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OV3017 Eye Disease > 21 - Systemic drugs 1: cardiovascular > Flashcards

21 - Systemic drugs 1: cardiovascular Flashcards

1
Q

modifiable risks of cardiovascular disease

A

-smoking
- hypertension
-hyperlidaemia
-diet+exercidse

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2
Q

non modifiable risks of CVD

A
  • age
  • gender
  • genetics
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3
Q

lifestyle measures to reduce risk of CVD

A
  • stop smoking
  • normal BMI 20-25
  • reduce salt intake to <6g
  • limit alcohol consumption <14 a week
  • 5 a day
  • reduce intake of total and saturated fat
  • regular excerie
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4
Q

hypertension is a major risk factor for

A
  • stroke
    -myocaridal infarction
  • heart failure
  • chronic kidney disease
  • cognitive decline
  • premature death
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5
Q

what can untreated hypertension cause

A
  • vascular and renal damage
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6
Q

diagnosing hypertension

A

if clinic bp higher than 140/90

offer bp monitoring at home to confirm diagnosing

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7
Q

stage 1 HTN

A
  • clinic BP is 140/90 or above and ABPM or HBPM average is 135/85 or above
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8
Q

stage 2 HTN

A

clinic BP > 60/100
and
ABPM/HBPM > 150/95

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9
Q

stage 3 HTN

A
  • clinic bp is 180 >
    or
    clinic diastolic bp is >110
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10
Q

why do we treat HTN

A
  • reduces cerebeovascular disease by 40-50%
  • reduces myocardial infarction by 16-30%
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11
Q

how do we treat HTN

A

stepped approach
- low doses of several drugs

minimises adverse events + maximises patient compliance

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12
Q

what is the aim of treatment

A
  • reduce diastolic BP <90
  • reduce systolic BP <140
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13
Q

younger 55 and stage 1 - which type of drug

A

ACE

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14
Q

Over 55 stage 1/ or black patients of any age - which drug

A
  • calcium channel blocker
  • diuretic
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15
Q

if px becomes stage 2

A

do not inrease dose of ACE - it can increase side effects

instead - add low doses of other drugs

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16
Q

suffix of ace inhibitors

A

PRIL

e.g ramipril

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17
Q

kidney produces renin, what is it and what does it do

A

an enzyme that converts angiotensin to angiotensin I, catalysing conversion

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18
Q

what is antigensin I the substrate for

A

angiotensin converting enzyme (ACE)

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19
Q

what does the angiotensin coverting enzyme do

A

converts angitotensin I to active angiotensin II

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20
Q

what is angiotensin II

A
  • potent vasoconstrictor
  • constricts blood vessels: increasing peripheral resistance + increasing blood volume

we want to STOP vasoconstriction as that will increase blood pressure

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21
Q

side effects of ace inhibtors

A
  • persistent dry cough
  • taste disturbance
  • angiodema
    -1st dose hypotension
  • hyperkalaemia
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22
Q

angiotensin II receptor antagonist

A
  • they completley inhibit the receptor at which angiotensin II acts

-fewer side effects than ACE

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23
Q

Angiotensin II receptor antagonists examples

A
  • candesartan
  • losartan
  • valsartan

TAN SUFFIX

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24
Q

calcium channel blockers

A

CCB all inhibit inward movement of calcium ions through the slow L-type calcium channels in active membranes:

—cells of the myocardium

—Cells within the his-purkinje system of the heart

—cells of the vascular smooth muscle

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25
Q

what do CCB affect - and cause as a result

A
  • cardiac contractability
    causes vasodilation
  • cause vasodilation of large and small arteries and also reduce cardiac output
26
Q

what are calcium channel blockers useful in the treatment of

A

hypertension and angina

27
Q

examples of CCB

A
  • Nifedipine,
  • Amlodipine
  • Verapamil
  • Diltiazem
28
Q

what do diuretics promote

A
  • excretion of water and salt: this is done by increasing urine production and increasing salt consumption
29
Q

how do diuretics reduce the re uptake of salt

A
  • increase the amount of urine
    thereby reducing blood volume
  • thus lowering blood pressue
30
Q

