Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Boards Pathology > Cell Adaptations, Injury, and Death > Flashcards

Cell Adaptations, Injury, and Death Flashcards

1
Q

An increase in stress leads to an increase in organ size. This occurs by one of two mechanisms.

______ is an increase in cell size.

______ is an increase in number of cells.

A

Hypertrophy

Hyperplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Of hyperplasia and hypertrophy, _______ involves gene activation, protein synthesis, and production of organelles

A

Hypertrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Of hyperplasia and hypertrophy, _____ involves production of new cells from stem cells

A

Hyperplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

T/F: Hyperplasia and hypertrophy generally occur together

A

True; example: uterus in pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What type of tissue does not have the ability to undergo hyperplasia?

A

Permanent tissues — cardiac myocytes, skeletal muscle, and nerve tissue

THESE UNDERGO HYPERTROPHY ONLY

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Pathologic hyperplasia can progress to ____ and ____

A

Dysplasia; cancer

[examples: endometrial hyperplasia progessing to endometrial carcinoma]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Pathologic hyperplasia can progress to dysplasia and cancer…with the exception of _________

A

Benign prostatic hyperplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

A decrease in stress on an organ leads to a decrease in size — a process called _____ in which there is a decrease in cell size and cell number. The decrease in cell number occurs via _______.

The decrease in cell size occurs via ____________ and _________________

A

Atrophy; apoptosis

Ubiquitin-proteosome degradation of cytoskeleton; autophagy of cell components

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

A change in stress on an organ leads to a change in cell type, called _______

A

Metaplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Metaplasia most commonly involves _______ epithelium Metaplastic cells are better able to handle new stress

A

Surface

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Barrett esophagus is a classic example of what growth adaptation? What change has taken place?

A

Metaplasia

Squamous epithelium —> columnar epithelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Mechanism of metaplasia and its reversal

A

Metaplasia occurs by a reprogramming of stem cells

Typically reversible with removal of driving stressor (ex: treatment of GERD)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Like hyperplasia, metaplasia can progress to dysplasia and cancer. An example of this is Barrett esophagus progressing to adenocarcinoma of the esophagus. An exception to this process is ______ metaplasia, which is seen with fibrocystic change of the breast and is not associated with increased risk of cancer

A

Apocrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

________ deficiency can result in metaplasia (i.e., keratomalacia)

A

Vitamin A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Myositis ossificans is an example of ______ of mesenchymal tissue

A

Metaplasia

[bone being produced in the place of muscle tissue; important to distinguish from osteosarcoma in that imaging of adjacent bone will be normal with myositis ossificans]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

______ = disordered cellular growth referring to proliferation of precancerous cells (e.g., CIN); arises from longstanding pathologic hyperplasia or metaplasia

A

Dysplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

T/F: dysplasia is irreversible

A

False — Dysplasia is reversible with alleviation of inciting stress. If stress persists, dysplasia progresses to carcinoma which is irreversible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

_____ = failure of cell production during embryogenesis

A

Aplasia (classic example is unilateral renal agenesis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

______ = decrease in cell production during embryogenesis resulting in a relatively small organ

A

Hypoplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Streak ovary in turners syndrome is an example of

A. Metaplasia
B. Dysplasia
C. Hypertrophy
D. Hyperplasia
E. Hypoplasia
A

E. Hypoplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Common causes of cell injury include inflammation, nutritional deficiency or excess, hypoxia, trauma, genetic mutations, etc.

Hypoxia occurs when there is low oxygen delivery to tissue. What are the 3 major causes of hypoxia?

