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PHRM824 > Exam 4 > Flashcards

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.

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2
Q

What is the term for programmed cell death? Non-programmed?

A

Programmed: apoptosis
Non-programmed: necrosis

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3
Q

Increase in cell and organ size

A

hypertrophy

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4
Q

What is the cell response: a woman’s uterus enlarges when pregnant?

A

hypertrophy

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5
Q

What type of cells can undergo hypertrophy?

A

Non-dividing cells (striated muscle)

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6
Q

Increase in number of cells

A

hyperplasia

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7
Q

What is the cell response: An increase in terminal ending buds (TEB) in the mammary gland

A

hyperplasia

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8
Q

Decrease in cell size by loss of substance

A

atrophy

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9
Q

What happens to protein degradation and protein synthesis in atrophy (incr/decr)

A

Protein degradation increases, protein synthesis decreases

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10
Q

Reversible form of one cell type to another cell type

A

Metaplasia

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11
Q

Deranged cell growth varying in size, shape and organization

A

dysplasia

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12
Q

What are the two types of oxygen deprivation?

A

hypoxia: low O2 supply
ischemia: loss completely of O2 blood to tissues

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13
Q

Which are chemical agents:
a. poisons
b. viruses
c. CO2
d. asbestos

A

a, c, and d

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14
Q

Which are infectious agents:
a. poisons
b. viruses
c. autoimmune diseases
d. parasites

A

b and d

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15
Q

Which are immunological reactions:
a. autoimmune diseases
b. viruses
c. sickle cell anemia
d. trauma

A

a

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16
Q

Which are genetic defects:
a. autoimmune diseases
b. hypercholesterolemia
c. sickle cell anemia
d. ischemia

A

b and c

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17
Q

Which are physical agents:
a. trauma
b. heat/cold
c. electric shock
d. ischemia

A

a, b, and c

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18
Q

What conditions are associated with nutritional imbalances?

A

Deficient and excessive nutrients, diabetes by obesity, and atherosclerosis

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19
Q

What are the two conditions associated with aging?

A

accumulated damage by reactive oxygen species (ROS) and loss of telomerase function

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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

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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

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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

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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

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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

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25
Q

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

A

c. Metaplasia of the squamous epithelial cells in the lower part of the esophagus

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26
Q

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

A

C. Cells are organized as normal cells

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27
Q

T/F: The hyperplasia associated with formation of terminal end buds (TEBs) and ductal elongation in breast during puberty is a pathological process.

A

False- physiological

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28
Q

T/F: During menopause, breast cancer may develop due to aberrant estrogen receptor activation.

A

True

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29
Q

T/F: Estrogen binding to its cytoplasmic receptor leads to activated estrogen receptor moving to the nucleus where it functions to enhance gene transcription.

A

True

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30
Q

T/F: (T/F) Hyperplasia in the smooth muscles cells of the uterus is primarily responsible for uterine enlargement during pregnancy.

A

False

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31
Q

T/F: Hormone (excess estrogen)-induced hyperplasia in endometrium occurs during menopause due to reduced progesterone signaling

A

True

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32
Q

T/F: (T/F) Dysplasia is characterized by abnormal changes in cell
structure/number and can be a precursor to cancer.

A

True

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33
Q

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

A

D. Lack of ATP generation

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34
Q

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

A

E. All of the above

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35
Q

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

A

E. Detachment of ribosomes

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36
Q

T/F: Cellular swelling accompanies both reversible and irreversible cell injury

A

True

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37
Q

T/F: Hypoxia is described as inadequate oxygenation of the body.

A

True

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38
Q

T/F: Myocardial cell death following an ischemic episode is visualized within minutes on a light microscopy.

A

False

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39
Q

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

A

E. Decreased protein degradation

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40
Q

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

A

E. All of the above

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41
Q

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

A

E. A, B and C

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42
Q

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

A

D. ER membrane

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43
Q

T/F: Free radical formation following in cells following laser irradiation chemically reduces cell structures like lipids, proteins, and nucleic acids.

A

False

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44
Q

T/F: Calcium overload is an injurious agent that can inappropriately activate enzymes that damage cellular homeostasis.

A

True

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45
Q

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

A

D. Binding of Fas ligand to its receptor

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46
Q

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

A

C. Activate initiator caspases

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47
Q

Which of the following molecules can increase mitochondrial membrane
permeability?
A. Bcl-2
B. Bax
C. Cytochrome c
D. TNF
E. Caspase-3

A

B. Bax

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48
Q

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.

