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case 2 - wrap up Flashcards

1
Q

what does stable angina have with coronary arteries?

A

stable angina is caused by atherosclerosis

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2
Q

what does unstable angina have with coronary arteries?

A

unstable angina is caused by atherosclerosis and blood clots in the coronary arteries

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3
Q

what does variant/Prinzmetal’s angina have with coronary arteries?

A

variant/Prinzmetal’s angina is caused by coronary artery spasm

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4
Q

what are the effects of scarring?

A

Gap junctions allow direct communication between adjacent cells, but in scar tissue this communication can be lost - Scar tissue has no cells so there’s no gap junctions, and so less Ca2+ flow

Replacement of the myocardium with scar tissue will alter/reduce the ability of the heart to pump blood.

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5
Q

component of S1 heart sound?

A

closure of tricuspid and mitral valves

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6
Q

component of S2 heart sound?

A

clousre of aortic (A2) and pulmonic (P2) valves.
split S2 occurs during inspiration, with a slight delay in P2

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7
Q

component of S3 heart sound?

A

young patients - rapid ventricular filling in diastole
older patients - blood rushing into an already filled ventricle that does not empty properly

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8
Q

component of S4 heart sound?

A

forceful atrial contraction into a stiff left ventricle

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9
Q

is S1 heart sound being heard normal or abnormal?

A

normal

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10
Q

is S2 heart sound being heard normal or abnormal?

A

normal

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11
Q

is S3 heart sound being heard normal or abnormal?

A

normal - in young patients
abnormal - in older patients

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12
Q

is S4 heart sound being heard normal or abnormal?

A

abnormal

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13
Q

CLINICAL MANAGEMENT OF
HYPERCHOLESTEROLAEMIA?

A
  • Further family information/testing
  • Refer for genetic testing for LDL-Receptor mutations
  • Reinforce benefits of lipid treatment for patient and other family
    members
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14
Q

Genetic testing for familial hypercholesterolemia (FH)looks for what?

A

Genetic testing for familial hypercholesterolemia (FH)looks for inherited genetic changes in three different genes (LDLR, APOB, and PCSK9) known to cause FH

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15
Q

If your doctor suspects that you have FH or a family member has been diagnosed with FH, what will they do?

A

your doctor may refer you for genetic counseling and testing for FH

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16
Q

adverse drug reactions (ADR) of warfarin?

A

haemorrhage, hepatic dysfunction, jaundice, pancreatitis (treat warfarin with vitamin K supplements)

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17
Q

adverse drug reactions (ADR) of APIXABAN?

A

increased risk of bleeding

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18
Q

adverse drug reactions (ADR) of CLOPIDOGREL?

A

abdominal pain, GI and intracranial bleeding, diarrhoea, dyspepsia

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19
Q

adverse drug reactions (ADR) of ALTEPLASE?

A

serious bleeds, reperfusion pathologies (e.g. cerebral oedema)

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20
Q

when would you be opposed to/against using ALTEPLASE?

A

if bleeding, if on ACs or antiplatelet drugs, if aortic dissection or aneurysm

21
Q

when would you be opposed to/against using CLOPIDOGREL?

A

if active bleeding prior
to elective surgery

22
Q

when would you be opposed to/against using APIXABAN?

A

if prosthetic heart valves, if pre-existing coagulopathy or bleeding

23
Q

when would you be opposed to/against using WARFARIN?

A

if haemorrhagic CVA, excessive bleeding, if on NSAIDs, if INR>4.5 (AF patient should be HAS-BLED assessed prior to medication)

24
Q

WARFARIN is a competitive inhibitor of vitamin K epoxide reductase (VKOR). Why is this relevant?

A

Normally, vitamin K is required to mediate the carboxylation of clotting factors II, VII, IX & X.
Warfarin inhibition of VKOR prevents formation of these clotting factors

25
APIXABAN is a highly selective reversible inhibitor of Factor Xa. Why is this relevant?
APIXABAN:highly selective reversible inhibitor of Factor Xa which prevents the conversion of prothrombin to thrombin(thrombin is the terminal step in fibrin clot formation)
26
CLOPIDOGREL is an inhibitor of the platelet P2Y12 ADP receptor. Why is this relevant?
CLOPIDOGREL:an inhibitor of the platelet P2Y12 ADP receptor Normally, the platelet ADP receptor sensitises collagen receptors on the platelet which subsequently trigger activation, aggregation & degranulation. Platelets are only exposed to collagen through vascular trauma. Clopidogrel suppresses platelet collagen responses
27
ALTEPLASE is a recombinant form of tissue plasminogen activating factor (tPA). Why is this relevant?
ALTEPLASE:a recombinant form of tissue plasminogen activating factor (tPA) tPA mediates the conversion of plasminogen to plasmin which rapidly dissolves clots by causing fibrinolysis
28
what is the first-line treatment in patients with angina?
Guidelines recommend beta blockers as first-line treatment in patients with angina either on their own or in combination with a calcium channel blocker
29
how do beta blockers treat angina?
Treatment of angina, by slowing the heart rate, beta blockers reduce the oxygen demand of the heart and reduce the frequency of angina attacks.
30
Antianginal drug therapy: how should acute attacks of angina be managed?
Acute attacks of stable angina should be managed with sublingualglyceryl trinitrate, which can also be used as a preventative measure immediately before performing activities that are known to bring on an attack.
31
Antianginal drug therapy: How should long-term prevention of chest pain in patients with stable angina be managed?
For long-term prevention of chest pain in patients with stable angina, a beta-blocker (such as atenolol, bisoprolol, fumarate, metoprolol. tartrate or propranolol hydrochloride) should be given as first-line therapy.
32
Antianginal drug therapy: What should be considered as an alternative if beta-blockers are contra-indicated, for example in patients with Prinzmetal's angina or decompensated heart failure?
A rate-limiting calcium-channel blocker (such as verapamil hydrochloride or diltiazem hydrochloride)
33
Antianginal drug therapy: What may be effective in patients with Prinzmetal's angina?
Dihydropyridine derivative calcium-channel blockers (such as amlodipine) may be effective in patients with Prinzmetal's angina.
34
If a beta-blocker alone fails to control symptoms (of angina) adequately, what should be considered?
If a beta-blocker alone fails to control symptoms adequately, a combination of a beta-blocker and a calcium-channel blocker should be considered. If this combination is not appropriate due to intolerance of, or contra-indication to, either beta-blockers or calcium-channel blockers, NICE CG126 recommends to consider addition of either a long-acting nitrate, ivabradine, nicorandil, or ranolazine.
35
when should a long-acting nitrate, ivabradine, nicorandil, or ranolazine also be considered?
A long-acting nitrate, ivabradine, nicorandil, or ranolazine, should also be considered as monotherapy in patients who cannot tolerate beta-blockers and calcium-channel blockers, if both are contraindicated, or when they both fail to adequately control angina symptoms.
36
how often should response to treatment be assessed, following initiation or change of drug therapy?
response to treatment should be assessed every 2-4 weeks following initiation or change of drug therapy
37
drug doses should be titrated to the what?
drug doses should be titrated to the maximum tolerated effective dose.
38
If a combination of two drugs at a maximum therapeutic dose fails to control angina symptoms, patients should be considered for what?
patients should be considered for referral to a specialist.
39
what is The mechanism of action of loop diuretics?
The mechanism of action of loop diuretics is the reversible inhibition of the sodium/potassium/chloride co-transporter in the thick ascending limb of the loop of Henle.
40
how can an MI lead to heart failure?
A myocardial infarction (MI), commonly known as a heart attack, can lead to heart failure because the damage to the heart muscle caused by the blocked coronary artery significantly impairs the heart's ability to pump blood effectively, eventually causing heart failure to develop.
41
what does FUROSEMIDE treat?
FUROSEMIDE (LOOP DIURETICS) TREATS HIGH BLOOD PRESSURE, HEART FAILURE AND OEDEMA
42
An MI means that cardiac tissue is being acutely starved of oxygen due to a clot blocking a coronary blood vessel. The priority is to quickly unblock the vessel or bypass it (“time is myocardium!”) so downstream ischaemic tissue can be re-perfused with oxygenated blood. The options for unblocking a compromised coronary artery can be:
(i)Using a fibrinolytic drug to dissolve the clot that’s causing the blockage. (ii)Using primary percutaneous coronary intervention(PCI), also called ‘angioplasty’, to expand the blocked vessel internally using a balloon (often followed by deploying a stent within the vessel to keep it open). The choice of which to use is a function of the location/size of the blockage and how quickly the patient can get to a centre offering PCI. If this can happen rapidly, PCI is considered the gold standard. If PCI is not available, then thrombolysis may be considered but again, the sooner the better after the initial diagnosis of an MI.
43
hypertension (HT) with consequent organ damage is a what now?
HT with consequent organ damage = hypertensive emergency.
44
what is the criteria for stage 1 hypertension?
Clinical BP 140/90 w/ subsequent 135/85 ABPM average daytime reading or HBPM average
45
what is the criteria for stage 2 hypertension?
Clinical BP 160/100 w/ subsequent 150/95 ABPM/HBPM
46
what is the criteria for stage 3 hypertension?
Clinical >180 systolic OR Clinical >110 Diastolic
47
what about Visceral Pain?
*Deep sensation *Discomfort, pressure, tightness, squeezing, dull, aching, boring * Poorly localized * Sense of malaise * Strong autonomic reflexes eg. Sweating, nausea, dizziness
48
what about referred Pain?

Case 2 (7 decks)

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