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respirator 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
Large cel ca presenation
Gynecomastia and galactorrhea
26
asbestosis presetation
progr dyspnoea, cough, and chest pain. Unilateral pleural thickening or plaque .HEMORRHAAGIC pleural effusion
27
histopath of asbestosis
Long slender microvilli and abundant | tonofilaments
28
what is lofrgen syndrome
fever, erythema nodosum, and bilateral hilar adenopathy
29
what causes centrilobular necrosis
• Right HF, drugs, toxins, and fulminant | hepatitis
30
what is compliction of surfactant treatment
Complications of surfactant treatment may include transient hypoxia and hypotension, blockage of an endotracheal tube, and pulmonary hemorrhage.
31
cmplication of b2 treatment in fetus
increased risk of neonatal intraventricular hemorrhage, hypoglycemia, hypocalcemia, and ileus.
32
distinguish CF from hirschprung
cf-meconium ileus=-squirt sign= Pneumonia, bronchiectasis or cor pulmonale are MCC of death nephrolithiasis and nephrotoxic drugs (aminoglycoside)
33
Hirscprung disease
``` Rectosigmoid obstruction • Normal meconium consistency • Positive squirt sign (forceful explusion of stool after DRE) • Enterocolitis is MCC of death ```
34
unique consequences of vit e deficiency
n, infertility, decreased serum phospholipids and increase lipid peroxidation
35
where other can you find bronchiectasis
large-cell lung ca, TB, CF, and suppurative lung diseases such as empyema,
36
cardiac complication of systemic sclerosis
Pericardial fibrosis • Impaired ventricular dilation, kussmaul sign and pulsus paradoxus impaired diastolic fillng
37
wht is difference between ghon complex and ranke complex
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
where does infection of tb occur
lower obe passed by aerolization= ghon focus=fibrosis+nodule =complex
39
4 factors that activate tb
(corticosteroids, anti TNF, calcineurin | inhibitors, HIV)
40
hematogenous spread of tb
Hematogenous spread • Basal meninges, lumbar spin, psoas muscle, pericardium and pleura, kidneys
41
pathophys of ards in sepsis
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
what causes focal necrosis of alveolar walls
Focal necrosis of alveolar walls | • Goodpastures, Wegners, SLE
43
what causes mononuclear inflitrate of lung | if neutrophils in alveoli
• Early stage of interstitial lung disease | pneumonia +aspiration
44
why dlco increased in asthma
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
NEutropeia
CAMR(candida,asper,mucor,rhizophus)
46
histolgic findings in ILD
``` s mix of chronic inflammation and patchy interstitial fibrosis, focal fibroblast proliferation, and formation of fibrotic cystic spaces in a honeycomb pattern ```
47
how is siadh charcterized
hyponatremia, decreased serum osmolality, and urine osmolality >100 mOsm/kg H2O.
48
why does massive pe cause scd
a sudden loss of CO. Less commonly, SCD may result from cardiac arrhythmia triggered by RV strain and ischemia.
49
where are emoheymatous blebs seen
e lung apices/it is a result of alveolar desrucion
50
how does aaat look of hist
``` 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
why excercise intolerance in emphysema
Dynamic hyperinflation: extra time required for exhalation, increase the amount of air trapped in the lungs and thus reducion tidal volume
52
how does smoking affect aA1AT
Release ROS that inhibit A1AT
53
2 diseases caused byionising radiation
xeroderma | pigmentosum, ataxia telangiectasia
54
major cause f chni lung dmage in asthma
MBP also dmgs epithelial and endothelial cells and is a major cause of chronic lung dmg in asthma.
55
function of il3
Bone marrow stem cell proliferation
56
causes of increase in paco2
poor ventalation,poor muscle effort,poor chest wall compliance, and airway obstruction
57
what are the two steps involved in PAH
abnormal bmpr2--->excessie endothelial prolif, +infection
58
histo of PAH
Medial hypertrophy and intimal hyperplasia/fibrosis (onion skinning) > plexiform lesions
59
RF for OSA
Obesity • Tonsillar hypertrophy • Hypothyroidis
60
pulmonary edema causes decreased compliance why
diluts surfactan
61
sweat glands in Cf
``` • CFTR reabsorbs Cl and Na follows (normally) making sweat hypotonic • CF pt experience severe hypovolemia due to excessive Na loss ```
62
what is the most common decrease in obesitry in pfe
• MC indicator of obesity related dz: | reduced expiratory reserve volume
63
what are the mediators in copd
Neutrophils, macrophages, and CD8+ T lymphocytes are the 1° mediators of disease in COPD
64
what causes dead space in o2 copd
``` The major cause is reversal of hypoxic pulm vasoconstriction, which ↑ physiologic dead space as blood is shunted away from wellventilated alveoli. ```
65
why a a patient with asthma can have dysphonia
• Dysphonia can also occur due to myopathy of laryngeal muscles and mucosal irritation
66
explain pathophys of pneumocicossis
Macrophages release PDGF and IGF causing fibroblast proliferation and collagen production (
67
what size of particles enter the broncioles
Particles larger than 10 micrometers get trapped at the terminal bronchioles and above cleared via mucociliary escalator • Particles smaller than that reach
68
how does cerberal blood flow alter wtth hypoxemia and hypercapnia
``` 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
why is fev/fvc ratio high in ILD
because increased fibrotic tissue, increased radial traction= increased outward flow of air:D
70
patients being weaned of mechanical ventalation
``` 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
use of glucocorticods can lead to dysphonia why
• Dysphonia can also occur due to myopathy of laryngeal muscles and mucosal irritatio
72
mechanism of mg sulfate
Magnesium sulfate: inhibits Ca influx promoting bronchodilation, stabilize T cells and mast cells
73
how to distinguis ectopic acth vs other acth
preence of lung cancer signs cough dyspnea and hemopysis
74
how to diagnose active and latent tb
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
how do we know when to use magnesium sulfate or endotracheal intubation
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
how to differentiate a normal viral infection from influenza (take an example of pharyngitis)
uncomplicated pharyngitis will have no myalgia and chills compared to influenza( you give osteomalvir
77
manifestation seen in stre pyo
NO cough, sore throat/ and cervical lAD
78
how do you approach a patient with mesentric ischemia
do ct angiography then do balloon stenting
79
what position would a person be in epiglottitis and in retropharyngeal abscess
tripod position extending neck
80
how is early phase mesothelioma what is the staining
``` 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
when do you hear expiratory stridor
always tracheal pathology tracheomalacia inspiration widens trachea expiration collapse trachea therefor sounds heard
82
what does aperillgosus does in asthma (predesposition to asperigollosus)
Asthma (especially if pt uses corticosteroids) or CF • Recurrent fleeting infiltrates • Bronchiectasis
83
symotoms of strongyloides stercalis
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
Pathophys of ards
cytokine recuritment neutrophil recruitment damage to the endothelium of lung therefore shock
85
MOA of profolol
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
second smoke history
Impaired mucociliary clearance Impaired phagocytosis by alveolar macrophages Immune & inflammatory cell recruitment to lung tissue
87
why patient with cystic fibrosis get pseudomonas infection
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
why do we have bronchioectasis
massive colonization of bacteria causes increased endobronchial protease activity
89
Acute pulmonary edema vs chronic pulmonary edema
``` 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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