A

Ischemia

Hypoxemia

Decreased O2 carrying capacity of the blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

_______ = decreased blood flow through an organ

A

Ischemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Define hypoxemia

A

Low partial pressure of O2 in the blood (PaO2 < 60 mm Hg, SaO2 < 90%)

[Remember FiO2 is partial pressure of O2 in the atmosphere. PAO2 is partial pressure of oxygen in alveolar air sacs, while PaO2 is partial pressure of oxygen in the arterioles. SaO2 is the partial pressure of oxygen associated with Hb. So the sequence is FiO2 —> PAO2 —> PaO2 —> SaO2]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Anemia is a decrease in RBC mass. This is associated with a _____ PaO2 and a ______ SaO2

A

Normal; normal

[PaO2 reflects the ability of oxygen to cross from alveolar air sacs into capillaries. SaO2 reflects the percentage of Hb is bound by oxygen. Neither of these is altered by anemia]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Carbon monoxide binds Hb more avidly than O2, resulting in CO poisoning. CO poisoning is associated with a ____ PaO2 and a ______ SaO2. Exposures include smoke from fires and exhaust from cars or gas heaters
Normal; decreased [Hb can’t hold as much oxygen bc some spaces are now taken up by CO]
26
Classic finding is cherry red appearance of the skin Early sign of exposure is headache; significant exposure can lead to coma and death
CO poisoning
27
_______ refers to the situation in which iron in heme is oxidized to Fe3+, which cannot bind O2
Methemoglobinemia [REMEMBER Fe2+ binds O2]
28
Methemoglobinemia refers to the situation in which iron in heme is oxidized to Fe3+, which cannot bind O2. This is associated with a ______ PaO2 and a ______ SaO2.
Normal; decreased
29
In what conditions might you see methemoglobinemia?
Methemoglobinemia is associated with oxidant stress (e.g., sulfa and nitrate drugs) or in newborns
30
Classic findings are cyanosis with chocolate-colored blood
Methemoglobinemia
31
Treatment for Methemoglobinemia
IV methylene blue — helps reduce Fe3+ back to Fe2+ state
32
Hypoxia impairs ______ _____ —> decreased ATP
Oxidative phosphorylation [O2 is final acceptor in electron transport chain]
33
Low ATP resulting from hypoxia disrupts what 3 key cell functions?
Na/K pump — lack of ATP results in buildup of Na in cell, water follows, cell swelling Ca2+ pump — usually keeps intracellular Ca low; increased Ca activates enzymes in the cell that you don’t want activated Aerobic glycolysis — leads to lactic acid buildup
34
Initial phase of cell injury due to hypoxia is cellular ______ which leads to loss of microvilli, membrane blebbing, and swelling of RER
Swelling [remember that consequence of swelling of RER is that ribosomes will disassociate and protein can no longer be synthesized]
35
The initial phase of cell damage due to hypoxia is cell swelling which is reversible. Eventually, the damage becomes irreversible and the hallmark of this is membrane _______
Damage Example: a sign of irreversible damage is plasma membrane damage, so that is what you’re testing when you look for cardiac enzymes, liver enzymes, etc.
36
3 main cell membranes that are damaged by longstanding hypoxia
Plasma membrane — release of enzymes; calcium floods in Mitochondrial membrane — Cyt C escape and cell death Lysosomal membrane — calcium flooding in activates escaped lysosomal enzymes causing further cell damage
37
Morphologic hallmark of cell death
Loss of nucleus [occurs via pyknosis, karyorrhexis, and karyolysis]
38
Pyknosis
Shrinkage of nucleus
39
Karyorrhexis
Breakage of nucleus into pieces
40
Karyolysis
Pieces of nucleus are further broken down
41
Death of a large group of cells followed by acute inflammation; due to underlying pathologic process and is NEVER physiologic
Necrosis
42
Characteristic type of necrosis for ischemic infarction of any organ except the brain
Coagulative necrosis
43
Describe tissue changes associated with coagulative necrosis (i.e., shape, structure, nuclear changes, etc)
Necrotic tissue remains firm; area of infarcted tissue is usually wedge-shaped and pale Cell shape and organ structure are preserved by coagulation of cellular proteins Nucleus disappears
