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)
1.2.1.1. Parenchymal undergo reactive change
1.2.1.2. CT cells experience inflammation
1.2.2. Lethal (severe)
1.2.2.1. Parenchymal & CT experience necrosis
1.3. Necrosis
1.3.1. Coagulative
1.3.1.1. Most common; solid organs
1.3.2. Colliquative (Liquefactive)
1.3.2.1. Occuring in brain due to autolysis (brain infarct) completing with little coagulation
1.3.2.2. Occurring in suppuration due to neutrophils lysing pyogenic bacteria (e.g. pimple)
1.3.3. Caseous
1.3.3.1. Tuberculosis, due to hypersensitivity reaction
1.3.4. Haemorrhagic
1.3.4.1. Result of ischaemia leading to necrosis infiltrated with RBC
1.3.5. Gummatous
1.3.5.1. Tertiary syphilis (treponema pallidum)
1.3.6. Fat
1.3.6.1. Enzymatic
1.3.6.1.1. Occurs around pancreas & associated adipose tissue (e.g. alcoholics)
1.3.6.2. Traumatic
1.3.6.2.1. Occurs when adipose tissue is injured (e.g. breast tissue after surgery)
1.3.7. Fibrinoid
1.3.7.1. Occurs in CT, blood vessel walls in hypertension & autoimmune diseases; collagen degenerates to resemble fibrin
1.3.8. Gangrenous
1.3.8.1. 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
2.2.1.1. e.g lobar pneumonia
2.2.2. Formation of an abscess
2.2.2.1. e.g. brain abscess
2.2.3. Repair (healing)
2.2.3.1. e.g. bronchopneumonia
2.2.4. Chronic inflammation
2.2.4.1. e.g. chronic peptic ulcer
2.3. Types of chronic inflammation
2.3.1. Chronic fibrous inflammation
2.3.1.1. Collagen scar; can lead to stenosis
2.3.2. Chronic serous inflammation
2.3.2.1. Serous fluid made by serous membrane; cold swelling; bursitis
2.3.3. Chronic suppurative inflammation
2.3.3.1. Too much pus; chronic abscess
2.3.4. Chronic ulcerative inflammation
2.3.4.1. Deep excavation in tissue e.g. ulcer
2.3.5. Chronic granulomatous inflammation
2.3.5.1. Tissue destroyed by specialised microbes/immunity; granuloma is formed
2.3.5.2. Example: Hansen's disease
2.3.6. Active chronic inflamamtion
2.4. Tuberculosis
2.4.1. Bronchopneumonia
2.4.1.1. bronchial spread
2.4.2. Miliary tuberculosis
2.4.2.1. 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 10
4.1. Congenital disorders
4.1.1. Bronchial atresia - narrowed bronchus
4.1.2. Hypoplasia of lung
4.1.3. Bronchogenic cysts - usually attached to trachea
4.1.4. Bronchopulmonary sequestration - portion of lung not communicating
4.1.5. Kartagener's syndrome - defective cilia
4.1.6. Neonatal respiratory distress syndrome (NRDS) - deficiency of surfactant, aveoli collapse
4.1.7. Cystic fibrosis
4.1.7.1. multisystem disease
4.1.7.2. CF gene causes production of abnormal viscid mucus that cannot be cleared from lungs
4.1.7.3. recurrent infections
4.1.7.4. hyperinflation & pneumothorax
4.1.7.5. necrosis, scarring
4.2. Circulatory disorders
4.2.1. Chronic venous congestion
4.2.1.1. reduced LV output leads to rupture of alveolar capillaries, haemorrhage, necrosis & fibrosis
4.2.2. Pulmonary oedema
4.2.2.1. Congestive heard failure, infections, toxic gas inhalation
4.2.2.1.1. leads to dys
4.2.2.2. leads to dyspnoea, hypostatic pneumonia
4.2.3. Pulmonary embolism
4.2.3.1. Arise in deep leg vein
4.2.3.2. Leads to dyspnoea, tachycardia, shock
4.2.3.3. Infarction or fatal
4.2.4. Pulmonary infarction
4.2.4.1. elderly/post-op patients with heart failure may develop thromboemboli
4.2.4.2. Leads to dyspnoea/scarring/death
4.2.5. Pulmonary hypertension
4.3. Chronic obstructive pulmonary disease (COPD)
4.3.1. Disease state characterised by persistent airflow limitation that is not fully reversible
4.3.2. Leads to dyspneoa/shortness of breath, cough and/or sputum production
4.3.3. Causes
4.3.3.1. Emphysema
4.3.3.1.1. increase in size of alveolar space and loss of recoil
4.3.3.2. Bronchiectasis
4.3.3.2.1. permanent, abnormal dilation of bronchi and bronchioles
4.3.3.2.2. cough and sputum present
4.3.3.3. Chronic bronchitis & bronchiolitis
4.3.3.3.1. airway narrowing caused by mucous hypersecretion, inflammation of ariways
4.3.3.3.2. due to inhalation of dust/smoke etc.
