Professional Documents
Culture Documents
Causes of death
Leading causes of death, Australia, 2014
Cause of death Rank Number
Ischaemic heart diseases 1 20 173
Dementia and Alzheimer disease 2 11 965
Cerebrovascular diseases 3 10 765
Trachea, bronchus, lung cancer 4 8 251
Chronic lower respiratory diseases 5 7 810
Diabetes 6 4 348
Blood and lymph cancer (including leukaemia) 7 4 275
Colon, sigmoid, rectum and anus cancer 8 4 169
Heart failure 9 3 447
Urinary system 10 3 136
Data from Australian Bureau of Statistics, 3303.0 Causes of Death Australia 2013, Mar 2016 2
Cause of death Rank Number Males
Ischaemic heart diseases 1 11 082
Trachea, bronchus, lung cancer 2 4 947
Cerebrovascular diseases 3 4 279
Chronic lower respiratory diseases 4 4 164
Dementia, including Alzheimer disease 5 4 106
Prostate cancer 6 3 102
Blood and lymph cancer (including leukaemia) 7 2 413
Colon, sigmoid, rectum and anus cancer 8 2 279
Diabetes 9 2 213
Intentional self harm 10 2 157 Females
Cause of death Rank Number
Ischaemic heart diseases 1 9 091
Dementia and Alzheimer disease 2 7 859
Cerebrovascular diseases 3 6 486
Chronic lower respiratory diseases 4 3 646
Trachea, bronchus, lung cancer 5 3 304
Breast cancer 6 2 814
Diabetes 7 2 135
Heart failure 8 1 975
Colon, sigmoid, rectum and anus cancer 9 1 890
Data from Australian Bureau of Statistics, 3303.0
Causes of Death Australia 2013, Mar 2016 Blood and lymph cancer (including leukaemia) 10 1 3862
http://www.abs.gov.au/ausstats/abs@.nsf/Lookup/by%20Subject/3303.0~2014~Main%20Features~
4
Summary%20of%20Findings~1, Last accessed July 2016
5
Systemic and pulmonary circuits
Systemic circuit
Blood supply to and
from all body tissues
Pulmonary circuit
Blood supply to and
from lungs (for
oxygenation)
6
Craft & Gordon, Understanding Pathophysiology 2nd ed 2015, Fig 22-1
Pathway of blood through the circulation
7
Craft & Gordon, Understanding Pathophysiology 2nd ed 2015, Fig 22-2
Structure of capillaries
Booth & Wyman, Anatomy, physiology, and pathophysiology for allied health. 2nd edn, 2009, Fig 5-9 and 5-10. 8
Anatomy of the heart
9
Craft & Gordon, Understanding Pathophysiology 2nd ed 2015, Fig 22-16C
Coronary arteries
Branch off the aorta
Lead into capillaries
supply cardiac tissue
10
Craft & Gordon, Understanding Pathophysiology 2nd ed 2015, Fig 22-16A
Coronary veins
Drain into coronary sinus (posterior surface of
heart)
Empties into right atrium
11
Craft & Gordon, Understanding Pathophysiology 2nd ed 2015, Fig 22-16 B
Cardiac conduction system
Sequence of excitation
Sinoatrial node: pacemaker, 100
impulses per minute
Atrioventricular node
Atrioventricular bundle (Bundle of His)
Right and left bundle branches
Purkinje fibres
12
Telser, Elseviers integrated histology, 2007, Fig 7-2
Electrocardiogram (ECG)
13
Craft & Gordon, Understanding Pathophysiology 2nd ed 2015, Fig 22-25
ECG and cardiac mechanical events
14
Fox, Human Physiology, 8th edn, 2004, Fig 13.21
ECG and cardiac mechanical events
ECG deflection Electrical Mechanical event
event
P wave Atrial depolarisation Atrial contraction
19
Adrenergic receptors
Receptor type Location Effect of adrenaline or
noradrenaline binding
Alpha ()1 Arteries supplying Vasoconstriction
receptors skin and visceral
organs
Beta ()1 receptors Heart (muscle) Increases heart rate;
increases force of
contraction
Beta ()2 receptors Coronary arteries Vasodilation
22
Craft & Gordon, Understanding Pathophysiology 2nd ed 2015, Fig 22-38
Peripheral resistance
Opposition to blood flow due to friction
Depends on:
Diameter of blood vessel
Adjusted constantly
Vasoconstriction increases resistance and BP
Blood viscosity
Thicker blood increases BP
23
Control of arterial blood pressure
Determined by:
cardiac output
peripheral resistance,
by altering blood
vessel diameter Vasoconstriction: Vasodilation:
decreases diameter increases diameter
increases resistance decreases resistance
increases BP decreases BP
BP = CO x PR
Blood pressure = cardiac output x peripheral resistance
24
https://www.physicool.co.uk/wp-content/uploads/2014/04/vasoconstriction.jpeg, Last accessed Feb 2016
Oxygen and cardiac muscle
Cardiac muscle uses 75% of oxygen in coronary
circulation at rest
Compared with overall body usage of 25% of
oxygen
25
Short-term control of blood pressure:
Nervous system (1)
Chemoreceptor reflex
Chemoreceptors (in aortic arch and carotid sinus)
