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Patho I > Powerpoint-Chap1 > Flashcards

Powerpoint-Chap1 Flashcards

1
Q

What are the main contributors to cellular aging

A

telomere shortening, environmental insults, DNA repair defects, Abnormal growth facto signaling

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2
Q

How is it hyposthesized that sirtuins reduce aging

A

insulin sensitization, decreasing free radicals and prevention of apoptosis

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3
Q

What to sirtuins require for action

A

NAD

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4
Q

What pharm agent induces Sirt1 activity

A

resveratrol

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5
Q

What is the first line of defense against cell injury

A

atrophy, hypertrophy, hyperplasia, metaplasia for ways of adaptation

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6
Q

inability of a cell to adapt leads to what

A

irreversible or reversible injury

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7
Q

Addition of growth factors and hormones can lead to what cell adaptations

A

hyperplasia and hypertrophy

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8
Q

decreased nutrients and stimulation can lead to what cell adaptations

A

atrophy

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9
Q

chronic irritation whether physical or chemical can lead to what cellular adaptation

A

metaplasia

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10
Q

actue transient hypoxic or injurious attacks lead to what type of cell injury

A

reversible. cell may swell or there are fatty changes

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11
Q

progressive and severe hypoxic or chemical attacks lead to what type of cell injury

A

irreversible

cell death by necrosis or apoptosis

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12
Q

metabolic alterations can lead to what type of cell response

A

intracellular accumulation, calcification

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13
Q

cumulative sublethal injury results in what type of cell response

A

cellular aging

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14
Q

having a cast causes what type of atrophy

A

decreased workload/disuse

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15
Q

what can cause denervation

A

disease or lack of use

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16
Q

what is worse, hypoxia or ischemia

A

ischemia

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17
Q

what is marasmus

A

really total malnutrition

breakdown fat really well still

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18
Q

what is cachexia

A

wasting away from diseases that cannot be reversed nutritionally

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19
Q

how does atrophy happen from endocrine system

A

loss of stimulation from those hormones

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20
Q

what is a pressure atrophy

A

presses on surrounding structures causing atrophy in surrounding areas

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21
Q

what is a common cause of pressure atrophy

A

decubitus ulcers

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22
Q

what are types of atrophy from inflammatory and immunologic processes

A

atrophic gastritis, celiac sprue

autoimmune!

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23
Q

what is atrophy senility

A

senile osteoporosis

aging!

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24
Q

What are the main mechs of atrophy

A

ubiquitin-proteasome protein breakdown pathway

accelerated proteolysis in catabolic conditions

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25
Q

What is lipofuscin

A

left over cell components after breakdown–> aging pigment

golden brown

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26
Q

what is brown atrophy

A

atrophy with lots of lipofuscin

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27
Q

What are the autophagy bodies called

A

residual bodies

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28
Q

what is kwashiorkor. signs?

A

moon face, swollen abdomen, thin muscles.
deficiency only in proteins.
(watered down formula)
massive edema

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29
Q

what occurs in cell metabolism in the casted limbs

A

lose proteoglycans in articular cartilage
decrease strength ligaments(atrophy)
osteopenia(loss of bone mass)

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30
Q

what causes fat atrophy

A

starvation or dissuse. replaced m with fat

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31
Q

when can function return after motor denervation of skel m

A

3-5 weeks

useless after 20-24 months

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32
Q

what are the cellular changes in hypertrophy

A

increased cytoplasm, increased ribosomes, more protein, nucleolus enlarged ( increased RNA, DNA)

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33
Q

what are the cellular changes in hyperplasia

A

nucleus enlarged but less basophilic(chromatin is dispersed)

increased DNA transcription

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34
Q

What are some causes of hypertrophy and hyperplasia

A 
increased functional demands
patholdy
compensation
excessive nutrition
increased blood flow
endocrine stimulation
mechanical factors
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35
Q

