MoD Session 1- Cell Injury Flashcards Preview

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Flashcards in MoD Session 1- Cell Injury Deck (56):
0

What is disease a failure of?

Homeostasis

1

What 4 factors does the degree of cell injury depend on?

-type of tissue
-type of injury
-duration of injury
-severity of injury

2

What is hypoxia and how does it cause cell injury?

It is oxygen deprivation.
It can cause decreased aerobic respiration and therefore cell injury.

3

What is Ischaemia and why is it more dangerous than hypoxia?

It is a reduction blood supply, therefore causing a reduced supply of oxygen and metabolic substrates.

4

What are the four causes of hypoxia?

-hypoxaemic hypoxia- less arterial oxygen
-histiocytic hypoxia- disabled oxidative phosphorylation enzymes
-anaemia hypoxia- inability of haemoglobin to carry oxygen
-ischaemic hypoxia- reduced blood supply.

5

What are some of the physical agents that cause cell injury? (5 max)

Temperature extremes
Radiation
Direct trauma
Electric currents
Atmospheric pressure changes

6

What are toxins that cause cell injury? (4 max)

-insecticides, herbicides
-pollutants, poisons, asbestos
-alcohol and drugs
-high oxygen conc.

7

What are micro-organisms that cause cell injury? (3)

-fungi
-bacteria
-viruses

8

What two immune mechanisms can cause cell injury?

-hypersensitivity reactions
-autoimmune reactions

9

What are the 7 causes of cell injury?

-hypoxia
-immune mechanisms
-dietary imbalance
-genetic abnormalities
-toxins
-micro-organisms
-physical agents

10

What are 4 target sites for cell injury?

-nucleus
-mitochondria
-cell membranes
-proteins

11

What are the three main consequences of reversible hypoxia injury?

-ribosomes detach from the ER as there is less ATP therefore less protein synthesis and increased lipid deposition.
-NA+/K+ pump activity is reduced therefore high intracellular sodium and water follows= swelling.
-more glycolysis- more lactic acid production. Low pH affects enzyme activity.

12

Why does irreversible injury eventually occur as a result of hypoxia?

Membrane integrity is disturbed and it becomes increasingly permeable.
Entry of calcium activates enzymes which destroy the cell.

13

What is ischaemic reperfusion injury?

When a tissue injury is worsened by the return of blood flow to a damaged, but not yet necrotic tissue.

14

What are free radicals and give the three most important examples.

They are reactive oxygen species with a single unpaired electron in their outer orbit that can react with other molecules to produce more free radicals.
H2O2, OH. , O2-

15

What are the body's defence against free radicals? (2)

-heat shock proteins - increased production when the body is in oxidative stress. They repair misfolded proteins to maintain cellular viability.
-anti-oxidants- SOD, catalase and peroxidases remove free radicals, scavengers such as Vit A,C and E, and glutathione neutralise them.

16

What are the reversible and irreversible cytoplasmic changes under the L microscope?

-reversible- reduced pink staining due to increased water accumulation
-irreversible- dark oink staining due to detached ribosomes and protein denaturation.

17

What acre the reversible and irreversible nuclear changes seem under the L microscope?

-reversible- chromatin clumping
-irreversible- pyknosis, karryolysis, karryohexis

18

What are some of the reversible features seen under the electron microscope?

-blebbing
-swelling- sodium potassium pump failure
-chromatin clumping
-ribosome separation

19

What are some of the irreversible features seen under the electron microscope?

-myelin figures
-membrane defects
-ER lysis
-cell swelling
-pyknosis, karryohexis, karryolysis

20

Define oncosis

Cell death with swelling.
It is a change that occurs in cells prior to death.

21

Define apoptosis

Cell death with shrinkage.
Cell suicide

22

Define necrosis

It is not a process, but an appearance of cell death. Morphological changes that occur 4-24 hours after cell death.
Also sees swelling.

23

Which the of necrosis appears white, is denatured proteins and therefore is firm and has a ghost outline?

Coagulative

24

Which type of necrosis occurs due to neutrophil death and is digestion of tissues?

Liquefactive

25

Where is Liquefactive necrosis typically found?

The brain

26

What type of necrosis has amorphous debris and a cottage cheese like appearance?

Caseous

27

What is caseous necrosis associated with?

