Cardiovascular Medicine 1 Flashcards

1
Q

what are the risk factors for cardiovascular disease

A

> irreversible

  • age
  • sex
  • family history

> reversible

  • smoking
  • obesity
  • diet
  • exercise
  • hypertension
  • hyperlipidaemia
  • diabetes
  • stress
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2
Q

what does the patient need to do to change their risk modification

A
  • need to have information on why they should change
  • need to believe they can change
  • need to have motivation to change
  • need to have a behavioural change
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3
Q

what is primary prevention

A

stop the risk that is going to give you the disease before you actually have the disease
this is often more difficult as if the patient doesnt believe they will get the disease they have no motivation to make the changes - its not real to them

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4
Q

what is secondary prevention

A

once you have the disease, this is to stop it getting worse

this is easier as the patient wont want the disease to get any worse, they now have motivation as it is real to them

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5
Q

what can be done in primary prevention

A
> exercise
> diet
> not smoking
> assess total risk
- medical treatment if risk is high
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6
Q

what can be done in secondary prevention

A

> diet
exercise
not smoking
medical treatment to reduce risk

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7
Q

what type of approach should be taken with primary prevention

A
opportunistic approach
> family history
> diet
> smoking 
> test cholesterol
> test blood pressure
> test for type 2 diabetes
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8
Q

what problems are likely to arise after presenting with CV disease

A

> angina
heart attack
stroke
claudication

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9
Q

what is included in the approach to prevention?

A

> lifestyle changes

> control total cholesterol

  • statin treatment
  • reduce cholesterol (<5.0mmol/L or 25%)

> control hypertension

  • moderate hypertension
  • mild hypertension with evidence of CV disease
  • reduce blood pressure to target <140/85

> antiplatelet drugs - aspirin

  • when identified CV disease
  • when high risk with no identified disease
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10
Q

why are drugs used in CV system

A

> to prevent further disease

> to reduce symptoms of current disease

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11
Q

what drugs can be used to prevent further disease in the CV system

A
  • anti-platelet drugs
  • lipid lowering drugs
  • anti-arrhythmics
  • anticoagulants
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12
Q

what drugs can be used to reduce symptoms of current disease in CV system

A
  • diuretics
  • anti-arrhythmics
  • nitrates
  • calcium channel blockers
  • ace inhibitors
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13
Q

what does aspirin do

A

inhibits platelet aggregation (dont want to stick to blood vessel walls)
alters the balance between thromboxane A2 and prostacyclin
irreversible for the life of the platelet (platelets last a week)
taking a aspirin every day means it will act on every new platelet being made in the body

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14
Q

how much aspirin should be taken to prevent platelet function

A

75mg

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15
Q

how much aspirin should be taken for painkiller function

A

300mg

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16
Q

what does clopidogrel do

A

inhibits ADP induced platelet aggregation

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17
Q

what does dipyridamole do

A

inhibits platelet phosphodiesterase

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18
Q

name new antiplatelet drugs

A

prasugrel and ticagrelor

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19
Q

when are new antiplatelet used

A

only prescribed in conjunction with aspirin
only licensed for acute coronary syndromes
poor evidence of bleeding risk in dentistry

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20
Q

what is atherosclerosis

A

> happens in arteries
more common as you get older
depends on biochemical factors in blood vessel walls and how you metabolise things
affected by diet and lifestyle
platelets stick to walls which narrows the artery and limits the blood flow

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21
Q

what do antiplatelets do

A

stop platelets sticking to walls and to each other

platelet helps to initiate clot formation but clot happens due to clot factors

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22
Q

name oral anticoagulants

A

> warfarin
(cheapest and most common, needs to be monitored and each patient has a tailored dose)

> rivaroxiban
apixaban
dabigatran
(these 3 drugs dependent on size of patients, these are preferred now but still more expensive but may work out that the cost of care is less overall as a result)

