Flashcards in Pathology Deck (311)
Explain the species differences between absorption of Igs in colostrum of ruminants vs horses and pigs
Ruminants: all Igs absorbed by intestine
Horses and pigs: IgG and IgM are selectively absorbed; IgA stays in intestine (acts like an antibiotic lining)
Intestine is only permeable for a short period, declines after 6 hours, by 24 hours almost nil absorption
When are the peak levels for circulating Igs reached in the neonate?
12-24 hours after birth
What do IgG and IgA prevent?
IgG prevents septicaemia
IgA prevents enteric disease
Why do non-suckled calves make antibodies sooner than suckled calves?
Maternally-derived antibodies inhibit Ab production
How can you assess neonate Ig levels?
Zinc sulphate turbidity test (cloudier=precipitated protein of immunoglobulin)
Measure serum levels of Igs by radial immunodiffusion
What is the difference between hyperplasia and hypertrophy?
Hyperplasia=increase in organ size due to increase in number of cells
Hypertrophy=increase in organ size due to increase in size of cells
What is meant by metaplasia?
Reversible change-replacement of one adult cell type by another
Due to reprogramming of stem cells
What are chaperones?
Interact with proteins, aid proper folding, transport and degradation of proteins
What is haemosiderin a storage form of?
In tissues, ferritin is transferred to haemosiderin granules
What are the causes of jaundice?
Severe hepatic injury
Obstructed bile flow
What is hypercalcaemia seen with?
Increased PTH secretion
Destruction of bone tissue
Vitamin D intoxication
Renal failure (secondary hyperparathyroidism)
What is an amyloid?
A pathological proteinaceous substance deposited between cells
What factors cause cell injury?
Decreased O2 availability
Chemicals and toxins
Physical agents (trauma, temperature, pH, radiation)
Genetic derangement (specific enzyme derangement)
What are the effects of oxygen free radicals in cell injury?
Protein cross-linking and fragmentation
Membrane lipid peroxidation
Which enzymes are activated by increased intracellular Ca2+?
What are the consequences?
ATPase: decreased ATP
Phospholipase: decreased phospholipids
Endonuclease: nuclear chromatin damage
Protease: disruption of membrane and cytoskeletal proteins
Give 4 potential causes of cell membrane damage that lead to irreversible injury
Progressive loss of membrane phospholipids due to activation of phospholipase by Ca2+
Cytoskeletal abnormalities due to activation of proteases and cell swelling
Toxic oxygen radicals after restoration of blood flow
Lipid breakdown products from phospholipid degradation
ULTIMATELY A MASSIVE INFLUX OF CALCIUM
What is the difference between apoptosis and necrosis?
Apoptosis= programmed cell death. Phagocytosis of apoptotic cells and fragments. No inflammation. Cells shrink. Plasma membrane stays intact. Cellular contents stay intact.
Necrosis= enzymatic digestion and leakage of cellular contents. Cells swell. Plasma membrane is disrupted. Cellular contents undergo enzymatic digestion.
What are the 4 types of necrosis?
Coagulative necrosis: Hypoxic cell death, preservation of cell outline
Liquefactive necrosis: Enzymatic digestion, complete digestion of cells -> liquid mass
Caseous necrosis: Complete obliteration of tissue architecture, surrounded by inflammatory cell border
Fat necrosis: focal destruction of adipose tissue, released fatty acids combine with calcium
Describe the morphology of apoptosis
1) Cell shrinkage
2) Chromatin condensation
3) Formation of cytoplasmic blebs and apoptotic bodies
4) Phagocytosis of apoptotic cells (by adjacent parenchymal cells and/or macrophages)
Why do neurones have to die in an apoptotic way?
We don't want inflammation of neurones in the brain. Instead they shrink and microglia quickly remove them.
What is involved in primary haemostasis?
Formation of a platelet plug
The release of what induces rolling of platelets and leukocytes?
P-selectin (from endothelial cells) on the endothelium
von Willebrand factor on the extracellular matrix
What does von-Willebrand factor bind to?
Platelets and collagen
Platelets adhere to endothelium via what?
GPI to von Willebrand factor or collagen
How do platelets aggregate with other platelets?
GPIIb/IIa through fibrinogen or vWF bridges
What do platelets release after activation?
Thromboxan, serotonin, factor V, ADP, ATP and plasminogen
Give some examples of platelet agonists?
ADP, thrombin, collagen, PAF
Secreted vWF serves as a carrier for which factor?
Where is vWF released from?