Question 1
Question
Ischaemic heart disease (IHD) is the same thing as coronary artery disease (CAD) and coronary heart disease (CHD).
Question 2
Question
Atherosclerosis, a [blank_start]lipid[blank_end] deposition in the subendothelial space, causes IHD. There is endothelial dysfunction with [blank_start]decreased[blank_end] production of NO, less [blank_start]vasodilation[blank_end], increased risk of platelet [blank_start]adhesion[blank_end]. An influx of lipid scavenger cells ([blank_start]macrophages[blank_end]) cause inflammation, calcification and [blank_start]narrowing[blank_end] of the blood vessel by increasing plaque formation.
Answer
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lipid
-
decreased
-
vasodilation
-
adhesion
-
macrophages
-
narrowing
Question 3
Question
Atherosclerotic plaque rupture causes a release of [blank_start]tissue[blank_end] factor (TF) and von Willebrand factor (vWF)
vWF. More [blank_start]platelets[blank_end] adhere, activate, and aggregate. The coagulation cascade activates resulting in [blank_start]fibrinogen[blank_end] binding platelets to one another causing clot ([blank_start]thrombus[blank_end]) formation.
Answer
-
tissue
-
platelets
-
fibrinogen
-
thrombus
Question 4
Question
Which of these is not a risk factor for IHD?
Answer
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Diabetes
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Obesity
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Smoking
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Being a woman over 45
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Alcohol overconsumption
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Being a man over 45
Question 5
Question
Choose the incorrect statement.
Answer
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Stable angina is a chronic form of IHD.
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Unstable angina is an acute coronary syndrome.
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Acute coronary syndromes are forms of IHD.
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A STEMI is an acute coronoary syndrome while and NSTEMI is a chronic form of IHD.
Question 6
Question
Chronic stable angina is the initial manifestation of IHD in about 50% of patients. It is often caused by obstructive [blank_start]atherosclerotic[blank_end] lesions in the coronary arteries. Vasospasm at the site of an atherosclerotic plaque may further [blank_start]constrict[blank_end] blood flow and contribute to angina.
Stable angina is characterised by a plaque with a thick fibrous cap and relatively [blank_start]small[blank_end] lipid core.
Patients are generally in no acute distress and describe stable angina pain as a sensation of pressure, heaviness, tightness, or squeezing in the anterior [blank_start]chest[blank_end] area. Pain may radiate to the neck, jaw, shoulder, back, or arm and may be accompanied by dyspnoea, nausea, vomiting, or diaphoresis. Pain lasts a few [blank_start]minutes[blank_end] and is often provoked by [blank_start]exertion[blank_end] (e.g. walking, climbing stairs, gardening) or emotional stress; and relieved within minutes by [blank_start]rest[blank_end] or with sublingual nitroglycerin.
Answer
-
atherosclerotic
-
constrict
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small
-
chest
-
minutes
-
exertion
-
rest
Question 7
Question
Acute coronary syndrome is the first sign of IHD in about 50% of patients.
Question 8
Question
Principles of treatment:
1. Angina:
Increase myocardial O2 supply (by [blank_start]dilating[blank_end] the cardiac vasculature) and
decrease O2 demand (by decreasing heart [blank_start]rate[blank_end], myocardial [blank_start]contractility[blank_end], and afterload)
2. ACS:
Re-vascularisation/re-perfusion with mechanical or chemical Tx.
- Mechanical:
Percutaneous coronary intervention ([blank_start]PCI[blank_end]) = Angiography or [blank_start]angioplasty[blank_end] (using a balloon or a stent), or Coronary artery bypass graft (CABG)
- Chemical:
Anti-platelets or
Anti-coagulants or
Fibrinolytics
Answer
-
dilating
-
rate
-
contractility
-
PCI
-
angioplasty
Question 9
Question
Match the drug treatment to the purpose for IHD.
- Dilate blood vessels and reduce cardiac load: [blank_start]nitrates, CCBs, ACEIs/ARBs, B-blockers[blank_end]
- Stabilise atherosclerotic plaques: [blank_start]statins and other lipid-lowering meds[blank_end]
- Prevent platelet aggregation: [blank_start]anti-platelets[blank_end]
- Prevent propagation of thrombus: [blank_start]anti-coagulants[blank_end]
- Break down thrombus: [blank_start]fibrinolytics[blank_end]
- Pain relief: [blank_start]morphine[blank_end]
Answer
-
nitrates, CCBs, ACEIs/ARBs, B-blockers
-
statins and other lipid-lowering meds
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anti-platelets
-
anti-coagulants
-
fibrinolytics
-
morphine
Question 10
Question
Nitrates are [blank_start]prodrugs[blank_end] that donate nitric oxide, NO. NO increases intracellular [blank_start]cGMP[blank_end], which relaxes [blank_start]smooth[blank_end] muscle cells and causes vasodilation. Frequent or high doses are associated with [blank_start]tolerance[blank_end].
Answer
-
prodrugs
-
cGMP
-
smooth
-
tolerance
Question 11
Question
Which of these is not a side effect of nitrates?
Answer
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Hypotension
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Flushing
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Headache
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Dizziness
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Hypertension
Question 12
Question
Common DHP CCBs are [blank_start]amlodipine and felodipine[blank_end]. Non-DHP CCBS are [blank_start]verapamil and diltiazem[blank_end].
[blank_start]CCBs[blank_end] can cause headache, flushing, dizziness/postural hypotension, peripheral oedema, and constipation. [blank_start]Non-DHP CCBs[blank_end] can cause bradycardia (caution if patient is on a beta blocker).
Question 13
Question
ACE inhibitors can cause cough due to the build up of bradykinin (which is broken down by ACE).
Question 14
Question
If we give a β-blocker then we anticipate an increase in HR, and bronchial relaxation.
Question 15
Question
Anti-platelets:
1. Aspirin: Inhibits [blank_start]COX-1[blank_end] which decreases [blank_start]TxA2[blank_end] meaning less activation and aggregation.
2. Thienopyridines (e.g. [blank_start]clopidogrel, ticagrelor[blank_end]): Inhibits [blank_start]ADP[blank_end] receptor P2Y12 to decrease [blank_start]activation[blank_end]
3. GPIIb/IIIa inhibitors (e.g. [blank_start]abciximab, tirofiban[blank_end]): Inhibit [blank_start]GPIIb/IIIa[blank_end] receptor to decrease [blank_start]aggregation[blank_end]
Answer
-
COX-1
-
TxA2
-
clopidogrel, ticagrelor
-
ADP
-
activation
-
abciximab, tirofiban
-
aggregation
-
GPIIb/IIIa
Question 16
Question
Anti-coagulants inhibit formation and propagation of thrombi in arteries and veins. In ACS mainly the heparins are used.
1. Unfractionated heparin (UFH) increases the [blank_start]inhibitory[blank_end] action of anti-thrombin (AT) on factors [blank_start]Xa and IIa[blank_end] (and to some extent XIIa, XIa, and IXa).
2. Low molecular weight heparins (LMWHs) increase the inhibitor action of AT on factor [blank_start]Xa >> IIa[blank_end]. LMWH (e.g. enoxaparin) have a [blank_start]smaller[blank_end] molecular weight than UFH, a longer [blank_start]half-life[blank_end], and can be administered [blank_start]subcutaneously[blank_end] (self-administered).
Answer
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inhibitory
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Xa and IIa
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Xa >> IIa
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smaller
-
half-life
-
subcutaneously
Question 17
Question
Fibrinolytics break down fibrin stabilised clots. They are used more in pulmonary [blank_start]embolism[blank_end] or stroke than in IHD. Examples are [blank_start]alteplase and reteplase[blank_end], synthetic tissue plasminogen activators ([blank_start]tPAs[blank_end]).
Answer
-
embolism
-
alteplase and reteplase
-
tPAs