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Therapeutics > Hypertension > Flashcards

Hypertension Flashcards

1
Q

How is hypertension defined?

A

Hypertension is defined as persistently elevated blood pressure measured on 3 separate occasions, a minimum of 2 days apart, with systolic BP ≥ 140 mmHg and/or diastolic BP ≥ 90 mmHg.

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2
Q

What should be done when blood pressure is severely elevated?

A

When blood pressure is severely elevated, at least 3 readings should be taken during the same visit.

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3
Q

Why is it important to ensure the correct cuff size?

A

Using the correct cuff size is crucial for accurate blood pressure measurements.

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4
Q

What role does the sympathetic nervous system play in hypertension?

A

Increased sympathetic nervous system activity can lead to vasoconstriction, which contributes to elevated blood pressure. This includes:

  • Increased large arterial stiffness
  • Increased systemic resistance
  • Inappropriately high cardiac output
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5
Q

How does abnormal venoconstriction affect blood pressure?

A

Abnormal constriction of veins increases venous return to the heart, which raises cardiac output and blood pressure

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6
Q

What is the effect of inappropriate renin release on blood pressure?

A

Overactivation of the Renin-Angiotensin-Aldosterone System (RAAS) increases blood volume and systemic vascular resistance. Elevated renin release leads to:

  • Increased angiotensin II, causing vasoconstriction
  • Aldosterone release, which promotes sodium and water retention
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7
Q

How does impaired renal salt and water handling contribute to hypertension?

A

Impaired renal function can cause inappropriate salt and water retention, leading to increased blood volume and elevated blood pressure.

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8
Q

What is the formula for calculating blood pressure (BP)?

A

BP = CO × PVR, where:

CO (Cardiac Output) = SV × HR

BP = SV × HR × PVR

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9
Q

What factors influence blood pressure?

A
  1. Volume Overload/Salt Overload: Increased blood volume can elevate blood pressure.
  2. Systemic Vascular Resistance (PVR): Increased resistance in the systemic circulation raises blood pressure.
  3. Central Drive to Increase BP: Increased central drive to elevate blood pressure impacts cardiac output and vascular resistance.
  4. Sympathetic Nerve Stimulation: Increased sympathetic activity leads to vasoconstriction, raising blood pressure.
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10
Q

How do volume overload and systemic vascular resistance affect blood pressure?

A

Both factors contribute to elevated blood pressure by increasing the total blood volume or the resistance against which the heart pumps.

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11
Q

How does sympathetic nerve stimulation affect BP?

A

Sympathetic nerve stimulation increases heart rate (HR) and systemic vascular resistance (PVR), which collectively raise blood pressure.

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12
Q

Optimal blood pressure

A

systolic: <120
diastolic: <80

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13
Q

Normal blood pressure

A

systolic: <130
diastolic: <85

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14
Q

Prehypertension

A

systolic: 130 to 139
diastolic: 85 to 89

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15
Q

Grade 1 hypertension (mild)

A

systolic: 140 to 159
diastolic: 90 to 99

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16
Q

Grade 2 hypertension (moderate)

A

systolic: 160 to 179
diastolic: 100 to 109

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17
Q

Grade 3 hypertension (severe)

A

systolic: >180
diastolic: >110

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18
Q

Isolated systolic hypertension (Grade 1)

A

systolic: 140 to 159
diastolic: <90

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19
Q

Isolated systolic hypertension (Grade 2)

A

systolic: >160
diastolic: <90

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20
Q

Lifestyle changes

A
  • Weight reduction
  • Restrict salt, dietary sugars, and saturated fat
  • Limit alcohol consumption
  • Increase fruit and vegetable
  • Increase physical activity
  • Stop all tobacco products
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21
Q

If BP 140- 159/ 90 -99 mmHg with <3 risk factors, no TOD or complications

A

Lifestyle modifications for 3-6 months

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22
Q

If BP 140- 159/ 90 -99 mmHg with >=3 risk factors, diabetes, TOD or complications

A

Commence monotherapy, review in 4-6 weeks

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23
Q

BP>= 160/100 mmHg

A

Commence 2 drugs preferably in fixed drug combination, review in 4-6 weeks

Not a goal

Add third drug/ optimise doses of drugs

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24
Q

Summary algorithm of clinical management

A
  1. Lifestyle modification
  2. Add hydrochlorothiazide
  3. Add CCB or ACEI
  4. Increase dose of CCB or ACEI
  5. Add 3rd medication: CCB/ ACEI
  6. Increase dose of 3rd medication
  7. Increase dose of hydrochlorothiazide and add 4th antihypertensive
  8. Refer
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25
Q

Initial choice of therapeutic agent

A
  1. ACEI or ARB
  2. Thiazide or thiazide- like
  3. CCB
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26
Q

What percentage of hypertension cases are classified as primary (essential)?

