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MAMS > Path Exam 1 > Flashcards

Path Exam 1 Flashcards

1
Q

hyperplasia

A

increase in # cells resulting in increased volume of the organ or tissue

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2
Q

where can hyperplasia be initiated?

A

in a cell pop that is capable of division and proliferation

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3
Q

what kind of adaptation is the lactating breast?

A

hormonal hyperplasia

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4
Q

what kind of adaptation is post-hepatectomy regeneration?

A

compensatory hypertrophy

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5
Q

what is the stimulus for liver regeneration after a hepatectomy?

A

growth factor produced by residual hepatocytes

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6
Q

what causes follicular hyperplasia of lymph nodes?

A

exposure to an infectious agent leads to B cell proliferation in the follicles of lymph nodes

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7
Q

what causes benign prostatic hyperplasia?

A

testosterone metabolite, dihydrotestosterone induces nodular enlargement of the gland

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8
Q

what causes squamous hyperplasia?

A

response to chronic inflammation, squamous mucosa thickens

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9
Q

what is the molecular mediator of squamous hyperplasia?

A

TGF-alpha

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10
Q

hypertrophy

A

increase in size of cells leading to increased tissue volume

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11
Q

alveolar spaces

A

terminal air spaces within the lung

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12
Q

autoimmune disease

A

a disease where immune response incorrectly attacks normal tissue

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13
Q

chemotaxis

A

directed movement of leukocytes or other cells in a specific direction

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14
Q

cytokines

A

protein mediators which activate and orchestrate the inflammatory response

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15
Q

leukocytes

A

white blood cells from bone marrow

critical part of inflammatory response

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16
Q

endothelial cells

A

cells that line blood vessels

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17
Q

hyperemia

A

increased blood flow inside vasculature

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18
Q

integrin

A

molecules on surface of white blood cells responsible for their adherence to the lining of blood vessels

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19
Q

margination

A

moving to the edge

usually leukocytes moving from center of bloodstream to edge

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20
Q

opsins

A

proteins that bind the outside of bacteria or dead tissue

usually antibodies or complement fragments

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21
Q

selectins

A

adhesion molecules that direct leukocytes to sites of inflammation

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22
Q

atrophy

A

shrinkage of a tissue due to loss of a cell substance/#

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23
Q

what drives atrophy?

A

imbalance between protein degradation and syntesis

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24
Q

what pathway is responsible for proteolysis in atrophied tissues?

A

ubiquitin-proteasome pathway

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25
Q

autophagic vacuoles

A

lysosomes that contain fragments of cell components

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26
Q

residual bodies

A

shrunken lysosomes that contain lipofuscin

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27
Q

brown atrophy

A

residual bodies cause atrophic organs to appear brown

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28
Q

metaplasia

A

reversible change in which one adult cell type is replaced by another

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29
Q

what does metaplasia result from?

A

reprogramming of tissue stem cells by actions of cytokines and growth factors

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30
Q

causes of reversible cell injury

A

cellular swelling

fatty change

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31
Q

what causes cellular swelling (cell level)?

A

loss of function of PM energy dependent ion pumps that leaves the cytoplasm distended but membranes intact

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32
Q

what causes cellular swelling(body level)?

A

anoxic injury

hepatocyte injury due to viral infection

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33
Q

what causes fatty change in cells?

A

excessively stressing the fat metab process in the liver

leads to accumulation in vacuoles in hepatocytes

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34
Q

what is the appearance of necrosis ultrastructurally?

A

disruption/fragmentation of cell membranes that can form myelin bodies
absence of nucleus

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35
Q

what injury would cause coagulative necrosis?

A

ischemic injury

MI

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36
Q

what is the ultrastructural appearance of coagulative necrosis?

A

ghost outlines of cells preserved due to Ca infusion and denaturation of proteins
eosinophilia

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37
Q

what injury causes liquefactive necrosis?

A

bacterial infection

infarction of CNS

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38
Q

what is the appearance of fat necrosis ultrastructurally?

A

formation of soap due to release of FA from the necrotic tissue

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39
Q

fibrinoid necrosis

A

deposits of complexes of antigens and antibodies with fibrin in the vessel wall

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40
Q

what usually causes ATP depletion in cells?

A

anoxia

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41
Q

what does accumulation of free radicals in the cell cause?

A

membrane damage from lipid peroxidation
denaturation of structural pro and NZs
DNA damage

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42
Q

mechanism of apoptosis

A

activation of caspases

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43
Q

what do caspases do?

A

denature cytoskeleton and nuc

activate DNAses

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44
Q

extrinsic pathway of apoptosis

A

ligands engage death receptors

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45
Q

what is the receptor of the extrinsic path of apoptosis

A

TNF type 1

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46
Q

intrinsic pathway of apoptosis

A

anti-apoptotic proteins are replaced by pro-apoptotic pro in the mito matrix, which leads to increased membrane perm which causes cytochrome C to bind to Apaf-1 leading to the caspase cascade

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47
Q

inflammation

A

host response to injury or infection

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48
Q

what cells respond first in inflammation?

A

neutrophils

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49
Q

length of acute inflammation

A

0-7 days

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50
Q

length of sub acute inflammation

A

7-30 days

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51
Q

length of chronic inflammation

A

> 30 days

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52
Q

cellular infiltrate of chronic inflammation

A

macrophages

lymphocytes

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53
Q

5 aspects of inflammation

A 
recognition of the offending agent
recruitment of cells and mediators
removal of offending agent
regulation of inflammation 
resolution
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54
Q

granulocytes

A

neutrophils
basophils
eosinophils

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55
Q

helper T cells

A

CD4

help B cells produce antibodies and activate macrophages thru secretion of cytokines

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56
Q

cytotoxic T cells

A

CD8

kill virally infected cells

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57
Q

B cells

A

mature in bone marrow
become plasma cells
secrete antibodies

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58
Q

where do macrophages originate?

