Brainscape's Knowledge GenomeTM

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


See full index

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

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

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

What happens when you get chest pains?

A

release of K, H and adenosine

disease progress insidiously until these symptoms

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

What is chest pain?

A

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

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

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

Risk factors

A
  1. non modifiable
    - age sex gender
    - family history
  2. modifiable
    - diet obesity and diabetes
    - smoking
    - high BP
    - high cholesterol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Epidemeology of ACS

A

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

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

amount of STEMI/NSTEMI in England

A

STEMI- 5/1000

Nstemi- increasing

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

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

Stable angina treatment

A

reduce cardiac work

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

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

unstable angina treatment

A

treat with MI strategy

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

Which types would have GTN relief?

A

Stable angina and unstable angina- not N/STEMI

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

Which would have a normal ECG?

A

Unstable and stable angina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Which types would have raised troponin?

A

NSTEMI

STEMI

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

What is the crucial door balloon time?

A

120 min
for STEMI
immediate procedure

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

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

A

Nitrates- they restore flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Medical treatments after stenting

A

DAPT- dual antiplatelet therapy- incidience of thrombosis 1%

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

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

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions