respiratory Flashcards
1
Q
diaphragm structures
A
- T8 = IVC
- T10= esophagus, vagus (CN 10)
- T12= aorta, thoracic duct and azygos vein
- at T-1-2 it’s the red white and blue
- innervated by C3,4,5 (phrenic nerve) –> pain from diaphgragm irritation ca be referred to shoulder (C5) and trapz (C3,4)
2
Q
lung volumes
- TV
- IRV
- ERV
- RV
- IC
- FRC
- VC
- TLC
A
- TV- air that mvoves into and out lung with each quiet breath (500 mL)
- IRV- air that can still be breathed in after normal inspiration
- ERV- air that still be breathed out after normal expiration
- RV- air in lung after maximal expiration (can’t be measured on spirometry)
- IC = IRV + TV
- FRC = RV+ERV (amount of air left in lungs after normal expiraton – it is functional bc this what you normally have left)
- VC= TV + IRV + ERV (max volume of gas that can be expired after a max inspiration)
- TLC = IRV + TV + ERV + RV (volume of air present in lungs after maximal inspiration)
3
Q
- determinationof physiologic dead space
- pulmonary vascular restance
- alveolar gas eqn
A
- VD=VTVx (PaC02 - PECO2)/PaCO2
- PECO2 = expired air PCO2
- P = Q x R (change in P = flow x resistance)
- PAO2 = 150 - PaCO2/0.8
4
Q
- Hb basics
- Methemoglobin
- Carboxyhemoglobin
A
- T form has low O2 affinity; R form has high O2 affinity
- increase in Cl, H, CO2, 2,3-BPG + temp favor T form
- Fe3+ – oxidized form of Hb that does not bind O2 readily but has increased affinity for cyanide
- caused by nitrites (ie: nitroglycerin)
- tx with methylene blue
- tx cyanide poisoning with nitrites to oxidize Hb to methemoglobin –> then use thiosulfate to bind this CN which is renally excreted
- Hb bound to CO instead of O2 –> less O2 unloading
5
Q
Hb level, Hb sat, PaO2, total O2 content of..
- CO poisoning
- anemia
- polycythemia
A
Hb Level
% O2 sat
of Hb
PaO2
Total O2 content
CO poisoning
Normal
low
Normal
low
Anemia
low
Normal
Normal
low
polycythemia
High
Normal
Normal
high
6
Q
pulmonary circulation: perfusion vs diffusion limited
A
- healthy lungs are perfusion limited
- gas equilibrates early along length of capillary
- emphsema or fibrosis are diffusion limited
- gas does not equilibrate by the time it reaches the end of the capillary
- SA decreases in emphysema
- diffusion barrier thickness increases in fibrosis
7
Q
hypoxemia (decreased PaO2)
- high altitude
- hypoventilation
- V/Q mismatch
- diffusion limitation
- R–> L shunt
- increased FiO2
A
- Normal A-a
- high altitude
- hypoventilation
- increased A-a
- V/Q mismatch
- diffusion limitation (pulmonary fibrosis)
- R—> L shunt
- increased FiO2 (you can only add so much O2 to the blood)
8
Q
- low CO
- hypoxemia
- anemia
- CO poisoning
- impeded arterial flow
- decreased venous drainage
A
- hypoxia (low O2 delivery to tissue)
- normal A-a: low CO, hypoxemia
- high A-a: anemia, CO poisoning
- ischemia
- normal A-a: impeded arterial flow and low venous drainage
9
Q
V/Q mismatch
- V/Q at apex of lung
- V/Q at base of lung
- airway obstruction
- blood flow obstruction
A
- V/Q = 3 (wasted ventilation)
- becomes more uniform with exercise –> increased perfusion at apex
- V/Q = 0.6 (wasted perfusion)
- both V and Q are greater at base of lung but increase in Q is greater than increase in V
- V/Q = 0 (shunt) – PO2 does not improve with 100% O2
- V/Q = infinity – PO2 improves with 100% O2
- lung prefentially perfuses areas that are getting O2
10
Q
- 3 forms of CO2 transport
- Haldane effect
- Bohr effect
A
- HCO3- (90%)
- CO2 and H20 diffuse into RBC and are converted into H+ and HCO3- via CA
- HbCO2 (carbaminohemoglobin) –
- CO2 bound to Hb at N-terminus of globin (not heme)
- CO2 bound favors T form
- dissolved CO2 (5%)
- Haldane effect: Oxygenation of Hb promotes dissociation of H+ from Hb –> CO2 formation –> CO2 released from RBC
- Bohr effect: H+ from tissue metabolism shifts curve to the R –> unloading more O2
11
Q
- diphenhydramine, dimenhydrinate, chlorpheniramine
- Loratidine, fexofenadine, desloratidine, cetirizine
- Guaifenesin
- N-acetylcysteine
A
- 1st gen H1 blockers: “en/ine” or “en/ate”
- toxicity: sedation, antimuscarinic, anti-alpha-adrenergic
- uses: allx, motion sickness, sleep aid
- 2nd gen H1 blockers (“-adine”)
- uses: allx
- far less sedating than 1st gen bc less CNS penetration
- expectorant
- mucolytic and antidote for tylenol OD
12
Q
- dextromethorphan
- pseudoephedrine, phenylephrine
- Albuterol, Salmeterol, Formoterol
A
- antitussive; synthetic codeine analog
- alpha-agonists
- nasal decongestants
- sudafed used to make meth
- can cause CNS stimulation (anxiety, HTN)
- B2 agonists
- albuterol = 1st line tx for acute asthma
- salmeterol and formoterol are long acting agents for prophylaxis
13
Q
- Theophylline
- Ipratropium
- beclomethasone, fluticasone
A
- methylxanthine: inhibits PDE –> increases cAMP levels
- bronchodilation for asthma
- low TI: low doses acts like caffeine, high doses causes abd pain, seizures and tachy
- muscarinic antag –> prevent bronchoconstriction
- tx asthma + COPD
- tiotropium is long-acting muscarinic antag
- corticosteroids
- 1st line tx for chronic asthma (prophylaxis)
14
Q
- Montelukast, zileuton
- omalizumab
- methacholine
- bosentan
A
- antileukotrienes (“lu” or “leu”)
- asthma prophylaxis
- IgE mAb
- allergic asthma resistant to steroids and B2 agonists
- muscarinic agonist
- bronchial provocation challenge to dx asthma
- tx pulmonary HTN
- antagonizes endothelin-1 receptors
15
Q
HIV
A
- diploid genome (2 molecules of RNA)
- 3 structural genes
- env –> forms gp41 (fusion and entry) + gp120 (attachment to host CD4+ T cell)
- gag –> capsid protein
- pol –> reverse transcriptase, integrase + protease
- virus binds CCR5 (early- macros) or CXCR4 (late) co-receptor + CD4 on T cells
- homozygous CCR5 mutation = immunity