A

in bone marrow as monoblasts

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59
Q

what do alternatively activated macrophages do?

A

shut off inflammatory process

induce fibrosis

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60
Q

where are eosinophils found?

A

local sites of inflammation in individuals with allergies

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61
Q

what activates basophils and mast cells?

A

binding of antigen of surface bound IgE

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62
Q

components of the innate humoral immune system

A

cytokines

complement

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63
Q

components of the innate cellular immune system

A 
neutrophils
NK cells
mast cells
dendritic cells
eosinophils
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64
Q

components of the adaptive humoral immune system

A

antibodies

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65
Q

components of the adaptive cellular immune system

A

T cells

B cells

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66
Q

which cells are the best APCs?

A

dendritic

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67
Q

when are tissues considered inflamed?

A

when leukocytes are present where they aren’t normally found

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68
Q

4 cardinal signs of acute local inflammation

A

rubor- redness
tumor- swelling
calor- heat
dolor- pain

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69
Q

cell derived mediators

A

produced within cells and then exported

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70
Q

plasma protein derived mediators

A

generated from proteins found in plasma and normally circulate in the blood

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71
Q

3 basic steps of acute inflammation

A

hyperemia
increased vascular permeability
emigration, accumulation, activation of leukocytes

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72
Q

hyperemia

A

dilation of blood vessels

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73
Q

vasoactive amines

A

histamine

serotonin

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74
Q

where is histamine stored?

A

mast cells
basophils
platelets

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75
Q

histamine actions

A

arteriolar dilation

increased venule permeability

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76
Q

what causes release of histamine?

A 
trauma/heat
reactions with IgE
C3a
C5a
leukocyte derived histamine releasing proteins
neuropeptides
cytokines
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77
Q

where is serotonin stored?

A

platelets

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78
Q

arachidonic acid metabolites

A

prostaglandins
leukotrienes
lipoxins

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79
Q

action of prostaglandins

A

vasodilation

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80
Q

action of thromboxane

A

vasoconstriction

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81
Q

action of leukotrienes

A

increased permeability

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82
Q

action of LTB4 and HETE

A

chemotaxis

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83
Q

action of NO

A

vasodilation

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84
Q

how is NO synthesized?

A

from L-arginase and oxygen by NO synthase

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85
Q

what is PAF derived from?

A

membrane phospholipids

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86
Q

actions of PAF

A 
platelet aggregation 
vasoconstriction
bronchoconstriction 
leukocyte oxidative burst
leukocyte adhesion
chemotaxis
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87
Q

actions of PAF at low concentrations

A

vasodilation

increased vascular permeability

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88
Q

bradykinin

A

vasoactive peptide derived from plasma proteins

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89
Q

bradykinin actions

A

vascular permeability
contraction of smooth muscle
dilation of blood vessels
pain

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90
Q

mediators of vasodilation

A

prostaglandins
NO
histamine

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91
Q

mediators of increased vascular permeability

A 
histamine
serotonin
C3a
C5a
bradykinin
leukotrienes
PAF
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92
Q

mediators of chemotaxis, leukocyte recruitment and activation

A 
TNF
IL-1
chemokines
C3a
C5a
leukotriene B4
bacterial products
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93
Q

mediators of fever

A

IL-1
TNF
prostaglandins

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94
Q

mediators of pain

A

prostaglandins

bradykinin

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95
Q

mediators of tissue damage

A

lysosomal NZs of leukocytes
ROS
NO

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96
Q

what causes swelling?

A

leakage of proteins from plasma to interstitium

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97
Q

where does leakage of proteins from plasma occur?

A

microcirculation, post-cap venules

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98
Q

transudate

A

fluid that passes due to hydrodynamic forces

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99
Q

what does the presence of transudate imply?

A

endothelial barrier to passage of plasma proteins is intact

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100
Q

exudate

A

fluid that escaped from the blood vasculature, usually as a result of inflammation

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101
Q

what does the presence of exudate imply?

A

damage of inflammatory changes to vascular endothelium

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102
Q

edema

A

accumulation of fluid within the interstitium of tissues

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103
Q

is edema transudate or exudate?

A

can be either

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104
Q

effusion

A

accumulation of fluid in a sealed body cavity

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105
Q

is effusion transudate or exudate?

A

can be either

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106
Q

serous exudate

A

contains few cells and resembles serum

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107
Q

what does a serous exudate suggest?

A

mild vascular injury

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108
Q

purulent exudate

A

cloudy appearance, pus

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109
Q

what does a purulent exudate suggest?

A

large concentration of neutrophils due to bacteria

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110
Q

hemorrhagic exudate

A

contains RBCs due to cap damage

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111
Q

fibrinous exudate

A

typically see on serosal surfaces

white layer of fibrin occurs as a result of polymerization of fibrin

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112
Q

what is the most important histologic sign of inflammation?

A

leukocyte infiltration

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113
Q

steps of leukocyte recruitment to tissues

A

margination
rolling
tight adhesion
migration

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114
Q

margination

A

leukocytes must move into the margin of the bloodstream to come into contact with the vascular wall

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115
Q

what regulates the specificity of cellular inflammation?

A

rolling phase

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116
Q

what mediates rolling?

A

selectins and integrins

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117
Q

what allows tight adhesion?

A

ability of integrin molecules to rapidly increase molecular avidity for integrin ligands on endothelial cell surface

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118
Q

neutrophil chemotactic agents

A 
bacterial products
C5a
Leukotriene B4
IL-8 CXC chemokines
PAF
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119
Q

vascular effects of C3a and C5a

A

release histamine from mast cells –> vasodilation, increased permeability

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120
Q

C5a roles

A

chemotaxis

activation of lipoxygenase pathway of

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121
Q

C3b role

A

opsonize bacteria for phagocytosis

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122
Q

what causes fever?

