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Pathology I Test I > Disease at the cellular level > Flashcards

Disease at the cellular level Flashcards

1
Q

What is hypertrophy?

A

1) General increase in the bulk, not due to tumor formation

2) increase in size of cells not #

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2
Q

What happens to tissue once it stretches or stress is put on a tissue?

A

It will adapt to the stress

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3
Q

What is atrophy or hypotrophy?

A

wasting of tissue from death and reabsorption of cells, diminished cellular proliferation, decreased cellular volume, pressure, ischemia or malnutrition that leads to lessened function or hormonal changes

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4
Q

What causes atrophy in the brain?

A

Aging and reduced blood supply

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5
Q

How does a brain that has undergone atrophy appear grossly?

A

The brain has narrowed gyri and widened sulci

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6
Q

What causes atrophy of the thyroid gland?

A

Longstanding autoimmune disease

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7
Q

What is hyperplasia?

A

increase in # cells excluding tumor formation

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8
Q

What causes endometrial hyperplasia?

A

Estrogen.

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9
Q

What causes calluses on the heels of feet?

A

Stresses due to constant wear on feet (ie: tight shoes)

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10
Q

What is BPH?

A

Benigh Prostatic hyperplasia

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11
Q

What is hypoplasia?

A

incomplete development of tissue (ie: neural fold defects)

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12
Q

What is metaplasia?

A

reversible replacement of one differentiated cell type with another differentiated cell type (ie: barrett’s esophagus where cells have migrated from the stomach to the esophagus due to constant stress)

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13
Q

What is anaplasia?

A

A change in the structure of cells and a change in their orientation to each other.

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14
Q

What is aplasia?

A

The defective development, or congenital absence of an organ or tissue

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15
Q

What is dysplasia?

A

Abnormal tissue growth with loss of cell orientation, shape, and size

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16
Q

Dysplasia is always what?

A

Pre-cancerous

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17
Q

What is cell injury?

A

When the limits of adaptive response is exceeded

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18
Q

What are the two types of cell injury?

A

Reversible and irreversible

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19
Q

What is reversible cell injury?

A

When the abnormal stress/stimuli persists for a short period of time

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20
Q

What is irreversible cell injury?

A

When the stress/stimuli persists or is severe

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21
Q

Is time a factor in cell injury?

A

Yes, it is a major factor for example drinking 1 beer will cause some reversible change but drinking 1 beer everyday for 30 years will be a persistent stimulus leading to irreversible change

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22
Q

What will swelling be like for reversible damage?

A

Generalized cell swelling

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23
Q

What is a bleb?

A

A bubble or outpouching of plasma membrane

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24
Q

Cells that bleb signify what type of cell injury?

A

Reversible

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25
Q

How does swelling of cells change for irreversible damage?

A

Increased swelling

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26
Q

What type of cell injury is plasma membrane damage?

A

Irreversible

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27
Q

What occurs in the ER with reversible Cell injury?

A

Swelling of the ER

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28
Q

What occurs in the ER with irreversible Cell injury?

A

Increased swelling of the ER

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29
Q

What happens to the ribosomes with reversible Cell injury?

A

Ribosomes detach from the ER

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30
Q

Cells with both reversible and irreversible damage have swollen mitochondria, but what is the difference in cells with irreversible damage?

A

They have vacuolization which is a Ca 2+ influx. due to membrane permeability

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31
Q

What happens to the nucleus in cells with reversible damage?

A

Reversible- chromatin clumps.

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32
Q

What happens to the nucleus in cells with irreversible damage?

A

Irreversible- Nuclear condensation, fragmentation and dissolution.

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33
Q

What is the term for nuclear condensation?

A

Pyknosis

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34
Q

What is the term for nuclear framentation?

A

Karyorrhexis

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35
Q

What is the term for nucleus dissolution?

A

karyolysis

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36
Q

What is the pH like for cells with reversible or irreversible damage?

A

Reversible has low intracelluar pH. Irreversible- continued low intracellular pH.

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37
Q

What type of cell injury is found with lysosome swelling and rupture?

A

Irreversible as necrosis will occur

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38
Q

What cell injury occurs when fat calcification begins?

A

Irreversible

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39
Q

What happens to reversible damaged cells when looking at them with light microscope?

A

They have fatty changes (steatosis).

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40
Q

Is nuclear clumping the same as nuclear condensation?

A

NO!

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41
Q

What is the difference between necrosis and apoptosis?

A

Necrosis- common after ischemia and chemical injury CELL SWELLING.
Apoptosis- is programmed cell death and CELL SHRINKAGE.

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42
Q

Does necrosis or apoptosis has neighbor or adjacent cell inflammation?

A

Usually necrosis

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43
Q

What happens to the plasma membrane during necrosis?

A

It is disrupted

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44
Q

What happens to the plasma membrane during apoptosis?

A

Intact/altered.

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45
Q

What happens with the cells contents with necrosis ?

A

enzymatically digested

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46
Q

What happens with the cells contents with apoptosis?

A

intact and packaged to be phagocytosed

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47
Q

What causes necrosis?

A

Inavriably pathologic

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48
Q

What causes apoptosis?

A

Often physiological

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49
Q

What does serum CK-MB check for?

A

Cardiac tissue ischemia

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50
Q

What does serum CK-BB check for?

A

Brain Tissue ischemia

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51
Q

What does serum CK-MM check for?

A

Generic muscle ischemia

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52
Q

What are the causes of cell injury?

A

1) O2 deprivation
2) Physical agents
3) Chemical agents/drugs
4) Infectious agents
5) Immunologic reactions
6) Genetic derangements
7) Nutritional imbalances

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53
Q

What are the two types of O2 deprivation cell injury?

A

Hypoxia and ischemia

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54
Q

What is hypoxia?

A

Inadequate oxygenation

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55
Q

What is ISchemia

A

Loss of blood supply

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56
Q

Can hypoxia occur without ischemia?

A

Yes, like in CO poisoning

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57
Q

Can ischemia occur without hypoxia?

A

No, hypoxia always occurs

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58
Q

What are some physical agents that cause cell injury?

A

trauma, burn, freeze

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59
Q

What are some chemial agents that cause cell injury?

A

cyanide, carbon monoxide, acetaminophen

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60
Q

What is an example of a genetic derangement that causes cell injury?

A

Sickle Cell Anemia

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61
Q

What is an example of a nutritional imbalances that causes cell injury?

A

Decreased calorie/protein, niacin, riboflavin

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62
Q

What are the types of biochemical mechanisms of cell injury

A

1) ATP depletion
2) Mitochondrial damage
3) High intracellular calcium
4) O2 deprivation & O2-derived free radicals
5) defects in membrane permeability

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63
Q

Mitochondrial damage that causes cell injury is due to what?

A

Increased Ca2+, oxidative stress, activated phospholiapase A2, Free fatty acids and ceramide

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64
Q

What is mitochondrial permeability transition?

A

Leakage of cytochrome c into the cytosol

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65
Q

Aerobic respiration gives us how much ATP?

A

36 atp

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66
Q

What do we get from anaerobic respiration?

A

2 ATP, and lactic acid.

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67
Q

Where does Kreb’s Cycle Occur?

A

In the mitochondrial matrix

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68
Q

What does cytochrome c do once it is outside of the mitochondrial membrane?

A

It induces secondary apoptotic effects

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69
Q

What are the sources of internal calcium?

A

1) mitochondrial damage
2) cell injury (external calcium enters cell)
3) ER damage

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70
Q

Where will Vitamin E be doing free radical protection?

A

In the membranes.

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71
Q

Glutothione is stored mostly where and to do what?

A

Stored in the retina to protect against all redox reactions.

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72
Q

What is the role of P-450?

A

Detox. It is enzymes that increase the solubility of compounds and help excrete them.

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73
Q

What is the down side of P-450?

A

While detoxing it can make some reactive oxygen intermediates which can injure cells.

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74
Q

Where are the P-450 enzymes found?

A

In the Smooth ER of hepatocytes.

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75
Q

What process is NADPH oxidase found in?

A

Pentose Shunt

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76
Q

Is iron required in the human body?

