MOD clinical Flashcards
Definition of hypoxia and the 4 different types.
Deficiency in oxygen levels to the tissues. Main cause of cell injury/cell death.
- Hypoxaemic hypoxia: oxygen content in blood is low (lung disase, high altitude)
- Anaemic hypoxia: decreased ability of Hb to carry oxygen (anaemia, CO poisoning)
- Ischaemic hypoxia: interruption in blood supply, oxygen isnt reaching the cells
- Histiocytic hypoxia: inability to utilise oxygen (cyanide poisoning)
Ischaemic reperfusion injury
Blood flow returned to tissue which is ischaemic but not yet necrotic -> makes it worse because of increased production of oxygen free radicals, increased number of neutrophils, and delivery of complement pathway
Excessive alcohol intake on the liver
Steatosis(fatty change) & acute alcohol hepatitis (inflammation of hepatocytes) are early stages of alcoholic liver disease. Fibrosis then occurs, causing alcoholic cirrhosis
Hereditary haemochromatosis
Hepcidin deficiency (Fe2+ storage molecule). Fe2+ deposited around body. Problems with pancreas, heart, etc. Treat with phlebotomy (remove some blood)
Carbon monoxide poisoning
Causes anaemic hypoxia -> Hb cant carry oxygen as it is bound to CO
Paracetamol poisoning
Production of NAPQI (strong oxidant) + depletion of glutathion (antioxidant) cause hepatocyte death/liver failure.
Treat with acetylcysteine within 8 hours to replenish GSH levels
Coal workers pneumoconiosis
Pulmonary fibrosis -> damaged lung. Reduced air entry -> cough/breathlessness/faint.
Due to accumulation of microscopic coal dust in lungs (high conc)
Alpha1 antitrypsin deficiency
Autosomal recessive. Lack of antitrypsin -> increased elastase -> breakdown of elastin in lung/liver tissue (destroys alveoli-> emphysema)
Bacterial meningitis
Acute inflammation of meninges of brain -> rise in intracranial pressure -> occludes blood vessels supplying blood to brain -> brain damage. Causes: Neonates- streptococcus B Children- neisseria meningitides Adults- enterovirus (VIRUS) Elderly- streptococcus pneumonae
Hereditary angio-oedema
Autosomal dominant. C1esterase inhibitor usually inhibits bradykinin and C1 (so inhibits C3 production).
Hereditary angio-oedema= c1 esterase inhibitor deficiency-> c3 and bradykinin no longer inhibited -> increased endothelial permeability -> oedema
Treat with fresh frozen plasma or c1 inhibitor
Chronic granulomatous disease
Neutrophils unable to form superoxide radicals -> no respiratory burst -> cant kill some bacteria. Forms granulomas in attempt to store the bacteria
Inflammatory bowel disease
Ulcerative colitis: chronic autoimmune inflammation of colon. Crypt abscesses, destruction of mucosa, attacks submucosa. Increases risk of colon cancer.
Crohns disease: chronic inflammation of any part of GI tract (mouth to anus). Many granulomas and a cobblestone bowel appearance. Anal lesions and bowel fistulae. Treat with steroids.
Difference between UC and crohns: crohns isnt limited to the colon and doesnt show crypt abscesses, and it doesnt increase the r isk of colon cancer.
Both cause abdominal pain, diarrhoea (may be bloody) and unexplained weightloss
Tuberculosis
Chronic infection in lungs (myobacterium tuberculosis). Spread by droplet infection. Macrophages phagocytose but cant destroy -> granulomas form -> bacteria multiply within the granulomas. Can lead to pulmonary fibrosis and death (and systemic infection) if not treated with antibiotics.
Sarcoidosis
Idiopathic granulomatous disease of the lungs. Granuloma formation with no caseous necrosis. Steroids.
Rheumatoid arthritis
Autoimmune attack of synovial membrane in joints -> granuloma formation -> erodes the articular surface of bone -> painful joints. Treat with steroids. Rheumatoid nodes- clumps of granulomas across the body
Wegener’s granulomatosis
Autoimmune chronic inflammation of epithelia in ear/nose/throat/lungs/kidney -> granuloma formation and fibrosis -> renal failure if untreated. Treat with steroids.
Leucocytosis
Increased number of leucocytes in blood
Macrophages and endothelia produce colony stimulating factors -> bone marrow produces more neutrohpils
Acute phase response
Change in protein synthesis in the livr (decreased albumin, increased fibrinogen). Caused by cytokines (released by macrophages). Causes sleepiness and lack of appetite
Collagen synthesis defects
Scurvy: vit c deficiency -> cant hydroxylate proline -> weakened collagen -> unable to heal wounds adequately (seen with bleeding gums)
Ehlers-Danlos syndrome: decreased tensile strength. Hypermobility of joints,stretchy skin, susceptible to dislocations.
Osteogenesis imperfecta: type 1 collagen deformity/deficiency -> less bone tissue -> prone to fractures. Blue sclera.
Alport syndrome: x linked dominant. Type 4 collagen defect
Keloid scars: overgrown scar that spreads outside he original area of skin damage. (Made of collagen)
Deep vein thrombosis
Formation of thrombus within a deep vein. Caused by inactivity, obesity, oral contraceptives, heart conditions.
Fragt can break off and migrate to lung causing a PE
Prevented with SC heparin and stockings to reduce likelihood of thrombus formation.
Treat with IV heparin/oral warfarin.
Embolism
Blockage of a blood vessel by a solid/liquid/gas at a site distant from the origin.
Most arise from thrombus (thromboembolism)
Types: gas, nitrogen, cerebral, air, amniotic, fat, paradoxical
Pulmonary embolism
Embolism that migrates to the pulmonary arteries, occluding the vessels and leading to respiratory problems. >60% reduction in lung function is fatal.
Can cause right sided heart failure due to severe pulmonary hypertension, mechanical shock due to severely decreased preload of the left heart, or critical ischaemic hypoxia to a huge part of the lung
Atheroma
Accumulation of intracellular and extracellular lipids in the tunica intima and tunica media of medium/large arteries
Atherosclerosis
Thickening and hardening of arterial walls due to atheroma
Artiosclerosis
Thickening of arterial/arteriolar walls due to hypertension/ diabetes
Consequences of Ischaemic heart disease
Death, MI, angina, cardiac failure, arrhythmias
Consequences of cerebral ischaemia
Transient ischaemic attack (TIA), stroke, multi-infarct dementia
Consequences of mesenteric ischaemia
Malabsorption, intestinal infarction, ischaemic colitis
Consequences of peripheral vascular disease
Intermittent claudication (intermittent leg cramps due to arterial obstruction), Leriche syndrome (aortoiliac occlusive disease), critical limb ischaemia (ischaemic rest pain and gangrene)
Examples of pathological hyperplasia
Hyperplasia: increased organ/tissue size due to increased cell numbers.
Psoriasis: extreme proliferation of skin cells-> deposition of keratinocytes at stratum corneum -> scaling
Thyroid goitre: hyperplasia of thyroid gland to compensate for inefficiency