Quiz
L41,42 Background/Pathology IHD
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Questions in this quiz (17)
1Ischaemic heart disease (IHD) is the same thing as coronary artery disease (CAD) and coronary heart disease (CHD).
- ATrue
- BFalse
2Atherosclerosis, 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.
- Alipid
- Bdecreased
- Cvasodilation
- Dadhesion
- Emacrophages
- Fnarrowing
3Atherosclerotic 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.- Atissue
- Bplatelets
- Cfibrinogen
- Dthrombus
4Which of these is not a risk factor for IHD?
- ADiabetes
- BObesity
- CSmoking
- DBeing a woman over 45
- EAlcohol overconsumption
- FBeing a man over 45
5Choose the incorrect statement.
- AStable angina is a chronic form of IHD.
- BUnstable angina is an acute coronary syndrome.
- CAcute coronary syndromes are forms of IHD.
- DA STEMI is an acute coronoary syndrome while and NSTEMI is a chronic form of IHD.
6Chronic 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.- Aatherosclerotic
- Bconstrict
- Csmall
- Dchest
- Eminutes
- Fexertion
- Grest
7Acute coronary syndrome is the first sign of IHD in about 50% of patients.
- ATrue
- BFalse
8Principles 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- Adilating
- Brate
- Ccontractility
- DPCI
- Eangioplasty
9Match 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]- Anitrates, CCBs, ACEIs/ARBs, B-blockers
- Bstatins and other lipid-lowering meds
- Canti-platelets
- Danti-coagulants
- Efibrinolytics
- Fmorphine
10Nitrates 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].
- Aprodrugs
- BcGMP
- Csmooth
- Dtolerance
11Which of these is not a side effect of nitrates?
- AHypotension
- BFlushing
- CHeadache
- DDizziness
- EHypertension
12Common 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).- Aamlodipine and felodipine
- Bverapamil and diltiazem
- CCCBs
- DNon-DHP CCBs
13ACE inhibitors can cause cough due to the build up of bradykinin (which is broken down by ACE).
- ATrue
- BFalse
14If we give a β-blocker then we anticipate an increase in HR, and bronchial relaxation.
- ATrue
- BFalse
15Anti-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]
- ACOX-1
- BTxA2
- Cclopidogrel, ticagrelor
- DADP
- Eactivation
- Fabciximab, tirofiban
- Gaggregation
- HGPIIb/IIIa
16Anti-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).- Ainhibitory
- BXa and IIa
- CXa >> IIa
- Dsmaller
- Ehalf-life
- Fsubcutaneously
17Fibrinolytics 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]).
- Aembolism
- Balteplase and reteplase
- CtPAs
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- User has deleted their subject information Quiz on L41,42 Background/Pathology IHD, created by Deleted user on 26/05/2019.
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- Created on 26 May 2019 · updated on 26 May 2019
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