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Cardiovascular MBCHB2 > Lecture 23: Acute chest pain > Flashcards

Lecture 23: Acute chest pain Flashcards

1
Q

What are the symptoms of acute chest pain?

A

Chest pain +/- Shortness of Breath

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2
Q

What are some of the chest pain differentials?

A

Cardiac
- MI, Myocarditis, Pericarditis, HF

Vascular
- Aortic stenosis

Respiratory
- PE, Infection; Pneumonia, Bronchitis, COPD, Asthma, Pneumothorax

Vascular
- Aortic dissection

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3
Q

What are the investigations to make for diagnosis of acute chest pain?

A
  • History and examination
  • Blood tests; Full blood count, blood gases, troponin, D dimer
  • ECG
  • Radiology (CXR, CTPA)
  • Coronary angiogram
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4
Q

What are the two types of acute MI?

A

ST elevation MI (STEMI)

Non-ST elevation MI (Non-stemi)

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5
Q

What triggers a STEMI?

A

Full occlusion of CA

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6
Q

What triggers a non-stemi?

A

Very dynamic situation, can open, vasospasm, closed, clot

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7
Q

What is the pathophysiology of vascular occlusion?

A
  • Plaque fissure
  • Platelet adhesion
  • Platelet activation
  • Platelet aggregation

(Anti-platelet medications)

  • Thrombotic occlusion (LMWH + Thrombolytics)
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8
Q

What does non-STEMI lead to on ECG?

A

ST depression

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9
Q

What is non-STEMI initial management?

A
  • Pain relief (morphine, anti-emetic)
  • Nitrate (Coronary vasodilator)
  • Aspirin (+/- other platelets)
  • Beta-blockers
  • Low Molecular Weight Herapin (LMWH)
  • Stent
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10
Q

What is the initial treatment of STEMI MI?

A
  • Pain relief (morphine, anti-emetic)
  • Nitrate (Coronary vasodilator)
  • Aspirin (+/- other platelets)
  • Beta-blockers
  • Thrombolytic + LMWH
  • NB Stent (Urgent) (Current standard)
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11
Q

What was found when streptokinase and aspirin were given together?

A

Synergistic effect

i.e thrombolysis and aspirin

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12
Q

What are some thrombolytics?

A
  • Streptokinase
  • Alteplase (human t-PA)
  • Tenecteplase (t-PA variant) (More specific human types)
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13
Q

Describe the action of thrombolytics;

A

Plasminogen in blood (endogenous thrombolytic)
(Streptokinase activates)
Plasminogen binds to fibrin
(alteplase, reteplase - activates plasminogen on fibrin)
Plasmin produced on fibrin. Fibrin broken down.

Fibrin degredation products

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14
Q

When are thrombolytics given? and how are they given

A

Within 12 hrs of chest pain

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15
Q

Describe streptokinase;

A

Streptokinase

  • Streptococci-synthesised protein
  • Streptokinase-plasminogen complex
  • Renal excretion
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16
Q

Describe tenecteplase:

A

Tenecteplase

  • Bolus
  • Liver metabolised
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17
Q

What are the thromoblysis risks?

A

All:
- Bleeding
+ Local (To lure site)
+ Intracerebral

Streptokinase

  • Allergy / anaphylaxis
  • Hypotension
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18
Q

What are contraindications for thrombolysis?

A

Surgery
Bleeding

and many more

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19
Q

What are the anti-platelet agents?

A

Aspirin
Clopidogrel
Ticagrelor

20
Q

What is the action of aspirin?

A
  • Inhibits platelet aggregation
  • Anti-inflammatory
  • Analgesic
  • Anti-pyretic
21
Q

What is the mechanism of action for aspirin?

A

Inhibits platelet COX 1 (Irreversible)

  • Acetylates serine residue at active site
  • Arachidonic acid unable to access active site
  • Prostaglandin / thromboxane production inhibited (decreased bioavailability)

Aspirin metabolised to salicylic acid

22
Q

What is the secondary prevention of aspirin?

