Flashcards in VP1 Deck (41)
Histological stain in pink and purple where acidic parts turn pink, such as proteins, and basic parts turn purple, such as nuclei. Fat, glycogen and water cannot be distinguished.
Oil Red O
A histology stain that turns fats red.
A histology stain that turns glycogen dark pink.
Histological stain that colours collagen green.
Histological stain that turns basement membranes dark brown. Great to the the organisation of the stoma in the tissue or protection (eg tumorous growths)
Histological stain with antibodies for specific sequences, like viral genetic material.
Increase in the number of cells compared to normal.
Enlargement of the cells.
Incomplete or underdevelopment of a tissue or organ.
An organ not developing past the embryonic state. A rudiment will be present.
An organ that has not developed at all in an animal.
Abnormal differentiation of adult cells
Abnormal organisation of cells. Pre-stage of neoplasia.
The sequence of events occurring after exposure to the inciting agent or event - disease development.
A pathological or traumatic discontinuation of a tissue or a partial loss of its function. Includes wounds, sores, ulcers, tumours, cataracts, eczema, scars, abscesses and bacterial or viral changes.
Cellular swelling/hydropic change
Cellular swelling is due to two things:
1) Dysfunction of membrane proteins eg the Na/K-ATPase-pumps. This will cause sodium to travel into the cells and water will follow, causing the cell to swell.
2) Hypoxia —> less aerobic output(ie ATP) —> switch (if possible)to anaerobic metabolism —> deplete glycogen and accumulate lactate and phosphate
Cellular swelling appears as clear vacuoles no matter the stain (no stain for water).
Cell death due to cell swelling (onco meaning swelling). Cell swelling is reversible but if stimuli is not removed then it will lead to cell death. Oncotic necrosis is divided into:
Diagnosis based on the predominant lesions - referring to the structural changes rather than the causative agent.
A diagnosis that specifies the aetiology, ie the causative agent. This could be done by eg immunohistochemistry stains.
A lesion that is so typical for a disease that you can diagnose based on it
Acute lesion caused by ischemia (inadequate blood supply) or infarction (obstruction of blood supply) —> think blood clot. Basic cell outlines are preserved.
Typically occurs in tissues with a high blood demand, eg the kidneys, adrenals and heart.
Caused by a chronic lesion. Tissue becomes friable (non-resistant to pressure) and cheese-like (Tip, caseous sounds like casein... cheese-ish). Can develop into dystrophic calcification.
Dead cells turn into a liquefied debris since there’s not enough tissue framework to support the dead cells, eg in the CNS, or by pyogenic (pus-generating) bacteria, eg in abscesses.
The chronic stage of a coagulative necrosis. Can either be
- moist/gas, invaded by saprophyte (something living on dead/decaying organic matter).
- dry, mummification
Specific for when there is extracellular fat accumulations (rather than oncotic necrosis).
During necrosis (cell death), the nucleus is divided into several small fragments.
During necrosis (cell death), the nucleus fades as it is destroyed. Common at coagulative necrosis.
During cell death, the cell and nucleus shrinks, flattens and the nucleus becomes densely stained- more asociated with apoptosis than necrosis.
Intracellular accumulation of fat. Hepatocytes (liver cells) are especially susceptible of their role in lipid metabolism. Heart muscle, skeletal muscle and kidney cells are all also at higher risk.
Tissue will have a greasy texture. Histologically you will need an Oil Red O stain to differentiate from glycogen and water.
Lipidosis happens of two reasons
1) Excessive free fatty acids into the liver
- Too much in the diet
- Adipose tissue breakdown due to starvation, eg during late multiple-offspring pregnancy
2) Toxic damage to cells so that they cannot handle (even normal) levels of fatty acids, eg alcoholism
Adipocytes replacing tissue-specific cells due to old age or obesity.
Abnormal amounts of glycogen in the cells, eg hepatocytes.
Glycogen accumulation can be due to three things:
1) Corticosteroid therapy why
2) Diabetes mellitus,
3) Glycogen storage disease
Calcium is deposited in tissues that are already dead/dying. A crippling noice can be hear in macro. Serum calcium levels will be normal.
Due to hypercalcaemia that will damage the intracellular organelles.
Occurs early in inflammatory lesions, eg burns, blisters and allergic reactions.
The exudate is clear to yellow and watery. It has non to few cells and acts to separate connective tissue fibres.
Arise in areas with mucus producing cells like the respiratory and GI tract.
Thick and gelatinous consistency. Some connective tissue and hyperplastic (swollen) epithelial cells.
Due to acute bacterial or viral infection, ie more severe damage.
White to yellow, soft and viscous, easy to remove and expose hyperaemic organs/tissues (active increase of blood supply). Fluid has high concentration of plasma proteins and a fibrin network (escapes from the blood vessels at high vascular permeability (hyperaemia)) but no/few cells (eosinophils).
Chronic reaction. Scar formation, fibroblasts laying down collagen to replace specialised cells.
Suppurative or Purulent exudate
Bacterial origin, especially staphylococcus, streptococcus and e. coli.
Thick white to yellow, liquid or dried out (lamination). High in plasma proteins and neutrophils, dead/dying cells, debris, fibrin, bacteria...
Purulent exudate that has been walled off
A hollow in the viscera filled with purulent exudate