“Find the key to yourself and every door in the world

is open to you”Mother..

Know your Strengths, Weakness, Interests etc..

2013 Term 1 CPC 1 Title: Cardiovascular System 1/3 – Valvular Heart DiseaseSystem: 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 CPC-1.1

– 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*.

Ms JM, 19-year-old woman living in a remote community who drops out of the local basketball team

Summary: ARF

Pancarditis + systemic(skin, joints, CNS)

Chronic RHD

ARF Microscopy: Aschoff body.

Aschoff Body

ARF- MicroscopyAschoff body

1. Necrosis2. Macrophages3. T Lymphocytes4. Giant cells(Near a BV)

ARF- GrossPancarditis

1. Fibrinous Pericarditis2. Myocarditis3. Endocarditis4. Valve Vegetations.

RHD: Clinical Correlations:

?

?

?

AT BIRTH (%)• Ventricular Septal Defect 42*• Atrial Septal Defect 10• Pulmonary Stenosis 8• Patent Ductus Arteriosus 7• Fallot’s Tetralogy 5• Coarctation Of Aorta 5

Adults % *ASD 47VSD 34FT 11COA 10

Congenital Heart Disease:

Classification:LR Shunts: ASD, VSD & PDA.RL Shunts: Fallot’s, Trans.GA.Obstructions: COA, PS.

Etiology: Toxic, Gen, infecPathogenesis: EmbryogenesisMorphology: Clinical:

Infective Endocarditis:

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.

Intro: ABE- Staph, SBE- StrepEtiology: Abnormal valve, infecPathogenesis: EmbryogenesisMorphology: Valve destruction, bacterial growth.Clinical: Fever, flu, murmur, petechiae.

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

Cardiomyopathy:

• Intrinsic myocardial dysfunction, Primary structural abnorm.

• Congenital / Acquired.• Types:

– Dilated 90%– Hypertrophic– Restrictive.

10

“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!

2013 Term 1 CPC 2 Title: Cardiovascular System 2/4 – IHDSystem: 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.

CPC12: Week overview:

CPC13-1.2 – Chest pain.

• 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,

Mrs. J.B 45 year old Aboriginal woman Presents for an urgent visit complaining of SOB, ‘oppressive feeling’ in her chest

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.

DANGER FACTORS• Low SMC.• Thin cap.• High Inflammation.• Large lipid core.

Plaque Biology:

Morphologic types:

Dots/streaks Soft Plaques Complicated Pl.

Atheroma types:

IHD Pathogenesis:

Stable

Unstable

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

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*

No Q wave - Q wave

Why spared?

What is important in this world is not where we are, but in which direction we are moving.

-- Oliver Wendell Holmes, Jr.

Location of MI & Involved Coronary A.

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

Myocardial Infarction: duration

Old & Recent

MI – stages.

Normal <1day Coagulative necrosis <7 days Acute inflam.

1-3 wk Granulation 3-6 wk Scar 3-6wk scar.

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

“Be like a postage stamp”Stick to one thing until you get there...!

- Josh Billings…

2013 Term 1 CPC 3

Title: Cardiovascular 3/4 - PVD

System: Cardiovascular System, SkinAim: 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.

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

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.

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..

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.

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.

Infectious ulcers: multiple,

• Cause: TB, Treponema (Yaws, Pinta), etc.

• Location: not particular, multiple.• Features:

– irregular, non specific. – Lymphadenitis.

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,

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.

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*

Leg Veins & varicosity:

Common Immune Vasculitis:

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

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. Fibrin

oid NecrosisIn

flam

mato

ry cells

Wegener’s granulomatosis:

Granulomatous inflammation around small vessels with epitheloid cells and giant cells. Lung specimen showing cavitating grey white lesions. (similar to TB)

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.

Giant cell arteritis:

Aorta Temporal Art. Nodular segmental thickening, Most common in adults, T-cell Granuloma + Giant cells, Ophthalmic artery blindness

That person who declares that there is always something wrong is

always doing something to make things wrong.

— Christian Larson

CPC14: Week overview:2013 Term 1

CPC 4Title: Respiratory 1/3 - Pneumonia

System: Respiratory SystemAim: 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).

Pneumonia

47

Pathogenesis of Pulmonary Infections

Aspiration, Inhalation, Inoculation, Colonization, Hematogenous & Direct spread

Pneumonia

48

Pneumonia Types:

Etiologic Types: Infective

Viral Bacterial Fungal Tuberculosis

Non Infective Toxins chemical Aspiration

Morphologic types: Lobar Broncho InterstitialDuration: Acute ChronicClinical: Primary /

secondary. Typical / Atypical Community a /

hospital a

Pneumonia

49

Types of Pneumonias & Causative agents

Community-Acquired Typical Pneumonia: Strep, H.influenzae, Staph aureus, Klebsiella.

Community-Acquired Atypical Pneumonia: Mycoplasma, Chlamydia, Legionella, SARS*, Q

Fever Nosocomial Pneumonia:

Klebsiella spp., Serratia, E coli, Pseudomonas Aspiration Pneumonia:

Anaerobic oral flora (Bacteroides) Chronic Pneumonia:

Nocardia, Actinomyces, Atyp. Mycob, Fungal (TB) Necrotizing Pneumonia and Lung

Abscess: Anaerobic bacteria

Pneumonia in the Immunocompromised: CMV, Pneumocystis, Atyp. Mycob. Fungal.

CongestionRed Hepatisation

Grey HepatizationResolution

Pathogenesis of Pneumonia

Pneumonia

51

Stages of pneunomia:

Pneumonia

52

Broncho – Pneumonia - Lobar

Extremes of age. Secondary, in sick. Both genders. Staph, Strep, H.infl. Patchy consolidation Around Small Bronchi Not limited by anatomic

boundaries. Usually bilateral.

Middle age – 20-50 Primary in a healthy adult. males common. 95% pneumococcus

(Klebs.) Entire lobe consolidation Diffuse Limited by anatomic

boundaries. Usually unilateral

Pneumonia

53

Chronic Pneumonia Chronic, lymphoid infiltrate, No classic stages. Lung destruction. Organisms

TB, Fungal etc.

Interstitial pneumonia

Viral

NON INFECTIVE PNEUMONIA:• Aspiration pneumonia

• Lower lobe, sec infection, abscess.

• Lipid pneumonia• Airway obstruction,

atelectasis.• Eosinophilic pneumonia

• Asthma, Löffler's syndrome.

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

CPC15: Week overview:2013 Term 1 CPC 5 Title: Respiratory 2/2 - Asthma & COPD

System: Respiratory SystemAim: 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.

Pathogenesis of COPD

1. Smoke, irritants, carcinogens.

2. Tissue irritation & destruction

3. Inflam Mucous production.

4. Airway thickening narrowing.

5. Alveolar damage widening.• Increase in

– Alveolar marcrophages– CD8 Lymphocytes– Neutrophils– Proteases.

• Airway damage Bronchitis• Alveoli damage Emphysema.• Both COPD.

α1AT def.. Emphysema

Bronchitis Emphysema

Both affected commonly COPD

COPD: Overlap of Clinical syndromes

COPD

Normal - COPD

CB

Emphysema

Restrictive lung disorders:Definition: Reduced expansion.

A. Intrinsic Lung Disorders:– Sarcoidosis, pneumoconiosis.– TB, Interstitial Pneumonia

B. Extrinsic Dis. (chest wall):– Scoliosis, Kyphosis, Obesity,– Pleurisy, rib fracture etc.

C. Neuromuscular Disorders:– Paralysis of the diaphragm,

Myasthenia Gravis, Poliomyelitis.

Pathogenesis

Silicosis:• Inorganic – sand & stone

dust.• Toxic to macrophages –

destruction fibrosis.• Scattered multiple small,

fibrotic Nodules• Surrounding Irregular

emphysema.• Restrictive pattern of

PFT.

Asbestosis:• Asbestos bodies in sputum.

– (Protein & Hemosiderin)

• “Inconsumable”, Beaded 5-100mm x 0.25mm.

• Within alveoli at lung bases.• Dyspnoea, dry cough• Clubbing is common.• Diffuse effusion consolidation*,

fibrosis Honey comb lung.

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.

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.

Restrictive vs Obstructive• Interstitial - (stiff lung)• Increased tissue •Relatively normal FEV1:FVC ratio

•Normal PEFR. •Types:•Acute – ARDS,Viral.•Chronic - pneumoconioses & sarcoidosis, Int. fibrosis.

•Obstructive (soft lung)•Destruction of tissue.•Low FEV1:VC ratio

•Low PEFR.•Types:

–Localised & Diffuse–Reversible & progressive.–COPD –Asthma–Bronchiectasis,

Asthma : Pathogenesis

Early phase (immediate) and late phase reactions

Asthma Morphology:

Asthma Microscopy1.Mucous Plugs +eosinophils2.Goblet cell hyperplasia3.Inflammation + Eosinophils4.Smooth muscle hyperplasia5.Mucous gl. Hyperplasia.

Lung Function Tests:

Whether you think that you can or that you can't,

you are usually right…!

– Henry Ford

CPC16: Week overview:2013 Term 1 CPC 6 Respiratory 3/3 – Lung cancer

System: Respiratory SystemAim: 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).

Pathogenesis – Lung Cancer.

3pK-RasC-myc

p53

Irritation Carcinogens Initiation Promotion Ca.

Pathogenesis:1. Smoking – carcinogens2. 3p – tumor suppressor gene loss3. Mutations (p53, KRAS, EGFR..)4. Dysplasia5. Infiltration6. Spread7. Metastases.

Biology of Cancer:• Grading Differentiation Microscopic• Staging Progression Clinical - TNM

Low Grade high

• T – Tumor (T1-4)

• N – Node (N1-3)

• M – Metastasis (M0-1)

Stage

Lung tumors Classification:

• Bronchogenic Carcinoma: (95%)– Small cell carcinoma SCC 20%– Non Small Cell Carcinoma NSCC 80%

• Adeno carcinoma ~40%*• Squamous carcinoma ~35%• Large cell anaplastic ~5%

• Other Tumours (5%)– Bronchial Carcinoid Tumor– Lung Hamartoma

• Metastatis (more common)• Tumors of Pleura - Mesothelioma• Mediastinal Tumours

– Thymic & other Lymphoma, Teratoma.

SCCSq

Big 3

Ad

SCC NSCC

SCC Sq. Ca Ad. Ca

Common types of Lung Ca: Biopsy

Adeno carcinoma Squamous Ca. Small Cell CaPeripheral Central CentralLocalised Localised DiffuseFemale Males MalesNon smokers Smokers SmokersGlands Keratin Oat cellPale Blue Pink Dark Blue

Lung Ca – Cytology

Adeno carcinoma Squamous Ca. Small Cell CaGland formation Pink Cytoplasm little cytoplasmMucin Keratin nil

EGFR (bevacizumab) Epithelial marker NeuroendocrineALK, KRAS PTH-rp, ACTH, ADH, Calcitonin

Clinical features & complications.• Local:

– Obstruction– Effusion– Pneumonia* lipid, other.– Bronchiectasis– Atelectasis– Haemoptysis– COPD (risk)

• Systemic:– Cachexia– Paraneoplastic sy– Clubbing– Pulm. Osteoarthropathy.– Bone pain– CNS dysfunction

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)

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.

“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!

CPC17: Week overview:

2013 Term 1 CPC 7 Title: Cardiovascular System 4/4 – Hypertension & CCFSystem: 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 CCF4. Anatomy of CVS5. Complications of Hypertension---CCF, AF, CVA, Renal

Failure, Retinal changes, Central vein thrombosis, Aortic Aneurysm and Aortic Dissection.

Blood Pressure:

82

(Aorta)

Cerebral / Coronary arteries

Resistant chamber

• Pressure = Pump + Resistance.• BP = Cardiac Output + BV. Res.• BP = CO + PR• Heart function, Blood volume, BV

elasticity control BP.• Kidney function important control.• Water*, Sodium* & BV tone*• Renin & Angiotensin system.

Measurements

BP

mmHg

• Pulse Pressure: 120-80 = 40 mmHg• Central Venous Pressure: 6 mmHg• Mean Arterial Pressure: DP+1/3PP = 93• Pulmonary Pressure: 20/10 mmHg• Cardiac Output: 4-8 L/min

Control of Blood Pressure:

83

Kidney BP Control:• Heart• Kidney• Hormones• Nerves

Complications: • BV thickening – Ischemia – Claudication.• Chronic, end organ & vascular damage.• Infarction(MI), Hemorrhage, Stroke & Aneurysm.

Heart Failure- PathophysiologyRenin Angiotensin Aldosterone BP & Fluid retention.

85

12

3

Low BloodLow GFR

High Fluid & High PR = High BP

Neurohormonal Mechanisms in HF

86

Inciting event

Hypertension

87

Ventricular Hypertrophy

88

LVH RVH

Systemic Hypertension Pulmonary Hypertension

>2 cm

Microangiopathy in Hypertension:• Hyaline arteriolosclerosis:

– Pink, hyaline thickening of vessel walls – narrowing of lumen

• Hyperplastic arteriolosclerosis:

– malignant hypertension : definition?– concentric laminated thickening of walls (“onion skin”) – Narrowing of lumen - smooth muscle proliferation

89

“onion skin”

Benign Nephrosclerosis

“Grain-leather kidney”

Hyaline arteriolosclerosis

Subarachnoid HaemorrhageIntracerebral haemorrhage (Stroke)

Hypertensive Intracranial haemorrhage

Hypertensive Retinopathy

• Grade I – Thickening of arterioles.

• Grade II – Focal Arteriolar spasms. Vein constriction. (AV nipping)

• Grade III – Hemorrhages (Flame shape), dot-blot and Cotton wool (ischemia) and hard waxy exudates (lipid deposition).

• Grade IV - Papilloedema

“Intelligence plus character, that is the goal of true education”

- Martin Luther King Jr.

Terminal cancer vs CHF

94

Worsening & compensatory mechanisms.

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

LVF: Pulmonary odema, Brown induration

96“Heart-failure cells”

Brown induration of lung.

“To educate a person in the mind but not in morals is to educate a menace to society.”

-Theodore Roosevelt

“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

What am I doing? - Where am I going?(Where I want to be in 5 years?)

Wish you all Success, Health,

& Happiness in life.

Need help for exams? You can still contact me..