Pathology Flashcards
Hypoxia?
Decreased oxygen supply to tissues
Ischaemia?
Decreased blood supply to tissues
Oncosis?
Cell death with swelling, changes occurring in injured cells before death
Necrosis?
Morphological changes occurring in a cell after it has been dead for 12-24 hours
- Coagulative (protein denaturation & clumping - solid tissue)
- Liquefactive (enzyme degradation - loose CT tissue e.g. Brain and infected areas with lots of neutrophils)
- Caseous (TB) and fat (adipose tissue)
Apoptosis?
Controlled cell death with shrinkage, induced by caspases
Gangrene?
Necrosis visible to naked eye
- Dry (coagulative necrosis - air exposure)
- Wet (Liq necrosis - infections)
Infarction?
Necrosis caused by reduction in blood supply
Infarct-area of necrotic tissue due to loss of blood supply
- White –> occlusion of end artery
- Red –> dual blood supply, loose tissue
Ischaemia reperfusion injury?
When blood flow is returned to a damaged but not necrotic tissue, it can cause further damage, worse than if no blood flow had been returned to tissue at all.
Causes: oxygen free radicals, more neutrophils leading to more inflammation, complement proteins and pathway
Anthracosis?
Caused by long exposure to coal dust
Inhaled and phagocytosed by alveolar macrophages
Travel to peribrochial lymph nodes - blackened lungs and nodes
Usually harmless
Coal worker’s pneumoconiosis?
Large amounts of anthracosis - fibrosis and emphysema
Blackened lungs and peri bronchial nodes
Hepatitis?
Acute or chronic (over 6 months) inflammation and necrosis of liver
Tests:
High ALT, AST, LDH, bilirubin, PT, ammonia
Low albumin
Alcoholic liver disease?
Acute: similar to hepatitis Chronic: fulminant liver failure -Mallory's hyaline (damaged keratin) Tests: high bilirubin, alkaline phosphatase, gamma GT, Low
Acute pancreatitis?
Inflammation of pancreas
Tests
High: serum amylase (24hrs), lipase (72-96hrs)
Could lead to hypocalcaemia - due to precipitation of Ca salts in fat necrosis
Acute appendicitis?
Swelling of appendix
Causes coag. necrosis -> perforation -> spreading of inflammation through peritoneum > peritonitis -> septicaemia
Complications: septic shock, fistula
Predisposing factors: family history, high fibre diet, CF, gender
Steatosis?
Accumulation of triglycerides
Often seen in liver
Due to: alcohol, diabetes mellitus, obesity, toxins
Inherited angio-oedema?
Rare AD deficiency of C1-esterase inhibitor (part of complement). Causes reduced level of C2/4, C3 normal
Symptoms: acute inflammation - non itchy cutaneous angio-oedema (dermis , subcutaneous tissue, mucosa, submucosal tissue), recurrent abdo pain
Chronic granulomatous disease?
X-linked or AR genetic deficiency of NADPH oxidase responsible for generating ROS
No ROS for oxygen dependent killing in phagocytes (neutrophils, macrophages)
Causes:
-Chronic suppurative granulomas, abscesses of skin & lymph nodes & lung & liver -> cirrhosis
-Increased susceptibility to bacterial infections, pneumonia, impetigo, cellulitis
Alpha1-antitrypsin deficiency?
Liver produces incorrectly folded protein
Accumulates within ER
Does not break down elastase - so elastase breaks down alveolar walls resulting in emphysema
Leads to acute inflammation -> cirrhosis
Hereditary haemochromatosis?
AR genetic disorder
Mutation in gene HFE on chromosome 6
Normally HFE competes with Transferrin to bind to receptor. Mutated-> doesn’t bind, transferrin has no competition
Too much Fe absorbed in intestine/cells -> Fe then deposited by skin, liver, pancreas, heart causing haemosiderosis
Symptoms: liver damage, heart dysfunction, pancreatic failure
Treatment: venesection/repeated bleeding
Cirrhosis?
Chronic inflammation with fibrosis of the liver, with no normal function
Due to: alcohol, HBV infection, immunological, fatty liver disease, drugs, toxins, obesity
Microscopic: regenerating nodules surrounded by fibrotic tissue
Jaundice?
Accumulation of bilirubin - bright yellow
Bile flow obstructed - bilirubin levels rise
It is a breakdown product of haem, stacks of porphyrin rings, formed in all body cells
Usually bilirubin taken from tissues by albumin to liver - excreted in bile
Signs: yellow sclera
Dystrophic calcification?
Localised calcification occurring in area of dying tissue, atherosclerosis plaque, ageing/damaged heart vessels, lymph nodes
It is a local change which favours nucleation of hydroxyapatite crystals
Metastatic calcification?
Generalised calcification due to hypercalcaemia, which in turn is due to calcium metabolism problems
Hydroxyapatite crystals deposited in normal tissues
Hypercalcaemia?
High calcium Due to: Increased secretion of PTH resulting in bone resorption - primary, secondary and ectopic Destruction of bone tissue