Week 2 25/01/21-29/01/21 Flashcards

1
Q

What does hypertrophy of cells mean?

A

↑ed cell size, ==> ↑ organ size
↑ed production of cellular proteins
Hypertrophied organ X new cells, just larger cells
Synthesis of more structural components of cell

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2
Q

What three factors can induce hypertrophy of cells?

A

Mechanical sensors, triggered by ↑ed work load
Growth factors incl: TGF-β, IGF-1, fibroblast growth factor
Vasoactive agents e.g. α-adrenergic agonists,
endothelin-1, angiotensin II

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3
Q

What is hyperplasia of the cells?

A

↑ cell no in organ/tissue ==> ↑ed mass of organ/tissue

Occurs if cell pop is capable of dividing

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4
Q

What are the two types of physiological hyperplasia?

A

Hormonal hyperplasia, ↑ functional capacity of a tissue when needed
Compensatory hyperplasia, ↑ tissue mass after damage/partial resection

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5
Q

What is the cause of pathological hyperplasia?

A

Excesses of hormones/growth factors acting on target cells

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6
Q

What is cellular atrophy?

A

↓ed organ/tissue size resulting from ↓in cell size + no

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7
Q

What are the different types of atrophy?

A

↓ed workload (atrophy of disuse)
Loss of innervation (denervation atrophy)
Diminished blood supply (senile atrophy)
Inadequate nutrition (marasmus, cachexia)
Loss of endocrine stimulation (endometrium, breast)
Pressure (tissue compression)

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8
Q

What are the mechanisms of atrophy?

A

↓ed protein synthesis + ↑ed protein degradation in

cells cos of reduced metabolic activity

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9
Q

What is metaplasia of cells?

A

Reversible change, one differentiated cell type (epithelial/mesenchymal) replaced by another cell type

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10
Q

What is cell necrosis?

A

Morphological changes that follow cell death in a LIVING tissue/organ, largely resulting from progressive, degradative action of enzymes on lethally injured cell

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11
Q

What are 2 causes of cell necrosis? (Types of enzymes)

A

Cell’s own degradative enzymes = Autolysis

Enzymes released by white cells + complement = Heterolysis

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12
Q

What is apoptosis of cell?

A

Chromatin condensation + DNA fragmentation

e.g. deletion of cells in: normal development, organogenesis, immune function, tissue growth

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13
Q

What are the 4 types of necrosis?

A

Coagulative necrosis e.g. MI/ paracetamol overdose in liver
Liquefactive necrosis e.g. cerebral infarct/abscess
Caseous necrosis e.g. tuberculosis
Fat necrosis e.g. in acute pancreatitis

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14
Q

What is gangrene?

A

Necrosis + putrefaction (i.e. rotting)

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15
Q

What are the 3 main types of diuretics? What are they used for?

A

Oedematous conditions - loop diuretics, K+ sparing diuretics

Hypertension - thiazide type diuretics

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16
Q

How do hydrostatic and osmotic pressures work in microvasculature? (kidneys)

A

Hydrostatic - pushes H2O out

Osmotic - pushes water in

17
Q

Where do the different diuretics act on?

A

Loop diuretics - ascending loop of Henle
Thiazide diuretics - DCT
K+ sparing diuretics - collecting ducts

18
Q

What drugs are loop diuretics?

A

Furosemide, Torsemide

19
Q

What conditions are loop diuretics used for?

A

Oedematous conditions e.g. heart failure. hepatic cirrhosis, glomerulonephritis

20
Q

What are potential adverse affects of loop diuretics?

A
Hypokalaemia, 
Metabolic acidosis
Depletion of plasma Ca2+, Mg 2+
Ototoxicity (deafness, uncommon)
Hypovolaemia
21
Q

What drugs are thiazide type diuretics?

A

Bendroflumethiazide, Indapamide

Metolazone (thiazide like)

22
Q

What type of diuretics should be used to treat hypertension? How much?

A

Low doses of thiazide-like drugs

23
Q

What are the adverse effects of thiazides?

A

Hypokalaemia
Hyperglycaemia
Hyperuricaemia
Metabolic alkalosis