A

yes but excess can cause oxidative changes

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77
Q

Is copper required in the human body?

A

Yes but only in trace amounts

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78
Q

Free radical injury is induced through what?

A

membrane lipid peroxidation, protein modification, DNA breakage.

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79
Q

How are free radicals degraded?

A

Through enzymes, spontaneous decay, and antioxidants.

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80
Q

Why is homogenated milk bad for us?

A

Xanthine oxidase is better absorbed in body and causes more free radicals in circulation

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81
Q

Reperfusion after anoxia (an abnormally low amount of oxygen in the body tissues) induces what?

A

Free radical production.

82
Q

What are some free radicals found in the body?

A

Super oxide, peroxide, hydroxide and nitrous oxide

83
Q

What are some antioxidants that neutralize the free radicals in the body that are found in the cytosol?

A 
Superoxide dismutase
Glutathione
Peroxidase
Ferritin
Ceruloplasmin
Quercitin
84
Q

What is the function of ferritin?

A

Moves iron around the body

85
Q

What is the function of ceruloplasmin

A

Transports copper around the body

86
Q

Where is quercitin found?

A

in orange peel (white part)

87
Q

What can initiate injury via free radicals?

A

Radiation exposure, metabolism of drugs (phase I), redox reaction, nitric oxide, transition metals, leukocyte oxidative burst

88
Q

How do free radicals cause cell injury?

A

Through membrane lipid peroxidation, protein modification and DNA breakage

89
Q

What are 2 types of toxic cell injury?

A
  1. Direct toxin.

2. Indirect toxin.

90
Q

Give an example of a direct toxin?

A

Heavy metals like mercury.

91
Q

How will heavy metals like mercury be toxic to cells?

A

It disrupts the S-S bonds.

92
Q

Give an example of an Indirect toxin?

A

Carbon Tetrachloride (CCl4) it is metabolized in the liver to Carbon trichloride (CCl3) and this is more toxic.

93
Q

The P-450 detoxes what?

A

Barbiturate.

94
Q

What is an example of induction (hypertrophy) of smooth ER?

A

Barbituate detox by P-450

1) can lead to cell adaptation therefore decreased efficacy of medications such as phenobarbital for epilepsy when taken with alcohol
2) chronic barbituate use can lead to cell adaptation of hyper-detox and therefore a decreased effect

95
Q

What will lysosomal catabolism do with a subcellular response to injury?

A

heterophagy and autophagy.

96
Q

How is phagocytosis mechanically possible?

A

Clatharin pulls in substance and the plasma membrane wraps around it

97
Q

What happens to the mitochondria with subcellular injury?

A

1) Increased number with cellular hypertrophy and decreased number with cellular atrophy.
2) Also mitochondria may assume extreme large and abnormal shapes with nutrient deficiency or EtOH use
3) abnormal cristae with mitchondrial myopathies (inherited)

98
Q

What happens when the cytoskeleton undergoes subcellular injury?

A

Impaired:

1) intracellular organelle and molecular transport
2) basic cell architecture/shape/polarity
3) cell-to cell and cell-extracellular signals
4) Tissue integrity/mechanical strength (ie: desmosome anchorage)
5) Cellular mobility
6) phagocytosis

** thick scaffold/structural impairments

99
Q

What are chaperones?

A

Heat shock proteins (HSP).

100
Q

What will HSP (heat shock proteins) respond to?

A

Discovered with increased temperature but they respond to a variety of chemical/physical stimuli.

101
Q

What are the 3 roles of HSP?

A
  1. Protein folding.
  2. Disaggregation of protein-protein complexes (unclumping).
  3. Protein transport to cell organelles (chaperones).
102
Q

What happens to albumin with increased temperature

A

It denatures

103
Q

Where will proteins mostly break down at?

A

At sistein where the s-s bridges are.

104
Q

What are the different types of necrosis?

A

1) Coagulative
2) Liquefactive
3) Caseous
4) Fat
5) Fibrinoid
6) Gangrenous

105
Q

Coagulative necrosis happens with necrosis to what areas?

A

Heart, liver, and kidney.

