Flashcards
Week 1: General pathology
Cards in this deck (50)
- 1What general requirements do cells have?Oxygen, nutrients, protection from toxins, intact membranes and enzyme systems
- 2What three processes cause disease in cells?Damaged organelles (mitochondria)
damaged membranes
damaged enzyme systems - 3What is a lesion?An abnormality of an organ or tissue
- 4Somatic death vs necrosis?Somatic death: Death of individual
Necrosis: cell death in living individual - 5Post mortem changes (4)Cooling
Rigor mortis
Blood changes
Degeneration - 6Factors influencing coolingInitial temperature (fever)
Insulation (clothing, fat, wool etc.)
Environment - 7What is rigor mortis, time and order of onset?Stiffening of muscles. Decreased energy causes muscle contraction
12-24 hours post mortem
head > heart > diaphragm > limbs - 8Blood changes (2)pooling
clotting - 9Degeneration processes (2)Autolysis: degradation via cellular enzymes
Putrefaction: degradation via bacteria inside or outside body - 10What factors determine rate of degeneration?Temperature
presence of bacteria
environment - 11Mechanisms of cell damage (5)Degeneration
Necrosis
Hypoxia
Free radicals
Chemical agents - 12What is hypoxia and what causes it?Lack of oxygen in tissue
-Reduced oxidative respiration
-Poor blood supply or oxygenation - 13Free radical damage, generation and protective mechanismsUnstable chemical compounds
Generated during cell function
Antioxidants protect: Vit A,C,E
Enzyme systems protect against FR damage - 14Mechanisms of chemical agents causing damage (2)Direct damage
Indirect damage via toxic metabolites - 15Other mechanisms of cell damageTrauma, heat, microbes, immune reactions, genetic defects, nutrition, ageing and obesity
- 16Significance of necrosis depends on? (4)Site (eg. brain is bad)
amount of tissue
speed of onset
scarring - 17Local reaction to necrosis (3)Inflammation
Mediator release
Neutrophil and macrophage involvement - 18Systemic reaction to necrosisEnzyme release from dead cells as they have leaky membranes
-quantified using biochemistry - 19Acute phase reaction to necrosis (3)Fever
Leukocytosis
Decreased appetite - 20LiquefactionDegradation of necrotic tissue into liquid. Large amounts of fluid, enzymes and neutrophils which are reabsorbed via lymphatic system
- 21suppurationLiquefaction and pus formation
- 22Components of pusnecrotic debris, neutrophils, tissue fluid and enzymes
- 23SequestrationEncapsulation of necrotic tissue in fibrous tissue in tissues with little bacteria and enzymes eg. bone
- 24Erosion and ulcerationin skin and luminal organs
desquamation: erosion of partial thickness of epithelia
Ulceration: severe, through basement membrane into connective tissue - 25OrganisationLeukocytes digest and remove necrotic tissues and fibroblasts form connective tissue to form a scar
- 26RegenerationCells that survive damage multiply and replace the scar - EXCEPT nervous and cardiac tissue
- 27GangreneNecrosis and bacterial involvement
Normal defences are ineffective and extremities are most susceptible - 28Characteristics of gangrenous tissue (6)no blood supply
cold
non responsive
no bleeding
stinks
discoloured - 29AtrophyDecrease in size of individual cells die to decrease in nutrients or stimulation
- 30Types of atrophy (2) and other causesdisuse atrophy
denervation atrophy
ageing and hormonal changes - 31HypertrophyIncrease in size of cells, tissues and organs
eg. pregnant uterus and heart valve disease - 32HypoplasiaIncomplete tissue growth or development of tissue. Congenital
- 33AtresiaAbsence of lumen
- 34HyperplasiaIncrease in number of cells, can coexist with hypertrophy
eg. goitre
can have cystic or nodular prefix - 35DysplasiaAbnormal architecture or structure of tissue
congenital - hip dysplasia
acquired - healing epithelium - 36MetaplasticChange from one cell type to another, usually a protective mechanism eg. columnar to stratified squamous epithelium in resp tract
- 37What controls normal blood flow?baroreceptors in carotid sinus and aortic arch
Renin-angiotensin-aldosterone system
ADH - 38circulation disturbances caused by increased blood in terminal vascular bed (2)Hyperaemia
Congestion - 39circulation disturbances caused by decreased blood in terminal vascular bed (2)Ischaemia
Infaction - 40HyperaemiaIncreased erethyocytes in vessels
active process
Dilution of arteriole but not venule
Inflammation - 41CongestionPathological, passive process
Impeded blood flow out of tissue due to compression, blockages and impeded flow
Build up of poorly oxygenated venous blood in tissue - turns blue - 42Types of congestion (3)Localised - obstructed veins
Generalised - cardiac failure
Hypostatic - gravity and peripheral circulation failure - 43Effects of congestiongradual onset leads to colateral circulation
Chronic congestion can lead to haemorrage , hypoxia and edema - 44IschaemiaInadequate blood supply to tissue relative to needs causing hypoxia, malnutrition and toxic build up of waste.
- 45Causes of ischaemiaShock, capillary damage, venous obstruction, cardiac arrest and arterial obstruction (embolism, collapse, arteritis).
Eg. bed sores, atherosclerosis and intestinal torsion - 46Modifying factors of ischaemiaSensitivity of tissue - brain most sensitive
Duration and speed of onset - slow onset can lead to colateral circulation
Anaemia - worse due to already poor oxygenation
Body temp: Low temp = better as lower metabolism - 47InfarctionLocalised area of necrosis due to ischaemia. Occurs more in organs with poor colateral circulation. Appears as a wedge shape. Sterile or septic
- 48Acute infarction appearanceDeep discoloured lesion, swollen due to cell degeneration.
- 49Sub-acute infarctionFluid forced from lesion area, becomes paler with a line of hyperaemia and inflammation
- 50Chronic infactionTissue pale and shrunken due to fibrosis and scarring.
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- Pathology Flashcards on Week 1: General pathology, created by Kelly Scott on 27/01/2020.
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- Kelly Scott
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