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23
Q

explain warfarin and its actions

A
  • coumarin based anticoagulant
  • inhibits synthesis of vitamin K dependent clotting factors (2,7,9,10 [slow] and protein C and S [quick])
  • initial hypercoagulation
    > anticoagulation takes 2-3 days
    > often heparin used concurrently initially
    > need to go into hospital and receive injectable anticoagulant to allow the oral warfarin time to actually work in the body
  • once stabilised it will take 2-3 days to los effect if drug stopped
    > very easily upset
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24
Q

why must warfarin be monitored regularly

A

> drug and food interaction

  • plasma protein binding
  • liver metabolism
  • need to have a predictable level of medicines and types of food

> monitored with INR test
- standardised prothrobin time (PT)

> usually therapeutic range is 2-4

  • within range = no alteration needed for dental care
  • out of range = refer for medical range
  • less than 2 = risk of clot
  • over 4 = risk of bleed

> local haemostatic measures always

> ID Block - avoid if possible but not contraindicated

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25
Q

what does warfarin interact with

A
assume all drugs interact with warfarin
> amoxycillin
> metronidazole 
> erythromycin 
> NSAIDs
26
Q

how often should new oral anticoagulants (NOAC) be taken

A
rivaroxiban = 1x daily (aXi)
apixban = 2x daily (aXi)
dabigatran = 2x daily (dTi)
27
Q

explain activated factor X inhibitors

A

lol go check the graph i dunno how to put it into words ahahahhh but looks kinda important it involves intrinsic and extrinsic activation xxxxxx

28
Q

name direct thrombin inhibitors

A
dabigatran 
argatroban
bivalirudin 
lepirudin
diagram is helpful for this x
29
Q

explain NOACs

A

new oral anticoagulant
> short half life - effect lost rapidly
> no anticoagulant test used
- bioavailability predictable
> may only be a short course / short period of time - DVT
- postpone an extraction until treatment is stopped - wont be long
> More predictable and controllable

30
Q

what is NOAC like with dental drug interactions

A

> safe with dental antibiotics except macrolides
- erythromycin and clarithromycin

> safe with antifungals
- topical and fluconazole

> safe with LA

> safe with antivirals

> NSAID will prolong action and inhibit platelets - avoid

31
Q

what other drugs prevent CV disease

A
> statins
> beta-adrenergic blockers
> diuretics
> calcium channel blockers
> ACE inhibitors
32
Q

what are lipid lowering drugs

A

> HMG coA reductase inhibitors (“statins”)

  • simvastatin = a prodrug (metabolised in liver to give an active drug)
  • atorvastatin
  • rosuvastatin (stop taking these with antifungal drugs, long term medicine so can stop taking them then start them again when antifungal prescription is complete)

> inhibit cholesterol synthesis in the liver
= reduce total cholesterol and LDL-cholesterol
(stops body making so much cholesterol, this reduces risk of developing atherosclerosis and the risk gets lower the longer you take the drug - wont see a change next week but notice difference in 10 years)

33
Q

what are side effects of lipid lowering drugs

A

possible myositis with some drug interactions - includes antifungals

34
Q

what sort of treatment can you not be on when taking lipid lowering drugs

A

> antifungal treatment as there is fluconazole interaction

35
Q

name beta-adrenergic blockers (beta-blockers)

A

> atenolol

  • selective
  • beta 1 only

> propranolol

  • non-selective
  • beta 1 and beta 2

> many others that end in -olol

36
Q

what do beta blockers do

A

> stop arrythmias leading to cardiac arrest (VF)

  • blocks effect of adrenaline on heart
  • slows heart down and makes it function poorly

> reduces heart muscle excitement

> prevents increase in heart rate
= postural hypotension
= prevents unusual heart rhythms which can lead to heart attacks

> reduce heart efficiency
= makes heart failure worse

> block beta receptors in the lungs
- make asthma worse of difficult to treat

37
Q

where are beta 2 receptors found

A

in lungs (asthma) and in the brain (anxiety)

