BIOH12011 WEEK 6 CARDIOVASCULAR PATHOPHYSIOLOGY
AND PHARMACOLOGY EXAM QUESTIONS AND ANSWERS
WITH COMPLETE SOLUTIONS GRADED A++
Blood Pressure
The force exerted by blood against a unit area of the blood vessel walls; differences in
blood pressure between different areas of the circulation provide the driving force for
blood circulation.
Blood Pressure (BP) = Cardiac Output (CO) x Peripheral Resistance (PR)
BP can rise as a result of:
Increased cardiac output• CO = stroke volume (SV) x heart rate (HR).• If HR increases,
BP will rise.• If SV increases as a result of fluid accumulation, BP will rise
Increased peripheral resistance • Stiff arteries due to age (arteriosclerosis)..
Systolic Blood pressure
High pressure generated as the ventricles contract and push blood
into the aorta (and other major arteries).
Diastolic Blood Pressure
Lower blood pressure between contractions.
Blood pressure reading
,Recorded in mmHg and expressed as:
Systolic Pressure/ Diastolic Blood Pressure
Hypertension
Consistent elevation of systemic arterial blood pressure.
Consistently elevated resting blood pressure at or above 140mmHg systolic and/or
90mmHg diastolic.
SBP ≥ 140mmHg and/or DBP ≥ 90mmHg - measured on two different days (World
Health Organisation, 2020).
− Repeated blood pressure (BP) measurements at different times.
Types of Hypertension
1.Primary (essential/idiopathic) Hypertension
2. Secondary Hypertension
3.Pre-eclampsia
Primary (essential/idiopathic)
Majority of cases (90 - 95%).Unknown aetiology.
No identifiable underlying cause,
Contributing factors include genetics, diet, Lifestyle, Sedentary lifestyle, Excessive
alcohol consumption
Diet (high sodium intake), Smoking , Stress and
Genetics
Secondary Hypertension
,Caused by an underlying disease.
Hardening and thickening of artery walls:
− Increases peripheral resistance or
cardiac output.
− Reduced blood flow to organs.
− Leads to target organ damage.
➢ Heart disease: Enlargement of ventricles (cardiac hypertrophy) and heart failure.
➢ Kidneys: Renal failure.
➢ Brain: Hypertensive encephalopathy.
➢ Eyes: Hypertensive retinopathy.
Example: Renal, endocrine, neurogenic, drugs (e.g., oral contraceptives,
corticosteroids, antihistamines). Management of the underlying condition can reduce
blood pressure to near normal levels.
Pre-eclampsia
Elevated blood pressure and proteinuria associated with pregnancy.
Clinical Manifestations of Hypertension
Early: None - a 'silent' condition.
• Later: Symptoms arise due to associated damage of organs as well as vascular
changes.
- These include:o Heart diseaseo Renal insufficiencyo Brain dysfunctiono Impaired
visiono Impaired mobilityo Vascular occlusion and oedema
, Pathophysiology of Primary Hypertension
Interaction of genetics and environmental or lifestyle factors. − Neural and hormonal
effects.
Pathophysiology mechanisms:− SNS: Renin-angiotensin-aldosterone system
o ↑ HR and vasoconstriction.
o ↓ Release of nitric oxide (NO) and other vasodilators.
o Sodium and water retention → ↑ blood volume.
Increased peripheral resistance and blood volume=
− Natriuretic peptides
− Inflammation
− Endothelial dysfunction
− Insulin resistance
Patho of Hypotension: Sympathetic Nervous System (SNS)
Vasomotor center: control of vascular tone - vasoconstriction to maintain tissue
perfusion.
• Regulation of cardiac output and blood volume.• Balance: local mediators opposing
vascular tone → vasodilation
e.g., nitric oxide (NO) release from endothelial cells.
