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PHA 222 > hypertension 1&2 > Flashcards

hypertension 1&2 Flashcards

1
Q

define hypertension

A

sustained or persistent elevated arterial BP

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2
Q

what effects hypertension?

A

age, gender, race

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3
Q

is hypertension bimodal?

A

no, it is normal among BP population

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4
Q

what is normotensive and hypertensive?

A

normotensive- normal blood pressure

hypertensive- high blood pressure

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5
Q

what is the 2 things hypertension is based on?

A

associated CV risk

based on arbitrarily defined ‘normal’ BP levels

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6
Q

what does NICE define as hypertensive?

A

140/90mmHg

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7
Q

what does ACC/AHA define as hypertensive?

A

130/80 mmHg

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8
Q

what ways does misdiagnosis usually occur?

A

Poor sensitivity & specificity

‘White coat’ hypertension phenomenon

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9
Q

what do NICE recommend in order to avoid misdiagnosis?

A

Multiple clinic/office BP measurements >140/90 mmHg

Ambulatory BP monitoring (ABPM) orHome BP monitoring (HBPM) >135/85 mmHg

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10
Q

how is hypertension classified?

A

according to blood pressure level( moderate to severe)
traditional 1-3
nice stages 1-3

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11
Q

when does CVD risk double?

A

doubles with each BP increment of 20/10 mm Hg

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12
Q

what does target organ damage effect?

A 
Cerebrovascular disease
Hypertensive retinopathy
Left ventricular dysfunction
Coronary artery disease
Peripheral artery disease
chronic kidney disease
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13
Q

how is hypertension categorized based on the aetiology?

A

hypertension w/ known causes (secondary 5-10%)

hypertension w/ unknown causes(primary 90-95%)

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14
Q

what are the 4 secondary causes of hypertension?

A

renal/endocrine/pregnancy/ drugs

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15
Q

what does primary hypertension cause?

A

increase in total peripheral resistance

Hyper-reactivity of BP to stress, abnormal vascular reactivity & impaired circulatory homeostasis

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16
Q

is hypertension a disorder?

A

yes its a disorder or a syndrome

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17
Q

what are the 3 things that control BP?

A

cardiac output
peripheral resistance
blood volume

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18
Q

what are 4 sites of blood pressure control?

A

1-resistance arterioles
2-capacitance venules
3-pump output heart
4-vol in kidneys

19
Q

what are the major postulates of pathogenesis mechanisms?

A

role of:genetics/ kidney/vascular reactivity and remodelling/neurohormonal factors/central and sympathetic NS

20
Q

what kind of risks are there?

A

modifiable- e.g. diet

non- modifiable- e.g. genetics

21
Q

why do you treat hypertension?

A

to target organ damage
associated with CV mortality
lowering BP reduces CV mortality

22
Q

for treatment, what is the goal for maintaining BP?

A

> 140/90 mmHg (office/clinic)or>135/85 mmHg (ABPM/HBPM)for all adults under 80 years old
150/90 mmHg (office/clinic)or>145/85 mmHg (ABPM/HBPM)for adults 80 years old and over

23
Q

what are the 6 pharmacological treatments for hypertension?

A 
ACE Inhibitors (ACEIs)
Angiotensin II receptor antagonists (ARBs)
Calcium channel antagonists
Diuretics
b-Adrenoceptor antagonists (b-blockers)
Miscellaneous
24
Q

what are the aims of non-pharmacological therapy?

A

to help lower BP
to control other risk factors
to help reduce doses of other hypertensive drugs

25
Q

what are the 5 steps of modification of lifestyle?

A 
1- weight reduction
2- dash eating plan
3- dietary na+ reduction
4-physical activity
5-alcohol moderation
26
Q

what are the main mechanisms for lowering BP?

A

decrease plasma volume
decrease total peripheral resistance (TPR)
decrease cardiac output (CO)
or combinations of three mechanisms

27
Q

what is ACEIs mechanism of antihypertensive effect?

A

dec angiotensin II production dec vasoconstriction  dec PVR
 dec aldosterone secretion  dec fluid retention  dec PV
 dec sympathetic activation  dec vasoconstriction  dec PVR
these in turn inc bradykinin and PGI2 synthesis

28
Q

what is ACEIs first choice initial therapy for?

A

younger hypertensive patients (55 years old) of non-African or Caribbean descent
All diabetic patients, irrespective of age or ethnic origin

29
Q

what is the mechanism for ARBs?

A

reduction of BP via AT1-receptor blockade
dec vascular AT1-R activation  dec vasoconstriction  dec PVR
dec aldosterone secretion  dec fluid retention dec in PV
decsympathetic activation  dec vasoconstriction  dec PVR

30
Q

initial use of ARBs when:

A

younger hypertensive patients (55 years old) of non-African or Caribbean descent
All diabetic patients, irrespective of age or ethnic origin

31
Q

what is ARBs effective in combination with?

A

effective combination with CCBs & thiazide-type diuretics

32
Q

how do CCBs produce their antihypertensive effect?

A

reduction of BP viablock of Ca++influx into heart cells and/or blood vessels

33
Q

CCBs are first line when:

A

elderly hypertensive patients (aged 55 and over)black (African/Caribbean) patients of any age

34
Q

what are CCBs effective in combination with?

A

CEIs, ARBs, BBs & thiazide-type diuretics

35
Q

how do diuretics produce their antihypertensive effect?

A

reduction of BP via:

  • increased diuresis-reduced plasma volume and decrease in CO
  • reduced peripheral vascular resistance(vasodilation/ NA stores)
36
Q

how much can diuretics lower BP by?

A

10-15mmHg

37
Q

what are the main dose of diuretics given?

A

low dose thiazide & thiazide-like agents used

38
Q

diuretics recommended for an ALTERNATIVE first choice when

A

elderly hypertensive patients (aged 55 and over)

black (African/Caribbean) patients of any age

39
Q

diuretics effective when given with:

A

AEIs, ARBs & CCBs

40
Q

what is the mechanism for antihypertensive effect for B-adrenoceptor antagonists?

A 
unsure... postulate mechanisms:
reduction of CO
inhibition of renin release
modulation of central BP regulation
resetting of baroreceptors
readjustments of blood flow
41
Q

what are the initial effects of b-adrenoceptor antagonists?

A

decrease in BP due to decrease in CO

PRV may increase slightly

42
Q

what are the chronic effects of antihypertensive action?

A

CO may or may not return to normal sustained reduction in PVR  decrease BP

43
Q

how much can b-adrenoceptors reduce BP by?

A

15-20%

44
Q

when are b-adrenoceptors an effective therapy?

A

combination with DH-type CCBs

PHA 222 (41 decks)

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