Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Cardiovascular System > Angina, ACS and MI > Flashcards

Angina, ACS and MI Flashcards

1
Q

what is the main difference between stable and unstable angina?

A

stable predictable, comes on during exercise and relieved by rest
unstable can come on at any point (including rest) and can’t always be relieved by rest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are the conditions that make up acute coronary syndromes?

A

unstable angina
NSTEMI
STEMI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what are some of the causes of acute coronary syndromes?

A 
atherosclerosis
vasospasm
cocaine
emboli
coronary dissection
coronary vasculitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what investigations should be done to diagnose an ACD?

A

HR, BP
ECG
blood test for markers (troponin, CK)
chest xray

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

if troponin levels are elevated if a patient presents with chest pain, what can that be a sign of?

A

STEMI

NSTEMI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

if troponin levels are not elevated if a patient presents with chest pain, what can that be a sign of?

A

unstable angina
stable angina
non-cardiac reasons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what other conditions could show elevated troponin levels?

A

pulmonary embolism
sepsis
kidney failure
subarachnoid hemorrage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

where on an ECG would a lateral MI show abnormalities?

A

SLL1
aVF
might involve the Cx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

where on an ECG would an inferior MI show abnormalities, and which vessel would it normally involve?

A

aVF
SLL2
SLL3
might involve the RCA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

where on an ECG would an anterior MI show abnormalities, and which vessel would normally be involved?

A

V1-V4

might involve the LAD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is the pharmacological treatment management for ACS?

A 
morphine (pain relief)
oxygen if sats low
nitrates IV
aspirin 
\+ clopidogrel/ticagrelor/prasugrel
fondaparinux/heparin
beta blockers (when pt stable)
statins 
ACEIs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what are more invasive treatment options for ACS/MI?

A

PCI

CABG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is the main protocol for treating a STEMI?

A

PCI within two hours of event

if no PCI facility available (fast enough), thrombolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what are the thrombolysis options for MI and their characteristics?

A

tenecteplase, alteplase: fibrin-specific

streptokinase: older drug, not fibrin-specific

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is the mechanism of action of aspirin?

A

it stops production of Thromboxane A2 at the beginning of the platelet activation process

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is the mechanism of action of clopidogrel, and what are its pharmacological properties?

A

prodrug - activated in liver

it stops the ADP receptor, which in turn acts on the GP IIb/IIIa receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is the difference between clopidogrel and ticagrelor?

A

clopidogrel is a pro-drug, some patients don’t metabolise it
ticagrelor is not a prodrug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what are some signs/symptoms of ACS/MI?

A 
variable, especially with NSTEMI
crushing chest pain/discomfort
pain may radiate to neck/arms
cold/clammy/sweaty
SoB
nausea/vomiting
collapse
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

which layers of the heart muscle are affected in NSTEMI and STEMI?

A

NSTEMI - endocardial layer = mural/endocardial MI

STEMI - all three layers = transmural MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what are the possible changes on an ECG during and after a STEMI?

A

ST elevation
hyperacute T waves
Q waves after a few days (dead tissue)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what are the possible changes on an ECG during and after a NSTEMI?

A

ST depression
inverted T wave
normally no Q waves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

how can a posterior MI be diagnosed?

A

by putting V leads on the patient’s back in opposite places as V1/V2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is used to support the diagnosis of an MI?

A 
biomarker presence (CK, troponin) +
ECG changes, symptoms, autopsy changes, other imaging evidence of cardiac damage
24
Q

what is the pathological difference between an NSTEMI and a STEMI?

A

STEMI - complete occlusion of a vessel

NSTEMI - severe narrowing but not complete obstruction of vessel

25
Q

what are some of the risks associated with PCI?

A

coronary artery damage/perforation
MI/stroke
bleeding
kidney damage from contrast

26
Q

what is used for imaging during PCI?

A

radiography (XR) with contrast

27
Q

what are possible complications following an MI?

A 
arrythmias
mechanical damage (tears in myocardium, papillary muscle snapping, pericardial tamponade)
28
Q

why should patients be left on dual antiplatelet therapy for a while after a PCI?

A

because stopping them before the stent is covered in endothelium may cause clotting/risk of further MI/stroke

29
Q

what are disadvantages of giving dual antiplatelet therapy?