Detect low pH, low O2
Stimulates cardioexcitatory centre to increase HR, and
vasoconstriction
26
Short-term control of blood pressure:
Nervous system (2)
Baroreceptor reflex
Baroreceptors (in carotid arteries and aortic arch)
Detect changes in stretch eg when stretched less (due to
decreased blood pressure)
Stimulates cardioacceleratory centre to increase HR, and
vasoconstriction
27
Baroreceptor reflex for
low blood pressure
28
Marieb & Hoehn, Human Anatomy and Physiology, 8th edn, Fig 19.9
Baroreceptor reflex for
high blood pressure
29
Marieb & Hoehn, Human Anatomy and Physiology, 8th edn, Fig 19.9
Long-term control of blood pressure:
Renin-angiotensin-aldosterone
Decreased blood pressure detected by kidney
Kidney releases renin: converts angiotensinogen to
angiotensin l
Angiotensin converting enzyme (ACE): converts
angiotensin I to angiotensin II (mainly in lungs)
Angiotensin II: causes aldosterone secretion from
adrenal gland, resulting in:
Reabsorption of sodium and water by kidney
Increased blood volume
Increased blood pressure
30
Renin-Angiotensin-Aldosterone system
Decrease in BP Kidneys reabsorb
detected by kidneys Na and water
31
Craft & Gordon, Understanding Pathophysiology 2nd ed 2015, Fig 28-15
32
Medications for Cardiovascular system (1)
Type Generic name Action
Anticoagulants eg Heparin, Inhibits coagulation (prevent fibrin mesh)
Warfarin Inhibits thrombus formation
Antiplatelets eg Aspirin, Inhibit platelet aggregation
Cartia Inhibits thrombus formation
Angiotensin- eg Captopril, Inhibits conversion of angiotensin I to angiotensin II,
converting Enalapril so less aldosterone
enzyme (ACE) Decrease blood pressure
inhibitors
Angiotensin II eg Irbesartan, Blocks angiotensin II receptors, so less aldosterone
blockers (ARBs) Losartan Decrease blood pressure
Angiotensin I
ACE (angiotensin converting enzyme)
ACE Inhibitors
Angiotensin II
Angiotensin receptors (adrenal cortex)
Angiotensin II receptor blockers
Aldosterone 34
Medications for Cardiovascular system (2)
Type Generic name Action
Calcium eg Diltiazem, Block calcium influx into cytoplasm
channel Verapamil Coronary artery vasodilation, improving perfusion
blockers Decreases contractility, lowers blood pressure
Coronary eg glyceryl Reduces myocardial demand for oxygen
vasodilators / trinitrate (GTN), Widespread vasodilation
nitrates nitroglycerine Coronary artery vasodilation, decreases
afterload
Digoxin Digoxin Increases intracellular calcium levels
Increases contractility
Diuretics eg Frusemide, Increase renal excretion of sodium and water
Spironolactone Decreases blood pressure
Lipid lowering eg Simvastatin, Liver draws LDL from the peripheral blood vessels
drugs Atorvastatin Decreases plasma lipid levels
Thrombolytics eg Breaks down fibrin mesh
Streptokinase Breaks down existing thrombus
35
36
Dietary fats
Triglycerides
Monounsaturated fats (eg olive oil)
Polyunsaturated fats (eg fish)
Trans-unsaturated fats (eg processing of
polyunsaturated fats, deep fried foods)
Saturated fats (eg animal fats)
Phospholipids (eg plant and animal)
Cholesterol (eg animal fats, eggs)
37
Sources of cholesterol
1. Dietary cholesterol (as per previous slide)
2. Produced by liver
Cells require cholesterol for cell membrane
Liver produces more cholesterol when the diet is
high in saturated and trans fats, and high blood
glucose level
38
Production of cholesterol
Cholesterol is produced by
the liver
Modified from Nelms et al, Nutrition Therapy and Pahophysiology, 2nd ed, Fig 13-10 39
Cholesterol in bile
Liver removes cholesterol
from the circulation through
the bile salts
Digestive function in emulsifying
fats in the small intestine
Bile salts are recycled via the
enterohepatic circulation
40
Sherwood, Human Physiology, 2004, Fig 16-17
Cholesterol in hormones
Cholesterol is necessary for the production of
various hormones, including
Cortisol
Aldosterone
Testosterone
Oestrogen
41
Berg et al, Biochemistry 7th edn, Fig 26-27
Transport of dietary fats
Lipoproteins: transport lipids in the blood
Lipids are insoluble in plasma (water-based)
42
LDL = low density
Lipoproteins: LDL lipoprotein,
bad cholesterol
43
HDL : high density
Lipoproteins: HDL lipoprotein,
good cholesterol
44
Summary of LDL and HDL activity
45
Gould, Pathophysiology for Health Professionals, 3rd edn, Fig 18-11b
Dyslipidaemia
Abnormal levels of lipids in the blood
Major risk factor for atherosclerosis
