Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathology Exam 1 > Lectures 1-5 > Flashcards

Lectures 1-5 Flashcards

1
Q

what is cytopathology?

A

evaluation of cells removed from organ or fluid, usually via needle

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

describe lymphocyte morphology

A

large nucleus, barely any cytoplasm

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

describe plasma cell morphology

A

nucleus off to the side

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

describe macrophage morphology

A

small nucleus, big granular cytoplasm

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

labile cells

A

continuously dividing

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

define hypertrophy

A

increase in size of cells

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

causes of physiologic hypertrophy

A

increased functional demand or hormonal stimulation

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

increased size of skeletal muscle of weight lifting athlete and uterus during pregnancy are examples of what?

A

physiologic hypertrophy

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

enlargement of cardiac muscle due to hypertension is an example of what?

A

pathologic hypertrophy

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

define hyperplasia

A

increase in number of cells

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

enlargement of female breast at puberty and in pregnancy is an example of what?

A

physiologic hyperplasia

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

regeneration of liver after partial resection is an example of what?

A

physiologic hyperplasia

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

causes of pathologic hyperplasia

A

excessive stimulation by growth factors or hormones

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

what cellular adaptation increases risk for cancer?

A

pathologic hyperplasia

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

skin warts and mucosal lesions associated with papilloma virus is an example of what cell adaptation?

A

pathologic hyperplasia

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

what organ undergoes both hyperplasia and hypertrophy?

A

uterus

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

define atrophy

A

decrease in size of cell

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

define metaplasia

A

one cell type is replaced by another cell type that is better able to handle stress

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

Barrett esophagus

A

-example of metaplasia -squamous epithelium becomes glandular epithelium (stomach cells), protects against reflux of stomach acid -predisposes to development of adenocarcinoma

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

what is the difference between hypoxia and ischemia?

A

hypoxia is the inadequate oxygenation of blood and ischemia is lack of blood supply to a site

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

in what type of cell injury do you see karyorrhexis and karyolysis?

A

necrosis

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

in what type of cell injury do you see nuclear shrinkage?

A

necrosis

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

what kind of necrosis results from hypoxic/anoxic injury due to ischemia?

A

coagulative

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

cause of coagulative necrosis

A

hypoxic/anoxic injury due to ischemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

where does coagulative necrosis occur?

A

in all solid organs except the brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

dead cells with intact outlines but smudgy appearance, no nuclei –> what kind of necrosis?

A

coagulative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

common causes of liquefactive necrosis

A

1) bacterial/fungal infections 2) brain infarcts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

dead cells with no outlines, karyorrhexis (fragments of nuclei) –> what kind of necrosis?

A

liquefactive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

white/yellow raised focal abscesses on surface of organ –> what kind of necrosis?

A

liquefactive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

granuloma: what it looks like, what kind of necrosis?

A

amorphous granular material surrounded by a border of inflammatory cells; caseous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

term used for ischemic coagulative necrosis of lower or upper extremity

A

gangrenous necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

wet gangrene

A

ischemic coagulative necrosis with bacterial infection, also has liquefactive characteristics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

necrosis commonly seen in acute pancreatitis

A

fat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

necrosis associated with vasculitis syndromes

A

fibrinoid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

cell death in which plasma membrane stays intact

A

apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

intrinsic apoptosis pathway: mechanism

A

Bcl-2 proteins increase permeability of the mitochondria and allow cytochrome C to enter cytoplasm –> caspase activation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

common endpoint of intrinsic and extrinsic apoptosis pathways

A

both activate initiator caspases –> executioner caspases –> break down of cytoskeleton –> apoptotic body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

two types of reversible cell injury

A

fatty change, hydropic change/vacuolar degeneration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

when does fatty change happen?

A

when there is toxic and hypoxic injury in cells dependent on fat metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

common example of fatty change

A

fatty liver secondary to excess alcohol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

mechanism of fatty change in fatty liver secondary to excess alcohol

A

hepatocytes are injured –> intracellular accumulation of triglycerides –> liver enlargement and increased liver enzymes (they leak from injured hepatocytes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

hydropic change/vacuolar degeneration: cause, why do vacuoles appear, what happens to cell size

A

results from failure of membrane pump to maintain homeostasis so membrane blebs; vacuoles appear in cells corresponding to distended ER; cell swells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

what happens when there is mitochondrial damage?

