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2 - Diseases Of The Human System > CV Medicine - 1 > Flashcards

CV Medicine - 1 Flashcards

1
Q

What are irreversble risk factors for cardiovascular disease?

A

age
sex
family history

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2
Q

Why do males have a larger risk of CVD?

A

females are protected by their sex hormones (estrogen)

the risk increases after menopause

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3
Q

What are reversible risk factors that patients can change?

A

smoking
obesity
diet
exercise

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4
Q

What are reversible risk factors that medicine can change?

A
  • hypertension
  • hyperlipidaemia (increased lipids in blood)
  • diabetes
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5
Q

What is primary prevention and what does it include?

A

stopping a disease before it happens
* Exercise, diet & not smoking
* Assess total risk
* Medical treatment if high risk

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6
Q

What is secondary prevention and what does it include?

A

preventing further disease after a disease occurs i.e after a heart attack

all primary prevention
medicial treatment to reduce risk

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7
Q

What is the opportunistic approach to primary prevention that may be difficult?

A
  • Family history
  • Diet
  • Smoking
  • Test cholesterol
  • Test blood pressure
  • Test for diabetes (Type 2)
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8
Q

What are some CV diseases?

A
  • Coronary artery disease (leads to MI)
  • Heart failure
  • Arrhythmias
  • Congenital heart disease
  • Valvular heart disease
  • Peripheral arterial disease
  • Aortic disease
  • Deep vein thrombosis (DVT)
  • Pulmonary embolism (PE)
  • Stroke
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9
Q

What is the healthy cholestrol value?

A

<5.0mmol/L or 25%

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10
Q

What drug classes are used to prevent further CV disease?

A
  • Anti platelet drugs
  • Lipid lowering drugs
  • Anti-arrhythmics
  • Anticoagulants
  • Diuretics
  • Ace-inhibitors
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11
Q

What drug classes are used to reduce symptoms of current disease?

A
  • Diuretics
  • Anti-arrhythmics
  • Nitrates
  • Calcium channel blockers
  • Ace-inhibitors
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12
Q

What are the main anti-platelet drugs?
How do they work?

A

Aspirin - alters balance between prostacyclin and thromboxane
Clopidogrel - inhibits ADP
Dipyridamole - inhibits phosphodiesterase

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13
Q

What is the platelet half-life in plasma?

A

7 days

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14
Q

What do anti-platelet cause to bleeding?

A

Prolong the bleeding time following dental extraction

  • Not a significant problem individually
  • Drug combinations increase the risk
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15
Q

How do anti-platelet drugs affect ‘at risk’ populations?

A

significantly reduce chance of heart attack/ stroke

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16
Q

When are the new anti-platelet drugs used?

A
  • Only prescribed in conjunction with aspirin
  • Only licenced for Acute Coronary Syndromes
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17
Q

When would oral anticoagulants cause a bleeding problem?

A

post-operation

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18
Q

How do oral anticoagulants work?

A

inhibit the clotting casade reducing fibrin formed
therefore clot will not stabilse as less fibrin is present

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19
Q

What phenolic substance is the base of warfarin?

A

coumarin

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20
Q

How does warfarin work?

A

Inhibits synthesis of Vitamin K dependent clotting factors

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21
Q

What clotting factors does warfarin inhibit sythesis of and what is the time period?

A

2, 7, 9, 10 (slow - 2 days)
protein c, protein s (quick)

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22
Q

What happens intially with warfarin?

A

Initial Hypercoagulation
* Anticoagulation takes 2-3 days

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23
Q

What is often used concurrently initially?

A

heparin

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24
Q

When does the effect of warfarin wear off after drug is used?

A

2-3 days

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25
Q

Why must warfarin be monitored?

A

Drug and food interaction with
* Plasma protein binding
* Liver metabolism

26
Q

How is warfarin monitored?

A

with INR test
aim for 2-4

27
Q

What is INR?

A

International Normalised Ratio
which is a Standardised prothrobin time (PT)

28
Q

If out of INR range what could happen?

A

refer for medical advice
too high = risk of bleeding
too low = risk of clots, reduced protection

29
Q

What are haemostatic measures used?

A

Absorbent gauze

Haemostatic packing material (e.g. oxidized cellulose, collagen sponge)

Suture kit (needle holders, tissue forceps, suture material, scissors)

LA with vasoconstrictor

30
Q

What should you avoiding prescribing alongside warfarin?

A

NSAID analgesics

31
Q

What are the new oral anticoagulants predictable in?

