Exam 4 Flashcards
1
Q
How do cells respond to injury?
A
A normal, homeostatic cell either adapts or is unable to adapt leading to cell injury. Cell injury consists of reversible, subcellular alterations, and apoptosis. In Reversible cell injury, if it goes past the point of irreversibility it leads to necrosis.
2
Q
What is the term for programmed cell death? Non-programmed?
A
Programmed: apoptosis
Non-programmed: necrosis
3
Q
Increase in cell and organ size
A
hypertrophy
4
Q
What is the cell response: a woman’s uterus enlarges when pregnant?
A
hypertrophy
5
Q
What type of cells can undergo hypertrophy?
A
Non-dividing cells (striated muscle)
6
Q
Increase in number of cells
A
hyperplasia
7
Q
What is the cell response: An increase in terminal ending buds (TEB) in the mammary gland
A
hyperplasia
8
Q
Decrease in cell size by loss of substance
A
atrophy
9
Q
What happens to protein degradation and protein synthesis in atrophy (incr/decr)
A
Protein degradation increases, protein synthesis decreases
10
Q
Reversible form of one cell type to another cell type
A
Metaplasia
11
Q
Deranged cell growth varying in size, shape and organization
A
dysplasia
12
Q
What are the two types of oxygen deprivation?
A
hypoxia: low O2 supply
ischemia: loss completely of O2 blood to tissues
13
Q
Which are chemical agents:
a. poisons
b. viruses
c. CO2
d. asbestos
A
a, c, and d
14
Q
Which are infectious agents:
a. poisons
b. viruses
c. autoimmune diseases
d. parasites
A
b and d
15
Q
Which are immunological reactions:
a. autoimmune diseases
b. viruses
c. sickle cell anemia
d. trauma
A
a
16
Q
Which are genetic defects:
a. autoimmune diseases
b. hypercholesterolemia
c. sickle cell anemia
d. ischemia
A
b and c
17
Q
Which are physical agents:
a. trauma
b. heat/cold
c. electric shock
d. ischemia
A
a, b, and c
18
Q
What conditions are associated with nutritional imbalances?
A
Deficient and excessive nutrients, diabetes by obesity, and atherosclerosis
19
Q
What are the two conditions associated with aging?
A
accumulated damage by reactive oxygen species (ROS) and loss of telomerase function
20
Q
Uterus enlargement during pregnancy is mainly caused by:
a. Commonly caused by atrophy and protein degradation
b. Hormone-induced hypertrophy of uterus smooth muscle cells
c. Hormone-induced hyperplasia of endometrium
d. Hormone-induced metaplasia of uterus smooth muscle cells
e. A and B
A
b. Hormone-induced hypertrophy of uterus smooth muscle cells
21
Q
Uterus enlargement during pregnancy is mainly caused by:
a. Hormone-induced hypertrophy of endometrium
b. Hormone-induced hypertrophy of uterus smooth muscle cells
c. Hormone-induced hyperplasia of endometrium
d. Hormone-induced metaplasia of uterus smooth muscle cells
e. A and B
A
b. Hormone-induced hypertrophy of uterus smooth muscle cells
22
Q
Which of the following may develop into cancer?
