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Step 1 Flash Cards > Pulm > Flashcards

Pulm Flashcards

1
Q

Structures cross the diaphragm at what levels

A

I ate 10 eggs at 12

  • IVC - T8
  • esophagus - T10
  • aorta - T12
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2
Q

physiologic dead space equation

A

Vd = Vt x (PaCO2 - PeCO2)/PaCO2
taco, paco peco, paco
= tidal volume (arterial PCO2 - expired air PCO2)/arterial PCO2

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3
Q

things that favor the taught form of Hgb

A

Cl-, H+, CO2, 2,3BPG and temperature

- right shift favored by BAT ACE: BPG, altitude, temp, acid, CO2, exercise

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4
Q

methemoblobin

A
  • oxidized Hgb (Fe3+), doesnt bind Hgb as well, seen in newborns and with oxidative stress (cyanosis and chocolate covered blood)
  • binds cyanide well, so give nitrites to form methemoglobin in cyanide poisoning, then give thiosulfate to bind cyanide and be renally excreted
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5
Q

carboxyhemoglobin

A

CO binds Hgb, causes a left shift and pts have cherry red skin

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6
Q

perfusion limited vs. diffusion limited

A
  • perfusion limited: things that are perfusion limited equilibrate early: O2 in healthy ppl, CO2, N2O
  • diffusion limited: things that do not equilibrate by the time the blood reaches the end of the capillary: O2 in emphysema and fibrosis, CO
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7
Q

hypoxemia with normal Aa gradient

A

high alt, hypoventilation

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8
Q

hypoxemia with increased Aa gradient

A

VQ mismatch, diffusion limitation, RL shunt

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9
Q

V/Q = 0

A

shunt

- does not improve with 100% O2

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10
Q

V/Q = infinity

A

blood flow obstruction

- does improve with 100% O2

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11
Q

Haldane effect

A

oxygenation of Hgb promotes dissociation of H+ from Hgb, therefore CO2 is released

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12
Q

Bohr effect

A

increased H+ in the tissue causes a right shift, causing unloading of O2

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13
Q

response to high altitude

A

decreased PaO2 leads to hyperventilation

  • increased EPO
  • increased 2,3BPG for more O2 unloading
  • more renal excretion of bicarb to compensate for respiratory alkalosis
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14
Q

response to exercise

A

increased CO2 production and O2 consumption

  • increased ventilation rate, and V/Q becomes more uniform throughout the lung
  • no change in PaO2 and PaCO2, but increase in venous CO2 and decrease in venous O2 content
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15
Q

rhinosinusitis bugs

A

S. pneumo, H flu, M catarrhalis

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16
Q

virchow triad

A
  • predisposition to DVTs

- stasis, hypercoagulability, endothelial damage

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17
Q

different types of emboli and their classic findings

A
  • fat: hypoxemia, neurologic abnormalities and petechial rash
  • amniotic fluid: DIC
  • gas: divers, treat with hyperbaric O2
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18
Q

centriacinar vs. paracinar emphysema

A
  • centri - smokers

- para - alpha 1 antitrypsin

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19
Q

asthma path findings

A 
Curschman spirals (shed epithelium forms mucus plugs)
Charcot-Leyden crystals (formed from breakdown of eosinophils in sputum)
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20
Q

bronchiectasis

A
  • chronic necrotizing infection of bronchi –> permanently dilated airways, purulent sputum, recurrent infections and hemoptysis
  • assoc w/ bronchial obstruction, poor ciliary motility (smoking), Kartagener syndrome, CF, allergic bronchopulmonary aspergillosis
21
Q

asbestosis findings and increased risks

A
  • asbestos (ferrunginous) bodies are golden-brown fusiform rods resembling dumbells
  • increased incidence of bronchogenic carcinoma and mesothelioma
22
Q

silicosis findings

A
  • impairs macrophages, leads to fibrosis and increased susceptibility to TB
  • “eggshell” calcification of hilar lymph nodes
23
Q

pulm HTN

A
  • primary due to BMPR2 gene, leading to vascular smooth muscle cell proliferation, poor prognosis
  • secondary due to COPD, VTE, AI disease, L-R shunt, sleep apnea or high alt
24
Q

most common sites that metastasize TO the lungs

A

breast, colon, prostate, bladder

25
Q

most common sites that the lungs metastasize to

A

adrenals, brain, bone, liver

26
Q

lung adenocarcinoma

A
  • most common
  • peripheral
  • activating mutations include k-ras, EGFR, and ALK
  • clubbing
27
Q

squamous cell carcinoma of the lung

A
  • Central, Cavitation, Cigarrettes, hyperCalcemia (PTHrP)
  • SCa+++mous
  • keratin pearls and intercellular bridges
28
Q

small cell (oat cell) lung cancer

A
  • central, undifferentiated, aggressive
  • Acth, Adh, Antibodies (Lambert-Eaton), Amplification of myc
  • inoperable, treat with chemo
  • neoplasm of the neuroendocrine Kulchitsky cells –> small dark blue cells
29
Q

large cell carcinoma

A
  • peripheral
  • highly anaplastic undiff tumor, poor prognosis
  • removed surgically
  • pleomorphic giant cells
30
Q

bronchial carcinoid tumor

A
  • excellent prognosis
  • symptoms due to mass effect, occasionally carcinoid syndrome (flushing, diarrhea, wheezing)
  • nests of neuroendocrine cells, Chromagranin A +ve
31
Q

mesothelioma

A
  • malignancy of the pleura with hemorrhagic pleural effusions and pleural thickening
  • psammoma bodies
32
Q

pancoast tumor

A
  • Horner, SVC, sensorimotor defects, hoarseness, upper extrem edema
33
Q

transudate pleural effusion

A

low prot content

- CHF, nephrotic syndrome, hepatic cirrhosis

34
Q

exudate pleura effusion

A

high prot content

- malignancy, infection, collagen vascular disease, trauma

35
Q

lymphatic pleural effusion

A
  • milky fluid with high TG

- thoracic duct injury

36
Q

1st gen H1 blockers

A
  • diphenhydramine, dimenhydrinate, chlorpheniramine
  • used in allergy, motion sickness, sleep aid
  • tox - sedation, antimuscarinic, anti-adrenergic
37
Q

2nd gen H1 blockers

A
  • loratidine, fexodenadine, desloratidine, cetirizine
  • used in allergy
  • tox - less sedating because less CNS penetration
38
Q

guaifenesin

A

expectorant - thins resp secretions, does not suppress cough reflex

39
Q

NAC

A

mucolytic - can loosen mucous plugs in CF kids

40
Q

dextromothorphan

A
  • antitussive (NMDA antagonism)
  • synthetic codeine analog
  • mild opioid effect in excess, mild abuse potential
  • naloxone can be given for overdose
41
Q

pseudoephedrine, phenylephrine

A
  • alpha agonist nasal decongestants
  • reduce hyperemia, edema and nasal congestion
  • tox - HTN, can also cause CNS stimulation/anxiety
  • tachyphylaxis - rapidly declining effect after a few days due to decreased production of norepi at nerve terminals
42
Q

b2 agonists

A
  • albuterol (short), salmeterol, formoterol (long-acting)
  • relaexes smooth muscle
  • SE: tremor and arrhythmia
43
Q

theophylline

A
  • methylxanthine that causes bronchodilation by inhibiting PDE –> inc CAMP because of decreased breakdown
  • narrow TI, p450 metabolizes it, blocks adenosine actions
44
Q

beclomethasone, fluticasone

A

corticosteroids that inactivate NFkB, the transcription factor that induces the production of TNFa and other inflammatory cytokines

45
Q

monteleukast, zafirlukast

A

leukotriene receptor blocker, good for aspirin-induced asthma

46
Q

zileuton

A

5-lipoxegenase pathway inhibitor (blocks AA –> leukotriene conversion)

47
Q

omalizumab

A

monoclonal IgE Ab for allergic asthma

48
Q

bosentan

A

used to treat pulmonary arterial hypertension, competitively antagonizes endothelin-1 receptors, decreased pulmonary vascular resistance

Step 1 Flash Cards (36 decks)

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