Patho of Hypotension: Renin-Angiotensin- Aldosterone System (RAAS)
Controls vascular tone and blood volume.• Synthesis of angiotensin II by ACE →
vasoconstriction + ↓ NO
AND PHARMACOLOGY EXAM QUESTIONS AND ANSWERS
WITH COMPLETE SOLUTIONS GRADED A++
Blood Pressure
The force exerted by blood against a unit area of the blood vessel walls; differences in
blood pressure between different areas of the circulation provide the driving force for
blood circulation.
Blood Pressure (BP) = Cardiac Output (CO) x Peripheral Resistance (PR)
BP can rise as a result of:
Increased cardiac output• CO = stroke volume (SV) x heart rate (HR).• If HR increases,
BP will rise.• If SV increases as a result of fluid accumulation, BP will rise
Increased peripheral resistance • Stiff arteries due to age (arteriosclerosis)..
Systolic Blood pressure
High pressure generated as the ventricles contract and push blood
into the aorta (and other major arteries).
Diastolic Blood Pressure
Lower blood pressure between contractions.
Blood pressure reading
,Recorded in mmHg and expressed as:
Systolic Pressure/ Diastolic Blood Pressure
Hypertension
Consistent elevation of systemic arterial blood pressure.
Consistently elevated resting blood pressure at or above 140mmHg systolic and/or
90mmHg diastolic.
SBP ≥ 140mmHg and/or DBP ≥ 90mmHg - measured on two different days (World
Health Organisation, 2020).
− Repeated blood pressure (BP) measurements at different times.
Types of Hypertension
1.Primary (essential/idiopathic) Hypertension
2. Secondary Hypertension
3.Pre-eclampsia
Primary (essential/idiopathic)
Majority of cases (90 - 95%).Unknown aetiology.
No identifiable underlying cause,
Contributing factors include genetics, diet, Lifestyle, Sedentary lifestyle, Excessive
alcohol consumption
Diet (high sodium intake), Smoking , Stress and
Genetics
Secondary Hypertension
,Caused by an underlying disease.
Hardening and thickening of artery walls:
− Increases peripheral resistance or
cardiac output.
− Reduced blood flow to organs.
− Leads to target organ damage.
➢ Heart disease: Enlargement of ventricles (cardiac hypertrophy) and heart failure.
➢ Kidneys: Renal failure.
➢ Brain: Hypertensive encephalopathy.
➢ Eyes: Hypertensive retinopathy.
Example: Renal, endocrine, neurogenic, drugs (e.g., oral contraceptives,
corticosteroids, antihistamines). Management of the underlying condition can reduce
blood pressure to near normal levels.
Pre-eclampsia
Elevated blood pressure and proteinuria associated with pregnancy.
Clinical Manifestations of Hypertension
Early: None - a 'silent' condition.
• Later: Symptoms arise due to associated damage of organs as well as vascular
changes.
- These include:o Heart diseaseo Renal insufficiencyo Brain dysfunctiono Impaired
visiono Impaired mobilityo Vascular occlusion and oedema
, Pathophysiology of Primary Hypertension
Interaction of genetics and environmental or lifestyle factors. − Neural and hormonal
effects.
Pathophysiology mechanisms:− SNS: Renin-angiotensin-aldosterone system
o ↑ HR and vasoconstriction.
o ↓ Release of nitric oxide (NO) and other vasodilators.
o Sodium and water retention → ↑ blood volume.
Increased peripheral resistance and blood volume=
− Natriuretic peptides
− Inflammation
− Endothelial dysfunction
− Insulin resistance
Patho of Hypotension: Sympathetic Nervous System (SNS)
Vasomotor center: control of vascular tone - vasoconstriction to maintain tissue
perfusion.
• Regulation of cardiac output and blood volume.• Balance: local mediators opposing
vascular tone → vasodilation
e.g., nitric oxide (NO) release from endothelial cells.
Patho of Hypotension: Renin-Angiotensin- Aldosterone System (RAAS)
Controls vascular tone and blood volume.• Synthesis of angiotensin II by ACE →
vasoconstriction + ↓ NO
