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MOD > Chapter 2 Robbins/Pathoma > Flashcards

Chapter 2 Robbins/Pathoma Flashcards

1
Q

What is involved in cellular senescence? (2 things)

A

telomere shortening –> puts them in a non-dividing state

activation of tumor suppression genes

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2
Q

Myositis ossificans?

what do you see on Xray?

A

inflammation of the connective tissue (mesenchymal cells) in muscle results in a metaplastic production of bone in response to trauma.

Bone that is NOT connected to the original bone.

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3
Q

is pathological hyperplasia cancer?

exception?

A

no, but it can progress to cancer –> endometrial hyperplasia can become endometrial carcinoma

benign prostatic hyperplasia is NOT associated with cancer

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4
Q

Metaplasia is what?

1) what is the definition
2) what is the most common place to find metaplasia?
3) common pathology and what is the change going from? (what is the name to know)

A

stress on the organ changes, then the organ will respond by changing its tissue type

Lines body surfaces

Barrett Esophagus –> squamous to columnar (columnar metaplasia). –> stomach acid refluxing up

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5
Q

How does metaplasia occur?

key thing to note about metaplasia?

A

reprogramming of STEM cells

REVERSIBLE process. if you remove the stress, it will result in metaplasia

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6
Q

What are the two mechanisms by which chemicals induce cell injury?

what organ is chiefly affected?

A

Direct toxicity or Conversion to a toxic metabolite

liver –> it’s doing the conversion.

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7
Q

What is defects in membrane permeability consistent with? exception?

A

cell injury

except apoptosis

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8
Q

you see alkaline phosphatase and transaminase levels elevated in the blood, what does it indicate?

A

irreversible damage of the liver.

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9
Q

“dry cleaning industry”… what happened and what created this problem? what do you see?

what is another way this type of toxicity could be presented?

A

conversion of a toxic metabolite –> CCL4 to CCL3 free radical.. this was done by Cytochrome P450 –> because this is occurring in the liver and you’re destroying protein creation from the free radicals, you see less apolipoproteins so fat accumulation!

Acetominophen –> converted to a toxic product by the liver.. hence you die if you take too much

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10
Q

What are Russell bodies?

A

Plasma cells that are producing excessive amounts of Its results in the ER becoming distended, producing large, characteristically eosinophilic inclusions.. Russell bodies

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11
Q

5 common causes of injury?

A

Inflammation

Nutritional deficiency or excess

Hypoxia

Trauma

Genetic Mutations

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12
Q

why might decreasing vein flow cause ischemia?

2 examples?

A

block the vein –> block the flow of blood across the bed so decrease in amount of oxygen within the organ.

Bud Chiari Syndrome –> blocking hepatic vein going to the liver because of another possible thing (polycythemia vera)

hypercoaguable states

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13
Q

Explain Cellular swelling in injury

A

you cut the Na/K pump that needs ATP. so Na stays accumulating inside –> water comes in and swells

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14
Q

what are the three endogenous pigments to know?

what PATHOLOGIES ARE THEY ASSOCIATED WITH?

A

Lipofuscin granules –> “wear and tear”.. seen on old hearts and livers –> TELLTALE SIGN of free radical injury and lipid peroxidation

melanin –> only endogenous brown-black pigment

hemosiderin –> storage for iron.. present when there’s tons of iron and ferritin micelles come together and form hemosiderin. —> local excess is seen in tissue hemorrhage!!!! (bruise, or hemorrhaging after necrosis)

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15
Q

what three things are pathologic with regards to free radicals?

A

1) lipid peroxidation of membranes –> destroy membranes
2) modification of proteins
3) lesions in DNA (double strand or single strand breaks)

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16
Q

What is causing atherosclerosis?

A

smooth muscle cells and macrophages in arteries and the aorta fill up with lipid vacuoles –> made of cholesterol and cholesterol esters

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17
Q

Pyroptosis?

A

programmed cell death that is accompanied by the release of IL1.

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18
Q

What happens because of the swelling of the RER?

A

ribosomes pop off and so protein synthesis of

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19
Q

Hypoplasia:

1) what is it?
2) hallmark?

A

decrease in cell production during embryogenesis –> resulting in a small organ

streak ovary in turner syndrome

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20
Q

Aplasia?

A

failure of cell production during embryogenesis

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21
Q

when is hemosiderosis best seen?

A

common bruise

hemorrhaging after an infarct

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22
Q

What is used to removed free radicals?

