Pathology Review-Term1

1. Pathology Review-Term1 “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 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*. 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*.

4. Summary: ARF Chronic RHD Pancarditis + systemic (skin, joints, CNS) Summary: ARF Chronic RHD Pancarditis + systemic (skin, joints, CNS)

5. ARF Microscopy: Aschoff body. ARF- Microscopy Aschoff body 1. Necrosis 2. Macrophages 3. T Lymphocytes 4. Giant cells (Near a BV) 1. 2. 3. 4. ARF- Gross Pancarditis Fibrinous Pericarditis Myocarditis Endocarditis Valve Vegetations. ARF Microscopy: Aschoff body. ARF- Microscopy Aschoff body 1. Necrosis 2. Macrophages 3. T Lymphocytes 4. Giant cells (Near a BV) 1. 2. 3. 4. ARF- Gross Pancarditis Fibrinous Pericarditis Myocarditis Endocarditis Valve Vegetations.

6. RHD: Clinical Correlations: ? ? ?

7. Congenital Heart Disease: Etiology: Toxic, Gen, infec Pathogenesis: Embryogenesis Morphology: Clinical: AT BIRTH (%) • Ventricular Septal Defect • Atrial Septal Defect • Pulmonary Stenosis • Patent Ductus Arteriosus • Fallot‘s Tetralogy • Coarctation Of Aorta 42* 10 8 7 5 5 Classification: LR Shunts: ASD, VSD & PDA. RL Shunts: Fallot‘s, Trans.GA. Obstructions: COA, PS. Adults ASD VSD FT COA %* 47 34 11 10 Congenital Heart Disease: Etiology: Toxic, Gen, infec Pathogenesis: Embryogenesis Morphology: Clinical: AT BIRTH (%) • Ventricular Septal Defect • Atrial Septal Defect • Pulmonary Stenosis • Patent Ductus Arteriosus • Fallot‘s Tetralogy • Coarctation Of Aorta 42* 10 8 7 5 5 Classification: LR Shunts: ASD, VSD & PDA. RL Shunts: Fallot‘s, Trans.GA. Obstructions: COA, PS. Adults ASD VSD FT COA %* 47 34 11 10

8. Infective Endocarditis: Intro: ABE- Staph, SBE- Strep Etiology: Abnormal valve, infec Pathogenesis: Embryogenesis Morphology: Valve destruction, bacterial growth. Clinical: Fever, flu, murmur, petechiae. NON INFECTIVE VALVE DISORDERS: • Non bacterial thrombotic..NBTE – marantic. • Libman-Sacks endocarditis – autoimmune – APL sy. • Endocardial myofibrosis in Carcinoid syndrome. Prosthetic valves – Mech/Bio, infec, thromb, hemolysis. Infective Endocarditis: Intro: ABE- Staph, SBE- Strep Etiology: Abnormal valve, infec Pathogenesis: Embryogenesis Morphology: Valve destruction, bacterial growth. Clinical: Fever, flu, murmur, petechiae. NON INFECTIVE VALVE DISORDERS: • Non bacterial thrombotic..NBTE – marantic. • Libman-Sacks endocarditis – autoimmune – APL sy. • Endocardial myofibrosis in Carcinoid syndrome. Prosthetic valves – Mech/Bio, infec, thromb, hemolysis.

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 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

10. . Cardiomyopathy: • Intrinsic myocardial dysfunction, Primary structural abnorm. • Congenital / Acquired. • Types: – Dilated 90% – Hypertrophic – Restrictive. 10

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,

14. . Pathogenesis: 1. intimal injury (at bifurcations) 2. Inflammatory cells & macrophages. 3. Lipid deposition, Central Necrosis, more inflammation (soft plaque) 4. Fibrosis, smooth muscle proliferation (hard plaque) 5. Complications – activaton, Thrombosis, embolism, aneurism, dissection & rupture.

15. . DANGER FACTORS Plaque Biology:SMC. • Low • Thin cap. • High Inflammation. • Large lipid core.

16. . Morphologic types: Dots/streaks Pl. Soft Plaques Complicated

17. . Atheroma types:

18. . IHD Pathogenesis: Coronary block: • <70% - Asymptomatic. • >70-75% - Stable Angina (exersion) • 90% - Fixed stenosis (rest) Chronic IHD • Plaque change: (ACS) – Rupture, fissure, ulcer, thromb/embolism. – Unstable angina, MI / SCD Stable Unstable

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*

20. . No Q wave - Q wave Why spared?

21. . What is important in this world is not where we are, but in which direction we are moving. -- Oliver Wendell Holmes, Jr.

22. . Location of MI & Involved Coronary A.

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

24. . Myocardial Infarction: duration Old & Recent

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.

29. . Chronic leg ulcers: DD • • • • • • Venous : Varicose veins, Thrombophlebitis. Arterial : Atherosclerosis, Diabetes*. Neuropathic : Diabetes* Malignancy : BCC, SCC, MM Infections : leprosy, TB, Treponemal, (Yaws) Others : Dermatitis, Vasculitis, Lymphedema.. Leg ulcers 1%  Venous 80% - Arterial 10% * RACGP

30. . Venous ulcers: (Wet, Bleeding, Dermatitis. • Cause: Varicose veins. • Location: Gaiter region. • Features: – large, irregular, shallow. – Wet edematous, oozing. – Moist granulating base – bleeds on touch. – Surrounding eczematous stasis dermatitis. – Mild pain, relieved by elevation. – Compression bandage helps.

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,

36. . Risk Factors for DVT • Virchow‘s triad: (Flow– Blood - Vessel) – Stasis, Hypercoagulability & BV injury. • Stasis (flow) – Immobilization, paralysis, in-patients, heart failure. • Hypercoagulability (Blood): – – – – Congenital: AT III, Protein-C/S deficiency, F V Leiden Acquired: Lupus & anti cardiolipin anticoagulants, Drugs, Oral contraceptives, Hyperhomocysteinemia. Hyperviscosity – Polycythemia, paraproteins. • Tissue damage (Vessel): – Surgery, Trauma, MI, Stroke, Malignancy, Phlebitis.

37. . Varicose Veins: • Tortuous superficial veins due to valve defect in deep veins of lower limb. • Congenital / Acquired. • Tortuous prominent veins. • Gaiter region. • Thrombosis & ulceration. • Over Medial malleolus. • Note: No DVT* or PE*

38. . Leg Veins & varicosity:

39. . Common Immune Vasculitis:

40. . Raynaud‘s Phenomenon: • • • • Vasoconstriction of digital arteries. Cold/emotional trigger. Primary: R.disease – genetic 3-5% Secondary: Vasculitis, SLE, Buergers, atherosclerosis, cold Ab hemolytic anemia etc. Pallor Cyanosis

41. . Polyarteritis nodosa: • Rare, Immune, HBs ag. • Systemic vasculitis with necrotizing inflammation. • Nodules over arteries. • Acute fever, muscle & joint pain, asymetric polyarthritis • Malaise rash & weight loss. • Neuropathy, kidney failure,. • High ESR, CRP, WBC. • Treat: Immunosuppression.

42. . Wegener‘s granulomatosis: Granulomatous inflammation around small vessels with epitheloid cells and giant cells. Lung specimen showing cavitating grey white lesions. (similar to TB)

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).

47. . Pneumonia Pathogenesis of Pulmonary Infections Aspiration, Inhalation, Inoculation, Colonization, Hematogenous & Direct spread 47

48. . Pneumonia Pneumonia Types: Etiologic Types:  Infective      Viral Bacterial Fungal Tuberculosis Non Infective    Toxins chemical Aspiration Morphologic types:  Lobar  Broncho  Interstitial Duration:  Acute  Chronic Clinical:  Primary / secondary.  Typical / Atypical  Community a / hospital a 48

49. . Pneumonia Types of Pneumonias & Causative agents  Community-Acquired Typical Pneumonia:   Community-Acquired Atypical Pneumonia:   Nocardia, Actinomyces, Atyp. Mycob, Fungal (TB) Necrotizing Pneumonia and Lung Abscess:   Anaerobic oral flora (Bacteroides) Chronic Pneumonia:   Klebsiella spp., Serratia, E coli, Pseudomonas Aspiration Pneumonia:   Mycoplasma, Chlamydia, Legionella, SARS*, Q Fever Nosocomial Pneumonia:   Strep, H.influenzae, Staph aureus, Klebsiella. Anaerobic bacteria Pneumonia in the Immunocompromised:  CMV, Pneumocystis, Atyp. Mycob. Fungal. 49

50. . Grey Hepatization Resolution Pathogenesis of Pneumonia Congestion Red Hepatisation