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CVS pathophysiology > Hypertension > Flashcards

Hypertension Flashcards

1
Q

Complications of hypertension

A

Slide2

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2
Q

What is hypertension?

A

The blood pressure above which the benefits of treatment outweighs the risks in term of morbitiy and mortality

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3
Q

NICE 2011 definitions of hypertension ( Stage 1, 2 + severe hypertension)

A

Stage 1 hypertension

  • Clinic BP 140/90mmHg/higher
  • ABPM daytime average 135/85mmHg or higher

Stage 2 Hypertension

  • Clinic BP 160/100mmHg/higher
  • ABPM daytime average 150/95mmHg/higher

Severe hypertension
-Clinic systolic BP 180mmHg/higher OR diastolic BP 110mmHg/higher

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4
Q

Causes of secondary hypertension

A
  • chronic renal disease
  • renal artery stenosis
  • endocrine disease, cushing’s, conn’s syndrome, Phaeochromocytoma, GRA
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5
Q

Causes of primary hypertension

A

-unknown

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6
Q

Factors that increases risk of hypertension

A
  • smoking cigarrrete (adds 20/10mmHg)
  • diabetes mellitus
  • renal disease
  • Male (2x risk)
  • hyperlipidaemia
  • previous MI / stroke
  • left ventricular hypertrophy(2x risk)
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7
Q

Sympathetic system activation

A

Causes:

  • vasocostriction
  • reflex tachycardia
  • increased CO

These actions account for second to second blood pressure control

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8
Q

Function of Renin-angiotensin-aldesterone system

A
  • maintanience of sodium balance
  • control of BV
  • control of BP
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9
Q

What activates RAAS?

A
  • fall in BP
  • fall in circulating volume
  • sodium depletion
  • Renin released by juxtaglomerular apparatus + convets Agiotensinogen>angiotensin I
  • Angiotensin l >angiotensin ll ( via angiotensin converting enzyme
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10
Q

What is angiotensin II? State its function

A

A potent:

  • vasoconstrictor
  • anti-natriretic(sodium) peptide
  • hypetrophic agent which stimulates myocyte + SM hypertrophy in arterioles
  • stimulator of aldesterone release from adrenal glands
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11
Q

What is aldesterone? State tis

A

A potent:

-antinatriutetic + antidiuretic peptide

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12
Q

Aetiology of hypertension

A

Polygenic
-major/poly genes

Polyfactorial

  • environment
  • individual and shared
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13
Q

Likely causes of hypertension

A

-increased reactivity of resistance vessels + increase in peripheral resistance as a result of hereditary defect of the smooth muscle lining arterioles

A sodium homeostatic
- kidneys are unable to excrete appopriate amounts of sodium for any given BP. As a result, sodium + fluid are retained and BP increases

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14
Q

Other factors of Hypertension

A
  • age
  • genetics + FH
  • environment
  • weight
  • alcohol intake
  • race
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15
Q

The effect of age on BP

A
  • BP increases with age due to decreased arterial compliance

- Hyper

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16
Q

The effect of genetics on BP

A
  • history of BP
  • correlation between siblings rather than parent-child
  • > 30 genes account for 0.5mmHg each
17
Q

The effect of the environment on BP (stress)

A
  • mental/physical stress
  • removing stress may not return BP back to normal
  • True stress responders who have high BP when they attend doctor but normal BP will be resistant to treatment
18
Q

The effect of sodium intake and diet

A
  • correlation between sodium intake and BP
  • reduction in sodium in hypertensive individuals will lower BP but in normotensives will have little effect
  • reducing intake to <6gm/day
19
Q

The effect of alcohol on BP

A
  • small amounts decreases BO
  • large amouns increases BP
  • reversible
20
Q

The effect of weight on BP

A
  • obesity=higher BP

- reversible

21
Q

The effect of birth weight on BP

A

-lower the birth weight, the higher the chance of hypertension and HD in future

22
Q

The effect of race on BP

A
  • caucasions have lower BP than black populations living in same environment
  • Black populations living in rural africa have a lower BP than those living in towns
23
Q

Secondary hypertension features

A
  • removal of cause may/may not be reversible

- sustained Hypertension causes end organ damage to BV’s, heart and kidney

24
Q

Causes of secondary hypertension

A

Renal disease

  • chronic pyelonephritis
  • fibromuscular dysplasia
  • renal artery stenosis
  • polycystic kidneys

Drug induced

  • NSAIDs
  • oral contraceptive
  • corticosteroids

Pregnancy
-preeclampsia

Endocrine

  • Conn’s syndrome
  • Cushing’s disease
  • phaepchromocytoma
  • hypo/hyperthydroidism
  • acromegaly

Vascular
-coarction of aorta

Sleep apnoea

25
Q

Assesing the risk of BP

A 
Assess end organ damage
ECG			LVH
Echocardiogram	LVH
Proteinuria
Renal ultrasound
Renal function
Screen for treatable causes
Renal artery stenosis/FMD
Cushings disease
Conn’s Syndrome
Sleep apnoea
Previous MI, stroke, IHD
Smoking
Diabetes mellitus
Hypercholesterolaemia
Family history
Physical Examination
26
Q

Treatment of hypertension

A

slide 78

27
Q

Stage 1 hypertension treatment

A
  • Antihypersensitive drug treatment <80yrs with ABPM >135/85 with 1/more:
  • target organ damage
  • CVD
  • renal disease
  • diabetes
  • 10 year CV risk 20% or greater

If <40 yrs seek specialist evalation of secondary causes of hypertension + target organ damage assestment

If ovwe 80 yrs pressure target is <145/85

28
Q

Stage 2 hypertension treatment

A

ABPM>150/95

-antihypersensitive drug treatment of any age

29
Q

Step 1 to choosing antihypersensitive drug treatment

A

STEP 1

  • offer antihypertensive treatment with CCB to people >55yrs and to black people of any age
  • alternative to CCB ( oedema, intolerance, HF) offer thiazide-like diuretic
  • If <55yrs offer ACEI/ARB ( not to blacks, women of child bearing age)

If diuretic treatment is to be initiated/changed, offer thiazide-like diuretic such as chlortalidone or indapamide

30
Q

Step 2 to choosing antihypersensitive drug treatment

A

-add thiazide-type diuretic such as clortalidone/indapamide to CCB/ACEI/ARB

31
Q

Step 3 to choosing antihypertensive drug treatment

A

-add CCB, ACEI, diuretic together

32
Q

Step 4 to choosing antihypertensive treatment

A

if potassium blood <4.5 offer low dose spironolactone. ( caution in people with estimated GFR beacuse risk of hyperkalaemia)
-If high Blood potassium, offer higher dose thiazidide-like diuretic

33
Q

State angiotensin converting enzyme inhibitors

A

Ramipril

  • prevents ACE from converting angiotensin I>Angiotensin II
  • prevents mechanism of angiotensin II ( vasoconstrictor and hypertrophogenic agent)

CVS pathophysiology (23 decks)

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