bladder hypertrophy is an example of what cause of hypertrophy

A

mechanical

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36
Q

prostatic hyperplasia is an example of what cause of hyperplasia

A

endocrine stimulation

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37
Q

Hypertrophy without hyperplasia occurs where**

A

heart and skel m

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38
Q

what organs of body commonly have increased functional demands

A

kidney, striated m, smooth m

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39
Q

how does the kidney respond to increase demand

A

hypertrophy and hyperplasia

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40
Q

how does striated m respond to increased demand

A

endurance- increased number and volume mitochondria

resistant- hypertrophy of contractile elements and increased capillary network

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41
Q

how does smooth m respond to increased demand

A

hypertrophy and hyperplasia

VASCULAR smooth muscle polyploidy

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42
Q

what is polyploidy

A

increase number DNA content

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43
Q

What are the two main pathways for mycardial hypertrophy

A

phosphinositide3-kinase/AKT pathway

GPCRs

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44
Q

what is the main pathway of myocardial hypertrophy from exercise

A

Phosphinositide 3-Kinase/AKT pathways

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45
Q

what is the main pathway for pathologic myocardial hypertrophy

A

GPCR downstream cascade signaling increase

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46
Q

What are the main changes in myocardial hypertrophy

A

switch of contractile protein to fetal forms

early development genes re-expressed

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47
Q

what is the fetal form of myocardium contractile protein

A

alpha heavy to beta heavy chain (energy economical)

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48
Q

what are the early development cardiac genes

A

increased ANF

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49
Q

what does increased ANF cause

A

increased Na excretion in kidney

decrease intravascular volume and pressure (vasodilates)

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50
Q

What can cause myocardial hypertrophy

A

mechanical stress worload
agonists like alpha adrenergic and Angiotensin
Growth factors like IGF-1

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51
Q

What are permanent changes from reversible cardiac hypertrophy

A

increased nuclear size and the scarring remains from initial insult- decreased compliance

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52
Q

what causes subcellular hypertrophy

A

cytochrome P450 activation can break down toxins(drugs and ethanol)

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53
Q

what happens with increased use of drugs and toxins

A

hypertrophy of the ER so can detoxify more of the toxins. Products from breakdown process may be more injurious because release ROS

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54
Q

What are physiologic causes hyperplasia

A

hormonal and compensatory

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55
Q

what are pathologic causes hyperplasia

A

hormonal (gigantism)
increased functional demand
persisten cell injury
infectious agents

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56
Q

what type of injury is from lichen simplex chronicus

A

pathologic hyperplasia due to persisten cell injury

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57
Q

what are the main mech of hyperplasia

A

GF driven proliferation of mature cells

Increased output of new cells from stem cells

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58
Q

What happens after you remove a lobe of liver

A

the rest of the liver hypertrophies and hyperplasia. “compensatory”

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59
Q

What are the stem cells in liver

A

oval cells or “satellite”

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60
Q

if the hepatocytes in a liver cannot replicate what happens

A

the oval cells take over and regenerate new lineage of cells

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61
Q

In the menstrual cycle what occurs to cells in proliferative, secretory and menstrual phases

A

proliferative is hyperplasia
secretory is hypertrophy
menstrual is atrophy

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62
Q

what metaplasia occurs from smoking

A

squamous metaplasia of ciliated columnar epithelium

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63
Q

chronic irritation to the endocervix leads to what metaplasia

A

squamous metaplasia of endocervical glandular epithelium

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64
Q

chronix reflux esophagitis leads to what metaplasia

A

intestinal and gastric glandular metaplasia

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65
Q

what layer of epithelium undergoes the metaplasia

A

begins at the base where the less differentiated cells are

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66
Q

What vitamin is critical for regulating gene transcription

A

Vit A thru retinoid R

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67
Q

Where is the main problem caused by Vit A deficiency

A

eye and the production of keratinizing metaplasia of the specialized epithelium

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68
Q

What is the most common example of metaplasia

A

switch from columnar to squamous as a protective measure

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69
Q

What is the double edged sword of squamous metaplasia

A

dec cilia in bronchi inc in mucus

malignant transformation may occur

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70
Q

What causes periductal mastitis

A

keratin trapped after metaplasia
ruptures the duct resulting in inflammatory response
fistulas occur recurrently thereafter

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71
Q

what is a common example of glandular metaplasia

A

barretts esophagus

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72
Q

What is Barretts esophagus

A

at gastroesophageal junction there is gastric acid that refluxes and transitions the squamous cells into columnar with lots of goblet cells

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73
Q

What are the structures of the cell that change in cell injury

A 
nuclei
ER
mitochondria
PM
other cell structures
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74
Q

What is oncosis

A

cell death with swelling (associated with necrosis)

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75
Q

What pathway occurs from ischemia that goes directly to irreversible injury

A

membrane damage

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76
Q

decrease ATP production ultimately leads to what if it is persistent

A

necrosis

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77
Q

If you turn off Na K pump what happens

A

increase intracellular Na, water follows

swelling

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78
Q

What is the sequence Ca after membrane dysfunction.

A

increase intracell Ca- activation phospholipases, digest cell

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79
Q

What does the mitochondrail release

A

cytochrome C which ultimately signals apoptosis

80
Q

What do mitochondria look like when injured

A

megamitochondria

81
Q

what commonly causes megamitochondria

A

alcoholic liver disease

82
Q

If oxygen acceps one electron what is it

A

superoxide O2negative

83
Q

If oxygen accepts two electrons what is it

A

hydrogen peroxide H2O2

84
Q

if hydrogen peroxide is presence of divalent Fe2+

A

hydroxyl radical OHelectron

85
Q

What is the fenton rxn

A

Fe2+ +H2O2 –> Fe3+ +OH- +OHelectron

86
Q

What radical causes most damage

A

hydroxyl radical

87
Q

what are natural mech to remove free radicals

A 
antioxidants
storage and transport proteins
superoxide dismutatses
Glutathione peroxidases
catalase
88
Q

What are our antioxidants

A

Vit E and A, ascorbic acid and glutathione (cytosol)

89
Q

what are our storage proteins for free radicals

A

transferrin, ferritin, lactoferrin, ceruloplasmin

90
Q

what are the superoxide dismutases that we have

A

manganese SOD (mitochondria
copper-zinc SOD (cytosol)
these all convert O2- to H2O2

91
Q

what is the glutathione peroxidase

A

mitochondria converts Ohelectron to H2O2 and O2

92
Q

what is clinically important of the ratio of oxidized glutathione GSSG to reduced form GSH

A

reflects cells ability to oxidize free radicals

93
Q

What does the catalase do

A

peroxisomes

decompose H2O2 to H2O and O2

94
Q

What do free radicals do in cytosol (ROS)

A

disrupt PM lipids
misfolded proteins
DNA damage

95
Q

What is the hydroxyl radical from

A

H2O by hydrolysis

H2O2 by fenton reaction

96
Q

what is the mechanism of innactivation of hydroxyl radical

A

conversion to H2O by glutathione peroxidase

97
Q

What happens if CCl4 gets in ER

A

P450 oxidases act and form CCl3- which inhibits protein synthesis and inhibits apoprotein synthesis and damages PM

98
Q

what can occur if apoprotein synthesis is inhibited

A

steatosis

99
Q

What is hydropic degeneration

A

swollen cells with bubbles inside (vacuoles) from hypoxic injury

100
Q

Why does repercussion cause injury

A

letting O2 back in so increase amount of ROS, also adding iron into area. everything is leaky = inflammation

101
Q

what is the prime time to do recatheterization

A

within 20 minutes is prime time

102
Q

Describe differences in PM between necrosis and apoptosis

A

necrosis has disrupted PM

apoptosis the PM still intact, maybe in apoptotic bodies

103
Q

Is necrosis both physiologic and pathologic

A

strictly pathologic

104
Q

what is karyolysis

A

no more DNA, it was all chewed up

before it would be karyorrhexis

105
Q

What are morphologic features of necrosis

A

eosinophilia because loss ribosomes(basophilic)
eosin dye is taken up by denatured proteins
swelling of mitochondria with Ca bodies
pyknosis, karyorrhexis and karyolysis

106
Q

what does early cell injury from reperfusion look like

A

microvilli loss and blebbing

107
Q

what do cells look like after irreversible ischemic injury

A

swollen mitochondria with densities
disrupted cell membranes
ruptured lysosomes
dense pyknotic/fragmented nucleus

108
Q

best sign for irreversible morphologic feature

A

PM is ruptured

109
Q

What is coagulative necrosis

A

denaturation of protein is the primary pattern

myocardial infarct

110
Q

what is caseous necrosis

A

distinct amorphous necrosis

mycobacterium TB

111
Q

what is liquefactive necrosis

A

enzyme digestion is dominant

bacterial abscess, cerebral infarct

112
Q

what is gangrene

A

necrosis with or without putrefaction

113
Q

Where does fat necrosis happen

A

in acute pancreatitis saponification

114
Q

when does fibrinoid necrosis take place

A

hypertension
immune complex deposition
vasculitis

115
Q

where is coagulative necrosis seen

A

hypoxic death of cells in tissues, NOT brain

116
Q

what is the morphology of coagulative necrosis

A

homogenous glassy eosinophilic appearance due to loss of cytoplasmic RNA(basophilic) and glycogen
Pinker than normal

117
Q

what is an hemorrhagic infarct

A

dual blood supply with large amounts of loose CT into which hemorrhage may occur

118
Q

what is a pale or anemic infarct

A

sudden arrest of circulatory blood flow. usually from thrombus or embolus

119
Q

What type of degradation is dominant in liquefactive necrosis

A

enzyme digestion- completely

120
Q

What is Pus

A

the left over from neutrophils and WBCs in the area

121
Q

What can lead to abscess propagation

A

bacteremia

local expansion

122
Q

what plane does pus travel along

A

fascial planes

123
Q

why is affected tissue from gangrene black

A

deposition of iron sulfide from degraded Hb

124
Q

what is dry gangrene

A

black brown, mummified appearance (coagulative necrosis)

125
Q

what is wet gangrene

A

bacterial superinfection of necrotic material with liquefactive necrosis

126
Q

what is gas gangrene

A

wet gangrene with infarction of bowel since rapid bacterial superinfection happens

127
Q

diabetics have what type gangrene usually

A

wet

128
Q

what usually causes gas gangrene

A

clostridium welche and Cl perfringes

129
Q

what conditions can gas gangrene live in

A

anaerobic conditions

130
Q

under microscope what does caseous necrosis look like

A

granular debris, fragmented coagulated cells

inflammatory granulamtous reaction

131
Q

fibrinoid is what color histo

A

light pink

132
Q

what can cause fibroid necrosis

A

aging, HTN or immune complex deposition in arteriolar walls

133
Q

what causes pancreatic fat necrosis

A

large amounts of hydrolytic enzymes

phospholipase and proteases attacking adipocyte PM

134
Q

How does saponification occur in pancreatic fat necrosis

A

pancreatic lipase hydrolyzes triglycerides

producing FFA which combine with Ca to form soaps

135
Q

When does traumatic fat necrosis occur.

if occurs in breast tissue can be mistaken for?

A

after crushing injury

breast cancer

136
Q

What are causes of pancreatitis

A

steroids, alcohol, trauma

137
Q

what are complications of pancreatitis

A

pancreatic pseudocyst
fat necrosis
can be fatal

138
Q

what does pancreatitis look like under microscope

A

adipocytes show loss of nuclei and blueish color

basophilic calcium deposits

139
Q

What can we measure necrosis by in the liver?

A

GGT AST ALT from liver

alkaline phosphatase from biliary obstruction

140
Q

how do we measure necrosis of CV system

A

creatine kinases, LDH and troponins from myocardial cells

141
Q

how do we measure necrois in pancreas

A

lipase and amylase levels

142
Q

how do we measure necrosis from RBC

A

LDH and Hb

143
Q

What are cell injuries that lead to apoptosis

A

DNA damage, abnormal protein accumulations

144
Q

what mechanisms in body trigger apoptosis

A

mitochondrial cytochrome C

p53 if DNA damage is unrepairable

145
Q

What is the intrinsic pathway of apoptosis

A

mitochondrial

action of sensors and effectors of the Bcl-2 family inducing leakage of the mitochondrial proteins

146
Q

What is the extrinsic pathway of apoptosis

A

death receptor mediated caspase activation

147
Q

What are the pro-apoptotic proteins that form channels in the mitochondria

A

Bax and Bak

148
Q

what proteins leak from mitochondrial layers

A

cytochrome c and other proteins that lead to caspase activation

149
Q

What ligands and proteins are included in the death receoptor pathway of apoptosis

A

FasLigand binds tot he Fas-associated death domain which downstream activates caspase 8

150
Q

What inflammatory mediator is capable of inducing apoptosis

A

cytokine TNF

151
Q

what does TNF do to tumor blood vessels

A

induces thrombosis

152
Q

Describe the CTL mediated apoptosis

A

CTL secrete perforin so that granzymes can enter and activate caspases to initiate effector phase

153
Q

what protein prevents cell replication when DNA damage is detected

A

p53

154
Q

what main type of disease is characterized by defective apoptosis

A

cancer

155
Q

what type of diseases/injuries involve increased apoptosis

A

neurodegenerative diseases- misfolded proteins build up
ischemic injury
death of virus infected cells

