Pathology

Question 1

ALL organ injury and clinical disease arise from what?

Answer 1

defects in cell structure and function (in response to something in the environment disrupting homeostasis).

Question 2

What are four types of adaptations

Answer 2

1. Hypertrophy (increase in size)
2. Hyperplasia (increase in cell number)
3. Atrophy (cell shrinkage leading to organ shrinkage)
4. Metaplasia (cell type replaced by another better able to withstand the stress).

Question 3

Example of physiological (normal) hypertrophy? example of pathological (sick condiction) hypertrophy?

Answer 3

Uterus during pregnancy (enlarges)

Ischemia in cardiac muscle (myocytes increase in size to remain viable).

Question 4

What signals are used to initiate hypertrophy in the pathological example of ischemia in cardiac muscle?

Answer 4

stretch of cells (mechanical stimulus) and changes in protein synthesis alter cell.

Question 5

Uterus enlarging during pregnancy is not only an example of hypertrophy but also?

Answer 5

hyperplasia (increase in number of cells).

Question 6

Another example of physiological hyperplasia besides uterus in pregnancy?

Answer 6

compensatory. example if we remove a piece of tissue i.e. liver damage or surgery, cells are able to regenerate (from G0->G1). also needs a stimulus which would be groth factors by hepatocytes.

Question 7

Examples of pathological hyperplasia? is this normally reversible or irreversible?

Answer 7

excessive hormonal/growth factor production.

if stimulus is removed this is normally reversible.

Question 8

Example of physiological atrophy?

Answer 8

aging. comparing a young brain to an old brain we can see atrophy occuring which is normal.

Question 9

Some examples of pathological atrophy?

Answer 9

decreased workload, loss of innervation or blood supply, nutritional deficiency or endocrine deficiency or cell size must diminish to maintain survival.

Question 10

Example of pathological Metaplasia?

Answer 10

smoking. in lungs the epithlial layer made up of simple columnar epithelium and has cilia on apical surface. with smoking this can transform to simple stratified squamous which has a loss of cilia (can no longer expel contents) and loss of goblet cells (only located in columnar).

Question 11

Is Metaplsia often reversible or irreversible?

Answer 11

reversible, if stimulus is removed.

Question 12

Another example of pathological metaplasia which has some positive effects?

Answer 12

chronic gastric reflex. transforms from squamous to columnar (esophagus to intestinal tissue) which becomes a more protective layer due to the goblet cells.

Question 13

What are the two types of cell death?

Answer 13

apoptosis and necrosis.

Question 14

Differences between apoptosis and necrosis?

Answer 14

apoptosis: membrane does NOT fragment, NO inflammatory response, membrane in tact with various bubbles released.
Necrosis: cell membrane fragments (starts by blebbing), releases contents into extracellular space and causes inflammatory response.

Question 15

What are seven common causes of cell injury?

Answer 15

1. Hypoxia (Ischemia, pneumonia, anemia or CO poisoning)
2. Chemicals (air pollutants, ethanol. issues in membrane perm, osmotic homeo and enzyme damage)
3. Infections (viruses, bacteria, parasites)
4. Genetic (i.e. sickle cell, enzyme abnormalties).
5. Nutritional imbalance
6. Physical Agents (i.e. trauma, temperature, shock, pressure)
7. Aging (replication and repair abilities damaged).

Question 16

Is mitochondrial dysfunction reversible?

Answer 16

NO

Question 17

What is a factor that determines point of no return?

Answer 17

disturbances in membrane function.

Question 18

What are the three histological patterns in changes of the nucleus?

Answer 18

breakdown DNA and chromatin.

1. Basophilia fades (Karyolysis)- increase in eosinophilia.
2. Pyknosis: shrinkage and increased basophilia (DNA solid mass)
3. Karyorrhexis: fragmentation of nucleus (nucleus disappears in 2-3 days).

Question 19

Three types of responses to injury?

Answer 19

1. Tissue level (necrosis)
2. Cellular level (nuclear changes, lipid accumulation)
3. Subcellular (molecular) levels (mitochondrial changes, cytoskeleton changes, etc).

Question 20

Coagulative necrosis is what?

Answer 20

usually found in kidney tissues, causes an infarct (irreversible injury). cells are dead.

Question 21

Common characteristics of infarcts are what? present in all tissues except what?

Answer 21

1. structural proteins, enzymes denatured
2. no proteolysis
3. persist days/weeks
4. eventual phagocytosis by infiltrating WBCs

EXCEPT BRAIN.

Question 22

Liquifactive necrosis is what?

Answer 22

happens in brain infarcts, hole is filled with liquid. caused by bacteria/fungi. accumulation of inflammatory cells which cause pus.

Question 23

liquefactive necrosis occurs in brain always when what?

Answer 23

hypoxia occurs.

Question 24

Caseous Necrosis is what?

Answer 24

mainly occurs in lung tissue due to a tuberculosis infection. tissue destroyed, surrounded by inflammation.

