Respiratory Flashcards

1
Q

type I pneumocytes

A

97% of aveoli surface, just thin and don’t do shit

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

type II pneumocytes

A

screte surfactant, cuboidal, differentiate into type I cells, they proliferated in response to injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what in amniotic fluid indicates fetal lung maturity

A

lecithin:sphingomyelin ratio >2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

of lobes of each lung

A

left has 2

right jhas 3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

which lung more commonly gets inhaled foreign body

A

right

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

aspirate peanut while standing, where does it go?

A

lower portion of right inferior lung

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

aspirate peanut while lying (supine), where dose it go?

A

superior portion of right inferior lobe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

location of pulmanary arteries in relation to hilum of bronchus?

A

RALS: Right Anterior Left Superior

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

perforates diaphram at T8

A

IVC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

perforates diaphragm at T10

A

esophagus and vagus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

perforates diaphragm at T12

A

aorta, thoracic duct, azygos vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

diaphragm pain refers to?

A

C3, 4, 5 shoulder and trapzius

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

muscles used during maximal inspiration?

A

external intercostals, scalene muscles, sternocleidomastoids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

muscles used during maximal expiration

A

rectus abdominis, internal/external obliques , transversus abdominus, internal intercostals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

functional vs anatomical dead space

A

functional is aveoli not being perfused (apex of lung), anatomical is conducting system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

hemoglobin two states

A

tense: low affinity for oxygen (periphery)
relaxed: high affinity for oxygen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

conditions which favor taut form of Hb?

A

high: Cl, H, CO2, 2,3-BPG and temp (shifts curve right)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

how to treat cyanide poisoning?

A

Nitrates oxidize hemoglobin to methemoglobin which favors binding cyanide. then treat with thiosulfate to form thiocyanate to excrete

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is methemoglobin and how to treat methemoglobin?

A

methemoglobin is oxidized hemoglobin that favor cyanide. give methylene blue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what creates methemoglobin?

A

nitrates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

histology of conducting zone vs respiratory zone (respiratory bronchioles and aveoli)

A

conducting zone is pseudostrat columnar ciliated
respiratory bronchioles are cuboidal
aveoli are simple squams
(no cilia cause macrophages clear)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

oxygen binding curve after carbon monoxide

A

left shift cause CO binds waaaaaay stronger

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

hemoglobin vs myoglobin multimer state?

A

4 vs 1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

effects of CO2 and O2 on pulmanary circulation

A

opposite of the rest of the body. hypoxia = vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

is normal gas exchange diffusion or perfusion limited?

A

perfusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

cor pulmonale

A

enlargment of right heart due to increased pulmanary circulation resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

normal pulm artery pressure?

A

10-14

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

gene responsible for primary pulmonary hypertension (and defect?)

A

BMPR2 w/ inactivating mutation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

ventilation and perfusion are greatest where?

A

base of lung

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Haldane effect

A

oxygenated hb dump H which causes biocarb to become CO2 at lungs (opposite of bohr effect/shift)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

virchows triad of DVT risk factors

A

Stasis, hyper coagulability, endothelial damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

dorsiflexion of foot elicits calf pain

A

sign for a deep vein thrombosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

heparin vs warfarin for DVT treatment

A

Heparin is acute prevention and treatment. warfarin is for chronic prevention of recurrance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

sudden onsent dyspneia, chest pain, tachypnea

A

Pulm embolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

high altitutde compensation mechanisms

A

acute: increase ventilation
chronic: high epo to increase hct, high 2,3-BPG, high bicarb excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

types of pulmonary emboli

A

FAT BAT: Fat, Air, Bactera, Amniotic, Tumor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Fat emboli etiology and triad

A

long bone fractures/liposuction

triad: hypoxemia, neurological abnormalities, and petechial rash

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

how to distinguish between post and premortum emboli via histology?

A
pink = plates (pre)
red = RBCs (post)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Chronic Bronchitis mechanism?

A

hypertrophy of mucus secreting glands, thick bronchi

40
Q

Reid index (thickness of glands/bronchial wall) to diagnose chronic bronchitis?

A

> 50%

41
Q

Mechanism of Emphysema

A

enlargment of airspaces due to destruction = less recoil so can’t collapse lungs to remove old air

42
Q

two type of Emphysema and their respective asssociations

A

Centriacinar: smoking
Panacinar: alpha1-antitrypsin deficency

43
Q

Emphysema elastase activity

A

increased resulting in loss of elastic fibers. they exhale through pursed lips

44
Q

Methacholine challenge

A

asthma test (causes asthma acutely)

45
Q

Asthma histology (3)

A

smooth muscle hypertrophy, Curschmann’s spirals (mucus/epi plugs), CHarcot-Leyden crystals (eosinophil breakdown product)

46
Q

bronchiectasis

A

chronic necrotizing infxn of bronchi -> dialated airways, hemoptysis, purulent sputum. Seen in CF, obstruction, kartageners

47
Q

Asthma is obstructive or restrictive?

A

obstructive

48
Q

obstructive vs restrictive

A

obstructive: air trapping
restrictive: lung expansion restricted

49
Q

what can cause pneumoconioses?

A

coal (anthracosis), silica (silicosis), asbestos (asbestosis)

50
Q

anthracosis cause and where it effects

A

coal (BLACK LUNG), affects upper lobes

51
Q

Silicosis effects where in the lungs?

A

upper lobes

52
Q

who might get silicosis

A

silica exposure: foundries, sandblasting, mines

53
Q

what does silicosis do to the lungs?

