Patho chap 1 - block 1 test
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1.
Acid reflux from the
stomach causes
metaplasia to?
non-ciliated, mucin-producing
columnar cells
18.
Carbon tetrachloride
(CCL4) will be converted
to?
CCL3 free radical by P450
system of hepatocytes
2.
acute ischemia results in?
injury
19.
Caseous necrosis
3.
After the dying cell
shrinks, nucleus will then?
condense and fragments in an
organized manner
soft and friable necrotic tissue
with "cottage cheese like"
appearance
4.
After the nucleus
condenses and
fragments?
apoptotic bodies fall from the
cell and are removed by
macrophages
20.
caseous necrosis is a
combination of?
coagulative and liquefactive
necrosis
21.
Alzheimer disease
Alpha-beta amyloid deposits in
the brain forming amyloid
plaques
caseous necrosis is
characteristic of?
granulomatous inflammation
due to TB or fungal infection
22.
caspases that mediate
apoptosis, will activate?
1. proteases
2. endonucleases
23.
catalase results in?
O2 and H2O
24.
causes of hypoxia,
include?
1. ischemia
2. hypoxemia
3. decreased O2-carrying
capacity of blood
25.
Cellular injury, occurs
when?
stress exceeds the cell's ability
to adapt
26.
the change of tissue in
vitamin A deficiency, is
known as?
keratomalacia
27.
Classic findings of
systemic amyloidosis?
1. nephrotic syndrome
2. restrictive cardiomyopathy or
arrhythmia
3. tongue enlargement,
malabsorption, and
hepatosplenomegaly
28.
Coagulative necrosis is?
necrotic tissue that remains firm
and nucleus disappears
5.
6.
Amyloid
misfolded protein that deposits
in the extracellular space,
damaging tissues
7.
Aplasia
failure of cell production during
embryogenesis
8.
Apoptosis is?
genetically programmed, cell
death
involving single cells or small
groups of cell
9.
Apoptosis is? energydependent or energyindependent?
energy (ATP)-dependent
10.
apoptosis is followed by/
not followed by
inflammation?
not followed by inflammation
11.
Apoptosis is mediated
by?
caspases
12.
Atrophy
decrease in stress that leads to a
decrease in organ size
13.
atrophy occurs via?
decrease in the size and number
of cells
14.
autophagic vauoles will
fuse with?
lysosomes, whose hydrolytic
enzymes breakdown cellular
components
15.
autophagy of cellular
components involves?
generation of autophagic
vacuoles
16.
Barrett esophagus is a
classic example of?
metaplasia
Carbon tetrachloride
(CCL4) results in?
cell injury with swelling of RER
17.
cell shape and organ structure
are preserved by coagulation of
proteins
29.
coagulative necrosis is an
area of?
infarcted tissue that often
wedge-shaped and pale
30.
common causes of
cellular injury, include?
1. inflammation
2. nutritional deficiency/ excess
3. hypoxia
4. trauma
5. genetic mutations
31.
cytosolic enzymes leak
into the serum, during?
cardiac troponin
32.
cytosol swelling, results
in?
1. loss of microvilli
2. membrane blebbing
33.
Cytotoxic CD8+ T cellmediated pathway
pathway that activates caspases
51.
Elimination of free
radicals occurs via?
1. antioxidants
2. enzymes
3. metal carrier proteins
52.
Endonucleases
break down DNA
53.
the end result of
liquefaction, of
liquefactive necrosis?
lysis of cells and proteins
54.
the end results of
irreversible injury?
cell death
55.
enzymes that help
with the elimination of
free radicals?
1. superoxide dismutase
2. glutathione peroxidase
3. catalase
56.
esophagus is normally
lined with?
non-keratinizing squamous
epithelium
57.
examples of apoptosis
include?
1. endometrial shedding during
menstrual cycle
2. removal of cells during
embryogenesis
3. CD8+ T cell-mediated killing of
virally infected cells
58.
examples of
decreased O2 carrying
capacity
1. anemia
2. carbon monoxide poisoning
3. methemoglobinemia
59.
examples of localized
amyloidosis?
1. senile cardiac amyloidosis
2. familial amyloid cardiomyopathy
3. non insulin dependent diabetes
mellitus
4. alzheimer disease
5. dialysis-associated amyloidosis
6. medullary carcinoma of the
thyroid
lactic acid buildup results in low
pH, which denatures proteins and
precipitates DNA
60.
exception of
pathologic
hyperplasia?
benign prostatic hyperplasia
Due to low ATP, what
will happen with the
Ca2+ pump
resulting in Ca2+ buildup in the
cytosol of the cell
61.
Extrinsic receptorligand pathway
pathway that activates caspases
62.
Due to low ATP, what
will happen with the
Na+/K+ pump
sodium and water buildup in the
cell
Familial amyloid
cardiomyopathy
mutated serum transthyretin
deposits in the heart leading to
restrictive cardiomyopathy
63.
fat necrosis
47.
dysplasia
disordered cellular growth
48.
dysplasia is
reversible/irreversible?
reversible
necrotic adipose tissue with chalkywhite appearance due to
deposition of calcium
64.
49.
dysplasia most often
refers to?
proliferation of precancerous cells
fat necrosis is
characteristics of?
trauma to fat and pancreatitismediated damage of
peripancreatic fat
dysplasia often arises
from?
longstanding pathologic
hyperplasia or metaplasia
65.
fibrinoid necrosis
50.
necrotic damage to blood vessel
wall
34.
Cytotoxic CD8+ T cellmediated pathway
occurs when?
perforins secreted by CD8+T cell
creates pores in membrane of
target cell and granzyme from
CD8+T cell enters pores ->
activates caspases
35.
decreased
apolipoproteins leads
to?
fatty change in the liver
36.
decreased arterial
perfusion can occur
with?
atherosclerosis
37.
Decreased O2 carrying
capacity arises with?
hemoglobin (Hb) loss or
dysfunction
38.
decreased venous
drainage occurs with?
budd-chiari syndrome
39.
decrease in cell
number occurs via?
apoptosis
40.
decrease in cell size
occurs via?
1. ubiquitin-proteosome
degradation of the cytoskeleton
2. autophagy of cellular
components
41.
deposition of
amyloidosis can be?
systemic or localized
42.
Dialysis-associated
amyloidosis
Beta-2 microglobulin deposits in
joints
43.
DNA damage is
implicated in?
aging and oncogenesis
44.
Due to low ATP, what
will happen with
aerobic glycolysis
results in a switch to anaerobic
glycolysis
45.
46.
66.
fibrinoid necrosis is
characteristic of?
1. malignant hypertension
2. vasculitis
67.
free radicals cause
cellular injury via?
peroxidation of lipids and
oxidation of DNA and proteins
68.
Gangrenous necrosis
coagulative necrosis that
resembles mummified tissue
69.
gangrenous necrosis is
characteristic of?
ischemia of lower limb and GI tract
70.
glutathione peroxidase
results in?
GS-SG and H2O
71.
the hallmark of
irreversible injury is?
membrane damage
how are drugs and
chemicals associated
with free radicals?
P450 system of liver metabolite
drugs, generating free radicals
73.
how are metals
associated with free
radicals?
Fe2+ generates hydroxyl free
radicals
74.
how is inflammation
associated with free
radicals?
NADPH oxidase generates
superoxide ions during oxygendependent killing by neutrophils
75.
how is ionizing
radiation associated
with free radicals?
water is hydrolyzed to hydroxyl
free radical
76.
hyperplasia
increase in the number of cells
77.
Hyperplasia involves?
production of new cells from stem
cells
78.
hypertrophy
increase in the size of cells
79.
Hypertrophy involves?
gene activation, protein synthesis,
production of organelles
80.
Hypoplasia
decrease in cell production during
embryogenesis
81.
Hypoplasia usually
results in?
relatively small organ
82.
Hypoxemia
low partial pressure of oxygen in
the bloos
83.
Hypoxemia, arises
with?
1. high altitude
2. hypoventilation
3. diffusion defect
4. V/Q mismatch
72.
84.