A

1) antioxidants –> vitamin E or vitamin A
2) transport proteins of metals (transferrin, lactoferrin, ceruloplasmin) –> minimizes reactivity of metals
3) free radical scavenging systems

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23
Q

What is Hyaline Change?

A

alteration within cells or in the extracellular space that gives a homogenous, glassy, pin, appearance.

in long standing hypertension and diabetes mellitus, walls of arterioles (especially in the kidney) become hyalinized from so much deposition of basement membrane stuff.

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24
Q

What can Barrett Esophagus become if left untreated?

A

Adenocarcinoma

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25
Q

what is the morphologic hallmark of cell death?

what is the mechanism by necrosis?

what about apoptosis?

A

loss of nucleus

Pyknosis –> nucleus shrinks
Karyorrhexis –> breaks it into pieces
Karyolysis –> final stuff broken down

fragmentation into nucleosome-size fragments

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26
Q

what are the free radical scavenging systems (enzymes)

A

1) Catalase –> present in peroxisomes –> decompose H2O2 to O2 and H2O

Superoxide dismutase (SOD) –> converts O2- to H2O2

Glutathione peroxidase

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27
Q

Fat Necrosis

1) what is it
2) main appearance? what is this called?
3) what 2 places is this associated with?

A

necrosis of adipose tissue

chalky white appearance –> saponification

  • -woman in car accident –> destruction of fat cells in the breast.
    • peripancreatic fat
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28
Q

common types of physiologic hyperplasia?

A

female breast glandular epithelium hypertrophy during pregnancy

liver transplant people –> grows back to original side.

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29
Q

What are three examples of pathologic hyperplasia?

A

endometrial hyperplasia (estrogen)

Benign Prostatic Hyperplasia (androgens)

Papillomaviruses/other viruses

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30
Q

Niemann Pick Disease, type C?

A

lysosomal storage disease –> problem with cholesterol trafficking so cholesterol accumulation.

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31
Q

30 y/o woman presents fibrinoid necrosis, what could it be?

A

preeclampsia –> 3rd trimester women have elevated BP and they have fibrinoid necrosis of the placenta

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32
Q

What is the most common genetic abnormality found in human cancers?

A

TP53

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33
Q

What are the major triggers for physiologic hypertrophy?

pathologic?

A

mechanical sensors + mechanical stretch

growth factors and agonists or hormones

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34
Q

Werner Syndrome?

A

defective gene product in DNA helicase

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35
Q

What is the term for large, whorled phospholipid masses that are derived from damaged cell membranes?

what is their fate?

A

myelin figures

phagocytose or degraded to fatty acids –> saponification

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36
Q

Physiologic examples of apoptosis (2)

A

endometrial shedding

removal of cells during embryogenesis

elimination of potentially harmful self-reactive lymphocytes

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37
Q

say there’s ischemia in the brain or spinal cord, what is the most useful thing that is done in response?

A

inducing hypothermia –> lower metabolic demands and suppresses the formation of free radicals.

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38
Q

what three things can happen that lead to cellular aging?

what 3 ways can this happen?

A

1) telomeres are too short –> cell loss
2) DNA damage –> mutations
2) damaging of proteins –> decreased cell function

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39
Q

Main consequence of hypoxia?

what’s the immediate result because of this?

What 2 things cannot work because of this?

what is unregulated?

A

Impairs oxidative phosphorylation –> so no ATP being generated

1) Na-K pump, so you see high K+ outside, high Na+ inside (3 out, 2 in)
2) Ca2+ pump –> can’t hide ca2+ anywhere in the cell, so it’s going to activate a bunch of stuff
3) aerobic glycolysis –> creates a little bit of ATP but tons of lactic acid, so lowers the pH and destroys DNA and protein.

40
Q

2 mechanisms of atrophy?

A

Apoptosis –> decrease # of cells

Ubiquitin-proteosome degradation pathway and Autophagy –> decreasing cell size

41
Q

What quality shows that the cell injury is now irreversible?

A

Membrane damage

42
Q

what 6 things help lead to atrophy?

1) someone in a cast
2) diabetics
3) atherosclerosis in old people (what is it called?)
4) impoverished countries
5) 55y/o female with a pituitary tumor
6) large benign tumor

A

1) muscle atrophy
2) loss of innervation
3) decreased blood supply (ischemia) leads to atrophy –> senile atrophy
4) nutritional problems
5) loss of endocrine stimulation –> no estrogen means atrophy of breast, endometrium, vaginal epithelium
6) pressure cam atrophy on surrounding tissues

43
Q

Necrosis:

1) cells
2) what is it followed by?
3) generally, is it physiologic or pathologic

A

large groups of cells

acute inflammation

always pathologic

44
Q

Keratomalacia is what?

A

metaplasia of the eye due to a vitamin A deficiency

45
Q

Fibrinoid Necrosis

1) what is it?
2) what does it cause?
3) what are the two characteristics of it?

A

damage to the blood vessel wall

leaking of proteins of the blood vessel into the wall –> bright pink staining

Malignant hypertension + Vasculitis

46
Q

What are the 4 types of adaptation cells do under stress to maintain a steady state of homeostasis?

A

Hypertrophy
Hyperplasia
Atrophy
Metaplasia

47
Q

What happens with protein in most renal diseases? what findings are there and what do you see histologically?

is it reversible?

A

proteinuria –> excessive protein loss in the urine due to heavy glomerular filtration

because you’re trying to keep as much as possible, your proximal tubule reabsorbs a ton more and you’ll see the protein as pink hyaline droplets within the cytoplasm

yes, proteinuria gone, these vesicles diminish

48
Q

What are the 3 major consequences of Mitochondrial damage?

A

1) creation of the Mitochondrial permeability transition pore
2) abnormal oxidative phosphorylation –> creates ROS
3) release cytochrome C to activate caspases

49
Q

I’m a virus and I want to get around the extrinsic pathway of apoptosis. what do I produce?

A

FLIP –> protein that binds to pro-caspase 8 but doesn’t allow it to be cleaved –> no start to the extrinsic apoptosis pathway

50
Q

What metaplasia goes from columnar to squamous? what also can lead to squamous metaplasia?

A

smokers, in which chronic irritation.

Vitamin A deficiency

51
Q

Classic findings of CO poisoning?

A

Cherry red appearance of skin –> hemoglobin tightly bound that it reflects red light looking like they’re red, but actually hypoxic

headache

52
Q

What are examples of Direct Toxicity?

A

Mercuric Chloride Poisoning

Cyanide Poisoning

53
Q

what are the three membranes that are responsible for “membrane damage” that results in irreversible injury?

what pathology can be explained by each (if applicable)? otherwise what’s going to happen?

A

Plasma membrane damage –> leaking of cardiac enzymes.. you can tell that there was irreversible damage

Mitochondrial membrane –> leakage of cytochrome C causes apoptosis

Lysosomal membrane –> leaks lytic enzymes, destroying the membrane.

54
Q

Caseous Necrosis

1) Characteristic appearance (2 names)
2) what 2 pathologies are associated with this?
3) characteristic to see on slide?

A

1) cottage cheese like, friable
2) fungal infection and mycobacterium TB
3) granulomatous inflammation

55
Q

In duration of injury, what what are the effects of things happening in order?

A

Cell function goes down

Biochemical alterations (lead to cell death)

ultrastructural changes (not so important)

light microscopic changes

gross morphologic changes last

56
Q

what is the major pathway of apoptosis in mammalian cells and how does it work?

1) what primary group is involved?

A

intrinsic pathway (hallmark is BCL2 family)

BH3 only cells “sense” that there is damage –> activate BAX and BAK, and inhibit BCL2/BCL-XL which are antiapoptotic stuff –> release cytochrome C

cytochrome C binds to APAF1 –> creates apoptosome –> binds to caspase 9 –> cleavage and activation of execution phase

this is the activation of Caspase 3 and 6 –> activate DNAse activity and destroy the insides

57
Q

Explain what happens whet happens when we have the mitochondrial permeability transition pore open?

A

leads to loss of mitochondrial membrane potential, so bad oxidative phosphorylation.

Protein Cyclophilin D –> targeted by cyclosporine which is used to close this channel (used to prevent graft rejection)

58
Q

say a mammalian cell is first dealing with hypoxic stress. what transcription factor is unregulated and what does it do?

A

hypoxia inducible factor 1

creates new blood vessels, stimulates cell survival pathways, and enhances anaerobic glycolysis.

59
Q

Hyperplasia

1) what is the definition?
2) mechanism?
3) what constitutes physiologic hyperplasia?
4) what constitutes pathologic hyperplasia?

A

increase in number of cells in an organ or tissue in response to a stimulus.

result of growth factor driven proliferation off mature cells and from tissue stem cells!

due to the action of hormones or growth factors (there’s a need to compensate for increase functional activity)

due to an inappropriate action of hormone or growth factors acting on target cells

60
Q

The uterus undergoes what type of growth? explain

A

Hyperplasia and hypertrophy

uterus increases in size when pregnant to accommodate for the space of the uterus

smooth muscle undergoes hyperplasia as well.

61
Q

What causes emphysema?

A

a1-antitrypsin deficiency –> mutations slow protein folding, so you have a buildup of partially folded intermediates in the ER and liver.

62
Q

3 causes of hypoxia?

A

Ischemia

Hypoxemia

Decreased O2 Carrying capacity of the blood

63
Q

what two phenomena consistently characterize irreversibility?

A

inability to reverse mitochondrial dysfunction

disturbances in membrane function.

64
Q

What’s different between apoptosis and Necroptosis?

what’s the general process of it?

A

necroptosis doesn’t result in the caspase pathway

TNFR1 is ligated –> recruits RIP1 and RIP3 –> generates ROS and damages mitochondria, reducing ATP

65
Q

Liquefactive Necrosis

1) why is it called that?
2) where does it occur (2 places)
3) what structure can be seen with this?

A

1) enzymatic lysis of cells that leaves it liquidy
2) brain due to microglia, and inner pancreas from pancreatitis
3) abscess

66
Q

Atrophy is what?

1) why is it?
2) what decreases?

A

results from decreased protein synthesis and increased protein degradation due to reduced metabolic activity

decreases both size of cell and number of cells

67
Q

Cyanide is an example of what?

A

damage to the mitochondria, resulting in low ATP and eventually cell injury

68
Q

Dystrophic vs Metastatic calcification?

where is dystrophic almost always found?

where are you going to find metastatic calcification?

A

dead or dying tissue, but calcium deposits on the tissue because it’s dying

metastatic means serum calcium or serum phosphate is elevated so it can deposit at all tissues of the body.

advanced atherosclerosis

people with hyperparathyroidism, bone tumors having higher bone resorption, vitamin D related stuff, renal failure

69
Q

What is the predominating biochemical pathway involving muscular hypertrophy?

what does it signal?

A

PI3K/aKT pathway

Gata4, NFAT, MEF2 –> work to increase synthesis of muscle prteins.

70
Q

what does TP53 do? what happens if its mutated?

A

it’s triggering p53 apoptosis when it sees that cells that are DNA damaged

cells with damaged DNA aren’t able to p53-mediated apoptosis –> and survive.

71
Q

what two things are helping with anti-aging?

specifically, what does caloric restriction do?

what are both doing to counteract aging?

A

chaperone proteins (without them, in mice they aged super fast)

caloric restriction –> reduces the IGF-1 pathway but increases sirtuins (increase longevity I guess)

both are helping increase DNA repair and increase protein homeostasis

72
Q

You want to remove the apoptotic bodies. what are two things that can coat these guys to help macrophages come and eat them?

A

thrombospondin

C1q from the complement system

73
Q

Dysplasia is considered what?

what are the classic examples of dysplasia

A

proliferation of precancerous cells

Barretts –> adenocarcinoma

endometrial hyperplasia –> endometrial carcinoma

74
Q

Hypertrophy:

1) what increases
2) what are the 2 mechanisms
3) what 3 tissues undergo hypertrophy only

A

Cell size

in order to accommodate a bigger cell, we need to increase the cytoskeleton –> so increased protein synthesis..

also we need to produce more organelles for larger cellular function

Cardiac myocytes, skeletal muscle, nerves

75
Q

What are the anti-apoptotic members of the BCL family?

what is their function?

what is the major “sensor” of the BCL family?

A

BCL2, BCL-XL, and MCL1

prevent leakage of cytochrome C and other death-inducing proteins into the cytosol

BCL3

76
Q

During autophagy, the autophagosomal membrane elongates, surrounds the cargo it wants to eat, and closes around it. what mediates this process and is also a good marker for identifying cells with autophagy?

what is autophagy prominent in?

A

LC3 (microtubule associated light chain 3)

atrophying cells

77
Q

Mammogram looks at what? why is this important?

A

can indicate ductal carcinoma in situ –> fat necrosis would show calcification in the mammogram

78
Q

what two diseases are associated with increased rates of autophagy?

A

huntingtons and alzheimers

79
Q

Failure to produce one kidney is an example of what “plasia”?

A

aplasia

80
Q

Autophagy?

A

cell consumes its own components in vacuoles

these vacuoles fuse with lysosomes to destroy it.

81
Q

What two features of reversible cell injury can be seen under the light microscope?

again, when are we going to see this in the duration of

A

cellular swelling and fatty change

2nd to last

82
Q

Where do we get free radicals from? (6)

A

1) normal redox reactions
2) ionizing radiation –> can hydrolyze water to OH and H free radicals –> Super dangerous
3) leukocytes during inflammation
4) chemicals and drug metabolism –> CCL4
5) Transition metals –> free iron and copper help form this.. think Fenton reaction
6) NO –> chemical mediator that can be converted to ONOO- or NO2 and NO3

83
Q

What can decrease Oxygen carrying capacity of the blood?

3 major pathologies

A

Anemia –> decreases the total amount of RBC so decreasing the amount of oxygen going to the tissue

CO poisoning –> CO binds Hb 100x more than O2 so binding sites are taken up.

Methemoglobinemia –> Fe2+ usually binds O2, but it’s oxidized to Fe3+ from sulfa or nitrate drugs –> can no longer bind iron

84
Q

Pathogenesis is what?

Etiology?

Morphology?

A

sequence of cellular, biochemical, and molecular events that follow the exposure of cells or tissues to an injurious agent.

Causes

structureal alteraltions

85
Q

What enzymes do Ca2+ activate when it’s at high levels in the failing cell?

A

Phospholipase

proteases

endonucleases

ATPases

86
Q

Most common exogenous pigments?

what do they present with?

what is an exogenous pigment found on the skin?

A

Carbon –> pollution, coal miner, smoking

anthracosis –> blackened tissues of the lungs

tattoos

87
Q

Hallmarks of initial phase of injury? 5 things

what’s important to know about these hallmarks?

A 
Cellular swelling
Loss of microvilli
Membrane blebbing
Swelling of RER
clumping of chromatin

show reversible stuff!

88
Q

Ubiquitin-proteosome degradation pathway?

A

If you have a cell that needs to shrink, you need to destroy the cytoskeleton –>

ubiquitin is tagged on the intermediate filaments of the cytoskeleton

proteasome organelle in THAT cell recognizes the ubiquitin tagged proteins and destroys the proteins in the cell.

89
Q

3 ways that ischemia happens? (examples of each)

A

Block in the arterial flow into the organ –> atherosclerosis

Decrease in flow through the vein

Shock –> septic, anaphylactic, neurogenic, etc.

90
Q

What is the Extrinsic Pathway of Apoptosis

A

1) FAS ligand (on T cells) finds FAS death receptor (CD95) on the target cell (or another death receptor is TNFR1)
2) activates the Fas associated death domain (FADD)
3) binds and cleaves caspase 8
4) lead to execution tase (activating caspase 3 and 6)

91
Q

Coagulative Necrosis?

1) texture
2) on a slide what do you see
3) what shape
4) where does it occur
5) what is the term for a localized area of coagulative necrosis?

6) what is coagulative necrosis called when it’s on the extremities? who is it associated with? what is to know about its characterization?

A

Firm and retain shape (coagulate)

no nucleus, but architecture still there.

3) wedge-shape
4) everywhere except the brain
5) infarct
6) Gangrenous –> it’s a clinical term, NOT A PATTERN. diabetics. dry without infection on top, wet with infection

92
Q

What can create hypoxemia?

3 pathologies

A

Hypoventilation (more CO2 than O2)

COPD –> air trapped in lungs

interstitial fibrosis

93
Q

What is the problem with reperfusion to ischemic tissues? (2 major consequences)

what if you reperfuse an ischemic heart?

A

deoxygenation to tissues –> have more blood go with more oxygen –> the tissues really aren’t able to use the oxygen correctly and instead make free radicals –> hurt the tissue more

more Ca2+ comes, favoring the opening of the mitochondrial permeability transition pore –> more ATP loss.

you’ll have even higher troponin and other cardiac. enzymes in blood work –> made it worse

94
Q

Findings of Methemoglobinemia?

treatment?

A

chocolate colored blood

newborns do not have enzymes to reduce iron to 2+ state.

IV methylene blue changes Fe3+ to 2+

95
Q

most common cause of signifiant fatty change in the liver?

A

alcoholic abuse, nonalcoholic fatty liver disease (from diabetes and obesity)

MOD (8 decks)

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