Personal Resilience in Project Management 2 - TV Edit 1a.pdf
Pathology Review-Term1
1. “Find the key to yourself
and every door in the world
is open to you”
Mother..
Know your Strengths, Weakness, Interests etc..
2. Week learning overview:
2013 Term 1 CPC 1 Title: Cardiovascular System 1/3 – Valvular Heart Disease
System: Cardiovascular System
Aim: To train students in:
Pathology, Clinical & population study of patients with
valvular heart disease.
Objectives: 1. History taking & clinical examination of patient with
valvular heart disease.
2. Physical examination - heart sounds both normal &
abnormal.
3. Pathophysiology of common valve disorders (congenital &
acquired) immune and developmental.
4. Review of basic sciences relating to embryogenesis of CVS
system, immune system & autoimmunity.
5. Study of population & community/rural issues in
rheumatic heart disease.
6. Understanding of cardiomyopathy (pathogenesis, common
presentations)
7. Understanding of cyanotic and non-cyanotic congenital
heart disease
3. 2013 CPC-1.1
Ms JM, 19-year-old woman living in a remote community who drops out
of the local basketball team
– Indigenous family from Cape York
– one of seven children. Love sports.
• ‗Short winded‘ since 6 months, worse since weeks,
‗heart pounding‘, cough – no blood
–
–
–
–
–
–
Smokes 5 cigarettes/day, ‗gunja‘ - occasional
Lives in a 4 bedroom house with 17 people *
fever & arthritis at 9y age*, off school for a month.
Brother gets injection every month since years *.
FH: Brother and mother have heart problems *...
Tall*, young*, JVP 4cm*.
9. Aortic valve calcification:
• most common cause of aortic
stenosis.
• Etiology: calcification from
progressive age-associated "wear
and tear".
• More in Congenital bicuspid aortic
valve, Rheumatic (10%).
• Pathology:
• Thick, irregular, fibrosed, with
nodules of calcification.
• LVH & Failure.
LVH
11. “Some people grumble that
roses have thorns; I am grateful
that thorns have roses.”
-- Alphonse Karr
Look for good in others, no one is without faults & every one
has some good quality!
12. CPC12: Week overview:
2013 Term 1 CPC 2 Title: Cardiovascular System 2/4 – IHD
System: Cardiovascular System
Aim: To train students in:
Basic Pathology, clinical skills & population study
of patients with ischaemic heart disease.
Objectives: 1. History taking & clinical examination of
patient with Acute Coronary Syndrome (ACS).
2. Pathophysiology of ischaemic heart disease.
3. Review of Basic sciences relating to CVS –
Anatomy, Physiology.
4. Study of Population & community/rural issues
in life style associated diseases.
13. CPC13-1.2 – Chest pain.
Mrs. J.B 45 year old Aboriginal woman Presents for an urgent visit complaining of
SOB, ‗oppressive feeling‘ in her chest
• While climbing steps* 15-20min, Pale, unwell, no pain now.
Burning sensation in her neck.
• Similar episodes - 2y, more frequent now. Centre of
sternum, no radiation*
• ↑Exertion, stress - ↓rest*
• HPTN 15y, Dyslipidemia 8y, GORD 7y,
• P/H: Chest pain, weak heart, no blocks.
• F/H: Smoker, 1pack/day 25y, IHD, DM2,
19. Common Sites:
• Large BV : Aorta, Carotid & Iliac.
(large vessels) – Bruit.
• Medium BV : Coronary,
Cerebral, Limbs, viscera –
ischemia.
Why?
* AS never affects veins or small
arteries.
* Microangiopathy is not due to AS
* AS is not a risk factor for DVT
* Alcohol is not a risk factor for AS.
* LDL is not bad type of cholesterol*
23. Morphology - Gross & Microscopic
Time (approx)
GROSS
MICROSCOPY
Up to 4 hour
None
None (loss of glycogen/LDH)
4 - 24 hours
Gradually deepening dark
area surrounded by
erythema. Oedema.
Beginning coagulation necrosis
contraction bands. Pyknotic
nuclei, Oedema, few acute
inflammatory cells.