A

E. None of the above.

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49
Q

T/F: Unlike necrosis, apoptosis is never observed physiologically.

A

False

50
Q

T/F: Common pathological causes of apoptosis include DNA damage and accumulation of misfolded proteins

A

True

51
Q

T/F: Procaspase-3 binds Cytochrome C to induce formation of the apoptosome.

A

False

52
Q

Which are the local signs of acute inflammation
a. heat
b. swelling
c. cyanosis
d. pain

A

a b and d

53
Q

What are the two major components of inflammation?

A

vascular changes and cellular events

54
Q

What is the leukocyte migration?

A

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
Q

Describe how phagocytosis occurs as well as how their host proteins play a role

A

Opsonins (host proteins) coat the microbes and target them for phagocytosis. Leukocytes then know to bind and ingest.

56
Q

What opsonins can bind to microbial cell-wall sugar groups?

A

Collectins: IgG, C3 breakdown products, and plasma carb-binding lectins

57
Q

Fusion of the phagosome with a lysosome

A

degranulation

58
Q

Phagocytosis stimulates what two oxidative bursts

A

Production of OFR (oxygen free radicals) and ROS (reactive oxygen species)

59
Q

Proteins that form holes in bacterial membranes

A

defensins

60
Q

What are the two principal mediators of inflammation?

A

plasma-derived and cell (local) derived

61
Q

What are the four systems in the liver’s mediators?

A

Plasma-derived: kinen cascade, clotting cascade, fibrinolytic system, and complement cascade

62
Q

Within the actions of the principal mediators of inflammation, what causes vascular smooth muscle relaxation?

A

nitric oxide

63
Q

Within the actions of the principal mediators of inflammation, what causes local endothelial activation?

A

cytokines (TNF, IL-1)

64
Q

Within the actions of the principal mediators of inflammation, what causes the killing of microbes?

A

nitric oxide and ROS

65
Q

Explain the mechanism of arachidonic acid in inflammation?

A

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
Q

Match the COX inhibitor with the drug:
aspirin
celebrex
naproxen
vioxx
ibuprofen

A

aspirin- COX 1 or 2
celebrex- COX 2
naproxen- COX 1 or 2
vioxx- COX 2
ibuprofen- COX 1 or 2

67
Q

What drug is a leukotriene receptor antagonist?

A

singulair

68
Q

What are the four major effects of TNF/IL-1?

A

Endothelial, fibroblast, systemic, and leukocyte

69
Q

What is activated by macrophages (and other cells) when bacterial products, immune complexes, toxins, physical injury, and/or other cytokines interfere?

A

TNF/IL-1

70
Q

What are the three acute inflammation outcomes?

A

Resolution, Fibrosis (either through pus formation or chronic inflammation), and chronic inflammation

71
Q

Inflammation of prolonged duration in which active inflammation, tissue injury, and healing process simultaneously

A

chronic inflammation

72
Q

Inflammation distinguished by vascular changes, edema, and a predominantly neutrophilic infiltrate.

A

acute inflammation

73
Q

What are the mononuclear cells caused by infiltration due to chronic inflammation?

A

macrophages, lymphocytes, and plasma cells

74
Q

What is the benefit of anti-PD-1 and anti-CTLA-4?

A

Targets cancer cells

75
Q

Leukocyte migration to the site of injury involves multiple steps. The step that involves the binding between integrin and ICAM-1 is called:

A

firm adhesion

76
Q

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

A. the coating of microbes by IgG or other components

77
Q

The mediator that can cause vascular smooth muscle relaxation and kill microbes is:
A. kinins
B. nitric oxide
C. TNF
E. IL-1

A

B. nitric oxide

78
Q

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

A

D. lymphocytes

79
Q

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

A

E. Chronic infection is always associated with viral infections

80
Q

Increased leukocyte settling along the inner surface of the blood vessels due to slowing of blood flow

A

margination

81
Q

Increased fluid flow through endothelial cells

A

transcytosis

82
Q

What is released?: small holes-plasma with little protein and no cells
Transudate vs exudate

A

transudate

83
Q

What is released?: bigger holes-protein rich fluid with numerous cells
Transudate vs exudate

A

exudate

84
Q

Innate or adaptive: B-cell, antibodies, T-cells

A

Adaptive

85
Q

Innate or adaptive: macrophages and neutrophils

A

innate

86
Q

Which defense mechanism has a dense, keratinized outer layer with low pH and fatty acids inhibiting microbial growth

A

Skin

87
Q

Defense using mucus, cilia, phagocytotic killing, and secreted IgA

A

respiratory tract

88
Q

Defense involving gastric pH, bile, mucus, defensins, IgA and gut flora

A

Intestinal tract

89
Q

Low pH in vagina from catabolism of _______ by lactobacilli

A

glycogen

90
Q

___________ can kill lactobacilli and make the vagina susceptible to infection

A

Antibiotics

91
Q

HBV, CMV and treponema pallidum are examples of _______ ______ within the body

A

vertical transmission

92
Q

What is the mechanism of viral entry to host cells in HIV

A

gp120 binds to CD4 (most T cells) and to the chemokine receptors CXCR4 (T cells) or CCR5 (macrophages)

93
Q

Virus type that binds to intercellular adhesion molecule-1 (ICAM-1)

A

rhinovirus

94
Q

A lipopolysaccharide (LPS) that is a major component of the outer cell wall of gram-negative bacteria

A

bacterial endotoxin

95
Q

How can diphtheria toxin inhibit protein synthesis

A

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
Q

functional cells of the organ (hepatocytes, myocytes, renal tubular cells)

A

parenchymal cells

97
Q

Supporting structure of organs (ECM, blood vessels, connective tissue)

A

stromal cells

98
Q

Replacement of injured tissue with cells of the same type and function

A

tissue regeneration

99
Q

Occurs when extent or nature of damage cannot be reversed by regeneration alone

A

tissue repair

100
Q

Arrange these injuries from lowest to highest healing time
Proliferation, Inflammation, Remodeling and Hemostasis

A

Hemostasis (minutes), inflammation (hrs), proliferation (days) and remodeling (weeks to months)

101
Q

Stage of healing resulting in local vasoconstriction and activation of platelets and clotting factors to form a fibrin clot from damaged cells

A

hemostasis

102
Q

Stage of healing driven by platelet-derived mediators, bacteria, and secreted chemoattractants (neutrophils and macrophages)

A

inflammation

103
Q

Stage of healing mediated by macrophage (endothelial cells and keratinocytes) and fibroblast-derived growth factors

A

proliferation

104
Q

Stage of healing transitions from type III to type I collagen, restoring tensile strength of tissue

A

remodeling

105
Q

Which stage of healing involves scab (eschar) formation

A

Proliferation

106
Q

epithelial proliferation and reduces inflammatory cells for proper remodeling

A

regeneration

107
Q

excessive scarring due to continued activation of inflammatory cells and excessive build up occuring

A

aberrant tissue repair

108
Q

Which stage (primary, secondary, tertiary) are where edges are brough together. Best choice for clean, fresh wounds, in sufficiently vascularized areas.

A

primary

109
Q

Which stage (primary, secondary, tertiary) would is left open and allowed to heal spontaneously; good for contaminated/infected wounds and increases scarring

A

secondary

110
Q

Which stage (primary, secondary, tertiary) delays primary closure and are good for wounds which are contaminated/infected initially

A

tertiary

111
Q

What are the three types of surface receptor responses to growth factors

A

P13k kinase pathway, MAP-kinase pathway -> Ras/Raf -> MAP kinase cascade, IP3 pathway -> IP3 release -> Ca release

112
Q

What is involved in the protein kinase cascade?

A

Ras -> MEKK-1, MKK-7, JNK to the nucleus to change gene expression (c-jun)

113
Q

What are the growth factors that regulate fibrosis?

A

PDGF, TGF-Beta and FGF-2

114
Q

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

a. sepsis, anaphylaxis and neurogenic

115
Q

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

A

d. myocardial infract, ventricular arrhythmia, cardiac myopathy, and valvular disease

116
Q

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

A

c. hemorrhage, severe burns, and severe vomiting, diarrhea

117
Q

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

A

b. cardiac tamponade, pulmonary embolism, pneumothorax

118
Q

What component of gram negative bacteria mediates septic shock?

A

endotoxin-producing: stimulates release of LPS

119
Q

Explain the role of adrenomedullin (ADM) and dipeptidyl dipeptidase 3 (cDPP3) in septic shock

A

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
Q

Primary driver of pushing fluid out of vascular space

A

hydrostatic pressure (mmHg)

121
Q

Draws fluid into the vascular space

A

colloid osmotic pressure (mmHg)

PHRM824 (6 decks)

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