Heart Week 1D

Question 1

Where is norepi used?

Answer 1

it is only used in the synapse between the post-ganglionic cell and the effector organs, everything else uses ACh.

Question 2

Where do the sympathetic nerves originate?

Answer 2

Thoracic and lumbar sections of the spine.

Question 3

Where do the parasympathetic nerve originate?

Answer 3

Brain stem and a few from the sacrum.

Question 4

Are muscarinic receptors excitatory or inhibitory? How do they act?

Answer 4

they can be either. They work via a G protein.

Question 5

What pathways do alpha receptors use? beta?

Answer 5

Alpha- IP3

Beta- cAMP

Question 6

What are two types of alpha receptors and where do they go?

Answer 6

Alpha 1: mostly on smooth muscle

Alpha 2: mostly on terminals of sympathetic NS

Question 7

What type of drug is amphetamine and how does it work?

Answer 7

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.

Question 8

What receptor does Ca++ work with to release more Ca++?

Answer 8

It attaches to ryanodine receptors.

Question 9

What does Ca++ bind to to help with smooth muscle contractions? What does that complex bind to?

Answer 9

Ca++ bind to calmodulin. The calmodulin complex binds to MLCK which exposes the binding sites for myosin.

Question 10

What does Ca++ bind to in smooth muscles? In skeletal muscles?

Answer 10

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.

Question 11

What do cAMP and cGMP do to smooth muscles?

Answer 11

relax them.

Question 12

What causes a smooth muscle to contract?

Answer 12

Sympathetic: NE binds to alpha receptor.

Parasympathetic: ACh binds to an M1 receptor

*also, some mechanical sensors, eg- baroreceptors and vasculature

Question 13

Does contraction of smooth muscles require a second messenger?

Answer 13

yes, always.

Question 14

How can a cell actively relax?

Answer 14

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)

Question 15

In order for a muscle to contract, must the myosin be P’ed or not P’ed?

Answer 15

Not phosphorylated.

Question 16

What are two ways for myosin to lose it’s phosphate? What helps myosin keep its phosphate?

Answer 16

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

Question 17

In a vascular bed (brain, GI, etc.), are arterioles in series or parallel?

Answer 17

Parallel.

1/R = 1/R + 1/R + 1/R…

Question 18

What is the relationship of compliance, volume and pressure?

Answer 18

delta V = C x (delta P)

Question 19

What is the pressure in the following vessels: aorta, VC, arterioles, capillaries, venules

Answer 19

aorta: 104 mmHg
arterioles: 70 mmHg
capillaries: 20 mmHg
venules: 10 mmHg
VC: 4 mmHg

Question 20

What is the main function of the baroreceptor?

Answer 20

Keep blood pressure constant on the time frame of seconds to minutes (at the most).

Question 21

What does angiotensis II do? Atrial natriuretic factor?

Answer 21

AFT II: increases vasoconstriction, reabsorption and aldosterone… all to increase blood pressure.

ANF: vasodilates, increases filtration and decrease absorption… all to reduce blood pressure.

Question 22

What are the layers of the vascular wall, proximal to lumen to distal?

Answer 22

1. endothelial cells (intima)
2. internal elastic lamina (intima)
3. media
4. external elastic lamina (adventitia)
5. conncetive tissue (adventitia)

Question 23

Where do atherosclerotic plaques usually first form?

Answer 23

most common in large arteries, eg- coronary, popliteal, internal carotid

Question 24

How does atherosclerosis progress?

Answer 24

1. fatty streaks
2. lipid core and fibrous cap
3. calcification
4. rupture
5. thrombosis

Question 25

How can macrophages affect plaques?

Answer 25

metalloproteinases > collagen degradation > weakened integrity of fibrous cap of plaque

Question 26

What can be some causes of aneurysms?

Answer 26

1. marfan's syndrome 2. loeys-dietz 3. abnormalities in elastin and collagens 1 and 3 4. vitamin C deficiency

Question 27

Is Type A or Type B aortic aneurysm more dangerous? Why?

Answer 27

Type A. Can involve ascending aorta. Type B is mostly descending/distal aorta.

Question 28

For ischemic heart disease, why is the LAD the most important artery?

Answer 28

It supplies 50% of the LV.

Question 29

What are the three arteries that are usually involved in ischemic heart disease?

Answer 29

LAD, LCX and RCA

Question 30

Explain the concept of myocardial oxygen supply and demand. (6 steps)

Answer 30

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

Question 31

What makes a plaque vulnerable? (4 things)

Answer 31

1. voluminouss 2. fibrous cap with macrophages and fewer smooth cells 3. necrotic core 4. large

Question 32

How long does it take a RBC to travel though a 1mm long capillary?

Answer 32

about 1-2 secs

Question 33

What are the three types of capillaries?

Answer 33

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

Question 34

What drives transport for O2 and CO2?

Answer 34

concentration gradient. CO2 and O2 can diffuse across membranes

Question 35

What happens within seconds, <2mins, 10mins, 40mins, 20-40mins and 1 hr of an MI?

Answer 35

``` 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 ```

Question 36

How can blood pressure affect fluid balance between vascular and interstitial compartments?

Answer 36

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

Question 37

How can vasoconstriction affect fluid balance between vascular and interstitial compartments?

Answer 37

a. vasodilation: decrease hydrostatic pressure, less filtration in arterioles b. vasoconstriction: more fluid in interstitium and can lead to edema (tissue swelling)

Question 38

How can osmotic pressure affect fluid balance between vascular and interstitial compartments?

Answer 38

a. cirrhosis and nephrotic syndrome: reduced protein concentration, leads to edema b. dehydration: increases effective osmotic gradient, increases absorption

Question 39

What happens when deltapf > 0? <0?

Answer 39

deltaPf > 0: filtration | deltaPf < 0: absorption