CVD, BONE METABOLISM, DIABETES, HERBALS Flashcards
(33 cards)
what are pacemaker cells of the heart
they have instable membrane potentials that allow them to reach threshold and generate action pot spontaneously
what movements maintain cardiac cell (3)
- constant diffusion of na and k down their gradiants
- 3 Na out for 2 k in
- ca out 3 NA in
what are the 5 (0+4) phases of ventricular action pot
0-depolarization (NA open)
1-rapid repolarization (na close k open n close)
2-plataue (ca open)
3-final repolarization (ca close, k open)
4-spontaneous depolarization (sod permeability increases)
What effect do catecholamines have on the heart
positive chronotropic effect
increase levels of cAMP
what effect does parasympathetic stim have on the heart
stim of muscarinic receptors cause reduced level of cAMP that produces an increase in outward K current (hyperpolarization)= decrease in pacemaker activity
what effect that ca have on non pacemaker cells
increase in intracellular ca= increase contraction strength
what is peripheral edema indicative of
heart failure
what are the cardiovascular consequenses of heart failure
increase venous pressure
increase sympathetic activity
increased renin, aldosterone etc
what is digitalis glycosides and how does it work
used for heart failure to have positive iontropic effect
inhibits na/k atpase pump with results in increase of intrcellular sodium conc= greater activation of contractile pros and less ca leaving
does digoxin affect skeletal mm
no just increases force and velocity of myocardial contraction
what is the cardiac side effects of digitalis glycosides
dose related arrhythmias
-premature atrial and ventricular contractions
what are the extracardiac toxicity of digitalis glycosides
most GIT
-vommiting due to stim of chemoreceptor trigger zone
What is the antidote for digitalis toxicity
administer potassium iv to decrease the slope of phase 4
or lidocaine
(the spontaneous depolarization portion)
What do class I anti arrhythmic drugs do
slow down rate of phase 0 (and 4) by blocking membrane sodium channels
–cause decrease in excitability + conduction velocity
What do class II anti arrhythic drugs do
B-adrenergic receptor antagonists- depress phase 4 depolarization by competing w catecholamine stim
what do class III anti arrhythmic durgs do
prolong the action potential with a consequent increase in the absolute and effective refractory period
What do call IV anti arrhytmic drugs do
Decrease inward current carried by calcium (in sa node decreases rate of phase 4 spontaneous depolarization)
what is the net calcium absorbtion when taken orally
15-40%
what is essential for calcium absorbtion
bile
effects of calcitonin
inhibits rate of bone turnover, increases exretion of sodium, pot and phosphate
what is raloxifene and what are its effects and the bioavailability
Selective estrogen receptor modulator (produces agonist effects)
only 2% oral bioavailability
How do bisphosphonates work and what is the oral bioavailability
10% bioavailability
-inhibit bone resorption by cellular effects on osteoclasts (inhibis recruitment, differentiation and activity)
what does flouride do
incorporated into bone as hydroxyfluroapatite which is resistant to resorption
What receptors do insulin bind to
binds to specific tyrosine kinase receptors to initatiate a series of enzyme reactions that impact on glucose homeostasis