Hypoxia
low oxygen delivery to tissue
85.
hypoxia impairs?
oxidative phosphorylation
resulting in decreased ATP
86.
if superimposed infection
of dead tissue occurs with
gangrenous necrosis?
then liquefactive necrosis
ensues
87.
in carbon monoxide
poisoning, what happens?
CO binds hemoglobin more
avidly than oxygen
Pao2 normal
Sao2 decreased
88.
in coagulative necrosis, red
infarction arises if?
blood re-enters a loosely
organized tissue
89.
in fat necrosis, fatty acids
are released by?
trauma or lipase
join with calcium via
saponification
90.
in fibrinoid necrosis, there
is leaking of?
proteins into vessel walls
91.
initial phase of cellular
injury? reversible/
irreversible?
reversible
92.
in methemoglobinemia,
what happens?
iron in heme is oxidized to
Fe3+, which cannot bind
oxygen
Pao2 normal
Sao2 decreased
93.
In the extrinsic receptorligand pathway, how does
the caspase activate?
1. FAS ligand binds FAS death
receptor (CD95) on the target
cell -> activates caspases
2. tumor necrosis factor (TNF)
binds TNF receptor on the
target cell -> activates
caspases
94.
Intrinsic mitochondrial
pathway
pathway that activates
caspases
95.
in vitamin A deficiency, the
thin squamous lining of the
conjunctiva undergoes?
metaplasia into stratified
keratinizing squamous
epithelium
96.
Ischemia arises with?
1. decreased arterial perfusion
2. decreased venous drainage
3. shock
97.
Ischemia is?
decreased blood flow through
an organ
98.
is systemic amyloidosis
treatable?
damaged organs must be
transplanted -> amyloid
cannot be removed
99.
lack of Bcl2 allows?
cytochrome c to leak from the inner
mitochondrial matrix into the
cytoplasm -> activate caspases
116.
metastatic
calcification occurs
when?
high serum calcium or phosphate
levels lead to calcium deposition
in normal tissue
100.
the leaking of
proteins in fibrinoid
necrosis results in?
bright pink staining of the wall
microscopically
117.
mitochondrial
membrane damage
results in?
1. loss of electron transport chain
2. cytochrome c leaking into
cytosol
101.
the likelihood of
injury depends on?
1. the type of stress
2. severity
3. type of cell affected
118.
the morphologic
hallmark of cell death
is?
loss of the nucleus
102.
liquefactive necrosis
is?
necrotic tissue that becomes
liquefied
119.
Necrosis is?
large groups of cells, followed by
acute inflammation
103.
liquefactive necrosis
is a characteristic
of?
1. brain infarction
2. abscess
3. pancreatitis
120.
Necrosis is divided
into?
several types, based on gross
features
121.
Necrosis is due to?
liquefactive necrosis
occurs with abscess
via?
proteolytic enzymes from neutrophils
liquefy tissue
some other underlying pathologic
process
105.
liquefactive necrosis
occurs with brain
infarction via?
proteolytic enzymes from microglial
cells liquefy the brain
106.
liquefactive necrosis
occurs with
pancreatitis via?
proteolytic enzymes from neutrophils
liquefy parenchyma
107.
Localized
amyloidosis
amyloid deposition usually localized
to a single organ
108.
loss of the nucleus,
occurs via?
1. nuclear condensation = pyknosis
2. fragmentation = karyorrhexis
3. dissolution = karyolysis
109.
Low ATP disrupts
key cellular
functions, including?
1. Na+/K+ pump
2. Ca+ pump
3. Aerobic glycolysis
Lysosome
membrane damage
results in?
hydrolytic enzymes leaking into the
cytosol -> activated by the high
intracellular calcium
111.
Medullary carcinoma
of the thyroid
calcitonin deposits within the tumor
112.
mesenchymal tissue
can undergo?
metaplasia
113.
Metaplasia
change in stress on an organ that
leads to a change in cell type
114.
metaplasia most
commonly involves?
change of one type of surface
epithelium to another
115.
Metaplasia occurs
via?
reprogramming of stem cells =
produce the new cell type
104.
110.
never physiologic
122.
neurons are highly
susceptible to?
ischemic injury
123.
Non-insulindependent diabetes
mellitus (type 2)
amylin deposits in the islets of the
pancreas
124.
partial reduction of O2
yields to?
1. superoxide (O2)
2. hydrogen peroxide (H2O2)
3. hydroxyl radicals (OH)
125.
pathologic generation
of free-radicals arises
with?
1. ionizing radiation
2. inflammation
3. metals
4. drugs and chemicals
126.
pathologic hyperplasia
can progress to?
dysplasia -> cancer
127.
permanent tissues
undergo?
only hypertrophy
128.
physiologic
generation of free
radicals occurs during?
oxidative phosphorylation
129.
plasma membrane
damage results in?
1. cytosolic enzymes leaking into
the serum
2. additional calcium entering the
cell
130.
Primary amyloidosis
systemic deposition of AL amyloid,
which is derived from
immunoglobulin light chain
131.
Primary amyloidosis is
associated with?
plasma cell dyscrasias
132.
Proteases
break down the cytoskeleton
133.
reperfusion injury is?
return of blood to ischemic tissue
149.
vitamin A is necessary for?
results in production of O2
derived-free radicals
134.
reperfusion injury leads
to?
continued rise in cardiac enzymes
after reperfusion of infarcted
myocardial tissue
135.
Saponification is an
example of?
dystrophic calcification, in which
calcium deposits on dead tissues
136.
Senile cardiac
amyloidosis
non-mutated serum transthyretin
deposits in the heart
137.
shared features of
amyloid, include?
1. beta-pleated sheet
configuration
2. congo red staining and applegreen birefringence when viewed
microscopically under polarized
light
differentiation of
specialized epithelial
surfaces
ex: conjunctiva covering the
eye
150.
What are examples of metal
carrier proteins used in the
elimination of free radicals
transferrin and
ceruloplasmin
151.
what are free radicals?
chemical species with an
unpaired electron in their
outer orbit
152.
what generally occurs
together?
hyperplasia and
hypertrophy
153.
What is a characteristics of
coagulative necrosis?
ischemic infarction of any
organ except the brain
154.
what is an example of acute
ischemia?
renal artery embolus
155.
what is an example of slow
developing ischemia?
renal artery atherosclerosis
156.
What is the hallmark of
reversible injury?
cellular swelling
157.
what leads to the inactivation
of Bcl2?
1. cellular injury
2. DNA damage
3. decreased hormonal
stimulation
158.
What occurs in ubiquitinproteosome degradation?
intermediate filaments of
the cytoskeleton are
"tagged" with ubiquitin
138.
shock occurs with?
generalized hypotension, resulting
in poor tissue perfusion
139.
slow developing
ischemia results in?
atrophy
140.
superoxide dismutase
results in?
H2O2
141.
swelling of the rough
endoplasmic reticulum
(RER) results in?
1. dissociation of ribosomes
2. decreased protein synthesis
142.
Systemic amyloidosis?
amyloid deposition in multiple
organs
143.
Systemic amyloidosis
can be divided into?
primary amyloidosis
secondary amyloidosis
159.
the two mechanisms of
cell death, are?
1. necrosis
2. apoptosis
When a dying cell shrinks,
what happens?
cytoplasma becomes more
eosinophilic
160.
Ultimately, what is the
end result in ubiquitinproteosome
degradation?
it is destroyed by proteosomes
why does high altitude cause
hypoxemia?
decreased barometric
pressure, results in
decreased PAO2
161.
why does hypoventilation
cause hypoxemia?
increased PACO2, results in
decreased PAO2
146.
ultimately what will
happen bc of Carbon
tetrachloride (CCL4)
ribosomes will detach and impair
protein synthesis
162.
why does the diffusion
defect cause hypoxemia?
147.
Under persistent stress,
metaplasia can
progress to?
dysplasia -> cancer
PAO2 not able to push as
much O2 into the blood
due to thicker diffusion
barrier
163.
why does V/Q mismatch
cause hypoxemia?
vitamin A deficiency
can also result in?
metaplasia
blood bypasses
oxygenated lung or
oxygenated air cannot
reach the blood
164.
why do permanent tissues
only undergo hypertrophy?
they cannot make new cells
144.
145.
148.