general patho Flashcards
(15 cards)
Familial adenomatous polyposis
- Most common polyposis syndrome
- Inheritable cancer presdisposition (mutation of APC gene)
- 95% will develop large numbers of colonic adenomas by 35
- 93% will develop into carcinoma if untreated
- oral manifestations: supernumerary teeth, congenitally missing teeth, odontomas
Pulmonary embolism
- Due to DVT of legs/pelvis
- breaks off, travels in venous system –> lodges in pulmonary arteries
- sudden death due to main trunk occlusion –> RH failure
- pulmonary necrosis
- pulmonary hypertension –> persistent vascular destruction
Dystrophic calcification
- Abnormal deposition of calcium in dead/dying tissue.
- Important component of atherosclerotic disease and valvular heart disease
- can occur intra- and extracellularly
Infective endocarditis
- Direct microbial infection of cardiac valves/endocardium –> vegetables on valves/myocytes
- Subacute (most common) –> viridans Strep
- Acute –> S. aureus
- Prosthetic valve endocarditis –> S. epidermidis
- Local complications: valve rupture, suppurative pericarditis
- Distant complications: organ infarction, abscess formation, vasculitis glomerulonephritis
Define oedema
Excessive extravascular accumulation of fluid found in interstitial and body cavities
Pathophysiological mechanisms that lead to oedema
- Due to change in Starling’s forces
- Increased hydrostatic pressure at arterial end
- Decreased oncotic pressure decreases reabsorption of fluid in interstitial spaces into capillaries via osmotic gradient created by plasma proteins
- Increased endothelial permeability –> leakage of fluid and proteins
- Lymphatic obstruction –> prevents reabsorption into lymph
- Sodium and water retention
Clinical example + explanation of LOCALISED oedema
- Impaired venous drainage –> increased hydrostatic pressure (eg. venous occlusion in thrombosis)
- Increased vascular permeability and hyperaemia (eg. inflammation)
- Obstruction/destruction of lymphatics (eg. filariasis, cancer)
Clinical example + explanation of GENERALISED oedema
Heart failure (forward and backward failure)
Nephrotic syndrome –> protein loss in urine due to glomerular disease + activation of RAAS
Liver disease –> hypoalbuminemia –> insufficient albumin, decreased oncotic pressure
Liver disease –> portal hypertension
Apoptosis + give example of physiological and pathological causes
Pathway of cell death induced by tightly regulated intracellular programs. Cells destined to die activate enzymes that degrade their own nuclear DNA and cytoplasmic proteins. Does not elicit inflammatory reactions, via phagocytosis. Usually only 1 or a few cells.
Physiological causes: embryogenesis, kill virus infected cells
Pathological causes: DNA damage due to radiation, cytotoxic anticancer drugs, accumulation of misfolded proteins leading to degenerative disease of CNS
Aspiration pneumonia
Inhalational lung injury due to impaired/unconscious swallowing.
Swallow mixed organisms, gastric acid, food –> infective pneumonia, chemical change of the lungs
Frequently leads to lung abscess
Causes of acute inflammation
Infection
Tissue necrosis
Foreign body
Immune reactions
5 cardinal signs of inflammation
Warmth, pain, swelling, redness, loss of function
What happens during acute inflammation?
- Hyperaemia caused by vasodilation –> reflex action by chemical mediators (eg. histamine) –> increased endothelial permeability
- Increased exudation/transudation –> exudation of proteins form fibrin meshwork
- emigration of leukocytes as there is margination of neutrophils via adhesion molecules –> pavementing of neutrophils, pass between endothelial cells and migrate into adventitia
2 consequences/outcomes after acute inflammation
Complete resolution –> clearance of stimuli, mediators, acute inflammatory cells –> replacement of injured cells, normal function –> minimal death and damage
Chronic inflammation –> prolonged duration, inflammation, tissue injury and repair coexist in varying combinations –> can follow acute inflammation/occur insidiously
Metaplasia
Adult cell that transforms into another type of cell. Reversible, can occur in mesenchymal tissue, often occurs in response to chronic inflammation
Direct metaplasia
Apparent conversion –> respecification of stem cell
Columnar to squamous –> smokers, stones in excretory ducts
Squamous to columnar –> chronic acid reflux (Barrett’s oesophagus)
