RMIT Classification

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RMIT Classification: Trusted
Learning objectives
1.Explain the causes, pathophysiology and complications of hypertension
2. Explain the causes, pathophysiology and complications of atherosclerosis
3. Explain the causes, pathophysiology and complications of thrombosis and
embolism
Essential Readings: Craft, Gordon, Huether, McCance and Brashers, Chapter 11
Alterations in cardiovascular function across lifespan, Understanding Pathophysiology
3rd Edition, 2018
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RMIT Classification: Trusted
Cardiovascular disorders
All diseases/conditions of heart and blood vessels
Stroke, coronary artery disease, hypertension, heart failure…
Leading cause of death -30% of all mortalities
1 death every 12 minutes
1:6 Australians (3.7 million)
Burden on economy, health care, families
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Blood pressure
Blood pressure is the measurement of force applied to
artery walls
Normal blood pressure is 120/80
Blood pressure is controlled by short and long term
mechanisms
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Blood pressure
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Blood pressure
Short term mechanism
Short term regulation of blood pressure is via the autonomic
nervous system
The baroreceptors located in the aorta and carotid sinus detect
changes in blood pressure.
When there is an increase in blood pressure, the
parasympathetic nervous system reduces heart rate and
cardiac contractility
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Blood pressure
When there is an decrease in blood pressure the sympathetic
nervous system increase the heart rate and cardiac
contractility
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Blood pressure
Long term mechanism
Decreased blood flow or sodium chloride delivery to the kidney
activates the renin-angiotensin aldosterone system.
Renin converts angiotensinogen to angiotensin I.
Angiotensin I is converted to angiotensin II by angiotensinconverting enzyme.
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Blood pressure
Angiotensin II cause vasoconstriction and increases sodium
absorption and releases aldosterone
Aldosterone increase sodium and water absorption
The result is an increase in blood pressure
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Blood pressure
Angiotension II will also stimulate the release of Anti diuretic
hormone
ADH increase the permeability of the collecting duct to water by
inserting aquaporin channels (AQP2) into the apical membrane
An increase in blood pressure will stimulate release of Atrial
natriuretic peptide.
ANP promotes sodium excretion
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Renin Angiotension
Aldosterone system
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Hypertension
An elevated blood pressure exceeding 140 over 90 mmHg
measured on 3 separate occasion
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Hypertension
There are two forms of hypertension
Primary hypertension is when there is no single cause but
there are several factors that contribute to high BP
These factors include genetics, diet, smoking, sedentary
lifestyle, excess alcohol consumption, ageing and stress
It accounts for 90% of cases
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Hypertension
Secondary hypertension is due to an underlying condition
Renal disorders (e.g. chronic pyelonephritis, diabetic
nephropathy).
Vascular disorders
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Hypertension
Endocrine disorders (e.g. primary hyperaldosteronism).
Drugs (e.g. alcohol, cocaine)
Miscellaneous causes (e.g. scleroderma, obstructive sleep
apnoea).
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Risk factors for Hypertension
Age (>50)
Smoking
Alcohol
Diabetes
Gender
(Men have higher risk)
Family history
Obesity
Sedentary lifestyle
Stress
Race ( Africans have a higher
risk)
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Pathophysiology of Hypertension
Blood pressure = Cardiac output x peripheral resistance
Factors that affect cardiac output and peripheral resistance will
lead to hypertension
1.Genetic factors eg defects in renal sodium homeostasis and
functional vasoconstriction
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Pathophysiology of Hypertension
2.Environmental factors eg stress obesity smoking
3. Overactive sympathetic nervous system
The release of catecholamines leads to overactive SNS
Leads to increased peripheral vascular resistance due to
vasoconstriction
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Pathophysiology of Hypertension
4. Overactivation of RAAS (eg renin secreting tumour, oral
contraceptive that increase angiotensinogen) can lead to the
following effects
Increase activity of SNS
Increased retention of sodium and water
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Pathophysiology of Hypertension
5. Endothelial dysfunction
Endothelium releases potent vasodilators in response to blood
flow
Endothelial damage leads to a decrease in these factors and
increase in vasoconstriction
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Symptoms of Hypertension
Asymptomatic
Severe headache
Blurred vision
Dizziness
Nausea
Vomiting
Fatigue
Chest pain
Shortness of breath
Irregular heart beat
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Complications of Hypertension
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Complications of Hypertension
Stroke- Hardening of blood vessel can lead to a stroke
Heart failure- Increase workload for heart can lead to heart failure
Damage to blood vessel can lead to a heart attack
Vision loss due to hardening and narrowing of blood vessels
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Complications of Hypertension
Kidney failure – Damage to blood vessel leads to kidney failure
and inability to filter wastes
Bone loss- High BP can lead to the loss of calcium in urine
Sexual dysfunction –High BP can restrict blood flow to penis and
cause erectile dysfunction
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Question 1
Anti diuretic hormone
A. Increases urine production and decrease blood pressure
B. Decrease urine production and blood pressure
C. Increase urine production and blood pressure
D. Decrease urine production and increase blood pressure
E. None of the above
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RMIT Classification: Trusted
Question 1
Anti diuretic hormone
A. Increases urine production and decrease blood pressure
B. Decrease urine production and blood pressure
C. Increase urine production and blood pressure
D. Decrease urine production and increase blood pressure
E. None of the above
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Question 2
Why does endothelial dysfunction lead to hypertension?
A. Endothelium damage activates SNS
B. Endothelium damages causes vasodilation
C. Endothelium damage decreases secretion of factors that promote
vasodilation
D. Endothelial damage increase renin secretion
E. Endothelial damages increase ADH secretion
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Question 2
Why does endothelial dysfunction lead to hypertension?
A. Endothelium damage activates SNS
B. Endothelium damages causes vasodilation
C. Endothelium damage decreases secretion of factors that
promote vasodilation
D. Endothelial damage increase renin secretion
E. Endothelial damages increase ADH secretion
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Question 3
Which hormone decreases blood pressure?
A. Anti-diuretic hormone
B. Aldosterone
C. Renin
D. Atrial natriuretic peptide
E. Vasopressin
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RMIT Classification: Trusted
Question 3
Which hormone decreases blood pressure?
A. Anti-diuretic hormone
B. Aldosterone
C. Renin
D. Atrial natriuretic peptide
E. Vasopressin
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RMIT Classification: Trusted
Arteriosclerosis and atherosclerosis
Arteriosclerosis is abnormal thickening and hardening of
artery walls
Atherosclerosis is a form of arteriosclerosis, with soft deposits
of intra-arterial fat and other variations depending on the
severity of the condition
Atherosclerosis is the main cause of coronary heart disease
and cerebrovascular disease.
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Atherosclerosis
Pathophysiology
1.Endothelium injury eg hypertension, smoking, viruses
2.Endothelium becomes inflamed
Inflammatory cells → further inflammation → more endothelial damage
Macrophages imbibe oxidised LDL and become foam cells and form fatty
streaks
endothelium changes → platelet aggregation and vasoconstriction →
decreased blood flow
3.Macrophages also release growth factors stimulating smooth muscle cell
(SMC) proliferation. SMCs migrate over the fatty streak and increased
collagen deposition to form a fibrous plaque.
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Atherosclerosis (cont.)
Pathophysiology
4.The fibrous plaque now formed may calcify, protrude into the
lumen, obstruct blood flow, and become an ‘unstable’ plaque.
5.An unstable plaque is prone to rupture and thus become a
‘complicated’ plaque. After rupture platelet adhesion occurs and
tissue clotting factors are also released. A thrombus rapidly forms,
and may cause complete blockage of the vessel.
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Atherosclerosis
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Atherosclerosis
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Complications of Atherosclerosis
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Thrombosis
What is a thrombus?
Blood clot inside a vessel
Narrows the vessel diameter = ↓ blood flow
How does it occur?
