myocardial infarction and stroke Flashcards

1
Q

3 phases of atherosclerosis (plaque build up)

A
  1. formation of fatty streaks
  2. atheroma formation (platelets attach to endothelium)
  3. plaque formation (high bp, low blood flow, damage vessel walls)
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2
Q

MOD risk for atherosclerosis

A

SOSTAD
- smoking
- obesity
- sedentery lifestyle
- type 2 diabetes
- alcohol
- diet

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3
Q

NON-MOD risk for atherosclerosis

A
  • age
  • gender
  • family history
  • personality charcterisitcs
  • increased trigylcerides
  • hypertension
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4
Q

risk of developing atherosclerosis for a given individual

A
  • High levels of blood lipids (total cholestrol greater than 6mmol/L increases risk 2x)
  • Hypertension (systolic SP>140mmHg and untreated, increases risk 5x)
  • Smoking (increase 2x)
  • Diabetes mellitus (increases risk 2x)
  • Genetics (influence HDL:LDL levels)
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5
Q

if hypoxia leads to death of a cell, by which mechanism is it mostly likely to die?

A

necrosis (cell swelling and bursts)

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6
Q

formations of thrombus includes:

A

formation of thrombus then MIS (agina), MIN,S
- large arteries - transport blood
- medium arteries - control blood to organs
- small arteries - regulate capilary blood flow

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7
Q

how macrophages contribute to inflammation and plaque formation in
atherosclerosis

A
  • monocytes form into Inflammatory macrophages enter the tunica initima and become foam cells which release proinflammatory cytokines then fatty streak to nerotic core formate in the intima causing plaques and inflammed reaction.
    The plaque is composed of:
  • thin fibrous cap
  • large lipid pool
  • cholesterol
    developing a weak cap due to low collagen.
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8
Q

clinical characteristics of angina pectoris

A
  • left side sharp chest pain lasting for 10-15min
  • temporary lack of blood to heart muscle
  • spasm of coronary arteries
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9
Q

ischaemic stroke

A

due to thrombosis in a cerebral vessel. 80% of strokes

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10
Q

clinical characteristic of myocardial
infarction

A

myocardial infarction- decrease or complete block of blood flow to the myocardium.
- not due to cardiac workload
- results in cell death (necrosis)
- blocking of arteries by thombi

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11
Q

causes of haemorrhagic stroke

A
  • hypertension
  • aneurysm (small berry in the artery)
  • thrombocytopenia (low platelets)
  • arteriovenous malformation
  • cerebral amyloid angiopathy
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12
Q

haemorrhagic stroke

A

due to ruptured vessel, resulting in bleeding.

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13
Q

3 causes of ischaemic strokes

A

SET
- sudden obstruction of cerebral artery
- embolism often from the heart or carotid artery
- thrombosis forming on an atherosclerotic narrowing of large artery.

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14
Q

what is a treatment of ischaemic stroke?

A
  • thrombolysis - a theraputic breakdown of fibrin within a blood clot.
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15
Q

What happens when a person has an ischaemic stroke?

A
  • blood flow reduced by 15% in ischaemic core and up to 40% in the ischaemic penumbra
  • too much release of glutamate (neurotoxic)
  • too much intracellular calcium causes the release of inflammatory mediators and destructive enzymes.
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16
Q

how is tPA given? what is TNK- tPA?

A

IET
- intravenously
- effective restoration for blood then it has to be given 4.5hrs of stroke symptoms.
- tPA has a short half life of 5 min.

TNK-tPA- is tenecteplase tPA which is a more rapid form of tPA and more fibrin specific.

17
Q

describe how tPA is used for fibrinolysis therapy

A

TRP
- tPA stands for tissue-type plasminogen activator (tPA).
- tPA is a regulatory for breaking down fibrin clots.
- plasminogen (pro enzyme) when tPA + uPA = Plasmin (active enzyme) for FIBRINOLYSIS.

18
Q

what secondary prevention treatments might be used following acute myocardial infarction or strokes?

A

DBAA
Diuretics - lower bp
Beta-blockers - lower bp
ACE inhibitors - lower bp
Angiotensin receptor antagonists - lower bp

These are all blood vessel relaxers.

19
Q

consequences of atherosclerosis?

A
  • narrowing of lumen in artery due too much fat forming a plaques
  • weakened cap due to decreased of smooth muscle cells, decreased collagen synthesis and increased macrophages and T-cells.
20
Q

What are some causes of vessel injury?

A

HSID
hypertension
smoking
inflammation
diabetes

21
Q

how is tPA (tissue plasminogen activator) given? what is TNK- tPA?

A

IET
- intravenously
- effective restoration for blood then it has to be given 4.5hrs of stroke symptoms.
- tPA has a short half life of 5 min.

TNK-tPA- is tenecteplase tPA which is a more rapid form of tPA and more fibrin specific.

22
Q

pathogenesis of MI

A

TAL
- thrombus deprives cells of oxygen
- anoxic cells us glycolysis to generate ATP to increase levels of lactic acid.
- lactic acid then reduces pH which damages heart muscles contractibility.

23
Q

Troponin diagnostic

A

used to determine the severity of myocardial infarct
- troponin which is a calcium released immediately after infarct which is a switch thats releases from necrotic tissue and can be found in blood.

24
Q

determines the severity of myocardial infarct

A

TCMCA
Troponins (high level)
Cardiac enzymes
Myoglobin
Chest X-ray (echo)
angiogram (dye in arteries and xray)

25
Q

clinical management of myocardial infarction

A

DIMDO
defib
intravenous saline
morphine (ease breathing)
diuresis
o2 therapy

26
Q

what is angina and how?

A

angina is a type of chest pain, due to low blood flow to heart (slow heart rate and irregular).

27
Q

3 phases of atherosclerosis (plaque build up)

A
  1. formation of fatty streaks
  2. atheroma formation (platelets attach to endothelium)
  3. plaque formation (high bp, low blood flow, damage vessel walls)
28
Q

3 phases of atherosclerosis (plaque build up)

A
  1. formation of fatty streaks
  2. atheroma formation (platelets attach to endothelium)
  3. plaque formation (high bp, low blood flow, damage vessel walls)