Human Biological Science 2 BIOL122: National Workshop Manual 2019

Human Biological Science 2
BIOL122
National Workshop Manual
2019
This document was prepared by past and present staff from the School of Science, ACU
Table of contents
Table of contents ........................................................................................................................................... 1

Workshop 1 – Pharmacological principles ...................................................................................................... 2
Workshop 2 – Pathophysiological principles / Anthropometry ..................................................................... 11
Workshop 3 – Infection control .................................................................................................................... 23
Workshop 4 – Haemodynamic derangements .............................................................................................. 29
Workshop 5 – Heart disease ........................................................................................................................ 36
Workshop 6 – Diabetes mellitus................................................................................................................... 44
Workshop 7 – Asthma and our immune system / In-class test ...................................................................... 52
Workshop 8 – Musculoskeletal disorders ..................................................................................................... 58
Workshop 9 – Mental illness ........................................................................................................................ 66
Workshop 10 – Cancer ................................................................................................................................ 73
 Page 1
Workshop 1 – Pharmacological principles
PRE-CLASS ACTIVITIES
Please complete the following before attending your allocated workshop class:
• Review last semester’s BIOL121 lecture ‘Principles of Pharmacology’. Available in week 1 class folder
on the BIOL122 LEO site
• Read pg. 189-202 in Bryant, B.J. & Knights, K.M. (2015) Pharmacology for health professionals, 4th
ed., Mosby/Elsevier, Chatswood, N.S.W. Chapter 9: Individual and lifespan aspects of drug therapy.
There is a link to this reading in the week 1 folder on LEO.
• Read pg. 203-214 in Bryant, B.J. & Knights, K.M. (2015) Pharmacology for health professionals, 4th
ed., Mosby/Elsevier, Chatswood, N.S.W. Chapter 10: Adverse drug reactions and drug interactions.
There is a link to this reading in the week 1 folder on LEO.
• Complete the activities below in the workbook and/or on LEO
1. Define the following terms:

Pharmacological term Definition
Pharmacokinetics
Pharmacodynamics
Absorption
Distribution
Metabolism
Excretion
Receptor
Ion channel
Carrier molecule
Enzyme
Bioavailability
Teratogen
Workshop 1 – Pharmacological principles  Page 2

2. The following question is designed to get you thinking about how your physiology changes as you age.
Circle the most appropriate response.
Liver enzyme activity of newborn baby Increased Decreased Same as healthy adult
Blood volume of heavily pregnant woman Increased Decreased Same as non-pregnant adult
Barrier function of skin in newborn baby Increased Decreased Same as healthy adult
Glomerular filtration rate of pregnant woman Increased Decreased Same as non-pregnant adult
Liver function of elderly person Increased Decreased Same as healthy adult
Renal function of elderly person Increased Decreased Same as health adult
Part A: Lifespan pharmacology

Lifespan pharmacology is important content in terms of Quality Use of Medicines (QUM). It is not presented
in lectures this semester, however, QUM is a learning outcome for this unit and therefore this topic is
assessable.
Physiological changes occur in our body systems as we age. These changes have a profound impact on how
drugs are absorbed, distributed, metabolised and excreted. As a consequence drug therapy in a pregnant
woman, infant, child and elderly person may differ from the adult population.
CASE SCENARIO ONE – A PREGNANT WOMAN

Nadia is a 29 year-old woman who is 17 weeks pregnant with her first child. Nadia works for a publishing
company and often sits working at her computer for long periods of time. She regularly develops ‘tension
headaches’ for which she takes a couple of 500 mg tablets of paracetamol. She decided to avoid taking
medications in the first trimester of her pregnancy but is happy to take ‘common medicines’ now that she is
in the second trimester.
1. Drug and complementary medicine use during pregnancy should be avoided or limited to those
women who absolutely require treatment. Explain why?

2. Nadia has decided that it is okay to take ‘common medicines’ now that she is in the second trimester
of pregnancy. Based on your reading for this class, explain why you agree or disagree with her.
3. Describe how pregnancy affects:

A. Drug absorption
B. Drug distribution
C. Drug metabolism
D. Drug excretion

Many drugs cross the placenta via simple diffusion and therefore the concentration of a drug in maternal
circulation can equal the concentration of a drug in fetal circulation. The fetus is therefore at risk of
pharmacological effects, adverse effects and teratogenic effects of the drug.
4. Why is the fetus at risk of the pharmacological effects, adverse effects and teratogenic effects of a
given drug?
5. Drugs consumed by breastfeeding women may also pass into breast milk. Why is it difficult to
determine how much drug a breastfeeding baby is consuming through breast milk?
CASE SCENARIO TWO – AN INFANT WITH A FEVER

Sam is a newborn (neonate) baby who has been irritable and hard to settle in the last 24 hours. His Mum,
Nadia, becomes increasingly concerned when Sam’s temperature starts to increase first to 38°C and then to
39.5°C in the space of a couple of hours. She rings her local maternal health nurse who recommends giving
baby Sam some paracetamol.
6. Discuss how pharmacokinetics changes differs for neonates under the following headings:
A. Absorption
B. Distribution

C. Metabolism
D. Excretion
7. Many drugs that are safe and effective for use in adults have not been tested for use in neonates and
children. Apart from ethical considerations, why else might this be problematic?
CASE SCENARIO THREE – AN ELDERLY WOMAN

Nadia is now 82-years old. She has generally experienced good health apart from being diagnosed with
osteoarthritis several years ago. One cold morning, Nadia goes outside to collect her mail and she slips over
and falls to the ground. In extreme pain, and unable to get up, she cries out for help. A passerby comes to
her aid and calls the ambulance. After initial assessment, the attending paramedics believe that she may
have broken her hip. She is transferred to an acute care hospital. Morphine is administered en route.
8. Discuss how pharmacokinetics changes in elderly people under the following headings:
A. Absorption
B. Distribution

C. Metabolism
D. Excretion
9. What is polypharmacy? Explain the effects of polypharmacy.
Part B: Adverse drug reaction (ADRs) and Drug interactions (DIs)

The pharmacology discussed in ADRs and DIs is important content in terms of Quality Use of Medicines
(QUM). It is not presented in lectures this semester, however, QUM is a learning outcome for this unit and
therefore this topic is assessable.
1. What is an adverse drug reaction (ADR)?

2. How does an adverse drug event (ADE) differ from an ADR?
3. There are four main types of ADRs. Describe each type and use examples to illustrate your answer.
4. Rose is a 78-year old woman who has had asthma since she was a teenager. Given your reading from
chapter 10 in Bryant and Knights (2015), explain why she is at risk of developing an ADR.

5. Drug X is a large molecule and is administered parenterally and frequently over a long period of time.
Given your reading from chapter 10 in Bryant and Knights (2015), explain why Drug X is likely to cause
an ADR.
6. What type of ADR are drug allergies?
7. How do drug allergies occur? Name two drugs that are known to drug allergies.
8. What is a drug interaction (DI)?

9. You are having a small mole removed from the skin on your arm. The dermatologist administers
lignocaine (a local anaesthetic) and adrenaline simultaneously via an injection to numb the area.
Adrenaline has numerous effects and in this instance it is administered to cause vasoconstriction.
Explain whether this reaction is a pharmacodynamics drug reaction or a pharmacokinetic drug
reaction.
10. How can you as a health professional minimise the incidence of ADRs and DIs?
Important instructions for next week’s workshop

• Avoid alcohol consumption for 24 hours before your workshop session
• It is also advisable not to eat/drink sugary drinks/exercise for 4 hours before this activity.
• Wear light clothing
Warning: You will not be able to participate in the activity next week if you are pregnant or have an
electric implant in your body

Workshop 2 – Pathophysiological principles / Anthropometry
• Please complete the following before attending your allocated workshop class:
• Read pg. 2-20 Bullock, S. & Hales, M. (2013). Principles of pathophysiology. Frenchs Forest, Australia.
Pearson. Chapter 1: Pathophysiological terminology, cellular adaption and injury.
1. Match the following terms with their correct definition:

Aetiology Anoxia Apoptosis Healing
Hypoxia Iatrogenic Idiopathic Infarction
Inflammation Ischemia Metaplasia Necrosis
Neoplasia Pathogenesis Pathology Risk factor
the study of disease
the cause of disease; why the disease arises
a disease/condition resulting from medical treatment or diagnostic procedures
an unknown cause
formation and progression of disease; how the disease progresses
when present, increases the likelihood of disease in the person, when absent/reduced,
lowers the likelihood of disease
cell death
programmed cell death
total lack of oxygen
decreased oxygen
reduction in blood supply/flow to an area
localised area of ischaemic necrosis
the body’s response to injury
the process of regeneration (replacing old/injured cells with new cells) or repair (laying
down collagen)
changing from one cell type into another (change in differentiation)
new growth; benign or malignant
Workshop 2 –Pathophysiological principles and Anthropometry  Page 11

Which of the following are examples of malnutrition? (tick correct boxes)
Protein deficiency
Toxicity due to excessive vitamin A
Obesity
Iron deficiency
2. Obesity is a metabolic disorder primarily induced and sustained by an over consumption or

underutilisation of calories. Which of the following are consequences of being overweight or obese?
(tick correct boxes)
Cancer Coronary heart disease Gallbladder disease
Hypertension Metabolic syndrome Osteoarthritis
Psychosocial problems Sleep apnoea Type II
3. Match the following fats with their respective descriptor below:

Essential fatty acids Fatty acids High density lipoprotein
Low density lipoprotein Monounsaturated Saturated
Trans fatty acids Polyunsaturated Triglycerides
Type of fat Descriptor
One double bond in the fatty acid chain; liquid at room temperature.
Two or more double bonds in the fatty acid chain; liquid at room temperature.
Fatty acid chain made up of single bonds; solid at room temperature; contribute
to heart disease by increasing LDLs.
Long hydrocarbon chain ‘capped’ by a carboxyl group (COOH) which makes the
molecules ‘acids’.
Type of polyunsaturated fat; either omega-3 FAs or omega-6 FAs; must be
obtained from our diet as body cannot make enough to supply its needs.
Industrially hardened fat created using heat and hydrogenation; behaves like
saturated fats and also impair how enzymes process essential fatty acids.
Contains a lot of cholesterol and not as much protein, and its role is to carry
cholesterol to all the body’s cells.
Contain lower amounts of cholesterol; it picks up unused cholesterol from the
bloodstream and artery walls and takes it back to the liver for storage or disposal.
Molecules that transport fat to the body’s cells.

4. Match the following foods with fat type that they contain.
Monounsaturated fat Omega-3 fatty acids Omega-6 fatty Saturated fat
Food Type of fat/lipid

Flax seeds, pumpkin seeds and walnuts, salmon, trout and tuna.
Corn oil, sunflower oil and soybean oil all contain them.
Butter, fat on/in meat
Olive oil
Part A: Pathophysiological principles

Pathology is the study of disease
The main pathological processes are:
1. Inflammatory disorders
2. Healing disorders
3. Immune
4. Infectious disorders
5. Fluid and haemodynamic derangements
6. Neoplasia
You will have lectures on each of these in more detail as the semester progresses.
Pathophysiology is the study of how our body responds to disease. We will use this term throughout the
semester and when we talk about the pathophysiology of a disease we follow a general framework.
General framework for discussing diseases

1. Underlying physiology - what happens normally in our body (so we will constantly be directing you
back to BIOL121 – you need a good understanding of how our body normally works before you can
examine a particular illness
2. Aetiology
3. Pathogenesis
4. Clinical manifestations

ACTIVITY ONE: CELL ADAPTATION AND INJURY
Our body’s cells are constantly exposed to a variety of stimuli in their environment. The stimuli are either
physiological (they help our body to maintain homeostasis) or pathological (disease processes). Cells
respond to these stimuli in a variety of ways depending on the:
• Cell type
• Type of stimulus
Cell types
Cells are generally categorised according to the following criteria:

• Labile cells – continually divide throughout life.
• Stable cells – low level of division (can undergo rapid division if stimulated by hormones or chemical
factors).
• Permanent cells – cannot undergo mitotic division in post-natal life.
Question
1. Give an example of a labile, stable and permanent cell based on the above definitions.
Type of stimulus
Cells respond to physiological stimuli such as hormones, chemical messages and increased or decreased
functional demands e.g. breast tissue enlarges during pregnancy. Cells also respond to pathological stimuli.
Question
2. Give some examples of pathological stimuli that can change cell structure and function.

Cell adaptation
Examine the flow diagram below from Kumar, V., Abbas, A.K., Aster, J.C. (2013) Robbins Basic Pathology (9th
ed.). Philadelphia, Elsevier. You will observe that when a cell is exposed to a stress/stimulus it either adapts
or becomes injured. Cells adapt via three main processes:
1. Hypertrophy – an increase in tissue/organ size due to an increase in cell size.
2. Atrophy – a decrease in tissue/organ size due to decrease in cell size.
3. Hyperplasia – an increase in tissue/organ size due to an increase in cell number.
Cell injury
Cell injury is a process that is either reversible or irreversible. Irreversible injury leads to cell death.
Picture below from: Kumar, V., Abbas, A.K., Aster, J.C. (2013) Robbins Basic Pathology (9th ed.). Philadelphia,
Elsevier

ACTVITY TWO: PHYSIOLOGICAL AND PATHOLOGICAL ADAPTATIONS 1
3. Figure 1a and 1b show a cross section of the myocardium.
A. In which Figure does the tissue look more “normal”; 1a or 1b? (Hint: look at the chamber size)
Justify your response.
B. Has the myocardial tissue in the abnormal figure undergone hypertrophy or hyperplasia? (Hint:
think of the cell type, page 27) Discuss.
C. Name a physiological stimulus that may have caused this adaptive change in myocardial cells.
D. Name a pathological stimulus that may have caused this adaptive change in myocardial cells.
E. What do you think happens when myocardial cells are injured?
F. What effect would scar tissue have in the heart?

ACTIVITY THREE: PHYSIOLOGICAL AND PATHOLOGICAL ADAPTATIONS 2
4. Figure 2a and 2b show a photograph of the brain.
A. In which Figure does the brain tissue look more “normal”; 2a or 2b? (Hint: look at the surface area)
Justify your response.
B. What has happened to the tissue in the abnormal figure?
C. Name a physiological stimulus that may have caused this adaptive change in neural cells.
D. Name a pathological stimulus that may have caused this adaptive change in neural cells.
ACTIVITY FOUR: PHYSIOLOGICAL AND PATHOLOGICAL ADAPTATIONS 3

5. Figure 3a and 3b show a histological section of the endometrial glands following the menses phase of
the menstrual cycle.
A. What are the differences between the tissues shown in Figure 3a in comparison to that of Figure
3b?
B. What physiological stimulus may have caused this?
C. Figure 3c shows a picture of a normal uterus (on the left) and a uterus from a recently pregnant
woman (on the right). Is this a physiological adaptation or a pathological adaption?
D. Is the adaptive change (in Figure 3c) best described as hypertrophy, hyperplasia or both?

Part B: Anthropometry
Important instructions to students
• Avoid alcohol consumption for 24 hours before your lab session

• It is also advisable not to eat/drink/exercise for 4 hours before this activity
• All measurements are to be taken with light clothing and your body in the anatomical position
• Wipe the scales and skin callipers with alcohol after each person’s measurement.
What is anthropometry?
“Anthropo” = human and “metron” = measurement

ANTHROPOMETRY is the science of measuring the human body as to height, weight and size of component
parts to study and compare the relative proportions under normal and abnormal conditions (Harris, Nagy, &
Vardaxis, 2006) 1.
Obesity and being overweight are conditions of excess body fat that cause significant burdens of ill health,
economic costs and mortality to the Australian community. There has been an increase in the number of
people who are overweight or obese in Australia and other nations. Apart from genetic factors, being
overweight or obese are caused by an energy imbalance, where a person’s energy intake exceeds energy
expenditure over a considerable period of time. This means when energy consumed is greater than
expended, weight increases and when energy consumed is less than expended, weight decreases.
Most researchers agree that the human body requires a certain amount of fat for good health. Fat helps
regulate body temperature, store energy, and cushion and insulate organs. The percentage of body weight
that makes up this "essential fat" is around 4% of body weight for men and 10% for women. Beyond that,
there's a somewhat wide range (15-18% in men and 20-25% in women) of what is considered a healthy
percentage of body fat.
1. List some of the common anthropometric measurements. Explain why there are different
anthropometric methods.

ACTIVITY FIVE: CALCULATE YOUR BMI
NB: you may prefer to do these measurements and calculations at home or not at all…that is perfectly fine,
as the measurement activities (5-7) are not compulsory. Please still attend the class, and participate as you
feel able.
BMI is the international standard for assessing body size in adults. Evidence shows that high BMI (obesity
level) is associated with metabolic syndrome, type II diabetes and high risk of cardiovascular morbidity and
mortality.
BMI formula = weight (kilograms)

height (meters2)
Body Mass Index
Classification Cut off points (kg/m2)
Underweight <18.5
Normal range 18.5 - 24.9
Overweight 25.0 - 29.9
Obese >30.0
Obese Class I 30.0 - 34.9
Obese Class II 35.0 - 39.9
Obese Class II >40.0
Adapted from WHO 2004
A. Weigh yourself to the nearest 0.1 kg with the bathroom (Bioimpedance) scales provided on level
flooring. My weight = kg
B. Use the tape and ruler to measure your height accurately to the nearest 0.1 cm in the anatomical
position. My height = m
C. My BMI = your weight in kg / height (m) x height (m) = kg/m2
2. What are the limitations of the BMI measurement?

https://www.healthdirect.gov.au/body-mass-index-bmi-and-waist-circumference

Body fat and its distribution
Upper-body fat is more common in men and lower body fat is more common
in women.
3. Explain why abdominal obesity is harmful.
Waist circumference (WC) provides a simple and practical diagnosis of intra abdominal adiposity (IAA) in
patients at elevated CV risk.
Waist Circumference is an indicator of fat distribution and abdominal fat:
≥ 80 cm is considered risk and ≥ 88 cm is high risk for women.
≥ 94 cm is considered risk and ≥ 102 cm is high risk for men.
Waist to Hip Ratio (WHR) is used to measure central obesity

Central obesity = Waist (cm)
Hip (cm)
Waist to Hip Ratio (WHR)

Category Men Women
Normal 1.0 0.9
Obesity & related diseases >1.0 >0.9
ACTIVITY SIX: CALCULATE WAIST-TO-HIP RATIO (WHR)

Work in pairs to measure each other. Use the tape measures with the zero end below the actual
measurement to measure waist and hip circumferences correctly to the nearest 0.1 cm. Breathe out
NORMALLY and keep your abdominal muscles relaxed. Measure the narrowest part of the abdomen (waist)
just below the ribcage and the widest part (hip) from one side (see image below). The tape should be parallel
to the floor and in close contact with the skin without compressing it, or over a thin layer of clothing.
A. My waist = cm
B. My hip = cm
C. My WHR = waist ÷ hip =

4. Are you an ‘apple’ or a ‘pear’? Why does it matter?
ACTIVITY SEVEN: ASSESS YOUR BODY COMPOSITION

Bioelectrical impedance (BI) is a measurement based on the electrical conductivity of fat and fat-free mass.
This instrument measures the impedance of an electrical current passed through the body which allows for
the calculation of various body volumes e.g. fat, bone, water. This technique is sensitive to the position of
the electrodes on the body, hydration status, and consumption of certain food and drink.
Warning: Please do not do this activity if you are pregnant or have an electric implant in your body.
The balance we are using has built-in electrodes and works best if you are bare-footed. You will need to
convert your percentage (fat, water, bone) to get your component weight.
A. Body weight: kg
B. Body Fat %: and Fat weight: kg
C. Bone mass % and Bone weight: kg
D. Body water %: and Body water weight: kg
Total body mass= fat mass + fat-free mass
Fat-free mass (lean body weight) = water + bone + muscle
E. Calculate your lean body weight (fat-free mass) from the information above.
My Lean Body Weight = Body weight - Fat weight kg
F. Calculate your muscle weight from the information above.
My Muscle Mass = (Lean body weight – (water + bone) kg
5. Check the manual for normal ranges of body fat and body water and explain your body composition.

6. Your sister, who is of normal weight, is concerned that she’s putting on weight, but her friend tells her
not to worry, as “it’s only a little bit…just an increase of 10%”. What may be some of the
consequences of this modest weight gain in such a person?
ACTIVITY EIGHT: RISK FACTORS

7. Work in groups to compile a list of risk factors for obesity. Use examples to support your answers
where possible.
8. Work is groups to compile a list of ways that reduce risk of being overweight/obese. Use examples to
support your answers where possible.
For those of you that are interested in finding out more about this topic, the link below is to a segment
entitled ‘Why am I still fat’; an episode on Catalyst (ABC production). The story looks at the relationships
between obesity and diet research, lap-band surgery and effects of BPA plastics. The content of this video
will not be assessed in this unit.
http://www.abc.net.au/catalyst/stories/4327346.htm

Workshop 3 – Infection control
1. Match the following terms with their correct definition.

Nosocomial infection Opportunistic infection Pathogenicity Virulence
Term Definition
A microorganism has taken advantage of host as there is either a lack of
competition from other microbes, reduced numbers of WBCs or it has
breached body defences
Hospital-acquired infection
Degree of pathogenicity
Ability to cause disease
2. Read the following before attending the workshop class

STEPS IN INFECTIOUS DISEASE
The body (the host) is generally well-equipped to avoid infection or to overcome an infection should one
occur, but obviously it is not always successful.
Infections follow this pattern (agent = the microbe, host = the person):
1. Encounter - agent meets host
2. Entry - agent enters host
3. Spread - agent spreads from site of entry
4. Multiplication - agent multiplies in host
5. Damage – damage is caused by the agent or the host response or both
6. Outcome - one or the other wins, or they learn to co-exist
Successful infection requires breaching of host defences; the microbe must either invade the host tissue or
produce a toxin that causes damage or interfere with the normal function of tissues or organs. What
distinguishes one microbe from another is the manner in which each triggers and fights the host’s defences;
to understand infection control it is essential that we understand how immunity works and what can affect
it.
It is important to understand that pathogenicity is the ability to cause disease and virulence is the degree of
pathogenicity.
Knowing where a microbe lives (its source or reservoir) and how it prefers to travel helps us to know how it
may enter and leave the body (its portal of entry and portal of exit, respectively). We are then better
equipped to protect ourselves and our patients.
For a disease to occur, five factors must occur simultaneously:

• a pathogen must be present
• it must have sufficient virulence
• the dose acquired must be large enough
• a portal of entry must be available
• the host must be susceptible
Workshop 3 – Infection control  Page 23

If any of these factors can be overcome, infection can be prevented. Infection control requires breaking the
chain of infection.
3. Before the workshop, complete the learning activities on LEO. You will need this information for the
activity in class.
ACTIVITY ONE: INFECTION CONTROL SUPER-QUIZ - “LAST PERSON STANDING”

This activity will allow you to evaluate your own knowledge of infection control, with a prize for the ‘winner’.
1. Completing the LEO activities will increase your chance of success.
2. Your tutor will show you a series of questions related to prevention and control of infection; those
who answer incorrectly will leave the game… the winner is “the last person standing”.
3. At the end of the series, we will review the questions, so please note down any that confused you, or
where you still cannot see why you were wrong.

ACTIVITY TWO: “THE DIRTY DOZEN” - IDENTIFICATION OF POTENTIAL RISKS
4. In groups use the image provided to identify twelve infection risks.
5. Write the risks that the students identify on the board.
6. For each, explain WHY it is a risk, and what, if any, alternative there may be.

ACTIVITY THREE: WHAT HAPPENS IN REAL (PROFESSIONAL) LIFE?
Infection control principles
At an inter-disciplinary professional development seminar, you meet a group of nurses working on a medical
ward. Two people in the ward have developed an infectious intestinal illness that is resistant to many
antibiotics: one is symptomatic and is being cared for in an isolation room in line with the hospital’s infection
control policy. The other has a sub-clinical case of the infection, and the nurses are debating whether this
woman should also be cared for in the same way. Some say that because she shows no symptoms, it is not
necessary to take any precautions as she is not going to be able to infect others.
7. Do you agree with them? Explain why or why not.
8. Explain to the group of nurses what ‘universal precautions’ (or an equivalent term) means and why it
is important that our practices obey these precautions.
Infection control in surgical settings

While many of us may never work in an operating theatre, we all know people who have had or will have
surgery – this includes ourselves. Also, many healthcare workers will care for people before or after surgery,
so it is important that we are aware of the practices that will reduce the chances of infection, to staff as well
as patients.
For each of the following, explain why this practice is necessary and how it would be carried out; i.e. what is
involved (remember to think of the staff as well as the patient).
9. Surgical attire/PPE (personal protective equipment)
A. Does it need to be fluid resistant? Why?
B. Why should a gown be changed after each case, if it is not dirty?

C. Are uncovered cloth shoes (e.g. runners) permitted? Why?
D. Is it good practice to wear long sleeves (i.e. your ordinary clothes) under surgical scrubs? Why?
E. Why are surgical masks used?
F. Should staff who are not directly involved in the surgery also wear PPE? Why?
10. Skin asepsis

A. Why is it necessary for staff to wash their hands for the appropriate length of time and with an
appropriate agent?
B. Is it necessary for the patient’s skin to be treated as well? Why?
11. Maintaining a sterile field is essential.

A. What is a sterile field?
B. Why is it necessary?
C. Unnecessary movement in the theatre should be avoided. Why?

Back in the ward
An audit of post-surgical wound infections has taken place in 2 wards in your hospital. The usual (and
acceptable) infection rate for this type of surgery in this hospital is 10%.
Ward 1 has 20 patients; there were 5 wound infections recorded during the period, all of them are in-
patients whose surgery was performed by one surgical team (team A). The same organism was the cause of
infection in all patients.
Ward 2, with 30 patients, had 3 infections over the same period; these patients had been operated on by a
different team (team B). The 3 patients each had a different microbe infecting the wound.
The wards are both under investigation and the Infection Control team is trying to establish the source of the
infection and the procedures/personnel in both the theatres and the wards.
12. Does either of these wards have a higher than acceptable rate of infection? If so, which one?
13. What do you think may be the likely source of infection for Ward 1? Explain.
14. Is the source likely to be the same for Ward 2? Explain.
15. Many post-surgical infections – in the wound, the respiratory tract and the urinary tract – are due to
the patient’s own normal flora (opportunistic infection). Explain why opportunistic infections occur
and what infection control practices can reduce the risk.

Workshop 4 – Haemodynamic derangements
• Bullock, S. & Hales, M. (2013). Principles of pathophysiology. Frenchs Forest, Australia. Pearson.
Chapter 29: Fluid imbalances pg. 718 - 728.
Chapter 21: Ischaemic heart disease pg. 474-483.

