Lectures 1-5 Flashcards

(141 cards)

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
where does coagulative necrosis occur?
in all solid organs except the brain
26
dead cells with intact outlines but smudgy appearance, no nuclei --\> what kind of necrosis?
coagulative
27
common causes of liquefactive necrosis
1) bacterial/fungal infections 2) brain infarcts
28
dead cells with no outlines, karyorrhexis (fragments of nuclei) --\> what kind of necrosis?
liquefactive
29
white/yellow raised focal abscesses on surface of organ --\> what kind of necrosis?
liquefactive
30
granuloma: what it looks like, what kind of necrosis?
amorphous granular material surrounded by a border of inflammatory cells; caseous
31
term used for ischemic coagulative necrosis of lower or upper extremity
gangrenous necrosis
32
wet gangrene
ischemic coagulative necrosis with bacterial infection, also has liquefactive characteristics
33
necrosis commonly seen in acute pancreatitis
fat
34
necrosis associated with vasculitis syndromes
fibrinoid
35
cell death in which plasma membrane stays intact
apoptosis
36
intrinsic apoptosis pathway: mechanism
Bcl-2 proteins increase permeability of the mitochondria and allow cytochrome C to enter cytoplasm --\> caspase activation
37
common endpoint of intrinsic and extrinsic apoptosis pathways
both activate initiator caspases --\> executioner caspases --\> break down of cytoskeleton --\> apoptotic body
38
two types of reversible cell injury
fatty change, hydropic change/vacuolar degeneration
39
when does fatty change happen?
when there is toxic and hypoxic injury in cells dependent on fat metabolism
40
common example of fatty change
fatty liver secondary to excess alcohol
41
mechanism of fatty change in fatty liver secondary to excess alcohol
hepatocytes are injured --\> intracellular accumulation of triglycerides --\> liver enlargement and increased liver enzymes (they leak from injured hepatocytes)
42
hydropic change/vacuolar degeneration: cause, why do vacuoles appear, what happens to cell size
results from failure of membrane pump to maintain homeostasis so membrane blebs; vacuoles appear in cells corresponding to distended ER; cell swells
43
what happens when there is mitochondrial damage?
ATP depletion, influx of calcium, anaerobic glycolysis, increased production of ROS and pro-apoptotic proteins
44
effects of influx of calcium in a cell
ER swelling, membrane and nuclear damage, increased mitochondrial permeability and therefore less ATP
45
why is there clumping of nuclear chromatin after mitochondrial damage?
mitochondrial damage causes increased anaerobic glycolysis --\> decreased pH --\> clumping of nuclear chromatin
46
does ischemia or hypoxia injure tissues faster? why?
ischemia (decreased blood flow), because there is no delivery of substrates for glycolysis (in hypoxia anaerobic glycolysis continues)
47
what cell type is particularly sensitive to lack of oxygen?
neurons
48
reperfusion injury: mechanism, in what organs does it frequently occur?
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
49
lipofuscin: what is it, in what organs is it found?
indigestible material resulting from lipid peroxidation, "wear and tear" pigment that occurs predominantly with aging; heart, liver, brain
50
Tay-Sachs disease: type of disease, mechanism
lysosomal storage disease; increased gangliosides because of lack of enzyme to degrade it, leads to decrease in cognitive function and death
51
what happens to mitochondria during starvation and alcohol consumption?
starvation: atrophy alcohol: enlarge
52
example of disease with cytoskeleton abnormalities and its mechanism
Alzheimer's: accumulations of neurofibrillary tangles --\> apoptosis
53
hemosiderin: what is it, where is it found
hemoglobin-derived pigment containing iron; occurs locally where there has been hemorrhage. if a patient has many blood transfusions systemic deposition can occur
54
characteristics of dystrophic pathologic calcification
occurs in dying tissues, typically inflammatory process, normal serum calcium
55
what kind of pathologic calcification occurs on aortic valves in the elderly?
dystrophic
56
what kind of pathologic calcification occurs with atheromas?
dystrophic
57
characteristics of metastatic pathologic calcification
occurs in normal tissues because of hypercalcemia due to increased parathyroid hormone, destruction of bone, or renal failure
58
what kind of pathologic calcification occurs with renal failure?
metastatic
59
what kind of pathologic calcification occurs with increased parathyroid hormone?
metastatic
60
CD4 T cells recruit/activate what cells and by what mechanisms?
macrophages and B cells by cytokine secretion or CD40:CD40L interaction
61
clonal expansion of T cells is driven by what cytokine?
