Midterm 3/Final Flashcards
what is the etiology of reperfusion injury?
- osmotic overload
- pH paradox
how does osmotic overload cause reperfusion injury?
- large increase in number of small molecules in the cytoplasm increases osmolarity from 300 mOsm/l to 400 mOsm/l
- causes water to enter the cell making them swell and rupture
- intracellular organelles also swell and rupture
how do the number of small molecules in the cytoplasm increase with reperfusion?
- breakdown to ATP -> ADP + Pi
- breakdown of phosphocreatine -> creatine + Pi
- breakdown of glycogen to lots of lactate molecules
what is the pH paradox?
rapid reperfusion causes further harm
- reperfusion washes away extracellular H+, creating a gradient for H+ to leave the cell (NHE1 - Na+/H+ exchanger)
- H+ in the cell inhibits Na/K-ATPase
- [Na+] in cell goes up, driving NCX to bring in Ca2+
- increased Ca2+ causes Ca2+ overload causing 1) activated proteases and 2) mitochondrial Ca2+ overload
- ultimately causes cell death
how does subendocardial ischemia present as a diastolic injury current?
- causes elevated (depolarized) RMP in injured subendocardium
- causes diastole to be more depolarized than systole (elevated T-Q segment)
- atrial depol. and ventricular repol. elevated (less potential difference between endo and epi)
how does subendocardial ischemia present as a systolic injury current?
occurs when ischemic injury prevents normal depolarization (Vepi > Vendo)
- net flow of positive charges is away from electrode during systole, displaying S-T depression
what is a transmural infarct? how does it show on ECG?
dead tissue from subendo to subepi
- some endocardial depol persists due to increased preconditioning in endocardium
- shows as S-T elevation (gradient towards electrode during systole)
what ECG changes are present with myocardial infarction?
- heightened T waves
- followed by T wave inversion (altered directionality of repolarization)
- ST segment elevation due to injury current
- deep Q waves
what serum changes occur during myocardial infarction?
- lactate dehydrogenase (LDH)
- creatine kinase (CK)
- Troponin I (TnI)
- cardiac myosin-binding protein C (CmyC)
how does TnI detect MI?
TnI:
- calpain degrades TnI
- blood TnI levels raise during infarct
what is preconditioning?
- repeated brief, mild ischemia
- multiple angina episodes may offer protection
- almost every insult (reduction in blood flow) in life offers protection
how does repeated brief, mild ischemia offer protection?
- increased Katp activity
- increased vasodilator metabolites (adenosine, CO2, hypoxia)
- release of NA, bradykin, opioids (activate G proteins, protein kinases (PKC, PI3-K))
what is postconditioning?
- restarting the flow in brief bursts rather than all at once
- short bursts of reperfusion produce the least damage
what consists of the upper and lower respiratory tracts?
upper:
- nasal cavity
- pharynx
- larynx
lower:
- trachea
- bronchi
what are the functions of the respiratory system?
1) gas exchange
2) conditioning inspired air
- warming and moisturizing
- filtering particles >10 um
3) secretion of mucus
- clear debris from airways
- host defense (immunoglobins, inflammatory mediators
4) filter small emboli from the blood (reduce blood clots)
5) secrete surfactant and ACE
6) acid-base balance of blood (CO2-HCO3- buffering)
7) vocalization at the larynx
8) olfaction (nerve endings in the roof of nose extend from olfactory epithelium to bulb)
9) heat loss
what makes up the physiological dead space?
- anatomical dead space: conducting airways
- alveolar dead space: alveoli that are ventilated but not perfused
what generations make up the conducting airways? have cartilage? have alveoli?
- conducting = 1-16
- cartilage = 1-10
- alveoli = 17-23
what makes up the respiratory epithelium in the conducting airways?
- goblet cells (make mucus, secrete mucin - lubrication, chemical barrier, virus protection) - present as
~ every 5th cell in epithelial layer - submucosal glands (secrete water, ions, mucus, bactericidal compounds)
- sol layer (allows free movement of cilia)
- mucus layer (traps airborne particles)
how do goblets change in smokers?
increases with smoking (why you have more mucus)
when does respiratory epithelium lose submucosal glands and goblet cells? how does airway epithelium change with size of conducting airway?
- submucosal glands and goblet cells absent after gen 11-12 (at bronchioles)
- airway epithelium thins in small conducting airways
what is the function of cilia? of microvilli?
cilia:
- trap particles
- contain ATPase thought to mediate beating motion (active movement of wafting particles up mucus elevator)
- sweep mucus out of airways
microvilli:
- brush cells
- increase surface area for secretion
how does air move within airways?
- by convection (air moves from high to low pressure areas) in conducting airways
- by diffusion in alveolar airways
what are type I alveolar pneumocytes?
- flat, elongated, 95% of alveolus surface
- primary site for gas exchange
- fused to endothelium (to vasculature)
what are type II alveolar pneumocytes?
- small, cuboidal, 2% of alveolus
- synthesize surfactant
- can replicate if alveoli are damaged