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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
3 steps to stenting
1. mounted on balloon 2. inside stent and inflated 3. stent positioned against wall and wire/ balloon is removed
26
Medical treatments after stenting
DAPT- dual antiplatelet therapy- incidience of thrombosis 1% | Aspirin-+ antiplatelet + abti-coagulant= continued years after stenting
27
Adverse effects and benefits of drugs after stenting
- excess bleeding - pleiotropic positive effects of neutrophils and therefore pulmonary infection- reduce cell growth and clotting, keep your artery open
28
What is the main aim of pharmalogical treatments of IHD?
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
two pharmacological treatment approaches?
1. symptomatic- reduce symptoms, reduce strain on heart and increase vasodilation 2. prognostic- improve outcomes and eleviate neg outcome in future
30
Symptomatic drugs
- nitrates - aspirin - Ca channel - K channel - Analgesia
31
Prognostic
- Aspirin - Statins - beta blockers or ACE inhibitors - anti-inflammation approaches are being developed
32
Nitrates- when they started, why we use them
- brunten 1867 | - first line agents, GTN as a short acting spray sublingually
33
What is the primary and secondary effect of nitrates???
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
Mechanism of action of nitrates
GTN metabolism activates GC and increases cGMP this activates PKG and causes relaxation of the smooth muscle
35
What are the main adverse effects of nitrates
- hypotension- administer slow - headaches - tolerance= depletion of SH group and is more common with longer acting agents
36
NITRATES-What is GTN activated by?
Hepatic metabolism
37
What is the delivery time and the length of effect of nitrates?
- 1-2 mins- conversion from di to mono in a min | - 30 mins it lasts
38
What is isosorbide mononitrate?
orally administered longer acting 2 a day with a nitrate free period at night to avoid tolerance
39
Mechanism of Ca channel blockers
block receptors, preventing ca channel opening therefore prevent influx of ca through membrane blocks smooth muscle contractions
40
What do Ca channel blockers act on ?
L type Ca channels
41
Ca channel drugs
-phenylalkylamine= verapamil - dihydropyridines= amlodipine benzothiazepines= diltiazem
42
What are the selective actions of the Ca channel drugs?
verapamil- more active on the heart nifedipine- smooth muscles drugs also dilate the coronary vessel
43
Side effects of Ca channel blockers
flushing and headaches due to vasodilator action | verapamil= constipation (effects GI nerves and smooth muscle)
44
What is aspirin, why is it given?
NSAID/ acetylsalicylic acid | - given immediately on presentation or daily thereafter
45
Mechanism of aspirin?
cardiovascular area because it inhibits the COX-1 receptor on platelets and reduces platelet aggregation irreversibly acetylates COX enzymes and platelet cannot replenish
46
Lifetime of a platelet
10 days | after that new ones form
47
Usage of aspirin? and risks?
First line CVD | GI bleeding, deafness, tinnitus, self poisoning and resistance
48
How was aspirin made?
One of the oldest drugs synthesesied derived from willow bark
49
Whats special about aspirin in comparison to other NSAIDS
non steroidal inflammatory drugs 75mg/day suppresses platelet aggregation
50
What does inhibiting COX1 effect?
it prevents the conversion of arachidonic acid to thromboxane A2 which causes platelet aggregation
51
Why can platelet replace enzyme?
Don't have a nucleus so cannot do de novo synthesis remain inactivated
52
Pharmacokinetics of taking aspirin
given orally hydrolysed in 30 mins by esterase from liver 1/2 life depends on dose
53
When happens to aspirin when taken orally
Week acid so protonated in stomach and able to pas through mucosa = major absorption site hydrolysed by salicylate in tissues
54
Anti-coagulant and platelet approach how does it work
prevents clotting by inhibiting clotting factors | heparins= enoxaparin- activate antithrombin which activates thrombin and factor xa - prevent stable clot formation
55
Side effects of anti- coagulant and platelet
bleeding
56
Analgesia
Given with acute coronary syndrome | heart attack= painful so give morphine
57
Different types of opiates
- Morphine | - codeine
58
What id morphine?
extracted from poppy juice used for 1000s years induce euphoria, analgesia and stop diarrhoea partial agonist
59
How does morphine work?
Binds to opiod receptor (GI/Go coupled to ion channel) | phenanthrene derivative
60
What is codeine?
opiate binds to Mu receptor as a partial agonist effective respiratory depressor
61
Side effects of opiates?
``` Respiratory depression nausea and vomiting reduced tone and motily in gut histamine released tolerance effects *morphine given slowly it doesn't have effects ```
62
Unstable angina treatments
DAPT heparin analgesia secondary prevention- ACE, statins, BB
63
Nstemi treatments
Antiplatelet analgesics PCI within 72 hours possibly additional platelet depending on changes in ECG
64
Treatments for STEMI
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
Personalisation of treatments
Platelet based- maybe inflammation | individual maps of the patients coronary arteries- help decide which lesions within which arteries need attention
66
PASTOR study
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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