Test
L41,42 Background/Pathology IHD
Este test tiene tipos de pregunta que se abren en el reproductor de siempre.
Preguntas del test (17)
1Ischaemic heart disease (IHD) is the same thing as coronary artery disease (CAD) and coronary heart disease (CHD).
- AVerdadero
- BFalso
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.
- AVerdadero
- BFalso
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).
- AVerdadero
- BFalso
14If we give a β-blocker then we anticipate an increase in HR, and bronchial relaxation.
- AVerdadero
- BFalso
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
Información
- Descripción
- El usuario ha eliminado su información de asignaturas Test sobre L41,42 Background/Pathology IHD, creado por Usuario eliminado el 26/05/2019.
- Autor
- Usuario eliminado
- Idioma
- English
- Visitas
- 34
- Historial
- Creado el 26 may 2019 · actualizado el 26 may 2019
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