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Step 1 > Pulmonary > Flashcards

Pulmonary Flashcards

1
Q

Epistaxis vessels

A

Most commonly occurs in anterior segment (Kiesselbach plexus)
Life threatening hemorrhage if in posterior (sphenopalatine aftery – branch of maxillary)

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2
Q

What does IL-5 do?

A

Calls in eosinophils (seen in asthma, and other stuff)

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3
Q

What does IL-4 do?

A

IgE class switch

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4
Q

What does Il-10 do?

A

inhibits TH1 cells and stimulates more TH2 cells (which release IL-4, 5, and 10

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5
Q

Gene associated w/ primary pulmonary HTN

A

Inactivation of BMPR2 (usually inhibits vascular sm muscle formation)

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6
Q

lung stem cell?

A

Type II pneumocyte. Also makes surfactant

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7
Q

Who are predisposed to lung abscess?

A

those at risk of LOC & aspiration. Oropharyngeal contents (esp alcoholics, epileptics) lead to anaerobes invading: Bacterioides, fusobacterium, peptostreptococcus and S aureus.
Tx: clinda

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8
Q

Bacteria likely in lung abscess (4)

A

Bacterioides
Fusobacterium
Peptostreptococcus
S. aureus

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9
Q

Tx for lung abscess

A

Clindamycin

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10
Q

Uses for H1 blockers

A

allergy, motion sickness, sleep aid

Diphenhydramine, dimenhydrinate, chlorpheniramine

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11
Q

Three H1 blockers (1st Gen)

A

Diphenhydramine
Dimenhydrinate
Chlorpheniramine

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12
Q

1st gen Histamine blocker toxicity

A

Sedation, antimuscarinic, anti-alpha adrenergic

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13
Q

2nd gen H1 blockers (four)

A

Loratidine
Fexofenadine
Desloratadine
Cetirizine

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14
Q

Use for 2nd gen H1 blockers

A

allergies

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15
Q

Benefit of 2nd gen H1 blockers

A

less sedating than 1st gen because decreased CNS entry

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16
Q

Guaifenesin use

A

expectorant, thins secretions; does not suppress cough

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17
Q

N-acetylecysteine uses

A

Mucolytic, loosens mucous plugs in CF patients by disrupting disfulfide bonds
- also used in acetaminophen overdose

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18
Q

Dextromethorphan use

A

antitussive ; synthetic codeine analog. Has mild opioid effect when used in excess
- give naloxone for OD.

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19
Q

Dextromethorphan MOA

A

NMDA glutamate receptor antagonist

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20
Q

Two adverse effects of dextromethorphan

A
  1. Overdose - needs naloxone

2. serotonin syndrome if combined w/ other serotonergic drugs

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21
Q

Pseudoephedrine, phenylephrine MOA

A

alpha adrenergic agonists, used as nasal decongestants

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22
Q

Pseudoephdrine and phenylephrine use

A
  • reduce hyperemia, edema, nasal congestion
  • open obstructed Eustachian tubes
    Note: illicitly used to make meth!!
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23
Q

Pseudoephedrine/phenylephrine toxicity

A
  1. HTN

2. CNS stimulation/anxiety (pseudoephedrine)

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24
Q

Endothelin receptor antagonists (use)

A

Pulmonary HTN (ex: Bosentan)

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25
Q

Bosentan

A

Endothelin receptor antagonist used in pulmonary HTN, decreases pulmonary vascular resistance

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26
Q

Bosentan / endothelium receptor adverse effect

A

Hepatotoxicity. Monitor LFTs

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27
Q

PDE-5 inhibitors

A

sildenafil - used in pulmonary HTN

Ihhibits cGMP PDE5 and prolongs the vasodilatory effect of NO.

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28
Q

Prostacyclin analogs (two)

A

Epoprostenol
Iloprost
PGI1 (prostacyclin) w/ direct vasodilatory effects on pulmonary and systemic arterial vascular beds
- inhibits platelet aggregation

29
Q

Epoprostenol and Iloprost (use)

A

Prostacyglin analog - used in pulp HTN for vasodilatory effects on both pulmonary and systemic arterial vascular beds
- also inhibits platelet aggregation

30
Q

Side effects of epoprostenol and iloprost

A

Flushing, jaw pain

31
Q

B2 agonists (3)

A

Albuterol, salmeterol, formoterol

32
Q

Albuterol MOA

A

Beta 2 agonist, relaxes bronchial smooth muscle

use for exacerbation

33
Q

Salmeterol MOA

A

Long acting Beta 2 agonist for prophylaxis

34
Q

Salmeterol adverse effects

A

Tremor, arrhythmia

35
Q

Fluticasone and Budesonide MOA

A

corticosteroids, inhibit cytokines
Inactivate NF-kB, which is the transcription factor that induces production of TNF-a and other inflammatory agents. 1st line for chronic asthma

36
Q

Ipratropium MOA

A

Muscarinic antagonist - competitive blocker of muscarinic receptors to prevent bronchoconstriction via parasympathetics. Also used in COPD.

37
Q

diff btw ipratropium vs tiotropium

A

tiotropium is long acting

38
Q

Montelukast, zafirlukast MOA

A

anti-leukotrienes. Block the CysLT1 leukotriene receptors. **Especially good for aspirin-induced asthma

39
Q

Zileuton

A

antileukotriene, blocks the 5-lipooxygenase pathway which converts arachidonic acid to leukotrienes. Hepatotoxic

40
Q

Zileuton SE

A

hepatotoxicity

41
Q

Omalizumab

A

Anti-IgE monoclonal antibody, binds mostly unbound serum IgE and blocks binding to FcERI. Used in allergic asthma resistant to steroids and long acting beta2 agonists

42
Q

Theophylline MOA

A

Methylxanthine - likely causes bronchodilation via inhibition of phosphodiesterase –> increased cAMP due to decreased cAMP hydrolysis.
NARROW THERAPEUTIC INDEX, can induce cardiotoxicity and neurotoxicity

43
Q

Theophylline SE

A

Narrow therapeutic window, can induce cardiotoxicity and neurotoxicity
Metabolized by cyp450. Blocks actions of adenosine

44
Q

Methacholine use

A

Muscarinic receptor agonist. Used in bronchial challenge test to help diagnosee asthma

45
Q

What is major basic protein?

A

released by eosinophils, a potent anti-helminthic toxin that can cause damage to epithelial and endothelial cells.

46
Q

What are in basophil granules?

A

heparin, histamine, SRS-A (mixture of leukotrienes)

47
Q

Mutation of Bruton tyrosine kinase causes

A

X-linked agammaglobulinemia; Causes failure of bone marrow pre-B cells (CD19+ and CD20+) to develop into mature B cells (CD19+, 20+ and 21+). They have low or absent B cells, increased risk of infection with pyogenic (encapsulated) bacteria. Also increased risk of viral and parasites like enterovirus and guardians 2/2 lack of neutralizing antibodies

48
Q

Where do you find CD15 cell marker

A

granulocytes

also Reed-Sternberg cells (useful for Hodgkins marker)

49
Q

Main CF mutation (70% of cases) does what?

A

three BP deletion of phenylalanine at AA 508, causes impaired post-translational processing (improper folding/glycosylation) - targeted for proteasomal degradation and never reaches the cell surface

50
Q

Mechanism of smoking on patients with AAT def?

A

Inactivates AAT through oxidation of a methionine residue - therefore devpt of emphysema happens at like 36 y/o instead of 51 in non-smokers

51
Q

Biostats question: what tests do you use to compare the means of different groups?

A

ANOVA - two or more

t-test - two groups

52
Q

Why does pO2 drop as blood goes from lungs into systemic circulation

A

addition of deoxygenated blood from bronchial circulation, intrapulm arteriovenous anastomoses, and Thebesian veins of the heart.

53
Q

Where should thoracentesis be performed?

A

8th rib in midClav line, 10th rib on mid ax line, 12th rib on post scapular or paravertebral line. Lower than this risk injury to abdominal structures, and insertion of needle on INFERIOR margin risks subcostal neurovascular bundle injury

54
Q

Tx for disseminated MAC

A

azithro w/ rifabutin or ethambutol.

Azithro is prophylaxis

55
Q

Which interleukins play a role in asthma

A

Th2 secrete IL4 (IgE class switch)
IL-5 (eosinophil recruitment)
IL-10 (increase TH2 cell proliferation)

56
Q

IL-3 Function?

A

stimulate bone marrow stem cells

57
Q

Symptoms of Selective IgA deficiency

A

Most are asymptomatic
Some have recurrent sinopulmonary and GI info
concomitant autoimmune disorder also common
Can cause reaction during blood txfusion due to formation of IgE against IgA

58
Q

C1 inhibitor deficiency causes what?

A

hereditary angioedema

59
Q

3 phases of pertussis

A

Catarrhal: like most URIs
Paroxysmal: severe cough w/ insp whoop or post tussive vomiting
Convalescent: cough improves

60
Q

What kind of bacteria is bordetella pertussis?

A

gram negative coccobacillus

Pertactin is what allows it to adhere to ciliated epithelium

61
Q

What inhibits neutrophil elastase?

A

alpha one antitrypsin

62
Q

what inhibits macrophage elastase?

A

tissue inhibitors of metalloproteinases (TIMPs)

63
Q

What are club cells?

A

Formerly Clara. Non-ciliated cells in terminal portions of bronchioles. Secrete proteins that protect against airway inflammation and oxidative stress, and surfactant components to prevent bronchiolar collapse

64
Q

What is IL-12?

A

When macrophage presents to a T cell, it produces IL-12 that will stimulate differentiation into TH1 subset.

65
Q

TH1 cells do what?

A

Cell-mediated immunity, activate macrophages and cytotoxic T cells. Secrete IL-2, IFN-gamma, and lymphotoxin beta. Result: Cytotoxicity, delayed hypersensitivity

66
Q

TH2 cells do what?

A

Humoral (antibody mediated), activate B cells and promote class switching. Release IL-4, 5, 10, and 13. Promotes secretion of antibodies.

67
Q

What does IFN-gamma do?

A

activate macrophages - these are necessary for delayed hypersensitivity rxn and cytotoxicity against intracellular organisms (like mycobacteria)

68
Q

IL-12 receptor deficiency predisposes to?

A

Severe mycobacterial infections. This is because IL-12 makes helper T cells differentiate into TH1, which release IFN-gamma to active macrophages.

Step 1 (6 decks)

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