106
Q

Coagulative necrosis is a result of what?

A

Protein denaturation.

107
Q

What will coagulative necrosis look like?

A

Preservation of basic cell outline for several days.

108
Q

Liquefactive necrosis happens where?

A

Brain

109
Q

Liquefactive necrosis is characteristic of what 2 things?

A
  1. Bacterial infection.

2. CNS stroke.

110
Q

Liquefactive necrosis is a result of what?

A

Enzymatic digestion.

111
Q

Gangrenous necrosis is associated with what area?

A

Limbs and GI tract.

112
Q

Gangrenous necrosis usually results in what?

A

limb with loss of blood and Coagulation necrosis.

113
Q

What is wet gangrene?

A

Coagulation necrosis with liquifactive action of bacterial infection and attracted leukocytes.

114
Q

Caseous necrosis occurs due to what?

A

It is seen in tuberculosis infections.

115
Q

What is the appearance of caseous necrosis?

A

Cheesy white appearance.

116
Q

Caseous necrosis is a distinct form of which type of necrosis?

A

Coagulative necrosis

117
Q

What is makes caseous necrosis a special form of coagulative necrosis?

A

Tissue architecture is obliterated unlike coagulative necrosis

118
Q

How does Caseous necrosis look microscopically?

A

1) amorphus granular debris of fragmented coagulated cell

2) amorphus granular debris enclosed within distinctive inflammatory border (granulmatous reaction)

119
Q

Can scarring from caseous necrosis be seen via x-ray? And how long does scarring last?

A

Yes it can be seen in x-ray and the scarring remains with the patient for life

120
Q

Fat necrosis occurs where?

A

In the pancreas

121
Q

Is fat necrosis a typical necrosis pattern?

A

No

122
Q

What will fat necrosis look like under microscope?

A

Foci of shadowy outlines of fat cells with basophilic calcium deposits surrounded by inflammatory reaction.

123
Q

What will fat necrosis look like grossly?

A

Chalky area due to fat saponification

124
Q

Is fat necrosis focal or widespread?

A

Focal area of fat destruction usually due to lipase release

125
Q

What does P-450 do? What is an unfortunate result?

A

P-450 neutralizes toxins but creates free radicals

126
Q

What is the stimulus for coagulative necrosis?

A

Hypoxia, toxins

127
Q

What is the stimulus for apoptosis?

A

Physiologic and pathologic

128
Q

What is the histology of the coagulative necrosis?

A

Cellular swelling
coagulative necrosis
organelle disruption

129
Q

What is the histology for apoptosis?

A

Cellular shrinkage
Chromatin condensation
Apoptotic bodies

130
Q

What is the DNA Breakdown in coagulative necrosis?

A

Random, diffuse

131
Q

What is the DNA Breakdown in apoptosis?

A

Internucleosomal

132
Q

What are the mechanisms of coagulative necrosis?

A

ATP depletion
Membrane injury
Free radical damage

133
Q

What are the mechanisms of apoptosis?

A

Gene activation
Endonucleases
Proteases

134
Q

What is the tissue reaction of coagulative necrosis?

A

Inflammation

135
Q

What is the tissue reaction of apoptosis?

A

No inflammation

Phagocytosis of ABs

136
Q

During what instances does apoptosis occur?

A

1) Embryogenesis
2) hormone induction (menstruation)
3) immune cell-mediated death
4) injurious stimuli (ie: radiation, hypoxia)
5) regulation of cell population and tumor suppression
6) atrophy (ie: endometrial lining during menopause)

137
Q

Which type of cell death is more controlled?

A

Apoptosis

138
Q

Which type of cell death involves more cells?

A

Necrosis

139
Q

What is the intrinsic (mitochondrial) pathway?

A

The permeabilisation of the mitochondria and release of cytochrome c into the cytoplasm. The cytocrome C then leads to caspase activation. Which then activates the executioner caspases and leads to apoptosis

140
Q

What is the process of extrinsic (Death Receptor-initiated) Pathway?

A

It uses Fas Ligand to bring death domains (3 of them) in proximity and the Fas associated death domain which will lead to autocatalytic caspace activation -> executioner caspases -> apoptosis

141
Q

Where is the brain of the cell?

A

Plasma membrane as it is the part that receives the information but (NB, it is the nucleus due to transcription and translation)

142
Q

What are the 4 general mechanisms of intracellular accumulations?

A

1) abnormal metabolism (fatty change in the liver)
2) Mutations causing alterations in protein folding and transport, so that defective molecules accumulate intracellularly
3) A deficiency of critical enzymes responsible for breaking down certain compounds which cause substrates to accumulate in lysosomes (lysosomal storage diseases)
4) An inability to degrade phagocytosed particles, as in carbon pigment accumulation

143
Q

What is an exogenous material for accumulation?

A

Coal particles (anthracosis)

144
Q

What are the endogenous metabolites of accumulation?

A

Hemosiderin

Lipids

145
Q

What are are some sources of intracellular accumulations?

A

1) lipids
- steatosis
- cholesterol and cholesterol esters
2) protein
3) hyaline change
4) glycogen
5) pigments

146
Q

Are the sources of intracellular accumulations exogenous or endogenous?

A

Endogenous although pigments can be both

147
Q

Are fats well absorbed?

A

Yes, they cycle, being absorbed in the intestines but expelled by the liver

148
Q

Does the heart use fats?

A

Yes, the heart uses fats and beta oxidation

149
Q

What is steatosis?

A

Fatty change leading to abnormal triglyceride accumulation in parenchymal cells

150
Q

What causes steatosis?

A

Alcohol abuse, toxins, protein malnutrition, diabetes mellitus, obesity and anorexia

151
Q

What enzyme is responsible for alcohol-induced fatty liver?

A

Alcohol dehydrogenase

152
Q

What does alcohol dehydrogenase do?

A

1) Interconversion between alcohols and aldehydes or ketones
2) Oxidizes methanol to produce formaldehyde
3) Oxidizes ethylene glycol to ultimately yield glycolic and oxalic acids

153
Q

What derivative of lipids can cause intracellular accumulations?

A

Cholesterol and cholesterol esters

154
Q

What is the microscopic appearance of lipid intracellular accumulations?

A

Foamy appearance

155
Q

What are some examples of lipid intracellular accumulations?

A

1) atherosclerosis
2) Xanthhomas
3) Inflammation
4) Cholesterolosis
5) Niemann-pick disease, type C

156
Q

Where does atherosclerosis due to lipid intracellular accumulation occur?

A

Plaque within the intima of large arteries

157
Q

Where does Xanthomas due to lipid intracellular accumulation occur?

A

Hyperlipidemia found in skin and tendon masses

158
Q

What occurs with inflammation due to lipid intracellular accumulation?

A

Phagocytosis of injured cell plasma membrane

159
Q

Where does cholesterolosis due to lipid intracellular accumulation occur?

A

Lamina propia of Gall Bladder

160
Q

What occurs with Niemann-Pick disease, type C due to lipid intracellular accumulation?

A

Lysosome storage disease

161
Q

Which of the lipid intracellular accumulations are found within macrophage

A

Xanthomas
Inflammation
Cholesterolosis

162
Q

What are some sources of protein intracellular accumulations?

A

1) Reabsorption droplets in the proximal renal tubules
2) Russell Bodies
3) Amyloidosis
4) Neuronal disease such as Alzheimer’s, Huntington’s, Parkinson’s and maybe Diabetes Mellitus Type 2

163
Q

What is the cause of reabsorption protein droplets in the proximal renal tubules?

A

kidney disease with protein loss

164
Q

What are Russell bodies?

A

Distended Endoplasmic Reticulumwith large eosinophilic inclusions (excess secretory protein synthesis)

165
Q

WHat is amyloidosis?

A

aggregation of abnormal proteins

166
Q

What is the cause of the neuro disease due to protein intracellular accumulations?

A

Glutathione stimulating hormone (GSH)

167
Q

What is hyaline change in terms of intracellular accumulations?

A

It is a pathologic descriptor meaning transparent appearance

168
Q

What causes hyaline intracellular accumulation change?

