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Year 2 Semester 2 > Pathology > Flashcards

Flashcards in Pathology Deck (311)
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211

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

212

When are the peak levels for circulating Igs reached in the neonate?

12-24 hours after birth

213

What do IgG and IgA prevent?

IgG prevents septicaemia
IgA prevents enteric disease

214

Why do non-suckled calves make antibodies sooner than suckled calves?

Maternally-derived antibodies inhibit Ab production

215

How can you assess neonate Ig levels?

Zinc sulphate turbidity test (cloudier=precipitated protein of immunoglobulin)
Measure serum levels of Igs by radial immunodiffusion

216

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

217

What is meant by metaplasia?

Reversible change-replacement of one adult cell type by another
Due to reprogramming of stem cells

218

What are chaperones?

Interact with proteins, aid proper folding, transport and degradation of proteins

219

What is haemosiderin a storage form of?

Iron
In tissues, ferritin is transferred to haemosiderin granules

220

What are the causes of jaundice?

Excessive haemolysis
Severe hepatic injury
Obstructed bile flow

221

What is hypercalcaemia seen with?

Increased PTH secretion
Destruction of bone tissue
Vitamin D intoxication
Renal failure (secondary hyperparathyroidism)

222

What is an amyloid?

A pathological proteinaceous substance deposited between cells

223

What factors cause cell injury?

Decreased O2 availability
Infectious agents
Immunological dysfunctions
Chemicals and toxins
Physical agents (trauma, temperature, pH, radiation)
Nutritional deficiencies
Genetic derangement (specific enzyme derangement)

224

What are the effects of oxygen free radicals in cell injury?

DNA fragmentation
Protein cross-linking and fragmentation
Membrane lipid peroxidation

225

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

226

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

227

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.

228

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

229

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)

230

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.

231

What is involved in primary haemostasis?

Formation of a platelet plug

232

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

233

What does von-Willebrand factor bind to?

Platelets and collagen

234

Platelets adhere to endothelium via what?

GPI to von Willebrand factor or collagen

235

How do platelets aggregate with other platelets?

GPIIb/IIa through fibrinogen or vWF bridges

236

What do platelets release after activation?

Thromboxan, serotonin, factor V, ADP, ATP and plasminogen

237

Give some examples of platelet agonists?

ADP, thrombin, collagen, PAF

238

Secreted vWF serves as a carrier for which factor?

Factor VIII

239

Where is vWF released from?

Endothelial cells

240

The platelet plug is stabilised by strands of what?

Fibrin