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Semester 1 Year 2 > Pathophysiology of hypertension > Flashcards

Pathophysiology of hypertension Flashcards

1
Q

Overview

A

• PRIMARY vs. SECONDARY HYPERTENSION

  • POSSIBLE MECHANISMS OF PRIMARY HYPERTENSION
  • SYMPATHETIC SYSTEM
  • RAAS
  • CIRCULATING FACTORS • GENETICS
  • MECHANISMS OF SECONDARY HYPERTENSION
  • CONSEQUENCES OF HYPERTENSION
  • TREATING HYPERTENSION
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2
Q

Discuss pulmonary hypertension

A

• Increased blood pressure in the arteries of the lungs

  • Cause often not known
  • Can be due to hypoxia, endothelial dysfunction, genetics, blockage/damage to blood vessels, side effects of drugs, left-sided HF
  • Right side of the heart has to work harder
  • Rare
  • More common in patients with another heart or lung condition
  • Usually only diagnosed when severe and symptomatic
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3
Q

Discuss systemic arterial hypertension

A

• Systemic arterial hypertension is the condition of persistent non-physiologic elevation of system blood pressure

  • Typically defined as:
  • Systolic > 140 mmHg and/or
  • Diastolic > 90mmHg
  • Identified as one of the major causal risk factors for cardiovascular disease
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4
Q

Discuss risk factors for hypertension

A
  • Hypertension is a complex phenotype
  • Multiple genetic risk factors
  • Multiple environmental risk factors
  • Age
  • Weight
  • Sex
  • < 60 years more prevalent in males
  • > 60 years more prevalent in females
  • Race
  • African Americans disproportionally affected
  • Education status
  • Diet
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5
Q

Discuss measurement of blood pressure in hypertension

A
  • All adults >40 years should have BP measured
  • <40 years with family history of atherosclerosis

• Minimum of 3-4 pairs of readings gathered over 3-4 months (unless severe HT)
RECOMMENEDED TO CONFIRM HT:

  • Ambulatory blood pressure monitoring (ABPM)
  • Measured twice per hour during waking hours
  • At least 14 measurements to calculate average
  • Home blood pressure monitoring (HBPM)
  • Monitored twice daily (day/night, sitting)
  • 2 recordings, 1min apart for 7 days (at least 4)
  • All recordings after 1st to calculate average
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6
Q

Discuss classification of systemic hypertension

A

Stage 1 hypertension
• Clinic BP is 140/90 mmHg or higher and subsequent ambulatory or home blood pressure monitoring (ABPM or HBPM) daytime average is 135/85 mmHg or higher

Stage 2 Hypertension
• Clinic BP is 160/100 mmHg or higher and subsequent ABPM or
HBPM daytime average is 150/95 mmHg or higher

Severe Hypertension
• Clinic systolic BP is 180 mmHg or higher
• OR clinic diastolic BP is 110 mmHg or higher

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7
Q

Discuss systemic arterial hypertension

A

Also known as primary hypertension

  • Also known as “essential” or “idiopathic” hypertension
  • Accounts for ~90 % of human hypertension
  • No apparent underlying cause
  • Weight
  • Lifestyle
    • Dietary sodium intake, lack of exercise, alcohol, smoking
  • Genetic factors
  • Multiple organ systems
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8
Q

What is the way to calculate blood pressure from cardiovascular states

A

BP = CO x TPR

CO = Stroke volume (SV) x Heart Rate (HR)

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9
Q

Discuss blood pressure control

A
  • Complex interactions of neurohormonal and local control systems that regulate BP and local tissue flow
  • BUT it also involves additional systems that regulate circulatory volume in relation to vascular capacitance
(?)
Short term: 
Cardiac output (CO)
Total peripheral resistance (TPR)
Long term: 
Effective circulating volume (ECV)
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10
Q

What are possible contributors to systemic hypertension

A
  1. INCREASED SYMPATHETIC ACTIVITY / SENSITIVITY
  2. RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM (RAAS)
  3. CIRCULATING FACTORS
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11
Q

How does the autonomic nervous system influence BP control

A 
• Blood vessel tone
• Heart rate and force of
contraction
• Adrenal gland secretion of
adrenaline
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12
Q

Discuss neurotransmission in the ANS

A

• SyNS and PaNS are the two major EFFERENT pathways controlling targets other than skeletal muscle
• Involves a two-synapse pathway
• SyNS and PaNS work SYNERGISTICALLY to control visceral activity (often working in opposite ways)
Sympathetic releases noradrenaline and adrenaline at postganglionic neuron
Parasympathetic releases ACh at postganglionic neuron

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13
Q

Discuss adrenergic receptors (adrenoceptors)

A

• Catecholamines bind adrenoceptors to elicit their actions

Adrenaline (A)

Noradrenaline (NA)

Isoprenaline (ISO) Synthetic b-agonist

  • Demonstrate different affinities to each receptor
  • Intracellular action of a specific catecholamine is determined by the complement of receptors expressed on the cell surface
  • Catecholamines bind adrenoceptors to elicit their actions
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14
Q

Discuss sympathetic contribution to hypertension

A

Increased blood pressure due to:

• Increased signalling to vascular smooth muscle cells of blood vessels (a1) so increase vasoconstriction so increaseTPR
• Increased signalling to pacemaker
and contractile cells in heart (b1) so increase HR and contraction so increase CO
• Adrenal gland secretion of adrenaline
• Renin secretion (b1 receptors) so increase Ang II so increase vasoconstriction so increase TPR
Ang II also increases Na+ and H2O absorption and so increase ECV

