Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Jason's Cardiovascular Block > Cholesterol + Drugs + IHD > Flashcards

Cholesterol + Drugs + IHD Flashcards

0
Q

Lateral portion of left ventricle is supplied by which artery?

A

Circumflex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

Anterior rounded section of a transverse cut heart is supplied by which artery?

A

left anterior descending

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

posterior descending artery supplies which segment of the heart?

A

posterior flattened area

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

LAD territory in the heart is where?

A

anterior 2/3 of heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

The circumflex artery supplies which heart segment?

A

Lateral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

When does the myocardial blood usually flow?

A

during diastole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

which heart area is most susceptible to ischaemia?

A

subendocardial muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

additional oxygen supply to meet demand must be met by:

A

an increase in blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is Laplace’s relationship?

A

ventricular wall stress is proportional to pressure and radius
inversely proportional to wall thickness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Define Ischaemic heart disease

A

group of conditions where heart demand is not being supplied

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Is stable angina acute or chronic?

A

chronic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Is unstable angina acute or chronic?

A

acute

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What prevents stenosis in initial stages of atherosclerosis?

A

vessel remodelling to accomodate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How much percentage narrowing of a vessel do you need to get symptoms?

A

70%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

If a vessel has atherosclerosis, what else is impaired in the endothelium?

A

vasodilators

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Why do you get pain in Acute myocardial ischaemia?

A

no ATP = anaerobic resp = acidosis = products = stim the pain nerves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Key features of unstable angina?

A

pain at rest, increasing in frequency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Key feature in stable angina?

A

pain only upon exertion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Acute plaque event happens when what tears and exposes what?

A

Fibrous cap tears and exposes tissue factor = thrombus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

if a thrombus starts, it’s it all or none?

A

Nope. It’s dynamic so there will be fibrinolysis too but the clotting may overtake and occlude the artery leading to infarction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Most common cause of Sudden Cardiac Death?

A

arrhythmic cardiac arrest d/t ventricular fibrillation/tachycardia = no blood pumped out = drop dead

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Can the heart beat at 400-500 beats per minute?

A

YES. in Ventricular fibrillation. mind blown

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is a mechanical mechanism for sudden cardiac death?

A

haemopericardium = tamponade (ECG is present but no CO)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Do you always get an infarction with arrhythmic sudden cardiac death?

A

Not necessarily.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How long does it take to get irreversible myocite injury?

A

20-40 minutes of severe ischaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How long for MI to go transmural? where does it start?

A

up to 24 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

99% cause of regional transmural MI is?

A

thrombosis post acute plaque event

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Subendocardium get damaged in two shapes:

A

regional

circumferential (not common)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What would you look for in MI diagnosis on ECG?

A

ST elevation MI

Non-ST elevation MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

How many days can you detect CK-MB and Troponins in the blood post MI?

A

CK-MB: 2-3 days

troponins: about 6 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

You usually die from complications of MI, they are: 3 things:

A

ventricular fibrillation = sudden death
cardiac failure
acute pulmonary oedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What can be ruptured in MIs? WHen do they usually occur?

A

papillary muscles

free wall of LV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Will a ventricular aneurysm risk bursting? what’s so dangerous about them?

A

Not likely to burst, but dilation increases risk of thrombus formation d/t decreased flow blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

3 other causes of ischaemic heart disease?

A

thromboemboli
vasculitis
aortic dissection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

4 None-coronary artery ischaemic heart disease

A

LV hypertrophy
rapid tachycardias
hypoxemia
shock

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

two surgical treatments for ischaemic heart disease?

A

stents

coronary bypass

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

How is cholesterol transported in blood as?

A

lipoproteins (the carriers)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is a waxy steroid metabolite found in cell membranes?

A

cholesterol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Chole- means?

A

Bile

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

stereos means?

A

solid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is the principle sterol synthesized by animals?

A

Cholesterol. duh.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

If the body is too hot or cold, what happens to cholesterol in the cell membrane?

A

Hot: fluidity/permeability increases too much
Cold: not fluid/permeable enough

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is the key component in vitamin D, steroid hormones and bile acids?

A

cholesterol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Name the 3 critical intermediates in cholesterol synthesis

A

HMG-CoA
Isoprene
Squalene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

4 types of lipoproteins involved in cholesterol transport?

A

chylomicrons
VLDL
LDL
HDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

How does HMG-CoA reductase affect arteriosclerosis?

A

If it’s hyperactive due to genetics, then you’ll get more LDL cholesterol in blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is the genetic disease for increased cholesterol ?

A

Familial hypercholesterolaemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

How many carbons in cholesterol ?

A

27

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Which carbon is the OH on in cholesterol ?

A

3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

describe cholesterol’s relationship with water

A

it’s amphiphilic. kinky.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Do plants make any cholesterol?

A

Nope. They have their own sterols

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Where is VLDL cholesterol made?

A

liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

cholesterol in liver has 3 fates:

A
  1. ester formation, stored as VLDL
  2. bile (recycled usage)
  3. membranes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

how much percent is cholesterol in the animal cell membrane?

A

8%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Where does cholesterol fit in the cell membrane’s Phospolipids?

A

In the cis-bond kink to decrease fluidity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What does cholesterol start off as?

A

Acetyl CoA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What has more energy? 1 ATP? or 1 NADPH?

A

NADPH yo.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Where in the cell is cholesterol made?

A

endoplasmic reticulum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What is ApoB-100?

A

protein that identifies LDL, attaches to receptor on liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Lipoproteins have a phospholipid bilayer?

A

Naw. Monolayer!

60
Q

HDL has what protein marker?

A

ApoA-I (HDL is good so it’s number one!)

61
Q

VLDL and LDL has what protein marker?

A

ApoB-100 (LDL is bad so it’s b for bad)

62
Q

what is the protein marker for chylomicrons and VLDL?

A

ApoC-II ( C for chylomicrons)

63
Q

ApoC-II marks what?

A

Chylomicrons and VLDL

64
Q

ApoA-I marks what?

A

HDL

65
Q

Where do you find ApoC-II usually?

A

Outside of muscles to break down fat anuse it as energy

66
Q

What’s the cholesterol donor?

A

LDL

67
Q

What’s the cholesterol scavenger?

A

HDL

68
Q

VLDL is created in liver, LDL is created?

A

In plasma from reminant chylomicrons

69
Q

What and where does LCAT and ACAT enzymes come into play regarding cholesterol ?

A

LCAT - in plasma for HDL

ACAT - liver for VLDL

70
Q

What’s in side LDL lipoprotein?

A

cholesterol ester, triacylglycerols, free cholesterol (no need to pay for them.)

71
Q

HDL does what to macrophages?

A

prevents foam cell formation

72
Q

What shape is Apo-AI

A

circular to make hydrophobic ring and round up cholesterol

73
Q

How much percent does cardiovascular disease account for?

A

40%!

73
Q

How much percent does cardiovascular disease account for?

A

40%!

74
Q

3 kinds of dyslipidaemia are?

A

hypercholesterolaemia
hypertriglyceridaemia
mixed hyperlipidaemia

75
Q

When are you considered high risk for hypercholesterolaemia?

A

> 7.5mmol/L cholesterol

76
Q

Is cholesterol important for hormones?

A

Yes. precursor to steroid hormones

77
Q

Whats the first statin discovered called?

A

Mevastatin

78
Q

What do all statins do?

A

inhibit HMG-CoA

derease mevalonic acid

79
Q

One dose of statin is great! TWO dose must double the effect right?

A

Nope.

80
Q

What conditions to you use statins?

A

hypercholesterolaemia

mixed hyperlipidaemia

81
Q

How long does it take for effect of statins?

A

1-2 years or use

82
Q

Grapefruit juice doesn’t mix well with:

A

Statins

83
Q

You need to be careful of these 3 things if you’re taking statins cause they’ll increase statin levels too much:

A

antibiotics
antifungals
fibrates

84
Q

Common adverse effects of statins?

A

mild GI, headahce, insomnia, dizzy

85
Q

When should you withhold statins? 3 scenarios:

A

infection
presurgery
post trauma

86
Q

What drug binds bile acid to treat hypercholesterolaemia?

A

Resins like Cholestyramine

87
Q

When should you give Resins if you have to give other drugs?

A

hours before or after resin

88
Q

Whats Ezetimibe?

A

selective inhibition of cholesterol absorption in intestine via sterol transporter

89
Q

does Ezetimibe affect bile acids, fat soluble vitamins, or cholesterol?

A

Cholesterol only, its like a cholesterol sniper.

90
Q

Can you combine Ezitimibe?

A

Yes, like statins and other agents too

91
Q

Which B-vitamin can you use to treat hypercholesterolaemia?

A

B3 - Niacin

92
Q

What are some adverse effects of Niacin treatment for hypercholesterolaemia?

A

Flushing, vasodilation, hypotension, BUT tolerance develops

93
Q

Would you use Niacin for hypercholesterolaemia alone?

A

Nope. Usually only in combos

94
Q

What are fibrates used to treat?

A

Hypertriglyceridaemia

95
Q

Gemfibrozil and fenofibrate are Hypertriglyceridaemia drugs, how do they work?

A

nuclear receptor agonistsm upregulate gene for lipoprotein lipase to lyse triglycerides in plasma

96
Q

Are fibrates for Hypertriglyceridaemia first line?

A

Second line after dietary and lifestyle changes

97
Q

Nausea, dry mouth, headache and rash are common side effects for which Hypertriglyceridaemia drug?

A

Fibrates

98
Q

Can you treat Hypertriglyceridaemia with fish oils?

A

Yep.

99
Q

What do you do if you have severe Hypertriglyceridaemia?

A

polytherapy: diet, fibrates, fish oils, statins, niacin, orlistat

100
Q

What does decreased Q10 symptoms?

A

cardiac and skeletal muscle pain and complications

101
Q

What’s the good thing that statins block out?

A

Q10 production

102
Q

how do statins work?

A

competitive inhibitors of HMG-CoA reductase

103
Q

how do you get elevated circulatory LDL in terms of a genetic reason?

