2 Lecture Flashcards

1
Q

Define Pathology

A

The study of suffering (Disease)

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2
Q

What is the difference between general pathology and systemic pathology?

A

general= basic reactions common to most tissues

systemic=specific responses in specific organs/tissues

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3
Q

what is the difference between the anatomic pathologist and the clinical pathologist?

A

anatomical= morphology based to figure out what etiology/pathogenesis mainly done under microscope.

Clinical= interpretation of laboratory data and very little morphology. This generally involves the study of body fluids even down to mutated genes.

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4
Q

What are the 4 aspects of a disease in order?

A

1) Etiology
2) Pathogenesis
3) Morphological changes
4) Clinical significance

(Note: of these 4, clinical pathologist generally focus on all except for #3. Anatomical pathologists focus on 3)

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5
Q

T/F All diseases start with abnormalities in cells?

A

True (for us)

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6
Q

What can we learn from the morphology of a cell?

A

The morphology of a cell can tell you a lot about the etiology/pathogenesis as well as the clinical behavior of the disease.

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7
Q

What are the two different categories of etiologies of a disease?

A

1) intrinsic= genetic problem from birth

2) acquired= hypoxia/ischemia, physical/chemical damage, nutritional defects, newly acquired mutations, etc.

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8
Q

What generally happens to cells when there is an added stress put on them? What will happen if this is long term?

A

The cells try to adapt to the situation by methods such as hypertrophy/atrophy, hyperplasia/dysplasia, etc.

If this goes on long term you generally get cell injury when the cells are no longer able to adapt to the situation.

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9
Q

If you have a severely injured cell, what 2 options does it have to die?

A

1) apoptosis

2) necrosis (the majority of the cells will undergo the necrosis method)

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10
Q

When can you see the morphological changes in cells under a light microscope?

A

Only after prolonged or severe injury.

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11
Q

What is the general trend (time frame) for noticing irreversible cell damage ?

A

1st in Labs
2nd in EM
3rd with Light microscope
4th with Autopsy/surgery/radiology

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12
Q

what is hyperplasia?

A

hyperplasia=more cells are produced

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13
Q

what is metaplasia?

A

metaplasia= cells change differentiation

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14
Q

what is dystrophic calcification?

A

calcification occurring in degenerated or necrotic tissue.

This is NI serum Ca+

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15
Q

what is metastatic calcification

A

Metastatic calcification=deposition of calcium salts in otherwise normal tissue because of elevated serum levels of calcium. (hypercalcemia)

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16
Q

What is a hyaline change? (intracellular and extracellular)

A

hyaline change =a pale, eosinophilic, homogeneous glassy appearance by H&E; it is a purely descriptive term and has a variety of causes.

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17
Q

Mechanisms of cell injury occur everywhere in the cell. However, there are 4 sites/processes that are more vulnerable than others which include?

A

1) cell membrane
2) aerobic respiration
3) protein synthesis
4) DNA integrity

18
Q

T/F hypoxia for 2 minutes in the liver will have the same effects as in the brain tissue?

A

False. The effect of cell injury depends on:

1) state of the cell
2) type of cell
3) duration/severity of injury

19
Q

There are 6 major mechanisms of biochemical injury to cells which include?

A

1) decreased ATP in cell
2) mitochondrial damage with Cytochrome C leakage
3) High intracellular calcium
4) High ROS
5) Membrane damage
6) Protein/DNA damage or misfolding

20
Q

CK-MB and troponin are increased in MI patients. Why do we see increases in these serum values?

A

It occurs because the cell membrane has been damaged due to the hypoxia/ischemia.

21
Q

A decrease in ATP leads to decreased function of the Na/K+ pump within the cell. What are the results of this?

A

1) increased Ca+,Na+, H2O influx, increased K+ efflux.

This leads to ER/cellular swelling, loss of microvilli, and blebbing of the cell.

22
Q

what affect does decreasing the pH of a cell have on chromatin?

A

it causes it to clump together

23
Q

If you have a decrease in ATP many ribosomes detach. This results in decreased proteins synthesis and ______?

A

lipid deposition

24
Q

Increased cytosolic Ca+, ROS, and lipid peroxidation have what affect on the cell?

A

Mainly mitochondrial injury. Mitochondrial dysfunction is frequently at the core of both necrosis and apoptosis.

25
Q

what is the normal cytoplasmic concentration of Ca+?

A

0.1 microMolar

26
Q

How does high/prolonged calcium inside the cell cause cell damage?

A

Calcium in high concentrations activates the enzymes that break down the cell. These include lipase, protease, ATPase, nucleases. (mainly target mitochondria)

27
Q

What are the 4 major ROS and their chemical breakdown?

A

1) super-oxide radical (02-)
2) Hydrogen peroxide (H2O2)
3) Hydroxide radical (OH-)
4) peroxynitrate anion (ONOO-)

28
Q

What is the function of NADPH Oxidase?

A

It generates ROS for use in killing bacteria such as in PMN’s.

29
Q

O2 is known to turn into superoxide (O2-) radical and cause damage. How does the body fix this problem?

A

It turns superoxide radical into H2O2 through the enzyme superoxide dismutase (SUD).

30
Q

H2O2 is also known to cause damage to the cell. How does the cell get rid of this ROS?

A

H2O2 is turned into H2O and O2 through the enzyme called catalase. Catalase is found in peroxisomes.

31
Q

How does your body get rid of the hydroxyl radical (OH-)?

A

The Hydroxyl radical can be converted into H2O2 by glutathione peroxidase. The H2O2 can then be converted into H2O and O2 through Catalase.

32
Q

T/F ROS contribute to atherosclerosis, cancer, and aging?

A

True. If you mess up the DNA it can lead to cancer and aging, and if you mess up lipid metabolism it can lead to atherosclerosis.

33
Q

T/F vitamin C and Vitamin E greatly reduce free radicals in the body?

A

False, to date few in any data has shown any benefit.

34
Q

What is NAC? What does it treat?

A

N-acetly cystine. It is used in tylenol overdoses to help enhance Glutathione pools in the liver.

35
Q

What is NAPQI?

A

NAPQI is a toxic byproduct produced during the xenobiotic metabolism of paracetamol (acetaminophen). It is normally produced only in small amounts, and then almost immediately detoxified in the liver.
However, under some conditions in which NAPQI is not effectively detoxified it causes severe damage to the liver.

36
Q

what is anoxia?

A

no oxygen delivery

37
Q

what is asphyxia?

A

No oxygen delivery due to an interruption of breathing.

38
Q

what is ischemia?

A

decreased blood flow. (note that this does not just limit oxygen)

39
Q

What are some of the characteristics of reversible cell injury? (6x)

A

1) loss of ATP
2) glycogen depletion
3) decreased pH (causes chromatin to clump)
4) failure of cell transport (causes edema)
5) detachment of ribosomes (decreases proteins syn.)
6) loss of microvilli
7) blebbing

40
Q

What are some of the characteristics of irreversible cell damage? (4X)

A

1) Membrane damage
2) intracellular loss of lysosomal enzymes
3) Large influx of calcium
4) Everything included under reversible cell injury.
a) loss of ATP
b) glycogen depletion
c) decreased pH (causes chromatin to clump)
d) failure of cell transport (causes edema)
e) detachment of ribosomes (decreases proteins syn.)
f) loss of microvilli
g) blebbing