A

pyrogens

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123
Q

what are the sources of pyrogens?

A

macrophage derived cytokines:
IL-1
IL-6
TNF-alpha

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124
Q

leukocytosis

A

increased number of leukocytes in peripheral blood

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125
Q

neutrophil extracellular nets

A

strands of chromatin derived from the neutrophil contain antimicrobial peptides and kill bacteria

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126
Q

causes of chronic infection

A

prolonged exposure to tissue injury, irritants, toxins
autoimmune diseases
allergic diseases
persistent infections

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127
Q

inflammatory mediators of chronic inflammation

A

acute phase proteins
cytokines- TNF
IL-6

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128
Q

what synthesizes acute phase proteins?

A

hepatocytes

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129
Q

what induces synthesis of acute phase proteins?

A

IL-6

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130
Q

ESR

A

erythrocyte sedimentation rate

clinically measures inflammation

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131
Q

what synthesizes IL-6?

A

macrophages
fibroblasts
endothelial cells
activated T cells

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132
Q

actions of IL-6

A

stimulates synthesis of acute phase reactants
fever
growth of B cells

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133
Q

granuloma

A

aggregate of macrophages arranged concentrically around a pathogen or irritant

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134
Q

characteristic cell of granuloma

A

epitheloid macrophage

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135
Q

epitheloid macrophage

A

large cell with abundant, pale, granular cytoplasm

in center of granuloma

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136
Q

distinctive feature of granuloma

A

multinucleated giant cells

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137
Q

causes of granuloma

A

bacterial inflammation
fungal/parasitic infections
aseptic foreign bodies
unknown causes

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138
Q

angiogenesis

A

formation of new blood vessels via extension or remodeling from existing cap

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139
Q

where are continuous cap?

A

skeletal muscle
heart
lung
brain

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140
Q

where are fenestrated cap?

A

endocrine glands
intestinal villi
glomeruli

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141
Q

where are discontinuous cap?

A

liver
spleen
bone marrow

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142
Q

what do endothelial cells secrete?

A 
prostacyclin
thrombomodulin
heparin
plasminogen activator
tissue factor
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143
Q

angiogenesis

A

formation of new blood vessels via extension or remodeling from existing cap

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144
Q

steps of sprouting angiogenesis

A 
increase vessel perm
loosening of pericytes
degradation of BM
EC proliferation
directed migration
sprouting/tubulogenesis
creation of lumen
pericytes attach
fuse with other sprouts
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145
Q

steps in vessel sprouting

A 
tip/stalk cell selection
tip cell navigation
stalk cell proliferation 
stalk elongation
tip cell fusion 
lumen formation 
perfusion and vessel maturation
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146
Q

what do tip cells form in response to VEGF?

A

filopodia

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147
Q

what regulates filopodia formation?

A

Cdc42
ephrinB2
VEGFR-2

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148
Q

what stabilizes the stalk cells?

A

notch activity

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149
Q

____ signaling promotes stabilization of the endothelial layer through the inhibition of SRC

A

Robo4/UNC5B

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150
Q

contact btwn cells that express Notch and Jagged1 induces expression of ____ in mural cell

A

Notch3

Jagged1

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151
Q

_____ are the major regulators of angiogenesis

A

VEGF ligands

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152
Q

____ promotes expression of VEGF

A

hypoxia

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153
Q

non-sprouting angiogenesis

A

involves formation of blood vessels by a splitting process in which elements of interstitial tissue invade existing vessels to form transvascular tissue pillars

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154
Q

vasculogenesis

A

de novo blood vessel development from vascular progenitor cells

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155
Q

what are hemangioblasts derived from

A

mesodermal cells

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156
Q

what causes mesodermal cells to differentiate into hemangioblasts?

A

high conc of bone morphogenetic proteins

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157
Q

phase 1 of vasculogenesis

A

mesodermal cells become hemangioblasts that condense into blood islands

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158
Q

phase 2 of vasculogenesis

A

angioblasts multiply and differentiate into endothelial cells

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159
Q

phase 3 of vasculogenesis

A

endothelial cells form tubes and connect to form the primary cap plexus

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160
Q

arteriogenesis

A

formation of mature blood vessels

differentiation into veins and arteries

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161
Q

2 elements of tissue repair

A

regeneration

fibrosis

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162
Q

labile cells

A

continuously dividing cells

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163
Q

stable cells

A

infrequently dividing cells

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164
Q

permanent cells

A

rarely or non dividing cells

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165
Q

tissue repair steps

A

inflammation
cell proliferation and migration
synthesis of ECM
remodeling of ECM

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166
Q

inflammation is equivalent to what layer of the chronic peptic ulcer?

A

necrosis and acute inflammatory exudate

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167
Q

cell proliferation and migration is equivalent to what layer of the chronic peptic ulcer?

A

granulation tissue

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168
Q

synthesis of ECM is equivalent to what layer of the chronic peptic ulcer?

A

granulation tissue and ECM

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169
Q

remodeling of ECM is equivalent to what layer of the chronic peptic ulcer?

A

fibrous scar

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170
Q

tissue elements of layer 1 acute inflammation and necrosis

A

fibrin
neutrophils
macrophages
platelets

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171
Q

molecular elements of layer 1 acute inflammation and necrosis

A

cytokines- IL, interferons, TNF

growth factors- PDGF, FGF

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172
Q

cellular elements of layer II granulation tissue

A

capillaries
fibroblasts
macrophages

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173
Q

molecular elements of layer II granulation tissue

A 
EGF/TGF-alpha
PDGF
FGF
VEGF
TGF-beta
angiopoietins
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174
Q

growth factors

A

polypeptides that signal cells to proliferate, migrate, and differentiate

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175
Q

EGF/TGF-alpha

A

bind ERB-B1 cell membrane receptors which generate a signal with tyrosine kinase that induces a wide variety of cells to divide

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176
Q

PDGF

A

dimer with A and B side chains where each molecule binds to 2 membrane receptors alpha and beta

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177
Q

where is PDGF stored?

A

platelet alpha granules

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178
Q

what produces PDGF?

A 
platelets
activated macrophages
smooth muscle cells
endothelial cells
some tumor cells
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179
Q

effects of PDGF

A

migration and proliferation of fibroblasts and endothelial cells

180
Q

FGFs

A

produced by a variety of cells and recognized by a family of cell surface receptors that have intrinsic protein kinase activity

181
Q

FGF actions

A

macrophage, fibroblast, endothelial cell migration

angiogenesis

182
Q

VEGF

A

family of growth factors essential to new blood vessel formation

183
Q

VEGF action

A

increased vascular permeability

184
Q

TGF-beta

A

family of homodimeric proteins that interact with cell surface receptors and trigger phosphorylation of Smads

185
Q

what produces TGF-beta

A

platelets
endothelial cells
lymphocytes
macrophages

186
Q

actions of TGF-beta

A

inhibits epithelial proliferation
stimulates fibroblasts chemotaxis
production of collagen and fibronectin

187
Q

2 distinct domains of the ECM

A

basal membrane

interstitial matrix

188
Q

what produces the basal membrane?

A

epithelial cells

some mesenchymal cells

189
Q

what composes the basal membrane?

A 
non-fibrillary collagens
laminin
heparan sulfate
proteoglycan 
glycoproteins
190
Q

interstitial matrix

A

fills spaces btwn cells and is the predominant element in CT

191
Q

what composes the interstitial matrix?

A 
fibrillary and non-fibrillary collagens
elastin
adhesive glycoproteins
fibronectin
gel of proteoglycans and hyaluronate
192
Q

what are the 3 groups of macromolecules that make up the ECM?

A

fibrous structural proteins
cell adhesion proteins
gel of proteoglycans and hyaluronan

193
Q

collagen

A

triple helix of 3 polypeptide alpha chains that have gly-x-y repeating sequence

194
Q

elastin

A

central core of elastin surrounded by a micro-fibrillary network of fibrilin

195
Q

cell adhesion proteins

A

glycoproteins that link cells and ECM components to each other

196
Q

cadherins

A

ca dependent adherence proteins that connect PM of adjacent cells

197
Q

how are cadherins linked to the cytoskeleton?

A

alpha and beta catenins

198
Q

integrins

A

family of cell surface receptors that mediate cell attachment to ECM by binding to CAMs

199
Q

fibronectin

A

large, adhesive glycoprotein that binds to ECM proteins and and to cells

200
Q

what produces fibronectin

A

fibroblasts
endothelial cells
monocytes

201
Q

laminin

A

spans the BM and binds specific cell surface receptors to collagen type IV and heparan sulfate

202
Q

proteoglycans

A

core of proteins linked to 1 or more disaccharide polymers

203
Q

role of proteoglycans

A

regulating ECM structure and permeability

204
Q

hyaluronan

A

large molecule consisting of numerous repeats of simple disaccharide

205
Q

role of hyaluronan

A

binds to water to give tissues turgor pressure

206
Q

how is remodeling achieved in layer IV?

A

degradation of collagen and pro by metalloproteinases and resynthesis

207
Q

what causes wound contraction?

A

myofibroblasts

208
Q

NK cells

A

large, non-phagocytic granular lymphocytes that kill abnormal host cells

209
Q

how do NK cells kill their target?

A

release perforins, granzymes and other cytotoxic chemical that induce apoptosis

210
Q

how do NK cells recognize their targets?

A

killer activation receptors

211
Q

origin of mast cells

A

bone marrow stem cells

212
Q

function of mast cells

A

mediates inflammatory process

213
Q

life span of mast cells

A

few months

214
Q

distribution of mast cells

A

CT conc along small blood vessels

subepithelium of resp and GI

215
Q

prestored mediators of mast cells

A

heparin
histamine
chondriotin sulfate
proteases

216
Q

heparin action

A

prevents clotting at site of infection

217
Q

lipid mediators of mast cells

A

prostaglandins
cysteinyl leukotrienes
PAF

218
Q

cytokines and chemokines of mast cells

A 
leukotrienes- IL-4,5,6
thromboxanes
TNF-alpha
eosinophil chemotactic factor
neutrophil chemotactic factor
219
Q

general functions of mast cell mediators

A 
recruitment of immune cells
activation of immune cells
phagocytosis
antimicrobial activity
tissue repair
vascular permeability
toxin degradation
220
Q

primary granules of neutrophils

A

lysosomes that contain myeloperoxidase

acid hydrolases

221
Q

myeloperoxidase

A

forms ROS that are toxic to bacteria

222
Q

specific granules of neutrophils

A

alkaline phosphatase collagenase
lactoferrin
bacterial phagocytins
lysozyme

223
Q

lysozyme

A

degrades components of bac cell walls

224
Q

tertiary granules of neutrophils

A

cathepsins
gelatinase
for cell migration

225
Q

what do eosinophilic granules contain

A

major basic protein

226
Q

major basic protein roles

A

potent toxin for helminth worms
induces histamine release
activates neutrophils and platelets
bronchospasm

227
Q

function of eosinophil

A

parasitic infestations

allergies

228
Q

primary granules of basophiles

A 
heparin
chondriotin sulfate
histamine
proteases
eosinophil chemotactic factor
neutrophil chemotactic factor
229
Q

secondary granules of basophils

A

leukotrienes- IL-4,5,6
thromboxanes
PAF
TNF-alpha

230
Q

monocytes are characterized by a high level expression of _____ surface receptor

A

CD14

231
Q

lacrimal apparatus

A

continual washing and blinking prevents microbes from settling on eye surface

232
Q

transferrins

A

iron binding proteins in blood that inhibits bacterial growth by reducing available iron

233
Q

pattern recognition receptors

A

receptors of the innate immune system that recognize broad structural motifs not in host but present on microbes

234
Q

what do pattern recognition receptors recognize?

