hypertension 1&2 Flashcards

(44 cards)

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
what are the 5 steps of modification of lifestyle?
``` 1- weight reduction 2- dash eating plan 3- dietary na+ reduction 4-physical activity 5-alcohol moderation ```
26
what are the main mechanisms for lowering BP?
decrease plasma volume decrease total peripheral resistance (TPR) decrease cardiac output (CO) or combinations of three mechanisms
27
what is ACEIs mechanism of antihypertensive effect?
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
what is ACEIs first choice initial therapy for?
younger hypertensive patients (55 years old) of non-African or Caribbean descent All diabetic patients, irrespective of age or ethnic origin
29
what is the mechanism for ARBs?
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
initial use of ARBs when:
younger hypertensive patients (55 years old) of non-African or Caribbean descent All diabetic patients, irrespective of age or ethnic origin
31
what is ARBs effective in combination with?
effective combination with CCBs & thiazide-type diuretics
32
how do CCBs produce their antihypertensive effect?
reduction of BP viablock of Ca++influx into heart cells and/or blood vessels
33
CCBs are first line when:
elderly hypertensive patients (aged 55 and over)black (African/Caribbean) patients of any age
34
what are CCBs effective in combination with?
CEIs, ARBs, BBs & thiazide-type diuretics
35
how do diuretics produce their antihypertensive effect?
reduction of BP via: - increased diuresis-reduced plasma volume and decrease in CO - reduced peripheral vascular resistance(vasodilation/ NA stores)
36
how much can diuretics lower BP by?
10-15mmHg
37
what are the main dose of diuretics given?
low dose thiazide & thiazide-like agents used
38
diuretics recommended for an ALTERNATIVE first choice when
elderly hypertensive patients (aged 55 and over) | black (African/Caribbean) patients of any age
39
diuretics effective when given with:
AEIs, ARBs & CCBs
40
what is the mechanism for antihypertensive effect for B-adrenoceptor antagonists?
``` unsure... postulate mechanisms: reduction of CO inhibition of renin release modulation of central BP regulation resetting of baroreceptors readjustments of blood flow ```
41
what are the initial effects of b-adrenoceptor antagonists?
decrease in BP due to decrease in CO | PRV may increase slightly
42
what are the chronic effects of antihypertensive action?
CO may or may not return to normal sustained reduction in PVR  decrease BP
43
how much can b-adrenoceptors reduce BP by?
15-20%
44
when are b-adrenoceptors an effective therapy?
combination with DH-type CCBs