pressure that this produces a hepatojugular reflux.

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11
Q

Lovitch Leukocytosis Flowchart

A
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12
Q

Lovitch Neutropenia Flowchart

A
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13
Q

Lovitch Pancytopenia Flowchart

A
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14
Q

General approach to leukopenia/leukocytosis

A
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15
Q

Cardiogenic pulmonary edema

A
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16
Q

Non-cardiogenic pulmonary edema

A
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17
Q

NYHA Heart Failure grading

A
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18
Q

Major factors that determine airway diameter (and therefore resistance)

A
  • Long size (changes throughout respiratory cycle)
  • Transmural pressure (Pin - Pout)
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19
Q

Hemoglobin dissociation curve

A
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20
Q

A patient with 60% oxygen saturation is put on oxygen and his oxygen improves, but his carbon dioxide increases substantially as well. What is the mechanism for his increased CO2?

A

Worsened V/Q mismatch

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21
Q

Etiology of combined pre and post capillary pulmonary hypertension

A

Started with high wedge pressure due to poor left heart function, developed increased PVR over time, and eventually led to pre-capillary pulmonary hypertension

22
Q

Why is elevated pre- and post- capillary pulmonary hypertension so hard to treat?

A

When you give a pulmonary vasodilator, their pulmonary artery will relax and fill with fluid, but then the fluid will get stuck! It can’t make it through the high pressure barrier of the capillaries.

You will just precipitate pulmonary edema.

Note that these are the patients with chronic L heart diastolic dysfunction.

23
Q

Why is pulmonary infarction usually towards the periphery of the lung?

A

Because these areas benefit the least from the dual blood supply of the lung. They are the least perfused by the bronchial arteries, and rely heavily on the pulmonary arteries.

24
Q

____ is a major cause of dyspnea in patients who breathe at dynamic hyperinflation and is a way of measuring whether or not someone is breathing at an EELV above their FRC.

A

Constrained inspiratory capacity is a major cause of dyspnea in patients who breathe at dynamic hyperinflation and is a way of measuring whether or not someone is breathing at an EELV above their FRC.

25
Q

When it comes no nitrates. . .

A

Low-dose nitrates are selective venodilators

High-dose nitrates are indescriminate vasodilators

26
Q

Full PAO2 equation

A

PAO2 = FiO2 ( Patm - 47 mmHg) - ( 1.25 * PaCO2 )

27
Q

The equation for estimated A-a gradient does not apply when. . .

A

. . . the patient is on supplemental oxygen

28
Q

Transfusion reaction summary

A
29
Q

Serologic types of autoimmune hemolytic anemia

A
30
Q

Model for drugging pulmonary hypertension

A
31
Q

Drug interactions for PAH

A
32
Q

What are some ways to differentiate TACO from TRALI?

A

Both produce an acute reaction involving severe dyspnea, tachycardia, and hypoxemia with new diffuse infiltrate on CXR.

However, TACO is not an inflammatory process, and so does not often cause hypotension or fever. TACO is also more likely if transfused blood was from an un-transfused male donor. More often, TACO causes hypertension

33
Q

Approach to community acquired pneumonia

A
34
Q

Considerations for nosocomial pneumonia

A
  • Patient gets pneumonia after ≥ 48 hours in the hospital
  • Identifying the pathogen is very important
  • CAP bugs + at risk for infection with a broader range of bacteria, including gram negatives (Escherichia coli, Klebsiella pneumoniae, Pseudomonas) and more resistant pathogens (MRSA)
  • Initial coverage often broad (ex. anti-pseudomonal cephalosporin + vancomycin)
  • Narrow regimen once pathogen identified
35
Q

Antibiotics that work against pseudomonas

A
36
Q

The HACEKs

A

A group of fastidious Gram-negative bacilli which normally live in the mouth, but which can also cause infective endocarditis.

37
Q

Treatment for HACEKs

A
38
Q

Treating outpatients for pneumonia

A
  • Treat empirically (i.e., no sputum cx)
  • Regimen:
    • If suspicion for possible S. pneumo (lobar infiltrate, high fever, or sick appearing): Beta-lactam (ex. amoxicillin)
    • If very low suspicion for S. pneumo* (interstitial infiltrate, not that sick): Tetracycline (ex. doxycycline) OR Macrolide (ex. azithro)
  • *Rates of macrolide resistant S. pneumo high
  • If very elderly or with substantial comorbidities, treat more aggressively with fluroquinolone or beta-lactam + macrolide
39
Q

Treating inpatients for pneumonia

A
  • Try to obtain sputum cx to guide treatment
  • Empiric Regimen while awaiting results:
  • Fluoroquinolone (ex. levofloxacin) OR Beta-lactam + macrolide

***These regimens cover atypicals (beta-lactams don’t cover Legionella, which is considered an “atypical organism” even though it generally causes a lobar infiltrate and makes people very sick) and provide extra coverage for macrolide-resistant S. pneumo

40
Q

Considerations for immunosuppressed states (impaired humoral, impaired cellular, AIDS, neutropemia, and asplenia)

A
  • Impaired humoral immunity = bacteria
  • Impaired cellular immunity = bacteria, viruses, fungi, PJP, TB
  • AIDS = combo of the above
  • Neutropenia = bacteria, aspergillus
  • Asplenic = increased risk for infection with encapsulated organisms
41
Q

Symptoms of cardiac tamponade

A
  • Beck’s triad: Hypotension, JVD, distant heart sounds
  • Tachycardia (compensatory)
  • Elevated pulsus paradoxus
  • Forward failure (cold extremities, lightheadedness, somnolence)
42
Q

Treating cardiac tamponade

A
  • Short term:
    • Positive inotropes and IV fluids if hypotensive
    • Allow tachycardia
    • Don’t do anything to decrease cardiac output (no nitrates, no diuretics, no beta blockers, no CCBs)
  • Pericardiocentesis as soon as possible
43
Q

Constriction vs tamponade

A
44
Q

Kussmaul’s Sign

A

A paradoxical rise in jugular venous pressure (JVP) on inspiration, or a failure in the appropriate fall of the JVP with inspiration.

This is due to the constrianing effects of a diseased pericardium in constrictive pericarditis. It can also be due to R ventricular infarct, cor pulmonale, or other R heart diastolic failure.

Present in 20-50% of patients with constrictive pericarditis

45
Q

Fick Equation

A
46
Q

Alveolar ventilation equation

A
47
Q

R and L axis deviation

A
48
Q

Why do patients with IPF have decreased oxygen saturation on exertion?

A

The primary mechanism for this is V/Q mismatch. Alveoli are partially destroyed due to fibrosis, and so the SA of any given alveolus is disrupted.

Diffusion barrier is also a contributor, but is not as important as V/Q mismatch.

49
Q

A patient with chronic hypertension presents with this ECG. What is likely the cause of these anomalies?

A

Left ventricular hypertrophy

Not necessarily ischemia

50
Q

Autoimmune hemolytic anemia table

A
51
Q

Endocarditis summary

A
52
Q

Modified Duke criteria

A
  • Designed to provide a good guess of whether or not someone has IE
  • 2 major, 1 major + 3 minor, or 5 minor establish presumptive diagnosis if no other explanation is available
  • Major: 1) positive blood culture + confirmation, 2) evidence of endocardial involvement
  • Minor: 1) Predisposing heart condition OR IV drug use, 2) Fever, 3) Vascular phenomena (evidence of embolism), 4) Evidence of type III hypersensitivity, 5) Microbiologic evidence other than positive blood culture

HMS Homeostasis I (62 decks)

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