Arteriosclerosis Atheroma Atherosclerosis Embolism
Embolus Thrombosis Thrombus
Detached thrombus (>99%), fat or air bubbles that travels in the bloodstream
A type of arteriosclerosis; formation of fibrofatty plaques in the walls of arteries
A fibrinous blood clot that has formed in an uninterrupted cardiovascular system
The thickening, hardening and loss of elasticity of blood vessel walls
The lodging of an embolus; can cause partial or total blockage of affected blood vessel
Process of forming a thrombus
Fibrofatty plaque
2. Differentiate between diffusion and osmosis.
3. Fill in the table below. Note; ECF = extracellular fluid, ICF = intracellular fluid
Body fluid Definition of body fluid Is this part of the Approximate
ECF or ICF? volume (L)
Plasma
Interstitial fluid
Workshop 4 –Haemodynamic derangements  Page 29

Part A: Atherosclerosis
Atherosclerosis significantly contributes to both morbidity and
mortality in Australia. The inner layer of artery walls (the tunica
intima, made of endothelial cells) allows blood to flow easily
through the artery. During atherosclerosis fatty deposits
accumulate in arterial walls over time.
Atherosclerosis starts to occur for many years without symptoms

but eventually leads to serious health problems. Most commonly a www.bhf.org.au
fatty plaque will rupture, causing the formation of a thrombus that rapidly limits or stops the blood flow to
organs, leading to the death of tissue. A thrombus that forms in a coronary artery may cause a heart attack.
A thrombus that forms in an artery to that supplies the brain may cause a stroke.
Atherosclerosis is the common cause of heart attacks, strokes, and peripheral vascular disease – together
these are known as "cardiovascular disease." Atherosclerosis is usually not detected until the disease is in an
advanced state. In some cases the first symptom is an anginal pain, heart attack or stroke.
NOW IT IS TIME TO BUILD YOUR OWN ATHEROSCLEROTIC PLAQUE

 Endothelial cells
 Erythrocytes
 Smooth muscle cells
 Monocytes
 Fibrin strands
 Platelets (thrombocytes)
 Collagen
 Low-density lipoproteins (LDLs)
Set up your board
I. Use the white board marker to label the tunica intima, tunica media and tunica externa on the right
of the page
II. Place the endothelial cells on the board, lining the intima. Note: this endothelial layer will need to be
moved frequently throughout
III. Place the smooth muscle cells onto the media. Note that there are already some smooth muscle
cells in the intimal layer
IV. Place the LDLs in the lumen of the vessel
V. Place 2 collagen strands in the intima
Prepare some ‘components’
VI. Take one colour of Play-doh® and make five 3 cm balls to be monocytes.
VII. Take the second Play-doh® colour and make ten 1 cm balls of thrombocytes.

VIII. Place monocytes, erythrocytes, and thrombocytes in the lumen of the blood vessel
IX. Leave your fibrin strands off the board at this stage
X. Place two collagen strands in the intima and leave the rest off the board at this stage
Process
As a result of shear stress to the endothelial cells (from hypertension or other factors), LDLs begin to move
out of the blood vessel lumen and into the tunica intima.
XI. Move the LDLs to the intima (between the endothelial cells and the basement membrane). You will
need to start making room so push the endothelial cells (away from the basement membrane so
that they begin to encroach into the vessel lumen)
The LDLs become oxidised and release a chemotactic agent which encourages monocytes to come to the
area.
XII. Move the monocytes from the lumen of the blood vessel to the intima (they become
“macrophages”)
The macrophages consume the oxidised LDLs and turn into “foam cells”
XIII. Place the LDLs inside the macrophages (flatten out the foam cell so now it is more 2 dimensional).
Fill the subendothelial area with these foam cells
The macrophages release chemicals which cause smooth muscle cell proliferation into the intima.
XIV. Place all of the smooth muscle cells from the tunica media and put them into the intima (just
underneath the endothelial cells).
XV. Fibroblasts (not demonstrated) produce collagen. Put the remaining collagen up in the intimal area.
This is called a “fibrous cap”
The fibrous cap hardens and can rupture.

XVI. Lift a couple of the endothelial cells up. Blood can now come into contact with non-endothelial
surfaces. This exposes blood to collagen and sets up a clotting cascade.
XVII. Bring the platelets down to the rupture. This is called platelet aggregation
XVIII. Bring the red blood cells down to the rupture. Form these cells into a mound on top of the
endothelium around the ruptured cap. Notice that this is occluding the lumen of the blood vessel
even further
XIX. Bring the fibrin strands onto the board and drape them across this haematoma. When the fibrin
strands develop the structure can now be called a ‘clot’
The lipid core can become necrotic.

• If the foam cells die and the smooth muscle cells at the centre of the plaque die this is called a
‘necrotic core’

1. List risk factors for atherosclerosis (ATH).
2. Explain why ATH causes hypertension, angina pectoris, myocardial infarction and stroke.
3. Explain why ‘statins’ are prescribed for people at risk of coronary artery disease.
4. Endothelial injury (and the subsequent development of ATH) is a major cause of thrombosis. What
are the other two major factors that cause thrombus formation? Explain how each of these contribute
to thrombus formation.
5. Discuss what is likely to happen to a thrombus after it has formed.
6. If a thrombus were to dislodge from a deep leg vein, where would it end up?

7. Compare and contrast the following groups of drugs that affect blood coagulation.
Drug group Pharmacological effect Adverse effect Example of drug

Anti-coagulants
Anti-platelets
Fibrinolytics
(Thrombolytics)
Part B: Oedema
1. Capillaries perform the ultimate function of the cardiovascular system – the exchange of gases,
nutrients and wastes. List some substances that are exchanged across the capillary wall (some text
books call the capillary wall the capillary membrane).
2. Many nutrients and wastes cross the capillary wall via diffusion. Another completely distinct process
takes place across the capillary wall as well. What is this process called?
3. Explain why the interstitial fluid can provide and receive fluid from plasma (and vice versa).
4. Are there any substances that do not pass from the capillary to the interstitial fluid? If so, what are
they? Where are they produced? Why don’t these substances cross the capillary wall?

5. Name the four forces that exist across the capillary wall. Draw your OWN diagram of the four forces
that exist across the capillary wall.
6. Describe the events that normally occur at the arteriole-end of a capillary.
7. Describe the events that normally occur at the venule end of a capillary.

8. What happens to any excess fluid that is not absorbed back into the capillary?
9. Explain why distribution of the ECF is vital for homeostasis?
10. Explain how the distribution of the ECF changes when there is significant blood loss.
11. Explain what oedema is.
12. Explain why oedema occurs in the following scenarios:

A. Injury
B. Heart failure
C. Cirrhosis of the liver
D. Lymphatic obstruction

Workshop 5 – Heart disease
Chapter 24: Circulatory shock and vascular disorders pg. 547-554.
• Review the renin-angiotensin-aldosterone system (RAAS) (BIOL121 lecture 26 Renal regulation)
1. In relation to the blood pressure, link a variable from Column A with its best match in Column B.
Column A Column B
Systolic pressure Increased heart rate; increased force of cardiac contraction;
vasoconstriction
Diastolic pressure Cardiac output multiplied by total peripheral resistance; DP + 1/3 (SP –DP)
Mean arterial pressure Determined by vessel length, vessel width and viscosity of blood
Increased sympathetic NS Heart rate multiplied by stroke volume

activity
Increased parasympathetic Peak arterial pressure during ventricular systole/ contraction
NS activity
Cardiac output Decreased heart rate
Total peripheral resistance Minimum arterial pressure during diastole/ relaxation
Refer to your week 9 BIOL121 notes to help you answer the following 5 questions
2. Which of the following triggers the release of renin?

A. ACE (angiotensin converting enzyme)
B. Decreased blood pressure
C. Angiotensin II
D. Increased blood pressure
3. Renin converts:
A. Angiotensin I to angiotensin II
B. Aldosterone to angiotensin II
C. Angiotensinogen to angiotensin I
D. ACE to angiotensin I
Workshop 5 – Heart disease  Page 36

4. ACE converts:
A. Angiotensin I to angiotensin II
B. Aldosterone to angiotensin II
C. Angiotensinogen to angiotensin I
D. ACE to angiotensin I
5. Which of the following are actions of angiotensin II?

A. Vasodilation
B. Vasoconstriction
C. Increased heart rate
D. Decreased heart rate
6. Which of the following hormonal changes occur when angiotensin II levels increase?
A. Aldosterone increases sodium retention
B. Aldosterone decreases blood pressure
C. Antidiuretic hormone decreases fluid retention
D. Antidiuretic hormone decreases blood pressure
Part A: Hypertension
1. What is ‘hypertension’? What blood pressure readings would lead to someone being diagnosed with
hypertension?
2. Why is hypertension often not diagnosed?
3. Describe the differences between primary hypertension, secondary hypertension and pre-eclampsia.
4. Explain why obesity increases your risk of hypertension. Name 5 other risk factors for hypertension.

overactive RAAS
overactive sympathetic nervous system activity
increased angiotensin I
increased fluid
retention
5. Fill in the rectangular boxes in the flow
diagram by using the following words:
a. increased aldosterone
b. increased HR; increased peripheral resistance
c. increased angiotensin II
d. increased release of noradrenaline
HYPERTENSION
e. increased blood volume
f. vasoconstriction

6. Discuss why the following medications are indicated for hypertension by referring to their
pharmacodynamics and pharmacological effects.
A. ACE inhibitors
Pharmacodynamics
Pharmacological effects
B. Angiotensin II antagonists
Pharmacodynamics
C. Beta blockers
Pharmacodynamics
7. Complete the figure on page 38 above by adding the following terms to the correct CIRCULAR shapes.
• ACE inhibitors
• Angiotensin II receptor antagonists
• Beta antagonists
8. Explain why hypertension can cause the following:

A. Atherosclerosis

B. Cardiac hypertrophy
C. Cerebral hemorrhage (type of stroke)
9. Suggest three non-pharmacological approaches in managing hypertension and explain why each help
to lower blood pressure.
Part B: CAD case study

Gary Jones is a 58-year-old Australian-born male. During the last few weeks he notices that he has become
more short of breath than usual when walking to the shops to buy his daily packet of cigarettes. He also
experiences sensations of pressure and tightness [sometimes accompanied by chest pain] when he has to
walk briskly to catch the train. Gary thinks to himself ‘I should probably go to the doctor’ but convinces
himself ‘it’s probably nothing’.
Other relevant information

Family history Father died 62 years of age from a heart attack. Mother still alive and has
type II diabetes mellitus. One sibling; reasonably healthy
Occupation IT specialist
Diet Reasonably balanced.
Alcohol intake 2-3 glasses of wine per night with dinner.
Smoker Has smoked since he was 19 years old; smoked a couple of packets/week
when he was 20-40 years old; quit for 2 years; and then started smoking
roughly a packet/day again since.
Exercise Walks occasionally.
Previous illness/surgery Nil.
Current medications Nil.
1. Do you think Gary should visit his doctor? Explain why or why not.

