Drugs + Hypertension Flashcards

(80 cards)

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
Name the three groups of Calcium Channel Blockers
1. Dihydropyridines 2. Phenylalkylamines (Verapamil and Diltiazem) 3. Diphenylalkylamines
26
What do all dihydropyridines end in
-dipine ``` E.g. Nifedipine Nicardipine Isradipine Lacidipine Lercadipine Amlodipine Nimodipine ```
27
How do nifedipine function
Reflex tachycardia
28
Advantages of Amlodipine
No effect on heart failure | Longer duration of action once daily doses
29
When is nimodipine given
Targets cerebral arteries
30
When is Verapamil given
Arrhythmias Hypertension Angina
31
When should Verapamil be avoided
If patient is being given B-blockers
32
When is Dilitiazem given
Angina | Hypertension
33
How does Verapamil effect DHP receptors
Inhibits binding (via allosteric site)
34
How does Dilitiazem effect DHP receptors
Enhances them
35
What metabolite of heart disease binds to DHP
Palmitoyl Carnitine
36
How does amlodipine function
Peripheral vasodilator
37
When is amlodipine given
Mild hypertension
38
To who is amlodipine given
55+ and afro/caribbean
39
When should amlodipine be avoided
Heart failure
40
Suffix of all Thiazide diuretics
-thialide
41
Formula for BP
CO x TPR
42
What diastolic range is considered mild hypertension
90-109 mmHg
43
How does a low BP effect hypertension
Means BP does not increase with age
44
What are Dahl Rat genes
Strains are sensitive and resistant to development on high salt diet
45
How can salt resistance by kidneys be solved
Renal transplant
46
What part of the kidney is effected by high salt diets
NaK2Cl transporters
47
What transporters do thiazides bind to
Na/Cl co-transporters in DCT
48
How do thiazides effect Na/K/2Cl pumps
No effect
49
What compound becomes an additive with thiazide
Frusemide
50
What substance inhibits thiazide binding
Cl
51
What substance stimulates thiazide binding
Na
52
How do thiazides effect urine production
Increased by 2l over first three days
53
Why is the diuretic effect of thiazides not sustained
RAAS is eventually activated
54
How and why does thiazides effect BP
Initial BP fall due to decreased CO, decreased TPR and CO returns to normal
55
How do diuretics effect Na/Ca exchange
Decreases it
56
How do diuretics effect blood vessel walls
1. Decreased Na/water content 2. Decreased wall thickness 3. Increased lumens diameter
57
Is diuretic effect on decreased TPR mainly direct or indirect
Indirect
58
Effect of thiazides on vasodilators
Inhibits vasoconstriction by Ang II, NE
59
How do thiazides effect cGP phosphodiesterase
Inhibits them
60
The action of which two molecules are potentiated by Thiazides
ANP and NO
61
How do Thiazides effect K-channels
Opens them
62
In what three cases are thiazides used for
1. Monotherapy hypertension 2. Oedema 3. Diabetes Insipidus
63
What advantages does Thiazides have in dealing with hypertension over amlodipine
1. Advantage if heart failure present | 2. Counterindicates Beta-blockers
64
6 Side-Effects of thiazides
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
Name three non-thiazide inhibitors
1. Chlorthalidone 2. Mefruside 3. Indapamide
66
Function of mefruside
Inhibits Na/K/2Cl
67
Function of Indapamide
Stronger vasodilator
68
What drug should be given to people with resistant hypertension
Spironolactone if hypokalaemic Thiazide if hyperkalaemic
69
Where are alpha-1 adrenoceptors found
Vascular smooth muscle (vasoconstrictor)
70
Role of the alpha adrenoceptor antagonists tamsulosin
Selective for bladder, relaxes prostate to inhibit hypertrophy
71
Name two alpha-adrenoceptor antagonists
Doxazosin | Indoramin
72
When are beta-blockers given
1. Angina 2. Heart Failure 3. Hypertension 4. Arrhythmia
73
Atenolol function vs Propranolol
Atenolol is selective for beta-1 receptors
74
How does Propranolol effect the CNS
Crosses BBB
75
How do beta-blockers effect Kidneys
Decreased renin secretion via beta-1
76
How do beta-blockers effect blood vessels
Enhances NE release on beta-2
77
Adverse effect of beta-blockers binding to B-1
Bradycardia
78
Adverse effects of beta-blockers on beta-2
1. Bronchoconstriction 2. Peripheral Vasoconstriction 3. Hypoglycaemia
79
Side-effect of verapamil
Constipation
80
Side-effect of most calcium-ion blockers
Dihydropyrodines 1. Headache 2. Palpitations Phenyl amines 3. Bradycardia Diphenylalkylamines Cardiac failure worsening