44
How does a “red” infarction occur?
Red infarction arises if blood reenters tissue and tissue is loosely organized Example: testicular infarction
45
Type of necrosis characteristic of brain infarction, abscess, and pancreatitis
Liquefactive necrosis [enzymatic lysis of cells and proteins results in liquefaction] NOTE: pancreatitis results in liquefactive necrosis of the pancreatic parenchyma and fat necrosis of the peripancreatic fat
46
Type of necrosis characteristic of ischemia of lower limb and GI tract
Gangrenous necrosis
47
Gangrenous necrosis is coagulative necrosis that resembles mummified tissue (dry gangrene). What happens to this type of necrosis if superimposed infection occurs?
Liquefactive necrosis (wet gangrene)
48
Characteristic type of necrosis associated with granulomatous inflammation due to TB or fungal infection
Caseous necrosis
49
Fat necrosis appears as necrotic adipose tissue with chalky-white appearance due to deposition of ______
Calcium (due to saponification)
50
Trauma to the breast may result in ____ necrosis
Fat [classic scenarios of fat necrosis = trauma to fat (i.e., breast), pancreatitis-mediated damage of peripancreatic fat]
51
_______ = example of dystrophic calcification in which fatty acids released by trauma or lipase join with calcium
Saponification
52
Characteristic type of necrosis associated with malignant hypertension or vasculitis
Fibrinoid necrosis
53
______ necrosis involves damage to blood vessel wall resulting in leaking of proteins into that vessel wall, characterized by bright pink staining
Fibrinoid necrosis
54
Hypertension associated with pre-eclampsia in a pregnant female may be lead to ______ necrosis of the placenta
Fibrinoid
55
Energy-dependent, genetically programmed cell death that involves single cells or small groups of cells
Apoptosis
56
Endometrial shedding during menstrual bleeding: Necrosis or Apoptosis?
Apoptosis
57
Removal of cells during embryogenesis: Necrosis or Apoptosis?
Apoptosis [failure results in syndactyly]
58
CD8+ T cell-mediated killing of virally infected cells: Necrosis or Apoptosis?
Apoptosis
59
Morphology of apoptosis
Dying cell shrinks and becomes eosinophilic Nucleus condenses and fragments Apoptotic bodies fall from cell and are removed by macrophages — NOT followed by inflammation! [contrast with necrosis]
60
Apoptosis is mediated by _____ which activate proteases that break down the cytoskeleton. They also activate ______ which break down the DNA
Caspases; endonucleases
61
Intrinsic mitochondrial pathway for caspase activation in apoptosis
Cell injury, DNA damage, or decreased hormone stimulation inactivates Bcl2 Cytochrome C leaks from inner mitochondrial matrix into cytoplasm [Bcl2 role is to stabilize mitochondrial membrane]
62
2 primary examples of extrinsic receptor-ligand pathway for caspase activation in apoptosis
FAS ligand binds FAS death receptor (CD95) on target cell [mechanism for negative selection of T cells that react too strongly to self-antigen] TNF binds TNF receptor on target cell
63
Cytotoxic CD8+ T-cell pathway for caspase activation in apoptosis
Perforins create pores in membrane of target cell Granzyme enters pores and activates caspases
64
Define free radical
Chemical species with unpaired electron in outer orbit
65
Generation of free radicals occurs during what physiologic process?
Oxidative phosphorylation [cytochrome C oxidase transfers electrons to O2; partial reduction yields O2*, H2O2, and OH* radicals] NOTE: of all the free radicals, OH* is most damaging
66
Examples of things that cause pathologic generation of free radicals
Ionizing radiation (typically produces OH*) Inflammation Metals (e.g., copper and iron) Drugs and chemicals (e.g., acetaminophen) NOTE: underlying pathologic mechanism of Wilson’s disease, Hemochromatosis, etc. is generation of free radicals
67
How do free radicals damage cells?
Peroxidation of lipids Oxidation of DNA and proteins [oxidation of DNA introduces mutations that may result in oncogenesis — this is the basis of taking anti-oxidants]
68
3 general mechanisms of eliminating free radicals = antioxidants, enzymes, and metal carrier proteins. What are the 3 major enzymes involved in eliminating free radicals?
Superoxide dismutase (SOD): converts O2* —>H2O2 Catalase: converts H2O2 —> OH* Glutathione peroxidase: converts OH* —>H2O
69
Free radical injury most commonly seen in dry cleaning industry
CCl4 [CCl4 is converted to CCl3 in the P450 system of the liver. CCl3 is a free radical that damages hepatocytes. The initial stage of damage is reversible — evidenced by cellular swelling. Recycling of fat by apolipoproteins cannot occur because protein synthesis has been affected by cell/RER swelling. Thus the primary change seen is fatty change of the liver]
70
Pathophysiology of reperfusion injury
When blood (containing inflammatory cells) returns to organ —> oxygen allows inflammatory cells react to dead tissue by generating free radicals leading to further damage Classic vignette is continued rise in cardiac enzymes after occluded vessel is reopened — this is due to FREE RADICAL injury
71
Misfolded protein that deposits in extracellular spaces, damaging tissues
Amyloid
72
Multiple proteins can deposit as amyloid. Misfolded proteins depositing as amyloid often deposit in _______________ configuration. They exhibit ____________ and _________ under polarized light
Beta-pleated sheet Congo red staining; apple-green birefringence
73
Deposition of amyloid can be systemic or localized. Systemic amyloidosis is divided into primary and secondary types. Primary amyloidosis is systemic deposition of ____ amyloid, derived from _________
AL; Ig light chain
74
Type of amyloidosis associated with plasma cell dyscrasias
Primary amyloidosis (AL amyloid derived from Ig light chains)
75
Secondary amyloidosis refers to systemic deposition of ___ amyloid derived from _________, an acute phase reactant that is increased in chronic inflammatory states, malignancies, and Familial Mediterranean fever
AA; SAA
76
Autosomal recessive dysfunction of neutrophils that presents with episodes of fever and acute serosal inflammation
Familial Mediterranean Fever (high SAA during attacks deposits as AA amyloid — secondary amyloidosis) Note: mimics various conditions depending on what serosa is affected — so if serosa of heart is affected, may look like an MI
77
Most common organ affected in amyloidosis
Kidney — presents with nephrotic syndrome
78
Classic clinical findings in amyloidosis
Nephrotic syndrome Restrictive cardiomyopathy or arrhythmia Tongue enlargement, malabsorption, and hepatosplenomegaly
79
Diagnosis of amyloidosis requires _______
Tissue biopsy [abdominal fat pad and rectum are easily accessible targets]
80
T/F: Amyloid cannot be removed, so damaged organs must be removed
True
81
Localized amyloidosis refers to amyloid deposition that is usually localized to a single organ. Examples of this phenomenon include senile cardiac amyloidosis and familial amyloid cardiomyopathy. What is the difference between these 2 conditions in terms of pathology, symptoms, and pt population affected
In senile cardiac amyloidosis, a NON-MUTATED serum transthyretin deposits in the heart. It is usually ASYMPTOMATIC and present in 25% of individuals >80 years of age. In familial amyloid cardiomyopathy, a MUTATED serum tranthyretin deposits in the heart and leads to RESTRICTIVE CARDIOMYOPATHY. 5% of African Americans carry the mutated gene
82
Describe the localized amyloidosis associated with type II diabetes
Amylin deposits in islets of pancreas Derived from insulin
83
Describe amyloidosis associated with Alzheimer disease
AB amyloid deposits in brain, forming amyloid plaques Derived from beta-amyloid precursor protein (on Chr 21) — important because there is increased risk of early onset Alzheimers in Down Syndrome
84
In dialysis-associated amyloidosis, _______ deposits in the ______
B2-microglobulin; joints [beta-2 microglobulin provides structural support to MHC class I molecules; in dialysis it is not filtered from the blood so it deposits as amyloid]
85
In what condition is there localized amyloidosis in which calcitonin deposits within tumor?
Medullary carcinoma of the thyroid [tumor of C-cells —> overproduction of calcitonin, which then deposits as amyloid. Histology is classically described as “tumor cells on an amyloid background”]

Boards Pathology (19 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions