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Cardio and Resp diseases > Essential hypertension > Flashcards

Essential hypertension Flashcards

1
Q

What is hypertension?

A

sustained elevation of systolic and diastolic blood pressure (> 140/90 mmHg)

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2
Q

What are the causes of hypertension?

A

Causes:
• primary (idiopathic/essential)
o No identifiable cause

• secondary:
o renal disease (salt/H2O imbalance)
o adrenal tumours (aldosterone)
o aortic coarctation (narrowing of aorta)
o Steroids, Rx
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3
Q

What are some hypertension related diseases?

A

Cerebrovascular
• Infarction: thrombotic – will cause ischaemic damage within the cerebral vessels

Cardiac
• Angina/MI
• CHF (congestive heart failure)
• Sudden death

Renal
• Chronic renal failure
• End stage renal disease

Retinopathy
• Sclerosis/Arterial
• Haemorrhage/Exudate

Large artery disease
• Carotid artery stenosis

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4
Q

How does hypertension cause organ damage in the blood vessels?

A

Blood vessels themselves undergo atheroma and aneurysm formation in large vessels, elastic reduplication in small vessels due to increased blood pressure

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5
Q

How does hypertension cause organ damage in the heart?

A

left ventricular hypertrophy, left heart failure (LHF).

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6
Q

How does hypertension cause organ damage in the lungs?

A

pulmonary oedema due to LHF

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7
Q

How does hypertension cause organ damage in the kidney?

A

nephrosclerosis, renal failure

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8
Q

How does hypertension cause organ damage in the eye?

A

retinal capillary damage, haemorrhages, exudates.

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9
Q

How does hypertension cause organ damage in the brain?

A

microaneurysms and stroke, ischaemic cortical atrophy/ dementia

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10
Q

What is hypertensive heart disease?

A

Increased load causes concentric left ventricular hypertrophy (increase in cell and muscle size in the heart) – causes weakening of the heart and reduced contractility, can lead to heart failure

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11
Q

How can a hypertensive patient experience massive intracerebral haemorrhage?

A

Massive intracerebral haemorrhage due to ruptured microaneurysm in the hypertensive patient

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12
Q

What affects blood pressure?

A

Cardiac output and the peripheral resistance

- CO x TPR = BP

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13
Q

What can high blood pressure arise from?

A
  • Increased ECFV (extracellular fluid volume) – venous return to the heart can affect it
  • Increased production of vasoconstrictor agents
  • Reduction in production of vasodilator agents
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14
Q

What are some of the factors to be considered when diagnosing hypertension?

A
  • BP cut off value (Usual value >140 and/or > 90 mmHg)
  • Age (increases with age)
  • Ethnic group (e.g. more common in African Americans
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15
Q

What are the causes of hypertension?

A

Causes of essential hypertension is still not known but genetic and environmental factors are believed to be important

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16
Q

What are important genetic/environmental factors for essential (primary) hypertension?

A

• Increased activity of hormonal system such as :
o Sympathetic nervous system (SNS)
o Renin-angiotensin-aldosterone system (RAA)

  • Obesity/ Insulin resistance – can lead to inflammatory changes
  • Endothelial dysfunction – big impact on atherosclerosis development
  • Capillary rarefaction – decrease in density of vessels, can have impact on vascular resistance
  • Defect in vascular smooth muscle contraction/relaxation
  • Defects in renal sodium handling
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17
Q

Why is treatment of hypertension important?

A

Reduction in blood pressure level reduces relative risk of consequences

A 5-mmHg reduction in diastolic BP for 5 years will:
• Reduce strokes by 42%
• Reduce MI by 16%
• Reduce vascular mortality by 21%

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18
Q

What are the goals of antihypertensive therapy?

A
  • Adequate Blood Pressure Control (< 140/90 mmHg)
  • Prevention of Target Organ Damage
  • Controlling other cardiovascular risk factors
  • No detrimental metabolic side-effects
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19
Q

Why is the classification of hypertension important?

A

It can impact on the care pathway

20
Q

What are the treatments and management for hypertension?

A
  • Nonpharmacological (Life-style modification)
  • Pharmacological treatment
  • Surgical e.g. for Conn’s syndrome (adrenal gland increases in aldosterone)
21
Q

What are the targets for life-style management for hypertension?

A
  1. Maintain normal weight (BMI 20-25%): can reduce by 1-2 mmHg/Kg
  2. ↓ Salt intake (≤ 100 mmol/day = 6 g NaCl): can reduce by 2-8 mmHg
  3. ↓ Alcohol intake (≤ 3 u/day men, ≤ 2 u/day women): can reduce by 2-4 mmHg
  4. Increase Fruits & vegetables intake (≥ 5 portions/day): can reduce by 8-14 mmHg
  5. Increase Regular exercise (≥ 30 min/day x 3 days/wk): can reduce by 4-9 mmHg
22
Q

What are the pharmacological treatments/major classes of antihypertensive drugs?

A
  • Renin inhibitors
  • ACE inhibitors
  • Angiotensin II receptor blockers
  • Calcium channel antagonists
  • Diuretics (loop diuretics, thiazides, potassium sparing)
  • Adrenergic (a1 /b1) receptor antagonists
  • Centrally acting a2 receptor agonists (rarely used for essential e.g. pregnancy)
  • Other vasodilators
23
Q

Some key issues to consider in selecting drug therapy?

A
  • Essential vs secondary hypertension
  • Evidence of efficacy
  • Side effects of drug
  • Drug interactions
  • Individual demographics
  • Coexisting diseases
  • Quality of life
  • Economic considerations
24
Q

What drugs are prescribed to under 55s?

A
  • Under 55 – ace inhibtors/angiotensin receptor blocker
  • Ca channel blocker added if ACE inhibitor wasn’t effective
  • Drugs are usually added to the already existing prescription until one works
25
Q

What drugs are prescribed to over 55s/Caribbean/African patients?

A
  • Ca channel blocker prescribed first because limited activity of drugs against the RAAS pathway
  • Combined with diuretic if it doesn’t work
26
Q

Examples of inhibitors of the renin-angiotensin system?

A
  • Renin inhibitors (rarely used) e.g. Aliskiren (risk of stroke)
  • ACE inhibitors (e.g. enalapril, ramipril)
27
Q

When should RAAS inhibitors not be used?

A

During pregnancy

28
Q

Why are RAAS inhibitors used for primary hypertension?

A

RAAS causes vasoconstriction and aldosterone secretion - causes increase in BP

RAAS inhibitors intervene and prevent vasoconstriction and aldosterone secretion

29
Q

How do calcium channel blockers treat hypertension?

A
  • Increase vasodilation

* By decreasing Ca influx – inhibition of the myosin light chain kinase

30
Q

What are the different types of Calcium channels blockers?

A

• Divided into 2 classes: Non-dihydropyridines and dihydropyridines

31
Q

Which calcium channel blockers are usually use for arrhythmias?

A

Non-dihydropyridines are usually used for arrhythmias

32
Q

What is the main effect of diuretics?

A

Increase in sodium and water excretion (but also direct effects on VSM tone)

33
Q

What are the different classes of diurectics?

A
  • Loop diuretics
  • Thiazides
  • Potassium sparing –
34
Q

How do loop diuretics act?

A

act on Na/Cl transporter in the thick ascending limb, inhibit sodium reabsorption into the epithelial cell and it’s lost through urine

35
Q

How do thiazides act?

A

most commonly used, act on Na/CL transporter to prevent Na reabsorption

36
Q

How do potassium-sparing diuretics act?

A

antagonises the aldosterone receptor to inhibit Na reabsorption in the collecting ducts, less Na/K transporter activity

37
Q

What are the side effects of diuretics?

A
  • Hypokalaemia (loop and thiazide diuretics, but not K+ sparing diuretics)
  • Lipid abnormalities
  • Glucose intolerance/Hyperglycemia
38
Q

What are the pharmacological targets for drugs acting on the sympathetic system and adrenergic receptors?

A
  1. Centrally acting agents
  2. Ganglion blockers
  3. Post ganglionic sympathetic neuron blocker
  4. Adrenoceptor blocker
39
Q

How do centrally acting agents work?

A

they’re a2 selective agonists

examples: methyldopa
- stimulates adrenoceptors in the brain stem and induces peripheral sympathoinhibition (vasodilation), reduces elevated BP and HR

40
Q

How do ganglion blockers work?

A

They’re nAChR (nicotinic acetylcholine receptor) antagonists

examples: Trimethaphan

41
Q

How do postganglionic sypmathetic neuron blockers work?

A

They block neurotransmission

Example: Reserpine

42
Q

How do adrenoceptor blockers work?

A

alpha and beta receptor antagonists

  • blocking the alpha receptors: relaxes the vascular smooth muscles (example: prazosin)
  • blocking the beta receptors: reduces cardiac output and inhibits renin release (examples: atenolol)
43
Q

What are the (10) side effects for beta blockers?

A
  • Acute bronchospasm – dangerous for asthma patients
  • Bradycardia
  • Raynaud’s syndrome (patients have reduced blood flow to periphery – fingers/toes) – patients who already have this need to be careful when taking the drugs
  • Claudication (cramp in leg resulting from reduced blood flow)
  • Increased triglycerides
  • Decreased HDL
  • Glucose intolerance
  • Lethargy
  • Nightmares
  • Impotence
44
Q

What are some other vasodilators used for hypertension?

A
  • Nitrovasodilators

- K+ channel openers/agonists

45
Q

Examples of nitrovasodilators and what is their mechanism?

A

Drugs: Nitroprusside
(Less frequently used, replaced by newer agents)

Mechanism of action:
• NO “donors”/NO enhancing effect
• Increase activation of soluble guanylate cyclase activity
• Increase in [cyclic GMP]
• Reduction in voltage-dependent Ca2+ channel activity
• Reduction in [Ca2+]
• Increased relaxation
• Inhibit myosin light chain kinase activity – reduce contractions

46
Q

Examples of K+ channel openers/agonists and what is their mechanism?

A

• Drugs: Minoxidil (severe hypertension)

Mechanism of action:
• Cause vascular smooth muscle hyperpolarization
• Reduction in voltage-dependent Ca2+ channel activity
• Reduction in [Ca2+]i
• Increased relaxation

Cardio and Resp diseases (29 decks)

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