USMLE World Flashcards

0
Q

In type 1 hypersensitivity, IgE binds to the antigen. What causes the anaphylactic reaction?

A

IgE’s cross link on pre-sensitized mast cells and aggregate, causing degranulation. Histamine is responsible for most of the effects, but tryptase is also elevated.

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1
Q

Pulmonary reaction to histoplasma

A

Similar to TB. Fungal spores from bat droppings are inhaled and ingested by alveolar macrophages, where they can be seen as ovoid cells. The immune response is to form granulomata.

Some pts may develop acute pulmonary disease, and those with underlying disease may develop chronic pulmonary histoplasmosis, which resembles TB.

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2
Q

What must always be equal in the systemic and pulmonary circulation?

A

Blood flow per minute. Doesn’t matter if it is rest or exercising.

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3
Q

How does N-acetylcysteine help in CF?

A

N-acetylcysteine is a mucolytic agent that cleaves disulfide bonds in mucus glycoproteins

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4
Q

Nosocomial pneumonia, visualized with silver stain, grows on charcoal yeast with cysteine supplementation.

May show hyponatremia, GI, and CNS symptoms

A

Legionella - contaminates water sources, transmitted by aerosol transmission from the water source.

Tx macrolide or quinolone

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5
Q

Epithelium of the respiratory tract: nose, paranasal sinuses, nasopharynx, oropharyxn, laryngopharynx, larynx, anterior epiglottis, vocal folds.

A

Pseudostratified columnar: nose, paranasal sinuses, nasopharyxn, larynx, tracheobronchial tree

Stratified squamous: oropharynx, laryngopharynx, anterior and part of posterior epiglottis, vocal folds.

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6
Q

Are the expiratory flow rates in restrictive lung disease increased or decreased? Why

A

Increased expiratory flow rate

Decreased lung compliance, and increased radial traction exerted on the conducting airways by fibrotic lung

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7
Q

What kind of sweat do you see in CF pts?

A

These patients cannot resorb Cl and Na in the eccrine ducts, sweat is relatively hypertonic.

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8
Q

What is Cheyne Stokes breathing?

A

A breathing pattern seen in CHF. Apnea, increasing tidal volume, decreasing tidal volume, apnea, etc. Due to delayed feedback, leading to overcompensation.

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9
Q

What cells are responsible for protease and elastase release in centriacinar emphysema?

A

Macrophages and neutrophils. Neutrophils also generate free radicals which inhibit anti-protease activity.

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10
Q

Pt presents with triad of hypoxemia, confusion, and petechial rash in the setting of long bone fracture. Dx?

A

Fat embolism. Can cause respiratory distress, thrombocytopenia, and anemia. Fat emboli can be stained with osmium tetroxide.

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11
Q

Middle aged patient with sudden onset dyspnea and calf swelling.

A

Pulmonary embolism

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12
Q

pH, PaO2, PaCO2, and plasma bicarb expected in PE

A

Hypoxemia leads to hyperventilation and respiratory alkalosis. Increased pH, decreased PaO2, PaCO2.

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13
Q

High altitude: pH, PaO2, PaCO2, plasma HCO3-

A

Hypoxia stimulates body to increase ventilatory drive. Leads to respiratory alkalosis, increasing pH and decreasing PaCO2. Low bicarb by compensation, and low-ish oxygen.

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14
Q

What is the driver of respiratory regulation in health people? In people with longstanding COPD?

A

Normal: PaCO2 is major stimulator through central medullary respiratory center (pH and PaO2 are less important until you get profound hypoxemia)

COPD: Prolonged hypercapnia leads to PaCO2 no longer driving. PaO2 sensed in the peripheral chemoreceptors (eg carotid body) stimulate respiration.

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15
Q

Bronchiolitis obliterans

A

Chronic rejection after lung transplant affecting small bronchioli. An obstructive lung disease.

Lymphocytic inflammation, necrosis of bronchiolar walls, and fibrosis. Finally leading to occlusion of bronchiolar lumen

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16
Q

Cause of spontaneous pneumothorax, classic presentation

A

Caused by rupture of apical subpleural blebs.

Sudden onset unilateral chest pain with hyperresonance and absent breath sounds in a tall, thin male around 20 y/o.

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17
Q

How might one’s lungs be hosting species such as peptostreptococcus and fusobacterium?

A

These are normal oral flora. Can get in by aspiration or seizure disorder, which can cause aspiration. Lung abscesses often contain oral flora

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18
Q

How do lung abscesses happen? (3 ways)

A
  1. Aspiration (increased risk with any loss of consciousness)
  2. Complication of bacterial pneumonia, especially in nosocomial pneumonias of old or immunocompromised. S aureus, E. coli, klebsiella, or strep pneumonia
  3. Hematogenous spread of infection from endocarditis. Staph, strep, ecoli, fungus
19
Q

Major causes of pulmonary artery hypertension

A

Idiopathic hereditary (BMPR2 gene, vascular smooth muscle proliferation); Left heart failure; Chronic hypoxia (COPD, OSA); chronic thromboembolism; HIV

20
Q

CF effects on pancreas

A

Sever CF may cause total obstruction and fibrotic atrophy. Pancreatic insufficiency then causes deficiency of fat soluble vitamins (ADEK).

