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respirator Flashcards

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USMLE® Step 1 flashcards
1
Q

what is the ansa cervicalis made up off? and how do you damage it

A

Ansa Cervicalis
• C1, C2, and C3
• Innervates sternohyoid, sternothyroid and
omohyoid
• Damaged with penetration above cricoid
cartilage
located at antrior wall of carotid sheath
superior root/inferior root combine-sup from hypoglossal nerve( ventral ramus of c1 join hypoglossal nerve

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2
Q

give anatomical relations with thyroid artery and laryngeal nerve
where does pec major insert?

A

• Runs posterior to carotid sheath and with
recurrent laryngeal nerve
-lat lip of humerus

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3
Q

what is haldane vs bohr effect

A

Deoxygenated Hb: buffers H+ very well
on His residues > stabilizes and
decreases affinity for oxygen
Bohr effect

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4
Q

how to examine erythroblastosis etalis

A

aminocentess

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5
Q

what activates fetal lung maturation

what can prevent cerebral palsy in preerm

A

dexomethasone+terbutaline

MG

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6
Q

acute lung transplant most common response
Hyperacute
what is resrictive allograft syndrome

A

Acute CMI perivascular and peribronchial(submucosal)
lymphocytic infiltrates
Will see perihilar and lower lobe
opacities
neutrophilic infitration wih fibronoid necrosis
-pleura fucked leads to restricion

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7
Q

why do we have anaphylaxis in IGA deficiency

A

IGE formed against IGA

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8
Q

wha is the marker of cd15

cd16

A

mcrophages / rs cells
nk cells,, neutrophils and
macrophages

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9
Q

what are the complications of pneumocoocal pneumonia
Allgric asprgiloosus
strongoglyiades

A

lung abscess, empyema and fibrosis
ABGA airwya dilation with infiltrates bronchioectasis
strongo-transient pneumonia

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10
Q

what is pneumolysin

A

toxin that causes pores in strep pneumo

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11
Q

what is the functionof cord factor
-sulfatides
what is the pathogenesis of tb

A

inactivates neutrohpils,
damaging mitochondria, and inducing
TNFalpha release
-fails phagosme and lysosome

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12
Q

what s mycobacterium scrofaleum

A

cervical lymphadenitis

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13
Q

mcc of cap in hiv and nonhiv

A

strep pneumo

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14
Q

risk factors of leiogenlla

A

immunocompromised, smokers,
alcoholics, COPD
Random Influenza A

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15
Q

what are the symptoms of leiogenlla

A

Abrupt onset fever, HA, myalgias that

improve 2• 5 days after

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16
Q

what can actinomycosis be confsued with

who is at bigger risk

A

tb,malignancy/lun abscess

alcoholics

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17
Q

how does pcp preent with

A

slowly worsening
cough and dyspnea, hypoxia, and
bilateral interstitial infiltrates

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18
Q

how does fat emboli release toxinc fa

A

Fat emboli activates the lipoprotein
lipase and intravascular release of toxic
levels of oleic acid

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19
Q

SYMPTOMS OF HTN

A

HA, visual symtpoms, N/V, proteinuria,

hematuria

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20
Q

main cause of nrds

A

lack of pneumo 2 development

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21
Q

what is macrophage ellastae inhibited by

what is neutrophil elastase inhibited y

A

TIMPS (metalloproteiases)

alat1

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22
Q

ARDS pathogenesis
wwhat causes hyalinization
what is the intial phase

A

fibrin deposition + protein cause hyaline
membrane
• Exudate

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23
Q

major difference between Red and gray hepaization

A

the major difference is the rbc component

both contain neutrophil,macrophages, fibrin

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24
Q

characterize rejection of lung

A

inflammation,
fibrosis, and, ultimately,
destruction of the bronchioles.