A. Hyperplasia
B. Hypertrophy
C. Metaplasia
D. A and C
E. All of the above
A
D. A and C
23
Q
Hyperplasia is likely caused by:
A. increased workload
B. Increased growth factors or hormones
C. Chronic irritation
D. Increased protein synthesis
E. All of the above
A
B. Increased growth factors or hormones
24
Q
The liver has a very high capacity to regenerate after surgical resection. This is caused by:
A. A significant increase in the cell size of remaining hepatocytes
B. A transdifferentiating of clotted platelets and other blood cells into hepatocytes
C. An increased proliferation of the remaining hepatocytes
D. A migration of regenerated hepatocytes in the bone marrow into the liver
E. None of the above
A
C. An increased proliferation of the remaining hepatocytes
25
Barrett's esophagus is the result of:
a. Hypertrophy of the squamous epithelial cells in the lower part of the esophagus
b. Hyperplasia of the squamous epithelial cells in the lower part of esophagus
c. Metaplasia of the squamous epithelial cells in the lower part of the esophagus
d. Atrophy of the squamous epithelial cells in the lower part of the esophagus
e. A and B
c. Metaplasia of the squamous epithelial cells in the lower part of the esophagus
26
Identify the FALSE statement about dysplasia:
A. Cells can have an increase in size
B. Cells can have a decrease in size
C. Cells are organized as normal cells
D. Dysplasia can be associated with chronic irritation
E. Dysplasia is considered as a precursor lesion
C. Cells are organized as normal cells
27
T/F: The hyperplasia associated with formation of terminal end buds (TEBs) and ductal elongation in breast during puberty is a pathological process.
False- physiological
28
T/F: During menopause, breast cancer may develop due to aberrant estrogen receptor activation.
True
29
T/F: Estrogen binding to its cytoplasmic receptor leads to activated estrogen receptor moving to the nucleus where it functions to enhance gene transcription.
True
30
T/F: (T/F) Hyperplasia in the smooth muscles cells of the uterus is primarily responsible for uterine enlargement during pregnancy.
False
31
T/F: Hormone (excess estrogen)-induced hyperplasia in endometrium occurs during menopause due to reduced progesterone signaling
True
32
T/F: (T/F) Dysplasia is characterized by abnormal changes in cell
structure/number and can be a precursor to cancer.
True
33
Which of the following is the typical characteristics of irreversible cell injury?
A. Cellular swelling
B. Lipid droplets in the cytoplasm
C. Swelling of endoplasmic reticulum
D. Lack of ATP generation
E. All of the above
D. Lack of ATP generation
34
Calcium influx during cell injury can cause the following:
A. Activation of ATPase
B. Activation of phospholipase
C. Activation of protease
D. Activation of endonuclease
E. All of the above
E. All of the above
35
ATP depletion can inhibit protein synthesis by the following mechanism:
A. Na pump does not function
B. Increased anaerobic glycolysis
C. Mitochondria swelling
D. Clumping of nuclear chromatin
E. Detachment of ribosomes
E. Detachment of ribosomes
36
T/F: Cellular swelling accompanies both reversible and irreversible cell injury
True
37
T/F: Hypoxia is described as inadequate oxygenation of the body.
True
38
T/F: Myocardial cell death following an ischemic episode is visualized within minutes on a light microscopy.
False
39
Increased oxidative stress often cause cell injury by the following mechanisms EXCEPT:
A. Disruption of plasma membrane
B. Disruption of organelles
C. Inactivation of some enzymes
D. Induction of DNA damages
E. Decreased protein degradation
E. Decreased protein degradation
40
The following may reduce oxygen free radicals and reactive oxygen species in
cells EXCEPT:
A. Superoxide dismutase
B. Glutathione peroxidase
C. Catalase
D. Vitamin E
E. All of the above
E. All of the above
41
Increased membrane permeability can be caused by the following:
A. Phospholipid loss
B. Lipid breakdown products
C. Damage to cytoskeletal proteins
D. A and B
E. A, B and C
E. A, B and C
42
The following sites of membrane damage are involved in cell injury EXCEPT?
A. Mitochondrial membrane
B. Plasma membrane
C. Lysosomal membrane
D. ER membrane
E. All of the above
D. ER membrane
43
T/F: Free radical formation following in cells following laser irradiation chemically reduces cell structures like lipids, proteins, and nucleic acids.
False
44
T/F: Calcium overload is an injurious agent that can inappropriately activate enzymes that damage cellular homeostasis.
True
45
Intrinsic apoptotic pathway may be activated by the following EXCEPT?