Low vitamin a causes squamous metaplasia

21
Q

How does the vagus nerve affect the lungs?

A

Increases bronchial smooth muscle constriction –> increases work of breathing. Increases bronchial secretions –> increases airflow resistance => increases work of breathing.

Via M3 receptor.

22
Q

What are the 4 stages of lobar pneumonia?

A

Congestion (first 24 hours)
Red hepatization (days 2-3)
Gray hepatization (days 4-6)
Resolution

23
Q

Lobar pneumonia congestion stage: macroscopic and microscopic appearance

A

Macroscopic: lobe is red, heavy, boggy
Micro: vascular dilation, edema, alveolar exudate of mostly bacteria

24
Q

Lobar pneumonia red hepatization stage: macroscopic and microscopic appearance

A

Macro: red, firm, liver-like
Micro: exudate contains RBCs, neutrophils, fibrin

25
Q

Lobar pneumonia, gray hepatization stage: macroscopic and microscopic

A

Macro: gray-brown, firm
Micro: RBCs lyse, exudate contains neutrophils and fibrin

26
Q

Lobar pneumonia, resolution phase

A

Restoration of normal architecture, enzymatic digestion of exudate

27
Q

What is the most common cause of meconium ileus?

A

CF

28
Q

Where is the fetal blood richest in oxygen content?

A

Mom - umbilical vein - liver (ductus venosus) - IVC - heart - tissues - umbilical arteries

29
Q

At what point is the fetal lung considered to be mature?

A

When the lecithin to sphingomyelin ratio is > 2.

Note: lecithin is aka phosphatidylcholine.

30
Q

What are Clara cells?

A

non-ciliated, secretory constituents of the terminal respiratory epithelium. Their secretion inhibits neutrophil recruitment/activation and neutrophil dependent mucin produciton. Also secrete surfactant precursors.

31
Q

What are lamellar bodies? What can destruction of them cause?

A

Lamellar bodies store and release sufactant in type II pneumocytes. Destruction leads to patchy atelectasis (collapse of alveoli), as in neonatal respiratory distress syndrome

32
Q

How does COPD affect EPO production?

A

Hypoxia is sensed and EPO production is increased.

33
Q

What measurement is a direct indicator of alveolar ventilation?

A

PaCO2.

Hypocapnea implies alveolar hyperventilation, and hypercapnea implies hypoventilation.

34
Q

What drug has a similar structure to pyroxidine?

A

Isoniazid, an anti-TB. Note that pyroxidine = B6

35
Q

Indications for rifampin

A

Used as part of multi-component therapy for mycobacterial pulmonary infections, leprosy, and staph endocarditis.

Prophylaxis for exposure to n. meningitidis and h.flu

36
Q

Mechanism of isoniazide

A

Inhibits mycolic acid synthesis, which is important in the cell wall of acid-fast bacteria.

37
Q

Mechanism of rifampin

A

inhibits transcription. Used for Tb but also for other things. Resistance is via altered binding site on RNA synthesis enzymes.

38
Q

Non-selective vs selective beta blockers

A

Non-selective: propanolol, timolol, nadolol

Selective: metoprolol, atenolol, emsolol (prefered in pts with asthma or copd)

39
Q

What is the alveolar gas equation and what is it used to calculate?

A

Calculate the partial pressure of oxygen in the alveolar air. Depends on PO2 in inspired air, PaCO2, and respiratory quotient (Co2 produced.O2 consumed).

PAO2 = 150 - PaCO2/0.8

40
Q

What is a normal A-a gap? What would a high A-a gap signify?

A

Normal is 10-15. High A-a occurs in hypoxemia due to shunting, V/Q mismatch, or fibrosis (impaired diffusion)

41
Q

What happens in a panic attack? Why do people get dizzy?

A

Hyperventilation –> decreased pCO2 –> vasoconstriction –> decreased cerebral blood flow

42
Q

What is the difference between panacinar and centriacinar emphysema?

A

Centriacinar: smoking, upper lobes
Panacinar: A1AT deficiency, lower lobes, can also develop liver cirrhosis.

43
Q

How do granulomatous diseases (sarcoidosis, tb, Hodgkin’s and non-Hodgkin’s) affect electrolytes?

A

Increased calcium absorption and bone resorption –> hypercalcemia

44
Q

What is the chloride shift?

A

CO2 taken up by RBCs in the tissues is converted by carbonic anhydrase to bicarb. The bicarb diffuses out of the cells, and Cl diffuses in to keep electroneutrality. High Cl in venous blood compared to arterial.

45
Q

What is the most potent cerebral vasodilator?

A

pCO2 –> decreases cerebral vascular resistance and increases cerebral perfusion in cases of hypoxia and hypercapnia.