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DS1102 > Week 3 - Hypertension > Flashcards

Week 3 - Hypertension Flashcards

1
Q

What is hypertension

A

Hypertension is also known as high blood pressure which is a condition where the force of the blood against the artery walls is consistently too high.

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2
Q

What blood pressure classifies as hypertension

A
  • sustained systolic > 140 mmHg

or

  • Sustained Diastolic > 90mmHg
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3
Q

What are the types of hypertension

A

Primary hypertension
Secondary hypertension

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4
Q

What is primary hypertension

A
  • High blood pressure due to no underlying cause or distinct anatomical pathology identified
  • Due to a combination of genetic and environmental factors (heredity, diet, age, diabetes mellitus, stress, smoking, obesity)
  • Approx 90% is primary hypertension
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5
Q

What is secondary hypertension

A

hypertension caused by an underlying condition e.g. kidney disease

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6
Q

How does obesity cause hypertension

A
  • Obesity causes mechanical stress - increased vessel length to sustain excess body mass
  • Physical stress on vasculature, impeding venous return
  • Impaired kidney function
  • Atherosclerosis due to poor diet
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7
Q

How does sympathetic activity influence blood pressure

A
  • vascular tone
  • local mediators and vasodilation - vascular dilation
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8
Q

What is Angiotensin II:

A

Angiotensin II is a peptide hormone that plays a critical role in the regulation of blood pressure and fluid balance.

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9
Q

What are the effects of angiotensin 2

A
  • Vasoconstriction: causes blood vessels to constrict which increases peripheral resistance
  • Aldosterone secretion: which leads to increased sodium reabsorption and an expansion of blood volume - increasing blood volume and hence blood pressure
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10
Q

What are non drug management strategies for hypertension

A
  • Physical Activity
  • Weight Control
  • Diet
  • Smoking cessation
  • Alcohol intake
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11
Q

What are antihypertensive drug therapy (5)

A
  1. Angiotensin coverting enzyme (ACE) inhibitors
  2. Angiotensin receptor blockers
  3. beta blockers (less effective - only used for patients with coronary heart disease)
  4. calcium channel blockers
  5. Diuretics
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12
Q

How do Angiotensin Converting Enzyme (ACE) Inhibitors work

A
  • They block angiotensin converting enzyme which converts antagonizing angiotensin 1 into angiotensin 2
  • This reduced constriction of arteries and reduces blood volume by reducing solidum and water retention by the kidneys
  • Has a dry cough as a side effect
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13
Q

How do Angiotensin 2 Receptor Blockers work

A
  • Inhibits the angiotensin 2 receptor
  • causing vasodilation of arteries (main effect)
  • Also reduces sodium and water retention by kidneys, decreasing blood volume (minor effect)
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14
Q

Where do Angiotensin 2 receptor blockers work

A

Works in the arteries

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15
Q

How do beta blockers work

A
  • Block the beta 1 receptors
  • Reduce the effect of noradrenaline (vasoconstricting)
  • reduce heart rate (main effect)
  • reduce cardiac output
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16
Q

Where do beta 1 receptor blockers work

A

works on the heart

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17
Q

What do beta 1 receptors normally respond to and what do they cause

A

adrenaline
they increase heart rate and cardiac output

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18
Q

How do calcium channel blockers work

A
  • Disrupts the movement of Ca2+ through calcium channels responsible for muscle contraction
  • Reduces force of contraction
  • Causes vasodilation
  • Reduces heart rate
  • Reduces aldosterone production = decreasing blood volume
  • Swelling of the lower limbs (ankles) are a side effect
19
Q

How do diuretics work

A
  • Works by altering urine production by decreasing water and sodium retention
  • Decreases blood volume
20
Q

What are the differences between dihydropyridine and non-dihydropyridine calcium channel blockers

A

Dihydropyridines affect blood vessels (more common) causing vasodilatation
Non-dihydropyridines affect the heart decreasing heart rate

21
Q

What are the effects of dihydropyridine calcium channel blockers

A
  • targets the L type calcium channels in the vascular smooth muscle
  • leads to vasodilation
  • reduces blood pressure
22
Q

What are the effects of non dihydropyridine calcium channel blockers

A
  • Also targets L type calcium channels but have more significant effects on the heart myocardium and AV node
  • Decreases heart rate and contractility
  • some vasodilation
23
Q

What can dihydropyridine calcium channel blockers cause

A

gastro-oesophageal reflux

24
Q

What is arteriosclerosis

A

Arteriosclerosis is a general term for the thickening, hardening and loss of elasticity of the walls of arteries. It is most concern in the coronary arteries but will occur in other arterial vessels.