A

Failure of LDL receptors to take LDL from circulation

104
Q

What is a xanthoma?

A

cholesterol deposits = yellow under skin

105
Q

Familial Hypercholesterolemia is suspected if? 2 things.

A

family history of early MI

>15mM choesterol

106
Q

How do you treat Familial Hypercholesterolemia?

A

statins

107
Q

What is mutated in Familial Hypercholesterolemia?

A

LDL receptor gene

108
Q

In Familial Hypercholesterolemia, is it dominant or recessive?

A

Dominant

108
Q

If you have Familial Hypercholesterolemia, what age can you get an MI?

A

mid twenties

108
Q

Whats so important about the end product cholesteryl ester droplet after the cell takes in the LDL?

A

If provides feedback inhibition of HMG-CoA reductase

108
Q

In Familial Hypercholesterolemia, what mechanism is messed up in the cholesterol production circuit?

A

HMG-CoA reductase is not inhibited and it just has a field day and over produces cholesterol

109
Q

” Bro, I feel like my breast is being strangled.”

A

“Dude, you have angina pectoris, go to the hospital.”

110
Q

What is variant angina?

A

coronary vasospasm at rest

unknown mediator

111
Q

Any coronary reserve with angina?

A

Nope. All used up.

112
Q

General drugs classes to affect:
Preload
Afterload
Mycardium

A

Preload: Nitrates
Afterload: Ca2+ blockers
Myocardium: B-adrenoceptor/Ca2+ blockers (Ivabradine)

113
Q

How does nitrates decrease preload?

A

relaxes veins

114
Q

how does nitrate decrease afterload?

A

relax large arteries

115
Q

What’s the short acting nitrate given for acute symptoms of angina?

A

GTN (glyceryl trinitrate)

116
Q

How do you administer GTN?

A

sublingually or transdermally

117
Q

What’s finicky about GTN? 3 things:

A

light sensitive
needs to be in glass vial
1st pass metabolism

118
Q

What’s the longer acting nitrate given for angina? how is it administered?

A

isosorbide dinitrate orally

119
Q

do you only take nitrates reactively?

A

You can take them proactively too.

120
Q

Why would you get reflex tachycardia with nitrate use alone? what can you do about it?

A

Baroreflex activates due to decrease in BP. So combine with B-blockers or Ca2+ blockers

121
Q

Nitrate and viagra is bad why?

A

Viagra is a phosphdiesterase inhibitor, breaks down cAMP and you’ll get over cGMP production and could be fatal.

122
Q

“I love GTN, I use it ALL the time Doc, that cool?”

A

“Bro, you’re gonna develop tolerance, your tissues are thiol depleted, here’s some N-acetyl cysteine, and take off the patch at night dummy.”

123
Q

What kind of channels do Ca2+ blockers block?

A

L-type channels

124
Q

What drugs to block Ca2+ into heart?

A

verapamil

diltiazem

125
Q

What’s nifedipine and felodipine used for?

A

block Ca2+ entry into vessels

126
Q

What’s verapamil

diltiazem used to do?

A

block Ca2+ into heart

127
Q

Drugs to block Ca2+ entry into vessels?

A

nifedipine and felodipine

128
Q

Should you combine verapamil and nifedipine in severe angina?

A

NO WAY. never combine two cardio depressive agents. You can combine it with a B-blocker instead Dr. House.

129
Q

How are Ca2+ blocker normally used? Reactively? or?

A

Prophylactically

130
Q

What type of Beta adrenoceptors are blocked?

A

Beta-1 adrenoceptors

131
Q

Two areas of the heart the beta blockers effect:

A

Nodes

myocardium

132
Q

Would you choose beta blockers or Ca2+ blockers for first line prophylaxis?

A

beta blockers

133
Q

What is the selective beta-1 blocker?

A

atenolol

134
Q

What’s a non-selective beta blocker?

A

propranolol

135
Q

“I’m on nitrates, Ca2+, and B-blockers Doc, my heart disease is a-ok right?”

A

“Actually those drugs aren’t disease modifying, your risks of MI and mortality is exactly the same, you’ll just be more comfortable before you drop dead.”

136
Q

Why is ivabradine so great?

A

‘pure’ heart rate reduction

137
Q

selective inhibition of inward Na-K current in sinus node is done by which drug?

A

ivabradine

138
Q

does ivabradine affect contractility, conduction, BP?

A

Nope. Just heart rate.

139
Q

Why give ivabradine if it ‘only’ decreases heart rate?

A

It preserves endothelium-mediated vasodilation to there is improved exercise tolerance

140
Q

What drug give you brightness in your visual field due to retinal effects?

A

ivabradine

141
Q

Does ivabradine work if your HR is >70bpm?

A

Yes! only if it’s <70 bpm!

142
Q

What is drug is contraindicated in variant angina?

A

B-adrenoceptor antagonists cause it may worsen the vasospasm

143
Q

How would you treat unstable angina?

A

Nitrate, Ca2+/B-blocker, and also aspirin

Jason's Cardiovascular Block (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions