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Hypertension Flashcards

1
Q

First line treatment

A

ABCD

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2
Q

Second line

A

Central alpha2 agonists
VDs
Alpha blockers

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3
Q

Diuretics

A

Diuretic action decreasing BV and CO
VD properties: k opener, depletion of Na and Prostaglandin
Indapamide (thiazide analogue that’s actually a CCB

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4
Q

Thiazide; Hydrochlorothiazide, chlorthalidone and indapamide

A

Mild and moderate

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5
Q

Loop
Furosemide Torsemide Ethacrynic acid Bumetanide

A

Severe HT
Ht emergencies
HT with renal insufficiency

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6
Q

Potassium Retaining
Spironolactone eplerenone amiloride triametrene

A

In combination with others to correct hypokalemia
Resistant hypertension

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7
Q

ACE Inhibitors

A

Inhibit VC and produce VD through kininase inhibition (directly through increase bradykinin and indirectly through PGs and NO

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8
Q

Hypertrophy and Cardiac Remodelling

A

Decreased by ACEis

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9
Q

Pharmacological actions of ACEis

A

Mixed Arterio > Venous VD
This decrease Cardiac work making ACEi ideal for HF angina as well

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10
Q

Venous VD

A

Decreased VR then EDV then Preload then BP

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11
Q

Arterial VD

A

Decreased TPR then BP

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12
Q

Increase Renal Blood Flow with decreased GFR

A

ACEi because of EFFERENT VD not afferent decreasing Glomerular HT
*doesn’t affect metabolites metabolism (including uric acid secretion) unlike diuretics do

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13
Q

No postural hypotension in ACEi

A

Less venodilation
*unlike nitrates with their postural hypotension and reflex tachycardia

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14
Q

Decreased baroreceptor reflex and sympathetic activity

A

No reflex tachycardia with ACEi

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15
Q

Dry irritant cough

A

Bradykinin and prostaglandin

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16
Q

Classification of ACEIs

A

S H containing - captopril
Non S H containing- active: lisinopril and pro drug: ramipril
* Fusinopril excreted in bile not urine so it’s dose doesn’t need to be readjusted with renal failure

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17
Q

Captopril
*Active
*Angio edema side effect

A

Oral absorption affected by meal so take 1 - 2 hrs before
No BBB
50% liver and 50% unchanged in urine
Short acting so give 2 - 3 times per day

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18
Q

Posses less side effects between cptopril and non SH

A

Non SH
*Absorption not even affected by meals

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19
Q

Active non S H

A

Lisinopril - NOat metabolised longest t1/2 so used once daily

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20
Q

Prodrugs

A

Enalapril - enalaprilat
Ramipril - ramiprilat
Perindopril - perindoprilat
Benazepril - benazeprilat
Quinapril
Fosinopril - excreted in bile not urine so impaired renal function doesn’t cause toxicity and stuff like that

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21
Q

First dose hypotension especially in

A

Na Depletes patients by diuretics
- treat with saline and stop diuretics before the ACEI

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22
Q

Take in patients with k Retaining diuretics or NSAIDS

A

Hyperkalemia

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23
Q

ACEIs are contraindicated jn bilateral renal artery stenosis

A

ACRIs cause EFFERENT not affer3nt VD which won’t help this situation at all

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24
Q

ACEI are only helpful in treatment of diabetes nephropathy with their efferent VD property

A

As with 1 you have BD arteries that need to be counterbalanced and with 2 the arteries are of normal diameter so no need

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25
Q

Decreased taste - disgeusia

A

ACEI side effect

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26
Q

ACEI s lush NSAIDS

A

Aspirins partially antagonise the hypotensive effects blocking PGs synthesis

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27
Q

ACEI plus anatcid

A

Poor absorption as they are week acids that require basic media

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28
Q

AT1receptor blockers
*compete with Ang for it’s receptors
*Two mechanisms :decreased VC and release prostacyclin(VD)

A

Losartan
Valsartan
Candesartan
Talmisartan
Irbesartan

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29
Q
A
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30
Q

Presynaptic AT1 receptors exists

A

Blocked by AT1 RB decreasing Noradrenaline release

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31
Q

Cause efferent DVD decreasing Glomerular Glomerular hypertension

32
Q

ATI RB plus diuretics

A

With diuretics because k Retaining
Mild uricosic
*therapeutic uses andside effects like ACEI minus dry irritant cough

33
Q

Dysgeusia neutropenia proteinuria

A

Side effects of ACE and AT1 Blockers

34
Q

Direct renin inhibitors

A

Aliskiren
*Better results (refmduced systolic and diastolic BP) with hydrochlorothiazide and AT1

35
Q

Adverse effects of Aliskiren

A

Headache fatigue dizziness diarrhea
Be careful moderate renal dysfunction patients because chymase takes over

36
Q

Sympathetic depressants as another line of treatment

37
Q

What are ganglion blockers?

A

Trimethaphan

38
Q

What are combined alpha- and beta-adrenergic blockers?

A

Examples include labetalol.

39
Q

What are beta adrenergic blockers?

A

Examples include propranolol.

40
Q

What are alpha adrenergic blockers?

A

Example includes Phentolamine.

41
Q

What are adrenergic neuron blockers?

A

Reserpine & Guanethidine.

42
Q

What are centrally acting sympathetic depressants?

A

Agonists such as Methyldopa & imidazoline.

43
Q

What is the use of sympathetic depressants?

A

They are used in the treatment of hypertension.

44
Q

Alpha 2 agonists inhibit NA release by stimulating the receptors in

A

The brain stem - decreasing flow from CNS
The kidney - decreasing renin
The adrenergic ending - decreasing NA
*plus they decrease renal vascular resistance so used in hypertension with renal failure

45
Q

Alpha methyldopa

A

BBB so a risk in pregnancy ĵ really

46
Q

Alpha methyl dopa inhibits NA through

A

Same general mechanisms plus inhibition of dopa decarboxylase and Serotonin biosynthesis

47
Q

Alpha methyl dopa fights with dopa for its Dopamine forming receptors

A

Giving methyl Noradrenaline (a false tesnsmitter) and not Noradrenaline with
*plus BBB

48
Q

Adrenergic blockers:
Selective al0ha

A

Two mechanisms
As an alpha blocker
And phosphodiesterase inhibi

49
Q

Uses of prazosin
3Hs

A

Hypertension
Heart Failure - mixed dilator
Benign prostatic Hyperplasia

50
Q

Beta blockers as adrenergic receptor blockers in HF

A

Can cause hypotension on Prolonged use

51
Q

Beta blockers in
The usual places

A

CNS
Kidney
Presynaptic endings
Heart
Baroreceptor - sensitivity
BV - PG and decreased PR
Plus VD beta blockers like celiprolol nebivolol carvedilol labetalol

52
Q

Beta and alpha blockers in treatment of hypertension

A

Labetalol
Beta : alpha - 3 : 1
No effect on CO plus no ISA like propranolol
No tachycardia- blocks both receptors

53
Q

Labetaproduces quick drop in bp because

A

Alpha 1 blocking
Anti renin
*so used in emergencies

54
Q

Combined Alpha and beta blockers are perfect for

A

Pheochromocytoma
And hypertension 😕: orally or IV in severe (emergency or toxemia(pre-eclampsia)) hypertension

55
Q

Carvedilol

A

Like labetalol but with antioxidant action apparently

56
Q

Calcium Channel Blockers

A

Also used in hypertension

57
Q

Vaso Ds as antihypertensives

A

Direct :
Veno - nitrates
Arterio - hydralazine minoxidil CCB
Mixed Na nitroprusside nesiritide
Others - affect endogenous mediators: raas antagonists autocoids sympathomimetics sympathetic depressants

58
Q

Special VD

A

Hydralazine - arterial through NO
Minoxidil
Diazoxide
Na nitroprusside

59
Q

Hydralazine

A

Coronary
Renal - increased RBF
Splanchnic
Decreased Diastolic more than systolic

60
Q

There can be slow acetylation of hydralazine

A

Peripheral neuritis(idiosyncracy) - treat with vit B6

61
Q

Decreased bp increased sympathetic reflex tachycardia
*Hydralazine

A

Contraindicated in angina
Contraindicated in kidney desease

62
Q

Anti hypertensive(maye with beta blockers or diuretics) drugs also used in

63
Q

Minoxidil, another arterio is a

A

Prodrug(K channel causing hyper p)
- active minoxidil sulphate

64
Q

Potent Oral Long acting Direct Arterio D

65
Q

Added disadvantage of minoxidil

A

Together with decreased BP
Hypertrichosis - All the hair growth

66
Q

Added therapeutic use of minoxidi

A

Topically in alopecia
Together with sever Hyper t and resistant HF

67
Q

Diazoxide

A

Two mechanisms:
Hyperpolarisation
Direct ArterioD

68
Q

Added disadvantage

A

It’s related to thiazide diuretics so can cause hyperglycaemia and hyperuricemia

69
Q

Therapeutic uses of diazoxide

A

Hypertension
Oral hypoglycemic in insulinomas

70
Q

Specia case of Diazoxide

A

Boud to plasma proteins so if to be used in emergencies:
Rapid IV of large doses
Repeated Iv of small doses till saturation of plasma proteins then IV infusion

71
Q

Na Nitroprusside- mixed VD plues inhibit platelet aggregation

A

RBCs and endothelium uptake the stuff then release NO which stimulates granulated cyclase and gives cGMP

72
Q

Na Nitroprusside

A

Arterio VD
Veno VD
Maintained CO because decreased TPR

73
Q

Na Nitroprusside

A

Taken IV:
Onset 0.5 minutes
Peak 2 minutes
Duration 3 minutes
Metabolised by Rhodanese enzyme - thiocyanate which is excerpted in urine

74
Q

Increase cyanide especially in old age

A

Acidosis and arrhythmia
Death

75
Q

Large doses of Na nitroprusside

A

Severe hypotension
Shock
*Teratogenic

76
Q

Don’t stop Na nitroprusside sudden

A

Rebound hyper t.

77
Q

Uses of Na nitroprusside
*Only by IV 0.5 to 10micrograms
* fresh
*cover with foil because photosensitive
*continuous monitoring
*never stop suddenly

A

Emergency HF HT
Controlled hypotension during some operations
In aortic Aneurysm together with Beta blockers

Pharmacology (17 decks)

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