A

Variety of alteration, not a specific pattern of accumulation

169
Q

How does hyaline change appear in the microscope?

A

Gives a homogenous, glassy, pink appearance on H&E staining

170
Q

What are some intracellular examples of hyaline change leading to intracellular accumulations?

A

1) Reabsorption droplets
2) Russel Bodies
3) Mallory alcoholic hyalin

171
Q

What are some extracellular examples of hyaline change leading to intracellular accumulations?

A

1) Collagenous/fibrous tissue (scars)

2) Arterial wall hyalinization (Hypertension or DM2)

172
Q

What are glycogen intracellular accumulations?

A

Clear Vacuoles within cytoplasm

173
Q

What are the causes of glycogen intracellular accumulations?

A

1) glucose metabolism disorders (diabetes mellitus)

2) Genetic disorder (glycogen storage disease)

174
Q

What are the two types of pigment intracellular accumulations?

A

1) Exogenous

2) Endogenous

175
Q

What are the sources of exogenous pigments of intracellular accumulations?

A

Carbon (coal)

Tatooing

176
Q

What are the sources of endogenous pigments of intracellular accumulations?

A

1) Lipofusin
2) Melanin
3) Hemosiderin

177
Q

What is lipofusin?

A

Lipids being oxidized or lipid peroxidation

178
Q

What is hemosiderin derived from?

A

Hemoglobin (stored and eaten)

179
Q

What is hemosiderosis?

A

Iron and RBC that are left (like the dark spots in a lung)

180
Q

What is hemachromatosis?

A

More severe version of hemosiderosis

181
Q

What are the two types of pathologic calcification?

A

Dystrophic calcification

Metastatic calcification

182
Q

Where does Dystrophic calcification occur?

A

Deposition occurring locally in dying tissue

183
Q

What happens to the serum calcium level of the dystrophic calcification?

A

Nothing, it is normal serum calcium level

184
Q

Is there any calcium metabolism pathology associated with dystrophic calcification?

A

No, no calcium metabolism pathology

185
Q

What are some examples of dystrophic calcification?

A

Atherosclerosis of arteries, damaged heart valves

186
Q

Where does metastatic calcification occur?

A

Deposition in otherwise normal tissue

187
Q

What happens to the serum calcium level of the metabolic calcification?

A

Systemic elevation calcium levels in the blood and all tissues

188
Q

What usually causes metastatic calcification?

A

Usually due to secondary hypercalcemia

189
Q

What is the most common cause of hypercalcemia?

A

Hyperparathyroidism

190
Q

What does calcitonin do?

A

Calcitonin is absorbed in the bone and decreases serum calcium

191
Q

What does parathyroid hormone do?

A

Decreases calcium in bone and increases serum calcium

192
Q

What are the causes of metastatic calcification?

A

1) increased parathyroid hormone
2) Bone destruction
3) vitamin D related
4) Renal failure

193
Q

What causes parathyroid hormone to increase?

A

Primary tumor

194
Q

What causes bone destruction?

A

Multiple myeloma and Paget’s disease

195
Q

What are some vitamin D related issues?

A

1) D toxicity
2) sarcoidosis
3) Williams Syndrome

196
Q

What causes renal failure?

A

Potassium retention leading to secondary hyperparathyroidism

197
Q

What ratio of calcium to phosphate does the body try to maintain?

A

2 Calcium to 1 Phosphate

198
Q

What does metastatic calcification principally affect?

A

The intersttial tissues of the vasculature, kidneys, lungs, and gastric mucosa

199
Q

How does multiple myeloma present in X-ray?

A

Widespread lucency in bone

  • discrete “punched out” lesions
  • uniform in size
200
Q

What is a distinctive x-ray appearance for multiple myeloma?

A

Lucent, elliptical, subcortical shadows especially in long bones or endosteal scalloping

201
Q

What happens to calcium levels in injured cells with dystrophic calcification?

A

The calcium levels will increase due to release from ER and mitochondria

202
Q

What happens to mitochondrial initiation with dystrophic calcification?

A

The mitochondrial permeability transition increases and therefore calcium diffuses through into the cell.

Pathology I Test I (5 decks)

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