A

bioavalibility

32
Q

What factor do most new oral anticoagulants inhibit?

A

factor 10

33
Q

What factor does dabigatran inhibit?

A

thrombin

34
Q

What is the duration of NOAC (new oral anticoagulants)?

A

short half life - effect rapidly lost

35
Q

Why is no anticoagulant test used with NOAC?

A

bioavilability predictable (warfin interacts with food therefore bioavalibity is unpredicatable)

36
Q

What are statins?

A

lipid lowering drugs - reduce cholosterol synthesis in the liver

37
Q

What drugs are HMG coA Reductase inhibitors?

A

-statin ending drugs

38
Q

What do statins reduce?

A

Reduce total cholesterol and LDL-cholesterol

39
Q

What are the side effects of statins?

A

if plasma drug levels becomes high/ interacts, this can cause inflammation in the muscle (myositis)

40
Q

What drug do statins interact with that has a significance in dentistry?

A

fluconazole

41
Q

What are beta-adrenergic blockers (beta-blockers)?

A

drugs that stop arrhythmias leading to cardiac arrest (Ventricular fibrillation – VF)
* Reduces heart muscle excitability

42
Q

Why is asthma relevant to beta blockers?

A

Salbutamol is used to relieve symptoms of asthma by relaxing muscles of airways

it works on beta-2 receptors

however if patient takes non selective beta-blocker, salbutamol is not effective as it cannot work on receptors

43
Q

What do b-blockers cause that can be dangerous?

A
  • Cause postural hypotension (decreased circulation)
  • Reduce heart efficiency, make heart failure worse
  • Block beta receptors in the lungs
44
Q

What are diuretics used for?

A

antihypertensive
heart failure

45
Q

What are the two types of diuretics?

A

thiazide
loop

46
Q

What do diuretics do systemically?

A

Increase salt and water LOSS
* Reduce plasma volume
* Reduce cardiac workload

47
Q

What are the side effects of diuretics?

A
  • Can lead to Na+/K+ imbalance if not monitored carefully
  • Can lead to dry mouth in the elderly
48
Q

What is an example of a short acting nitrate?

A

GTN

49
Q

Why is GTN administered sub-lingually/dermal patches?

A

extensively metabolised (inactivated) on first pass metabolised through liver

50
Q

When are short acting nitrates used?

A

Emergency management of angina pectoris

51
Q

What are long acting nitrates used?

A

Prevention of angina pectoris

52
Q

What is an example of a long-acting nitrate (transdermal patch)?

A

isosorbide mononitrate

53
Q

How are nitrates inactivated?

A

Inactivated by first pass metabolism–administer
by
Sublingual
Transdermal
Intravenous

54
Q

What do nitrates do systemically?

A
  • Vasodilation: This is the primary action. Nitrates work by relaxing smooth muscle cells in blood vessels, causing them to widen (dilate). This widens blood vessels throughout the body, particularly those supplying the heart (coronary arteries).
  • Reduced Blood Pressure:
  • Improved blood flow to the heart:
  • Reduced workload on the heart:
55
Q

What oral disease can calcium channel blockers lead to?

A

Can lead to gingival hyperplasia in some

  • Oral hygiene dependent – need to keep good OH
56
Q

What do calcium channel blockers do systemically and what are they used for?

A

Block Calcium channels in smooth muscle causing slow conduction of pacing impulses
* Relaxation and vasodilation

Used to treat hypertension and migranes

57
Q

What do ACE inhibitors do?

A
  • Inhibit conversion of angiotensin I to angiotensin II
  • Prevents aldosterone dependent reabsorption of salt and water.
58
Q

What do ACE inhibiotrs do systemically?

A
  • Reduce blood pressure
  • Reduce excess salt and water retention
59
Q

What are the side effects of ACE inhibitors?

A

cough (inhibit other enzymes causing irritation)
hypotension

60
Q

What do angiotensin 2 blockers do?

A

Directly block
Inhibit same system but by a different mechanism
do not cause ACE side effects

61
Q

What drug is most likely to be given to someone having an acute myocardial infarction FIRST?

A

aspirin

62
Q

How does aspirin work?

A

Aspirin works by irreversibly inhibiting an enzyme called COX-1 in platelets.
COX-1 helps make chemicals that promote clotting.

By blocking COX-1, aspirin reduces platelet clumping, helping to prevent further blood clot formation in heart attacks and reduce inflammation. This can limit damage to the heart muscle.

2 - Diseases Of The Human System (19 decks)

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