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Year 2 > Drugs + Hypertension > Flashcards

Drugs + Hypertension Flashcards

1
Q

What is the limit for hypertension suspicion

A

140/90 mmHg or higher

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2
Q

How do we confirm hypertension diagnosis

A

ABPM and HBPM

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3
Q

How do we use ABPM

A

Aka two measurements an hour during person’s usual waking hours, average of 14 measurements to confirm

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4
Q

How do we use HBPM

A
  1. Two consecutive seated measurements 1 minute apart
  2. BP is recorded twice a day for at least 4 days - 1 week
  3. Measurements on first dy discarded and average value of all remaining is used
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5
Q

What three-drug combination is used to treat hypertension

A

ACE
Calcium-channel blocker
Thiazide-like diuretic

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6
Q

What do we treat people aged under 55 with for hypertension

A

ACE

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7
Q

What do we treat people aged over 55, black of any age with for hypertension

A

Calcium-channel blocker

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8
Q

What is step 2 treatment of hypertension

A

ACE

Calcium-channel blocker

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9
Q

What is step 3 treatment

A

ACE
Calcium-ion channel blockers
Thiazide-like diuretic

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10
Q

What is step 4 hypertension

A

Resistant hypertension

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11
Q

How is resistant hypertension treated

A

ACE, Calcium, Thiazide and beta-blockers

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12
Q

Describe the RAAS system

A
  1. When renal blood flow is reduced, juxtaglomerular cells convert prorenin -> renin
  2. Renin converts angiotensinogen -> angiotensin I
  3. Angiotensin I converted to angiotensin II by ACE in lungs
  4. Angiotensin II stimulates secretion of aldosterone and causes vasoconstriction
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13
Q

Name the renin inhibitor drug

A

Aliskiren

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14
Q

How do beta-blockers effect RAAS

A

Prevent renin activation

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15
Q

What drug inhibits the angiotensin receptors

A

AT1 antagonists - ARB

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16
Q

What do all ACE inhibitor drugs end in

A
  • pril

e. g. Captopril, Cilanzapril

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17
Q

What effects to ACE Inhibitors have on the body

A
  1. Reduced vascular resistance due to:
    Decreased smooth muscle tone
    Neuronal NE release decreased
    CNS sympathetic tone decreased
  2. ECF volume reduced as less aldosterone and reabsorption of Na
  3. Bradykinin elevated No, PGI2 not involved
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18
Q

Advantages of using ACE inhibitors

A
  1. No effect on neutral lipids (caused by diuretics)
  2. No effect on insulin (b-blockers and diuretics)
  3. No Heart failure
  4. No peripheral vascular disease effect
  5. Increase QOL
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19
Q

Role of bradykinin

A

Compound that causes contraction of smooth muscles and dilation of blood vessels

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20
Q

What are three unwanted effects of ACE inhibitors

A
  1. Bradykinin-mediated
    - Persistent dry cough
    - Angioedema
  2. Lack of angiotensin can result in renal artery stenosis -> renal failure
  3. Lack of aldosterone can result in hyperkalaemia
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21
Q

What suffix do all Angiotensin Receptor Blockers have

A

-sartan

Candesartan
Eposartan

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22
Q

Unwanted side-effects of ARBs

A
  1. Renal Artery Stenosis
  2. Hyperkalaemia

No bradykinin-mediated effects

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23
Q

How do Calcium Channel Blockers function

A

Do not inhibit calcium but prevent opening of voltage-gates calcium channels.

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24
Q

How many groups of Calcium Channel Blockers are there

A

3

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25
Q

Name the three groups of Calcium Channel Blockers

A
  1. Dihydropyridines
  2. Phenylalkylamines (Verapamil and Diltiazem)
  3. Diphenylalkylamines
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26
Q

What do all dihydropyridines end in

A

-dipine

E.g. 
Nifedipine
Nicardipine
Isradipine
Lacidipine
Lercadipine 
Amlodipine 
Nimodipine
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27
Q

How do nifedipine function

A

Reflex tachycardia

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28
Q

Advantages of Amlodipine

A

No effect on heart failure

Longer duration of action once daily doses

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29
Q

When is nimodipine given

A

Targets cerebral arteries

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30
Q

When is Verapamil given

A

Arrhythmias
Hypertension
Angina

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31
Q

When should Verapamil be avoided

A

If patient is being given B-blockers

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32
Q

When is Dilitiazem given

A

Angina

Hypertension

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33
Q

How does Verapamil effect DHP receptors

A

Inhibits binding (via allosteric site)

34
Q

How does Dilitiazem effect DHP receptors

A

Enhances them

35
Q

What metabolite of heart disease binds to DHP

A

Palmitoyl Carnitine

36
Q

How does amlodipine function

A

Peripheral vasodilator

37
Q

When is amlodipine given

A

Mild hypertension

38
Q

To who is amlodipine given

A

55+ and afro/caribbean

39
Q

When should amlodipine be avoided

A

Heart failure

40
Q

Suffix of all Thiazide diuretics

A

-thialide

41
Q

Formula for BP

A

CO x TPR

42
Q

What diastolic range is considered mild hypertension

A

90-109 mmHg

43
Q

How does a low BP effect hypertension

A

Means BP does not increase with age

44
Q

What are Dahl Rat genes

A

Strains are sensitive and resistant to development on high salt diet

45
Q

How can salt resistance by kidneys be solved

A

Renal transplant

46
Q

What part of the kidney is effected by high salt diets

A

NaK2Cl transporters

47
Q

What transporters do thiazides bind to

A

Na/Cl co-transporters in DCT

48
Q

How do thiazides effect Na/K/2Cl pumps

A

No effect

49
Q

What compound becomes an additive with thiazide

A

Frusemide

50
Q

What substance inhibits thiazide binding

A

Cl

51
Q

What substance stimulates thiazide binding

A

Na

52
Q

How do thiazides effect urine production

A

Increased by 2l over first three days

53
Q

Why is the diuretic effect of thiazides not sustained

A

RAAS is eventually activated

54
Q

How and why does thiazides effect BP

A

Initial BP fall due to decreased CO, decreased TPR and CO returns to normal

55
Q

How do diuretics effect Na/Ca exchange

A

Decreases it

56
Q

How do diuretics effect blood vessel walls

A
  1. Decreased Na/water content
  2. Decreased wall thickness
  3. Increased lumens diameter
57
Q

Is diuretic effect on decreased TPR mainly direct or indirect

A

Indirect

58
Q

Effect of thiazides on vasodilators

A

Inhibits vasoconstriction by Ang II, NE

59
Q

How do thiazides effect cGP phosphodiesterase

A

Inhibits them

60
Q

The action of which two molecules are potentiated by Thiazides

A

ANP and NO

61
Q

How do Thiazides effect K-channels

A

Opens them

62
Q

In what three cases are thiazides used for

A
  1. Monotherapy hypertension
  2. Oedema
  3. Diabetes Insipidus
63
Q

What advantages does Thiazides have in dealing with hypertension over amlodipine

A
  1. Advantage if heart failure present

2. Counterindicates Beta-blockers

64
Q

6 Side-Effects of thiazides

A
  1. Volume depletion
  2. Hypokalaemia (fixed with K supplements/K sparing diuretics
  3. Pre-existing gout worsens
  4. Decreased calcium excretion
  5. Inhibits insulin release in diabetes
  6. Increased lipid levels
65
Q

Name three non-thiazide inhibitors

A
  1. Chlorthalidone
  2. Mefruside
  3. Indapamide
66
Q

Function of mefruside

A

Inhibits Na/K/2Cl

67
Q

Function of Indapamide

A

Stronger vasodilator

68
Q

What drug should be given to people with resistant hypertension

A

Spironolactone if hypokalaemic

Thiazide if hyperkalaemic

69
Q

Where are alpha-1 adrenoceptors found

A

Vascular smooth muscle (vasoconstrictor)

70
Q

Role of the alpha adrenoceptor antagonists tamsulosin

A

Selective for bladder, relaxes prostate to inhibit hypertrophy

71
Q

Name two alpha-adrenoceptor antagonists

A

Doxazosin

Indoramin

72
Q

When are beta-blockers given

A
  1. Angina
  2. Heart Failure
  3. Hypertension
  4. Arrhythmia
73
Q

Atenolol function vs Propranolol

A

Atenolol is selective for beta-1 receptors

74
Q

How does Propranolol effect the CNS

A

Crosses BBB

75
Q

How do beta-blockers effect Kidneys

A

Decreased renin secretion via beta-1

76
Q

How do beta-blockers effect blood vessels

A

Enhances NE release on beta-2

77
Q

Adverse effect of beta-blockers binding to B-1

A

Bradycardia

78
Q

Adverse effects of beta-blockers on beta-2

A
  1. Bronchoconstriction
  2. Peripheral Vasoconstriction
  3. Hypoglycaemia
79
Q

Side-effect of verapamil

A

Constipation

80
Q

Side-effect of most calcium-ion blockers

A

Dihydropyrodines

  1. Headache
  2. Palpitations

Phenyl amines
3. Bradycardia

Diphenylalkylamines
Cardiac failure worsening

Year 2 (155 decks)

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