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25
Q

Large cel ca presenation

A

Gynecomastia and galactorrhea

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26
Q

asbestosis presetation

A

progr dyspnoea, cough, and
chest pain. Unilateral pleural
thickening or plaque .HEMORRHAAGIC pleural effusion

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27
Q

histopath of asbestosis

A

Long slender microvilli and abundant

tonofilaments

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28
Q

what is lofrgen syndrome

A

fever, erythema nodosum, and bilateral hilar adenopathy

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29
Q

what causes centrilobular necrosis

A

• Right HF, drugs, toxins, and fulminant

hepatitis

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30
Q

what is compliction of surfactant treatment

A

Complications of surfactant treatment may include transient hypoxia and hypotension, blockage of an endotracheal tube, and pulmonary hemorrhage.

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31
Q

cmplication of b2 treatment in fetus

A

increased risk of neonatal intraventricular hemorrhage, hypoglycemia, hypocalcemia, and ileus.

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32
Q

distinguish CF from hirschprung

A

cf-meconium ileus=-squirt sign= Pneumonia, bronchiectasis or cor
pulmonale are MCC of death
nephrolithiasis and
nephrotoxic drugs (aminoglycoside)

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33
Q

Hirscprung disease

A 
Rectosigmoid obstruction
• Normal meconium consistency
• Positive squirt sign (forceful explusion of
stool after DRE)
• Enterocolitis is MCC of death
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34
Q

unique consequences of vit e deficiency

A

n, infertility,
decreased serum phospholipids and
increase lipid peroxidation

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35
Q

where other can you find bronchiectasis

A

large-cell lung ca,
TB, CF, and suppurative lung
diseases such as empyema,

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36
Q

cardiac complication of systemic sclerosis

A

Pericardial fibrosis
• Impaired ventricular dilation, kussmaul
sign and pulsus paradoxus
impaired diastolic fillng

37
Q

wht is difference between ghon complex and ranke complex

A

https://www.google.com/search?q=ranke+complex&rlz=1C1GCEB_enCZ924CZ924&sxsrf=ALeKk00YPt13NvHi1O7C5g556ozE9JDgGg:1604511960090&tbm=isch&source=iu&ictx=1&fir=gsm-60wlv7jOvM%252CGIRKlSIoK9la4M%252C_&vet=1&usg=AI4_-kTbdpgBoI4hUUZ4z6iaS5fQZcIJAA&sa=X&ved=2ahUKEwjX2azruOnsAhV6AGMBHd1yBWEQ9QF6BAgKEDQ#imgrc=gsm-60wlv7jOvM

38
Q

where does infection of tb occur

A

lower obe passed by aerolization= ghon focus=fibrosis+nodule =complex

39
Q

4 factors that activate tb

A

(corticosteroids, anti TNF, calcineurin

inhibitors, HIV)

40
Q

hematogenous spread of tb

A

Hematogenous spread
• Basal meninges, lumbar spin, psoas
muscle, pericardium and pleura, kidneys

41
Q

pathophys of ards in sepsis

A

IL 1, 6 and 8 circulate in response to
infection > activate pulmonary epithelium
> recruits neutrophils > lung damage >
alveolar space filled with fluid > ARDS

aspiration also causes ards

42
Q

what causes focal necrosis of alveolar walls

A

Focal necrosis of alveolar walls

• Goodpastures, Wegners, SLE

43
Q

what causes mononuclear inflitrate of lung

if neutrophils in alveoli

A

• Early stage of interstitial lung disease

pneumonia +aspiration

44
Q

why dlco increased in asthma

A

The high DLCO values [123, 124] have been explained by hyperinflation, increased intrathoracic pressure, and a more likely cause, increases in pulmonary capillary blood volume or extravasation of red blood cells into the alveolus.

45
Q

NEutropeia

A

CAMR(candida,asper,mucor,rhizophus)

46
Q

histolgic findings in ILD

A 
s mix of chronic
inflammation and patchy
interstitial fibrosis, focal
fibroblast proliferation, and
formation of fibrotic cystic
spaces in a honeycomb pattern
47
Q

how is siadh charcterized

A

hyponatremia,
decreased serum osmolality, and
urine osmolality >100 mOsm/kg
H2O.