A

pathogen associated molecular patterns

235
Q

pathogen associated molecular patterns

A

molecules associated with groups of pathogens

recognized by innate immune system

236
Q

toll like receptor role

A

mediate generation of defensive responses

237
Q

what triggers TLR

A

binding to a PAMP on an infectious organism

238
Q

stimulation of TLR leads to production of

A

inflammatory cytokines-IL-6,10,12
type I IFNs
chemokines

239
Q

B cells

A

recognize antigens via membrane bound IgM as part of the B cell R complex

240
Q

CD4 T cells interact with APCs expressing ___

A

MHC II

241
Q

CD4 T cell role

A

activate macrophages

activate B lymphocytes

242
Q

CD8 T cells interact with APCs expressing ___

A

MHC I

243
Q

CD8 T cell role

A

directly kill virus infected or tumor cells

244
Q

pleiotropic effects

A

1 cytokine can have diverse effects on many cell types

245
Q

redundant effects

A

multiple cytokines may have the same activity

246
Q

proinflammatory cytokines

A

IL-1
IL-6
TNF

247
Q

anti inflammatory cytokines

A

IL-10

TGF-beta

248
Q

growth factor cytokines

A

IL-2 secreted by helper T cells

249
Q

main chemokine cytokine

A

IL-8

250
Q

interferons

A

antiviral proteins that interfere with viral multiplication

251
Q

alpha and beta interferons

A

produced by virus infected cells and diffuse to neighboring cells to cause infected cells to produce antiviral proteins

252
Q

what produces gamma interferon

A

lymphocytes

253
Q

what does gamma interferon do?

A

causes neutrophils to kill viruses and some bacteria

254
Q

major histocompatibility complex

A

tightly linked cluster of genes whose products are associated with intracellular recognition and self/nonself discrimination

255
Q

what do class I MHC genes mediate?

A

immune responses against endogenous antigens

256
Q

what alleles encode class I MHC?

A

HLA-A,B,C

257
Q

what do class II MHC genes mediate?

A

immune response against exogenous antigens

258
Q

what encodes class II MHC?

A

HLA-D allele

DP, DQ, DR subregions

259
Q

where are MHC class II found?

A

APC cells

260
Q

professional APCs

A

dendritic cells
macrophages
B cells

261
Q

main function of dendritic cells

A

process antigen material and present it on the cell surface of the T cells of the immune system

262
Q

where are dendritic cells?

A

tissues that are in contact with the environment

263
Q

antigen processing

A

formation of peptide-MHC complexes that require a protein antigen be degraded into peptides and displayed within the cleft of the MHC molecule on the cell membrane

264
Q

antigen presentation

A

display of transported peptide-MHC molecules on the cell membrane

265
Q

cytokines produced by TH1 cells

A

IFN-g

266
Q

cytokines produced by TH2 cells

A

IL-4,5,13

267
Q

cytokines produced by TH17 cells

A

IL-17,22

chemokines

268
Q

immunologic reactions triggered by TH1

A

macrophage activation
stimulation of IgG
antibody production

269
Q

TH1 role in disease

A

immune-mediated chronic inflammatory diseases

270
Q

immunologic reactions triggered by TH2

A

stimulation of IgE production

activation of mast cells and eosinophils

271
Q

TH2 role in disease

A

allergies

272
Q

immunologic reactions triggered by TH17

A

recruitment of neutrophils, monocytes

273
Q

TH17 role in disease

A

immune-mediated chronic inflammatory diseases

274
Q

IL-4 action

A

stimulates B cells to differentiate into IgE secreting plasma cells

275
Q

IL-5 action

A

activates eosinophils

276
Q

IL-13 action

A

activates mucosal epithelial cells to secrete mucus and expel microbes
activates macrophages to secrete growth factors important for tissue repair

277
Q

chemotaxis

A

phagocytes are chemically attracted to site of infection

278
Q

complement system

A

large group of serum proteins that participate in the lysis of foreign cells, inflammation, phagocytosis

279
Q

classical pathway of complement activation

A

initiated by an immune reaction of antibodies

280
Q

alternative pathway of complement activation

A

initiated by direct interaction of complement proteins with microbial polysaccharides

281
Q

cytolysis

A

formation of a membrane attack complex that causes lesions in microbial membranes

282
Q

which part of the complement system is involved in opsonization?

A

C3b

283
Q

type I hypersensitivity

A

allergies

284
Q

what mediates type I hypersensitivity

A

IgE antibodies that activate mast cells

285
Q

cells involved in type I hypersensitivity

A 
B lymphocytes
plasma cells
mast cells
basophils
neutrophils
eosinophils
286
Q

type II hypersensitivity

A

antibody mediated diseases

287
Q

what causes type II hypersensitivity

A

antibodies directed against antigens present on cell surfaces or the extracellyular matrix

288
Q

autoantigen of myasthenia gravis

A

ACh R

289
Q

myasthenia gravis consequence

A

skeletal muscle weakness due to impaired contraction

290
Q

myasthenia gravis treatment

A

pyridostigmine (ACh inhibitor)

291
Q

autoantigen of immune thrombocytopenic purpura

A

platelet surface antigens

292
Q

Immune thrombocytopenic purpura consequence

A

premature destruction of platelets

293
Q

Thrombocytopenia

A

low levels of platelets

294
Q

Pemphigus vulgaris antibodies

A

formed against desomosomes

295
Q

Pemphigus vulgaris consequence

A

layers of skin separate and blisters form

296
Q

type III hypersensitivity

A

immune complex diseases

297
Q

type III hypersensitivity cause

A

antibodies formed against antigens leading to the formation of immune complexes

298
Q

3 possible factors precipitating type III HSR

A

Persistence of low grade microbial infection
Extrinsic environmental antigen
Autoimmune process

299
Q

type IV hypersensitivity

A

T cell mediated

300
Q

type IV hypersensitivity cause

A

tissue injury by T cell mediated response without formation of antibodies

301
Q

2 classes of type IV hypersensitivity

A

delayed type hypersensitivity

direct cell mediated cytotxicity

302
Q

delayed type hypersensitivity is characterized by ___

A

perivascular accumulation of CD4 T cells and macrophages

303
Q

TB test is what kind of HSR?