A

high risk of bleeding

30
Q

what are some contraindications to thrombolysis?

A

recent bleeding/menstrual bleeding
recent brain damage (structural, ischemic stroke, haemorrage,)
suspected aortic dissection

31
Q

what are the benefits and disadvantages of prasugrel compared to clopidogrel?

A

prasugrel works faster on ADP receptor
prasugrel doesn’t need to be metabolised for activation
prasugrel has higher incidence of bleeding

32
Q

what is the difference in administration between low molecular weight heparin and unfractionated heparin?

A

LMWH is administered subcutaneously

UFH is administered intravenously

33
Q

what are some types of low molecular weight heparin?

A

tinzaparin
deltaparin
fondaparinux

34
Q

what is the main symptom of stable angina?

A

chest pain on exertion

35
Q

what can be some symptoms of stable angina in absence of chest pain, and who might have them?

A

SoB/fatigue/syncope or presyncope on exertion

diabetics - they may not feel pain as much (diabetic neuropathy)

36
Q

what is the most common physiological cause of stable angina?

A

mismatch in O2 supply/demand because of narrowed coronary artery

37
Q

what are less common physiological causes of stable angina?

A

pathological increase in O2 demand

reduced O2 distribution (anemia)

38
Q

what are the main investigations done to diagnose stable angina?

A

Blood test (FBC, U&E, glucose, biochemistry)
ECG
CXR
ETT (stress test)
Myocardial perfusion imaging
if the above inconclusive: CT coronary angiogram

39
Q

what are possible signs of stable angina?

A

tar staining (smoking)
xanthalasma and corneal arcus (high cholesterol)
obesity
retinopathy (diabetic or hypertensive)
crackles, raised JVP, possible murmur (heart failure)
pallor (anemic)

40
Q

what are the non-pharmacological treatment options for stable angina?

A

manage underlying cause

smoking cessation, weight management

41
Q

what is the main aim of pharmacological treatment for stable angina?

A

aimed at controlling risk factors
reduction of symptoms
improve survival

42
Q

what are the pharmaceutical treatment options for stable angina?

A 
morphine, oxygen, nitrates, aspirin/clopidogrel
beta blockers
ivabradine (funny ion channel inhibitors)
nicorandil (K+ channel activators)
ranolazine (late Na+ channel blocker)
statins
CCBs
ACEIs
43
Q

what invasive treatment options are available for stable angina, when are they carried out and what is their purpose?

A

PCI and CABG
if investigations show severe stenosis
PCI - symptom relief
CABG - better prognostic but higher risks in procedure

44
Q

what should be the first line pharmaceutical therapy in stable angina?

A

GTN

beta blockers/CCB

45
Q

what should be the second line pharmaceutical therapy in stable angina?

A 
ivabradine
ranolazine
nicorandil
long acting nitrates
trimetazidine
46
Q

what should be the first line medical and non-medical prevention therapy in stable angina?

A
  • lifestyle advice, smoking cessation, weight loss
  • aspirin/clopidogrel
    statins
    ACEIs/ARB
47
Q

why should nifedipine never be given immediate release?

A

because it may precipitate MI/heart failure

48
Q

what are the mechanisms of action of nicorandil?

A

K channel opening

some nitrate effect (vasodilation)

49
Q

what is the mechanism of action of ranozaline?

A

closes late Na+ channels

50
Q

what are some contraindications for beta blockers?

A

asthma
peripheral vascular disease
sometimes heart failure
bradychardia/heart block

51
Q

what are some side effects of beta blockers?

A

fatigue
depression
lethargy
bradychardia

52
Q

what are possible side effects of nitrates and vasodilating CCBs?

A 
headache
flushing
dizzyness
hypotension
syncope (GTN syncope)
53
Q

what are the two main side effects of GTN and isosorbide mono/dinitrate?

A

headache!

hypotension (GTN syncope)

54
Q

which angina medication has side effects which can mimic Crohn’s disease?

A

nicorandil

55
Q

what is the lowest heart rate someone can have to be “safely” put on beta blockers?

A

60bpm

56
Q

which angina medications can interact with macrolide antibiotics?

A

ivabradine

ranolazine

57
Q

with what types of medication is drug-drug interaction of ivabradine important?

A

macrolides (eg clarythromycin)
antifungals
antivirals (HIV)

Cardiovascular System (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions