Flashcards in Pathology Deck (311)
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.
Platelets adhere to endothelium via what?
GPI to vWF or collagen
Platelets aggregate with other platelets via what?
GPIIb/IIa through fibrinogen or vWF bridges
Platelets can release what after activation?
Thromboxan, serotonin, factor V, ADP, ATP and plasminogen
Name some platelet agonists
PAF, collage, ADP, thrombin
What are vWF and P-selectin produced by?
Define secondary haemostasis
Formation of the fibrin clot
What are the 2 products of the coagulation cascade?
Thrombin (factor IIa) and insoluble fibrin
The steps of the coagulation cascade are carried out in the presence of what?
Which is the only factor involved in the extrinsic pathway of the coagulation cascade?
What is the intrinsic pathway activated by?
Intravascular causes- exposed damaged endothelium
What is the extrinsic pathway activated by?
Tissue factor released from damaged tissue
Which factor (combined with free calcium ions) causes cross-linking of fibrin?
Which coagulation factors are vitamin-K dependant?
II, VII, IX, X
(2, 7, 9, 10)
Which coagulation factors are in the contact group?
(11 and 12)
Which coagulation factors are in the highly labile fibrinogen group?
I, V, VIII, XIII
(1, 5, 8, 13)