A

Secondary prevention

  • Vascular events
  • Mortality
23
Q

What vascular events does aspirin prevent?

A

CAD

  • MI
  • Chronic Angina

Stroke
Peripheral vascular disease

24
Q

What are aspirin side effects?

A

Upper GI effects

  • Reduced production of protective prostaglandin E2 (bicarb and mucous)
  • Dyspepsia, upper GI ulcers

Asthma (sensitive people)

25
Q

What is the action of clopidogrel?

A
  • Antithrombotic / antiplatelet drug (irreversible)
  • Absorbed -> CYP P450 metabolism -> active metabolite.
  • > Inhibits P2Y platelet receptor
26
Q

What are the limits of clopidogrel?

A

Ceiling effect (50-60% platelet aggregation inhibition)

Time and dose dependant

27
Q

What are the side effects of clopidogrel?

A
  • GI bleeding
  • Upper GI symptoms
  • Rash
  • Beware if concurrently on warfarin
28
Q

When should you use clopidogrel?

A
  • Acute coronary syndromes
  • Aspirin allergy
  • Vascular stening (b.c foreign material)
29
Q

Write some notes on ticagrelor?

A

Efficacy > Clopidogrel

  • Reversible antagonist
30
Q

Whats the risk of ticagrelor?

A

Dyspnoea

Bleeding

31
Q

What are LMWH?

A

Take naturally occuring herapins which have varying KDA, and take the specific subset with LMW

32
Q

How do LMWH do?

A

Inhibit factor Xa

33
Q

When do you use LMWH?

A

Indications:

  • Non-STEMI
  • STEMI
34
Q

What are the adverse effects of LMWH?

A

Bruising/bleeding sites

  • Intra-cranial
  • Injection sites
  • Gastro-intestinal loss
  • Epistasis

Thrombocytopenia (Next year, autoimmune phenomenon)

35
Q

What really increases the risk of bleeding?

A 
Post MI
- Fibrinolysis
\+
- LMWH
\+
- Antiplatelet agent
36
Q

When do you use nitrates?

A
  • Acute coronary disease

- Chronic angina

37
Q

What are the potential mechanisms of nitrate administration?

A

Rapidly absorbed;

  • Oral
  • Intravenous
  • Sublingual
  • Transdermal
38
Q

What are the pharmacodynamics of nitrates?

A
  • Uncertain mechanism
    + Biotransformation
    + Denitration
    + Increased bioavailability/activity Nitric Oxide
39
Q

What do nitrates do?

A

Vascular smooth muscle relaxation

  • Arterial Dilation (Coronary and Peripheral)
  • Veno dilation (decreased cardiac work)
40
Q

What is nitrate tolerance?

A

Loss of haemodynamic and anti-anginal efficacy during sustained therapy

41
Q

How can nitrate tolerance be prevented?

A
  • Nitrate dosing

- Nitrate-free period

42
Q

What are the mechanisms of action for beta blockers?

A
  • Antagonise b adrenoreceptors
  • Reduced cardiac work
  • Negatively inotropic (acutely)
  • Negatively chronotropic
43
Q

Whats the relative selectivity of metoprolol / atenolol?

A

B1&raquo_space;» B2

44
Q

Whats the differences of the various Beta blockers?

A
  • Selectivity (B1 or B2)
  • Elimination (Renal vs Liver)
  • Half life
  • Solubility (water vs fat)
  • Additional properties / mechanisms
45
Q

What beta blockers are used in an acute MI?

A

Metoprolol

Carvedilol

46
Q

What are the potential adverse effects of beta blockers?

A

Resp.
- Asthma exacerbation

CVS

  • Hypotension
  • Bradycardia
  • CCF exacerbation
  • Vasospasm

Cardiovascular MBCHB2 (31 decks)

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