A

ATP depletion, influx of calcium, anaerobic glycolysis, increased production of ROS and pro-apoptotic proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

effects of influx of calcium in a cell

A

ER swelling, membrane and nuclear damage, increased mitochondrial permeability and therefore less ATP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

why is there clumping of nuclear chromatin after mitochondrial damage?

A

mitochondrial damage causes increased anaerobic glycolysis –> decreased pH –> clumping of nuclear chromatin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

does ischemia or hypoxia injure tissues faster? why?

A

ischemia (decreased blood flow), because there is no delivery of substrates for glycolysis (in hypoxia anaerobic glycolysis continues)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

what cell type is particularly sensitive to lack of oxygen?

A

neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

reperfusion injury: mechanism, in what organs does it frequently occur?

A

ischemia causes incomplete reduction of oxygen, so when oxygen is restored it allows for production of free radicals which lead to tissue damage; brain and heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

lipofuscin: what is it, in what organs is it found?

A

indigestible material resulting from lipid peroxidation, “wear and tear” pigment that occurs predominantly with aging; heart, liver, brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Tay-Sachs disease: type of disease, mechanism

A

lysosomal storage disease; increased gangliosides because of lack of enzyme to degrade it, leads to decrease in cognitive function and death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

what happens to mitochondria during starvation and alcohol consumption?

A

starvation: atrophy alcohol: enlarge

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

example of disease with cytoskeleton abnormalities and its mechanism

A

Alzheimer’s: accumulations of neurofibrillary tangles –> apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

hemosiderin: what is it, where is it found

A

hemoglobin-derived pigment containing iron; occurs locally where there has been hemorrhage. if a patient has many blood transfusions systemic deposition can occur

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

characteristics of dystrophic pathologic calcification

A

occurs in dying tissues, typically inflammatory process, normal serum calcium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

what kind of pathologic calcification occurs on aortic valves in the elderly?

A

dystrophic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

what kind of pathologic calcification occurs with atheromas?

A

dystrophic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

characteristics of metastatic pathologic calcification

A

occurs in normal tissues because of hypercalcemia due to increased parathyroid hormone, destruction of bone, or renal failure

58
Q

what kind of pathologic calcification occurs with renal failure?

A

metastatic

59
Q

what kind of pathologic calcification occurs with increased parathyroid hormone?

A

metastatic

60
Q

CD4 T cells recruit/activate what cells and by what mechanisms?

A

macrophages and B cells by cytokine secretion or CD40:CD40L interaction

61
Q

clonal expansion of T cells is driven by what cytokine?

A

IL-2

62
Q

role of TH1 cells

A

produces IFN-gamma, defends against intracellular microbes

63
Q

role of TH2 cells

A

produce IL-4, -5, -13, allergies

64
Q

role of TH17 cells

A

produce IL-17, -22, chemokines, defends against extracellular bacteria, fungi

65
Q

activates classical complement pathway

A

IgM and IgG

66
Q

role of IgM

A

low affinity, activates classical complement pathway

67
Q

role of IgG

A

main workhorse, abundant in blood, opsonize antigens, activates classical complement pathway, ADCC

68
Q

antibody responsible for ADCC

A

IgG

69
Q

role of IgA

A

produced in gut and respiratory tract, neutralize mucosal microbes and toxins

70
Q

role of IgE

A

allergy via mast cell degranulation, parasites

71
Q

starting point of alternative complement pathway

A

C3b

72
Q

live attenuated vaccination induces what type of response?

A

T cell

73
Q

inactivated vaccination induces what type of response?

A

B cell

74
Q

central tolerance: mechanism

A

after positive selection, any immature T/B cells that recognize high avidity self antigens presented on MHC are killed through apoptosis

75
Q

peripheral tolerance mechanisms

A

apoptosis via Fas/Fas ligand, anergy by APCs that lack costimulatory molecules, suppression by Tregs

76
Q

APECED: mechanism

A

defect in AIRE gene which normally induces expression of self antigens by thymic cells to lead to the deletion of self-reactive T cells

77
Q

low calcium, low PTH, low cortisol

A

APECED

78
Q

skin bronzing, fungal infections

A

APECED

79
Q

characterized by autoimmune adrenal and parathyroid disease

A

APECED

80
Q

ALPS: mechanism

A

mutations in Fas or Fas ligand; Fas normally transmits pro-apoptotic signals that result in lymphocyte death

81
Q

diffuse lymphadenopathy, splenomegaly, hemolytic anemia, high double negative T cells, hypergammaglobulinemia

A

ALPS

82
Q

IPEX: mechanism

A

mutation in Foxp3 –> loss of T regulatory cells

83
Q

IBD, severe eczema and food allergies, hemolytic anemia, high IgG and IgE

A

IPEX

84
Q

type 1 hypersensitivity: mechanism, examples

A

immediate hypersensitivity, IgE-mediated, requires TH2 cells; allergic rhinitis, asthma, eczema, food allergies

85
Q

type 2 hypersensitivity: mechanism, examples

A

antibody-mediated hypersensitivity: antibodies are made to self proteins –> complement activation (which may lead to lysis of RBCs), crosslinking of Fc receptors on macrophage/neutrophils, phagocytosis (of platelets in ITP); myasthenia gravis, Grave’s disease, acute rheumatic fever

86
Q

acute rheumatic fever: mechanism, hypersensitivity type

A

virulence factors expressed by S. pyogenes are structurally similar to heart muscle –> antibodies are made against heart muscle; 2

87
Q

JONES criteria: what disease and what does it stand for

A

acute rheumatic fever: joints, heart, nodules, erythema marginatum, Syndenham’s chorea (major manifestations)

88
Q

antibodies against proteins in intracellular junctions of epidermal cells causing skin vesicles

A

pemphigus vulgaris

89
Q

pemphigus vulgaris: mechanism, hypersensitivity type

A

antibodies against proteins in intracellular junctions of epidermal cells causing skin vesicles; 2

90
Q

antibodies against basement membranes of kidney glomeruli and lung alveoli causing nephritis and lung hemorrhages

A

Goodpasture’s syndrome

91
Q

Goodpasture’s syndrome: mechanism, hypersensitivity type

A

antibodies against basement membranes of kidney glomeruli and lung alveoli causing nephritis and lung hemorrhages; 2

92
Q

antibodies against acetylcholine receptor

A

myasthenia gravis

93
Q

myasthenia gravis: mechanism, hypersensitivity type

A

antibodies against acetylcholine receptor; 2

94
Q

antibodies against TSH receptor

A

Graves’ disease

95
Q

Graves’ disease: mechanism, hypersensitivity type

A

antibodies against TSH receptor; 2

96
Q

antibodies against intrinsic factor of gastric parietal cells causing macrocytic anemia

A

pernicious anemia

97
Q

pernicious anemia: mechanism, hypersensitivity type

A

antibodies against intrinsic factor of gastric parietal cells causing macrocytic anemia; 2

98
Q

treatment of antibody-mediated diseases

A

IVIG, corticosteroids (Prednisone), rituximab (kills B cells), plasmapharesis

99
Q

type 3 hypersensitivity: what is it called?

A

immune complex-mediated

100
Q

11 criteria of SLE

A

4 skin-related: discoid rash, malar rash, photosensitivity, oral/nasal ulcers 4 organ-related (-itises): arthritis, serositis, cerebritis, nephritis 3 lab: ANA, immune (dsDNA, anti-Sm), autoimmune cytopenias must have 4 out of 11 to be diagnostic

101
Q

antibodies against hepatitis B surface antigen causing vasculitis

A

polyarteritis nodosa

102
Q

polyarteritis nodosa: mechanism, hypersensitivity type

A

antibodies against hepatitis B surface antigen causing vasculitis; 3

103
Q

antibodies against streptococcal cell wall antigens causing nephritis

A

poststreptococcal glomerulonephritis

104
Q

poststreptococcal glomerulonephritis: mechanism, hypersensitivity type

A

antibodies against streptococcal cell wall antigens causing nephritis; 3

105
Q

type 4 hypersensitivity: what is it called?

A

immediate type (T cells)

106
Q

high ESR/CRP

A

rheumatoid arthritis

107
Q

rheumatoid arthritis: mechanism

A

T cells in synovial space activate monocytes, macrophages, and synovial fibroblasts which then release IL-1, IL-6, and TNF

108
Q

rash on eyelids, bridge of nose, cheeks, scaly plaques on knuckles, MCP, elbows, knees, toes, proximal muscle weakness, dilation of capillaries in nail bed, high AST, ALT, CK

A

dermatomyositis

109
Q

dermatomyositis: symptoms

A

rash on eyelids, bridge of nose, cheeks, scaly plaques on knuckles, MCP, elbows, knees, toes, proximal muscle weakness, dilation of capillaries in nail bed, high AST, ALT, CK

110
Q

dermatomyositis: mechanism

A

perivascular inflammatory infiltrate with CD4 T cells, necrosis of muscle in periphery (perifascicular atrophy)

111
Q

differences between polymyositis and dermatomyositis

A

polymyositis has diffuse muscle fiber death next to normal fibers (damage is spotty throughout muscle, not perifascicular) and is mediated by CD8 T cells not CD4

112
Q

chronic granulomatous disease: mechanism

A

absence of respiratory burst in neutrophils due to defect in an NADPH oxidase subunit

113
Q

absence of respiratory burst in neutrophils due to defect in an NADPH oxidase subunit

A

chronic granulomatous disease

114
Q

infant with adenopathy, liver abscesses, infection with catalase-positive organisms (Staph, Aspergillus, Nocardia)

A

chronic granulomatous disease

115
Q

chronic granulomatous disease: clinical presentation

A

infant with adenopathy, liver abscesses, infection with catalase-positive organisms (Staph, Aspergillus, Nocardia)

116
Q

diagnostic test for chronic granulomatous disease

A

dihyrorhodamine (DHR) test

117
Q

leukocyte adhesion deficiency: mechanism

A

mutation in common beta chain of LFA-1 preventing leukocyte adhesion to endothelium

118
Q

skin ulcers without pus, high neutrophil count

A

leukocyte adhesion deficiency

119
Q

leukocyte adhesion deficiency: clinical presentation

A

skin ulcers without pus, high neutrophil count

120
Q

late complement deficiency: mechanism

A

deficiency in C5-C9 which form the membrane attack complex, leads to increased susceptibility to Neisserial infections

121
Q

increased susceptibility to Neisserial infections

A

late complement deficiency

122
Q

X-Linked Agammaglobulinemia (XLA): mechanism

A

mutation in Btk = no B cells

123
Q

X-Linked Agammaglobulinemia (XLA): clinical presentation

A

early onset recurrent otitis, sinusitis, pneumonia

124
Q

bronchiectasis: what it is, which diseases it is seen in

A

widening of bronchi due to recurrent infections; X-Linked Agammaglobulinemia (XLA) and Common Variable Immunodeficiency (CVID)

125
Q

difference between XLA and CVID

A

XLA is early onset, CVID can be diagnosed at any age

126
Q

common variable immunodeficiency (CVID): diagnosis

A

low IgG AND low IgA or IgM

127
Q

low IgG AND low IgA or IgM

A

CVID

128
Q

CVID cause of death

A

pulmonary disease

129
Q

why can deficiency in IgA cause false positive pregnancy tests?

A

increased incidence of heterophile antibodies

130
Q

specific antibody deficiency: mechanism

A

developmental delay in antibody response to polysaccharide antigens

131
Q

specific antibody deficiency: clinical presentation

A

“abnormal” specific antibody response to immunization (especially polysaccharide antigens); recurrent sinopulmonary infections; normal IgG, IgA, IgM, normal T cell function

132
Q

X-linked SCID: mechanism

A

mutation in common gamma-chain of IL-2 receptor (shared component with other IL receptors) = lack of T cells and NK cells, B cells present but not functional

133
Q

mutation in common gamma-chain of IL-2 receptor

A

X-linked SCID

134
Q

SCID: clinical presentation

A

onset in infancy (4-5 mo), pneumonia, otitis media, thrush, intractable diarrhea, failure to thrive

135
Q

screening test for SCID; describe

A

TRECs are a surrogate marker for numbers of normal, naive T cells and is low for all forms of SCID

136
Q

onset in infancy (4-5 mo), pneumonia, otitis media, thrush, intractable diarrhea, failure to thrive

A

SCID

137
Q

DiGeorge syndrome: mechanism

A

microdeletion in chromosome 2q11.2: field defect first to sixth pharyngeal pouchs; deletion of TBX1 underlies many of the abnormalities

138
Q

DiGeorge syndrome: clinical presentation

A

CATCH22 mnemonic: cardiac defects, abnormal facies, thymic hypoplasia, cleft palate, hypocalcemia, 22nd chromosome

139
Q

cardiac defects, abnormal facies, thymic hypoplasia, cleft palate, hypocalcemia

A

DiGeorge syndrome

140
Q

all infants with congenital heart disease/significant heart defects should be tested for what?

A

DiGeorge syndrome

141
Q

DiGeorge syndrome: diagnostic test

A

chromosome microarray/DNA duplication deletion test

Pathology Exam 1 (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions