Respiratory Flashcards

1
Q

rhinitis

A

associated with asthma and eczema

allergic polyps develop in adults - long term allergy

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2
Q

acute epiglottitis

A

H. flu

inspiratory stridor

scenario - 3 mo old kid dies
- tracheal inflammation - parainfluenza virus

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3
Q

mesothelioma

A

Psammoma bodies

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4
Q

COPDs

A

chronic bronchitis
emphysema (for a1-antitrypsin - cirrhosis will develop first and kill the patient, globules will be PAS pos and diastase resistant, diastase breaks down glycogen)
asthma
bronchiectasis

you will see a ventilation/perfusion mismatch

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5
Q

TH2 cells release

A
IL4 - class switching to IgE
IL5 - calls in eos
IL10 - inhibits TH1 phenotype, promotes TH2 phenotype
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6
Q

asthma

A

TH2 cells

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7
Q

restrictive lung diseases

A

aka interstitial lung diseases

idiopathic pulmonary fibrosis
pneumoconioses
sarcoidosis
hypersensitivity pneumonitis
drugs
etc.
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8
Q

lobar pneumonia

A

S pneumo - middle-aged adults and elderly
- treat with penicillin G
Kleb
Legionella

nosocomial - E coli, Pseudomonas, S. aureus

lung consolidation - decreased percussion, increased tactile fremitus, E –> A
(v.s. pleural effusion - decreased percussion ONLY)

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9
Q

bronchopneumonia

A

S. aureus
H. flu
Pseudomonas aeruginosa - water-loving bacteria, will see this in pt on a respirator in the ICU
Moraxella
Legionella - water-loving bacteria, hyponatremia, knocks out JC apparatus, interstitial nephritis, liver disease
- treat with erythromycin
S pneumo
Kleb - alcoholic, mucoid appearing sputum (Kleb capsule), will cavitate in upper lobes

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10
Q

atypical pneumonia

A

aka walking pneumonia

Mycoplasma
Chlamydia (- if in newborns, staccato cough)
RSV
CMV - transplant pts
Influenza (+ increased risk for post bac pneumonia)
Coxiella

inflammation of interstitium

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11
Q

sarcoidosis

A

involves lungs

  • uveitis, skin (cutaneous nodules or erythema nodosum)
  • salivary and lacrimal glands - mimics sjogrens
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12
Q

pulmonary HTN

A

familial form - BMPR2 mutations –> increased proliferation of vascular smooth muscle

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13
Q

small cell carcinoma

A

arises from NE Kulchitsky cells

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14
Q

LABAs

A

salmeterol, formoterol - used in prophylaxis

ARDS - tremor, arrhythmia

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15
Q

inhaled corticosteroids

A

fluticasone/budesonide - 1st line therapy for chronic asthma
inhibit synthesis of all cytokines, inactivates NF-kB (which produces TNF-a, etc.)
may cause oral thrush

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16
Q

anti-LTs

A

-lukast
block LT receptors intracellularly
good for ASA-induced and exercise intolerant asthma

17
Q

methylxanthines

A

theophylline
causes bronchodilation by inhibiting PDE —> increased cAMP, blocks actions of adenosine
narrow therapeutic index (cardiotox, neurotox)
metabolized by CYP450

18
Q

ventilation/perfusion

A

both perfusion and ventilation are greater at the bases

  • perfusion > ventilation in lower lobes - infarcts occur in the lower lobes
  • why is ventilation greater at the bases? - at the end of expiration, alveoli are filled with air (and less compliant)
    - during inspiration - additional air is directed to the lung apex, alveoli there are more compliant
  • V/Q ratio decreases as you go down the lung - perfusion increases more than ventilation

ventilation greater at apex (? goljan)
- Tb reactivates in the apex - aerobe

zone are formed because of gravity’s effects on blood flow (all zone 3 when supine)
zone 1: alveolar pressure > arterial pressure > venous pressure
- zone 1 forms during hemorrhage, high alveolar pressure (pos-P ventilation)

zone 2: arterial pressure > alveolar pressure > venous pressure
- blood flows in a pulsatile fashion - arterial pressure rises during systole so capillary (..venous) pressure can overcome alveolar pressure

