Session 1 - Cell Injury

Question 1

What is hypoxaemic hypoxia?

Answer 1

Arterial concentration of oxygen is reduced

Question 2

What is Anaemic Hypoxia?

Answer 2

Decreased ability of Hb to carry oxygen

Question 3

What is Ischaemic Hypoxia?

Answer 3

Interruption of blood supply

Question 4

What is Histiocytic Hypoxia?

Answer 4

Inability to utilise oxygen

Question 5

Apart from hypoxia, what else can cause cell injury do death? (Long list)

Answer 5

• Physical agents
• Chemical agents
• Micro-organisms
• Immune mechanisms
• Dietary insufficiency
• Genetic abnormalities

Question 6

What are the four main targets for cell injury?

Answer 6

• Cell membranes (both plasma and organeller)
• Nucleus
• Proteins
• Mitochondria

Question 7

What is the general outline for hypoxia cell injury?

Answer 7

Cell is deprived of oxygen - No ATP production - Sodium potassium pump stops working - Sodium and water enter cell - Oncosis - pH decreases due to glycolysis - Calcium enters cell - Attacks on membranes, proteins, DNA and cytoplasmic comments - death

Question 8

What is Ischaemia-Reperfusion injury?

Answer 8

Oxygen returns to Ischaemic tissue, causes damage if cells are not yet necrotic. Increase in free radicals, neutrophils and complement pathway

Question 9

Name the three importance free radicals

Answer 9

• Superoxide
• Hydroxyl
• Hydrogen Peroxide

Question 10

What are the bodies defences against free radicals?

Answer 10

• Enzymes - SOD, catalases and perioxidases
• Free radical scavengers - glutathione, Vit A,C and E
• Storage proteins - sequest transition metals

Question 11

What are Heat shock proteins?

Answer 11

Proteins that recognise and repair mis-folded proteins

E.g Ubiquitin

Question 12

What cytoplasmic changes can we see with light microscopy?

Answer 12

• decrease in pinkness = accumulation of water

- increase in pinkness = accumulation of denatured proteins and ribosomes

Question 13

What nuclear changes can we see with light microscopy?

Answer 13

• Clumped chromatin
• Pyknosis - shrinkage
• Karryohexis - fragmentation
• Karryolysis - dissolution

Question 14

What reversible changes can be seen with electron microscopy?

Answer 14

• Swelling
• Blebs
• Clumped chromatin
• Ribosome separation from ER

Question 15

What irreversible changes can be seen with electron microscopy?

Answer 15

• Big cell swelling
• Nuclear changes
• Membrane defects
• swollen mitochondria

Question 16

What is Oncosis?

Answer 16

Cell death with swelling

Question 17

What is Apoptosis?

Answer 17

Cell death with shrinkage

Question 18

What is Necrosis?

Answer 18

Morphological changes that occur after a cell has been dead for some time

Question 19

What are the four types of necrosis?

Answer 19

• Coagulative
• Liquifactive
• Caseous
• Fat

Question 20

What is Coagulative necrosis?

Answer 20

• More desaturation of proteins that release of proteases
• Solid consistency
• Appears white
• Proteins become less soluble

Question 21

What is Liquifactive necrosis?

Answer 21

• more enzyme degradation that denaturation
• neutrophil infiltration
• seen in bacterial infections
• seen in brain
• viscous mass

Question 22

When is Caseous necrosis seen?

Answer 22

In tuberculosis; amorphous debris with cheesy appearance

Question 23

What is Fat necrosis?

Answer 23

• destruction of adipose
• Can be caused by acute pancreatitis = lipase release
• also from direct trauma
• in breast tissue can be confused for cancer

Question 24

What are the two types of gangrene and how are they caused?

Answer 24

Dry - exposure to air

Wet - infection with bacteria

Question 25

What is Infarction?

Answer 25

- Cause of necrosis, namely ischaemia - Caused by thrombosis of embolism - can also be through external compression of blood vessels

Question 26

What is a White infarct?

