Lecture 1

Question 1

Pathogenesis?

Answer 1

Developing a disease

Question 2

Cellular response to injury depends

Answer 2

on the type, the duration and the severity of the injury

Question 3

Consequences depend on

Answer 3

the type, the condition and the adaptability of the cell

Question 4

The most important attack points in the cell:

Answer 4

plasma membrane, aerobic respiration, protein synthesis, genome

Question 5

What follows the functional changes of a damaged cell?

Answer 5

Morphological changes

Question 6

What kind of tissue or damage can a cell undergo?

Answer 6

Causes:

2. Physical agents (mechanic, irradiation, electric, burn, thermic etc.)
3. Chemical agents (toxins, drugs, bacterial toxins)
4. Biological agents (microbes)
5. Genetic defects
6. Nutritional effects (qualitative/ quantitative malnutrition)
7. Oxigen and nutrition deficiency (ischemia, hypoxia)

Question 7

Difference between ischemia and hypoxia?

Answer 7

Ischemia: deficient blood supply
Hypoxia: deficient oxygen supply
Ischemia leads to nutrition deficiency and of course oxygen deficiency
Then again anaemia can reduce the oxygen transport by the blood and be a reasons as well

Question 8

what biological function is turn off in ischemia?

Answer 8

Aerobic function is turned off and glycolysis/anaerobic function are turned on (2 ATP instead of 34 ATP per glucose)

Question 9

What can we see in necrotic cells?

Answer 9

Lipids and fatty acid release leading to calcification of necrotic cells

Question 10

Difference between reversible and irreversible injury

Answer 10

The reperfusion won’t aid

Question 11

Reperfusion injury

Answer 11

ROS are produced during hypoxia that then destroy more tissue

Question 12

Necrosis

Answer 12

Pathological, irreversible cell or tissue death in a living organism

Question 13

Morphology of necrosis

Answer 13

Swelling: Transport mechanisms that require ATP are not working as intended and the build up of ions lead to increased water uptake
Eosinphilic: more acidic compounds are created e.g. lactate, the mitochondria swell and break leaking lysosomes that break down other parts of the cell leading to neutral and eventual acidic pH in the cytoplasm staining eosine
The ER also swell leading to removal of membranes and clumping of chromatin

Question 14

Karyorrhexis

Answer 14

Fragmentation of nucleus

Question 15

Pyknosis

Answer 15

Shrinkage of nucleus

Question 16

Karyolysis

Answer 16

lysis of nucleus

Question 17

Irreversible signs

Answer 17

Autolysis, heterolysis, and karyolysis cause by lysosome enzymes

Question 18

Reversible damage

Answer 18

The nucleus is swollen but still present.

Question 19

Necrosis at the level of an organ

Answer 19

Infraction

Question 20

Coagulative necrosis

Answer 20

See a yellow wedge area in e.g. spleen and kidney surrounded by a hyperaemic are due to dilated capillaries. The yellow are neutrophil granulocytes.
Also firm and dry.

Question 21

Congestion

Answer 21

Reduced outflow leading to hemorrhagic infraction

Question 22

Double blood supply and infraction

Answer 22

Double blood supply can save the organ, but if not, the area will be red rather than yellow. Lungs and Bowels have double blood supply e.g.

Question 23

Liquefactive necrosis

Answer 23

Release of enzymes liquifying the organ e.g. brain and pancreas.

Question 24

Different stroke mechanisms

Answer 24

Infraction and aneurism

Question 25

Abscess

Answer 25

Typical bacterial infection leading to accumulation of neutrophils that then leave an empty cyst e.g. liver

Question 26

What forms the brown coloured inside macrophages?

Answer 26

breakdown of haemoglobin to haemosiderin

Question 27

Caseating necrosis

Answer 27

Granular resembles cheese, don't see the border of the destructed tissue but you see T cells and other inflammatory cells around the area

Question 28

Fat necrosis

Answer 28

Damage to organs containing a lot of fat, acute pancreatitis, see tiny soap like lesions with blurred borders

Question 29

Fibrinoid necrosis

Answer 29

Necrosis of the vessel wall insudated plasma proteins into the vessel wall

Question 30

Apoptosis

Answer 30

Programmed cell death occurring in normal or pathological individual cells and is regulated by pro and anti apoptotic proteins

Question 31

2 pathways:

Answer 31

* Intrinsic (mitochondrial) pathway– Bcl-2 family proteins | * Extrinsic (death-receptor) pathway– Fas and Fas-L interactions

Question 32

Morphology of apoptosis

Answer 32

``` Cytoplasmic eosinophilic condensation of chromatin Karyorrhexis apoptotic bodies Phagocytosis with inflammatory response ```

Question 33

Adaptation of cellular growth and differentiation

Answer 33

atrophy hypertrophy hyperplasia metaplasia

Question 34

Atrophy

Answer 34

pathological or physiological cellular/organ shrinkage

Question 35

Physiological atrophy

Answer 35

removal of embryonic structures e.g thyroglossal duct and thymus

Question 36

Pathological atrophy

Answer 36

ischemia./hypoxia leading to renal atrophy. Short time reversible, longer leads to replacement with fat and connective tissue

Question 37

Hypertrophy

Answer 37

Enlargement of an organ or tissue due to increase in cell size e.g. heart and skeletal muscle

Question 38

physiological atrophy

Answer 38

Working out, uterus enlargement

Question 39

Pathological hypertrophy

Answer 39

enlargement of heart due to chronic hypertension

Question 40

Hyperplasia

Answer 40

Enlargement of an organ or tissue due to increase in cell number

Question 41

Physiological hyperplasia

Answer 41

uterus during pregnancy (both hyperplasia and hypertrophy)

Question 42

Pathological hyperplasia

Answer 42

imbalance of hormones, inflammation, or following surgical resection e.g. adrenal cortex

Question 43

Metaplasia

Answer 43

Adaptive process of a tissue characterised by transformation to another type of matured tissue. e.g. bronchial squamous metaplasia due to chronic irritation of the tissue by smoking

Question 44

Intracellular accumulation

Answer 44

abnormal synthesis/metabolism leads to more product, accumulation of exogenous substances, pigments. E.g. the metabolism isn't enough and the overload causes damage. e.g. Excess triglycerides in the liver and inhibition of fatty acid oxidation Alpha 1 antitrypsin deficiency accumulation of Tau protein in Alzheimer's disease, glycogen storage disease in diabetes mellitus

Question 45

Pigments

Answer 45

Anthracosis (exogenous pigments), Tattoos | Hemosiderin (endogenous pigments)

Question 46

Amyloidosis

Answer 46

Abnormal accumulation of specific extracellular proteins causing firmness, enlargement and malfunction of the involved organs associated with chronic and hereditary diseases can be due to abnormal folding of proteins

Question 47

Amyloid material

Answer 47

Fibril proteins that bind to proteoglycans glycosaminoglycan and plasma protein diagnosed with Congo red staining

Question 48

Systemic amyloidosis

Answer 48

``` chronic inflammation (reactive systemic amyloidosis) hemodialysis ```

Question 49

localised amyloidosis

Answer 49

Alzheimer's diseases, atrial, endocrine amyloid in medullar carcinoma or type 2 diabetes