4.4. Asthma
4.4.1. Reversible bronchospasm causing wheezing & excess mucus mediated by type 1 hypersensitivity
4.4.2. Extrinsic - allergen/enivronment
4.4.3. Intrinsic - exercise/stress
4.4.4. Sequelae
4.4.4.1. mild disease
4.4.4.2. status asthmaticus (chronic inflated lungs because air cannot escape)
4.4.4.3. chronic asthma
4.4.4.4. COPD
4.5. Infections & inflammation, ARDS
4.5.1. rhinitis
4.5.2. sinusitis
4.5.3. laryngitis
4.5.4. tracheitis
4.5.5. tracheo-bronchitis
4.5.6. bronchiolitis
4.5.7. pneumonia
4.5.7.1. lobar pneumonia - whole lobe
4.5.7.2. bronchopneumonia - patchy
4.5.8. pleurisy
4.5.9. viral infections
4.5.10. fungal infections
4.5.11. tuberculosis
4.5.11.1. acid fast bacilli stain pink with Ziehl-neelsen stain
4.5.12. sarcoidosis
4.5.12.1. idiopathic, non caseating, granulomatous inflammation
4.5.13. ARDS
4.5.13.1. diffuse alveolar damage & inflammation
4.5.13.2. Causes
4.5.13.2.1. septicaemia, major trauma
4.5.13.2.2. toxic smoke/fume inhalation
4.5.13.2.3. amniotic fluid embolism, DIC
4.5.13.2.4. radiation injury, chemotherapy
4.5.13.3. 70% die in acute phase, 10% recover, 20% due due to chronic impairment
4.6. Organic & inorganic pneumoconioses
4.6.1. Dust inhalation disease
4.6.2. Organic
4.6.2.1. Byssinosis - cotton
4.6.2.2. Bagassosis - sugar cane refuse
4.6.2.3. Farmers' lung - mouldy hay
4.6.2.4. Suberosis - cork dust
4.6.3. Inorganic
4.6.3.1. Anthracosis - carbon
4.6.3.2. Silicosis - silica
4.6.3.3. Silicoanthracosis - carbon & silica
4.6.3.4. Berrylliosis - berryllium
4.6.3.5. Silicosiderosis - silica & iron
4.6.3.6. Asbestosis - asbestos
4.6.3.6.1. leads to asbestosis, COPD, mesothelioma of pleura
4.7. Primary & secondary tumours
4.7.1. Mesothelioma of the pleura
4.7.1.1. exposure to asbestos
4.7.1.2. highly malignant, death usually within 10 months of diagnosis
4.7.2. Carcinoma of the bronchus
4.7.2.1. due to smoking, x-rays, asbestosis etc.
4.7.2.2. peripheral masses may give rise to para-neoplastic syndromes
4.7.2.2.1. e.g. pancoast syndrome - pain in shoulder, arm & hand
4.7.2.2.2. e.g. horner's syndrome - nerves supplying eye are damaged
4.7.2.3. Diagnosis
4.7.2.3.1. chest x-ray
4.7.2.3.2. bronchoscopy & biopsy
4.7.2.3.3. needle biopsy of lymph nodes
4.7.2.3.4. sputum sytology
4.7.3. breast, bone, skin, kidney tumours commonly metastasise into lungs
5. Week 11
5.1. Inflammation & carcinoma of oral cavity
5.1.1. Inflammation
5.1.1.1. Mainly due to HSV type 1, EBV, coxsackievirus
5.1.1.2. e.g. stomatitis, cheilitis, glossitis, gingivitis, peridontitis, dental caries, sialadenitis, pharyngitis
5.1.2. Carcinoma of oral cavity
5.1.2.1. lips, tongue, buccal mucosa, pharynx, males more common
5.1.2.2. morphology - squamous cell carcinoma
5.1.2.3. treatment - surgical excision; radiotherapy (poor prognosis)
5.2. Hiatus hernia & oesophagitis
5.2.1. Oesophagitis
5.2.1.1. Due to gastro-oesophageal reflux disease (GORD) or infections
5.2.1.1.1. GORD may lead to dyspepsia, dysphagia or Barrett's oesophagus (which can lead to adenocarcinoma)
5.2.2. Hiatus hernia
5.2.2.1. protrusion of part of stomach into thoracic cavity through diaphragmatic hiatus
5.2.2.2. rolling (5%)
5.2.2.3. sliding (95%)
5.2.2.4. Causes
5.2.2.4.1. congenital weakness in diaphragm
5.2.2.4.2. obesity/overloading of the stomach
5.2.2.5. Symptoms same as GORD
5.2.2.6. Treatment - surgery/small meals/weight reduction
5.3. Oesophageal varices & carcinoma of oesophagus
5.3.1. Oesophageal varices
5.3.1.1. Dilated veins due to cirrhosis of the liver and portal hypertension
5.3.2. Plummer-Vinson syndrome
5.3.2.1. Sideropenic dysphagia & abnoral peristalsis and mucosal webs
5.3.2.1.1. F.I.D.A.C.K.S
5.4. Gastritis & gastric atrophy
5.4.1. Acute (erosive) gastritis
5.4.1.1. Due to alcholo, aspirin, H.pylori, NSAIDS
5.4.1.2. Characterised by erosions
5.4.1.3. usually resolves
5.4.2. Chronic gastritis
5.4.2.1. Chronic helicobacter-associated gastritis (most common; good prognosis)
5.4.2.2. Chronic atrophic (autoimmune) gastritis (poor prognosis)
5.4.2.2.1. may lead to gastric Ca
5.4.2.3. Reactive gastritis due to reflux of NSAIDS or bile into lower part of stomach (good prognosis)
5.5. Peptic ulceration & carcinoma of the stomach
5.5.1. Acute peptic ulcers
5.5.1.1. Progression of acute (erosive) gastritis (usually heal)
5.5.1.1.1. may progress to chronic peptic ulcer
5.5.2. Chronic peptic ulcers
5.5.2.1. 30-45 years - due to genetics, smoking, low blood supply
5.5.2.2. Gnawing pain in epigastrium 1-3 hrs after meal
5.5.2.3. Steady pain in epigastrium 2-4 hrs after meals
5.5.2.4. Most heal; melaenal haematemesis;perforation
5.5.2.4.1. malignancy may supervene
5.5.3. Adenocarcinoma of the stomach
5.5.3.1. Commonly males 50yrs~ with poor prognosis
5.5.3.2. Contributing factors
5.5.3.2.1. Diet
5.5.3.2.2. Genetics (blood group A)
5.5.3.2.3. H.pylori
5.5.3.2.4. Malignant disease
5.6. Small intestine
5.6.1. Diverticula
5.6.1.1. True of false outpouchings in walls of tubular organs
5.6.1.1.1. Diverticula present = diverticulosis
5.6.1.1.2. inflamed diverticula present = diverticulitis
5.6.1.1.3. True outpouches involves all layers of wall and is usually congenital
5.6.2. Meckel's Diverticula
5.6.2.1. True civerticulum
5.6.2.2. Congenital in ileum
5.6.2.3. May appear as left-sided appendicitis
5.6.2.4. Pancreatic/gastric choristoma
5.6.3. Crohn's disease
5.6.3.1. anywhere in GIT, common in ileum
5.6.3.2. idiopathic/autoimmune pathgensis
5.6.3.3. Relapsing-remitting granulomatous inflammtion
5.6.3.4. Skip lesions/cobblestone pattern; rubber hose intestine
5.6.3.5. Ileo-colic and ileovesical fistulae
5.6.3.6. Steatorrhea (foul smelling, pale faeces
5.6.4. Malabsorption syndrome
5.6.4.1. Poor absorption
5.6.4.2. Causes
5.6.4.2.1. Pancreatic insufficiency
5.6.4.2.2. Parasites/worms
5.6.4.2.3. Ileal resection
5.6.4.2.4. Crohn's disease
5.6.4.2.5. Liver disease
5.6.4.2.6. Coeliac disease (gluten enteropathy)
5.6.5. Tumorurs
5.6.5.1. Rare
5.6.5.1.1. Lipomas
5.6.5.1.2. Leiomyomas
5.6.5.1.3. Carcinoid tumour (APUD cells secrete serotonin
5.7. Appendix
5.7.1. Acute appendicitis
5.7.1.1. Acute abdomen
5.7.1.2. Obstruction, the secndary infection
5.7.1.3. Surgical emergency
5.7.2. Mucocoele of appendix
5.7.2.1. Accumulation of mucus due to obstruction
5.7.2.2. usually resolves
5.8. Large (and small) intestine
5.8.1. Infection
5.8.1.1. Transmitted by contaminated food/water causing diarrhoea, fever etc.
5.8.1.2. Protozoa
5.8.1.2.1. giardia, entamoeba
5.8.1.3. Bacterial
5.8.1.3.1. salmonella tyhpi, camplyobacter, escherichia coli
5.8.1.4. Viruses
5.8.1.4.1. rotavirus, calicivirus
5.8.2. Obstruction
5.8.2.1. Volvulus - twisting or rotation of a loop of bowel
5.8.2.2. Meconium ileus - obstruction by meconium
5.8.2.2.1. seen in 10-20% of CF cases
5.8.2.3. Intussusception - invagination of one part of bowl into lumen distally
5.9. Colon
5.9.1. Ulcerative colitis
5.9.1.1. Chronic inflammation/ulceration of colon mucosa - pseudopolyps
5.9.1.2. idiopathic, non-granulomatous, autoimmunity impliacted
5.9.1.3. Symptoms include diarrhoea, anaemia, weight loss, iritis/stomatitis/arthritis/skin rashes/ anaemia
5.9.1.3.1. Can progress to colon Ca
5.9.1.3.2. Pseudopolyps may lead to haemorrhage, perforation
5.9.2. Diverticulosis of the colon
5.9.2.1. False diverticula (sigmoid, rectum)
5.9.2.2. Due to western died, chronic constipation, abnormal peristalsis
5.9.3. Benign tumours
5.9.3.1. Premalignant
5.9.3.2. Sigmoid, rectum most commonly
5.9.3.3. Males ~55yrs
5.9.4. Familial polyposis coli
5.9.4.1. Autosomal dominant
5.9.4.1.1. hundreds of genign adenomatous polyps form in GIT (mostly rectum)
5.9.4.2. predisposed to carcinoma with 15-20 yrs
5.9.5. Peutz-Jehghers syndrome
5.9.5.1. Autosomal dominant
5.9.5.2. Benign polyps
5.9.5.2.1. predispose to carcinoma of colon
5.9.5.3. Increased melanin pigmentation
5.9.6. Gardner's syndrome
5.9.6.1. Autosomal dominant; benign polyps
5.9.6.1.1. predisposes to carcinoma of colon
5.9.6.2. Osteomas
5.9.7. Turcot's syndrome
5.9.7.1. Autosomal recessive; benign polyps
5.9.7.1.1. predisposes to carcinoma of colon
5.9.7.2. Gliomas
5.9.8. Colonic carcinoma
5.9.8.1. Common in men ~55yrs, rectum and sigmoid
5.9.8.2. Due to western diet, chronic constipation, genetic factors, premalignant diseases
5.9.8.3. Mucus secreting adencarcinomata
5.9.8.4. Symptoms include changes in bowel habit, occult faecal blood, haemochezia, anaemia, ileus, perforation
5.9.8.4.1. prognosis: TNM score combined with Duke's staging system
5.9.9. Haemorrhoids
5.9.9.1. Varicosities due to diet, chronic constipation, obesity, pregnancy, portal hypertension
5.9.9.1.1. may lead to rectal prolapse
6. Week 4
6.1. Variations of growth
6.1.1. Hyperplasia
6.1.1.1. Increase in mass due to increase in number of cells
6.1.1.2. E.g. remaining kidney after nephrectomy
6.1.2. Hypertrophy
6.1.2.1. Increase in mass due to increase in size of cells
6.1.2.2. E.g. athletes and their big muscles
6.1.3. Atrophy
6.1.3.1. Decrease in mass due to decrease in size/number of cells
6.1.3.2. E.g. uterus after menopause/childbirth
6.1.4. Agenesis
6.1.4.1. Failure of organ to develop at all
6.1.4.2. E.g. Anencephaly
6.1.5. Aplasia
6.1.5.1. Sudden cessation of growth (traumatic)
6.1.5.2. E.g. Thymus gland after childhood
6.1.6. Hypoplasia
6.1.6.1. Tissue fails to attain full size due to deficient growth
6.1.6.2. E.g. cryptochidism (undescended testis)
6.1.7. Metaplasia
6.1.7.1. Fully differentiated adult cells change into another more resilient but less specific cell type
6.1.7.2. E.g airways of a smoker
6.1.8. Dysplasia
6.1.8.1. Abnormal growth and differentiation; pre-malignant
6.1.8.2. E.g. oral cavity (smoking or dentures), respiratory tract (smoking), cervix (HPV
6.1.9. Hamartoma
6.1.9.1. Focal overgrowth of normal cells where they are normally present
6.1.9.2. E.g. mole (benign naevus)
6.1.10. Choristoma (ectopia)
6.1.10.1. Focal overgrowth of normal cells found where they are not supposed to be
6.1.10.2. E.g. endometriosos
6.1.11. Neoplasia
6.1.11.1. Formation of abnormal, uncontrolled tissue growth with no coordinated function
6.1.11.2. E.g. tumour
6.2. Neoplasms
6.2.1. Clinical classification
6.2.1.1. Benign
6.2.1.2. Malignant
6.2.1.3. Differentiation
6.2.1.3.1. Well differentiated
6.2.1.3.2. Poorly differentiated
6.2.1.3.3. Non differentiated
6.2.1.3.4. Anaplastic tumours
6.2.2. Histogenic classification
6.2.2.1. -oma for benign tumours
6.2.2.2. carcinoma for tumours of epithelial origin
6.2.2.3. sarcoma for tumours of mesenchymal origin
6.2.2.4. Exceptions
6.2.2.4.1. Glioma - glial cells in brain
6.2.2.4.2. Melanoma - melanocytes
6.2.2.4.3. Mesothelioma - mesothelium
6.2.2.4.4. Myeloma - plasma cells
6.2.2.4.5. Leukaemia - bone marrow
6.2.2.4.6. Blastoma - primitive stem cells
6.2.2.4.7. Teratoma - pluripotential cells (benign or malignant)
6.2.3. Morphological classification
6.2.3.1. Polyp/polypoid - toadstool
6.2.3.2. Papillary (fungating) - cauliflower
6.2.3.3. Ulcerating - excavating
6.2.3.4. Infiltrating - rapidly spreading
6.2.3.5. Nodular - lump
6.2.3.6. Cystic - fluid filled cyst
6.2.3.7. Scirrhous - hard on palpation due to much collagenous stromal tissue
6.2.3.8. Encephaloid - soft on palpation due to little collagenous stromal tissue
6.3. Types of cell
6.3.1. Labile cells
6.3.2. Stable cells
6.3.3. Permanent cells
7. Week 5
7.1. Carcinogenesis
7.1.1. Targets for genetic damage
7.1.1.1. Growth promoting proto-oncogenes
7.1.1.2. Growth-inhibiting tumour suppressor cells
7.1.1.3. Genes that regulate apoptosis
7.1.1.4. Genes involved in DNA repiar
7.1.2. Intrinsic factors
7.1.2.1. Genetic
7.1.2.1.1. e.g. trisomy 21 & leukaemia
7.1.2.2. Racial and geographical
7.1.2.3. Immunological
7.1.2.3.1. e.g. AIDS & higher incidence of cancer
7.1.2.4. Sex & hormonal
7.1.2.4.1. e.g. hormonal stimulation leading to cancer
7.1.2.5. Age
7.1.2.6. Pre-existing benign neoplasm
7.1.3. Extrinsic factors
7.1.3.1. Chemical agents
7.1.3.1.1. e.g. soot exposure causing carcinoma of the scrotum
7.1.3.2. Physical agents
7.1.3.2.1. e.g. radiation, trauma, inert substances
7.1.3.3. Biological factors
7.1.3.3.1. Parasite
7.1.3.3.2. Fungi and bacteria
7.1.3.3.3. Virus
7.2. Immunodeficiency
7.2.1. Primary
7.2.1.1. Present at birth
7.2.1.2. E.g. Bruton's disease - agammaglobulinemic
7.2.1.3. E.g. Di George - congenital thymic aplasia
7.2.1.4. E.g. Swiss-type - combined immunodeficiency
7.2.2. Secondary
7.2.2.1. Miscellaneous
7.2.2.1.1. e.g. Aging - erysipelas
7.2.2.1.2. e.g. Infection
7.2.2.1.3. e.g. Neoplasm - Hodgkin's disease of the spleen
7.2.2.2. AIDS
7.2.2.2.1. Virus infects CD4 cells
7.3. Hypersensitivity
7.3.1. Type 1 - immediate
7.3.1.1. mast cells and IgE
7.3.1.2. e.g. allergic reaction
7.3.2. Type 2 - antibody
7.3.2.1. IgG or IgM damage cells
7.3.2.2. e.g. erythroblastosis
7.3.3. Type 3 - immune complex
7.3.3.1. antigens and Abs form immune complexes
7.3.3.2. e.g. serum sickness
7.3.3.3. e.g. glomerulonephritis
7.3.4. Type 4 - t-cell mediated
7.3.4.1. t-cell immune response
7.3.4.2. e.g. mosquito bites
7.4. Autoimmune disorders
7.4.1. Organ-specific
7.4.1.1. e.g. hashimoto's disease
7.4.1.2. e.g. atrophic gastritis
7.4.2. Systemic
7.4.2.1. e.g. systemic lupus erythematosus
7.4.2.2. e.g. rheumatoid arthritis
8. Week 7
8.1. Oedema
8.1.1. Localised
8.1.1.1. Special terms