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15
Q

Discuss a quick overview of the kidneys

A
  • Functional unit of kidney is a nephron
  • Filters blood and produces urine
  • Filter ~ 180 L blood/day
  • REABSORPTION

• Na+ is predominant cation in ECF
• Movement of Na+ established osmotic
gradients for H2O movement • Na+ is freely filtered across
glomerulus, 99% will be reabsorbed
• The kidneys must balance Na+ intake with Na+ excretion
• This maintains ECF volume and therefore long-term BP
• Critical target for anti-hypertensives

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16
Q

Discuss RAAS

A
  • Angiotensinogen:
  • a2 globulin
  • synthesized by the liver
  • released into circulation

• Renin:
• proteolytic enzyme
• released by granular cells in the juxtaglomerular apparatus (JGA) of the kidney
Angiotensin converting enzyme (ACE)
• cleaves Angiotensinogen to Angiotensin I
Angiotensin II
• Renin is cleared rapidly from the plasma

  • Angiotensin I:
  • appears to have no biological activity
  • is a precursor to Angiotensin II
  • Angiotensin converting enzyme (ACE):
  • enzyme
  • found in vascular endothelium in the lungs and the renal afferent and efferent arterioles
  • converts Angiotensin I to Angiotensin II
17
Q

Discuss low renin hypertension

A
  • Subset of patients with primary hypertension
  • It becomes secondary if the cause is known e.g. Conn’s syndrome
  • More prevalent in patient who are:
  • Older
  • Of Afro-Caribbean descent
  • Diagnosed using plasma aldosterone:renin ratio
  • Low renin, normal aldosterone
  • Different treatment strategy
18
Q

Discuss circulating factors

A

ENDOTHELIN
• Most potent endogenous vasoconstrictor
• Endothelin-1 (ET-1) predominant isoform in cardiovascular system
• Circulating concentrations of ET-1 are NOT commonly increased in primary hypertension
• BUT local levels may be increased
• Can bind ETA receptors on vascular smooth muscle cells
• VASOCONSTRICTION
• Can bind ETA receptors in cardiomyocytes and increase contractility
• But also bind ETB receptors
• Production of nitric oxide causing VASODILATION
• In the kidneys promotes Na+ and H2O excretion (natriuresis and diuresis, respectively)

NITRIC OXIDE
• Lipophilic gas released from endothelial cells in response to stimuli
• Most potent endogenous VASODILATOR
• Very short half-life
• Usually acts in the tissues where it is secreted
• Chronic regulator of RENAL blood flow and increases Na+ excretion

REACTIVE OXYGEN SPECIES
• Including superoxide, hydrogen peroxide (H2O2) and peroxynitrite
• Patients with essential hypertension have increased circulating H2O2
• ROS in the vasculature may uncouple the enzymes which produce NO
• BUT chronic treatment with antioxidants does NOT lower pressure

19
Q

Discuss genetics

A
  • Studies of BP pressure patterns in families suggest genetic factors may account for as much as 30-50% of BP variance
  • Whilst many studies have shown associations of gene polymorphisms and BP, the genetic alterations that contribute to primary HT remain elusive
  • Is this surprising?
  • Complex interplay between multiple neural, hormonal, renal and vascular mechanisms for short- and long-term BP regulation
20
Q

Discuss systemic hypertension

A

Also known as secondary hypertension

  • ~5 % of cases
  • Identifiable underlying cause
  • Often in patients < 25 years

Renal
• Renal parenchymal disease: glomerularnephritis, diabetic nephropathy, lupus nephritis, polycystic kidney disease
• Renal vascular: renal artery stenosis, vasculitis, fibromuscular dysplasia

Endocrine
• Adrenal gland:
• Zona glomerulosa (aldo) – Conn’s syndrome
• Zona fasiculata (cort) – Cushing’s syndrome
• Adrenal medulla (E/NE) - Pheochromocytoma

21
Q

Discuss some causes of systemic (secondary) hypertension

A 
PREGNANCY
• Eclampsia, pre-eclampsia
COARCTATION OF THE AORTA
DRUGS
• Contraceptive pill, cocaine, amphetamine, NSAIDs, alcohol
OBSTRUCTIVE SLEEP APNOEA
22
Q

What are the consequences of systemic hypertension

A 
HEART
• Heart failure
• Pressure overload from increased TPR, left ventricular hypertrophy
• Myocardial infarction
VASCULATURE
• Accelerated atherosclerosis
• Smaller arteries and arterioles
• Stroke
• Retinopathy
KIDNEYS
• Continued hypertension
• Albuminuria
• End stage renal disease
23
Q

How does one treat systemic (secondary) hypertension

A

Meta-analyses of large-scale randomized controlled trials (RCTs) show:
10/5 mmHg reduction in BP is associated with
• 15% reduction in all-cause mortality
• 35% reduction in stroke
• 40% reduction in heart failure
• 20% reduction in myocardial infarction

24
Q

Learning outcomes

A
  • Define primary and secondary hypertension and recognise their grades and features.
  • Relate the proposed causes and risk factors to the pathogenesis of primary hypertension.
  • Identify causes of secondary hypertension across different organ systems and clinical conditions.
  • Describe the major consequences of uncorrected, chronically elevated hypertension.

Semester 1 Year 2 (69 decks)

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