IL-2
62
role of TH1 cells
produces IFN-gamma, defends against intracellular microbes
63
role of TH2 cells
produce IL-4, -5, -13, allergies
64
role of TH17 cells
produce IL-17, -22, chemokines, defends against extracellular bacteria, fungi
65
activates classical complement pathway
IgM and IgG
66
role of IgM
low affinity, activates classical complement pathway
67
role of IgG
main workhorse, abundant in blood, opsonize antigens, activates classical complement pathway, ADCC
68
antibody responsible for ADCC
IgG
69
role of IgA
produced in gut and respiratory tract, neutralize mucosal microbes and toxins
70
role of IgE
allergy via mast cell degranulation, parasites
71
starting point of alternative complement pathway
C3b
72
live attenuated vaccination induces what type of response?
T cell
73
inactivated vaccination induces what type of response?
B cell
74
central tolerance: mechanism
after positive selection, any immature T/B cells that recognize high avidity self antigens presented on MHC are killed through apoptosis
75
peripheral tolerance mechanisms
apoptosis via Fas/Fas ligand, anergy by APCs that lack costimulatory molecules, suppression by Tregs
76
APECED: mechanism
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
low calcium, low PTH, low cortisol
APECED
78
skin bronzing, fungal infections
APECED
79
characterized by autoimmune adrenal and parathyroid disease
APECED
80
ALPS: mechanism
mutations in Fas or Fas ligand; Fas normally transmits pro-apoptotic signals that result in lymphocyte death
81
diffuse lymphadenopathy, splenomegaly, hemolytic anemia, high double negative T cells, hypergammaglobulinemia
ALPS
82
IPEX: mechanism
mutation in Foxp3 --\> loss of T regulatory cells
83
IBD, severe eczema and food allergies, hemolytic anemia, high IgG and IgE
IPEX
84
type 1 hypersensitivity: mechanism, examples
immediate hypersensitivity, IgE-mediated, requires TH2 cells; allergic rhinitis, asthma, eczema, food allergies
85
type 2 hypersensitivity: mechanism, examples
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
acute rheumatic fever: mechanism, hypersensitivity type
virulence factors expressed by S. pyogenes are structurally similar to heart muscle --\> antibodies are made against heart muscle; 2
87
JONES criteria: what disease and what does it stand for
acute rheumatic fever: joints, heart, nodules, erythema marginatum, Syndenham's chorea (major manifestations)
88
antibodies against proteins in intracellular junctions of epidermal cells causing skin vesicles
pemphigus vulgaris
89
pemphigus vulgaris: mechanism, hypersensitivity type
antibodies against proteins in intracellular junctions of epidermal cells causing skin vesicles; 2
90
antibodies against basement membranes of kidney glomeruli and lung alveoli causing nephritis and lung hemorrhages
Goodpasture's syndrome
91
Goodpasture's syndrome: mechanism, hypersensitivity type
antibodies against basement membranes of kidney glomeruli and lung alveoli causing nephritis and lung hemorrhages; 2
92
antibodies against acetylcholine receptor
myasthenia gravis
93
myasthenia gravis: mechanism, hypersensitivity type
antibodies against acetylcholine receptor; 2
94
antibodies against TSH receptor
Graves' disease
95
Graves' disease: mechanism, hypersensitivity type
antibodies against TSH receptor; 2
96
antibodies against intrinsic factor of gastric parietal cells causing macrocytic anemia
pernicious anemia
97
pernicious anemia: mechanism, hypersensitivity type
antibodies against intrinsic factor of gastric parietal cells causing macrocytic anemia; 2
98
treatment of antibody-mediated diseases
IVIG, corticosteroids (Prednisone), rituximab (kills B cells), plasmapharesis
99
type 3 hypersensitivity: what is it called?
immune complex-mediated
100
11 criteria of SLE
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
antibodies against hepatitis B surface antigen causing vasculitis
polyarteritis nodosa
102
polyarteritis nodosa: mechanism, hypersensitivity type
antibodies against hepatitis B surface antigen causing vasculitis; 3
103
antibodies against streptococcal cell wall antigens causing nephritis
poststreptococcal glomerulonephritis
104
poststreptococcal glomerulonephritis: mechanism, hypersensitivity type
antibodies against streptococcal cell wall antigens causing nephritis; 3
105
type 4 hypersensitivity: what is it called?
immediate type (T cells)
106
high ESR/CRP
rheumatoid arthritis
107
rheumatoid arthritis: mechanism
T cells in synovial space activate monocytes, macrophages, and synovial fibroblasts which then release IL-1, IL-6, and TNF
108
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
dermatomyositis
109
dermatomyositis: symptoms
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
dermatomyositis: mechanism
perivascular inflammatory infiltrate with CD4 T cells, necrosis of muscle in periphery (perifascicular atrophy)
111
differences between polymyositis and dermatomyositis
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
chronic granulomatous disease: mechanism
absence of respiratory burst in neutrophils due to defect in an NADPH oxidase subunit
113
absence of respiratory burst in neutrophils due to defect in an NADPH oxidase subunit
chronic granulomatous disease
114
infant with adenopathy, liver abscesses, infection with catalase-positive organisms (Staph, Aspergillus, Nocardia)
chronic granulomatous disease
115
chronic granulomatous disease: clinical presentation
infant with adenopathy, liver abscesses, infection with catalase-positive organisms (Staph, Aspergillus, Nocardia)
116
diagnostic test for chronic granulomatous disease
dihyrorhodamine (DHR) test
117
leukocyte adhesion deficiency: mechanism
mutation in common beta chain of LFA-1 preventing leukocyte adhesion to endothelium
118
skin ulcers without pus, high neutrophil count
leukocyte adhesion deficiency
119
leukocyte adhesion deficiency: clinical presentation
skin ulcers without pus, high neutrophil count
120
late complement deficiency: mechanism
deficiency in C5-C9 which form the membrane attack complex, leads to increased susceptibility to Neisserial infections
121
increased susceptibility to Neisserial infections
late complement deficiency
122
X-Linked Agammaglobulinemia (XLA): mechanism
mutation in Btk = no B cells
123
X-Linked Agammaglobulinemia (XLA): clinical presentation
early onset recurrent otitis, sinusitis, pneumonia
124
bronchiectasis: what it is, which diseases it is seen in
widening of bronchi due to recurrent infections; X-Linked Agammaglobulinemia (XLA) and Common Variable Immunodeficiency (CVID)
125
difference between XLA and CVID
XLA is early onset, CVID can be diagnosed at any age
126
common variable immunodeficiency (CVID): diagnosis
low IgG AND low IgA or IgM
127
low IgG AND low IgA or IgM
CVID
128
CVID cause of death
pulmonary disease
129
why can deficiency in IgA cause false positive pregnancy tests?
increased incidence of heterophile antibodies
130
specific antibody deficiency: mechanism
developmental delay in antibody response to polysaccharide antigens
131
specific antibody deficiency: clinical presentation
"abnormal" specific antibody response to immunization (especially polysaccharide antigens); recurrent sinopulmonary infections; normal IgG, IgA, IgM, normal T cell function
132
X-linked SCID: mechanism
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
mutation in common gamma-chain of IL-2 receptor
X-linked SCID
134
SCID: clinical presentation
onset in infancy (4-5 mo), pneumonia, otitis media, thrush, intractable diarrhea, failure to thrive
135
screening test for SCID; describe
TRECs are a surrogate marker for numbers of normal, naive T cells and is low for all forms of SCID
136
onset in infancy (4-5 mo), pneumonia, otitis media, thrush, intractable diarrhea, failure to thrive
SCID
137
DiGeorge syndrome: mechanism
microdeletion in chromosome 2q11.2: field defect first to sixth pharyngeal pouchs; deletion of TBX1 underlies many of the abnormalities
138
DiGeorge syndrome: clinical presentation
CATCH22 mnemonic: cardiac defects, abnormal facies, thymic hypoplasia, cleft palate, hypocalcemia, 22nd chromosome
139
cardiac defects, abnormal facies, thymic hypoplasia, cleft palate, hypocalcemia
DiGeorge syndrome
140
all infants with congenital heart disease/significant heart defects should be tested for what?
DiGeorge syndrome
141
DiGeorge syndrome: diagnostic test
chromosome microarray/DNA duplication deletion test