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PED2007 > ischaemic heart disease > Flashcards

ischaemic heart disease Flashcards

1
Q

how does the respiration differ in myocytes between healthly patients and patients with Ischaemic heart disease (IHD)

A

normal= aerobic
IHD = anaerobic

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2
Q

how does Ischaemic heart disease effects the heart

A

-reduces generation of ATP which inpairs interaction of contractile proteins
-reduction (transient) of ventricular systolic contraction + diastole relaxation
(occurs within 60s, reversible if repurfusion occurs

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3
Q

what changes to cell structure happens during IHD

A

-glycogen depletion
-mitocondrial swelling
develops withing minutes

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4
Q

when does irreversible cell death occurs

A

20-40 minutes after onset

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5
Q

build up of local metabolites is caused by - and what do they cause

A

due to lack of blood supply/removal
-Activates pain receptors in C7-T4 distribution (Angina)
-dangerous arrhythmias

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6
Q

what are the factors of myocardial oxygen supply

A

-O2 carrying capacity
-coronary blood flow (coronary perfusion pressure + vascular resistance
-external compression
-intrinstic factors (local metabolites, endothelial factors, nueronal innervation)

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7
Q

what are the factors of myocardial oxygen demands

A

wall stress
heart rate
contractibility

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8
Q

there are multiple drugs to treat myocardial infarctions

A

-oxygen (mask)
-Morphine/diamorphine with an antiemetic
-Nitrates
-antiplatelets
-beta blockers
-ACE inhibitos
-Anti-coagulants
-Antiarrhythmia
-statins

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9
Q

how does oxygen help MI

A

relieves hypoxia

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10
Q

how does morphine treat MI

A

-pain relief
-relief from nausea
-venodilation

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11
Q

which drug class reduced the risk of another MI

A

anti-platelets = aspirin, clopidogrel

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12
Q

how do beta blockers treat MI

A

improves perfusions and reduce risk of arrhythmias
lengthens diastole

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13
Q

how does ACE inhibitors treat IM

A

useful in risk of heart failure, left ventricular dysfunction

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14
Q

how do anti-coagulants treat MI

A

protection from thrombus in at risk patient

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15
Q

give an example of a short acting and long acting nitrates

A

-GTN (short acting)
-Isosorbide mononitrate (long activity)

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16
Q

what is the mechanism of action of nitrates

A

-relaxes vascular smooth muscle, some reduction of afterload
-relaxes veins, decrease central venous pressure and redcues preload
-The therapeutic doses have less effect on small resistance arteries than on veins

17
Q

what is the cellular effects of nitrate

A

it is metabolised and the released Nitric oxide (NO)
this activates guanylyl cyclase, this increase cGMP, this causes desphosphorylation of myosin light chain
this decrease cytoplasmic Ca2+ which reduction of smooth muscle contraction
-Vasodilates collateral arteries

18
Q

what is Nitrates used to treat

A

Angina
IHD & MI

19
Q

what are the adverse effects of nitrates

A

postural hypotension
headache

20
Q

what is angina caused by

A

caused by the arteries suppling blood to the heart muscles becoming narrowed by a build-up of fatty substances (atherscleosis)

21
Q

what are the symptoms of angina

A

-chest pain = tight, dull or heavy. May spread to your arms, neck, jaw or back. Triggered by physical exertion or stress. Stops within a few minutes of resting
-Feeling sick or breathless

22
Q

what are the risk of angina

A

-risk of atherosclerosis
-unhealthy diet, lack of exercise, smoking, increased age and family history

23
Q

what is the difference between stable and unstable angina

A

-Stable = attacks have triggers (stress/exercise) and stops during rest
-unstable = attacks are more unpredictable (no trigger) and can continue despite resting
Unstable can develop from stable

24
Q

what are the tests used to confirm angina

A

Blood pressure
BMI + waist size
Blood test to check cholesterol
ECG/ exercise ECG
coronary angiography - scan after injection of a dye to highlight heart and blood vessels

25
Q

what does NSTEMI mean

A

Non ST elevated myocardial infraction

26
Q

what is a NSTEMI, how does it present and how is it detected

A

-Its a subendocardial infraction = caused by incomplete occlusion of artery
-clinically presents as Angina (more severe), unrelieved by rest
-detected by biochemical makers - Troponin T

27
Q

what is STEMI

A

ST elevated myocardial infraction

28
Q

what is a STEMI

A
  • complete occlusion of coronary artery by thrombotic rapture
    atheromatous plaque
  • transmural infarction = full thickness myocardial necrosis
  • prolonged occlusion leads to myocardial necrosis within 15-30
    mins
29
Q

what is the lifestyle changes used to treat with angina

A

balanced diet, cutting down on alcohol, stopping smoking, losing weight, regular exercise

30
Q

what the main medicine can be used treat angina

A

Nitrate - Glyceryl trinitrates (mouth spray)

31
Q

Other medicine that can be used to treat angina

A

Beta blockers
Calcium channel blockers

PED2007 (8 decks)

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