A

macrophages release fibrogenic factors. risk of TB and carcinoma

54
Q

eggshell calcifications of hilar lymph nodes

A

Silicosis

55
Q

Ivory white calcified pleural plaques

A

pathognomonic of asbestosis

56
Q

golden-brown fusiform rods that look like dumbells

A

asbestosis

57
Q

who might get asbestosis

A

shipbuilders, roofers, plumbers

58
Q

risks of asbestosis?

A

carcinoma and mesothelioma

59
Q

where does asbestosis effect?

A

lower lobes (only one of the pneumoconioses to hit lower lobes)

60
Q

Neonatal respiratory distress syndrome cause and test

A

surfactant deficency. lecithin: sphingomyelin ratio

61
Q

risks of neonatal respiratory distress syndrome and risk of treatment

A

PDA (low O2). But O2 supp leads to retinopathy of prematurity and bronchopulmonary dysplasia.

62
Q

acute respiratory distress syndrome causes

A

trauma, uremia, sepsis, shock, gastic aspiration, acute pancreatisis, amniotic fluid embolism

63
Q

ARDS pathophys

A

chronic: diffuse aveolar damage causes increase capillary permeability causes proteinacous fluid in aveoli which forms hyalin membrane in aveoli.
acute: neutrophils, coag cascade, oxygen derived free radicals

64
Q

FEV1/FVC for normal, obstructive and restrictive

A

normal: 80%

Obstructive

65
Q

what is sleep apnea and causes

A

stop breathing >10sec repeatedly while sleeping. typically very tired cause they wake up a lot. also hypoxia leads to high RBC. can be central or obstrucutive (snoring/fat/resistance present)

66
Q

sleep apnea treatment

A

weight loss, CPAP, surgery

67
Q

leading cause of cancer death? (ie type)

A

lung cancer

68
Q

coin lesion in lung on xray or ct

A

lung cancer

69
Q

most common lung cancer

A

met from another tumor

70
Q

where do lung cancers met?

A

adrenals, brain, bone (path fracture), liver

71
Q

lung cancer complications

A

SPHERE of complications: Superior vena cava syndrome, Pancoast tumor, Horners syndrome, Endocrine (paraneoplastic cause of ACE and stuff), Recurrenty laryngeal symptoms, Effusions

72
Q

which lung cancers aren’t smoking associated?

A

bronchioloalveolar and bronchial carcinoid

73
Q

lung adenocarcinoma location and histology

A

peripheral. bronchioalveolar subtype grows along septa so septal thickening

74
Q

lung adenocarcinoma characteristics

A

most common lung cancer in non smokers. activation of k-ras. displays clubbing.

75
Q

Bronchioloaveoloar subtype of lung adenocarcinoma findings and prognosis

A

histology has “septal thickening”, CXR has hazy infiltrates like pneumonia. Excellent prognosis

76
Q

lung squamous cell carcinoma

A

centrally located. hilar mass from broncus. Cavitation, Cigarettes, hyperCalcemia.

77
Q

keratin pearls and intercellular bridges histology in lung

A

squamous cell carcinoma of lung

78
Q

small dark blue cells “oat cells”

A

small cell carcinoma of lung

79
Q

small cell carcinoma of lung

A

located centrally. very aggressive undifferentiated neuroendocrine cells. produce ACTH, ADH, Antibodies against presynaptic Ca channels, Amplification of myc oncogenes

80
Q

large cell carcinoma of lung

A

peripherally located. anaplastic undiff tumor with poor prognosis, surgery is only option… giant cells

81
Q

bronchial carcinoid tumor

A

neuroendocrine cells which has great prognosis and no mets. just mass effect is dangerous (and maybe carcinoid syndrome)

82
Q

lung cancer with chromogranin positive cells

A

bronchial carcinoid tumor

83
Q

Lung Psammoma bodies

A

mesothelioma

84
Q

mesothelioma

A

pleural tumor associated with asbestosis. hemorrhagic effusions

85
Q

pancoast tumor

A

carcinoma in the apex of the lung which impinges on cervical sympathetic plexus causing Horners (ipsilateral ptosis, miosis, anhidrosis)

86
Q

superior vena cava syndrome

A

obstructed SVC - blood cant drain from head - JVD - upper extremity edema. Caused by malig and thrombosis for catheters. Medical emergency cause high ICP causes aneurysms

87
Q

lobar pneumonia

A

S. pneumo (Klebsiella rare). Intra-aveolar exudate/consolidation (may involve all lung but typically in one lobe)

88
Q

Bronchopneumonia

A

S. pneumo, S. aureus, H. influ, Klebsiella. acute inflammatory infiltrates from bronchioles into aveoli = patchy distribution in 1 or more lobes

89
Q

interstitial (aytpical) pneumonia

A

viruses, mycoplasma, legionella, chlamydia. diffuse patchy inflammation localized to interstitial areas at alveolar walls. slow indolent course

90
Q

lung abscess organisms

A

S. aureus or anaerobes (bacteroides, fusobacterium, peptostreptococcus)

91
Q

hypersensitivity pneumonitis

A

mixed type 3/4 hypersensitivity due to antigen causing dyspnea, cough, chest tightness. seen in farmers and bird exposures

92
Q

transudate pleural effusion

A

low protein content due to CHF, nephrotic syndrome, or cirrhosis

93
Q

exudate pleural effusion

A

high protien content. cloudy. due to malignancy, pneumoia, collagen cascular disease, trauma. MUST BE DRAINED

94
Q

lymphatic pleural effusion

A

aka chylothorax. thoracic duct injury so milky pus filled

95
Q

spontaneous pneumothorax

A

air gets into thorax despite intact chest wall. in tall thin guys cause of apical blebs rupturing. trachea deviates TOWARD lesion

96
Q

tension pneumothorax

A

trauma or infxn causes air to enter thorax. trachea deviates AWAY from affected lung.