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Pathology by Mind Map: Pathology

1. Week 1

1.1. Genetically determined disorders

1.1.1. Cytogenic

1.1.2. Mendelian

1.1.3. Multifactorial inheritance

1.1.4. Congenital malformation

1.2. Response to cell injury

1.2.1. Sublethal (mild) Parenchymal undergo reactive change CT cells experience inflammation

1.2.2. Lethal (severe) Parenchymal & CT experience necrosis

1.3. Necrosis

1.3.1. Coagulative Most common; solid organs

1.3.2. Colliquative (Liquefactive) Occuring in brain due to autolysis (brain infarct) completing with little coagulation Occurring in suppuration due to neutrophils lysing pyogenic bacteria (e.g. pimple)

1.3.3. Caseous Tuberculosis, due to hypersensitivity reaction

1.3.4. Haemorrhagic Result of ischaemia leading to necrosis infiltrated with RBC

1.3.5. Gummatous Tertiary syphilis (treponema pallidum)

1.3.6. Fat Enzymatic Occurs around pancreas & associated adipose tissue (e.g. alcoholics) Traumatic Occurs when adipose tissue is injured (e.g. breast tissue after surgery)

1.3.7. Fibrinoid Occurs in CT, blood vessel walls in hypertension & autoimmune diseases; collagen degenerates to resemble fibrin

1.3.8. Gangrenous Result of ischaemia & infection of necrotic tissue with anaerobic bacteria

2. Week 2

2.1. Cardinal signs

2.1.1. Calor (heat)

2.1.2. Rubor (redness)

2.1.3. Dolor (pain)

2.1.4. Tumor (swelling)

2.1.5. Functio laesa (loss of function)

2.2. Acute inflammation outcomes

2.2.1. Resolution e.g lobar pneumonia

2.2.2. Formation of an abscess e.g. brain abscess

2.2.3. Repair (healing) e.g. bronchopneumonia

2.2.4. Chronic inflammation e.g. chronic peptic ulcer

2.3. Types of chronic inflammation

2.3.1. Chronic fibrous inflammation Collagen scar; can lead to stenosis

2.3.2. Chronic serous inflammation Serous fluid made by serous membrane; cold swelling; bursitis

2.3.3. Chronic suppurative inflammation Too much pus; chronic abscess

2.3.4. Chronic ulcerative inflammation Deep excavation in tissue e.g. ulcer

2.3.5. Chronic granulomatous inflammation Tissue destroyed by specialised microbes/immunity; granuloma is formed Example: Hansen's disease

2.3.6. Active chronic inflamamtion

2.4. Tuberculosis

2.4.1. Bronchopneumonia bronchial spread

2.4.2. Miliary tuberculosis blood spread

3. Week 3

3.1. Soft tissue wounds

3.2. Fracture types

3.3. Healing of a wound

3.4. Healing of a fracture

4. Week 4

4.1. Variations of growth

4.1.1. Hyperplasia Increase in mass due to increase in number of cells E.g. remaining kidney after nephrectomy

4.1.2. Hypertrophy Increase in mass due to increase in size of cells E.g. athletes and their big muscles

4.1.3. Atrophy Decrease in mass due to decrease in size/number of cells E.g. uterus after menopause/childbirth

4.1.4. Agenesis Failure of organ to develop at all E.g. Anencephaly

4.1.5. Aplasia Sudden cessation of growth (traumatic) E.g. Thymus gland after childhood

4.1.6. Hypoplasia Tissue fails to attain full size due to deficient growth E.g. cryptochidism (undescended testis)

4.1.7. Metaplasia Fully differentiated adult cells change into another more resilient but less specific cell type E.g airways of a smoker

4.1.8. Dysplasia Abnormal growth and differentiation; pre-malignant E.g. oral cavity (smoking or dentures), respiratory tract (smoking), cervix (HPV

4.1.9. Hamartoma Focal overgrowth of normal cells where they are normally present E.g. mole (benign naevus)

4.1.10. Choristoma (ectopia) Focal overgrowth of normal cells found where they are not supposed to be E.g. endometriosos

4.1.11. Neoplasia Formation of abnormal, uncontrolled tissue growth with no coordinated function E.g. tumour

4.2. Neoplasms

4.2.1. Clinical classification Benign Malignant Differentiation Well differentiated Poorly differentiated Non differentiated Anaplastic tumours

4.2.2. Histogenic classification -oma for benign tumours carcinoma for tumours of epithelial origin sarcoma for tumours of mesenchymal origin Exceptions Glioma - glial cells in brain Melanoma - melanocytes Mesothelioma - mesothelium Myeloma - plasma cells Leukaemia - bone marrow Blastoma - primitive stem cells Teratoma - pluripotential cells (benign or malignant)

4.2.3. Morphological classification Polyp/polypoid - toadstool Papillary (fungating) - cauliflower Ulcerating - excavating Infiltrating - rapidly spreading Nodular - lump Cystic - fluid filled cyst Scirrhous - hard on palpation due to much collagenous stromal tissue Encephaloid - soft on palpation due to little collagenous stromal tissue

4.3. Types of cell

4.3.1. Labile cells

4.3.2. Stable cells

4.3.3. Permanent cells

5. Week 5

5.1. Carcinogenesis

5.1.1. Targets for genetic damage Growth promoting proto-oncogenes Growth-inhibiting tumour suppressor cells Genes that regulate apoptosis Genes involved in DNA repiar

5.1.2. Intrinsic factors Genetic e.g. trisomy 21 & leukaemia Racial and geographical Immunological e.g. AIDS & higher incidence of cancer Sex & hormonal e.g. hormonal stimulation leading to cancer Age Pre-existing benign neoplasm

5.1.3. Extrinsic factors Chemical agents e.g. soot exposure causing carcinoma of the scrotum Physical agents e.g. radiation, trauma, inert substances Biological factors Parasite Fungi and bacteria Virus

5.2. Immunodeficiency

5.2.1. Primary Present at birth E.g. Bruton's disease - agammaglobulinemic E.g. Di George - congenital thymic aplasia E.g. Swiss-type - combined immunodeficiency

5.2.2. Secondary Miscellaneous e.g. Aging - erysipelas e.g. Infection e.g. Neoplasm - Hodgkin's disease of the spleen AIDS Virus infects CD4 cells

5.3. Hypersensitivity

5.3.1. Type 1 - immediate mast cells and IgE e.g. allergic reaction

5.3.2. Type 2 - antibody IgG or IgM damage cells e.g. erythroblastosis

5.3.3. Type 3 - immune complex antigens  and Abs form immune complexes e.g. serum sickness e.g. glomerulonephritis

5.3.4. Type 4 - t-cell mediated t-cell immune response e.g. mosquito bites

5.4. Autoimmune disorders

5.4.1. Organ-specific e.g. hashimoto's disease e.g. atrophic gastritis

5.4.2. Systemic e.g. systemic lupus erythematosus e.g. rheumatoid arthritis

6. Week 7

6.1. Oedema

6.1.1. Localised Special terms Ascites - peritoneum oedema Hydrothorax Hydropericardium Hydrocele - tunica vaginalis Causes Acute inflammation Type 1 hypersensitivity Lymphatic obstruction Impaired venous drainage

6.1.2. Generalised Special terms Anasarca Hydrops Causes Pathogenic Renal disorders Liver disease Malnutrition Other clinical states

6.1.3. Fluid types Transudate non-inflammatory tissue fluid with little protein Exudate inflammatory fluid with high protein Serous Fibrinous Haemorrhagic Suppurative

6.1.4. Life threatening forms Pulmonary - due to LV failure Cerebral - due to head trauma; infections

6.2. Haemorrhage

6.2.1. Types Ecchymosis Haematoma Petechiae Internal External

6.2.2. Colour changes Bright red - oxygenated Hb Cherry red - unoxygenated Hb Greenish - biliverdin Orange/yellow - bilirubin Brownish - haemosiderin

6.3. Purpura

6.3.1. Thrombocytopenia less platelet production from bone marrow

6.3.2. Non-thrombocytopenic vascular defects with normal platelet numbers

6.3.3. Thromboasthenia platelets are abnormal in function

6.4. Shock

6.4.1. Primary Injury Great pain Strong emotion Fluid balance not effected

6.4.2. Secondary Hypovolemic shock Cardiogenic shock Septic shock Fluid balance effected

6.5. Thrombosis

6.5.1. Types Pale - platelets and fibrin Dark - fibrin, RBW & WBC Mixed - regions of both (lines of Zahn)

6.5.2. Forms Mural adherent to one side of vessel wall Occlusive lumen totally attached Coralline irregular - may become occlusive Propagating progressive involvement of thrombus into other branches Ball unattached spherical thrombus Septic presence of infection Vegetations thrombi on heart valve

6.5.3. Virchow's triad Change in vessel wall Change in blood flow Changes in blood constituents

6.5.4. Fate of thrombi Propagation thrombus enlarges along vessel Lysis and resolution most favourable Calcification dystrophic calcification Infection septicaemia Retraction, organisation, recanalization thrombus shrinks, re-establishment of blood flow through scar tissue Thromboembolism detachment of thrombus travelling to a distant location Infarction thrombus interrupts blood flow, anoxia and necrosis

6.6. Thromboembolism

6.6.1. Venous emboli lodge in pulmonary vessels arise in deep leg veins

6.6.2. Arterial emboli arise in aorta, coronary & cerebral arteries lodge in any organ

6.6.3. Fat emboli Bone fracture type Atherosclerotic plaque type

6.6.4. Gas emboli Air emboli Nitrogen emboli - divers

6.6.5. Foreign body emboli

6.6.6. Tumour emboli arise in venules or veins due to malignant tumour infiltration

6.6.7. Amniotic fluid emboli occurs during childbirth

6.7. Embolism

6.7.1. Occlusion of vessel by mass of material transported into bloodstream

7. Week 8

7.1. Infarction

7.1.1. Classifications Pale infarct Arterial blood supply is obstructed Red infarct Venous drainage is obstructed Mixed infarct Begin as pale then blood supply is partially readmitted

7.1.2. Occlusion of arteries

7.1.3. Occlusion of veins

7.2. Hypertension

7.2.1. Aetiology Primary Secondary

7.2.2. Clinical Beningn most common kidney lesions develop over years Malignant can supervene on benign hypertension 'onion skin' arterioles petechial haemorrhages on kidney surface

7.2.3. 1st degree Idiopathic Genetic, environment, hormonal, neurogenic

7.2.4. 2nd degree excessive renin production renal atery stenosis endocrine causes (aldosterone, oestrogen, noradrenaline) iatrogenic causes (oestrogen)

7.3. Ateriosclerosis

7.3.1. Atherosclerosis aorta and major branches disorder of intima typical lesion is atheroma/atheromatous plaque Lesions fatty streaks musculoelastic lesions typical atheromatous plaques complicated atheromatous plaques Clinical effects Intermittent ischaemic effects Thrombosis, embolism, infarction Aneurysm formation

7.3.2. Monckeberg's medial calcification idiopathic with degeneration and necrosis of medial smooth muscle followed by dystrophic calicification intima is not affected

7.3.3. Arteriolosclerosis seen with systemic hypertension seen in normotensive, elderly people and people with diabetes mellitus

8. Week 9

8.1. Congentical

8.1.1. Left to right shunts Atrial septal defect Ventricular septal defect Patent ductus arteriosus

8.1.2. Pulmonary stenoic lesions Narrowing of the pulmonary artery/valve less oxygenation of blood leads to cyanosis Fallot's tetraology

9. Week 10

9.1. Congenital disorders

9.1.1. Bronchial atresia - narrowed bronchus

9.1.2. Hypoplasia of lung

9.1.3. Bronchogenic cysts - usually attached to trachea

9.1.4. Bronchopulmonary sequestration - portion of lung not communicating

9.1.5. Kartagener's syndrome - defective cilia

9.1.6. Neonatal respiratory distress syndrome (NRDS) - deficiency of surfactant, aveoli collapse

9.1.7. Cystic fibrosis multisystem disease CF gene causes production of abnormal viscid mucus that cannot be cleared from lungs recurrent infections hyperinflation & pneumothorax necrosis, scarring

9.2. Circulatory disorders

9.2.1. Chronic venous congestion reduced LV output leads to rupture of alveolar capillaries, haemorrhage, necrosis & fibrosis

9.2.2. Pulmonary oedema Congestive heard failure, infections, toxic gas inhalation leads to dys leads to dyspnoea, hypostatic pneumonia

9.2.3. Pulmonary embolism Arise in deep leg vein Leads to dyspnoea, tachycardia, shock Infarction or fatal

9.2.4. Pulmonary infarction elderly/post-op patients with heart failure may develop thromboemboli Leads to dyspnoea/scarring/death

9.2.5. Pulmonary hypertension

9.3. Chronic obstructive pulmonary disease (COPD)

9.3.1. Disease state characterised by persistent airflow limitation that is not fully reversible

9.3.2. Leads to dyspneoa/shortness of breath, cough and/or sputum production

9.3.3. Causes Emphysema increase in size of alveolar space and loss of recoil Bronchiectasis permanent, abnormal dilation of bronchi and bronchioles cough and sputum present Chronic bronchitis & bronchiolitis airway narrowing caused by mucous hypersecretion, inflammation of ariways due to inhalation of dust/smoke etc.

9.4. Asthma

9.4.1. Reversible bronchospasm causing wheezing & excess mucus mediated by type 1 hypersensitivity

9.4.2. Extrinsic - allergen/enivronment

9.4.3. Intrinsic - exercise/stress

9.4.4. Sequelae mild disease status asthmaticus (chronic inflated lungs because air cannot escape) chronic asthma COPD

9.5. Infections & inflammation, ARDS

9.5.1. rhinitis

9.5.2. sinusitis

9.5.3. laryngitis

9.5.4. tracheitis

9.5.5. tracheo-bronchitis

9.5.6. bronchiolitis

9.5.7. pneumonia lobar pneumonia - whole lobe bronchopneumonia - patchy

9.5.8. pleurisy

9.5.9. viral infections

9.5.10. fungal infections

9.5.11. tuberculosis acid fast bacilli stain pink with Ziehl-neelsen stain

9.5.12. sarcoidosis idiopathic, non caseating, granulomatous inflammation

9.5.13. ARDS diffuse alveolar damage & inflammation Causes septicaemia, major trauma toxic smoke/fume inhalation amniotic fluid embolism, DIC radiation injury, chemotherapy 70% die in acute phase, 10% recover, 20% due due to chronic impairment

9.6. Organic & inorganic pneumoconioses

9.6.1. Dust inhalation disease

9.6.2. Organic Byssinosis - cotton Bagassosis - sugar cane refuse Farmers' lung - mouldy hay Suberosis - cork dust

9.6.3. Inorganic Anthracosis - carbon Silicosis - silica Silicoanthracosis - carbon & silica Berrylliosis - berryllium Silicosiderosis - silica & iron Asbestosis - asbestos leads to asbestosis, COPD, mesothelioma of pleura

9.7. Primary & secondary tumours

9.7.1. Mesothelioma of the pleura exposure to asbestos highly malignant, death usually within 10 months of diagnosis

9.7.2. Carcinoma of the bronchus due to smoking, x-rays, asbestosis etc. peripheral masses may give rise to para-neoplastic syndromes e.g. pancoast syndrome - pain in shoulder, arm & hand e.g. horner's syndrome - nerves supplying eye are damaged Diagnosis chest x-ray bronchoscopy & biopsy needle biopsy of lymph nodes sputum sytology

9.7.3. breast, bone, skin, kidney tumours commonly metastasise into lungs

10. Week 11

10.1. Inflammation & carcinoma of oral cavity

10.1.1. Inflammation Mainly due to HSV type 1, EBV, coxsackievirus e.g. stomatitis, cheilitis, glossitis, gingivitis, peridontitis, dental caries, sialadenitis, pharyngitis

10.1.2. Carcinoma of oral cavity lips, tongue, buccal mucosa, pharynx, males more common morphology - squamous cell carcinoma treatment - surgical excision; radiotherapy (poor prognosis)

10.2. Hiatus hernia & oesophagitis

10.2.1. Oesophagitis Due to gastro-oesophageal reflux disease (GORD) or infections GORD may lead to dyspepsia, dysphagia or Barrett's oesophagus (which can lead to adenocarcinoma)

10.2.2. Hiatus hernia protrusion of part of stomach into thoracic cavity through diaphragmatic hiatus rolling (5%) sliding (95%) Causes congenital weakness in diaphragm obesity/overloading of the stomach Symptoms same as GORD Treatment - surgery/small meals/weight reduction

10.3. Oesophageal varices & carcinoma of oesophagus

10.3.1. Oesophageal varices Dilated veins due to cirrhosis of the liver and portal hypertension

10.3.2. Plummer-Vinson syndrome Sideropenic dysphagia & abnoral peristalsis and mucosal webs F.I.D.A.C.K.S

10.4. Gastritis & gastric atrophy

10.4.1. Acute (erosive) gastritis Due to alcholo, aspirin, H.pylori, NSAIDS Characterised by erosions usually resolves

10.4.2. Chronic gastritis Chronic helicobacter-associated gastritis (most common; good prognosis) Chronic atrophic (autoimmune) gastritis (poor prognosis) may lead to gastric Ca Reactive gastritis due to reflux of NSAIDS or bile into lower part of stomach (good prognosis)

10.5. Peptic ulceration & carcinoma of the stomach

10.5.1. Acute peptic ulcers Progression of acute (erosive) gastritis (usually heal) may progress to chronic peptic ulcer

10.5.2. Chronic peptic ulcers 30-45 years - due to genetics, smoking, low blood supply Gnawing pain in epigastrium 1-3 hrs after meal Steady pain in epigastrium 2-4 hrs after meals Most heal; melaenal haematemesis;perforation malignancy may supervene

10.5.3. Adenocarcinoma of the stomach Commonly males 50yrs~ with poor prognosis Contributing factors Diet Genetics (blood group A) H.pylori Malignant disease

10.6. Small intestine

10.6.1. Diverticula True of false outpouchings in walls of tubular organs Diverticula present = diverticulosis inflamed diverticula present = diverticulitis True outpouches involves all layers of wall and is usually congenital

10.6.2. Meckel's Diverticula True civerticulum Congenital in ileum May appear as left-sided appendicitis Pancreatic/gastric choristoma

10.6.3. Crohn's disease anywhere in GIT, common in ileum idiopathic/autoimmune pathgensis Relapsing-remitting granulomatous inflammtion Skip lesions/cobblestone pattern; rubber hose intestine Ileo-colic and ileovesical fistulae Steatorrhea (foul smelling, pale faeces

10.6.4. Malabsorption syndrome Poor absorption Causes Pancreatic insufficiency Parasites/worms Ileal resection Crohn's disease Liver disease Coeliac disease (gluten enteropathy)

10.6.5. Tumorurs Rare Lipomas Leiomyomas Carcinoid tumour (APUD cells secrete serotonin

10.7. Appendix

10.7.1. Acute appendicitis Acute abdomen Obstruction, the secndary infection Surgical emergency

10.7.2. Mucocoele of appendix Accumulation of mucus due to obstruction usually resolves

10.8. Large (and small) intestine

10.8.1. Infection Transmitted by contaminated food/water causing diarrhoea, fever etc. Protozoa giardia, entamoeba Bacterial salmonella tyhpi, camplyobacter, escherichia coli Viruses rotavirus, calicivirus

10.8.2. Obstruction Volvulus - twisting or rotation of a loop of bowel Meconium ileus - obstruction by meconium seen in 10-20% of CF cases Intussusception - invagination of one part of bowl into lumen distally

10.9. Colon

10.9.1. Ulcerative colitis Chronic inflammation/ulceration of colon mucosa - pseudopolyps idiopathic, non-granulomatous, autoimmunity impliacted Symptoms include diarrhoea, anaemia, weight loss, iritis/stomatitis/arthritis/skin rashes/ anaemia Can progress to colon Ca Pseudopolyps may lead to haemorrhage, perforation

10.9.2. Diverticulosis of the colon False diverticula (sigmoid, rectum) Due to western died, chronic constipation, abnormal peristalsis

10.9.3. Benign tumours Premalignant Sigmoid, rectum most commonly Males ~55yrs

10.9.4. Familial polyposis coli Autosomal dominant hundreds of genign adenomatous polyps form in GIT (mostly rectum) predisposed to carcinoma with 15-20 yrs

10.9.5. Peutz-Jehghers syndrome Autosomal dominant Benign polyps predispose to carcinoma of colon Increased melanin pigmentation

10.9.6. Gardner's syndrome Autosomal dominant; benign polyps predisposes to carcinoma of colon Osteomas

10.9.7. Turcot's syndrome Autosomal recessive; benign polyps predisposes to carcinoma of colon Gliomas

10.9.8. Colonic carcinoma Common in men ~55yrs, rectum and sigmoid Due to western diet, chronic constipation, genetic factors, premalignant diseases Mucus secreting adencarcinomata Symptoms include changes in bowel habit, occult faecal blood, haemochezia, anaemia, ileus, perforation prognosis: TNM score combined with Duke's staging system

10.9.9. Haemorrhoids Varicosities due to diet, chronic constipation, obesity, pregnancy, portal hypertension may lead to rectal prolapse