respi Flashcards
CF, nasal transepithelial test, describe flow of ions and why
increased absorption of sodium, because Cl- stays intracellularly, it comes toward epithelial surface creating a hyperpolarized voltage difference, also allows ENaC s to open bringing in sodium
recurrent pulmonary infiltrates and eosinophilia for patient with asthma on inhaled glucocorticoids, proximal bronchiectasis, organism and dx?
aspergillus fumigatus, allergic, bronchopulmonary aspergillosis (ABPA)
5 dimorphic fungi, which one has single bud
histoplasmosis, blastomycosis, sporothrix, coccidioides, paracoccidoides- blasto
smoker and occupational exposure to nickel, thickened bronchial walls, inflammatory infiltrates, mucous gland enlargement, patchy squamous metaplasia in dyspneic patient, dx and risk factor?
bronchitis, smoking
what is virulence factor for organism that causes epiglottitis and mechanism?
PRP capsule (polyribosylribitol phosphate), binds to factor H which is a circulating complement regulator, preventing H. Influenzae from being phagocytosed. Vaccine is this capsule conjugated to protein toxoid
subpleural blebs caused by and complicated by
emphysema and pneumothorax
fat embolism triad, when does it occur, mechanism of triad?
AMS, petichiae, hypoxemia. 24-72 hrs after long bone fracture, fat globule from marrow gets sucked up in circulation, gets stuck in lung, dermal capillaries, and CNS
how does acid-fast staining work for which bacteria? and why
mycobacterium and nocardia, dye with carbofuschin stain, but mycolic acid retains the dye
As hemoglobin becomes more saturated, what ions are released? what is the bohr and haldane effect?
hydrogen. Bohr (body)- Increased CO2 in peripheral tissues lead to unloading of O2; haldane (HALdane)- increased O2 binding leads to release of CO2 and Hydrogen ions
elastase why so stretchy, biochemically? how about collagen?
lysine cross links made by lysyl oxidase, disulfide bonds are in collagen
recent lung transplant, decreased FEV1, fibrotic obstruction in terminal bronchioles, dx?
chronic rejection characterized by bronchiolitis obliterans (primary affects small bronchioles)
why are patients with cerebral edema hyperventilated?
because hypocapnia causes decrease in cerebral blood flow, leading to lowered intracranial pressure. CO2 levels regulate CBF
what do eosoinophils fight off and how? and collaterla damage?
helminths, using major basic proteins, eats up epi and endothelial cells as well
woman with SOB and cough, seasonal allergies, pulmonary infiltrates, hilar adenopathy, non-caseating granuloma with tightly clustered epithelioid macropahges with pink cytoplasm, dx and immune mediators?
sarcoidosis, Th1, IL-2, IFN-gamma. CD4 helper T cell of Th1 type, differentiation activated by IL-12, causes IL2 release which promotes Th1 activation, and IFN-g activates macrophages, which secrete TNF-a
5 causes of hypoventilation and example
- low inspired FiO2 (hiking K2), 2. global hypoventilation (extrapulmonary pathology- MG), always T2RF. 3. V/Q mismatch (pulmonary pathology- pneumonia, PE), usually T1RF, sometimes T2, 4. Shunt (L-R is TOF, R-L is PDA- this happens because increased blood flow to lungs, not enough time to oxygenate. 5. Diffusion (ILD, sarcoid/amyloid, pneumoconiosis)
giardia infection, low serum Igs, what is dx and mechanism?
XLA (x-linked agammaglobulinemia)- BTK is absent, which prevents maturation of B cells
what mediates bronchoconstriction and what is a class of drugs and mechanism in preventing this from happening?
stimulation of Vagal nerve, activating parasympathetic response, acetylcholine acting on muscarinic receptor. Anticholinergic drugs such as ipratropium can stop this from happening as well as prevent mucus productino
subpleural areas of dense collagen depositition and areas of fibroblast proliferation with lymphocytic infiltration
histopathologic features of IPF, found in periphery
3 organisms after influenza pneumonia?
strep pneumo staph aureus h influenza
which chemoreceptors are involved in decreased respiratory drive after oxygen supplementation?
peripheral-aortic arch and carotid body chemoreceptors. The central chemoreceptor at the medulla is sensitive to CO2, but chronic CO2 retention in COPD makes it tuned to O2 more than CO2
acute PE, predict ABG
alkalosis, hypoxic, hypocapnic, bicarb normal
coccobacilli, septic arthritis, grows on hematin and NAD, what is virulence factor?
capsules (H. influenzae)
incidental finding of lung nodules and liver and spleen calcifications, dx?
histoplasma capsulatum is like TB but a fungal kind
person with heart failure, PaO2 70mmHg, what is the reason for increased hematocrit in 3days? normal RBC mass.
relative erythrocytosis (normal RBC mass) absolute is increased RBC mass. absolute can be primary (polycythemia vera) or secondary (CKD etc)
lower lung fibrosis, pleural plaques, dx and what do you find on pathological exam?
asbestosis- ferruginous bodies
severe dyspnea and chest pain in smoker, hypoxemia and hypocapnia, what is the dx and mechanism contributing to this?
PE, V/Q mismatch leading to alveolar hyperventilation, leading to increased loss of CO2, but O2 is capped by Hb saturation so remains stable
what is DLCO? what is it in obstructive and restrictive diseases? with exceptions
diffusing capacity of CO, because CO is an avid binder to RBC, and less dependent on cardiac output. in obstructive- asthma/chronic bronchitis can have normal or increased DLCO, but in emphysema it is decreased due to septa destruction. In restrictive- decreased in intrinsic (ILD, pneumoconiosis), increased in extrinsic (NMD, obesity)
immunocompromised, budding yeasts with thick capsules, organism and common infxn it causes?
cryptococcus neoformans, meningtits
cough, wheezing, liver enzymes mildly elevated, biopsy of liver shows PAS stains, what is causing shortness of breath, diagnosis?
A1AT deficiency, pathology is the destruction of alveolar septa because of unrestricted action of neutrophilic elastase (which A1AT blocks). mutated A1AT gets accumulated in liver ER, causing cirrhosis and HCC
antibiotic is a glycosyltransferase enzyme inhibitor, which bacteria is resistant to this and why? what do you treat with?
myocoplasma because lack of cell wall, macrolides/tetracyclines which are ribosomal inhibitor
when do you give iso, hypo, and hypertonic solution, and what is 5% dextrose in .45% saline
rapid volume resus, hypernatremia/maintenance hydration, SBP or HRS. initially hypertonic, then dextrose gets metabolized and becomes hypo
describe primary and secondary infection with pTB, and ghon and ranke
primary is when bacteria replicate in phagocytes and travel to ipsilateral hilar lymph node forming ghon complex, then CD4 activation causes granulomas to form and fibrose and calcify, making a ranke complex. Secondary is when usually immunocompromised, TB can escape granuloma
how does albuterol work?
increase cAMP levels in bronchial sm muscle
normal aging describe the lung volumes
TLC same, FVC decreases and RV increases
CF pathogenesis
3 base pair deletion F508, at CFTR, leading to faulty post-translational processing, leading to degradation of faulty CFTR
TB pathogenesis
go into alveolar macrophages, prevent phagolysosome formation and replicate intracellularly for many weeks, then eventually macrophages go to LN and activate Th1 to make interferon gamma (intracellular) which destroys and makes epithelioid cells that cause caseus necrosis
left heart failure, crackles in lungs, what is pathophysiology of lungs?
decreased compliance in lungs due to pulmonary edema, also due to intrapulmonary shunting because low V/Q ratio
woman with UTI started on meds who is also on theophylline, develops tachycardia, sweating, etc why?
ciprofloxacin inhibits the CYP450 enzyme, so theophylline toxicity
fever, chills, sputum- crackles in lung. xray shows round density with air-fluid level, dx and what pathology is contributing to this?
lung abscess; from neutrophils releasing cytotoxic granules (lysosomes) containing myeloperoxidase and other enzymes to kill bacteria and causes liquefying necrosis as collateral damage
major basic protein function
eosinophils secrete this to fight parasites
non-smoker, thick lung walls, dx and histopathological features?
mesothelioma, pleural nodules that grow to encase the lung, a/w asbestosis exposure, and positive for cytokeratin
a protein can degrade the elastase, where is this protein made?
alveolar macrophages
recurrent respi infections and dextrocardia
kartagener’s primary ciliary dyskinesia.
what happens to varous pulmonary cell types inIPF?
type 1 pneumocytes loss, type 2 pneumocytes hyperplasia
man with decreased FEV1/FVC, what is the cell that plays major role in pathogenesis and what do they do? what is COPD, emphysema and bronchitis’ main pathology?
neutrophils, macrophages and CD8- release elastase and MMP, proteases to destroy and remodel. COPD- chronic airway inflammation, emphysema- parenchymal destruction, bronchitis- mucus hypersecretion and remodeling of the airways
apical cavitary lesions, and pulmonary infiltrates, on glucocorticoids
secondary activation of TB
organelles containing parallel stacks of membrane lamellae, function
lamellar bodies (shown by EM) carries surfactant
5 catalase pos organisms involved in CGD
s.aureus, burkholderia cepacia, aspergillus, serratia, nocardia
woman with dyspnea, PAH in mother, loud S2, clear CXR, RAD on ECG, inherited disorder. What is diagnosis and gene responsible?
pulmonary arterial hypertension, BMPR2, sm. muscle proliferation of vessel wall
smoking cessation drugs and mechanism?
varenicline- a4b2 nicotinic acetylcholine receptor partial agonist, causing relief to withdrawal and competing with nicotine. bupropion- NDRI, unknown…
coal worker, with small reticular nodules, carbon particles in respiratory bronchioles and alveolar ducts, what is the mechanism to clear this?
phagocytosis by alveolar macrophages. small fine particles. mucocillary transport is for bigger ones
from trachea to alveoli, how is the graph of resistance?
airway resistance is inversely related to total cross sectional area, so trachea is high, medium bronchi are higher, then drops down drastically towards alveoli
why does TB affect MHC class II, not MHC class I?
because although intracellular, TB replicates in phagosome, which is classically class II. Class I is usually for intracellular organisms in the cytoplasm
alcoholic, poor dental health, pneumonia like illness, consolidation with air bronchograms and basophilic mucus like substance surrounded by neutrophils, organism?
actinomycosis
what does OSA cause and why?
pulmonary HTN and systemic- due to hypoxia, leads to vasoconstriction and sympathetic activation
what features of lung tissue is last to disappear?
cilia, glands and cartilage end before bronchiole and goblet cell end before terminal bronchiole
aspiration while supine goes to which lobe?
posterior portion of upper lobe and superior of lower lobe
common organisms for COPD exacerbation
rhinovirus, influenza, strep pneumo, moxarella, h. influenzae
chloride is changed in venous blood, what enzyme is the culprit?
carbonic enzyme due to chloride shift, using bicarbonate produced from Co2