38
Q

what does a patient with postural hypotension need

A

more time to get out of the chair
normally, the body changes in blood pressure when moving from lying down to sitting up by increasing the heart rate
but patients with this can’t do this so need to allow the time to adjust before actually getting up

39
Q

what effect does diuretics have on the body

A

makes you pee
the more you pee the less circulating blood volume you have
blood vessels adapt to this by constricting

40
Q

why would you take diuretics

A

antihypertensive and heart failure

41
Q

what are the 2 types of diuretics

A
  • thiazide diuretics
    (bendroflumethiazide)
  • loop diuretics
    (frusemide)
42
Q

what effect do diuretics directly have on the kidneys

A

increase salt and water loss
- reduce plasma volume
- reduce cardiac workload
(need to make sure patient’s electrolyte balance is acceptable)

43
Q

what are the side effects of diuretics

A
  • can lead to sodium / potassium imbalance if not monitored

- can lead to dry mouth in the elderly

44
Q

where does loop diuretics act on the nephron

A

ascending loop of henle

45
Q

where does thiazide diuretics act on the nephron

A

end of ascending loop of henle / start of distal convoluted tubule

46
Q

what are short acting nitrates

A

eg glyceryl trinitrate (GTN)
= emergency treatment of angina pectoris
- changes to blood vessels
- dilates blood pressure

47
Q

when patient has chest pain what should you do

A

spray GTN under the tongue
if pain goes away = angina attack
if pain doesnt go away = heart attack

48
Q

what are long acting nitrates

A

eg isosorbide mononitrate

prevention of angina pectoris

49
Q

what do nitrates dilate?

A

> dilate veins
- reduce preload to heart

> dilate resistance arteries

  • reduce cardiac workload (afterload)
  • reduce cardiac oxygen consumption

> dilate collateral coronary artery supply
- reduce anginal pain

50
Q

how should nitrates be absorbed

A

> inactivated by first pass metabolism

> sublingual (spray works in minutes)

> transdermal (works for many hours as a patch)

51
Q

what are the side effects of nitrates

A

headache

52
Q

what effect do calcium channel blockers have on the oral cavity

A

makes gums bigger
lumpy fibrous gums are a common side effect
need to have perfect oral hygiene to take this medication

53
Q

what do calcium channel blockers treat

A

hypertension

54
Q

how do calcium channel blockers work

A

block calcium channels in smooth muscle
- some more active on peripheral blood vessels
= relaxation and vasodilation
(drugs ending in -pine eg nifedipine, amlodipine)
- some more active on then heart muscle
= slow conduction of pacing impulses
(eg verapamil)

55
Q

what does ACE stand for in ACE inhibitors

A

angiotensin converting enzyme

56
Q

name ACE inhibitors

A

> enalapril
ramapril
lisinopril
ends in -pril

57
Q

what do ACE inhibitors do

A

> inhibit conversion of angiotensin I to angiotensin II

  • vasconstrictor
  • increases blood pressure

> prevents aldosterone dependent reabsorption of salt and water
(red diagram helpful xo)

> reduce blood pressure

> reduce excess salt and water retention

58
Q

what happens in the renin-angiotensin-aldosterone system

A

stimulus at the nephron causes renin to be released
renin converts angiotensinogen to angiotensin I
the angiotensin converting enzyme converts this to angiotensin II which acts on the adrenal cortex (also causes peripheral vasoconstrictor
this causes an increase in aldosterone release
which increases sodium absorption in cortical collecting ducts

59
Q

what are the side effects of ACE inhibitors

A
  • cough
  • hypotension
  • oral reactions
    > angio-oedema
    > Lichenoid reaction
60
Q

what are angiotensin II blockers

A

> losartan and others (-artan)
inhibit same system but by a different mechanism
doesnt stop you making it but will stop it doing anything