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CDL301 > Lecture 11 IHD > Flashcards

Lecture 11 IHD Flashcards

1
Q

What causes IHD?

A

when a fatty/fibrotic plaque (atherosclerosis) blocks the coronary artery lumen restricting blood flow (ischaemia) resulting in reduced nutrient supply to the tissues - oxygen and glucose

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2
Q

When does Ischaemia occur?

How does Ischaemia often present?

A

oxygen demand of the myocardium (heart muscle) exceeds the supply
chest pain - central in chest but can radiate to arms, neck and jaw

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3
Q

What can cause chest pain?

A

angina or myocardial infarction

due to release of potassium ions, H+ and adenosine that stimulate nociceptors

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4
Q

What is the epidemiology of IHD?

A

2013 IHD resulted in 7 million deaths
21,000 cases/year in UK
prevalence over 55-year olds

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5
Q

What are the modifiable risk factors of IHD?

A

high blood pressure
diabetes
smoking
high-cholesterol

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6
Q

What are the non-modifiable risk factors of IHD?

A

advanced age
male gender
family history of IHD and/or heart disease

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7
Q

What are probable risk factors of IHD?

A

poor diet
obesity
chronic kidney disease

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8
Q

What are the risks of IHD to patients?

A

acute coronary syndromes including
NSTEMI - type of MI
STEMI - blockage of one of the main coronary arteries
unstable angina - pre-MI condition

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9
Q

When does acute coronary syndrome (ACS) present?

A

when the flow in the artery is suddenly blocked leading to ischaemia normally due to platelet rupture forming platelet clots

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10
Q

What is the problem with IHD?

A

can be untraceable by ECG unless they have had a previous MI or currently having ischaemia/MI

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11
Q

What is angina characterised by?

A

heavy or central crushing pain on exertion

relieved by rest

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12
Q

What are the different treatments for stable angina?

A

nitrates and calcium-antagonists - reduce cardiac work
statin - treat underlying condition
prophylaxis - anti-platelet drugs

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13
Q

What are the different treatments for unstable angina?

A

treat as if MI - DAPT (dual-antiplatelet therapy) and nitrates

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14
Q

What is the difference between stable and unstable angina?

A

stable - predictable pain on exertion

unstable - pain occurring with less and less exertion

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15
Q

What is the difference between STEMI/NSTEMI and unstable angina?

A

unstable angina patients require GTN relief, have normal ECGs and do not have raised troponin levels

STEMI/NSTEMI patients do not require GTN relief, have abnormal ECGs and have raised troponin levels

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16
Q

What is the clinical importance of raised troponin levels?

How is raised troponin levels tested for?

A

troponins are specific to cardiac muscle and raised in STEMI/NTEMI patients
they allow diagnosis of MI and indicate myocyte death
blood test

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17
Q

What is the overall aim of ischaemic treatments?

What happens if this is not achieved?

A

restore blood flow and quickly

necrosis of the myocardium will occur along with MI leading to heart failure

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18
Q

What are the four broader aims of IHD treatment?

A

reopen blocked arteries
reduce blood coagulability
control risk factors
reduce myocardial oxygen demand

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19
Q

How is blood flow restored to the heart?

A

percutaneous coronary intervention (PCI)

nitrates

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20
Q

How does PCI work?

A

widens the artery using dilation from within via the radial, brachial or femoral arteries
use a metallic stent often coated with anti-platelet drugs

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21
Q

What is the crucial door-to-balloon time in STEMI cases?

A

120 minutes

22
Q

Why are treatments given before, during and after PCI?

A

risk of stent thrombosis ~1%

reduce the coagulability of blood to reduce risk

23
Q

What is the treatment given to patients after PCI? What is the aim of this pharmacological treatment?

A

DAPT (dual anti-platelet therapy)

to keep the coronary plaques as stable as possible to avoid an acute blockage

24
Q

What are the two approaches of pharmacological treatments?

A

symptomatic - reduce symptoms

prognostic - improve outcomes

25
Q

What treatments can be given to patients suffering with IHD?

A 
nitrates - glyceryl trinitrate (GTN), isosorbide mononitrate
antiplatelet drugs - aspirin 
calcium channel blockers - amlodipine
potassium channel activators - nicorandil 
analgesics - morphine 
statins/PCSK9 inhibitors
beta blockers - propranolol 
ACE inhibitors - ramipril
26
Q

What is the primary mechanism of nitrates?

A

relaxation of smooth muscle in vasculature leading to reduced blood pressure and coronary vasodilation
reduces central venous pressure, preload (venodilation) and reduces cardiac work

27
Q

When and who discovered nitrates?

A

Lauder Brunton 1867

28
Q

What are the secondary effects of nitrates?

A

reduces cardiac work
redirection of flow towards ischaemic areas of heart muscle
improves coronary artery spasms

29
Q

What are the adverse effects and disadvantages of nitrates?

A

hypotension - administer sitting down
headaches
tolerance - possibly depletion of -SH groups
no proof reduce mortality

30
Q

What are the pharmacokinetics of GTN?

A

short acting
sublingual delivery effective within 1-2 minutes
inactivated by hepatic metabolism
effective 30 minutes

31
Q

What are the pharmacokinetics of Isosorbide Mononitrate?

A

long acting
oral deliver twice a day
nitrate-free period overnight to avoid tolerance

32
Q

What are the pharmacokinetics of CCB - Amiloride?

A

dihydropyridine - long elimination time given max once/day

33
Q

What are the side effects of CCBs?

A

flushing and headache

verapamil - constipation (effect of GI nerves/smooth muscle)

34
Q

What is the advantage of aspirin?

A

reduces mortality

reduces risk of future MI

35
Q

How does aspirin work?

A

irreversibly inhibits the COX-1 enzymes through acetylation on platelets preventing conversion of arachidonic acid into thromboxane A2 reducing platelet aggregation
platelets have a lifetime of 10 days and are produced by the bone marrow

36
Q

What are the risks of aspirin?

A

gastrointestinal bleeding
tinnitus and deafness (larger dose/overdose)
risk of self-poisoning
interacts and increases [warfarin]

37
Q

What are the pharmacokinetics of aspirin?

A

weak acid - protonated in stomach allowing to pass through lining of mucosa
major site of absorption - ileum
rapidly hydrolysed to salicylate in tissue by esterases in liver (or plasma)

38
Q

Give an example of an anticoagulant

What is their function?

A

Heparins - glycosaminoglycans found in mast cells and basophils
prevent venous thrombus and thrombus propagation

39
Q

What is the mechanism of action of heparins?

A

activation of antithrombin IIIa which inactivates thrombin and factor Xa preventing the formation of a stable clot

40
Q

What is a heparin antidote?

A

protamine sulphate

41
Q

What is an adverse effect of heparins?

A

bleeding

42
Q

Give examples of antiplatelet drugs

A

thienopyridines
clopidogrel (PLAVIX)
tricagrelor

43
Q

Give example of an analgesic
What else can it be used for?
How does it work?

A

morphine
inducing euphoria and stop diarrhoea
binds to opioid (mu) receptors in the brain - Gi/Go coupled to ion channels

44
Q

Define: Antiemetic

Give an example

A

anti-vomiting drug

metoclopramide

45
Q

What are the side effects of morphine?

A 
respiratory depression 
nausea and vomiting - acting on postrema (medulla)
reduced gut tone and motility 
histamine release
tolerance
46
Q

What treatments are given for unstable angina?

What secondary treatments are given as preventatives?

A

DAPT
heparin
analgesics
planned PCI (once stable)

statins
ACE inhibitors
beta blockers

47
Q

What treatments are given for NSTEMI?

A

DAPT + additional anti-platelet if unstable ECG
analgesics
PCI (72 hours)

48
Q

What happens if you can’t complete PCI for STEMI patients within 120 minutes?
What should be noted about this treatment?

A

give patient a clot-buster to stimulate breakdown of stable fibrin clots, e.g. streptokinase
can’t use antiplatelets and clot buster drugs at the same time

49
Q

What treatments are given for STEMI?

A

PCI - 120 minutes
antiplatelet medications - aspirin and ticagrelor
ACE inhibitors and beta blockers - aid myocardial recovery

50
Q

What is the mortality for a STEMI patient?

A

4.4% if reach hospital

30% do not make it to hospital

CDL301 (14 decks)

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