zone 3: arterial pressure > venous pressure > alveolar pressure

19
Q

A-a gradient

A

normal = 5-15

> 30 = something is wrong in the lungs
- high specificity

depression of respiratory center will NOT increase A-a gradient

  • ALS, Guillan-Barre, barbiturates
  • but you will have hypoxemia

PAO2 = PO2,inspired - PCO2/0.8

20
Q

triad asthma

A

scenario: 35 yo woman with chronic headaches or fibromyalgia - point is she has pain

pt develops occasional bouts of asthma - mechanism is LTC,D,E4 are still formed
- non-type1 HSR asthma

triad = ASA + asthma + nasal polyps

21
Q

anabolic steroids

A

produce benign liver cell adenomas - tendency to rupture

- well-built male who presents with liver/intraparenchymal hemorrhage

22
Q

vocal cords

A

1) false vocal cords - squamous epithelium
2) commisure
3) true vocal cords - ciliated pseudostratified columnar epithelium

laryngeal carcinoma - 1 smoking, 2 alcohol (synergism - do both, develop carcinoma faster)
- hoarseness of throat

23
Q

hyaline membrane disease

aka RDS

A

massive atelectasis

causes - prematurity (surfactant production peaks at 32-35 week)

corticosteroids, thyroxine, and prolactin all increase surfactant production

C-section produces respiratory distress syndrome - absence of stress - ACTH and cortisol are not increased –> surfactant is not being made

NRDS - often will have PDA (because of hypoxemia, machine-like murmurs)

  • ventilation defect - lungs wont open
  • shunt problem
  • treat with PEEP therapy

hyaline membranes are due to degeneration of type 2 pneumocytes - fibrinogen leaks through membrane

ARDS - neutrophil related injury
- neutrophils destroy type 2 pneumocytes and capillaries
- most common cause is septic shock ( E coli)
(- side note - septic shock is the most common cause of DIC)

24
Q

type 2 pneumocytes

A

contain lamellar bodies - pump out surfactant

25
Q

pneumothorax

A

spontaneous - subpleural bleb (hole in pleural)
- tracheal deviation TO side of collapse

tension - TEAR of pleura, makes it so that air is introduced and stays in the pleural cavity

  • increase in pressure in pleural space pushed lung and mediastinum to the other side
  • lung is compressed by
26
Q

bronchiolitis

A

RSV

wheezing - small airway disease

27
Q

influenza

A

vaccine against A

28
Q

conjunctivitis (in a newborn)

A

can also be caused by erythromycin drops

29
Q

systemic fungi

A

Candida - indwelling catheters

non-productive coughs:
Histoplasmosis, midwest - bats (spelunker), starlings, pigeons
- yeast phagocytosed by macrophages

Blasto, great lakes - skin + lung

Coccidio, SW US - spherules filled with endospores

Cryptococcus - pigeon, halo

treat with actinomycin

30
Q

dysgeusia

A

Zn deficiency- can also cause anosmia

31
Q

S. pneumo

A

alveolar hepatization….gray hepatization (fibrinopurulent exudates)

32
Q

obliterative lower airway inflammation

A

organizing pneumonia –> granulation tissue will obstruct small bronchioles and consolidate the alveoli
- idiopathic - treat with corticosteroids

33
Q

corticosteroids and asthma

A

eosinophil degranulation impaired by corticosteroids

34
Q

secondhand smoke

A
placenta previa and abruption
premie, low birthweight
SIDs - likely due to impaired arousal and abnormal CV response
middle ear disease (otitis media)
asthma 
respiratory tract infections 

toxins in smoke - nicotine, CO, ammonia

35
Q

sarcoidosis

A

cough, dyspnea, extrapulmonary findings (skin lesions, uveitis, Lofgren syndrome)

  • bilateral hilar LAD
  • hypercalcemia/hypercaluria
  • elevated serum ACE - granulomas produce ACE
  • non-caseating granulomas

difficult to distinguish from other lung disease

  • use CD4/CD8 lavage - sarcoidosis will have CD4:CD8 > 2
  • CD8 predominates in HS pneumonitis
36
Q

rhonchi

A

~snoring - occurs due to obstruction of large airways

37
Q

aspiration pneumonia

A

Peptostreptococcus, Bacteroides, Prevotella, Fusobacterium

dependent locations - R, posterior upper lobes, superior lower lobes

  • altered consciousness
  • impaired cough reflex, dysphagia (think stroke), GERD
  • NG, endotracheal tubes
  • protracted vomiting
  • large volume feedings when recumbent