As is our Pathology,
so is our Practice.
-- Sir William Osler, M.D.
(Father of Modern Medicine & Founding professor of John Hopkins,
developed first residency program for physicians.)
Pathology: The science of medicine !
CPC31: Week Overview
2013 Term 3 CPC 1 Title: Endocrine 1/1 Thyroid
Aim: To educate students in Clinical, pathology & population
study of patients with Endocrine disorders (using example
of thyroid disorder).
Learning Outcomes: 1. Demonstrate an ability to take a focused History &
Students will be able
carry out a focused clinical examination of patients
with neck swelling and systemic symptoms
2. Describe the Pathophysiology of common endocrine
3. Describe the pathophysiology of thyroid disorders.
4. Outline the basic sciences relating to
hypothalamic/pituitary/thyroid axis; thyroid function
testing; role of anti thyroid antibodies in differentiating
5. Outline first line treatment of thyroid disorders.
Nontoxic-Multi Nodular Goitre.
A: conspicuous neck mass. B: Coronal section showing
numerous irregular nodules, some with hemorrhage.
C: Microscopy: variation in the size of the follicles.
TSH, T3,T4 Normal
Carcinoma of Thyroid
young adults 20-40
Young-middle 4050 (>45)
Good with radioespecially to bone iodine therapy.
SIADH: Sy of Inappropriate ADH secretion
Too Much ADH
Low Serum Sodium
Low Serum Osmolality
High Urine Osmolality
Too Little ADH
High Serum Sodium
High Serum Osmolality
Low Urine Osmolality
Tumor of medullary Chromaffin cells.
May be familial (MEN syndrome).
Increased Urinary VMA
Acute hemorrhagic necrosis (apoplexy).
Lack of aldosterone
Salt & water loss
The adrenals from a child dying of
meningococcal septicaemia are destroyed
Education is what remains after we have
forgotten all the facts taught in the class!
CPC32: Week Overview
2013 Term 3 CPC 2 Endocrine 2 - Diabetes
Aim: To educate students in: Clinical, Pathology & population
study of patients with Diabetes Mellitus
Learning 1. Demonstrate an ability to carry out a focused History &
clinical examination of patients with diabetes.
Students will be 2. Describe the pathophysiology of Diabetes Mellitus
Types 1 + 2 and their complications.
3. Outline the Basic sciences relating to endocrine
4. Explain the abnormalities of Blood supply common in
diabetic patients including - ischaemia, infarction &
5. Outline the epidemiology and aetiology of Diabetes
Mellitus in Australia and world wide.
6. Outline first-line management and demonstrate an
understanding of the process of care of a diabetic
Most likely .. What type of DM ?
1. 56 year male obese
2. 30 year female following pregnancy
3. 8 year old boy, poor growth, DKA.
4. 24 year female Cushing‟s sy
5. 68 Year male following Ca. pancreas.
6. 32 male, DM, BMI 18, Anti-GAD +ve.
7. 34 year male, extensive tuberculosis.
8. 12 year old female following viral fever
9. 41y DM2, BMI 17.1, HbA1c 14.1, DKA
10.15y male, BMI 16.2, recurrent infect.
Definition? types common? Diagnosis?
Primary & Sec? Congenital? Gestational?
Monogenic? MODY, LADA, drugs?
List functions of Insulin? Antagonists?
Etiology & Pathogenesis of Type 1 & 2.
Stages of DM & their pathological basis?
Obesity & Insulin resistance *
– FFAs, PKC, Adipkines, PPARγ
– Inflammation & Insulin resistance.
• Mechanism of β cell destruction type 1, 2.
• Islet Amyloid PolyPeptide (IAPP)?
“A man must be big enough to admit his
mistakes, smart enough to profit from
them, and strong enough to correct
--John C. Maxwell
CPC33: Week over veiw
2013 Term 3 CPC 3 Title: Neurology 1 – Head injury, Stroke.
Aim: To educate students in:
Clinical, Pathology & population study of patients with Head Injury,
including non traumatic brain injury & stroke.
Learning 1. Demonstrate an ability to take a focused history & perform a relevant
and focused clinical examination of patients with loss of
Students will be
consciousness/alteration in neurological function
able to 2. Describe the Pathophysiology of cerebrovascular accidents.
3. State the Pathophysiology of hypertension (review).
4. Recall the components of Basic sciences relating to function of the
5. Define the Epidemiology and Pathology of cerebrovascular disease
6. Describe the Epidemiology of neurological diseases in Australia and
7. Define the first line management of patients with impaired Glasgow
8. Demonstrate an understanding of the complications of intra-cerebral
Left (Dominant) Hemisphere Stroke: Clinical
Right-sided sensory loss
Right visual field defect
Poor right conjugate gaze
Difficulty reading, writing, or
Diagnosis: Recent cerebral infarction in left MCA distribution.
