Revision Part2

8/12/2019 Revision Part2

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REVISION

PART2PATHOLOGY OF THE H EMOPOEITIC & LYMPHOID

SYSTEM , BLOOD V ESSELS, HEART, LUNG, K IDNEY,GIT, LIVER, GALL BLADDER, PANCREAS


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Hematopoietic system


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Diagnostic approach to

ANEMIA


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First of all- Think of the

followingWhat are the symptoms of the patient ?What is the level of Hemoglobin?

What does the MCV reveal ?

What does the peripheral blood smear reveal ?

What is the type of anemia ?

What is the cause of this anemia?

What is the pathogenesis ?

What are the investigations for this type of anemia ?


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To make it as simple as possible ?

Is this an IRON DEFICIENCY anemia?

Is this ANEMIA OF CHRONIC DISEASE?

Is this HEMOLYTIC ANEMIA ?

Is this MEGALOBLASTIC ANEMIA ?


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A simple formula Anemia + Microcytic hypochromic red cells = try to think of irondeficiency anemia first.

Anemia + Normocytic red cells + chronic disease = try to think ofanemia of chronic disease.

Anemia + evidence of red cell destruction = try to think of haemolyticanemia

Anemia + macrocytes = try to think of Megaloblastic anemia

Note : The MCV value will give you an idea about the size of the RBC (normocytic/ microcytic/ macrocytic )


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Aplastic anemiaCaused by bone marrow failure.Pancytopenia

Bone marrow- hypocellular


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Polycythemia Increase in red cells/unit volume of peripheral bloodTypes : absolute, relative

Type of absolute polycythemia : Primary, secondary

Investigation: Serum erthropoietin


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Neoplastic proliferation of

white cells LYMPHOID NEOPLASMS : ALL, LYMPHOCYTIC leukemias , NHL,Hodgkin lymphoma, myeloma

MYELOID NEOPLASMS : AML, Myeloproliferative neoplasms (CML,polycythemia vera etc.), myelodysplastic syndrome.

HISTIOCYTIC NEOPLASMS: rare


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How do we make a diagnosis ofleukemia ?

The WBC count is markedly raised. Acute leukemias show many blasts.

Then we have to find out : Is this AML

Is this ALL

Is this CML

Is this CLL

Bone marrow examination is absolutely essential for the diagnosis ofleukemia.

Blast count > 20% = acute leukemias

Depending on the type of blast we classify it as myeloblastic/ lymphoblastic

ALL- more common in children

AML- more common in adults


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Bone marrow

aspiration/biopsy

Absolutely essential for thediagnosis of leukemia / aplasticanemia/ other neoplasticdisorders of marrow etc.


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LymphomaHODGKIN LYMPHOMA :Malignant REED STERNBERG CELL.

surrounded by reactivelymphocytes, macrophages etc.

Orderly spread by contiguity

Morphological types : Fivesubtypes

WHO classification: morphology+

immunophenotypeClinical staging : ANN ARBORClassification

NON HODGKIN LYMPHOMA

Several types

Extranodal involvement common

Clinical staging : ANN ARBOR

WHO classification : morphology +immunophenotype


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Investigation for lymphomaHistopathological study of the affected lymph nodeImmunophenotype

Karyotype etc.


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BLEEDING DISORDERS Due to PLATELET abnormalities THROMBOCYTOPENIA ( Example: ITP)

Due to CLOTTING FACTOR abnormalities

Hemophilia

Von Willebrand disease

Due to vessel wall abnormalities : example: Scurvy


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Tests for bleeding disorders (

basic)Platelet countProthrombin time(PT)

APTT


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DIC

Discussed in the previous revision session.

Recap- Thrombohemorrhagic disorder caused by the systemicactivation of coagulation resulting in systemic microthrombi &activation of fibrinolysis.

Pathogenesis

triggered by either releases of tissue factor/ thromboplastic substance or bywidespread endothelial damage

Results in platelet aggregation & formation of widespread microvascularthrombosis

This results in ischemic tissue damage

The depletion of platelets & clotting factors along with the activation ofplasmin results in an associated bleeding diathesis.


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Heart CONGENITAL HEART DISEASEISCHEMIC HEART DISEASE

HYPERTENSIVE HEART DISEASE

VALVULAR HEART DISEASE

HEART FAILURE

Cardiomyopathy

pericarditis


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Congenital heart diseaseLeft to right shuntASD

VSD

PDA etc

RIGHT TO LEFT SHUNT

early cyanosis is a feature

Tetralogy of Fallot

Transposition of the greatarteries etc.


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Ischemic heart disease Angina pectorisAcute myocardial infarction

Chronic IHD

Sudden cardiac death


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MORPHOLOGIC CHANGES IN

MICOAGULATION NECROSIS- begins at >4 hrs12-24 HOURS- NEUTROPHILIC INFILTRATE APPEARS

7 10 days granulation tissue

> 2 months- collagenous scar


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Investigations for MIELECTROCARDIOGRAPHTROPONIN/CK-MB


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Consequences/ complications

of MIVENTRICULAR RUPTUREVENTRICULAR ANEURYSM

ARRHYTHMIA etc


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ACUTE RHEUMATIC FEVER Rheumatic fever is an acute immunologically mediated multisysteminflammatory disease that occurs after group A beta haemolyticstreptococcal infection

Symptoms: Carditis, arthritis , fever etc

Jones criteria: Carditis, migratory polyarthritis, subcutaneous nodules ,erythema marginatum along with raised ASLO.

Morphology : ASCHOFF BODIES , pancarditis

Pericarditis

MyocarditisValve involvement verrucae


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hypertensive heart disease Systemic ( left sided )hypertensive heart disease.

Left ventricular hypertrophy

Complications- heart failure, IHDetc

Pulmonary hypertensive heartdisease

Right ventricular hypertrophy &dilation

Etiology : pulmonaryhypertension due to disorders oflung parenchyma or pulmonaryvasculature

Types : acute , chronic corpulmonale

Complication : right heart failure


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LUNG Pneumonia, lung abscess

Obstructive lung diseases

Restrictive lung diseases

Pulmonary embolism

Lung tumors

Pleural effusions

Acute lung injury

Atelectasis


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Obstructive lung diseasesBronchial asthma

Chronic bronchitis

Emphysema

Bronchiectasis


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Bronchial asthmaA clinical syndrome characterized by episodic reversible airwayobstruction, bronchial hyperreactivity & airway inflammation.

Types of asthma : atopic , non atopic, drug induced, occupational

Pathogenesis : Type 1 hypersensitivity, acute & chronic airwayinflammation, bronchial hyperesponsiveness.

Triggering of asthma ( sensitization) followed by immediate phase &the late phase

Morphology: Eosinophils ,Mucous plugs, Charcot Leyden crystals,

Curschmann spirals

Clinical features : dyspnea + wheezing


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Chronic bronchitisPersistent production of cough for at least 3 consecutive months intwo consecutive years.

Risk factor_ cigarette smoking

Morphology- marked thickening of mucous gland layer


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EmphysemaChronic obstructive airway disease

Permanent enlargement of airspaces distal to terminal bronchiole

Types : Centriacinar smoking,

Panacinar- alpha 1 antitrypsin deficiency


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Bronchiectasis permanent dilation of bronchi & bronchioles caused by destruction ofthe muscle & elastic tissue , resulting from or associated chronicnecrotizing infection.

Pathogenesis : persistent infection + obstruction


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Restrictive lung diseases (some examples)Pneumoconiosis

Sarcoidosis

Hypersensitivity pneumonitis


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PneumoniaInfection of lung

Types :

Community acquired pneumonia : Types - Acute , atypical

Hospital acquired pneumonia

Morphology: congestion, red hepatisation, grey hepatisation,resolution

Complications: lung abscess, empyema, meningitis, arthritis, infective

endocarditis


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Pulmonary tuberculosis Chronic granulomatous diseases caused by Mycobacteriumtuberculosis.

Pathogenesis :

Unexposed immunocompetent host : Primary pulmonary TB ( Ghoncomplex)

Secondary tuberculosis : arises in a previously sensitized host- upperparts of lung, caseation, cavitation


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AtelectasisLung collapse

Types :

Resorption atelectasis

Compression atelectasis

Contraction atelectasis


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Lung tumors Risk factor for carcinomas- smoking

Types of lung tumors : adenocarcinoma, squamous cell carcinoma,large cell carcinoma, small cell carcinoma, carcinoids.

Small cell carcinomas- best treated by chemotherapy.

Carcinoid- malignant tumors


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Oral cavityOral inflammatory lesions

Proliferative & neoplastic lesions


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EsophagusObstructive diseases

Reflux esophagitis

Esophageal tumors


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Stomach Inflammatory diseases : Gastritis

Neoplastic diseases :

polypsAdenocarcinoma:

INTESTINAL TYPE OF GASTRIC ADENOCARCINOMA ( PRESENTS AS AN EXOPHYTIC MASS)

DIFFUSE TYPE OF GASTRIC ADENOCARCINOMA ( LINITIS PLASTICA)


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Small & large intestines Intestinal obstruction

diarrheal disease

Inflammatory bowel disease

Colonic polyps

Adenocarcinoma


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Liver, gall bladder, biliary tract Jaundice

Hepatic failure

Cirrhosis

Porta hypertension

Fatty liver

Tumors

Cholelithiasis

Cholecystitis

Tumors


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Patterns of hepatic injuryHepatic degeneration

Intracellular accumulation

Hepatic necrosis & apoptosis

Inflammation

Regeneration

Fibrosis


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Pancreas Congenital anomalies

Acute & chronic pancreatitis

Pancreatic neoplasma


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Etiologic factors in acutepancreatitisMetabolic example: alcoholism

Genetic

Mechanical- gallstones, trauma

Vascular- shock

Infection- mumps


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Pathogenesis of acutepancreatitisInappropriate activation of trypsin is the key triggering event

Net result: proteolysis, lipolysis, hemorrhage


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Chronic pancreatitisInflammation with irreversible parenchymal destruction & fibrosis.

Etiology: long term alcohol abuse

Pathogenesis : recurring bouts of acute pancreatitis. Events include

ductal obstruction, toxic effects, oxidative stressMorphology: replacement of pancreatic acinar tissue by dense fibrousconnective tissue,


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Kidney Glomerular diseasesNephrotic syndrome

Nephritic syndrome

RPGN

Tubulointerstitial diseases Tubulointerstitial nephritis

Acute tubular necrosis

Cystic diseases of kidney : Simple cysts, autosomal dominant & recessivepolycystic kidney disease

Obstructive diseases : renal stones, hydronephrosis

Tumors : renal cell carcinoma


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Pathology of BLOOD VESSELSARTERIOSCLEROSIS

ATHEROSCLEROSIS : EPIDEMIOLOGY, RISK FACTORS, PATHOGENESIS ,MORPHOLOGY, CONSEQUENCES

HYPERTENSIVE VASCULAR DISEASE

ANEURYSMS AND DISSECTIONS

VASCULITIS

TUMORS


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Types & causes ofhypertension Essential hypertension

Secondary hypertension

Renal example acute glomerulonephritis

Endocrine- example Cushing syndrome

Cardiovascular- example- coarctation of aorta

Neurologic


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Vascular pathology inhypertension Hyaline arteriosclerosis

Hyperplastic arteriosclerosis


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AtherosclerosisRisk factors: Modifiable, non modifiable

Slowly progressive disease

affects large to medium sized muscular & elastic arteries

Pathogenesis : endothelial injury ,Smooth muscle proliferation

Morphology: atheromatous plaque

Atheromatous plaque = necrotic core, superficial fibrous capcomposed of smooth muscle cells, inflammatory cells

Consequences of atherosclerosis

Stenosis

Thrombosis


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Aneurysm Abnormal vascular dilation

Types of aneurysms: Abdominal aortic aneurysm, thoracic aortic aneurysm

Thoracic aortic aneurysm

Most common etiology- hypertension. Others Marfan syndrome, syphilis

Abdominal aortic aneurysm

Etiology: Most common cause of abdominal aortic aneurysm is atherosclerosis .Other causes include vasculitis, trauma ,mycotic aneurysms, inflammatory

Complication: rupture, compression of adjacent structures etc

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