156
Q

What causes dysregulated apoptosis

A

unable to cope with a large number of misfolded proteins

157
Q

What is the main mechanism of DNA breakdown in apoptosis

A

Gene activation and endonucleases

158
Q

how does apoptosis and necrosis appear on a gel electrophoresis

A

apoptosis in laders

necrosis in large smear

159
Q

What is the role of alpha1-antitrypsin

A

inhibits neutrophil elastase

160
Q

what occurs in an alpha1-antityrpsin deficiency

A

accumulation of abnormally folded protein in ER
causes hepatocyte death(apoptosis)
lung disease(enzymatic digestion)

161
Q

What is Reye syndrome

A

children with viral infection and concomitant use of aspirin results in mitochondrial injury leading to decreaed FFA oxidation

162
Q

What occurs to organs in Reye syndrome

A

liver develops steatosis with micro vesicular pattern

163
Q

What are signs of Reye syndrome

A

vomiting, liver failure and neurologic symptoms

164
Q

What can cause accumulation of triglycerides

A

diabetes, starvation, ethanol, hypoxia and Reye syndrome, toxins, malnutrition CCL4

165
Q

how does diabetes and starvation lead to accumulation triglycerides

A

increased supply of FFA

166
Q

how does ethanol lead to accumulation triglycerides

A

increased supply of FFA
increased esterification of FFA to triglyceride
decreased oxidation of FFA

167
Q

how does hypoxia and reye syndrome lead to accumulation of triglycerides

A

decreased oxidation of FFA

168
Q

how do toxins lead to accumulation of triglycerides

A

decreased oxidation of FFA

reduced apoprotein availability

169
Q

how does malnutrition and CCl4 lead to accumulation of triglycerides

A

reduced apoprotein availability

170
Q

thin filaments are targets for what

A

toxins like mushrooms

171
Q

what filament is responsible for rigor mortis

A

thin

172
Q

what filaments are responsible for mallory alcoholic hyaline

A

intermediate

173
Q

What protein in our bodies inactivates toxins

A

cytochrome p450

174
Q

what induce cytochrome p450

A

ethanol, phenobarbital and tobacco

175
Q

what surgery protects against second drug effect of cytochrome p450

A

partial hepatectomy

176
Q

What occurs with cell injury due to alcohol

A 
cytochrome p450 induction
hydropic changes
fatty changes
hyaline degeneration leaving mallory bodies
also causes pancreatitis
177
Q

how do mallory bodies stain with H&E

A

eosinophilic

178
Q

what is the genetic syndrome with defective dynein arms

A

kartagener syndrome

179
Q

what happens with kartagener syndrome

A 
primary ciliary dyskinesia
leading to brochiectasis
chronic sinusitis
infertile males
subfertile females
180
Q

What other strange anomaly occurs with kartagener syndrome

A

situs inversus

181
Q

What is steatosis

A

accumulations of FA and triglycerides

182
Q

What occurs with intracellular accumulations of cholesterol

A

atherosclerosis, xanthomas, cholesterolosis and Niemann-Pick type C

183
Q

what occurs wih intracellular accumulations of proteins

A

proteinuria, plasma cell dyscrasias, cytoskeletal proteins, abnormal proteins

184
Q

what occurs with intracellular accumulations of glycogen

A

DM and glycogenoses

185
Q

What is mallory hyaline

A

keratin intermendiate filaments building up

186
Q

what are neurofibrillary tangles

A

accumulations of neurofilaments

187
Q

What occurs in diabetic hepatopathy

A

glycogenosis (accumulation glycogen)

188
Q

Lipofuscin granules accumulate in what tissue

A

cardiac myocyte

189
Q

What is hemosiderin

A

breakdown of Hb, ferritin micelles

190
Q

what stain is used to visualize iron in Hb

A

prussian blue stain

191
Q

accumulation of melanin presents how on epidermis

A

blue nevus

192
Q

What stain is used to visualize copper

A

rhodamine

193
Q

what is anthracosis

A

accumulation of coal

194
Q

what is it called when there is accumulation of lead and where is this seen in people

A

plumbism
gingival lead line
hemolytic anemia and renal tubular necrosis from toxic effects of lead

195
Q

what is dystrophic calcification

A

in site of previous tissue damage

may end up with bony metaplasia

196
Q

Where does metastatic calcifaication show up

A

in alkaline environment

interstitium of acid secreting organs (stomach, kidney, lung)

197
Q

What other pathologies usually exist with metastatic calcification

A

HyperPTH
vit D excess
bone destruction
idiopathic hypercalcemia of infant, aluminum intoxication, milk alkali syndrome

Patho I (6 decks)

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