Left cerebral hemisphere shows swelling with compression of the lateral
ventricle mainly in the frontal area, due to recent infarct in the Middle Cerebral
Artery (MCA) distribution. The brain in the MCA area shows discoloration of
the cortex and also blurring between the cortex and white matter.
• Paralysis of contralateral foot
• Sensory loss over toes, foot
• Impairment of gait and stance
• Abulia (slowness and
prolonged delays to perform
• Flat affect, lack of spontaneity,
• Cognitive impairment, such as
perseveration and amnesia
• Urinary incontinence
Wikipedia: GNU Free Documentation license
CNS AV Malformations:
• Many types:
AV Malformation *
• Cause of Seizure
disorders & hemorrhage.
• Most common
• Typically located in the
outer cerebral cortex
underlying white matter.
Our greatest glory is not in never
falling, but in rising every time
CPC34: Week over view
2013 Term 3 CPC Title: Neurology 2
Aim: To educate students in:
Clinical, Pathology & population study of patients with dementia
Learning 1. Demonstrate an ability to take a relevant and focused history and
carry out a relevant clinical examination of patients with dementia.
(Students will be 2. Carry out a competent physical examination of neurological system.
able to) 3. Describe the Pathophysiology & Pathology of common causes of
dementia (Alzheimer’s Disease, multi infarct dementia)
4. Recognsise rare neurological causes of dementia (Huntington’s
disease, CJD, HIV).
5. Outline the basic sciences relating to structure and function of the
6. Describe the difference between age associated memory
impairment, mild cognitive impairment and Alzheimer’s disease
7. Outline the epidemiology of Alzheimer’s disease and other causes
of dementia in Australia.
8. Explain the first line management of common causes of dementia
9. Outline ethical dilemmas in caring for patients with dementia
Broca‟s area - Cingulate and Parahippocampal gyri.
are converted to longterm memories
sensory and limbic
information and sends
to cerebral cortex
Limbic system: controls
hippocampus and parts
of the cortex)
Diffuse Lewy body Dementia: DLD
• 10-15% of Parkinsons with
dementia within a year of
• impaired memory of recent
events, confusion, language
• Dementia + visual
• Lewy body (α-synuclein) in
many part of cortex &
substantia nigra (global)
• Atrophy of cortex like AD.
• Rapidly progressive – early
cortical Lewy bodies (αsynuclein) special stain.
• "shaking palsy"
• Parkinsonism: Clinical sy.
– Drugs: dopamine antagonists
– Toxins: MPTP(heroin),
– Diseases: Multiple system atrophy, Post encephalitic.
• Parkinson‟s disease – Primary atrophy of substantia nigra.
Dopaminergic nerves with α-synuclein - Lewy body.
• Clinical features:
– Adults (45-60y), tremor, bradykinesia & rigidity
– Diminished facial expressions, stooped posture,
– Slow voluntary movements, festinating gait, & fine rolling resting
tremors. Dementia in some cases.
– When dementia arises within 1 year of the onset of motor
symptoms, it is referred to Lewy body dementia (LBD).
Pathology of Parkinson‟s disease:
• Gross: Loss of
pigment in substantia
• Neuronal loss,
• Loss of neurons
replaced by gliosis
• Loss of neuromelanin.
• Reactive gliosis.
• Lewy bodies (αsynuclein) in neurons.
• Dementia, depression,
• 5th decade. Autosomal dom.
• Huntington gene on 4p –
• Excess CAG tandem
repeats = severity.
Atrophy of caudate & putamen (striatum)
Compensatory hydrocephalus of lateral ventricles*.
Metabolic CNS Disorders: Alcohol
• Vit. B1 (thiamine) def.
• In Chronic alcoholics,
• Wernicke encephalopathy
ataxia, confusion, double
• Korsakoff psychosis: memory
loss with confabulations.
• Cortical atrophy.
• Central pontine myelinolysis.
• Atrophy of vermis of the
Recurrent petechial hemorrhages in
the hypothalamus, mamillary bodies
with atrophy. Central pontine
• Common 1:1000, adults,
females 2:1, HLA DR2, <50y.
• Autoimmune (Gen+Env+AI)
• Episodes of Limb Weakness,
• Relapsing & remitting.
• Progressive death in years.
• Multiple soft pink plaques of
• Inflammation, perivascular T
lymphocytes & plasma cells.
• CSF - oligoclonal IgG.
• Reactive gliosis.
Multiple Sclerosis: Demyelinated plaques
Microscopy showed loss of
myelination with many lipid
macrophages around BV.
ALS: Amyotrophic Lateral
Also known as Lou Gehrig's disease,
is the most common type of Motor
Neurone Disease (MND).
Genetic: Mutations in SOD1 gene on
Progressive neuron loss.
Middle age, men, sporadic common,
Muscle weakness, fasciculations,
Degeneration of lateral and ventral
spasticity, Sensation normal.
corticospinal tracts (myelin stain).
Degeneration of LMN tracts in the
lateral portion of the spinal cord
• Amyotrophic Lateral Sclerosis*
("lateral sclerosis"). and of UMN • Progressive muscle atrophy (LMN)
Betz cells in the motor cortex.
• Primary lateral sclerosis (UMN)
• Progressive bulbar palsy
Dementia Cases: Disease
49y woman, chronic cognitive difficulty,
irritability, depression, poor movememnts,
no significant memory loss, muscle
rigidity, wide gait, choriform movements of
trunk & limbs. (Father & many of relatives
had involuntary movements.)
74y man, mild cognitive decline, slow gait,
depression, resting tremors, visual
hallucinations, episodes of “absent”
“confused” MMSE 27/30, ACE-R score
78/100. Rigid muscles,
Parkinson‟s with Dementia
75y man, rapid decline in cognitive function
with fluctuations, MMSE 22/30. Ten point
clock face drawing test - 0. Day time
sleepiness. Apathy, visual and auditory
Diffuse Lewy body Dementia
Fronto-Temporal / Pick‟s
56y man, progressive speech difficulty 2y.
Slow to respond, paucity of words. Lack of
judgement, disorganized, aggression,
impulsive. Good memory. Left hand
weakness, progressive motor weakness.
MMSE 27/30. FH of dementia.
58y man, mild cognitive impairment,
weakness of distal limbs, loss of muscle
mass, fasciculations, rigidity. Babinski sign
+ve. Recurrent respiratory infections.
59y professional foot ball player.
Progressive dementia & tremor.
67y man, previously healthy, 3m h/o rapid
dementia, weakness of hands & fingers,
insomnia, irritability, inability to find his way
home. visual hallucinations and tremor, speech
difficulty, admitted with Gen. seizure.
Amyotropic Lateral Sclerosis
CJD – Mad Cow Disease
Alzheimers Pathogenesis: YouTube
The only real mistake is the one,
from which we learn nothing!
CPC35: Week over view
2013 Term 3 Title: Neurology 3
Aim: To train students in :
History taking + clinical examination of post ictal/acutely unwell
patient; pathology of brain tumours; pathology of meningitis;
pathology of epilepsy; process of care + population health
especially rural and remote
Learning 1. Demonstrate an ability to take a relevant and focused History
& clinical carry out a relevant examination of patients after a
be able to 2. Describe the Pathophysiology of primary and secondary brain
tumours; meningitis; epilepsy
3. Recall the relevant basic sciences including normal anatomy
and blood supply of the brain
4. Recall the differential diagnoses for a patient with a first fit
5. Describe first line management in a patient with a first fit or
altered level of consciousness.
Septic Meningitis-Spinal fluid
• Increased intracranial pressure.
• CNS infarctions (A),
abscess (C) or
Perivascular cuffs of lymphocytes and Microglial nodules
Acute, Self limiting, Less severe than bacterial.
Clear CSF, sugar normal, lymphocytes, protein.
Cerebral edema, perivascular lymphocyte cuffing.
Reactive microglial nodules.
Arbovirus*, Herpes, Varicella Zoster, CMV, Polio, Rabies.
0-4 lympho 0.1-0.4(n)
The 10-10-10 rule…
Think about effect of your decision in….
10 – 10 – 10
"I wasn't living my life. My life was living me. I realised I made many of my decisions without thinking their
consequences… “I realised all I really had to do to reclaim my life was to Start making decisions by considering their
consequences in the immediate present, near term and distant future.. i.e . In ten minutes, in ten months and in ten years”.
-- The 10-10-10 rule, Suzy Welch.
Most common CNS Tumors:
spindle cells in whorls
and psammoma bodies
Astrocytomas - Glioma
– Commonest 80%, Cerebral.
– Low Gr: Solid, Fibrillary glioma
– High Gr: glioblastoma multiforme Varigated,
Hemorrhagic - Malignant,.
– Cystic, Low grade*, Pilocytic
– Infratentorial (Cerebellum),
mutations of the metabolic enzyme Isocitrate DeHydrogenase (IDH1 and IDH2) are
common in lower-grade astrocytomas. As a result, immunostaining for the mutated
form of IDH1 has become an important diagnostic tool for low grade gliomas.
Low high grade.
Chromosome 10 (80%)
Most GBMs have lost one
entire copy of C – 10
• Pleomorphic astrocytes,
Why pupils dilate?
Sympathetic / parasympathetic Balance.
“Sympathetic system shows sympathy to your dress!”
One of the first duties of the
physician is to educate the
masses not to take medicine!
-- Sir William Osler (1849 - 1919),
Aphorisms from his Bedside Teachings (1961) p. 105
CPC36: Week over view
2013 Term 3 CPC 6 Title: Infections & PUO
System: Infectious disease
Aim: Develop understanding pathology & clinical diagnosis of
patient with pyrexia of unknown origin
Learning Outcomes: 1. Demonstrate competency in taking a focused History
Students will be able
taking & clinical examination of patients with pyrexia
to 2. Demonstrate relevant focused physical examination of
all systems relevant to a patient with PUO
3. Demonstrate competency in formulating the differential
diagnoses of patients with PUO
4. Outline the Management of PUO
5. Outline the Basic sciences applicable to PUO including
– Infection & Immunity.
6. Describe the pathology of arboviruses including
transmission of disease. (Tropical diseases)
Viral Infections •
• Ross River Fever
• Australian Encephalitis.
Ross River Fever
Malaria, Q fever,
– Ross River Virus (RRV) – epidemic arthritis
– Barmah Forest Fever
– Equine Encephalitis – many types.
Dengue – Hemorrhagic fever.
Murray Valley Encephalitis – meningitis like.
– LaCrosse encephalitis
– Reo viruses
– Colorado tick fever
The major arboviruses of concern
in Australia are:
Ross River Virus
Barmah Forest Virus
Murray Valley Encephalitis
Ross River Fever - Symptoms:
Warning Signs for Dengue Shock
Four Criteria for DHF:
• Hemorrhagic manifestations
• Excessive capillary
• 100,000/mm3 platelets
• Disappearance of
• Drop in platelets
• Increase in
• Severe abdominal pain
• Prolonged vomiting
• Fever to hypothermia
• Change in level of
When Patients Develop
• 3 to 6 days after onset of
A: Cutaneous melioidosis
B: lung abscesses on Chest X-Ray
C: corresponding CT Scan
Intracellular gram-neg Burkholderia
pseudomallei, Saprophyte in Soil.
Northern Australia -"hyperendemic"
seasonal peaks in the wet seasons.
Inhalation / inoculation / soil or water.
D: Skin in a fatal disseminated melioidosis.
E: splenic abscesses abdominal CT
F: Aspirated pus- Prostatic abscess
G: Abscesses on a CT scan.
• Severe jaundice, fever,
hemorrhage with renal
involvement - Weil‟s disease.
• Leptospira icterohemorrhagica..
• Zoonotic: Pri. hosts - mammals,
birds, reptiles, Contact with water,
food, soil containing urine of
• No spread from person to person.
• NQ - Banana & dairy farmers.
• Biphasic: Flu like first phase
followed in a week by
Hemorrhage meninges, liver,
renal failure - Weil‟s disease.
Jaundice + Hemorrhage
“Q - ? In an abattoir in Brisbane.
Coxiella burnetii, highly infectious
Cattle, sheep,goat and other live stock.
Biphasic:Acute & Chronic phase.
Acute: Fever, headache, fatigue, muscle & joint
• Most recover - life long immunity but some
become chronic fatigue, hepatitis, endocarditis,
pneumonia - serious.
• Meningitis/encephalitis: in both acute and chronic
form in 1% patients.
• Vaccine – pre vaccine testing is important.
We can change our lives. We
can do, have, and be exactly
what we wish.
- - Anthony Robbins
CPC37: Week over view
2013 Term 3 Title: Multiple Co-morbidities
System: Musculoskeletal, Neurological , CVS, Endocrine
Aim: Educate students in clinical and pathological processes in
patients with bone abnormalities.
Learning 1. Demonstrate competency in History taking skills & focused
clinical examination of patients who have sustained trauma
Students will be 2. Describe the pathophysiology of fractures, osteoporosis,
able to to
bone tumours (primary and secondary)
3. Describe the risk factors of osteoporosis.
4. Describe the Healing in bone and other tissues following
5. Describe the Basic sciences specific to tissue injury and
6. Outline the clinical approach to patient with multiple comorbidities and polypharmacy