A. Radiation-induced DNA damages
B. Protein missfolding-induced ER stress
C. Growth factor withdrawal
D. Binding of Fas ligand to its receptor
E. All of the above
D. Binding of Fas ligand to its receptor
46
The role of cytochrome C in apoptosis is to:
A. Increase mitochondrial membrane permeability
B. Degrade Bcl-2
C. Activate initiator caspases
D. Phosphorylate and activate endonucleases
E. All of the above
C. Activate initiator caspases
47
Which of the following molecules can increase mitochondrial membrane
permeability?
A. Bcl-2
B. Bax
C. Cytochrome c
D. TNF
E. Caspase-3
B. Bax
48
Which of the following statements about apoptosis and necrosis is TRUE?
A. Apoptosis and necrosis can occur under both physiological and
pathological conditions.
B. Cell size is enlarged when apoptosis or necrosis occurs.
C. Inflammation in surrounding cells and tissue can be seen
when cells undergo apoptosis.
D. DNA is fragmented into nucleosome size when necrosis occurs.
E. None of the above.
E. None of the above.
49
T/F: Unlike necrosis, apoptosis is never observed physiologically.
False
50
T/F: Common pathological causes of apoptosis include DNA damage and accumulation of misfolded proteins
True
51
T/F: Procaspase-3 binds Cytochrome C to induce formation of the apoptosome.
False
52
Which are the local signs of acute inflammation
a. heat
b. swelling
c. cyanosis
d. pain
a b and d
53
What are the two major components of inflammation?
vascular changes and cellular events
54
What is the leukocyte migration?
Leukocyte has Sialyl-Lewis glycoprotein and integrin that roll and attach onto the cell surfaces receptors P and E-selectin. and ICAM-1 respectfully. Once at cell gap, they squeeze through to move to tissue damage location.
55
Describe how phagocytosis occurs as well as how their host proteins play a role
Opsonins (host proteins) coat the microbes and target them for phagocytosis. Leukocytes then know to bind and ingest.
56
What opsonins can bind to microbial cell-wall sugar groups?
Collectins: IgG, C3 breakdown products, and plasma carb-binding lectins
57
Fusion of the phagosome with a lysosome
degranulation
58
Phagocytosis stimulates what two oxidative bursts
Production of OFR (oxygen free radicals) and ROS (reactive oxygen species)
59
Proteins that form holes in bacterial membranes
defensins
60
What are the two principal mediators of inflammation?
plasma-derived and cell (local) derived
61
What are the four systems in the liver's mediators?
Plasma-derived: kinen cascade, clotting cascade, fibrinolytic system, and complement cascade
62
Within the actions of the principal mediators of inflammation, what causes vascular smooth muscle relaxation?
nitric oxide
63
Within the actions of the principal mediators of inflammation, what causes local endothelial activation?
cytokines (TNF, IL-1)
64
Within the actions of the principal mediators of inflammation, what causes the killing of microbes?
nitric oxide and ROS
65
Explain the mechanism of arachidonic acid in inflammation?
Steroids inhibit the release of phospholipases to the cell membrane phospholipids. Arachidonic acid is formed and releases Prostaglandin G2 (PGG2). This is due to the inhibition of COX through COX 1 and 2 inhibitors or aspirin.
66
Match the COX inhibitor with the drug:
aspirin
celebrex
naproxen
vioxx
ibuprofen
aspirin- COX 1 or 2
celebrex- COX 2
naproxen- COX 1 or 2
vioxx- COX 2
ibuprofen- COX 1 or 2
67
What drug is a leukotriene receptor antagonist?
singulair
68
What are the four major effects of TNF/IL-1?
Endothelial, fibroblast, systemic, and leukocyte
69
What is activated by macrophages (and other cells) when bacterial products, immune complexes, toxins, physical injury, and/or other cytokines interfere?
TNF/IL-1
70
What are the three acute inflammation outcomes?
