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Chapter 1 Flashcards

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1
Q

What are the two ways that an organ can increase in size?

A

Hyperplasia and hypertrophy

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2
Q

Steps involved in hypertrophy?

A

Gene activation, protein synthesis, production or organelles

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3
Q

What kind of growth is undergone by permanent tissues?

A

Only hypertrophy in cardiac muscle, skeletal muscles, and nerves

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4
Q

What can pathologic hyperplasia lead to?

A

Dysplasia and possibly cancer

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5
Q

What tissue hyperplasia has no increased risk of cancer?

A

BPH

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6
Q

What are the two forms of atrophy?

A

Decrease in cell number via apoptosis

Decrease in cell size via ubiquitin proteosome degradation of the cytoskeleton or autophagy.

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7
Q

How does ubitquitin proteosome degradation occur?

A

intermediate filaments of the cytoskeleton are tagged with ubiquitin and destroyed by proteosomes

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8
Q

Autophagy

A

autophagic vacuoles fuse with lysosomes containing hydrolytic enzymes to breakdown cellular components

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9
Q

a increase in stress leads to _________
a decrease in stress leads to ___________
a change in stress leads to ___________

A

an increase in size
a decrease in size
a change in cell type

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10
Q

most common cells to undergo metaplasia?

A

surface epithelium

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11
Q

Barret’s esophagus is an example of metaplasia?

A

esophagus is normally lined by nonkeratinizing squamous epithelium and acid reflux causes it to change to nonciliated mucin–producing columnar cells

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12
Q

metaplasia occurs via_______ ≈

A

reprogramming cells

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13
Q

Is metaplasia reversible?

A

Yes, with removal of stressor

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14
Q

what is one tissue that can become metaplastic with no increased risk of cancer?

A

apocrine metaplasia of the breast (fibrocystic change)

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15
Q

vitamin A deficiency can cause metaplasia in ____

A

thin squamous lining of the conjunctiva– becomes stratified keratinizing squamous epithelium= keratomalcia

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16
Q

Mesenchymal(connective tissue) metaplasia example?

A

Myositis ossifican in which CT in muscle changes to bone during healing after trauma.

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17
Q

dysplasia

A

disordered cell growth, most often refers to proliferation of precancerous cells

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18
Q

is dysplasia reversible?

A

in theory, it is reversible with alleviation of inciting stress, if it persists, dysplasia becomes carcinoma

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19
Q

Aplasia vs hypoplasia

A

Aplasia: failure of cell production during embryogenesis
Hypoplasia: decrease in cell production during embryogenesis, resulting in small organ

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20
Q

what occurs when a stress exceeds the cells ability to adapt?

A

cellular injury

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21
Q

slowly vs. acutely developing ischemia

A 
Slow= atrophy: renal atherosclerosis
Acute= ischemia: renal artery embolus
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22
Q

What is the final electron acceptor in the electron transport chain?

A

Oxygen

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23
Q

How does decreased oxygen lead to lack of ATP?

A

Impairment of Oxidative phosphorylation

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24
Q

3 causes of ischemia

A

Decreased arterial perfusion- arteriosclerosis
Decreased venous drainage- budd chiari- PV thrombosis seen with polycythemia vera
Shock- generalized hypotension= poor perfusion

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25
hypoxemia
PaO2 <60 mmHg, SaO2 < 90%,low partial pressure of oxygen in the blood
26
Causes of Hypoemia
High altitude, hypoventilation, difusion defect, V/Q mismatch
27
cherry–red appearance of the skin and headache
CO poisoning, leads to coma and death
28
cyanosis with chocolate colored blood
Methemogolinemia
29
Why can't heme bind O2 in methemoglobin
Fe3+ is present, only Fe2+ binds O2.
30
Treatment for methemoglobin
methylene blue
31
Labs in Carbon Monoxide posioning
Normal PaO2, decreased Sao2
32
Labs in Methemoglobinemia
PaO2 normal, Sao2 decreased
33
why do newborns get methemoglobinemia
there is oxidant stress (sulfa or nitratae drugs) and adults have enzymes to reduce but newborns are immature.
34
broad effects of low ATP on cellular functioning
Na–K pump dysfunction: water and sodium buildup in the cell Ca pump: calcium build up in the cell anaerobic glycolysis impaired– switch to anaerobic causing lactic acidosis, which denatures proteins and precipitates DNA
35
What is the hallmark of reversible injury?
Swelling
36
What happens with cellular swelling?
cytosol swells: loss o microvilli and membrane blebbing and swelling of RER, causing the dissociation of ER and ribosomes and decreased protein synthesis
37
hallmark of irreversible injury
membrane damage (plasma membrane, mitochondrial membrane, and lysosome membrane)
38
plasma membrane damage results in?
cytosolic enzymes leaking into the serum and additional calcium entering the cell
39
mitochondiral membrane damage results in?
loss of the electron transport chain (inner membrane) and cytochrome c leaking into cytosol and activating apoptosis
40
lysosome membrane damage results in
hydrolytic enzymes leaking into the cytosol and being activated by calcium
41
normal calcium concentration in the cell
Very low– calcium is a messenger and turns on lots of pathways
42
hallmark of cell death
loss of nucleus condensation (pyknosis) fragmentation (karyorrhexis) dissolution (karyolysis)
43
necrosis is always followed by
acute inflammation
44
necrotic tissue that remains firm with cell and organ structure preserved, but nucleus disappears
coagulative necrosis
45
area of infarcted tissue in coagulative necrosis
wedge–shaped and pale
46
red infarction
if blood reenters a loosely organized tissue
47
necrotic tissue with no structure or solidity– enzymatic lysis of cells and proteins
liquefactive necrosis
48
characteristic of ischemia anywhere except the brain
coagulative necrosis
49
name 3 places where liquefactive necrosis characteristically occurs
brain infarction: proteolytic enzymes from microglial cells liquefy the brain abscess: neutrophil proteolytic enzymes liquefy tissue pancreatitis: proteolytic enzymes from pancreas liquefy parenchyma
50
coagulative necrosis that resembles mummified tissue
"dry grangrene", gangrene necrosis
51
example of gangrene necrosis
lower limb ischemia
52
Caseous necrosis
soft and friable necrotic tissue with cottage cheese–like appearance. Combination of coagulative and liquefactive necrosis. Sign of tb or fungal infection
53
characteristic of granulomatous inflammation due to tuberculosis or fungal infection necrotic adipose tissue with a chalky–white appearance due to deposition of calcium
fat necrosis with saponification
54
dystrophic calcification
necrotic tissue acts as a nidus for calcium deposition in the setting of normal serum calcium
55
metastatic calcification
high serum calcium or phosphate levels lead to calcium deposition in normal tissue (like getting kidney stones from high serum calcium
56
fat necrosis caused by
trauma or pancreatitis–mediated damage of peripancreatic fat
57
fibrinoid necrosis
necrotic damage to blood vessel walls; leaking of proteins into vessel walls leads to bright pink staining of the wall microscopically
58
apoptosis
energy–dependent, genetically programmed cell death involving single cells or small groups of cells
59
what does a cell undergoing apoptosis look like?
dying cell shrinks and cytoplasm becomes eosinophilic | nucleus condenses and fragments
60
apoptotic bodies
as the cell dies, apoptotic bodies fall from the cell and are removed by macrophages; apoptosis is not followed by inflammation
61
apoptosis is mediated by
caspases
62
caspases activate
proteases: break down cytoskeleton endonucleases: break down DNA
63
what are the ways caspase are activated?
intrinsic mitochondrial extrinsic receptor–ligand pathway cytotoxic CD8+ T cell–mediated pathway
64
intrinsic mitochondrial pathway of caspase activation
- cellular injury, DNA damage or loss of hormonal stimulation leads to inactivation of Bcl2 - cytochrome c leaks from the inner mitochondrial membrane into the cytoplasm and activates caspases
65
Bcl 2
inhibits cyt c from leaking from the inner mitochondrial membrane into the cytoplasm extrinsic receptor–ligand pathway of caspase activation Fas ligand binds FAS death receptor (CD95) to activate caspase tumor necrosis factor (TNF) binds TNF receptor on the target cell to activate caspases
66
CD95
Fas death receptor
67
cytotoxic T cell mediated pathway of caspase activation
perforins secreted by CD8+ T cells create pores in membrane of target cell granzyme from CD8+ T cell enters pores and activates caspases
68
free radicals
chemical species with an unpaired electron in their outer orbit
69
physiologic generation of free radicals
oxidative phosphorylation, cyt c oxidase, partial reduction of O2 yields superoxie, hydrogen peroxide, and hydroxyl radicals
70
4 ways that free radicals are generated pathologically
ionizing radiation inflammation– NAPDPH oxidase generates superoxide ions in O2 dependent killing by neutrophils metals drugs and chemicals
71
free radicals cause cellular injury by
peroxidation of lipids and oxidation of DNA and protein
72
enzymes that eliminate free radiations
superoxide dismutase glutathione peroxidase catalase
73
carbon tetrachloride
organic solvent used in dry cleaning that is converted to a free radical in the liver and causes swelling of RER ribosomes detach and protein synthesis is impaired and fatty change occurs
74
reperfusion injury
return of blood to ischemic area results in O2–derived free radicals, which continue to damage tissue ***this is the reason that there is a continued rise in cardiac enzymes after reperfusion of infarcted tissue
75
a misfolded protein that deposits in extracellular space and damages tissues
amyloid
76
Features of amyload
beta pleated sheet configuration | congo red staining and apple green birefringence with polarized light
77
primary amyloidosis
systemic deposition of AL amyloid- derived from Ig light chains
78
primary amyloidosis is associated with
plasma cell dyscrasia (multiple myeloma)
79
secondary amyloidosis
AA amyloid deposition systemically of SAA (serum–associated amyloid protein)
80
SAA
acute phase reactant increased in chronic inflammatory states, malignancy and familial mediterranean fever***
81
Familial Mediterranean fever
dysfunction of neutrophils presents with: fever, acute serosal inflammation (mimics appendicitis, arthritis, myocardial infarction)
82
clinical findings of sysmteic amyloidosis
nephrotic syndrome (most common)\nrestrictive cardiomyopathy or arrhythmia\ntongue enlargement, malabsorption, hepatosplenomegaly
83
treatment for amyloidosis?
damaged organ must be transplanted
84
localized amyloidosis
single organ
85
senile cardiac amyloidosis
non–mutated serum transthyretindeposits in the heart, usually asymptomatic
86
familial amyloid cardiomyopathy
mutated serum transthyretin deposits in the heart and causes a restrictive cardiomyopathy***
87
non–insulin–dependent diabetes mellitus amyloidosis
amylin deposits in the islets of the pancreas (amylin is derived from insulin)
88
alzheimer's amyloidosis
A–beta amyloid deposits in the brain | ***gene is on chromosome 21
89
dialysis associated amyloidosis
B2 microglobulin (component of MHC–I) deposits in joints
90
medullary carcinoma of the thyroid amyloidosis
calcitonin (produced by tumor cells) deposits in the tumor
91
FNA of thyroid shows tumor cells in amyloid background
medullary carcinoma of the thyroid

Pathoma (2 decks)

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