When normal process of Haemostasis is inappropriately
activated ie in an uninjured or slightly injured blood vessel
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Haemostasis
Three phases occur in rapid sequence
Vasoconstriction in response to injury
Clumping (aggregation of platelets = plug)
Coagulation (blood clotting)
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Risk factors for Thrombosis
1. Blood vessel endothelial damage
Endothelial cell dysfunction
CVD risk factors ie Diabetes, Smoking Cholesterol
Hyperlipemia Hypertension
=Slow blood flow caused by narrowed arteries
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Thrombosis
2. Venous stasis = ‘low blood flow’ in the veins
Immobilisation (eg prolonged bed rest following surgery, sitting in
aircraft, obesity)
Venous thrombosis more common than arterial due to low flow and
low pressure
3. Enhanced coagulation
Pregnancy, polycythemia, Cancer, Inherited clotting disorders
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Thrombosis
A thrombus can be classified as arterial or venous
Venous thrombi are further classified by their location ie Deep
vein thrombosis or Portal vein thrombosis
The complications of thrombosis include stroke, myocardial
infarction
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Outcomes of Thrombosis
Positive outcomes
Lysis – dissolved by plasmin system
Retraction – shrinkage
Organisation & recanalisation – new vessels grow through lesion,
allowing some blood flow to organ.
Negative outcomes
Propagation – larger and moves towards heart
Thromboembolism breaks off and floats freely until it lodges or
dissolves
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Embolism
Embolus: Usually a mass (bolus) which forms in one location,
dislodges and moves through the circulation
90% are dislodged thrombi (thromboemboli)
Fat (broken bones)
Air, Amniotic fluid
Foreign substances
Bacterial
The complications of embolism include stroke, myocardial
infarction
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RMIT Classification: Trusted
Question 1
Which of the following is a negative outcome for patient with
thrombosis?
A. Lysis of the thrombus
B. Retraction of the thrombus
C. Organisation & recanalization of the thrombus
D. Formation of a thromboembolus
E. None of the above
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RMIT Classification: Trusted
Question 1
Which of the following is a negative outcome for patient with
thrombosis?
A. Lysis of the thrombus
B. Retraction of the thrombus
C. Organisation & recanalization of the thrombus
D. Formation of a thromboembolus
E. None of the above
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RMIT Classification: Trusted
Question 2
What are foam cells?
A. Macrophages that engulf oxidised LDL
B. T cells that engulf oxidised LDL
C. B cells that engulf oxidised LDL
D. Injured endothelium
E. Proliferating smooth muscle
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RMIT Classification: Trusted
Question 2
What are foam cells?
A. Macrophages that engulf oxidised LDL
B. T cells that engulf oxidised LDL
C. B cells that engulf oxidised LDL
D. Injured endothelium
E. Proliferating smooth muscle
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RMIT Classification: Trusted
Case study 1
Emily wong, aged 32, suffers from headaches. She visits her doctor
and is diagnosed with hypertension.
Q1 She has recently begun taking an oral contraceptive that
increases the amount of angiotensinogen in her body. Explain how
this could contribute to hypertension.
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RMIT Classification: Trusted
Case study 1
Emily wong, aged 32, suffers from headaches. She visits her doctor
and is diagnosed with hypertension.
Q1 She has recently begun taking an oral contraceptive that
increases the amount of angiotensinogen in her body. Explain how
this could contribute to hypertension.
Angiotensinogen is part of the renin angiotensin aldosterone system. The
increase in angiotensinogen would lead to an increase in angiotensin II
(see diagram). This would lead to increase sodium absorption directly and
aldosterone secretion that leads to sodium absorption and water
reabsorption and ADH secretion that leads to water reabsorption
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Case study 1
Q2 Emily finds that she has started to lose her vision. This has
resulted in multiple falls and subsequent fractures. Explain why
Emily suffer from vision loss and fractures.
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RMIT Classification: Trusted
Case study 1
Q2 Emily finds that she has started to lose her vision. This has
resulted in multiple falls and subsequent fractures. Explain why
Emily suffer from vision loss and fractures.