2. Is Gary at risk of coronary artery disease (CAD)? What are the risk factors of CAD?
CASE STUDY CONTINUED

One day whilst Gary was walking up the stairs in his house he felt a dull, aching pain coming from the left-
side of his chest. The pain also seemed to be radiating down the left-side of his neck. It really hurt. Gary
wondered what was wrong. He hadn’t played sport since he was a teenager, so why would his neck be sore?
Gary called out to his wife, Lucinda, and told her the he had bad pain is his chest and neck. Lucinda called an
ambulance. After arrival at the Emergency department, a team of health professionals speculated that Gary
had coronary artery disease (CAD).
3. Discuss the aetiology of coronary artery disease?
4. What advice would you give Gary to reduce his risk of cardiovascular disease?
5. Explain why atheromas accumulate in arteries.

6. Explain what caused Gary’s chest and neck pain. Explain why it subsided.

A few months later Gary and Lucinda went on holidays. They decided to spend a few weeks in tropical north
Queensland relaxing by the coast. Gary had been feeling reasonably well since his time in hospital, apart
from the occasional bout of angina, which was relieved with glyceryl trinitrate (GTN). He had also cut his
smoking down to 3 cigarettes per day. At around 10 am on Tuesday, Gary and Lucinda hired some bikes and
rode to the top of the headland overlooking the coast. When they were nearly at the top roughly 2 hours
later, Gary experienced severe, crushing chest pain. He clambered off his bike and thought that he was going
to pass out. Lucinda helped him to the ground and called an ambulance with her mobile phone. The
Paramedics arrived and determined the following:
Information from Paramedics

General appearance Distressed, overweight, sweaty, in pain (9 out of 10)
Blood pressure 127/90 mm Hg
Heart rate 88 bpm
Auscultation Chest clear
Respiration rate 24/min
Paramedic action
Oxygen administration 40% via a facial mask
GTN 1 tablet sublingually
IV cannula Inserted
Morphine 7.5 mg IV
7. What do you think has happened to Gary? Describe the main pathogenic mechanisms of this event.

8. The symptoms of a heart attack vary from person to person. Describe some of these variations.
9. Explain why Gary was administered (GTN).
10. Does GTN have any direct effect on the coronary vasculature? Explain your response.
11. Explain why GTN is administered sublingually by referring to its pharmacokinetics properties.
12. List two other categories of drugs which are used in the management of angina/myocardial ischemia.
Explain briefly the mechanism of action of drugs of each of these categories.

Workshop 6 – Diabetes mellitus
Pre class work: Please read the following before attending this tutorial class
• Diabetes Australia website: http://www.diabetesaustralia.com.au/
Chapter 19: Diabetes mellitus pg. 418-439.
• Bryant, B.J. & Knights, K.M. (2015) Pharmacology for health professionals, 4th ed., Mosby/Elsevier,
Chatswood, N.S.W. Chapter 36: The endocrine pancreas and Management of Diabetes Mellitus pp.
765-778.
1. Compare and contrast type I and type II diabetes mellitus by using the list of variables to fill in the
table below.
autoimmune disease early age onset (< 20 years) gradual and asymptomatic
high risk of ketoacidosis mature age onset (> 53 years) sudden and symptomatic
ketoacidosis is rare strong family history low-normal-high insulin levels
often obese require insulin for survival low/no plasma insulin
usually non-obese usually managed by diet, exercise, oral hypoglycaemics (may
progress to requiring insulin)
Type I DM Type II DM
Part A: Complications of diabetes mellitus

CASE STUDY
Marcus is an 18 year-old university student whom after 4 weeks of classes feels very tired. He initially
attributed this to increased alcohol consumption and too many late nights, but his tiredness persisted, even
when he went to bed early and didn’t drink. He also noticed that he needed to urinate more frequently
during the day and night (sometimes 8 times a night) and that he was increasingly thirsty. He would regularly
go to bed with a big glass of cordial to quench his thirst. His clothes were also too big for him. Marcus went
to the University’s health centre and the following was noted:
Workshop 6 – Diabetes mellitus  Page 44

Assessment/Examination Results
Blood pressure 118/76 mm Hg
Pulse rate 83 bpm
Respiration rate 29 breaths/min (deep and rapid)
Appearance Red and dry skin
Breath Sweet, fruity odour
Height 1.75 m
Weight 60 kg
Urine dipstick test – glucose +++
Urine dipstick test – ketones ++
1. Glucose is normally reabsorbed by the kidney. Explain why people with diabetes might have glucose in
their urine.
2. Marcus has glucose in his urine. What is the difference between the glucose transporters in nephrons
and GLUTs?
3. Explain why Marcus urinates frequently.
4. What are ketones and how are they normally formed? Explain why their levels rise in plasma and
urine?

Marcus was admitted to hospital for monitoring and was not allowed to eat anything so his fasting plasma
glucose levels could be measured. He developed an infection in hospital. His blood test results are shown
below:
Assessment/Examination Results
Plasma glucose (fasting) 22 mmol/L
Plasma insulin < 5 mU/L
Hb1Ac 9%
5. Are Marcus’s fasting plasma glucose levels normal? What are normal fasting blood glucose levels?
6. Describe how insulin normally decreases blood glucose levels including the role of glucose
transporters.
7. Sometimes diabetes mellitus is referred to as ‘starvation in the midst of plenty’. Explain why?
8. Diabetic ketoacidosis is an acute complication of diabetes mellitus. What is it?
9. Which type of diabetes mellitus (DM) does diabetic ketoacidosis (DKA) commonly occur in?
10. Explain why DKA is more likely to occur in people with type I DM.

11. What are some other acute complications of DM?
12. Describe some chronic complications of DM that Marcus is at risk of developing in the future.
13. Explain how chronic hyperglycaemia leads to CV disease.
14. Explain how chronic hyperglycaemia leads to peripheral neuropathy.
15. Explain why Marcus is more susceptible to infection, and why it takes longer to clear an infection.

Part B: Control of diabetes mellitus
1. Explain why it is important for Marcus to regularly test his blood glucose levels (BGLs).
2. What do you think happens to Marcus’ BGLs when he is stressed? Explain why this occurs.
3. The HBA1c is used to diagnose diabetes mellitus and to monitor blood glucose levels. Explain what
specifically this test measures and why it is a very good indicator of long-term blood glucose control.
4. Exogenous insulin is commonly indicated in type 1 diabetes mellitus but not type 2 diabetes mellitus.
True or false? Discuss.
5. Explain why Marcus administers insulin via a subcutaneous injection rather than orally. (Think back to
your pharmacokinetics lecture in week 1 – factors that affect drug absorption).

6. Explain why insulin absorption either increases or decreases in the following scenarios:
A. Injecting into an exercised area such as the thigh
B. Smoking
C. A high body temperature caused by a hot bath/shower/spa/sauna/hot water bottle
D. Scarring/using same injection site
E. Massaging the area around the injection site
F. Injecting cold insulin immediately after taking from the fridge
G. Giving an IM injection as opposed to a SC injection
7. Where are common subcutaneous injection sites for insulin?
8. Insulin is formulated in a number of ways such as short-acting and long-acting insulins. Explain why
there are number of different formulations.

9. What are the differences between these formulations?
10. Which of these formulations is best administered half an hour before a meal?
11. The following table provides instructions for administering insulin. In the ‘Rationale’ column explain
why these instructions are stipulated.
INSTRUCTIONS FOR ASDMINSTRATION OF RATIONALE

INSULIN
Vials
- store away from heat and sunlight
- check clarity of vial solution
Needles
- inject at 90° into subcutaneous tissue
Syringes
- use only insulin syringes for injection
Check insulin requirements when patient is:

1) Sick
2)Pregnant
3)Experiencing developmental changes

e.g. approaching adolescence or adulthood
Check BSL, Urinalysis

12. There are a number of types or oral hypoglycaemic drugs. Match each drug group with its mechanism
of action (some drug groups may have more than one action).
Biguanides Glitazones Glucosidase inhibitors Sulphonylureas
Drug group Mechanism of action
Inhibits hepatic synthesis of glucose
Stimulates insulin release from pancreas
Slows glucose absorption in gut
Improves insulin sensitivity
13. Marcus decides to go out with his friends. He drinks two beers and an hour later experiences blurred
vision, confusion, drowsiness and shakiness. One of his friends notices that he is slumped over in a
chair somewhat unresponsive. His friend calls 000. What is Marcus experiencing? What is the effect of
alcohol on BGLs?
14. Discuss the treatment for someone who is experiencing mild to moderate hypoglycaemia.
15. Describe the actions of glucagon and explain why it was administered to Marcus. Refer to the route of
administration in your answer.

Workshop 7 – Asthma and our immune system / In-class test
Term Definition
Hypersensitivity reaction Antigen that causes type 1 hypersensitivity reactions
Inflammation Constriction of bronchioles
Antibody Immune system ‘over-reacts’ after exposure with an antigen (a
trigger)
Allergen Limitation of airflow due to increased resistance caused by partial or
complete obstruction
Bronchoconstriction Reduced expansion of lungs accompanied by decreased total lung
capacity
Obstructive airway disease A protein produced by WBC in response to the presence of a
harmful substance.
Restrictive airway disease Body’s response to injury
Part A: Type I Hypersensitivity reaction

The first time an allergen enters the body there is no reaction…but an antibody is created. Next time that
antigen enters the body the antibodies can respond quickly. One of the antibodies made is IgE, this
antibody’s job is to bind to a mast cell or a basophil (these are two of the granular leukocytes). It will now
stay there and it cannot be removed; although it is inactive until it is required. Mast cells and basophils are
very similar, but mast cells are ‘fixed’ in tissues while basophils are move freely in the blood.
The mast cell (or basophil) is now ‘primed’ or ‘sensitised’ by IgE, so that if it comes into contact with the
antigen that IgE is made to fight, it can respond instantly by ‘degranulating’ or blowing apart and releasing
the chemicals that are contained in its granules e.g. histamines.
One of the main chemicals is histamine, which is a potent mediator of inflammation (i.e. it is very good at
producing an inflammatory reaction): this reaction begins very soon after the antigen is encountered, peaks
at 15 minutes, and is usually finished within an hour. This response is a normal one, however in some
people, certain antigens cause the immune system to overreact and so the response is much bigger than
necessary.
Remember that antigens enter the body through portals of entry; it makes sense for the body to concentrate
its defence in those areas, and so the nasal membranes, skin, tongue, airways in lungs and GI tract contain
many mast cells. Leukotrienes are other inflammatory mediators released by mast cells.
An allergic or atopic response occurs when the body over-reacts to an antigen by releasing far more
histamine and other mediators than necessary. The antigen that triggers this is called an allergen. Atopy is a
genetic predisposition to type 1 hypersensitivity reaction, and there is a 50% chance of a child being affected
if one parent is affected and a 75% chance if both are. About 5-10% of the population, when exposed to
Practical 7 – Asthma and our immune system  Page 52

airborne allergens, becomes sensitised. Asthma, eczema, hay fever and hives (urticaria) are all type 1
hypersensitivity reactions.
In some people, the response occurs throughout the respiratory tract, and may lead to anaphylaxis; in
others, it is localised in the bronchus, and this results in allergic (extrinsic) asthma.
Questions
Your friend Harry has been diagnosed with allergic asthma, and at lunchtime today, he suffered a severe
attack. He thinks that it is due to your cat’s hair and you feel bad because he visited your house last night.
1. Why is type 1 hypersensitivity known as “immediate hypersensitivity”?
2. Do you think that Harry is correct in blaming his asthma on your cat? Explain what you would tell him
and why.
3. Using the diagram below as a guide, explain the steps that occur in a type 1 hypersensitivity reaction.
http://www.freshlife.com/files/freshmail/allergy%20graphic.png
4. What are the three major pathophysiological problems faced by asthmatics?

5. What is the primary determinant of airflow resistance?
6. What is the response of the airways to increased sympathetic nervous system activity? What
neurotransmitters are involved, and what class of receptors respond? Precisely where in the lungs are
these receptors located?
7. What is salbutamol and how does salbutamol work?
8. What is the response of the respiratory system to parasympathetic nervous system stimulation? What
neurotransmitters are involved, and what class of receptors responds? Precisely where in the lungs
are these receptors located?
9. What are the signs and symptoms of Harry’s asthma attack?
10. What is the role of histamine in an allergic reaction?

11. Use your knowledge of histamine and inflammation to explain some of the signs/symptoms described
in Q9.
12. The following are common triggers of asthma. In groups, use your knowledge of physiology try to
determine how each one can lead to asthma.
• Allergies, such as those due to house dust mites, animal dander (microscopic, flecks of skin shed by
animals with fur or feathers, such as cats, dogs, rodents and birds), moulds and pollen.
• Tobacco smoke
• Air pollution, strong odours
• Emotional anxiety and stress
• Certain medications, including aspirin or other non-steroidal anti-inflammatory drugs (NSAIDs) such
as ibuprofen, and beta-blockers, used to treat heart disease, high blood pressure, migraine
headaches or glaucoma.
• Viral and bacterial infections
• Exposure to cold, dry air or weather changes

Part B: Asthma and exercise
Many people with asthma (or their families) are unsure of the role of exercise in the condition. Exercise is a
common trigger for asthma, and so many people avoid it: however, controlled exercise in those with stable
asthma can lead to a reduction in both symptoms and reliance on medication.
ACTIVITY ONE: EXERCISE AS BENEFIT

Read the stories of two athletes, Amy Van Dyken and Paula Radcliffe to help you answer the
questions below. (Taken from http://www.health.com/health/gallery/0,,20306639_3,00.html)
Amy Van Dyken
‘When she was a child, Amy Van Dyken’s asthma was so bad that she couldn’t climb a flight of stairs. At age 6
she took up swimming on the advice of a doctor, who said that the rhythmic breathing and humid air might
help stretch out her lungs.
It was slow-going at first—Van Dyken couldn’t swim 100 meters until she was a teenager—but with the help
of a regimen of medications (and despite frequent asthma attacks), Van Dyken crawled her way to the top of
her sport. She won four gold medals at the Athens Olympics and collected two more in Sydney four years
later.’
Paula Radcliffe
‘The marathon is among the most gruelling athletic events known to man. Completing one is difficult,
winning one is very difficult, and winning one with asthma is near impossible.
But that’s what British long-distance runner Paula Radcliffe has done—seven times. The current world
record holder in the marathon, Radcliffe was diagnosed with exercise-induced asthma as a teenager, shortly
after she began training seriously.
"I always take my reliever inhaler before and after I run, and am extra careful when I have a cold, as that can
make the symptoms more severe" she told an interview.’
Questions
1. Using your knowledge of the body and the pathophysiology of asthma, suggest how exercise in
general, and swimming in particular, may benefit people with this condition. (Hint: remember that
when you consider a person with asthma, you need to think of more than just the respiratory system)

ACTIVITY TWO: EXERCISE-INDUCED ASTHMA (EIA) OR EXERCISE-INDUCED
BRONCHOCONSTRICTION (EIB)
Some of the material below was derived from Asthma Australia’s website
(http://www.asthmaaustralia.org.au/default.aspx) which has useful information and links to other
resources.
Shortness of breath during or after activity is normal, depending on an individual’s fitness; however,
exercise-induced asthma may be present if the symptoms below occur during or immediately after exercise,
and do not improve within 10 minutes of resting and cool-down. The symptoms may persist for 15-30
minutes if untreated.
• cough
• chest tightness
• shortness of breath
• wheeze
Questions
2. During normal breathing, explain what happens when air enters the respiratory tract; what occurs in
the nose and why is this beneficial?
3. How does our breathing change when we exercise?
4. What sport or exercise is best for people with asthma? Is there a single answer to this question? Why
or why not?

Workshop 8 – Musculoskeletal disorders
Please complete the following before attending workshop class
Chapter 42: Joint disorders pg. 1016 – 1029
• Complete questions 1 and 2 as pre-class activity.
1. Label a picture of a typical synovial joint to review the location of:

Synovial fluid Fibrous capsule Articular cartilage
Synovial cavity Synovial membrane
2. Match the following structures with their corresponding function.

Synovial fluid Fibrous capsule Articular cartilage
Synovial cavity Synovial membrane
Structure Function
slippery viscous fluid for lubrication of joint; allows movement; nourishes
cartilage
tough dense tissue that surrounds and encapsulates the synovial fluid
smooth surface that covers bones to reduce friction and protect underlying
bone, dissipates load evenly across the joint
gap between two articulating bones; contains synovial fluid
epithelial lining of fibrous capsule; produces and secretes synovial fluid
Practical 8 – Musculoskeletal disorders  Page 58

3. Compare and contrast osteoarthritis and rheumatoid arthritis in terms of their definition, aetiology,
onset, pathogenesis and clinical manifestations.
Osteoarthritis Rheumatoid arthritis

Definition
Aetiology
Onset
Pathogenesis
Clinical
manifestations
4. Explain how chondrocytes in the avascular articular cartilage receive nutrients and oxygen and rid
wastes. What type of tissue is articular cartilage?
CASE STUDY
Mrs. Chapman is a slightly overweight 52 year old receptionist who has type 1 diabetes mellitus and is a
regular smoker. In her spare time, she enjoys knitting clothes for her grandchildren but the last few years,
she has found it difficult to continue her hobby because her ‘fingers on both hands are so sore and stiff,
especially in the mornings’ and her knuckles appear to be swollen and feel warm.