3-7 days
Pale / Yellow centre with
haemorrhagic border
Obvious necrosis of muscle and
plenty of Neutrophils
hemorrhage (more if
reperfusion injury) few
macrophages.
1-3 weeks
Pale, thin (loss of tissue
mass) pale grey area with
red border.
No muscle, Granulation tissue,
macrophages prominent
capillaries, fibroblasts.
3-6 weeks
(permanent)
Small Silvery white scar .
Replacement of granulation
tissue by dense fibrosis
25. MI – stages.
Normal
1-3 wk Granulation
<1day Coagulative necrosis
3-6 wk Scar
<7 days Acute inflam.
3-6wk
scar.
26. Complications of MI:
A Anterior myocardial rupture . B Rupture ventricular septum C Rupture papillary muscle.
D Fibrinous pericarditis (dark, rough) E Thinning and mural thrombus. F aneurysm
27. “Be like a postage stamp”
Stick to one thing until you get there...!
- Josh Billings…
28. 2013 Term 1 Title: Cardiovascular 3/4 - PVD
CPC 3
System: Cardiovascular System, Skin
Aim: To train students in :
Clinical, Pathology & population study of patients with arterial +
venous disorders + skin lesions.
Objectives: 1. History taking & clinical examination of patients with peripheral
vascular disease
2. Clinical examination of peripheral circulation.
3. Clinical examination of skin & skin lesions.
4. Pathophysiology of common arterial and venous disorders.
Atherosclerosis & Deep vein thrombosis.
5. Pathophysiology of common skin disorders Infection,
inflammation & malignancy. (Review MB3-TIN)
6. Pathophysiology of Ischemia, infarction, and necrosis. (Review
MB3-TIN)
7. Review of Basic sciences relating to structure and function of
blood vessels. Fluid balance and dynamics of micro capillary
circulation & Pathophysiology of oedema formation.
8. Epidemiology of lifestyle diseases, population & community/rural
issues in life style disorders specifically atherosclerosis.
31. Arterial Ulcers: (Dry & Painful)
• Cause: AS (PVD, DM2)
• Location: distal & dorsal foot or toes.
• Features:
– Cold, pale feet, absent or weak pulses.
– Dry, Irregular clear border, grey black
necrotic.
– Pale granulation, Does not bleed on
touch.
– Painful (Nocturnal) partly relieved by
dependency.
– Skin: Shiny, loss of hair – atrophy.
* Note: Angiogram, no compression bandage..
32. Neuropathic ulcers: (Clean, Caving, Callus)
• Cause: Nerve damage.
• Location: Distal leg, pressure points.
• Features:
– Punched-out ulcers, deep caving.
– Frequently painless, loss or weak pulses.
– Often with surrounding calluses
(hyperkeratosis)
– Probing or debriding leads to brisk bleeding.
– May also have Impaired sensation and
diminished positional sense or 2-point
discrimination.
33. Malignant ulcers: (Exposed, tumour)
• Cause: UV-rays, Idiopathic.
• Location: Sun exposed*.
• Features: (remember ABCDE…!)
– irregular, Punched-out, deep, caving or with
tumour.
– Frequently painless.
– Lymphnodes, spreading, metastases.
– Cancer cachexia – weight loss etc.
34. Infectious ulcers: multiple,
• Cause: TB, Treponema (Yaws, Pinta), etc.
• Location: not particular, multiple.
• Features:
– irregular, non specific.
– Lymphadenitis.
35. DVT: Typical Clinical History:
• 34 year male – sudden chest pain and
collapse while recovering 12 days after
orthopaedic surgery for comminuted # of
femur.
• 68 year male AS, past MI, chest pain
following 24 hour flight travel.
• 28 year female, recurrent abortions.
• 54 year obese female, tender calf muscles.
• Pregnancy, OCP, flight, surgery,
43. Buerger‘s Disease:
• Thromboangiitis
obliterans
• Strong association with
smoking.
• Common Males, Jews.
• Peripheral gangrene
• Small artery in limbs
thrombosis & fibrosis.
• Also involves veins &
surrounding tissue.
44. Giant cell arteritis:
Aorta Temporal Art. Nodular segmental thickening, Most common in adults, T-cell
Granuloma + Giant cells, Ophthalmic artery blindness
45. That person who declares that there
is always something wrong is
always doing something to make
things wrong.
— Christian Larson
46. CPC14: Week overview:
2013 Term 1 Title: Respiratory 1/3 - Pneumonia
CPC 4
System: Respiratory System
Aim: To train students in :
Clinical, Pathology & population study of patients with pneumonia COPD, and
pneumoconiosis.
Objectives: 1. History taking & clinical examination of patients with a chronic lung disease (COPD,
asthma, TB, fungal & other chronic infections) and acute infection (pneumonia).
2. Review of Basic sciences relating to structure and function of lungs. Blood gas
physiology, measurement of blood gasses and lung function tests, sputum cytology
and serology in lung infection.
3. Pathology of chronic obstructive airway disorders.
4. Pathophysiology of acute respiratory infection.
5. Pathophysiology of occupational, environmental & smoking related lung disorders.
6. Pathophysiology of common and important rare causes of pneumonia, particularly
tropical illnesses.
7. Physical examination of Respiratory system.
8. Complications of pneumonia.
9. Interpretation of Chest X-rays.
10. Epidemiology of pneumonia in Australia, South East Asia and The Tropics.
11. Role of health promotion, screening, public health in acute and chronic pneumonic
conditions.
12. Smoking & lung disease. Role of health promotion, Population & community/rural
issues in smoking & work related lung disorders (pneumoconiosis).
54. The ability to concentrate and to use your
time well is everything if you want to
succeed in business, or anywhere else for
that matter!
-- Lee Iacocca
55. CPC15: Week overview:
2013 Term 1 CPC 5 Title: Respiratory 2/2 - Asthma & COPD
System: Respiratory System
Aim: To train students in :
Clinical, Pathology and Population studies of patients with
Upper Airway Disease Processes. Asthma, Chronic Cough,
Emphysema, COPD, Chronic Bronchitis and Acute
Bronchitis. [Epiglottitis, Croup]
Objectives: 1. History taking & clinical examination of patients with
obstructive airway disease, upper airway disease.
2. Physical examination of Respiratory system.
3. Review of Basic sciences relating to structure and
function of lungs. Blood gas physiology, measurement
of blood gasses and lung function tests,
4. Pathophysiology of acute upper airway injury.
62. Asbestosis:
• Asbestos bodies in sputum.
– (Protein & Hemosiderin)
• ―Inconsumable‖, Beaded 5100mm x 0.25mm.
• Within alveoli at lung bases.
• Dyspnoea, dry cough
• Clubbing is common.
• Diffuse effusion consolidation*,
fibrosis Honey comb lung.
63. Coal Miner‘s Lung:
• Athraco-Silicosis:
• Dense cardon
pigmentation –
Anthracosis and
nodules of silicosis.
• Commonly seen in
coal miners.
• Only anthracosis
no fibrosis or
damage.
64. Sarcoidosis:
• Granulomatous, immune,
multisystem disorder.
• Unknown Etiology.
• Multiple fine nodules.
• Like TB (no caseation).
• Smokers – Uncommon
• SOB, Erythema nodosum,
lymphadenopathy, hypercalcemia,
nephrocalcinosis, occular, skin &
nerve damage.. Etc.
• Stage I asymptomatic to Stage IV –
Pulm fibrosis.
65. Restrictive vs
• Interstitial - (stiff lung)
• Increased tissue
• Relatively normal
FEV1:FVC ratio
• Normal PEFR.
• Types:
•Acute – ARDS,Viral.
•Chronic pneumoconioses &
sarcoidosis, Int. fibrosis.
Obstructive
• Obstructive (soft lung)
• Destruction of tissue.
• Low FEV1:VC ratio
• Low PEFR.
• Types:
–Localised & Diffuse
–Reversible & progressive.
–COPD
–Asthma
–Bronchiectasis,
69. Whether you think that you can
or that you can't,
you are usually right…!
– Henry Ford
70. CPC16: Week overview:
2013 Term 1 CPC 6 Respiratory 3/3 – Lung cancer
System: Respiratory System
Aim: To train students in:
Clinical, pathological & population study of patients with lung
cancer & smoking related lung diseases.
Objectives: 1. History taking & clinical examination of patients for chronic lung
disease & smoking (COPD, cancer etc)
2. Physical examination of patient with respiratory symptoms.
3. Pathophysiology of smoking related lung diseases.
4. Pathophysiology of lung cancers.
5. Review of basic sciences relating to structure and function of
lungs. Blood gas physiology, measurement of blood gases and
lung function tests.
6. Pathophysiology of environmental & smoking related cancer
development (carcinogenesis, chemical, radiation, viral etc.)
7. Epidemiology of smoking related disorders in Australia.
8. Role of health promotion, population & community/rural issues
in smoking & work related lung disorders (pneumoconiosis).
75. Common types of Lung Ca: Biopsy
Adeno carcinoma
Peripheral
Localised
Female
Non smokers
Glands
Pale Blue
Squamous Ca.
Central
Localised
Males
Smokers
Keratin
Pink
Small Cell Ca
Central
Diffuse
Males
Smokers
Oat cell
Dark Blue
76. Lung Ca – Cytology
Adeno carcinoma
Gland formation
Mucin
Squamous Ca.
Pink Cytoplasm
Keratin
Small Cell Ca
little cytoplasm
nil
EGFR (bevacizumab)
ALK, KRAS
Epithelial marker
PTH-rp,
Neuroendocrine
ACTH, ADH, Calcitonin
78. Carcinoid Tumour:
•
•
•
•
Young <40y,
No relation to smoking.
Bronchus, Small polypoid submucosal (<4cm)
Neuroendocrine cells, secrete seratonin carcinoid
syndrome (intermittent attacks of diarrhea, flushing and
cyanosis).
• behave benign even with nodal spread (no distant
metastases).
• Uniform clusters with capillaries (endocrine pattern)
79. Mesothelioma:
•
•
•
•
•
50% history of asbestos exposure.
Latent period of 25-40 years.
Preceded by pleural fibrous plaques.
Encases lungs from pleura.
Biphasic: (Carcinoma+Sarcoma)
Epithelial and fibrous components.
80. ―A good scare is worth more to
a man than good advice."
- Edgar Watson Howe - Country Town Sayings (1911)
That‘s why we have….
Exams!
81. CPC17: Week overview:
2013 Term 1 CPC 7 Title: Cardiovascular System 4/4 – Hypertension & CCF
System: Cardiovascular System
Aim: Clinical presentation, pathology and population studies of
patients with Hypertension and Cardiac Failure.
Objectives: 1. History taking and Clinical examination of patients with
hypertension.
2. Clinical examination of patients with Heart Failure.
3. Pathophysiology of HT and CCF
4. Anatomy of CVS
5. Complications of Hypertension---CCF, AF, CVA, Renal
Failure, Retinal changes, Central vein thrombosis, Aortic
Aneurysm and Aortic Dissection.
95. Compensatory Mechanisms:
• Frank-Starling mechanism:
– More stretch – more contraction.
• Neurohumoral activation:
– Vaso constrictors – norepinephrine
– Renin-Angiotensin system.
– Atrial Natriuretic Peptide – (opposite effect)
• Compensatory Hypertrophy of Heart:
– Pathologic Hypertrophy:
• concentric, pressure, high mortality.
– Physiologic Hypertrophy
• Eccentric, Volume, more BV, e.g. exercise.
95
96. LVF: Pulmonary odema, Brown induration
Brown induration of lung.
―Heart-failure cells‖
96
97. “To educate a person in the mind but not in
morals is to educate a menace to society.”
-Theodore Roosevelt
98. What am I doing? - Where am I going?
(Where I want to be in 5 years?)
“Identifying your Goal is like identifying the
North Star, you fix your compass on it and then
use it as the means of getting back on track when
you tend to stray”
-- Marshall Dimock
99. Wish you all Success,
Health, & Happiness
in life.
Need help for exams?
You can still contact me..