Resolution, Fibrosis (either through pus formation or chronic inflammation), and chronic inflammation
71
Inflammation of prolonged duration in which active inflammation, tissue injury, and healing process simultaneously
chronic inflammation
72
Inflammation distinguished by vascular changes, edema, and a predominantly neutrophilic infiltrate.
acute inflammation
73
What are the mononuclear cells caused by infiltration due to chronic inflammation?
macrophages, lymphocytes, and plasma cells
74
What is the benefit of anti-PD-1 and anti-CTLA-4?
Targets cancer cells
75
Leukocyte migration to the site of injury involves multiple steps. The step that involves the binding between integrin and ICAM-1 is called:
firm adhesion
76
Opsonization refers to:
A. the coating of microbes by IgG or other components
B. Phagocytosis of microbes by leukocytes
C. Migration of leukocytes to microbes
D. Production of NO and ROS in phagolysomes
A. the coating of microbes by IgG or other components
77
The mediator that can cause vascular smooth muscle relaxation and kill microbes is:
A. kinins
B. nitric oxide
C. TNF
E. IL-1
B. nitric oxide
78
The multiple effects of IL-1 during inflammation are mediated by acting on the following cells EXCEPT:
A. endothelial cells
B. fibroblasts
C. leukocytes
D. lymphocytes
D. lymphocytes
79
Which of the following statements about inflammation is FALSE:
A. Edema is one of the early signs for acute inflammation
B. Neutrophils are the major cells infiltrated during acute inflammation
C. Mononuclear cell infiltration is a typical feature of chronic inflammation
D. Angiogenesis and fibrosis are seen in chronic inflammation
E. Chronic infection is always associated with viral infections
E. Chronic infection is always associated with viral infections
80
Increased leukocyte settling along the inner surface of the blood vessels due to slowing of blood flow
margination
81
Increased fluid flow through endothelial cells
transcytosis
82
What is released?: small holes-plasma with little protein and no cells
Transudate vs exudate
transudate
83
What is released?: bigger holes-protein rich fluid with numerous cells
Transudate vs exudate
exudate
84
Innate or adaptive: B-cell, antibodies, T-cells
Adaptive
85
Innate or adaptive: macrophages and neutrophils
innate
86
Which defense mechanism has a dense, keratinized outer layer with low pH and fatty acids inhibiting microbial growth
Skin
87
Defense using mucus, cilia, phagocytotic killing, and secreted IgA
respiratory tract
88
Defense involving gastric pH, bile, mucus, defensins, IgA and gut flora
Intestinal tract
89
Low pH in vagina from catabolism of _______ by lactobacilli
glycogen
90
___________ can kill lactobacilli and make the vagina susceptible to infection
Antibiotics
91
HBV, CMV and treponema pallidum are examples of _______ ______ within the body
vertical transmission
92
What is the mechanism of viral entry to host cells in HIV
gp120 binds to CD4 (most T cells) and to the chemokine receptors CXCR4 (T cells) or CCR5 (macrophages)
93
Virus type that binds to intercellular adhesion molecule-1 (ICAM-1)
rhinovirus
94
A lipopolysaccharide (LPS) that is a major component of the outer cell wall of gram-negative bacteria
bacterial endotoxin
95
How can diphtheria toxin inhibit protein synthesis
Toxin is held by two subunits (a&b) In the cytoplasm, disulfide broken releasing active amino A. Subunit A catalyzes transfer of ADP-ribose from NAD to the EF-2, thus inactivating it. This kills the cells rapidly.
96
functional cells of the organ (hepatocytes, myocytes, renal tubular cells)
parenchymal cells
97
Supporting structure of organs (ECM, blood vessels, connective tissue)
stromal cells
98
Replacement of injured tissue with cells of the same type and function
tissue regeneration
99
Occurs when extent or nature of damage cannot be reversed by regeneration alone
tissue repair
100
Arrange these injuries from lowest to highest healing time
Proliferation, Inflammation, Remodeling and Hemostasis
Hemostasis (minutes), inflammation (hrs), proliferation (days) and remodeling (weeks to months)
101
Stage of healing resulting in local vasoconstriction and activation of platelets and clotting factors to form a fibrin clot from damaged cells
hemostasis
102
Stage of healing driven by platelet-derived mediators, bacteria, and secreted chemoattractants (neutrophils and macrophages)
inflammation
103
Stage of healing mediated by macrophage (endothelial cells and keratinocytes) and fibroblast-derived growth factors
proliferation
104
Stage of healing transitions from type III to type I collagen, restoring tensile strength of tissue
remodeling
105
Which stage of healing involves scab (eschar) formation
Proliferation
106
epithelial proliferation and reduces inflammatory cells for proper remodeling
regeneration
107
excessive scarring due to continued activation of inflammatory cells and excessive build up occuring
aberrant tissue repair
108
Which stage (primary, secondary, tertiary) are where edges are brough together. Best choice for clean, fresh wounds, in sufficiently vascularized areas.
primary
109
Which stage (primary, secondary, tertiary) would is left open and allowed to heal spontaneously; good for contaminated/infected wounds and increases scarring
secondary
110
Which stage (primary, secondary, tertiary) delays primary closure and are good for wounds which are contaminated/infected initially
tertiary
111
What are the three types of surface receptor responses to growth factors
P13k kinase pathway, MAP-kinase pathway -> Ras/Raf -> MAP kinase cascade, IP3 pathway -> IP3 release -> Ca release
112
What is involved in the protein kinase cascade?
Ras -> MEKK-1, MKK-7, JNK to the nucleus to change gene expression (c-jun)
113
What are the growth factors that regulate fibrosis?
PDGF, TGF-Beta and FGF-2
114
What are the causes of distributive shock
a. sepsis, anaphylaxis and neurogenic
b. cardiac tamponade, pulmonary embolism, pneumothorax
c. hemorrhage, severe burns, and severe vomiting, diarrhea
d. myocardial infract, ventricular arrhythmia, cardiac myopathy, and valvular disease
a. sepsis, anaphylaxis and neurogenic
115
What are the causes of cardiogenic shock?
a. sepsis, anaphylaxis and neurogenic
b. cardiac tamponade, pulmonary embolism, pneumothorax
c. hemorrhage, severe burns, and severe vomiting, diarrhea
d. myocardial infract, ventricular arrhythmia, cardiac myopathy, and valvular disease
d. myocardial infract, ventricular arrhythmia, cardiac myopathy, and valvular disease
116
What are the causes of hypovolemic shock?
a. sepsis, anaphylaxis and neurogenic
b. cardiac tamponade, pulmonary embolism, pneumothorax
c. hemorrhage, severe burns, and severe vomiting, diarrhea
d. myocardial infract, ventricular arrhythmia, cardiac myopathy, and valvular disease
c. hemorrhage, severe burns, and severe vomiting, diarrhea
117
What are the causes of obstructive shock?
a. sepsis, anaphylaxis and neurogenic
b. cardiac tamponade, pulmonary embolism, pneumothorax
c. hemorrhage, severe burns, and severe vomiting, diarrhea
d. myocardial infract, ventricular arrhythmia, cardiac myopathy, and valvular disease
b. cardiac tamponade, pulmonary embolism, pneumothorax
118
What component of gram negative bacteria mediates septic shock?
endotoxin-producing: stimulates release of LPS
119
Explain the role of adrenomedullin (ADM) and dipeptidyl dipeptidase 3 (cDPP3) in septic shock
ADM binds to endothelium and closes itself in the intravascular compartment. Being unable to cross the space allows ADM to trigger vasodilation and sepsis to occur
When cDPP3 is stuck in the intravascular compartment, this breaks cleaves angiotension II ( that causes vasoconstriction) and promotes vasodilation, increasing shock
120
Primary driver of pushing fluid out of vascular space
hydrostatic pressure (mmHg)
121
Draws fluid into the vascular space
colloid osmotic pressure (mmHg)