Dyslipidaemia includes:
Increased triglycerides
Increased LDL
Decreased HDL
Lipids (mmol/L)
LDL < 2.0
HDL > 1.0
Triglycerides <2.0
Total cholesterol <4.0
Adapted from Craft & Gordon, Understanding Pathophysiology 2nd ed 2015, Table 23.4 48
Prevention and Management
Dietary
Modifying amount and type of fat intake
Decreasing total energy intake
Increasing dietary fibre
Decreasing intake of simple carbohydrates
Exercise
Lipid-lowering drugs
49
50
Atherosclerosis
Atherosclerosis: fatty deposits and hardening of artery
wall
Progressive accumulation of
lipids
inflammatory cells
smooth muscle cells
connective tissue
52
http://media-2.web.britannica.com/eb-media/83/98483-004-FD45DAA5.jpg, Last accessed Feb 2016
53
Craft & Gordon, Understanding Pathophysiology 2nd ed 2015, Fig 23-12A
Risk factors for atherosclerosis
Modifiable risks Non-modifiable risks
Dyslipidaemia Increasing age
Male gender;
Hypertension
female after menopause
Obesity, sedentary lifestyle Family history of heart disease
Diabetes mellitus, insulin
Familial hyperlipidaemia (genetic)
resistance
Cigarette smoking Aboriginal and Torres Strait Islander
Inflammation
Stress 54
Dyslipidaemia
Abnormal amounts of lipids in the blood
High total cholesterol, high LDL, or low HDL
55
Hypertension
Consistent elevation of systemic arterial blood
pressure
Causes endothelial cell injury
56
Obesity, sedentary lifestyle
Obesity: contributes to dyslipidaemia and
altered fat metabolism
Abdominal fat decreases HDL and increases BP
57
Diabetes mellitus
Diabetes mellitus and insulin resistance:
characterised by hyperglycaemia
Cholesterol production is high during
hyperglycaemia
Hyperglycaemia: high blood glucose level
Hyperglycaemia causes:
Endothelial cell injury
Inflammation
58
Smoking
Nicotine stimulates release of adrenaline and
noradrenaline
Increases HR, vasoconstriction, and BP
59
Inflammation
Chronic inflammation contributes to heart
disease
60
Stress
Increases production of cortisol
Cortisol promotes dyslipidaemia and increases blood pressure
61
Fox, Human Physiology, 2010, 11th ed, Fig 13-32
Aboriginal and Torres Strait Islander
Higher prevalence of risk factors for heart disease
62
https://heartfoundation.org.au/images/uploads/publications/aust-cardiovascular-risk-charts.pdf,
63
Last accessed Jul 2016
Progression of atherosclerosis
1. Endothelial cell injury and inflammation
2. Fatty streak
3. Hard / Fibrous plaque
4. Soft / Complicated plaque
64
1. Endothelial cell injury and inflammation
Injured endothelial cells:
Allows LDL to enter the subendothelium
Macrophages enter the subendothelium,
enhancing the inflammatory response
Unable to mediate vasodilation
65
Craft & Gordon, Understanding Pathophysiology 2nd ed 2015, Fig 23-11A
Endothelial cells
Normal physiology: Pathophysiology:
Low levels of NO also promotes LDL entry into the vessel wall
66
2. Fatty streak
LDL in the subendothelium is engulfed by
macrophages
Macrophages become foam cells
67
Craft & Gordon, Understanding Pathophysiology 2nd ed 2015, Fig 23-11B
3. Fibrous / hard plaque
Macrophages release growth factors
Stimulate smooth muscle growth
Increased deposition of collagen
Loss of vasodilation
68
Craft & Gordon, Understanding Pathophysiology 2nd ed 2015, Fig 23-11C
4. Soft and Complicated plaques
Thrombosis formation of a
Soft plaque: prone to rupture blood clot
The surface promotes thrombosis
Thrombus unstable, perfusion restored
quickly
Platelets promote vasoconstriction
Complicated plaque: Soft plaque + thrombus
69
Craft & Gordon, Understanding Pathophysiology 2nd ed 2015, Fig 23-11D
Atherosclerosis
Soft plaque Fibrous / hard plaque
70
Damjanov, Pathophysiology, 2009, Fig 4-36
Consequences of atherosclerosis
Heart: chest pain, heart attack, death
Brain: stroke, death
Arms and legs: peripheral artery disease,
gangrene and amputation
Kidneys: kidney failure
Genitals: erectile dysfunction, vaginal dryness
71
Formation of an embolus
o Embolus travels
downstream and lodges
in a smaller diameter
vessel, blocking
perfusion to the organ
72
Gould, Pathophysiology for the Health Professions, 3rd edn, Fig 18-12e
Prevention and management
Addressing risk factors, including dietary
Decreasing saturated and trans fats
Increasing mono-, poly-unsaturated fats and dietary
fibre
Medications
Antiplatelets
Anticoagulants
Lipid lowering
ACE inhibitors, angiotensin II blockers
73