Answer 26

- occurs in solid organs after occlusion of end artery | - Limits to amount of haemorraging that occurs

Question 27

What is a red infarct?

Answer 27

Extensive haemorrhage into dead tissue, occurs when: - Dual blood supply eg lungs - Numerous anastomoses eg intestine - loose tissue eg lung - where previous congestion has occurred - where there is raised venous pressure

Question 28

What affects the consequences of the infarct?

Answer 28

- Whether tissue has an alternative blood supply - How quickly ischaemia developed - how vulnerable tissue is to hypoxia

Question 29

What three molecules are released after cell injury?

Answer 29

Potassium, Enzymes and Myoglobin

Question 30

What is special about DNA breakdown in apoptosis?

Answer 30

It is not random, it is cut in specific places

Question 31

When does apoptosis occur?

Answer 31

- Can be a normal physiological process - Can be hormone controllers - cytosol T-cells killing virally infected cells - cell damage especially if to DNA

Question 32

Which organelle is the central player for intrinsic apoptosis?

Answer 32

The mitochondria

Question 33

What is external apoptosis triggered by?

Answer 33

External Ligands such as TRAIL and Fas

Question 34

What can we see in electron microscopy in apoptosis?

Answer 34

- Cytoplasmic budding - Fragmentation - No league of cellular contents

Question 35

What can we see under a light microscope in apoptosis?

Answer 35

- Shrunken cells - Chromatin condensation - Pyknosis and Karryorrhexis - Affects on only single cells or small clusters

Question 36

Name some important apoptotic molecules (long list)

Answer 36

- p53; mediates response to DNA damage - Cytochrome c, APAF 1 + cascade 9 - Bel-2 - prevents cytochrome c release - TRAIL - death ligand - TRAIL-R - death receptor - Caspases

Question 37

Name the 5 main groups of intra cellular accumulations

Answer 37

- Water and electrolytes - Lipids - Proteins - Pigments - Carbs

Question 38

How can fluid accumulation appear in cells?

Answer 38

Either as small vacuoles or as Hydropic swelling

Question 39

Where is Hydropic swelling most dangerous?

Answer 39

The brain; it does not have room to expand and can cause pressure on the blood vessels

Question 40

What are the two types of lipid accumulation?

Answer 40

Steatosis and Cholesterol

Question 41

What are two main types of protein accumulation?

Answer 41

Mallory's Hyaline - damaged protein in hepatocytes due to alcohol liver disease Alpha-1-antitrypsin - Mis-folded protein accumulates in ER and means no regulation of proteases in lung so can cause emphysema

Question 42

Where are exogenous pigment residues found?

Answer 42

Lung and Lymph Nodes

Question 43

Name three endogenous pigments

Answer 43

Lipofuscin, Haemosiderin, and Bilirubin

Question 44

What is Lipofuscin?

Answer 44

Brown pigment found in ageing cells, found in long-living cells

Question 45

What is Haemosiderin?

Answer 45

An iron storage molecule, most commonly found in bruising. Also very common in Hereditary Haemochromatosis where Iron absorption in the intestine is increased. (Treated with regular bleeding)

Question 46

What is Bilirubin?

Answer 46

Bright yellow bile pigment If levels too high = Jaundice Transported to liver to be excreted

Question 47

Name the two types of Pathological Calcification?

Answer 47

Dystrophic and Metastatic

Question 48

What are the two main causes of Metastatic Calcification?

Answer 48

- Increased PTH release | - Destruction of bone

Question 49

Why can cells not divide indefinitely?

Answer 49

- Accumulative damage of cell comments and DNA | - Shortened telomeres

Question 50

What enzyme do stem cells and cancer cells have enabling them divide continually?

Answer 50

Telomerase

Question 51

What are the three main effects on the liver as a result of chronic excess alcohol intake?

Answer 51

- Fatty change - Acute alcohol hepatitis - Cirrhosis

Question 52

What is hypoxia?

Answer 52

Deficiency of oxygen reaching the tissues