Flashcards in Heart Week 1D Deck (39):
Where is norepi used?
it is only used in the synapse between the post-ganglionic cell and the effector organs, everything else uses ACh.
Where do the sympathetic nerves originate?
Thoracic and lumbar sections of the spine.
Where do the parasympathetic nerve originate?
Brain stem and a few from the sacrum.
Are muscarinic receptors excitatory or inhibitory? How do they act?
they can be either. They work via a G protein.
What pathways do alpha receptors use? beta?
What are two types of alpha receptors and where do they go?
Alpha 1: mostly on smooth muscle
Alpha 2: mostly on terminals of sympathetic NS
What type of drug is amphetamine and how does it work?
sympathomimetic. it is released in the synapse with norepi, reverses some of the transporters to get norepi out of the synpase (back into the cell) and back into vesicles (VMAT transporter). In effect, it increases the duration that norepi is in the synapse.
What receptor does Ca++ work with to release more Ca++?
It attaches to ryanodine receptors.
What does Ca++ bind to to help with smooth muscle contractions? What does that complex bind to?
Ca++ bind to calmodulin. The calmodulin complex binds to MLCK which exposes the binding sites for myosin.
What does Ca++ bind to in smooth muscles? In skeletal muscles?
Smooth: Ca++ binds to calmodulin, which then binds to MLCK, which allows myosin to bind.
Skeletal: Ca++ binds to actin filaments and allows for the myosin to bind.
What do cAMP and cGMP do to smooth muscles?
What causes a smooth muscle to contract?
Sympathetic: NE binds to alpha receptor.
Parasympathetic: ACh binds to an M1 receptor
*also, some mechanical sensors, eg- baroreceptors and vasculature
Does contraction of smooth muscles require a second messenger?
How can a cell actively relax?
1. hyper-polarization by opening K+ channels (either use cAMP or cytoplasmic Ca++
2. cAMP inactivates myosin light chain (MLCK gets phosphed, and MLCK-P can't bind to actin... no contraction)
In order for a muscle to contract, must the myosin be P'ed or not P'ed?
What are two ways for myosin to lose it's phosphate? What helps myosin keep its phosphate?
cAMP: PKA makes MLCK-P which prevents myosin from being phosphorylated
cGMP: PKG prevents myosin from being phosphorylated
Rho kinase: helps myosin to be phosphorylated
In a vascular bed (brain, GI, etc.), are arterioles in series or parallel?
(1/R = 1/R + 1/R + 1/R...)
What is the relationship of compliance, volume and pressure?
delta V = C x (delta P)
What is the pressure in the following vessels: aorta, VC, arterioles, capillaries, venules
aorta: 104 mmHg
arterioles: 70 mmHg
capillaries: 20 mmHg
venules: 10 mmHg
VC: 4 mmHg
What is the main function of the baroreceptor?
Keep blood pressure constant on the time frame of seconds to minutes (at the most).
What does angiotensis II do? Atrial natriuretic factor?
AFT II: increases vasoconstriction, reabsorption and aldosterone... all to increase blood pressure.
ANF: vasodilates, increases filtration and decrease absorption... all to reduce blood pressure.
What are the layers of the vascular wall, proximal to lumen to distal?
1. endothelial cells (intima)
2. internal elastic lamina (intima)
4. external elastic lamina (adventitia)
5. conncetive tissue (adventitia)
Where do atherosclerotic plaques usually first form?
most common in large arteries, eg- coronary, popliteal, internal carotid
How does atherosclerosis progress?
1. fatty streaks
2. lipid core and fibrous cap
How can macrophages affect plaques?
metalloproteinases > collagen degradation > weakened integrity of fibrous cap of plaque
What can be some causes of aneurysms?
1. marfan's syndrome
3. abnormalities in elastin and collagens 1 and 3
4. vitamin C deficiency
Is Type A or Type B aortic aneurysm more dangerous? Why?
Type A. Can involve ascending aorta. Type B is mostly descending/distal aorta.
For ischemic heart disease, why is the LAD the most important artery?
It supplies 50% of the LV.
What are the three arteries that are usually involved in ischemic heart disease?
LAD, LCX and RCA
Explain the concept of myocardial oxygen supply and demand. (6 steps)
1. low blood/O2 supply
2. cessation of aerobic respiration
3. anaerobic glycolysis
4. not enough high-energy phosphate reserves
5. lactate accumulation, reduced pH
6. ATP depletion
What makes a plaque vulnerable? (4 things)
2. fibrous cap with macrophages and fewer smooth cells
3. necrotic core
How long does it take a RBC to travel though a 1mm long capillary?
about 1-2 secs
What are the three types of capillaries?
1. continuous- unbroken endothelial cells, skeletal muscle
2. fenestrated- special holes, 500-600 Angs, designed for rapid fluid transfer
3. discontinuous- wide holes, 10,000 Angs, proteins can cross
What drives transport for O2 and CO2?
concentration gradient. CO2 and O2 can diffuse across membranes
What happens within seconds, <2mins, 10mins, 40mins, 20-40mins and 1 hr of an MI?
seconds: onset of ATP depletion
<2mins: loss of contractility
10mins: ATP reduced by 50%
40mins: ATP reduced by 90%
20-40mins: irreversible cell injury
1hr: microvascular injury
How can blood pressure affect fluid balance between vascular and interstitial compartments?
a. hypotension: molarity in arterioles increases, so less fluid released
b. CHF: R side of heart malfunctions, venous pressure increases leads to edema of liver and extremities
c. portal hypertension: increased pressure in splanchnic circulation, leads to edema of abdomen and ascites
How can vasoconstriction affect fluid balance between vascular and interstitial compartments?
a. vasodilation: decrease hydrostatic pressure, less filtration in arterioles
b. vasoconstriction: more fluid in interstitium and can lead to edema (tissue swelling)
How can osmotic pressure affect fluid balance between vascular and interstitial compartments?
a. cirrhosis and nephrotic syndrome: reduced protein concentration, leads to edema
b. dehydration: increases effective osmotic gradient, increases absorption