3 main classes of diuretics and where do they mainly work

A

distal convulated tube

  • thiazides
  • loop diuretic
  • potassium sparing
31
Q

what are thiazides commonly used for

A

blood pressure

32
Q

Ignore

A
33
Q

how do thiazides work

A
  • inhibit absorbtion of Na in the DCT
  • can lead to K deficiency
34
Q

how do thiazides reduce BP

A
  • vasodilation
  • reduction in blood volume
35
Q

examples of thiazides

A

bendrofluazide,

Hydrochlorothiazide

Indapamide

36
Q

what do loop diuretics do

A
  • inhibit absorption of sodium and potassium in TAL of loop of henle
  • fast acting
37
Q

when are loop diuretics used

A
  • renal failure + heart failure
38
Q

examples of loop diuretcs

A

Furosemide, Bumetanide

39
Q

where does potassium sparing act

A

DCT

40
Q

What do potassium sparings do

A
  • retain potassium
  • used in conjunction with thiazide and loop diuretics
41
Q

examples of potassium s-paring

A
  • amiloride
  • spironolactone
42
Q

when are beta blockers used

A

treatment of angina

  • increased risk of side effects
43
Q

examples of beta blockers

A
  • atenolol
  • metoprolol
  • propanolol
44
Q

what does the mechanism of beta blockers involve

A
  • reduction of heart rate + force of contraction
  • reduction of peripheral resistance
  • ihibition of renin release
    reduce sympathetic activity
45
Q

less commonly used in anti-hypertensive agents

A

used when other drugs are not bringing down blood pressure that easily even with combination drugs. Or if the patient had bad side effects with some drugs.

-Alpha-adrenoceptor antagonists
Doxazosin

-Centrally acting agents
Methyldopa
Moxonidine

-Vasodilators
Hydralazine
Minoxidil

46
Q

other cardiovascular disease

A
  • ischaemic heart disease
  • cardiac failure
  • cardiac arrythmias
47
Q

Ischaemic heart disease: Angina pectoris

A

-presents with intermittent chest pain on excretion or stress (stable angina)
-caused by insufficient oxygen supplied to cardiac muscle due to narrowing of coronary arteries

48
Q

how is angina pectoris treated

A

–>single acute attack (Glyceryl trinitrate-potent vasodilator)
–>Prophylaxis (Sublingual GTN, Aspirin, Beta- blockers, calcium channel blockers). All patients should receive lipid lowering therapy.

stent inserted to widen blood vessel.`

49
Q

what is atheroma

A
  • Atheroma deposited in the wall of blood vessels
  • Atheroma is problematic because it narrows the blood vessels
    Also linked to formation of clots
50
Q

Ischaemic heart disease: Myocardial infarction

A

-ST elevation on ECG

Immediate:

-Analgesia, Thrombolysis, Aspirin

Prophylaxis:

  • Beta blockers

-ACE inhibitors

  • Aspirin
  • Lipid lowering therapy
51
Q

Heart failure - due to what

A

-Usually the result of damage to the myocardium e.g. MI, Myocardiomyopathy, heart valve damage

-results in poor tissue perfusion and eodema of the lungs or peripheral tissue

52
Q

treatment of heart failure

A
  • Diuretics
  • ACE inhibitors
  • Nitrates
  • Beta blockers
  • Ionotropic drugs e.g. Digoxin
53
Q

Cardiac arrythmias

A

too long and confusing to write]

Just know causes changes in the cardiac action potential

54
Q

what is lipid modification

A
  • cholesterol and triglycerdes transported in the blood from the liver in association with lipoproteins
55
Q

what is low density lipoprotein LDL

A

bad cholestrol

56
Q

what is high density lipoprotein HDL

A

good cholesterol

57
Q

what is LDL cholesterol associated with

A

atheroma and cardiovascular disease

58
Q

what are statins used for

A

to lower cholesterol

59
Q

Enzyme: HMG-CoA

A

rate limiting step in the synthesis of cholestrol in liver

60
Q

what do statins do to this Enzyme: HMG-CoA

A

inhibit this enzyme increasing uptake of LDL from blood

61
Q

statin examples

A

-Simvastatin
- Atorvastatin
- Pravastatin

62
Q

by inhibiting cholesterol synthesis in the liver

A

you get more uptake of LDL cholesterol

OV3017 Eye Disease (19 decks)

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