Question 25

Fat necrosis is what?

Answer 25

usually occurs in pancreas, caused by lipases released from pancreas (leaked enzymes) causes fatty deposits. FA combine with Ca2+ to form saponification.

Question 26

Fibrinoid Necrosis is what?

Answer 26

usually occurs in blood vessel walls, inflammatory response

Question 27

Gangrenous Necrosis is what? type of what necrosis?

Answer 27

loss of blood supply to limb. form of coagulative necrosis however it involves many more layers than coagulative. sometimes bacteria can get involved causing liquefaction (pus).

Question 28

What are two subcellular responses to injury?

Answer 28

1. autophagy (self digestion): these have the contents needed to be digested, they fuse with primary lysosomes with degradative enzymes and then material is degraded. 2. heterophagy: macros ingest substance and destroy

Question 29

When would we see hypertrophy of SER?

Answer 29

in response to drugs or toxins in the body, hypertrophy allows for tolerance.

Question 30

two disorders of the mitochondria are?

Answer 30

1. megamitochondria disorder: in the liver, due to alcohol abuse or nutrition deficiency. mitos become large to deal with stress. 2. Mito myopathies: inherited disorder in skeletal muscles, defects into mito metabolism, mitos get large and increase in number.

Question 31

cell injury can cause issues in what four things? which are part of necrosis pathway/apoptosis?

Answer 31

1. decrease in ATP 2. membrane damage 3. cytoskeletal damage 4. DNA damage, accumulation of misfolded proteins. All are part of necrosis pathway EXCEPT DNA damage which goes through cell death (apoptosis).

Question 32

decreased ATP causes what?

Answer 32

1. Na/K pump activity reduced 2. increased glycolysis (anaerobic) 3. influx of Ca2+ (into cytoplasm) 4. reduced protein synthesis (due to detachment of ribos)

Question 33

What happens in response to EVERY type of cell injury? what does this cause?

Answer 33

mitochondrial damage. in response to cell injury, mito activates apoptosis pathways by releasing cytochrome c and ca2+ which are main drivers of apoptosis.

Question 34

Increased cytosolic Ca2+ causes what?

Answer 34

decreased ATP, decreased phospholipids, disruption of membrane and cytoskeletal proteins and nucleus chromatin damage.

Question 35

Pathological effects of ROS from cell injury and death?

Answer 35

1. ROS react with FA leading to disruption of PM and organelles. 2. ROS react with proteins causing loss of enzymatic activity and abnormal folding. 3. ROS react with DNA causing mutations and breaks.

Question 36

What are the most common causes of cell injury? which injures faster?

Answer 36

ischemia and hypoxic injury. | ischemia does because it decreases substrates for glycolysis where hypoxia can still use glycolysis.

Question 37

ischemia-reperfusion injury is due to?

Answer 37

myocardial and cerebral infarctions. increased ROS generation in parenchymal, endothelial and WBCs. increased inflammation.

Question 38

Chemical toxic injury can be what two types?

Answer 38

1. direct (combine with molecule or organelle) i.e. mercury combines with sulfur groups and inhibits active transport, membrane perm 2. converted to toxic metabolites i.e. CCl4 (used to be used in cleaning products now banned).

Question 39

Examples of physiological apoptosis?

Answer 39

1. embryongenesis 2. hormone deprivation 3. proliferating populations 4. cells served their purpose 5. elimination of harmful self reactive lymphocytes 6. cytotoxic T lymphocytes

Question 40

Examples of pathological apoptosis?

Answer 40

1. DNA damage 2. misfolded proteins in ER 3. infection-induce injury 4. atrophy due to clogs

Question 41

what are capases?

Answer 41

special enzymes only used in apoptosis, they activate nucleases which destroy nucleoproteins, cytoskeletal proteins.

Question 42

Which two pathways converge on capases?

Answer 42

mitochondrial intrinsic pathway and death receptor extrinsic pathway.

Question 43

Which pathway mito intrinsic or death receptor extrinsic is reliable on receptors? what is another difference between the two pathways?

Answer 43

extrinsic pathway is receptor mediated (TNF binds to a specific receptor on membrane). onset, death extrinsic is from viral or toxic onset where intrinsic is due to cell injury.

Question 44

abnormal intracellular accumulations is common for what tissue? What is an example in the liver? is it reversible?

Answer 44

RPE. build up of triglycerides (called steatosis) can occur in the liver (can also occur in heart, kidney, skeletal muscle) which is usually in response to alcohol abuse. reversible unless severe (if severe it will go to cell death)

Question 45

cholesterol is also another example of abnormal accumulations intracellularly which can happen where?

Answer 45

in the walls of smooth muscle and macrophages will fill with cholesterol droplets. this occurs in atherosclerosis.

Question 46

Protein reabsorption can be due to excess leakage which is common in which disease?

Answer 46

diabetes.