48
Q

why does massive pe cause scd

A

a sudden loss of CO. Less
commonly, SCD may result from
cardiac arrhythmia triggered by
RV strain and ischemia.

49
Q

where are emoheymatous blebs seen

A

e lung apices/it is a result of alveolar desrucion

50
Q

how does aaat look of hist

A 
AATD can
demonstrate reddish-pink
globules on PAS stain; these
globules represent un-secreted,
polymerised AAT in the
periportal hepatocytes.
 resist
digestion by diastase
51
Q

why excercise intolerance in emphysema

A

Dynamic hyperinflation: extra time
required for exhalation, increase the
amount of air trapped in the lungs and
thus reducion tidal volume

52
Q

how does smoking affect aA1AT

A

Release ROS that inhibit A1AT

53
Q

2 diseases caused byionising radiation

A

xeroderma

pigmentosum, ataxia telangiectasia

54
Q

major cause f chni lung dmage in asthma

A

MBP also dmgs epithelial and
endothelial cells and is a major
cause of chronic lung dmg in
asthma.

55
Q

function of il3

A

Bone marrow stem cell proliferation

56
Q

causes of increase in paco2

A

poor ventalation,poor muscle effort,poor chest wall compliance, and airway obstruction

57
Q

what are the two steps involved in PAH

A

abnormal bmpr2—>excessie endothelial prolif, +infection

58
Q

histo of PAH

A

Medial hypertrophy and intimal
hyperplasia/fibrosis (onion skinning) >
plexiform lesions

59
Q

RF for OSA

A

Obesity
• Tonsillar hypertrophy
• Hypothyroidis

60
Q

pulmonary edema causes decreased compliance why

A

diluts surfactan

61
Q

sweat glands in Cf

A 
• CFTR reabsorbs Cl and Na follows
(normally) making sweat hypotonic
• CF pt experience severe hypovolemia
due to excessive Na
loss
62
Q

what is the most common decrease in obesitry in pfe

A

• MC indicator of obesity related dz:

reduced expiratory reserve volume

63
Q

what are the mediators in copd

A

Neutrophils, macrophages, and
CD8+ T lymphocytes are the 1°
mediators of disease in COPD

64
Q

what causes dead space in o2 copd

A 
The major cause
is reversal of hypoxic pulm
vasoconstriction, which ↑
physiologic dead space as blood
is shunted away from wellventilated alveoli.
65
Q

why a a patient with asthma can have dysphonia

A

• Dysphonia can also occur due to
myopathy of laryngeal muscles and
mucosal irritation

66
Q

explain pathophys of pneumocicossis

A

Macrophages release PDGF and IGF
causing fibroblast proliferation and
collagen production (

67
Q

what size of particles enter the broncioles

A

Particles larger than 10 micrometers get
trapped at the terminal bronchioles and
above cleared via mucociliary escalator
• Particles smaller than that reach

68
Q

how does cerberal blood flow alter wtth hypoxemia and hypercapnia

A 
Cerebral blood flow
• pCO2 increase from 25 >100: linear
increase in blood flow
• After pCO2 gets over 100, there is
little chance in blood flow
• pO2 of 50 or more: no change in blood
flow
• pO2 under 50: linear increase is blood
flow
69
Q

why is fev/fvc ratio high in ILD

A

because increased fibrotic tissue, increased radial traction= increased outward flow of air:D

70
Q

patients being weaned of mechanical ventalation

A 
Pts being weaned from mech vent
typically breathe at low TVs, w/
a comp incr in RR to maintain
min vent. B/c at low TVs a
higher proportion of each breath
is composed of dead space, this
type of breathing leads to an incr
in wasted vent (inefficient
breathing).
71
Q

use of glucocorticods can lead to dysphonia why

A

• Dysphonia can also occur due to
myopathy of laryngeal muscles and
mucosal irritatio

72
Q

mechanism of mg sulfate

A

Magnesium sulfate: inhibits Ca influx
promoting
bronchodilation, stabilize T cells and mast
cells

73
Q

how to distinguis ectopic acth vs other acth

A

preence of lung cancer signs cough dyspnea and hemopysis

74
Q

how to diagnose active and latent tb

A

The analysis of sputum specimens is the easiest and least invasive way to confirm suspected active pulmonary TB. Patients with suspected active TB are required to submit 3 sputum specimens, with each one used for culture, acid-fast bacilli smear microscopy, and nucleic acid amplification. The last two tests are useful for rapidly identifying active tuberculosis. Bacterial culture is necessary to confirm the diagnosis and test for drug sensitivity.

