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CVS > CVS 5 Control Of Blood Presure+ Hypertension > Flashcards

CVS 5 Control Of Blood Presure+ Hypertension Flashcards

1
Q

Normal range of blood pressure

A

Systolic - 90-120
Diastolic - 60-80

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2
Q

BP in stage 1 hypertension

A

> 140/90 mmHg

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3
Q

BP in stage 2 hypertension

A

160/100 mmHg

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4
Q

BP in severe hypertension

A

> 180 systolic or > 110 diastolic

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5
Q

Difference in the changes of the stages of hypertension

A

+ 20 systolic: - normal 90-120
- stage 1 140
- stage 2 160
- severe 180

+ 10 diastolic: - normal 60-80
- stage 1 90
- stage 2 100
- severe 110

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6
Q

Causes of primary hypertension

A

Idiopathic - Unknown

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7
Q

Causes of secondary hypertension

A

ROPED
- Renal disease e.g. renal artery stenosis
- Obesity
- Pregnancy induced or Pre-eclampsia
- Endocrine e.g. Cushing’s syndrome, hyperaldosteronism
- Drugs e.g. alcohol, steroids, NSAIDS, oestrogen

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8
Q

What organs should be assessed by clinical history + physical exam in relation to hypertension?

A

Brain
Eyes
Heart
Kidneys
Arteries

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9
Q

What controls short term regulation of blood pressure?

A

Baroreceptors reflexes

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10
Q

Why can baroreceptors only work in short term regulation of BP?

A

Threshold for baroreceptor firing resets
So not long term

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11
Q

Where are baroreceptors located?

A

Carotid sinus
Aortic arch

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12
Q

What are the neurohumoral pathways that control blood pressure?

A

1- renin-angiotensin-aldosterone-system
2- sympathetic nervous system
3- anti diuretic hormone
4- atrial natriuretic peptide

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13
Q

Where is renin released from?

A

Granular cells of juxaglomerular apparatus (JGA) in kidney

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14
Q

What is renin release stimulated by?

A
  • decreased NaCl delivery to distal convoluted tubule
  • decreased kidney perfusion
  • sympathetic stimulation of JGA
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15
Q

What is kidney perfusion detected by?

A

Baroreceptors in afferent arteriole to kidney

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16
Q

What can a decrease in kidney perfusion be due to?

A

Renal artery stenosis
Decrease circulating volume

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17
Q

What is the pathway in RAAS?

A

Angiotensinogen > angiotensin I > angiotensin II
renin. ACE

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18
Q

What is angiotensinogen produced by?

A

Liver

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19
Q

What type of receptor is angiotensin receptor 1/2?

A

G protein coupled receptor

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20
Q

Action of angiotensin II

A
  • increases BP
  • vasoconstriction of arterioles
  • increased Na+ reabsorption at kidney
  • stimulates sympathetic NS to release more NA
  • acts on hypothalamus to increase thirst + increase ADH release
  • aldosterone release from adrenal cortex
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21
Q

Where is aldosterone released from?

A

Adrenal cortex
Zona glomerulosa

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22
Q

Action of aldosterone on kidney

A
  • increased expression of Na/K ATPase > increased Na reabsorption > H2O follows - H2O reabsorption
  • activates apical Na+ and K+ channels
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23
Q

ACE action on bradykinin

A

Breaks down bradykinin into peptide fragments

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24
Q

Function of bradykinin

A

Vasodilator

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25
Q

Why do ACE inhibitors cause dry coughs?

A

Prevent breakdown of bradykinin
Build up bradykinin cause cough

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26
Q

What is the sympathetic nervous system stimulated by for regulating BP?

A

RAAS directly (AngII)
A decrease in BP

27
Q

What do high levels of sympathetic stimulation cause?

A
  • Decreased renal blood flow by vasoconstriction of afferent arterioles
  • stimulates renin release from JGA - ^ AngII levels > ^ aldosterone
  • activates apical NHE + basolateral Na/K ATPase

All cause increased Na + fluid reabsorption > ^ BP

28
Q

Where is ADH released from?

A

Posterior pituitary

29
Q

What stimulates ADH release?

A

Severe hypovalaemia
Increase in plasma osmolarity

30
Q

What does ADH do?

A
  • increase water reabsorption
  • increase Na+ reabsorption
  • vasoconstiction

Increased BP

31
Q

How does ADH cause increase water reabsorption?

A
  • insertion of aquaporins into collecting duct of kidney nephron
  • forms concentrated urine
32
Q

What do atrial natriuretic peptides do?

A

Promotes Na+ excretion > water follows > decreased BP

33
Q

How does ANP promote Na+ excretion?

A

Inhibits Na+ reabsorption
Stimulates vasodilation of afferent arterioles

34
Q

Where are atrial natriuretic peptides synthesised + stored?

A

Atrial myocytes

35
Q

Where are atrial natriuretic peptides released from?
In response to what?

A

Atrial cells
In response to stretch (increased BP)

36
Q

What inhibits atrial natriuretic peptides?

A

Decreased filling of heart due to low BP > less stretching > ANP release inhibited > increased BP

37
Q

What is dopamine made from?

A

L-DOPA

38
Q

Effects of dopamine

A

Vasodilatation
Increased renal blood flow
Decreased reabsorption of NaCl

39
Q

What do prostaglandin act as?

A

Vasodilators
Buffers to excessive vasoconstriction by SNS + RAAS

40
Q

Treatment of hypertension

A
  • Exercise
  • Diet - decrease salt intake
  • Decreased alcohol intake
  • Drugs targeting RAAS - ACE inhibitors + AngII receptor antagonist
  • Vasodilators - L-type Ca2+ channel blockers + a1 receptor blockers
  • Diuretics
41
Q

Examples of ACE inhibitors

A

Suffix -pril

Captopril
Lisionpril
Perindopril
Enalapril

42
Q

Examples of AngII receptor antagonists

A

Suffix -artan

Losartan
Valsartan
Temisartan

43
Q

Examples of a1 receptor blockers

A

Doxazosin

44
Q

Examples of L-type Ca2+ channel blockers

A

Verapamil
Nifedipine

45
Q

Adrenal causes of secondary hypertension

A
  • conn’s syndrome
  • cushing’s syndrome
  • phaeochromocytoma
46
Q

What is Conn’s syndrome

A

Aldosterone secreting adenoma

47
Q

What is Cushing’s syndrome?
How does it cause secondary hypertension?

A
  • Excess secretion of cortisol from Zona fasiculata
  • at high levels, acts on aldosterone receptors > Na+ and H2O retention
48
Q

What is a phaeochromocytoma?

A

Tumour of adrenal medulla
Secretes catecholamines (NA + adrenaline)

49
Q

Triad of symptoms for phaeochromocytoma

A
  • episodic headache
  • sweating
  • tachycardia
    (Patients often do not have all three)
50
Q

what is the most common symptoms of phaeochromocytoma?

A

Sustained or paroxysmal hypertension

51
Q

Treatment of phaeochromocytoma

A
  • resection
  • before surgery a + B blockers are needed phenoxybenzamine 10mg od/bd
52
Q

Diagnosis of phaeochromocytoma

A
  • 24 hour urine collection
  • Abdominal CT or MRI to detect tumours
    .
  • confirmed by measuring urinary + plasma fractionated metanephrines + catecholamines
53
Q

What drug is most commonly used during treatment of phaeochromocytoma?

A

Phenoxybenzamine
(alpha blocker)

54
Q

Hypertension management for:
- type 2 diabetics (regardless of age)
- under 55

A
  • step 1: ACEi or ARB
  • **step 2 **: add CCB or thiazide like diuretic
  • step 3: add the other one (ACEi/ARB + CCB + thiazide like diuretic)
  • step 4 if K+ <4.5mmol/L: spironolactone
  • step 4 if K+ >4.5mmol/L: alpha blocker or beta blocker
55
Q

Hypertension management for:
- over 55 years old
- black African or African-Caribbean family origin (regardless of age)

A
  • step 1: CCB
  • step 2: add ACEi/ARB or thiazide like diuretic
  • step 3: add the other one (CCB + ACEi/ARB + thiazide like diuretic
  • step 4 if K+ is <4.5mmol/L: spironolactone
  • step 4 if K+ is >4.5mmol/L: alpha blocker or beta blocker
56
Q

What is the target blood pressure for those <80 on treatment?

A

<140 systolic
<90 diastolic

57
Q

What is the target blood pressure for those >80 on treatment?

A

<150 systolic
<90 diastolic

58
Q

What is accelerated/malignant hypertension?

A

BP >180/120 with retinal haemorrhages or papilloedema

59
Q

IV options in hypertensive emergency

A
  • sodium nitroprusside - vasodilator
  • labetalol - B blocker
  • glyceryl trinitrate - vasodilator
  • nicardipine - CCB
  • esmolol - B blocker
60
Q

What are the two ways patients can present in hypertensive crisis?

A
  • emergency: high BP associated with a critical event e.g. encephalopathy, pulmonary oedema, MI, AKI
  • urgency: high BP without critical illness but may include malignant hypertension
61
Q

What is the aim of therapy for hypertensive crisis:
- emergency
- urgency

A

To reduce diastolic BP to 110mmHg:
- in 3-12 hours for emergency
- in 24 hours for urgency

62
Q

What is the safest treatment for most patientsof hypertensive urgency?

A
  • nifedipine 20mg MR BD + amlodipine10mg OD for three days
  • continue amlodipine 10mg OD after
63
Q

What is a hypertensive emergency?

A

High BP with assocaited critical event
e.g. MI, AKI, pulmonary oedema, encephalopathy

64
Q

What is hypertensive urgency?

A

High BP without critical event
But may include malignant hypertension

CVS (21 decks)

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