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CDL301 > Ischaemic heart disease > Flashcards

Ischaemic heart disease Flashcards

1
Q

What is ischaemic heart disease?

A

Disease of the coronary arteries
occurs when fatty/ fibrotic plaque blocks the coronary lumen
and blood flow is restricted= ischaemia

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2
Q

How does IHD occur and present?

A

Chest pains
When O2 demand of myocardium exceeds supply
less nutrients to tissue so cell death
presents when plaque ruptures and flow to artery is suddenly blocked

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3
Q

What happens when you get chest pains?

A

release of K, H and adenosine

disease progress insidiously until these symptoms

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4
Q

What is chest pain?

A

typically centered in the chest
radiates to neck and arm
levines sign
patients fist is clenched

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5
Q

Progression of coronary atherosclerosis

A 
0-10= foam cells 
10-20= fatty streak 
20-30= intermediate lesion 
30-40= atheroma 
40-50= complicated lesion or rupture
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6
Q

Stats about IHD

A

leading cause of death
2013-7 million deaths
UK- 21,000 cases
>55 12% of men and 5% women

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7
Q

Risk factors

A
  1. non modifiable
    - age sex gender
    - family history
  2. modifiable
    - diet obesity and diabetes
    - smoking
    - high BP
    - high cholesterol
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8
Q

What are the risks to patients with IHD?

A
  • suspectible to acute coronary syndromes-ACS
  • unstable angina
  • Non-ST elevation MI (NSTEMI)
  • ST elevation MI (STEMI)
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9
Q

ECG of IHD patients

A

The ECG can be normal in patients with IHD unless they have had a previous MI. To see the ECG changes – need to have current ischaemia or have had an MI

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10
Q

What are the differences in unstable angina, NSTEMI and STEMI?

A

unstable angina = pre MI condition
NSTEMI =a type of MI (more minor forms)
STEMI =caused by a complete blockage of one of the main coronary arteries. (can occur in emotional or physical stress and can progress as a full heart attack)

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11
Q

Lumen of stable angina and Non- stemi

A

stable angina, above plaque normal wall (thickened) ischemia (stable form
N ST- complete and permanent blockage

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12
Q

Epidemeology of ACS

A

Rare under 35
0.6%- 35-74
2.3%-75+
England= 233,600 new cases annually

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13
Q

amount of STEMI/NSTEMI in England

A

STEMI- 5/1000

Nstemi- increasing

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14
Q

How would a myocardial ischaemia be apparent and dealt with?

A

Chest pain- heavy or crushing

treatment would be based on the type of angina

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15
Q

Stable angina treatment

A

reduce cardiac work

treat the underlying condition- atherosclerosis (statin) or prohylaxis (anti-platelet)

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16
Q

unstable angina treatment

A

treat with MI strategy

  • DAPT
  • nitrates
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17
Q

Which types would have GTN relief?

A

Stable angina and unstable angina- not N/STEMI

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18
Q

Which would have a normal ECG?

A

Unstable and stable angina

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19
Q

Which types would have raised troponin?

A

NSTEMI

STEMI

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20
Q

What are the 4 steps for treating ischaemia?

A

restore blood flow asap

  1. reopen blocked arteries
  2. reduce the coagulability of blood
  3. control risk factors
  4. reduce myocardial O2 demand
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21
Q

Restoring blood flow method- PCI

A

PCI-percutaneous coronary intervention

  • non surgical technique- aim to widen the artery using dilation from within
  • place stent
  • popular drugs attached to stent to inhibit cell regrowth
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22
Q

What is the crucial door balloon time?

A

120 min
for STEMI
immediate procedure

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23
Q

What would you use if there wasn’t uncontrolled angina?

A

Nitrates- they restore flow

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24
Q

What is combined treatment for IHD?

A 
Use catheter and track into heart 
add dye 
see pictures 
-dilate vessels from veins and increase vessel size 
\+
- push away plaque
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25
Q

3 steps to stenting

A
  1. mounted on balloon
  2. inside stent and inflated
  3. stent positioned against wall and wire/ balloon is removed
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26
Q

Medical treatments after stenting

A

DAPT- dual antiplatelet therapy- incidience of thrombosis 1%

Aspirin-+ antiplatelet + abti-coagulant= continued years after stenting

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27
Q

Adverse effects and benefits of drugs after stenting

A
  • excess bleeding
  • pleiotropic positive effects of neutrophils and therefore pulmonary infection- reduce cell growth and clotting, keep your artery open
28
Q

What is the main aim of pharmalogical treatments of IHD?

A

to keep the coronary plaque stable as possible to avoid an acute clot blockage (occlusion) which can be partial or full
and to reduce pain

29
Q

two pharmacological treatment approaches?

A
  1. symptomatic- reduce symptoms, reduce strain on heart and increase vasodilation
  2. prognostic- improve outcomes and eleviate neg outcome in future
30
Q

Symptomatic drugs

A
  • nitrates
  • aspirin
  • Ca channel
  • K channel
  • Analgesia
31
Q

Prognostic

A
  • Aspirin
  • Statins
  • beta blockers or ACE inhibitors
  • anti-inflammation approaches are being developed
32
Q

Nitrates- when they started, why we use them

A
  • brunten 1867

- first line agents, GTN as a short acting spray sublingually

33
Q

What is the primary and secondary effect of nitrates???

A

primary- to relax smooth muscle and veins, main effect on larger muscular arteries
secondary- reduce Cardiac work, redirection of flow towards ischaemic areas of heart muscle, improves coronary spasm

34
Q

Mechanism of action of nitrates

A

GTN metabolism
activates GC and increases cGMP
this activates PKG and causes relaxation of the smooth muscle

35
Q

What are the main adverse effects of nitrates

A
  • hypotension- administer slow
  • headaches
  • tolerance= depletion of SH group and is more common with longer acting agents
36
Q

NITRATES-What is GTN activated by?

A

Hepatic metabolism

37
Q

What is the delivery time and the length of effect of nitrates?

A
  • 1-2 mins- conversion from di to mono in a min

- 30 mins it lasts

38
Q

What is isosorbide mononitrate?

A

orally administered
longer acting
2 a day with a nitrate free period at night to avoid tolerance

39
Q

Mechanism of Ca channel blockers

A

block receptors, preventing ca channel opening therefore prevent influx of ca through membrane
blocks smooth muscle contractions

40
Q

What do Ca channel blockers act on ?

A

L type Ca channels

41
Q

Ca channel drugs

A

-phenylalkylamine= verapamil
- dihydropyridines= amlodipine
benzothiazepines= diltiazem

42
Q

What are the selective actions of the Ca channel drugs?

A

verapamil- more active on the heart
nifedipine- smooth muscles
drugs also dilate the coronary vessel

43
Q

Side effects of Ca channel blockers

A

flushing and headaches due to vasodilator action

verapamil= constipation (effects GI nerves and smooth muscle)

44
Q

What is aspirin, why is it given?

A

NSAID/ acetylsalicylic acid

- given immediately on presentation or daily thereafter

45
Q

Mechanism of aspirin?

A

cardiovascular area because it inhibits the COX-1 receptor on platelets and reduces platelet aggregation
irreversibly acetylates COX enzymes and platelet cannot replenish

46
Q

Lifetime of a platelet

A

10 days

after that new ones form

47
Q

Usage of aspirin? and risks?

A

First line CVD

GI bleeding, deafness, tinnitus, self poisoning and resistance

48
Q

How was aspirin made?

A

One of the oldest drugs
synthesesied
derived from willow bark

49
Q

Whats special about aspirin in comparison to other NSAIDS

A

non steroidal inflammatory drugs 75mg/day suppresses platelet aggregation

50
Q

What does inhibiting COX1 effect?

A

it prevents the conversion of arachidonic acid to thromboxane A2 which causes platelet aggregation

51
Q

Why can platelet replace enzyme?

A

Don’t have a nucleus
so cannot do de novo synthesis
remain inactivated

52
Q

Pharmacokinetics of taking aspirin

A

given orally
hydrolysed in 30 mins by esterase from liver
1/2 life depends on dose

53
Q

When happens to aspirin when taken orally

A

Week acid so protonated in stomach and able to pas through mucosa = major absorption site
hydrolysed by salicylate in tissues

54
Q

Anti-coagulant and platelet approach how does it work

A

prevents clotting by inhibiting clotting factors

heparins= enoxaparin- activate antithrombin which activates thrombin and factor xa - prevent stable clot formation

55
Q

Side effects of anti- coagulant and platelet

A

bleeding

56
Q

Analgesia

A

Given with acute coronary syndrome

heart attack= painful so give morphine

57
Q

Different types of opiates

A
  • Morphine

- codeine

58
Q

What id morphine?

A

extracted from poppy juice used for 1000s years
induce euphoria, analgesia and stop diarrhoea
partial agonist

59
Q

How does morphine work?

A

Binds to opiod receptor (GI/Go coupled to ion channel)

phenanthrene derivative

60
Q

What is codeine?

A

opiate
binds to Mu receptor as a partial agonist
effective respiratory depressor

61
Q

Side effects of opiates?

A 
Respiratory depression 
nausea and vomiting 
reduced tone and motily in gut 
histamine released tolerance effects
*morphine given slowly it doesn't have effects
62
Q

Unstable angina treatments

A

DAPT
heparin
analgesia
secondary prevention- ACE, statins, BB

63
Q

Nstemi treatments

A

Antiplatelet
analgesics
PCI within 72 hours
possibly additional platelet depending on changes in ECG

64
Q

Treatments for STEMI

A

PCI- If centre is too far away then clot buster
antiplatelet medications- aspirin
lifelong medications= aspirin 75mg/day for 1 year, statins, ace, BB

65
Q

Personalisation of treatments

A

Platelet based- maybe inflammation

individual maps of the patients coronary arteries- help decide which lesions within which arteries need attention

66
Q

PASTOR study

A

used bedside device at the time of PCI after STEMI to measure individual platelet activity and assign anti-platelet medication on this basis

CDL301 (7 decks)

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