A

type IV

304
Q

hashimoto’s thyroiditis

A

condition characterized by autoimmune destruction of thyroid

305
Q

pathophysiology of hashitmoto’s

A

destruction of thyroid tissue by CD8 T cells and macrophages

306
Q

hashimoto’s symptoms

A 
Weight gain 
Fatigue 
Paleness or puffiness of face
Constipation 
Cold intolerance
Difficulty getting pregnant
Joint and muscle pain 
Hair loss
Depression
307
Q

central tolerance

A

antigen induced deletion of self-reactive T and B cells during maturation

308
Q

mechanisms of peripheral tolerance

A

anergy
suppression by Treg
activation induced cell death

309
Q

anergy

A

functional inactivation

310
Q

type II autoimmune disease

A

antibodies against cell surface or matrix antigens

311
Q

examples of type II autoimmune diseases

A 
autoimmune hemolytic anemia
immune thrombocytopenic purpura
Goodpasture's syndrome
pemphigus vulgaris
Graves disease
myasthenia gravis
312
Q

symptoms of autoimmune hemolytic anemia

A

fatigue
exertional dyspnea
palpitation

313
Q

autoantigen of autoimmune hemolytic anemia

A

RBC surface antigens

314
Q

autoimmune hemolytic anemia consequene

A

premature destruction of RBC by complement and phagocytes leading to anemia

315
Q

how do you diagnose autoimmune hemolytic anemia

A

Coombs test

316
Q

immune thrombocytopenic purpura autoantigen

A

platelet surface antigens

317
Q

immune thrombocytopenic purpura consequence

A

premature destruction of platelets

318
Q

Goodpasture’s syndrome autoantigen

A

non-collagenous domain of BM collagen type IV

319
Q

Goodpasture’s syndrome consequence

A

pulmonary hemorrhage

glomerulonephritis

320
Q

pemphigus vulgaris autoantigen

A

epidermal cadherin

321
Q

pemphigus vulgaris consequence

A

blistering of skin

322
Q

Grave’s disease autoantigen

A

thyroid stimulating hormone receptor

323
Q

Grave’s disease consequence

A

hyperthyroidism

324
Q

myasthenia gravis autoantigen

A

ACh R

325
Q

myasthenia gravis consequence

A

progressive weakness

326
Q

type III autoimmune disease

A

immune complex disease

327
Q

type III autoimmune disease examples

A

systemic lupus erythematosus

328
Q

systemic lupus erythematosus pathophysiology

A

autoantibodies form circulating immune complexes that deposit in tissues and cause a type III HSR

329
Q

systemic lupus erythematosus autoantigen

A 
DNA
histones
ribosomes
snRNP
scRNP
330
Q

systemic lupus erythematosus consequence

A

glomerulonephritis
vasculitis
arthritis
systemic inflammation

331
Q

type IV autoimmune disease

A

T cell mediated disease

332
Q

type IV autoimmune disease examples

A

type 1 diabetes
rheumatoid arthritis
multiple sclerosis
Sjogren syndrome

333
Q

type 1 diabetes autoantigen

A

pancreatic beta cell antigen

334
Q

type 1 diabetes consequence

A

beta cell destruction

335
Q

rheumatoid arthritis autoantigen

A

unknown synovial joint antigen

336
Q

rheumatoid arthritis consequence

A

joint inflammation and destruction

337
Q

rheumatoid arthritis treatments

A

anti TNF-a monoclonal antibodies

antibody dependent cell mediated cytotoxicity treatment

338
Q

multiple sclerosis autoantigen

A

myelin basic protein

proteolipid protein

339
Q

multiple scleorsis consequence

A

demyelination
brain degradation
paralysis

340
Q

Sjogren syndrome autoantigen

A

unknown antigens in ductal epithelial cells of exocrine glands

341
Q

Sjogren syndrome consequence

A

destruction of lacrimal and salivary glands

342
Q

what causes Sjogren sydnrome

A

CD4+ T cell reactions

systemic B cell hyperreactivity

343
Q

what is the dominant factor affecting susceptibility to autoimmune disease?

A

HLA

344
Q

sympathetic ophthalmia

A

physical trauma to 1 eye results in release of sequestered intraocular protein antigen –> T cell attack antigen in both eyes

345
Q

what is the most hazardous time for infant disease?

A

neonatal period

first 4 weeks of life

346
Q

congenital abnormalities

A

structural defects present at birth

347
Q

malformations

A

primary errors of morphogenesis

intrinsic abnormal developmental processes

348
Q

3 major causes of malformation

A

genetic
environmental
multifactorial

349
Q

Zika

A

severe malformations of the CNS

350
Q

rubella embryopathy

A

cataracts
heart defects
deafness
mental retardation

351
Q

what characterizes fetal alcohol syndrome?

A 
growth retardation
microcephaly
short palpebral fissures
maxillary hypoplasia
psychomotor disturbances
352
Q

what is associated with nicotine (teratogen)

A 
spontaneous abortions
premature labor
placental abnormalities
low birth weight
SIDS
353
Q

what does exposure of heavy doses of radiation during the period of organogenesis lead to?

A

microcephaly
blindness
skull defects
spina bifida

354
Q

incidence of malformations in diabetic mothers

A

6-10%

355
Q

what does maternal hyperglycemia-induced fetal hyperinsulinemia result in?

A

fetal macrosomia
cardiac anomalies
neural tube defects
CNS malfunctions

356
Q

multifcatorial causes

A

implies the interaction of environmental influences with 2+ genes of small effect
most common genetic cause of congenital malformations

357
Q

2 phases of intrauterine development

A

embryonic

fetal

358
Q

when is the embryo susceptible to teratogenesis?

A

btwn 3-9 weeks

peaks at 4 and 5

359
Q

what does valproic acid disrupt?

A

expression of HOX proteins- implicated in patterning of limbs, vertebrae, craniofacial structures

360
Q

syndactyly

A

fusion of digits

361
Q

polydactyly

A

extra digits

362
Q

what characterizes hand-foot-genital syndrome

A

distal limb and urinary tract malformations

363
Q

absence of all trans retinoic acid causes

A

many malformations including eyes, genitourinary, CVS, diaphragm, lungs

364
Q

excess of all trans retinoic acid causes

A

reinoic acid embryopathy- CNS, CVS, craniofacial defects

365
Q

prematurity

A

Infants born before completion of the normal gestational period or who have failed to grow normally during gestation have higher morbidity and mortality rates than full-term infants

366
Q

what defines prematurity

A

gestational age <37weeks

weight <2500g

367
Q

major risk factors of prematurity

A

Preterm premature rupture of placental membranes.

  • Intrauterine infection leading to inflammation of placental membranes
    (chorioamnionitis) .
  • Structural abnormalities of the uterus, cervix, and placenta (placenta previa, and abruptio
    placentae) .
  • Multiple gestation (twin pregnancy).
368
Q

what complications are premature babies vulnerable to?

A

 Respiratory distress syndrome of the newborn (RDS)
 Necrotizing enterocolitis (NEC)
 Intraventricular and germinal matrix hemorrhage
 Sepsis

369
Q

respiratory distress syndrome of the newborn cause

A

immaturity of the lungs

370
Q

main defect of RDS

A

deficiency of pulmonary surfactant leading to collapsed lungs, progressive atelectasis and reduced lung compliance resulting in a protein/fibrin-rich exudate in the alveolar spaces with the formation of hyaline membranes

371
Q

treatment

A

maternal steroids before birth

artificial surfactant

372
Q

Necrotizing enterocolitis presentation

A

abdominal distention
absent bowel sounds
bloody stools

373
Q

what do abdominal radiographs of infants with NEC show

A

gas within the intestinal wall (pneumatosis intestinalis)

374
Q

Germinal Matrix-Intraventricular Hemorrhage

A

Subependymal (germinal matrix) hemorrhage, with secondary bleeding into the ventricles

375
Q

SIDS

A

the sudden death of an infant under 1 year of age which remains unexplained after a thorough case investigation, including performance of a complete autopsy, examination of the death scene, and review of the clinical history

376
Q

most common findings in SIDS autopsies

A

petechiae on the thymus, visceral and parietal pleura, and epicardium

377
Q

most important modifiable risk factors in SIDS

A

prone sleeping position
sleeping on soft surfaces
thermal stress

378
Q

fetal hydrops

A

accumulation of edema fluid in the fetus during intrauterine growth

379
Q

causes of fetal hydrops

A

hemolytic anemia due to Rh blood group incompatibility between the mother and fetus (immune hydrops) and nonimmune hydrops

380
Q

immune hydrops

A

antibody-induced hemolytic disease in the newborn caused by blood-group incompatibility between mother and fetus

381
Q

causes of non immune hydrops

A

cardiovascular defects, chromosomal anomalies, and fetal anemia

382
Q

kernicterus

A

brain is enlarged and edematous and on cut section shows deposit of bright yellow pigment (bilirubin) particularly in the basal ganglia and brain stem

383
Q

2 types of hemangiomas

A

capillary

cavernous

384
Q

where are most hemangiomas located in children

A

skin- face and scalp

385
Q

von-Hippel-Lindau syndrome

A

autosomal dominant disorder with retinal angiomas, CNS hemangioblastomas, renal cell carcinomas; pheochromocytoma, tumors of the pancreas; endolymphatic sac tumors; and renal, pancreatic, and epididymal cysts

386
Q

Sturge Weber syndrome

A

congenital neurological and skin disorder associated with port-wine stains of the face, glaucoma, seizures, mental retardation, and ipsilateral leptomeningeal angioma (cerebral malformations and tumors)

387
Q

microscopic appearnace of lymphangiomas

A

cystic and cavernous spaces with pale fluid content lined by endothelial cells surrounded by lymphoid aggregates

388
Q

where do lymphangiomas mainly occur

A

deeper regions of the neck, axilla, mediastinum and retroperitoneum

389
Q

most common germ cell tumors of childhood

A

Sacrococcygeal Teratomas

390
Q

neuroblastoma defintions

A

tumor of the sympathetic ganglia and adrenal medulla

391
Q

how are neuroblastomas classified?

A

by neural differentiation

392
Q

Neuroblastoma

A

primitive stroma

393
Q

Ganglioneuroblastoma

A

primitive stroma and ganglion cells

394
Q

Ganglioneuroma

A

schwannian stroma and ganglion cells

395
Q

stage 1 Neuroblastoma

A

Localized tumor completely excised, with or without microscopic residual disease; representative ipsilateral non-adherent lymph nodes negative for tumor (nodes adherent to the primary tumor may be positive for tumor)

396
Q

stage 2A Neuroblastoma

A

Localized tumor with incomplete gross resection; representative ipsilateral non-adherent lymph nodes negative for tumor microscopically

397
Q

stage 2B Neuroblastoma

A

Localized tumor with or without complete gross excision, ipsilateral non-adherent lymph nodes positive for tumor; enlarged contralateral lymph nodes, which are negative for tumor microscopically.

398
Q

stage 3 Neuroblastoma

A

Unresectable unilateral tumor infiltrating across the midline with or without regional lymph node involvement; or localized unilateral tumor with contralateral regional lymph node involvement

399
Q

stage 4 Neuroblastoma

A

Any primary tumor with dissemination to distant lymph nodes, bone, bone marrow, liver, skin, and/or other organs

400
Q

stage 4S Neuroblastoma

A

Localized primary tumor (as defined for Stages 1, 2A, or 2B) with dissemination limited to skin, liver, and/or bone marrow (<10% of nucleated cells are constituted by neoplastic cells; >10% involvement of bone marrow is considered a stage 4). Stage 4S is limited to infants <1 yr.

401
Q

Children younger than ___ of age have a more favorable outlook for neuroblastomas

A

18 mo

402
Q

favorable histologic pattern of neuroblastomas

A

evidence of schwannian stroma or gangliocytic differentiation

403
Q

the greater the # of copies of ___ indicates a worse prognosis for neuroblastomas

A

N-myc

404
Q

what DNA ploidy is more favorable in neuroblastomas

A

hyperdiploid

405
Q

what mutations are unfavorable in neuroblastomas

A

ALK

406
Q

expression of. ___ is favorable in neuroblastomas

A

TrkA

407
Q

Approximately 40% of cases of retinoblastoma are associated with a germline mutation of the ___

A

RB1 gene

408
Q

retinoblastoma presentation

A

poor vision
strabismus
a whitish hue to the pupil (“cats eye reflex”)
pain, tenderness in the eye

409
Q

median age of presentation of retinoblastoma

A

2 years

410
Q

most common sites of metastases of retinoblastomas

A

central nervous system
skull
distal bones
lymph nodes

411
Q

Wilms Tumor

A

nephroblastoma

412
Q

Most cases of Wilms tumor occur in children between ages

A

2-5 years old

413
Q

WAGR syndrome

A

characterized by Wilms tumor, aniridia, genital anomalies, and mental retardation

414
Q

Denys-Drash syndrome

A

gonadal dysgenesis and renal abnormalities

extremely high risk for Wilms tumor

415
Q

Beckwith-Wiedemann syndrome

A

atients have an increased risk for the development of Wilms tumor
exhibit enlargement of individual body organs (organomegaly: tongue, kidneys or liver) or entire body segments (hemihypertrophy), and enlargement of adrenal cortical cells (adrenal cytomegaly)

416
Q

Beckwith-Wiedemann syndrome in an example of a disorder of ____

A

genomic imprinting

417
Q

genetic locus of Beckeith-Wiedemann

A

genetic locus is in band p15.5 of chromosome 11 distal to the WT1 locus

418
Q

___are precursor lesions of Wilms tumors

A

nephrogenic rests

419
Q

treatment of Wilms tumor

A

nephrectomy

chemotherapy

420
Q

benign pediatric tumors

A

hemangioma
lymphangioma
teratoma

421
Q

malignant pediatric tumors

A

neuroblastoma
retinoblastoma
wilms tumor

422
Q

first and second most common causes of neonatal mortality

A

congenital anomalies

prematurity

423
Q

RDS is most commonly observed in?

A

male preterm infants delivered by C-section

424
Q

what does RDS lead to?

A

increased surface tension
collapsed lungs
progressive atelectasis
reduced lung compliance

425
Q

fetal hydrops CV causes

A

malformations
tachyarrhytmia
high-output failure

426
Q

fetal hydrops chromosomal causes

A

turner syndrome
trisomy 21- down syndrome
trisomy 18- edward syndrome

427
Q

fetal hydrops infection causes

A

cytomegalovirus
syphilis
toxoplasmosis

428
Q

fetal hydrops fetal anemia causes

A

homozygous alpha-thalassemia
parvovirus B19
immunhydrops (Rh and ABO)

429
Q

what does parvovirus B19 attack

A

erythroblasts

430
Q

major causes of non immune hydrops

A
  • Cardiovascular defects

- Chromosomal anomalies - Fetal anemia

431
Q

capillary type of hemangioma

A

occurs in the skin, subcutaneous tissue, mucous membranes of the oral cavity and lips, liver, spleen and kidneys. Many instances they spontaneously regress

432
Q

cavernous type of hemangioma

A

less well circumscribed and more frequently involve deep structures
may be locally destructive and show no spontaneous tendency to regress, so surgery may be required

433
Q

cavernous hemangiomas are a component of ____

A

Hippel-Lindau disease

434
Q

Simple (capillary) lymphangiomas

A

composed of small lymphatic channels predominantly occurring in the head, neck, and axillary subcutaneous tissues

435
Q

Cavernous lymphangiomas (cystic hygromas)

A

typically found in the neck or axilla of children and rarely occur in the retroperitoneum

436
Q

what are cavernous lymphangiomas associated with?

A

turner syndrome

437
Q

what are neuroblastomas derived from?

A

derived from primordial neural crest cells that populate these sites

438
Q

blueberry muffin baby

A

in neonates
disseminated neuroblastomas may present with multiple cutaneous metastases with deep blue discoloration to
the skin

439
Q

overexpression of N-MYC is associated with ___

A

rapid tumor progression

440
Q

treatment of neuroblastomas

A

retinoids

inhibitors of ALK

441
Q

where is the RB allele located?

A

chromosome 13q14

442
Q

prognostic factors of retinoblastoma

A

stage of cnacer
age of pt
likelihood vision can be saved
size and # of tumors

443
Q

retinoblastoma treatments

A 
enucleation
radiation
cryotherapy
thermotherapy
chemotherapy
444
Q

wilms tumor presentation

A

huge, palpable flank mass

hematuria

445
Q

anaplasia

A

Presence of cells with large, hyperchromatic, pleomorphic nuclei and abnormal mitoses

446
Q

what causes wilms tumor

A

Deletion of tumor suppressor gene WT1 on chromosome 11.

MAMS (8 decks)

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