An interferon-gamma release assay can be used to diagnose latent TB. This patient has findings that potentially indicate active TB. His interferon-gamma release assay would most likely be positive but not provide any additional information.

FEEDBACK

75
Q

how do we know when to use magnesium sulfate or endotracheal intubation

A

if we have multiple bouts of asthma, doesn’t response BUT NO CONFUSION OR IT HAS MOVEMENT OF AIR you could give mg sulfate

76
Q

how to differentiate a normal viral infection from influenza (take an example of pharyngitis)

A

uncomplicated pharyngitis will have no myalgia and chills compared to influenza( you give osteomalvir

77
Q

manifestation seen in stre pyo

A

NO cough, sore throat/ and cervical lAD

78
Q

how do you approach a patient with mesentric ischemia

A

do ct angiography then do balloon stenting

79
Q

what position would a person be in epiglottitis and in retropharyngeal abscess

A

tripod position extending neck

80
Q

how is early phase mesothelioma what is the staining

A 
In early
mesothelioma, multiple nodules
form on the parietal pleura and
gradually encase the lung
parenchyma.
Immunohistochemistry is
important for diagnosis; nearly
all mesotheliomas stain positive
for cytokeratins and many also
stain positive for calretinin.
81
Q

when do you hear expiratory stridor

A

always tracheal pathology tracheomalacia inspiration widens trachea expiration collapse trachea therefor sounds heard

82
Q

what does aperillgosus does in asthma (predesposition to asperigollosus)

A

Asthma (especially if pt uses
corticosteroids) or CF
• Recurrent fleeting infiltrates
• Bronchiectasis

83
Q

symotoms of strongyloides stercalis

A

Strongyloidiasis is typically asymptomatic but can sometimes cause pulmonary symptoms (eg, cough, asthma-like bronchospasm, hemoptysis) or a transient pneumonia as the larvae migrate through the lungs on their way to the laryngopharynx. However, progression to bronchiectasis is not commonly reported.

84
Q

Pathophys of ards

A

cytokine recuritment neutrophil recruitment damage to the endothelium of lung therefore shock

85
Q

MOA of profolol

A

Propofol is highly lipid soluble and has a very short duration of action (seconds) because of rapid redistribution from the brain, where it activates the GABA-A receptor, to other tissues. Propofol is a hypnotic agent; it does not cause muscle paralysis.

86
Q

second smoke history

A

Impaired mucociliary clearance
Impaired phagocytosis by alveolar macrophages
Immune & inflammatory cell recruitment to lung tissue

87
Q

why patient with cystic fibrosis get pseudomonas infection

A

he microenvironment is particularly suitable to mucoid P aeruginosa because localized hypoxia within the airway mucus causes the bacterium to lose motility and produce alginate, a polysaccharide involved in biofilm formation. The biofilm acts as a protective matrix for the development of Pseudomonasmacrocolonies, which are difficult to eradicate and cause recurrent and persistent infection.

88
Q

why do we have bronchioectasis

A

massive colonization of bacteria causes increased endobronchial protease activity

89
Q

Acute pulmonary edema vs chronic pulmonary edema

A 
Acute pulm oedema is a common
conseq of AMI affecting the LV.
↑ hydrostatic pressure in the
pulm venous system leads to
engorged alveolar caps w/
transudation of fluid into the
alveoli, appearing as acellular
pink material on histo.
hemosiderin-laden macrophages
are indicative of chronic lung
congestion and aren't present
acutely.
MI

usmle (38 decks)

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