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M103 T3 > M103 T3 L13 > Flashcards

M103 T3 L13 Flashcards

1
Q

What is preload regulated by?

A

the sympathetic system

RAAS

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2
Q

What are the side effects of stable angina treatment?

A

Postural hypotension

Headache, Dizziness

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3
Q

What is an example of a stable angina treatment?

A

glyceryl trinitrate (GTN)

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4
Q

What is reflex tachycardia caused by?

A

the activation of the sympathetic NS

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5
Q

What should be done if stable angina treatment causes side effects?

A

should look to block effects of sympathetic NS using a beta blocker

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6
Q

What are the roles of beta blockers?

A

inhibit renin release from kidney - inhibit RAAS

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7
Q

What are the side effects of beta blockers?

A

Bronchoconstriction

Fatigue

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8
Q

How can CCBs reduce the heart rate?

A

by blocking L-type channels in the SA and AV-nodes

this slows the rate of depolarisation and of actpt generation

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9
Q

How can CCBs reduce the force of contraction of the ventricles?

A

by reducing calcium entry through L-type channels

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10
Q

What is the effect of Ivabradine?

A

blocks If in the nodal tissue of the heart

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11
Q

How does Ivabradin slow the rate of depolarisation of the SA node cells?

A

reduces Na+ entry through If channels
reduce firing frequency
reduce heart rate

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12
Q

What are alternative drugs to ivabradin? (Long Nights Rapping)

A

Long acting nitrates (isosorbide mononitrate)
Nicorandil
Ranolazine

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13
Q

What is the effect of long acting nitrates?

A

they decrease preload

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14
Q

Where is nitric oxide produced?

A

in the endothelial cells that line the blood vessel

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15
Q

What is one of the ways by which nitric oxide is produced in blood vessels?

A

stress / resistance is created between the flow of fluid against the walls of the blood vessels
the stress causes an influx of ca2+ into endothelial cells
ca2+ acts as a co factor to stimulate activity of NO synthase
NOS converts arginine to nitric oxide

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16
Q

What is a by product of NO production?

A

citrulline (amac)

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17
Q

What happens to NO after production?

A

passes across the cell membrane of the endothelial cells into the smooth muscle cell
binds to its muscle receptor - sGC

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18
Q

What is the function of sGC?

A

helps with the production of cyclic GNP

to act as a receptor for NO

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19
Q

What is the role of cyclic GMP?

A

relaxes the smooth muscle walls of the coronary vessels

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20
Q

How do nitrites increase oxygen supply to the heart?

A

they produce NO, which activates cyclic GMP

leads to muscle relaxation

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21
Q

What are the two effects of nitrates on the heart?

A

increase oxygen supply to the heart

decrease the work that the heart has to do

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22
Q

When can’t beta blockers be used?

A

if the patient is asthmatic

if the patient has poor peripheral circulation

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23
Q

What are alternative drugs when beta blockers can’t be used?

A

calcium channel antagonists

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24
Q

What main types of calcium channel antagonists are used for stable angina treatment?

A

phenyalkylamines

benzothiazepines

25
Q

What effects do phenyalkylamines and benzothiazepines have on the nodal tissues?

A

reduce calcium entry into nodal cells
therefore slow the frequency of actpt generation
slows heart rate

26
Q

What effects do phenyalkylamines and benzothiazepines have on the ventricular myocytes?

A

block calcium channels outside the calcium channels

reduce the force of contraction

27
Q

What happens if calcium channel antagonists and some beta blockers are used together in a mixture?

A

severe bradycardia

heart block

28
Q

Why can a mixture of calcium channel antagonists and some beta blockers be dangerous?

A

because they work in the same way and achieve the same effects

29
Q

What are the two causes of heart block?

A

a delay in the time it takes for the actpt to get from the atria to the ventricles
when some of the actpts generated in the SA node don’t make it through the ATP into the ventricles

30
Q

Which two heart channels does the funny current travel through?

A

HCN channel

pacemaker channel

31
Q

Why is it called the funny current?

A

because most channels are opened by depolarisation,

but this one’s opened by hyperpolarization

32
Q

How is glyceride trinitrate administered?

A

pill administered sublingually

33
Q

How does glyceride trinitrate enter the body?

A

absorbed through the oral mucosa

straight into the bloodstream

34
Q

How are Long acting nitrates administered?

A

orally - tablets

patch - a long slow release patch so it can be released into the blood system very slowly

35
Q

What is the effect of nicorandil based on its nitrate-like properties?

A

can dilate some of the coronary arteries

can open some k channels

36
Q

What is the effect of nicorandil based on ability to open some k channels in vascular smooth muscle cells?

A

dilate peripheral arterials
decrease after load by decreasing peripheral resistance
reduce myocardial oxygen requirements

37
Q

What are the consequences of the late current being over expressed?

A

affects the actpt shape

affects the hearts’ contraction

38
Q

How does the over expression of the late current affect the patient physiologically?

A

more na ions enter the cell in the normal healthy heart muscle cell
however lots more na ions enter the damaged cell

39
Q

How does the na-ca exchange protein in the late current remove ca ions?

A

uses the na ion gradient across the membrane as the driving force for the removal of ca gainst its concentration gradient

40
Q

Through which protein is calcium removed from the heart muscle cells?

A

the na-ca exchange protein

41
Q

What are the amounts of na ions inside and outside of the heart muscle cells?

A

outside - 140 mM

inside - 5 million mM

42
Q

Why is the removal of ca from the inside to the outside of heart muscle cells important?

A

it shortens the contraction that’s occurring in the heart muscle

43
Q

What happens to the late na+ channel when cardiomyocytes are damaged and CO is compromised?

A

it becomes overexpressed
lots of na ions enter the cell during the actpt
they are followed by some of ca ions
However, bc there are lots of na ions inside the cell, this pump doesn’t work in the normal way

44
Q

How can the late na+ channel work when it’s not working in the normal way?

A

less na and ca ions are removed

the pump can even work in reverse

45
Q

What happens when the late na+ channel is reversed?

A

the na ions are removed

there is an influx of ca ions

46
Q

How does the heart try to compensate when the late na+ channel is reversed?

A

it tries to generate more force

does more work

47
Q

What happens when the heart tries to work harder to compensate for reversed late na+ channels?

A

can cause the pain associated with ischaemic events

48
Q

What is the effect of Ranolazine?

A

it blocks the late na+ current
reduced influx of na ions through this current
reverses the pathological state where there is elevated intracellular ca and stronger contraction
causes contraction and intracellular ca levels to return to normal levels

49
Q

How is pacemaker current calculated?

A

Ih/f

50
Q

What are terms associated with an L-type channel?

A

high-voltage activated

voltage-dependent

51
Q

What does the “L” stand for in L-type channel?

A

long-lasting - length of activation

52
Q

In what condition are beta blockers contraindicated in?

A

patients with peripheral vascular disease

53
Q

What is the term for the feedback mechanism activated in response to low bp?

A

Reflex tachycardia

54
Q

What are features of sGC?

A

it’s soluble - completely intracellular

is involved in vasodilation

55
Q

Which amac is NO synthesised from?

A

arginine

56
Q

How are long acting-nitrates administered?

A

tabletz

57
Q

Which angina medication (ivabradin alternative) benefits men more than women?

A

Ranolazine

58
Q

What channels are targeted by CCBs?

A

L-type channels in the SA and AV-nodes

M103 T3 (21 decks)

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