A

80-90% of hypertension cases are classified as primary (essential).

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27
Q

Causes of primary hypertension

A
  • family history
  • obesity
  • environmental factors
  • fetal factors
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28
Q

What are some genetic or shared environmental influences that can lead to primary hypertension?

A

Family history of hypertension can be a genetic or shared environmental influence.

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29
Q

Environmental factors that can cause primary hypertension

A
  • alcohol intake
  • sodium intake
  • poor diet
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30
Q

How does a poor diet influence the risk of primary hypertension?

A

A poor diet, often leading to obesity or increased salt intake, can increase the risk of developing primary hypertension.

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31
Q

What fetal factor is linked to primary hypertension later in life?

A

Low birth weight is a fetal factor associated with a higher risk of developing primary hypertension.

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32
Q

What defines secondary hypertension?

A

Secondary hypertension is elevated blood pressure due to a specific and potentially treatable cause.

33
Q

Causes of secondary hypertension

A
  1. renal diseases
  2. endocrine
  3. vascular
34
Q

What percentage of secondary hypertension cases are related to renal diseases?

A

Over 80% of secondary hypertension cases are related to renal diseases.

35
Q

What renal diseases can cause secondary hypertension?

A
  • Diabetic nephropathy
  • Chronic GN
  • Polycystic kidney disease
  • Chronic tubulointerstitial nephritis
  • Renovascular disease, including renal artery stenosis
36
Q

Endocrine causes of secondary hypertension

A
  • Phaeochromocytoma
  • Cushing’s syndrome
  • Thyroid disease
  • Conn’s syndrome
  • Acromegaly
37
Q

How does phaeochromocytoma contribute to secondary hypertension?

A

Phaeochromocytoma is a catecholamine-secreting tumor that can cause secondary hypertension through the excessive release of catecholamines.

38
Q

How does Cushing’s syndrome lead to secondary hypertension?

A

Cushing’s syndrome causes secondary hypertension through excess cortisol production, which can increase blood pressure

39
Q

What is Conn’s syndrome and how does it affect blood pressure?

A

Conn’s syndrome, or primary hyperaldosteronism, is characterized by excessive aldosterone production, leading to increased sodium and fluid retention, which raises blood pressure.

40
Q

How does acromegaly contribute to secondary hypertension?

A

Acromegaly, caused by excess growth hormone, can lead to secondary hypertension through various mechanisms including increased fluid retention and vascular resistance.

41
Q

Vascular causes of secondary hypertension

A
  • Aortic coarctation
42
Q

Secondary hypertension: Medication induced

A
  1. Oestrogen
  2. Herbal (complimentary medicines/ OTCs)
  3. Stimulants (sympathomimetic)
  4. NSAIDs
  5. Psychiatrics
  6. Immunosuppressants
43
Q

Estrogen

A

Oral contraceptives

44
Q

Stimulants (sympathomimetic):
Prescription

A

Methylphenidate,
ephedrine in nasal decongestants,
diet pills

45
Q

Stimulants (sympathomimetic):
Illicit

A

Methamphetamines (‘tik’),
Cocaine,
Ecstasy

46
Q

Nonsteroidal anti-inflammatory

A

Ibuprofen,
non-selective cyclo-oxygenase inhibitors (Naproxen),
cyclo-oxygenase-2 inhibitors (Celecoxib).

47
Q

Psychiatric

A

Carbamazepine,
clozapine,
fluoxetine,
lithium,
tricyclic antidepressants

48
Q

Immunosuppressants

A

Steroids - Methylprednisolone (Depo-Medrol), prednisone

Tacrolimus

49
Q

Effect of liquorice

A
  • Glycyrrhizin - can induce pseudohyperaldesteronism
    – High BP
    – Fluid retention
    – Arrhythmias
50
Q

General Approach to management of HTN

A

Non-Pharmacological
Pharmacological
Holistic approach – Biopsychosocial assessment

51
Q

Therapeutic objectives:
of managing HTN

A
  • Reduce morbidity and mortality
  • Obtain target BP goals of <140/90 mmHg or <130/80 mmHg with diabetes or renal disease.
  • Prevent disease progression
  • Improve quality of life
52
Q

Non- pharmacological management of HTN

A
  • Exercise (>30 min/d at least 3/week)
  • Diet (low salt [<6g/d], low fat, vegetable & fruit)
  • Weight loss: Ideal bodyweight (BMI < 25)
  • Alcohol consumption reduction
  • Smoking cessation
  • Avoid use of stimulant drugs
53
Q

After how long do you change from non- pharmacological to pharmacological therapy

A

If no BP reduction after 3 months, consider pharmacological therapy

54
Q

Name the drugs used in hypertension

A
  • Diuretics (Low Ceiling and High Ceiling)
  • Angiotensin converting enzyme inhibitors (ACE-i) and Angiotensin receptor blockers (ARBs)
  • Calcium channel blockers
  • Mineralocorticoid antagonists
  • Sympatholytic agents
    – Beta blockers
    – ⍺2 -receptor agonist
  • Other:
    – Alpha-receptor blockers
    – Vasodilators
55
Q

Formula for excretion

A

Filtra ration- Reabsoprtion + Secretion

56
Q

Drugs that work at the glomerulus

A

NSAIDs: PGI2 and PGE2 vasodilators

Ang II Vasoconstrictor: ACEIs

57
Q

Drugs that work at the proximal convoluted tubule

A
  1. Carbonic anhydrase inhibitors
  2. Osmotic diuretics
58
Q

Carbonic anhydrase inhibitors

A

Stops the reabsorption of NaHCO3 and glucose at the proximal convoluted tubule

59
Q

Osmotic diuretics

A

Stops the reabsoprtion of H2O at the proximal convoluted tubule

60
Q

Drugs that work at the loop of henle

A

loop diuretics

61
Q

Loop diuretics

A

Stops the reabsoprtion of Na/ K/ 2Cl at the loop of henle

62
Q

Drugs that work at the distal convoluted tubule

A

Thiazide

63
Q

Thiazides

A

Stops the reabsoprtion of NaCl

64
Q

Drugs that work at the collecting duct

A

Aldosterone antagonists
ADH antagonists

65
Q

Aldosterone antagonists

A

Stops the reabsoprtion of Na by inhibiting the ENaC channel at the collecting duct

66
Q

ADH antagonist

A

Stops the reabsoprtion of H2O at the collecting duct

67
Q

What is the concept of high ceiling diuretics?

A

High ceiling diuretics are those where the effect of diuresis increases with increasing dose, causing substantial diuresis. An example is loop diuretics like Furosemide

68
Q

What is the main characteristic of high ceiling diuretics regarding their diuretic effect?

A

The diuretic effect of high ceiling diuretics increases with higher doses.

69
Q

Can you name an example of a high ceiling diuretic?

A

Furosemide is an example of a high ceiling diuretic.

70
Q

What is the concept of low ceiling diuretics?

A

Low ceiling diuretics are those where the effect of diuresis flattens with increasing dose, leading to an increased risk of adverse effects without significant additional diuretic benefit. An example is thiazide diuretics like Hydrochlorothiazide.

71
Q

What happens to the effect of diuresis with increasing doses of low ceiling diuretics?

A

The effect of diuresis flattens, meaning it does not significantly increase with higher doses.

72
Q

What is a potential risk when increasing the dose of low ceiling diuretics?

A

There is an increased risk of adverse effects without substantial additional diuretic benefit.

73
Q

Can you name an example of a low ceiling diuretic?

A

Hydrochlorothiazide is an example of a low ceiling diuretic.

74
Q

What transporter do thiazide diuretics block in the kidney?

A

Thiazide diuretics block the NaCl cotransporter in the distal convoluted tubule.

75
Q

How do thiazide diuretics affect sodium reabsorption?

A

Thiazide diuretics prevent Na+ reabsorption, thereby increasing Na+ excretion.

76
Q

What is the initial effect of thiazide diuretics on stroke volume (SV) and cardiac output?

A

Thiazide diuretics initially cause a decrease in stroke volume (SV) and cardiac output.

77
Q

How is the long-term effect of thiazide diuretics maintained?

A

The long-term effect of thiazide diuretics is maintained through reduced vascular resistance by the opening of Ca2+ activated K+ channels.

78
Q

What is the prototypical thiazide diuretic?

A

Hydrochlorothiazide (HCTZ) is the prototypical thiazide diuretic.

Therapeutics (15 decks)

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