8.1.1.1.1. Ascites - peritoneum oedema
8.1.1.1.2. Hydrothorax
8.1.1.1.3. Hydropericardium
8.1.1.1.4. Hydrocele - tunica vaginalis
8.1.1.2. Causes
8.1.1.2.1. Acute inflammation
8.1.1.2.2. Type 1 hypersensitivity
8.1.1.2.3. Lymphatic obstruction
8.1.1.2.4. Impaired venous drainage
8.1.2. Generalised
8.1.2.1. Special terms
8.1.2.1.1. Anasarca
8.1.2.1.2. Hydrops
8.1.2.2. Causes
8.1.2.2.1. Pathogenic
8.1.2.2.2. Renal disorders
8.1.2.2.3. Liver disease
8.1.2.2.4. Malnutrition
8.1.2.2.5. Other clinical states
8.1.3. Fluid types
8.1.3.1. Transudate
8.1.3.1.1. non-inflammatory tissue fluid with little protein
8.1.3.2. Exudate
8.1.3.2.1. inflammatory fluid with high protein
8.1.3.2.2. Serous
8.1.3.2.3. Fibrinous
8.1.3.2.4. Haemorrhagic
8.1.3.2.5. Suppurative
8.1.4. Life threatening forms
8.1.4.1. Pulmonary - due to LV failure
8.1.4.2. Cerebral - due to head trauma; infections
8.2. Haemorrhage
8.2.1. Types
8.2.1.1. Ecchymosis
8.2.1.2. Haematoma
8.2.1.3. Petechiae
8.2.1.4. Internal
8.2.1.5. External
8.2.2. Colour changes
8.2.2.1. Bright red - oxygenated Hb
8.2.2.2. Cherry red - unoxygenated Hb
8.2.2.3. Greenish - biliverdin
8.2.2.4. Orange/yellow - bilirubin
8.2.2.5. Brownish - haemosiderin
8.3. Purpura
8.3.1. Thrombocytopenia
8.3.1.1. less platelet production from bone marrow
8.3.2. Non-thrombocytopenic
8.3.2.1. vascular defects with normal platelet numbers
8.3.3. Thromboasthenia
8.3.3.1. platelets are abnormal in function
8.4. Shock
8.4.1. Primary
8.4.1.1. Injury
8.4.1.2. Great pain
8.4.1.3. Strong emotion
8.4.1.4. Fluid balance not effected
8.4.2. Secondary
8.4.2.1. Hypovolemic shock
8.4.2.2. Cardiogenic shock
8.4.2.3. Septic shock
8.4.2.4. Fluid balance effected
8.5. Thrombosis
8.5.1. Types
8.5.1.1. Pale - platelets and fibrin
8.5.1.2. Dark - fibrin, RBW & WBC
8.5.1.3. Mixed - regions of both (lines of Zahn)
8.5.2. Forms
8.5.2.1. Mural
8.5.2.1.1. adherent to one side of vessel wall
8.5.2.2. Occlusive
8.5.2.2.1. lumen totally attached
8.5.2.3. Coralline
8.5.2.3.1. irregular - may become occlusive
8.5.2.4. Propagating
8.5.2.4.1. progressive involvement of thrombus into other branches
8.5.2.5. Ball
8.5.2.5.1. unattached spherical thrombus
8.5.2.6. Septic
8.5.2.6.1. presence of infection
8.5.2.7. Vegetations
8.5.2.7.1. thrombi on heart valve
8.5.3. Virchow's triad
8.5.3.1. Change in vessel wall
8.5.3.2. Change in blood flow
8.5.3.3. Changes in blood constituents
8.5.4. Fate of thrombi
8.5.4.1. Propagation
8.5.4.1.1. thrombus enlarges along vessel
8.5.4.2. Lysis and resolution
8.5.4.2.1. most favourable
8.5.4.3. Calcification
8.5.4.3.1. dystrophic calcification
8.5.4.4. Infection
8.5.4.4.1. septicaemia
8.5.4.5. Retraction, organisation, recanalization
8.5.4.5.1. thrombus shrinks, re-establishment of blood flow through scar tissue
8.5.4.6. Thromboembolism
8.5.4.6.1. detachment of thrombus travelling to a distant location
8.5.4.7. Infarction
8.5.4.7.1. thrombus interrupts blood flow, anoxia and necrosis
8.6. Thromboembolism
8.6.1. Venous emboli
8.6.1.1. lodge in pulmonary vessels
8.6.1.2. arise in deep leg veins
8.6.2. Arterial emboli
8.6.2.1. arise in aorta, coronary & cerebral arteries
8.6.2.2. lodge in any organ
8.6.3. Fat emboli
8.6.3.1. Bone fracture type
8.6.3.2. Atherosclerotic plaque type
8.6.4. Gas emboli
8.6.4.1. Air emboli
8.6.4.2. Nitrogen emboli - divers
8.6.5. Foreign body emboli
8.6.6. Tumour emboli
8.6.6.1. arise in venules or veins due to malignant tumour infiltration
8.6.7. Amniotic fluid emboli
8.6.7.1. occurs during childbirth
8.7. Embolism
8.7.1. Occlusion of vessel by mass of material transported into bloodstream
9. Week 8
9.1. Infarction
9.1.1. Classifications
9.1.1.1. Pale infarct
9.1.1.1.1. Arterial blood supply is obstructed
9.1.1.2. Red infarct
9.1.1.2.1. Venous drainage is obstructed
9.1.1.3. Mixed infarct
9.1.1.3.1. Begin as pale then blood supply is partially readmitted
9.1.2. Occlusion of arteries
9.1.3. Occlusion of veins
9.2. Hypertension
9.2.1. Aetiology
9.2.1.1. Primary
9.2.1.2. Secondary
9.2.2. Clinical
9.2.2.1. Beningn
9.2.2.1.1. most common
9.2.2.1.2. kidney lesions develop over years
9.2.2.2. Malignant
9.2.2.2.1. can supervene on benign hypertension
9.2.2.2.2. 'onion skin' arterioles
9.2.2.2.3. petechial haemorrhages on kidney surface
9.2.3. 1st degree
9.2.3.1. Idiopathic
9.2.3.2. Genetic, environment, hormonal, neurogenic
9.2.4. 2nd degree
9.2.4.1. excessive renin production
9.2.4.2. renal atery stenosis
9.2.4.3. endocrine causes (aldosterone, oestrogen, noradrenaline)
9.2.4.4. iatrogenic causes (oestrogen)
9.3. Ateriosclerosis
9.3.1. Atherosclerosis
9.3.1.1. aorta and major branches
9.3.1.2. disorder of intima
9.3.1.2.1. typical lesion is atheroma/atheromatous plaque
9.3.1.3. Lesions
9.3.1.3.1. fatty streaks
9.3.1.3.2. musculoelastic lesions
9.3.1.3.3. typical atheromatous plaques
9.3.1.3.4. complicated atheromatous plaques
9.3.1.4. Clinical effects
9.3.1.4.1. Intermittent ischaemic effects
9.3.1.4.2. Thrombosis, embolism, infarction
9.3.1.4.3. Aneurysm formation
9.3.2. Monckeberg's medial calcification
9.3.2.1. idiopathic with degeneration and necrosis of medial smooth muscle followed by dystrophic calicification
9.3.2.2. intima is not affected
9.3.3. Arteriolosclerosis
9.3.3.1. seen with systemic hypertension
9.3.3.2. seen in normotensive, elderly people and people with diabetes mellitus
10. Week 9
10.1. Congentical
10.1.1. Left to right shunts
10.1.1.1. Atrial septal defect
10.1.1.2. Ventricular septal defect
10.1.1.3. Patent ductus arteriosus
10.1.2. Pulmonary stenoic lesions
10.1.2.1. Narrowing of the pulmonary artery/valve
10.1.2.1.1. less oxygenation of blood leads to cyanosis
10.1.2.1.2. Fallot's tetraology