Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

B SL ext. > 1 Myocardial Infarction > Flashcards

1 Myocardial Infarction Flashcards

(71 cards)

Start Studying
1
Q

Define an MI

A

Ischaemic necrosis of the myocardium as a result of acute occlusion of a coronary artery

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

What is included in the clinical definition of MI?

A
  1. Symptoms - characteristic of myocardial pain
  2. ECG changes - characteristic of myocardial infarct/ischaemia
  3. Cardiac enzymes - evidence for cardiac myocyte necrosis (without enzymes → Acute Coronary Syndrome)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is unstable angina and how should it be treated?

A

Change in character, duration, frequency, severity of chest pain

Treat as acute coronary syndrome

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

Name some common causes of MI

A

Atheroma,

Hypercoagulability,

Aortic dissection - flap occlusion,

Coronary artery dissection/aneurysm

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

What are the major symptoms of MI?

A

Chest pain - ususally sudden onset, crushing, >20 mins, may radiate

Sweating

Pallor

Nausea

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

What are the signs of MI?

A

Excess sympathetic tone - Tachycardia, Hypertension

or Excess parasympathetic tone - Bradycardia and Hypotension

Impaired left ventricle function → hypotension, lung crackles, murmur

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

What are the stages of ECG changes in MI?

A

ST depression - not always there - ischaemia + partial occlusion

T wave peaking - ischaemia (or hyperkalaemia)

ST elevation - ischaemia + total artery occlusion

T wave inversion - ST segment slowly → baseline

Q wave development

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

What is indicative of a LBBB?

A

Wide QRS

Broad +/- notched R wave - prolonged upstroke in V5, V6 (and 1, AVL)

Left axis deviation may/may not be present

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

What are the major cardiac enzymes implicated in MI?

A

Troponin (T or I)

Released within 4-6 hours, raised up 2 weeks after Infarction (but also rises in PE, septicaemia, renal failure, cardiac trauma)

Other enzymes: MB creatinine kinase, Lactate dehydrogenase-1

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

What is the immediate treatment of MI?

A

AMONAC

Antiemetic, Morphine, O2, Nitrate, Aspirin, Clopidogrel

Cyclizine, Morphine/Diamorphine, GTN, Aspirin, Clopidogrel

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

What is the treatment for STEMIs?

A

Reperfusion therapy <12 hours

Immediate Percutaneous Coronary Intervention (PCI) - most effective <90 mins

or

Thrombolysis

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

What does Percutaneous Coronary Intervention involve?

A

Balloon Angioplasty +/- stenting, with drugs:

Glycoprotein IIb/IIIa Inhibitors (Abciximab, Eptifibatide) - Antiplatelet - reduce risk of immediate vascular obstruction

Unfractioned Heparin

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

What does thrombolysis involve?

A

Recombinant tissue plasminogen activator: Plasminogen → Plasmin → Break down fibrin

Telecteplase

Given with LMWH

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

What is the treatment and management for an NSTEMI?

A

LMWH, or unfractioned Heparin

Take troponin 12 hours after onset

GRACE system >3% CV event risk → Coronary angiography +/- PCI (within 96 hours)

<3% → non-invasive ischaemia testing

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

For confirmed MI, what drugs should be given?

A

MI5 (AABCS)

Aspirin - Antiplatelet

ACE inhibitor - Decrease BP and cardiac workload

Beta blocker - Bisoprolol - Slow HR and contractility

Clopidogrel - Antiplatelet

Statin - Lower cholesterol

Also warfarin/fondaparinux (anticoagulants) and Insulin if required

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

Where are atheromas distributed?

A

Patchily in elastic arteries and large/medium muscular arteries

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

What are the layers of the arterial wall structure?

A

Intima - Endothelium (simple squamous), basal lamina, subendothelial connective tissue

Media - thickest, smooth muscle, elastic and collagen fibres

Adventitia - thin outer layer to prevent overstretch - contains vasa vasorum, nervi vascularis

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

What is the structure of a plaque?

A
  1. Fibrous cap - made of smooth muscle, with collagen and elastin
  2. Shoulder regions - accumulation of foam cells and T lymphocytes
  3. Lipid core - oxidised LDL and cholesterol, cell debris and some foam cells
  4. Weak vessel wall under plaque due to degeneration of vessel media
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the stages of plaque development?

A
  1. LDLs damage and enter the endothelium
  2. Monocytes attracted
  3. Foam cells die
  4. Cytokines encourage smooth muscle to form fibrous cap
  5. Continued growth and development of nectrotic core
  6. Deterioration of plaque
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How do LDLs damage and enter the endothelium?

A

Monocytes release free radicals → oxidise LDLs

oxLDL → damages endothelium at points of high shear stress and bind to basement membrane proteoglycans

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

How are monocytes attracted in plaque development?

A

Damaged endothelium expresses cell surface adhesion molecules for monocytes

Macrophages migrate to subendothelium and take up oxLDL → Foam Cells

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

What happens when foam cells die?

A

They cannot process LDL, the debris realases further free radicals and attracts more monocytes/T cells

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

How is the fibrous cap formed?

A

Cytokines cause SMCs to migrate → intima

  1. Secrete collagen and elastin → forms cap
  2. Encourage angiogenesis into plaque
  3. Encourage further SMC migration into plaque/cap
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How is the necrotic core formed?

A

Foam cells death → toxic free radicals and cytokines → induction of apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
How does the plaque deteriorate?
Macrophage/Foam cells produce factors → SMC death and fibrous cap breakdown Erosion: Cytokine-induced apoptosis and enzymes cutting basement membrane → endothelium erosion
27
How does thrombosis form?
Erosion/ rupture of the fibrous cap
28
How does rupture occur?
Unstable plaque development: 1. Thin fibrous cap with few SMCs 2. Increased inflammatory cell concentration (especially active macrophages instead of foam) 3. Eroded epithelium
29
How does NO play a role in plaque formation?
Undersecretion
30
When is NO normally secreted? and what are its actions?
In response to shear stress Vasodilation Antiatherogenic - inhibits: SMC proliferation, monocyte attraction, LDL oxidation; and antiplatelet effects Damaged endothelium less likely to be able to produce NO
31
What are the sources of cholesterol?
Diet and synthesised by liver from Acety CoA
32
How is cholesterol excreted?
Bile acids
33
How is cholesterol regulated in the body?
_Negative feedback_ - inhibits further synthesis of itself by inhibiting HMG-CoA reductase _Insulin/glucagon control_ - insulin → increases synthesis; glucagon → decreases synthesis _Long term control_ - inhibition of HMG-CoA reductase → decrease cholesterol also: reduced cellular uptake by inhibition of cholesterol receptor expression
34
What is the basic lipoprotein structure?
Non-polar lipid core - mostly TAGs and cholesterol esters Polar (hydrophilic) outer coat
35
What are the sources of cholesterol?
Diet and synthesised by liver from Acety CoA
36
How is cholesterol excreted?
Bile acids
37
How is cholesterol regulated in the body?
_Negative feedback_ - inhibits further synthesis of itself by inhibiting HMG-CoA reductase _Insulin/glucagon control_ - insulin → increases synthesis; glucagon → decreases synthesis _Long term control_ - inhibition of HMG-CoA reductase → decrease cholesterol also: reduced cellular uptake by inhibition of cholesterol receptor expression
38
What is the basic lipoprotein structure?
Non-polar lipid core - mostly TAGs and cholesterol esters Polar (hydrophilic) outer coat
39
What is a chylomicron?
Takes TAGs from small intestine → tissues
40
What do VLDLs do?
Take TAGs from liver → tissues
41
What is IDL?
Remnant of VLDL and can form LDLs
42
Diagram for major groups of lipoproteins and their actions
43
What are LDLs?
Take cholesterol esters from IDL → tissues
44
What is HDL?
Free cholesterol scavenger in periphery → liver
45
How are long chain FAs transported from the intestine?
Converted to TAGs, packaged into chylomicrons → secreted into lacteals (Exogenous pathway)
46
Diagram for major groups of lipoproteins and their actions
47
how are short and medium chain FAs transported from the intestine?
Secreted into bloodstream as FFAs Increase in FFAs in blood → insulin secretion → encourage uptake by liver/muscle/tissue Decrease FFAs in blood between meals → adipocyte release of FFAs
48
What is a chylomicron?
Takes TAGs from small intestine → tissues
49
What does the exogenous lipid transport pathway include?
_Takes lipids from small intestine → tissues via chylomicrons_ 1. Chylomicrons secreted into lymph system by intestinal mucosal cells 2. Chylomicrons acquire apolipoproteins from HDL circulating in blood (apoC and apoE) 3. CMs and TAGs broken down → FFAs by _lipoprotein lipase_ (apoC) for the tissues to absorb 4. Remnants taken up by liver (apoE)
50
What is involved in the endogenous pathway?