Vision loss due to hardening and narrowing of blood vessels
Bone loss due to high BP can lead to the loss of calcium in urine. This
would increase the chance of fractures
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RMIT Classification: Trusted
Case study 1
Q2 Emily finds that she has started to lose her vision. This has
resulted in multiple falls and subsequent fractures. Explain why
Emily suffer from vision loss and fractures.
Vision loss due to hardening and narrowing of blood vessels
Bone loss due to high BP can lead to the loss of calcium in urine. This
would increase the chance of fractures
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RMIT Classification: Trusted
Case study 1
Q2 Emily finds that she has started to lose her vision. This has
resulted in multiple falls and subsequent fractures. Explain why
Emily suffer from vision loss and fractures.
Vision loss due to hardening and narrowing of blood vessels
Bone loss due to high BP can lead to the loss of calcium in urine. This
would increase the chance of fractures
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RMIT Classification: Trusted
Case study 2
Andrew Biden is a 52 year old partner at Price Waterhouse Coopers. He is
obese due to a high fat diet, a sedentary lifestyle and no exercise. He
deals with the stressful job by being a heavy smoker. Andrew is diagnosed
with atherosclerosis.
Q1.What is the first event of atherosclerosis? Identify one factor that
would contribute to this event
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RMIT Classification: Trusted
Case study 2
Andrew Biden is a 52 year old partner at Price Waterhouse Coopers. He is
obese due to a high fat diet, a sedentary lifestyle and no exercise. He
deals with the stressful job by being a heavy smoker. Andrew is diagnosed
with atherosclerosis.
Q1.What is the first event of atherosclerosis? Identify one factor that
would contribute to this event
Injury to the endothelium is the first event. Smoking is likely to have
contributed to the event
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Case study 2
Q2. Identify one factor which would contribute to the formation of
foam cells.
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RMIT Classification: Trusted
Case study 2
Q2. Identify one factor which would contribute to the formation of
foam cells.
Any one of the following;
Smoking that causes endothelial cell damage would recruit macrophages
High fat diet will lead to Low density lipids. Macrophages imbibe the
oxidised LDL and become foam cells
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RMIT Classification: Trusted
Case study 2
A thrombus forms on Andrew’s atherosclerotic plaque in the
coronary artery.
Q3 What is a thrombus?
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RMIT Classification: Trusted
Case study 2
A thrombus forms on Andrew’s atherosclerotic plaque in the
coronary artery.
Q3 What is a thrombus?
When normal process of Haemostasis is inappropriately activated (ie in an
uninjured or slightly injured blood vessel ) and resulting in a blood clot in a
blood vessel
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RMIT Classification: Trusted
Case study 2
A thrombus forms on Andrew’s atherosclerotic plaque in the
coronary artery.
Q4 The thrombus grows over a period of time but does not cause a
myocardial infarction due to Organisation & recanalization. Explain
why
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RMIT Classification: Trusted
Case study 2
A thrombus forms on Andrew’s atherosclerotic plaque in the
coronary artery.
Q4 The thrombus grows over a period of time but does not cause a
myocardial infarction due to Organisation & recanalization. Explain
why
Organisation & recanalisation of the thrombus allows new vessels to grow
through lesion and some blood flow to organ. Hence Andrew will not suffer
from Myocardial infarction
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RMIT Classification: Trusted
Case study 2
Q5 A thrombus breaks off and forms a thromboembolism. Andrew
suffers a stroke. Explain how this would cause a stroke
.
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RMIT Classification: Trusted
Case study 2
Q5 A thrombus breaks off and forms a thromboembolism. Andrew
suffers a stroke. Explain how this would cause a stroke
An emboli is a mass which forms in one location, dislodges and moves
through the circulation. In this case a thrombus has broken off and formed
a thromboembolism. The thromboembolism has lodged in his carotid
artery. The narrowed lumen restricts blood flow to the brain. The ischemia
leads to hypoxia and cell death or a stroke.

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