Adaptive Tissues Responses, Pigments, Infiltrates and Storage Diseases Flashcards
What is Atrophy, the mechanisms of Atrophy and the some causes?
- A reduction in the size of amount of an organ, tissue or cell, due to a decrease in the size and/or number of its specialised cells/organelles.
- An increase in APOPTOSIS is responsible for the decrease in number of cells. The remaining cells survive at a smaller size with fewer mitochondria, myofilaments and ER.
- Causes of Atrophy
- • inadequate nutrition,
- • decreased blood supply,
- • loss of innervation,
- • decreased workload (disuse),
- • prolonged pressure,
- • decreased or aberrant hormonal stimulation,
- • physiological (eg: thymus),
- • aging.
What is Hypertrophy, its mechanisms and Causes?
- •increase in the size of an organ or tissue due to an increase in the size of its specialised cells.• cells with increased workload that cannot divide eg:muscle. • general increase in the number of organelles which increases the size of the cell (limited by SA:vol)
- Mechanisms of Hypertrophy:
• Trophic triggers: growth factors, hormones, cytokines. May be produced endogenously or exogenously –> increase gene expression.• Physical triggers.
- Causes of Hypertrophy:
- Compensatory:
- removal of a kidney,
- increased workload – striated and cardiac muscle.
- Hormonal:
- pregnancy causes uterine hypertrophy.
What is Hyperplasia
Explain Physiological Hyperplasia and Pathological Hyperplasia
- HYPERPLASIA
- an increase in the size of an organ or tissue due to an increase in the number of its specialised cells.
- may be due to physiological or pathological causes.
- Physiological hyperplasia:
-
compensatory/reactive:
- haematopoietic system after blood loss,
- mesenteric lymph nodes.
- hormonal:
- cyclical changes in mammary gland or endometrium.
- Pathological hyperplasia:
-
hormonal excess:
- XS erythropoietin – polycythemia,
- XS estrogen – dysmenorrhea.
- Reparatory - to restore architecture or function.
- infectious organisms.
What is Metaplasia
METAPLASIA
- change from one type of specialised, fully differentiated adult cell to another adult cell type (often less specialised).
- a protective response.
- however, some functions are lost.
- reprogramming of stem cells by cytokines, growth factors (TGF-b), ECM components.
What is Dysplasia
DYSPLASIA
- = “disordered growth”
- not an ATR; principally in epithelium
- often occurs in metaplastic/hyperplastic epithelium
- loss in uniformity of individual cells plus loss in architectural organisation
- may progress to neoplasia
What is the difference between Left Ventricular Concentric and Left Ventricular Dilation/eccentric hypertrophy?
- Concentric = Walls are thicker of the heart but the ventricular lumen is smaller. Seen when there is a problem with uni-directional bloodflow leaving the heart. Eg a Cat having a stenosis impeding the outflow.
- Eccentric = Left Ventrical lumen is much larger but the walls are much thinner than normal. If you weigh the heart there will be a noticable increase in size and weight. This happens due to the AV valve not closing properly which will then inclease preload stretching the ventrical.
What are 4 endogenous pigments?
- Melanin
- Lipofuscin
- Haemosiderin
- Bilirubin
How is Melanin produced ?
What happens when there is a congenital deficiency? What is this called?
What is an example of an Aquired Deficiency?
- The ozidation or Tyrosine by Tyrosinase to Melanin
- Albinism
- Local injury (Branding) or Dietary Copper deficiency
- What is Lipofuscin
Lipofuscin is the name given to fine yellow-brown pigment granules composed of lipid-containing residues of lysosomal digestion. It is considered to be one of the aging or “wear-and-tear” pigments, found in the liver, kidney, heart muscle, retina, adrenals, nerve cells, and ganglion cells.
- What would haemosiderin look like in the tissue?
- What is it the product of?
- What is Haemosiderosis? What colour is it grosely and what stain would you use to identify it?
- Course, granular, golden-brown pigment
- Breakdown of Haemoglobin
- The accumulation of Haemosiderin in the tissue. Its brown grossly and it stains blue with Perls Prussian Blue Stain
What is this? and what is the causes?
Alimentary Lipofuscionsis
The occurrence of lipofuscin is associated with:
a) aging - continuous exposure through life to environmental agents generating free radicals
b) diets high in fat
c) vitamin E deficiency. Vitamin E is incorporated into the membrane lipid bilayer and inhibits peroxidation.
What would an albino be deficient in?
Tyrosinase
The enzyme that transforms Tyrosine into Melanin
What are some causes for deficiency of Melanin
Deficient formation of melanin:
a) albinism: genetic deficiency of the enzyme tyrosinase (general)
b) Cu2+ deficiency (general)
c) gonad, thyroid and adrenal hormone imbalance (localised)
d) trauma or chemical injury, e.g. freeze branding (localised)
What would lead to an increase/excess of Melanin?
Increased formation of melanin:
a) stimulation by ultraviolet light - suntan
b) localised “melanosis”, e.g. in lung or liver for no apparent reason (incidental finding)
c) moles (naevi): dermal accumulations of melanoblasts
d) melanomas: tumours arising from melanoblasts.
What has caused this?
Pulmonary melanosis, lungs, pig. Note the areas of black (melanin pigment) discoloration of the pleural surface. This pigmentation extends into the lungs and is an incidental finding that has no clinical or pathologic significance. It is most common in “black-face” breeds of animals, especially sheep.
- What is hyperbilirubinaemia
- What are the 3 forms
- What are their causes
What are the 4 types of Photosensitivity?
What has caused this?
What Stains would you use to see what colours?
Amyloid is an extracellular deposit and when present in large amounts can cause organs to be large, pale and waxy. In H & E sections, amyloid appears as a homogenous pink staining material in extracellular locations. It stains orange / pale red with Congo Red. Amyloid also shows an apple green birefringence when sections stained with Congo Red are viewed under a polarising microscope.
What is Gout?
What does Anti-Freeze do in the body?
GOUT is a disease in which URIC ACID or URATE CRYSTALS are deposited in tissues, particularly around joints. The crystals initiate a low grade chronic inflammatory reaction with enlargement and distortion of joints. In birds, deposition is most common over visceral organs. Impaired purine metabolism, (alcoholics) may lead to gout. Uric acid is stored as the white spots in the skin of the green tree frog.
The ingestion of certain plants, e.g. Oxalis pes-capri (Sour Rob) containing OXALATE, results in the accumulation of calcium oxalate crystals in the kidney tubules and sometimes in the CNS. Antifreeze (ethylene glycol) when ingested is metabolised to oxalic acid and produces similar lesions. The patient usually dies of hypocalcaemia or acute renal failure.
What is the cause of this (at the arrows?)
Dog Kidney!
Oxalate nephrosis, kidney. Dog. Tubular dilation, necrosis, and early regeneration (increased numbers of epithelial cells lining several tubules). Numerous tubules contain oxalate crystals (arrows), which have dilated the tubules and compressed their epithelium. H&E stain.
