Cell Injury Flashcards

1
Q

What happens in hereditary haemochromatosis

A

Increased absorption of dietary iron

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2
Q

What does increased absorption of iron cause

A

Deposits in skin, liver, pancreas, heart and endocrine organs. Associated with scarring in liver and pancreas

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3
Q

Symptoms of hereditary haemochromatosis

A

Liver damage, heart dysfunction, (pancreatic) endocrine failure

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4
Q

Treatment for hereditary haemochromatosis

A

Repeated bleeding

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5
Q

Inheritance pattern of alpha-1 antitrypsin deficiency

A

Autosomal recessive

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6
Q

What is alpha-1 antitryspin

A

A protease inhibitor which deactivates enzymes released from neutrophils at the site of inflammation

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7
Q

What happens in alpha-1 antitrypsin deficiency

A

Liver produces incorrectly folded version, cannot be packaged by ER, accumulates here leading to hepatic damage/cirrhosis.
Systemic deficiency means proteases in lungs act unchecked, breaking down tissue, causing emphysema

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8
Q

What is coal-workers pneumoconiosis

A

Emphysema due to eg. Soot inhaled and phagocytosed by alveolar macrophages

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9
Q

What is anthracosis

A

Blackening of lungs

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10
Q

What does coal workers pneumoconiosis cause

A

Emphysema, anthracosis, blackened perinronchial lymph nodes (due to phagocytosis of soot/carbon by alveolar macrophages)

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11
Q

What would you see in serology for pancreatitis

A

Early- raised amylase

Late- raised lipase

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12
Q

Explain how pancreatitis can cause hypocalcaemia

A

Lipase leaks out of pancreatic cells into abdominal cavity, breaking down triglycerides, causing fat necrosis. Calcium salts precipitate here forming calcium soaps, decreasing systemic calcium.

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13
Q

What happens in 10% of cases of pancreatitis

A

Glycosuria

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14
Q

What would a LFT show in hepatitis

A

Raised ALT, ALP, AST
Raised bilirubin
Low albumin
Raised PT, APTT

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15
Q

Hepatitis B serology

A

Surface antigen -> E antigen -> core antibody (IgM) -> E antibody -> surface antibody -> core antibody (IgG)

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16
Q

FBC acute liver disease

A

Raised ALT, AST, ALP

Raised bilirubin

17
Q

FBC chronic liver disease

A

Low albumin

Raised PT, APTT

18
Q

What are symptoms of chronic liver disease (5)

A

Fatty liver, cirrhosis, gout, lactic acidosis, hypoglycaemia

19
Q

Symptoms hep b

A

Jaundice, fatigue, abdominal pain, athralgia, nausea

20
Q

Incubation period hep b

A

1.5-6 months

21
Q

When does an infection go from acute to chronic

A

6 months

22
Q

Difference in serology for acute vs chronic hep b

A

Acute - IgM

Chronic IgG

23
Q

What are free radicals produced by

A

Chemical/radiation injury
Ischaemia reperfusion injury
Cellular ageing
High oxygen conc

24
Q

What do free radicals cause

A

Membrane lipid peroxidation
Damage to proteins, nuclei acids, carbohydrates
Mutagenic

25
Q

Examples of enzyme free radical scavengers and what they do

A

Superoxide dismutase: superoxide -> h2o2

Catalase/peroxidases: h2o2-> o2 + h20

26
Q

Examples of non enzyme free radical scavengers

A

Vitamins a, c and e

Glutathione

27
Q

Examples of storage proteins

A

Transferrin, ceruloplasmin

28
Q

What do storage proteins do

A

Sequester transition metals eg iron, copper in the extracellular matrix

29
Q

14 steps of hypoxic cell injury pls ;) (roughly)

A

1- cell deprived of oxygen
2- mitochondrial atp production stops
2- decreased activity Na+k+ATPase
4- Na+ and water seep into cell
5- cell swells
6- glycolysis enables cell to limp on for short time
7- cell initiates heat shock/stress response
8- pH drops as lactic acid from glycolysis accumulates
9- Ca enters cell (due to reversal of NCX)
10- Ca activates: phospholipases (break down cell memb), proteases (break down cytoskeleton and membrane), ATPase (breakdown atp), endonucleases (chromatin clumps)
11- ER and other organelles swell
12- lysosomes leak enzymes, attack cytoplasm
13- blebs form
14- death (probs due to burst of a bleb)