25
Q

What is atherosclerosis

A

Atherosclerosis is a condition in which
- the arteries become narrowed and hardened due to a buildup of plaque on their inner walls - resulting in hypertension
- small patchy thickening (atheromas) form
- Atheroma’s can intrude into the lumen resulting in arterial spasms and cause blood clots

26
Q

What are the stages of development of atherosclerosis

A
  1. Endothelium is injured by (diabetes, toxins, hypertension..)
  2. Lipids accumulate and oxidize in the tunica intima - LDL accumulate and oxidases in an inflammatory environment
  3. Smooth muscle cells proliferate and a fibrous cap forms - forms atherosclerotic plaque
  4. Plaque protrudes into vessel lumen
    Additional
  5. Plaque becomes unstable - as plaque enlarges and cells at center die forming unstable plaque which is prone to rupture (thrombus)
27
Q

What are the 2 atherosclerotic plaque

A
  • stable
  • unstable
28
Q

What is stable plaque

A

Has a thick fibrous cap and is more stable and less likely to rupture

restricts blood flow and oxygen to heart

progressive weaking of heart pumping

29
Q

What is unstable plaque

A

Has a thin fibrous cap which is more prone to rupture or erosion. Plaque rupture exposes the lipid core to the blood stream, leading to blood clot formation (thrombis)

30
Q

What are consequences of atherosclerosis (4)

A
  • Stiffened artery walls (causing hypertension)
  • Damage arterial walls - thrombus (clot formation), injured epithelial cells make less anti-thrombotic chemicals
  • Increases risk of myocardial infarction (heart attack) and stroke
  • Responsible for pain occurring with Ischemic heart disease angina
31
Q

What is Angina

A

chest pain or discomfort that occurs when the heart muscle doesn’t get enough oxygen-rich blood. It is the pain associated with myocardial ischemia.

32
Q

What is myocardial Ischemia

A

when blood flow to the heart muscle (myocardium) is reduced, preventing it from receiving enough oxygen.

33
Q

What is Anginal pain

A

the pain associated with angina is typically described as being constricting, squeezing or suffocating

34
Q

What are the 3 types of angina

A
  • stable
  • unstable
  • variant
35
Q

what is stable angina

A

Result of atherosclerotic plaque constricting blood flow. Blood flow adequate at rest, exertion causing pain.

Symptoms occur predictably during physical exertion or stress and are relieved by rest or medication (e.g., nitroglycerin).

36
Q

What is unstable angina

A

Result of atherosclerotic plaque and an associated thrombus, greater degree of constriction. Compromised even at rest.

Symptoms occur unexpectedly and at rest, indicating a higher risk of heart attack. This requires immediate medical attention.

37
Q

What is variant angina

A

Unexplained spasms constricting blood flow. Can occur at any time, not just with exertion (exercise)

38
Q

What are some Lifestyle Modifications to reduce Angina

A
  • Stop smoking
  • Stress reduction
  • regular exercise
  • limit dietary intake of cholesterol and saturated fats
  • weight reduction
  • avoid cold and other physical stresses
39
Q

What main drug is used to manage angina

A

Glyceryl Trinitrate (GTN)

40
Q

What does Glyceryl Trinitrate (GTN) do

A

it is a potent vasodilator which is administered during an attack and should provide immediate relief

Vasodilator action:
- Acts on blood vessels
- dilates blood vessels
- inhibits calcium influx
- Decreases preload by increasing venous capacity
- Reduces ventricular filling pressure and arterial blood pressure
- Helps open collateral vessels in ischaemic areas of the myocardium, improving coronary blood flow

41
Q

What is the chemical messenger of GTN

A

nitric oxide

42
Q

Why does GTN work so fast

A

it is lipophilic and hence can easily travel through cell membrane and function

43
Q

What other drugs could be used to treat angina

A
  • ACE inhibitors
  • Angiotensin receptor blockers
  • Beta blockers
  • Calcium channel blockers
44
Q
A

DS1102 (30 decks)

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