Infection. E.g TB

28

When does fat necrosis occur? (2)

-as a result of direct trauma to adipose
-following acute pancreatitis as lipases are released which act on adipose.

29

What is a characteristic feature of fat necrosis?

Chalky deposits due to the release of fatty acids reacting with calcium.

30

What is gangrene?

A description of necrosis.

31

What is dry gangrene?

Coagulative necrosis modified by exposure to the air.

32

What is wet gangrene?

Liquefactive necrosis infected with a mixed bacterial culture.

33

Why is wet gangrene serious?

Because bacteria can easily get into the blood stream and cause septicaemia.

34

What is gas gangrene and when is it most common?

It is wet gangrene caused by anaerobic bacteria that produce visible, palpable gas bubbles.
Ischaemic limbs.

35

What is an infarct?

An ischaemic necrosis

36

When do white infarcts occur, and why are they white?

They occur in solid organs due to the occlusion of an end artery.
They are white because there is a lack of blood.

37

When do red infarcts occur?

They occur when there is extensive haemorrhage into dead tissue.

38

Why are molecules released during cell injury?

Because membrane integrity is lost.

39

What are the 3 molecules released by injured cells?

-potassium
-enzymes
-myoglobin

40

When are budding and blebbing seen?

-budding- apoptosis
-blebbing- oncosis

41

What are the three steps of apoptosis and what happens at each?

1. Initiation - intrinsic and extrinsic mechanisms activate caspases that cleave proteins and initiate DNA degradation.
2. Execution - intrinsic- mitochondria becomes more permeable and cytochrome C is therefore released. Extrinsic- Ligands bind to death receptors.
3. Degradation and phagocytosis - cell breaks down into apoptotic bodies which induce phagocytosis.

42

What are two important apoptotic molecules?

P53- mediates apoptosis in response to DNA damage
BC1-2- prevents cytochrome C release from mitochondria, therefore inhibits apoptosis.

43

Why can fluid accumulate in cellular damage?

Due to osmotic disturbances.

44

What lipids can accumulate abnormally? And where do they accumulate?

-triglycerides. - cause steatosis. Common in the liver as this is the site of metabolism.
-cholesterol. - excess is stored in membrane bound droplets and can cause xanthomas and atheromas.

45

What proteins can accumulate in cellular damage?
How do they accumulate?

-Mallorys hyaline- they accumulate due to damaged protein in hepatocytes as a result of alcoholic liver disease. It is an accumulation of altered keratin filaments.
-alpha-1-anti trypsin- deficiency of this is a genetic disorder in which the liver incorrectly folds it and therefore it can't be packaged by the ER, so accumulates and isn't secreted by the liver.

46

What exogenous pigments can accumulate in cells?

-tattoos- pigment placed into skin is phagocytosed by macrophages.
-carbon, coal dust and soot- are inhaled and then phagocytosed as above to give blackened lungs.

47

What endogenous pigments can accumulate? (3)

-lipofuscin
-haemosiderin
-bilirubin

48

What is haemosiderosis?

When there is deposition of haemosiderin due to a systemic iron overload.

49

What is hereditary haemochromatosis?

A genetically inherited disorder leading to increased intestinal iron absorption causing haemosiderosis in various organs.

50

Where do dystrophic and metastatic calcifications occur, respectively?

-dystrophic- dying tissues e.g atherosclerotic plaques and damaged heart valves.
-metastatic- body wide distribution.

51

What is pathological calcification?

Abnormal deposition of calcium salts (hydroxyapatite crystals) within tissues.

52

What is metastatic calcification due to?

Hypercalcaemia caused by disturbance in calcium metabolism.

53

What is replication senescence?

When cells can no longer replicate because they have reached their critical length.

54

What are the results of chronic alcohol intake and why do they arise? (3)

-fatty change- fat metabolism is affected, therefore steatosis occurs and hepatomegaly as a result.
-acute alcoholic hepatitis- alcohol and metabolites are toxic, therefore in high quantities they can cause hepatitis, necrosis, Mallory bodies and neutrophil infiltration.
-cirrhosis- a hard, shrunken, nobbly liver.

55

Which two consequences of excessive alcohol intake are often reversible and which one is irreversible?

-reversible- fatty change and hepatitis
-irreversible- cirrhosis

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