5. What condition do you think Mrs. Chapman has? Explain why.
6. Describe the risk factors that could have contributed to Mrs. Chapman developing this condition.
One morning, Mrs. Chapman feels particularly unwell so she decides to take herself off to see the doctors.
She describes her symptoms to the doctor who writes her a script for a NSAID and orders her a blood test.
7. How do NSAIDs act to decrease inflammation?

A week later, Mrs. Chapman returns to the clinic to hear her results. The doctor tells Mrs. Chapman that she
has rheumatoid arthritis which is an ‘auto-immune disease’. The doctor writes Mrs. Chapman a script for a
drug that is more likely to manage her condition and advises Mrs Chapman to stop smoking.
8. What did the doctor mean when they stated that Mrs Chapman had an ‘auto-immune disease’?

Thirteen years later Mrs. Chapman is still a regular smoker. Her knitting had stopped long ago and she no
longer works as a receptionist because of her sore back. She has since developed a noticeable hunch and her
grandchildren affectionately call her ‘granny hunchback’. She is still taking medications for her rheumatoid
arthritis and like most other people, has good and bad days. Right now however, it is a great day because
she is celebrating her 65th birthday with her family. She gets up to pour herself a drink and accidentally takes
a tumble. She feels excruciating pain in her left hip and cannot move from the floor. An ambulance is called
and Mrs. Chapman is immediately rushed off to the hospital.

At the hospital, it is confirmed that Mrs. Chapman has broken her ‘left hip’ and must undergo surgery to
remove the broken shards of bone. Bone scans reveal that her bone density is much lower than expected
which has contributed to her hip fracture. Mrs. Chapman is hospitalised where she is confined to bed-rest.
9. Describe some common causes of fractures and explain what influences the degree of their severity.
10. State the common sites of healthy bone fractures versus pathological fractures.
11. Does Mrs. Chapman’s continued smoking have an effect on her recovery from the hip fracture? If so,
explain how.
12. What does a ‘broken hip’ actually mean? i.e., what is actually broken?
13. Explain why Mrs. Chapman’s bone density is so low.

14. Explain how osteoporosis differs from osteoarthritis.
15. Kyphosis is the name given to the exaggerated spinal curvature of the thoracic vertebrae which leads
to the appearance of having a hunched back. Can you link this condition to Mrs. Chapman’s pre-
existing conditions?
16. What are the complications involved with kyphosis?
17. Hip fractures in the elderly are associated with a high mortality rate. Often what seems like a minor
fall can result in death very quickly. What are the complications involved with hip fractures?

18. Examine the laminated cards showing x-rays of various types of fractures. Distinguish between the
following: complete fracture, incomplete fracture, open fracture, closed fracture. Describe each of
these fracture types.
a.
b.
c.
d.
e.
19. Describe the symptoms of fracturing a bone.
20. ‘Breaking a hip’ increases mortality. Explain why?

21. Arrange the five steps of bone healing by writing numbers in the upper left corner and describe the
steps of bone healing at the bottom of each box.
HARD
SOFT
http://askabiologist.asu.edu/busy-bones

22. Describe what can happen when a fracture does not heal properly.
23. Mrs Chapman’s friend Iris visits her in hospital. Iris was pleased that she could visit her friend today as
she has osteoarthritis and sometimes experiences a lot of pain which limits her ability to get out and
about. Describe why osteoarthritis causes pain.

Workshop 9 – Mental illness
• ‘Nerves, Synapses and Neurotransmitters’ lecture from BIOL121
• Bryant, B.J. & Knights, K.M. (2015) Pharmacology for health professionals, 4th ed., Mosby/Elsevier,
Chatswood, N.S.W. Chapter 21: Drug dependence and social pharmacology pg. 441-481.
• Pennay, A., Lubman, D.I. & Miller, P. (2011) Combining energy drinks and alcohol. Aust Family Phys
40:3 104-107. http://www.racgp.org.au/download/documents/AFP/2011/March/201103pennay.pdf
• Pennay, A., Lubman, D.I. & MacLean, S. (2011) Risky drinking among young Australians. Aust Family
Phys 40:8 584-588.
http://www.racgp.org.au/download/documents/AFP/2011/August/201108pennay.pdf
Chapter 14: Depression, psychosis and anxiety disorders pg. 314-332.
1. Match the following structures with their corresponding function.

Pre-synaptic Synapse Synaptic cleft Synaptic Neurotransmitter
neurons vesicle/bulb
Structure Definition/function
Where an axon meets a target cell. This is where a signal is transmitted to either
another neuron or to an effector cell (e.g. cardiac muscle, smooth muscle, and
gland). In humans most synapses are chemical synapses (involving
neurotransmitters).
The synaptic cleft is the small gap between the neuron and subsequent effector
cell/s.
Synthesis and release of neurotransmitter
Storage of neurotransmitter
Chemical message release from nerve cell
Part A: Synaptic transmission

Preparation
I. Decide which Play-doh® colours will represent the various substances
II. Put a small piece of each colour in the circle beside the appropriate substance
III. Use a whiteboard marker to label the following structures
• Pre-synaptic neuron
• Synaptic cleft
• Post-synaptic neuron
• Calcium channel
• Sodium channel
• Receptor
Workshop 9 – Mental illness  Page 66

IV. Draw an arrow to identify the direction of the action potential
Finish your synapse

V. Using your chosen colour Play-doh® make 8-10 balls of calcium and put them outside the neuron
near the calcium channel
VI. Make 8-10 balls of sodium and put them inside the synaptic cleft
VII. Make 2-3 vesicles and put them in the presynaptic membrane (these should be big flat discs, but
think of these as a bag)
VIII. Make 8-12 balls of neurotransmitters and put these on the vesicles
Synaptic transmission
IX. An action potential arrives and causes calcium to enter the presynaptic neuron through the calcium
channels
X. The increased concentration of positive ions causes the vesicles to merge with the pre-synaptic
membrane and empty their contents into the synaptic cleft
XI. The neurotransmitters bind to the receptors on the post synaptic membrane
XII. This results in opening of the sodium channels
XIII. Sodium enters the post synaptic neuron through the sodium channels
XIV. The increase in positive ions in the post synaptic neuron results in depolarisation and causes a new
action potential to be generated
XV. Disconnect your neurotransmitters and put them back in the synapse
Prepare your board for neurotransmitter clearance

There are a number of ways to clear the synapse:
1. Destruction by enzyme
2. Reuptake back into the presynaptic neuron via a carrier molecule
3. Diffusion back into the presynaptic neuron
XVI. Draw a circle down the bottom of the page beneath the circles already there. Label it “MAO” and
draw a pair of scissors beside the circle
XVII. Draw a channel looking shape on the presynaptic neuron (or make it out of Play-doh) and label it a
“reuptake transporter protein”
Neurotransmitter clearance
XVIII. Take a pair of scissors and chop the neurotransmitter Play-do in half saying “MAO destroys
monoamine neurotransmitters like dopamine, noradrenaline and serotonin”, and then put those
neurotransmitter pieces off to the side.
XIX. Take some neurotransmitters and put them through the newly made reuptake transporter protein
and put them back in the vesicle.

Questions – Integration and application
1. Name the four types of primary drug targets.
2. Is it likely that the synapse is a target for drugs? Explain why or why not.
3. What do you think would happen at a typical synapse if someone was administered a drug that
caused calcium channels to close?
4. What do you think would happen at a typical synapse if someone was administered a drug that
caused sodium channels to close?
Part B: Addiction
Kerry and her workmates are out celebrating after successfully pitching a marketing strategy to Kraft. Kerry
usually drinks a few glasses of wine every evening but has decided to get rowdy and drink Red Bull and
vodkas. They all had an awesome time! Kerry’s face was very flushed and she needed to go to the toilet
frequently. After a few hours of drinking wine, Kerry decides that it was time for da na na na na na na na
TEQUILIA! She leaves the bar seriously drunk (her friends help her to walk) and in attempting to catch a taxi,
she misjudges the height of the curb, falls over and extends her right-arm to limit her fall – breaking her
radius in the process. Her friends call an ambulance and she is taken to hospital. She is somewhat dazed and
confused in the first 24 hours, after which time she feels very unwell – alternating with chills and sweating.
Later in the afternoon, Kerry becomes aggressive with the nurses and believes that her skin is crawling with
ants.

1. Alcohol is a CNS-depressant. Explain why people who consume a larger quantity of alcohol initially feel
confident and euphoric.
2. What are the central effects of alcohol?
3. Why was Kerry’s face flushed?
4. Why did Kerry need to urinate frequently?
5. What are some other peripheral effects of alcohol?

6. Is combining alcohol with energy drinks a recipe for trouble? Discuss.
7. What are some useful harm reduction messages with regards to combing energy drinks with alcohol?
8. What is Kerry suffering from in hospital?
9. What are other symptoms of this syndrome?
10. Is Kerry at risk of developing delirium tremens? Explain why or why not?
11. What is the delirium tremens?

12. What group of drugs might be administered to help alleviate the signs and symptoms of this
withdrawal syndrome and why?
13. Describe the difference between psychological and physical drug dependence.
Part C: Depression – Case study

A few years later Kerry presents at her GPs. She has experienced appetite loss and a low mood for the past 3
months. She tells the GP that she is teary, unable to sleep, and has loss of interest in work and leisure
activities. She feels stressed and unable to function but denies any suicidal thoughts. Physical examination
and other investigations are unremarkable and the diagnosis of depression is made. A series of
appointments are scheduled for counselling. The severity of her symptoms, which meet diagnostic criteria
for major depression, necessitate initiation of antidepressant therapy – a selective serotonin reuptake
inhibitor (SSRI) (20 mg daily).
1. Explain the mechanism of action of SSRIs.
2. Why is this group of drugs indicated in depression? Your answer should include reference to the
monoamine theory of depression.

3. SSRIs are known to have long half-life times. If a certain SSRI has a half-life time of 6 days, how long
does it take this drug to reach steady state concentration? What are the implications of this?
4. What are the adverse effects of SSRIs?
5. What is serotonin syndrome?
6. What information about antidepressant therapy are you likely to discuss with a person in your care?

Workshop 10 – Cancer
1. Match the following terms with their correct definition:
Term Definition
Anabolic reaction Energy intake is less than energy expenditure
Catabolic reaction Formation of fat
Hyper-catabolism Decreased anabolic reactions
Hypo-anabolism Breakdown of proteins
Negative energy balance Loss of appetite and/or inability to eat
Lipolysis ‘Breaking down’; release energy
Lipogenesis ‘Building up’; require energy to work
Anorexia Increased catabolic reactions
Proteolysis Breakdown of lipids
Part A: Neoplasm
1. Define neoplasm. State the differences between the two major types of neoplasms.
2. Risk factors contributing to cancer development can be biological, lifestyle and environmental factors.
List examples from each factor and make sure to provide at least one specific example of a carcinogen.
3. What is the involvement of genetic factors/ heredity in cancer?
Workshop 10 – Cancer  Page 73

4. What is meant by gene mutation?
Cancer is uncontrolled cell growth and replication. Our bodies have mechanisms to maintain normal growth
through regulatory genes. Two types of regulatory genes are called proto-oncogenes and tumor suppressor
genes. Proto-oncogenes normally regulate cell growth and division, to ensure that cell growth and
replication is normal. Tumor suppressor genes normally repair damaged DNA or cell cycle abnormalities,
preventing damaged cells from replicating through apoptosis if necessary. If these genes are mutated they
can lead to cancerous growth.
5. What are the consequences of a mutation in the BRCA genes? Which type of gene is it (proto-
oncogene or tumor suppressor gene)?
6. What role do hormones play in breast cancer?
7. What are some of the clinical manifestations of cancer?
PART B: CASE STUDY- Cancer cachexia
Fred is a 64-year old man who has been diagnosed with cancer. He is undergoing chemotherapy and may
have radiotherapy later. Fred was a fit and athletic man prior to this, and he and his wife Jan eat a healthy
diet (Fred normally does the cooking). Fred is losing weight, feeling tired and says he has “lost his appetite”.
He and Jan have come to talk to you about a condition called cancer anorexia-cachexia syndrome (CACS).

Cachexia in cancer
Cancer anorexia-cachexia syndrome (CACS) is a metabolic syndrome of involuntary weight loss associated
with malignancy. It is characterised by a decrease in the mass and/or strength of muscles; fatigue, anorexia;
anaemia; inflammation and low serum albumin levels. CACS is not uncommon and leads to death if left
untreated. The pathophysiologic and biochemical pathways involved are not well understood.
1. What is the definition of cancer cachexia?
2. How would you know that Fred has cachexia? Identify the signs and symptom of a person with
cachexia.
3. What are the outcomes of cachexia? Explain why this is bad for Fred.
Background
The hypothalamus receives and integrates visual, cognitive and sensory inputs from the body and forwards
these to relevant parts of the brain for action to be initiated. These signals bring information about the
body’s reserves of energy and nutrients, activity in the GI tract and the quantity and variety of nutrients
entering the body. In a healthy person, the balance between anabolism and catabolism is generally easily
maintained.
Systemic inflammation is linked with obesity and metabolic syndrome but it is also strongly implicated in the
development of cachexia through the action of particular cytokines. Cytokines are molecules that help cells
communicate with each other in immune responses (“cell signalling molecules” or “immunomodulating
molecules”). They help guide cells towards areas of inflammation, infection or trauma. There are many

factors that can increase the rate of catabolism, including tumour progression, comorbid conditions, old age,
physical deconditioning, nutritional deficiency, drugs (such as chemotherapy) and other medical
interventions (surgery, radiotherapy).
4. What effect do you think increased catabolism would have on Fred’s fat tissue and muscle mass? Is
this a positive or negative health outcome for him? Explain why
Pathophysiology
CACS is a multifactorial syndrome – as well as systemic inflammation, reduced food intake and changes in
metabolism contribute to a negative protein and energy balance that results in a loss of muscle mass and
reduction in body weight. Other contributors to CACS are changes in the ability of the liver and skeletal
muscle to synthesise (build) and degrade protein, and in the rate of lipolysis in adipocytes.
5. What does “a negative protein and energy balance” mean? Explain why it is not beneficial for Fred.
6. Muscle carries out many roles in eating and digesting food and excreting waste. Explain how these
roles might be affected if Fred has a reduction in the mass and strength of skeletal muscle.

Contributors to pathophysiology
Inflammation
Inflammation is a local event, but when it occurs in different tissues concurrently it can produce an
integrated response in the affected person. These effects can include including not only anorexia but also
fatigue, sleep disturbances, mood alteration, lethargy, depression, fever, anhedonia, cognitive impairment,
hyperalgesia and decreased social interaction.
Both the tumour and a range of host cells (e.g. skeletal muscle, adipose tissue and cells of the immune
system and liver) induce an inflammatory response; this acts both on the brain and on other organs in the
body.
Some patients with cancer have high levels of several cytokines, one of which is TNF-α (tumour-necrosis
factor α). Whether produced by the tumour or by the person’s immune response (this is not well
understood), cytokines are thought to cause the acute phase protein response (APPR) seen in many
malignancies and in CACS. APPR is the term given to the host’s normal response to infection, inflammation,
or trauma. It results in pyrexia, leukocytosis, hormone alterations, and depletion of muscle proteins; in
healthy individuals this minimises tissue damage while enhancing the repair process.
7. Do you think pyrexia would be beneficial or harmful to Fred? Explain why.
GOOD LUCK

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Human Biological Science 2

Table of contents ........................................................................................................................................... 1

1. Define the following terms:

Workshop 1 – Pharmacological principles  Page 2

Part A: Lifespan pharmacology

CASE SCENARIO ONE – A PREGNANT WOMAN

Workshop 1 – Pharmacological principles  Page 3

3. Describe how pregnancy affects:

Workshop 1 – Pharmacological principles  Page 4

CASE SCENARIO TWO – AN INFANT WITH A FEVER

Workshop 1 – Pharmacological principles  Page 5

CASE SCENARIO THREE – AN ELDERLY WOMAN

Workshop 1 – Pharmacological principles  Page 6

9. What is polypharmacy? Explain the effects of polypharmacy.

Part B: Adverse drug reaction (ADRs) and Drug interactions (DIs)

1. What is an adverse drug reaction (ADR)?

Workshop 1 – Pharmacological principles  Page 7

Workshop 1 – Pharmacological principles  Page 8

6. What type of ADR are drug allergies?

8. What is a drug interaction (DI)?

Workshop 1 – Pharmacological principles  Page 9

Important instructions for next week’s workshop

Workshop 1 – Pharmacological principles  Page 10

1. Match the following terms with their correct definition:

the study of disease

the cause of disease; why the disease arises

a disease/condition resulting from medical treatment or diagnostic procedures

formation and progression of disease; how the disease progresses

programmed cell death

total lack of oxygen

reduction in blood supply/flow to an area

localised area of ischaemic necrosis

the body’s response to injury

new growth; benign or malignant

Workshop 2 –Pathophysiological principles and Anthropometry  Page 11

2. Obesity is a metabolic disorder primarily induced and sustained by an over consumption or

3. Match the following fats with their respective descriptor below:

Type of fat Descriptor

Workshop 2 –Pathophysiological principles and Anthropometry  Page 12

Food Type of fat/lipid

Butter, fat on/in meat

Part A: Pathophysiological principles

General framework for discussing diseases

Workshop 2 –Pathophysiological principles and Anthropometry  Page 13

Cells are generally categorised according to the following criteria:

Workshop 2 –Pathophysiological principles and Anthropometry  Page 14

1. Hypertrophy – an increase in tissue/organ size due to an increase in cell size.

2. Atrophy – a decrease in tissue/organ size due to decrease in cell size.

3. Hyperplasia – an increase in tissue/organ size due to an increase in cell number.

Workshop 2 –Pathophysiological principles and Anthropometry  Page 15

E. What do you think happens when myocardial cells are injured?

F. What effect would scar tissue have in the heart?

Workshop 2 –Pathophysiological principles and Anthropometry  Page 16

B. What has happened to the tissue in the abnormal figure?

ACTIVITY FOUR: PHYSIOLOGICAL AND PATHOLOGICAL ADAPTATIONS 3

B. What physiological stimulus may have caused this?

Workshop 2 –Pathophysiological principles and Anthropometry  Page 17

• Avoid alcohol consumption for 24 hours before your lab session

“Anthropo” = human and “metron” = measurement

Workshop 2 –Pathophysiological principles and Anthropometry  Page 18

BMI formula = weight (kilograms)

2. What are the limitations of the BMI measurement?

Workshop 2 –Pathophysiological principles and Anthropometry  Page 19