_Takes TAGs and Cholesterol to tissues via VLDL → IDL → LDL_ 1. VLDL synthesised in the liver (TAGs + apolipoproteins/cholesterol) 2. TAGs removed by lipoprotein lipase in capillaries → IDL 3. Majority IDL donates apolipoproteins to HDL → becomes LDL 4. LDL taken up by peripheral tissues (provide cholesterol)
51
What does reverse cholesterol transport invovle?
Transports free/used cholesterol back to the liver HDL scavengers: free cholesterol in peripheries → liver Provides apolipoproteins to CMs, VLDL, IDL
52
What is xanthelasma?
Yellow flat plaques on upper/lower eyelids - lipid-containing macrophages condensing around the socket Usually due to high cholesterol/atheromatous disease
53
What is corneal arcus?
Grey opaque line surrounding margin of cornea Common in Type II Diabetes
54
What is the pathophysiology of Familial Hypercholesterolaemia?
Genetic disorder - autosomal dominant, though varying effect with homo/heterozygous Causes LDL Receptor dysfunction - prevents proper uptake of LDL by cells
55
What investigations can be used for diagnosis of Familial Hypercholesterolaemia?
Bloods Total cholesterol \>7.5mmol/l LDL \>4.9mmol/l Plus tendon xanthoma → diagnosis
56
What is the treatment for Familial Hypercholesterolaemia?
Diet/lifestyle Treatment of associated conditions Statins - decrease cholesterol synthesis and increase LDL uptake; increase atherosclerotic plaque stability Fibrates - decrease hepatic secretion + increase peripheral uptake → decrease serum triglyceride Increase gallstone risk by increasing choleseterol content of bile
57
What is the clinical definition of familial hypercholesterolaemia?
Increased total cholesterol or LDL + Tendon Xanthoma in patient or close relative
58
how are short and medium chain FAs transported from the intestine?
Secreted into bloodstream as FFAs Increase in FFAs in blood → insulin secretion → encourage uptake by liver/muscle/tissue Decrease FFAs in blood between meals → adipocyte release of FFAs
59
What is the treatment for Familial Hypercholesterolaemia?
Diet/lifestyle Treatment of associated conditions Statins - decrease cholesterol synthesis and increase LDL uptake; increase atherosclerotic plaque stability Fibrates - decrease hepatic secretion + increase peripheral uptake → decrease serum triglyceride Increase gallstone risk by increasing choleseterol content of bile
60
What investigations can be used for diagnosis of Familial Hypercholesterolaemia?
Bloods Total cholesterol \>7.5mmol/l LDL \>4.9mmol/l Plus tendon xanthoma → diagnosis
61
What is the pathophysiology of Familial Hypercholesterolaemia?
Genetic disorder - autosomal dominant, though varying effect with homo/heterozygous Causes LDL Receptor dysfunction - prevents proper uptake of LDL by cells
62
What is corneal arcus?
Grey opaque line surrounding margin of cornea Common in Type II Diabetes
63
What is xanthelasma?
Yellow flat plaques on upper/lower eyelids - lipid-containing macrophages condensing around the socket Usually due to high cholesterol/atheromatous disease
64
What is the clinical definition of familial hypercholesterolaemia?
Increased total cholesterol or LDL + Tendon Xanthoma in patient or close relative
65
What does reverse cholesterol transport invovle?
Transports free/used cholesterol back to the liver HDL scavengers: free cholesterol in peripheries → liver Provides apolipoproteins to CMs, VLDL, IDL
66
What is involved in the endogenous pathway?
_Takes TAGs and Cholesterol to tissues via VLDL → IDL → LDL_ 1. VLDL synthesised in the liver (TAGs + apolipoproteins/cholesterol) 2. TAGs removed by lipoprotein lipase in capillaries → IDL 3. Majority IDL donates apolipoproteins to HDL → becomes LDL 4. LDL taken up by peripheral tissues (provide cholesterol)
67
What does the exogenous lipid transport pathway include?
_Takes lipids from small intestine → tissues via chylomicrons_ 1. Chylomicrons secreted into lymph system by intestinal mucosal cells 2. Chylomicrons acquire apolipoproteins from HDL circulating in blood (apoC and apoE) 3. CMs and TAGs broken down → FFAs by _lipoprotein lipase_ (apoC) for the tissues to absorb 4. Remnants taken up by liver (apoE)
68
How are long chain FAs transported from the intestine?
Converted to TAGs, packaged into chylomicrons → secreted into lacteals (Exogenous pathway)
69
What is HDL?
Free cholesterol scavenger in periphery → liver
70
What are LDLs?
Take cholesterol esters from IDL → tissues
71
What is IDL?
Remnant of VLDL and can form LDLs
72
What do VLDLs do?
Take TAGs from liver → tissues

B SL ext. (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions