final studying Flashcards
(138 cards)
1
Q
autolysis
A
cell dissolution often by enzymes released from the cells themselves.
2
Q
pykorrhexis
A
nucleus shrinks, basophilic (blue/purple stain)
3
Q
karyorrhexis
A
fragmentation
4
Q
karyolysis
A
nucleus fades away, due to DNA nucleases
5
Q
main points of necrosis
A
increased eosinophilia (pink stain) due to denatured proteins
3 Nucleus patterns
autolysis
6
Q
coagulative necrosis main points
A
INFARCTS in SOLID ORGANS (not brain)
architecture is still visible
firm texture
cells own enzymes are denatured on the inside
7
Q
liquefactive necrosis
A
CNS INFARCTS (stroke) - brain
tissue liquifies
seen in bacterial and fungal infections
8
Q
caseous necrosis
A
IN GRANULOMAS (TB)
cheese-like
fragmented or lysed cells
no architecture
-body just walls off the problem and it is cut off from resources
9
Q
fat necrosis
A
TRAUMATIC INJURY to FATTY AREAS
or RELEASE OF PANCREATIC enzymes
lipolysis
phagocytes contain lipids
pancreatic = saponification (ca++ deposits)
10
Q
fibrinoid necrosis
A
IMMUNE COMPLEX DEPOSITION
fibrin-like appearance
damage in vasculature and kidneys
11
Q
how is embryogenesis related to apoptosis
A
Embryogenesis forms new structures, and apoptosis fine-tunes them, ensuring only the necessary and healthy cells survive to complete the organism’s development.
12
Q
steps of apoptosis
A
condensation of chromatin and blebbing of membrane
fragmentation creates apoptotic bodies - no spilling
phagocytes engulf apoptotic bodies that send out “eat me” signals
13
Q
what is the enzymes that drive apoptosis
A
caspases
14
Q
autophagy
A
digestion of cell’s own contents
Autophagy is a cellular process where a cell degrades and recycles its own components to maintain cellular homeostasis and provide nutrients during times of stress. - survival mechanism
15
Q
autophagy vs autolysis
A
Autophagy is a regulated, protective process used by living cells to maintain health and adapt to stress.
Autolysis is a destructive, uncontrolled process that happens after cell death, usually contributing to damage in surrounding tissues.
16
Q
5 cardinal signs in medical terms
A
calor - heat
rubor - Redness
tumor - swelling
dolor - pain
Virchow - LOF
17
Q
the complement component C5 and LTB4 is involved in what when it is activated
A
chemotaxis
18
Q
IgG antibody and C3 from the complement system and collectins are all considered what
A
opsonins
19
Q
what is elastase and what is it typically used for
A
protease enzyme that breaks down elastin, a key protein in connective tissue that gives it elasticity.
used in extracellular defense against foreign materials
20
Q
what do AMPs do in the gut
A
disrupt bacterial, fungal, and viral membranes, leading to cell lysis
21
Q
what is the last resort for cell defense
A
NETS: cell extrudes its nucleus to trap the problem and the cell releases enzymes that kill the bacteria
22
Q
what AA does COX make
A
prostaglandins and thromboxanes
23
Q
what is the action of prostaglandins and thromboxanes
A
All the TWOS: PGI2, PGD2, PGE2, TXA2
24
Q
what does PGI2 and which is opposite to this one?
A
vasodilation, inhibits platelet aggregation
TXA2
25
what does PGD2/PGE2 do
vasodilation and vascular permeablity
26
what AA does 5-lipoxygenase make
leukotrienes
27
what is the products of leukotriens
ALL the L4's
LTB4, LTC4,LTD4, LTE4
28
LTB4 is unique for what
chemotaxis
29
LTC4,LTD4, and LTE4 all do what
bronchoconstriction, increased vascular permeability
30
what AA does 12-lipoxygenase make
lipoxins
31
lipoxins do what action
inhibit chemotaxis of neutrophils, inhibit adhesion
32
steroids inhibit what part of the AA pathway
phospholipases that make AA = blocks all AA production
33
NSAIDs inhibit what part of the AA pathway
inhibit COX enzymes = no prostaglandin production = no pain or fever
34
what are the 2 kinds of COX inhibitors
COX 1 and COX2
35
COX1 is unique for what
its always on at low levels
36
COX2 is unique for what
blocks only harmful inflammation, but increases vasoconstriction = risk of stroke
37
PAF comes from where
membrane phospholipids of neutrophils, monocytes, basophils, endothelial cells and platelets
38
what is the action of PAF
through GPCR:
stimulates bronchoconstriction
vasodilation
vascular permeability
stimulates platelets
39
NO is produced from what
macrophages
40
name the 3 lysosomal enzymes
elastase, collagenase, cathsepsin
41
where are neuropeptides produced
secreted from nerve fibers (lung and GI tract)
42
what is the action of neuropeptides
transmit pain signals, regulate vessel tone and permeability
43
what are the 3 plasma-derived mediators that are all intertwined
complement, coagulation system, kinin system
44
C3a and C5a of the complement system both cause what
they are anaphylatoxins = cause mast cells to release histamine = vasodilation and vascular permeability
45
what does C3b in complement do
opsonization
46
C3a, C4a, and C5a all do what
recruit and activate WBCs
47
C5b-C9 all do what
forms MACs and lyses microbes
48
what is the important factor in the coagulation cascade
hageman factor 12
49
hageman factor ultimately results into what effect
prothrombin to thrombin: makes fibrin clot and cleaves C5 into C5a
Xa activation: increases vascular permeability and recruits WBCs
50
fibrinolytic system converts what to what
plasminogen to plasmin
51
what does the production of plasmin activate
complement system since plasmin cleaves C3 into C3a
52
the kinin system activates what system
fibrinolytic and coagulation
53
how does the kinin system activate the coagulation cascade
converts kininogen to kallikrein which activates hageman factor
54
how does the kinin system activate the fibrinolytic system
produces kallikrein which degrades plasminogen to plasmin which activates the fibrinolytic system.
55
what is the overall process of the kinin system
converts HMW kininogen to bradykinin = pain
and produces kallikrein which is chemotactic and activates hageman factor
56
which cytokine are involved in acute phase response
TNF, IL-1, IL-6, and acute phase proteins from liver
57
what are the main acute phase proteins involved in APR
CRP, fibrinogen, SAA
stimulated by IL-6
58
what is the role of the acute phase proteins
act as opsonins and induce complement
59
explain the CRP test to detect high levels of APR
measures Levels of CRP, an acute-phase protein made by the liver.
High levels = active inflammation or infection.
60
explain the ESR (fibrinogen) test to detect high levels
measure How fast red blood cells settle in a test tube over 1 hour.
Increased fibrinogen and other acute-phase proteins make RBCs clump → settle faster.
So a high ESR = presence of inflammation.
61
what are the two systemic effects, explain
Fever: pyrogens increase COX enzyme production which stimulate the prostaglandin production in the hypothalamus
Pyrogens (things that cause fever):
- exogenous (LPS) and endogenous (IL-1, TNF)
Leukocytosis: release of WBCs from bone marrow
- IL-1 and TNF promote the release of WBC from bone marrow, shift to the left
62
what are the cytokines involved in chronic inflammation that are new
IL-12, IFN-gamma, IL-4,, IL-5, IL-13
63
using what cytokines do helper T cells recruit other cells
IFN-gamma: activates macrophages
IL-4,IL-5, and IL-12 recruit and activate eosinophils
IL-17: recruit monocytes and neutrophils
64
what do eosinophils target
parasitic infections and chronic inflammation in allergic reactions
65
what are the two fates of macrophages in granulomatous inflammation
become an epitheloid cell: secrete cytokines
fuse mulitple macrophages together to form a giant cell
66
what are the two types of ECM
interstitial and basement membrane
67
what are the 3 components of the ECM
fibrous, gels, glycoprotein
68
what is the fibrous component made up of
collagen and elastin
69
what is the gel component made up of
proteoglycans and hyaluronan
70
what are the 3 glycoproteins of the ECM
fibronectin, laminin, integrins
71
what are the 3 basic steps of scarring
1) angiogenesis
2) migration and proliferation of fibroblasts and new connective tissue
3) maturation and organization of fibrous tissue
72
what are the growth factors that promote ECM
TGF-beta: collagen, fibronectin, proteoglycan production
PDGF: bring fibroblasts in
FGF-2: proliferation of endothelial cells, bring fibroblasts and macrophages in
cytokines: IL-1 and IL-3: collagen synthesis from fibroblasts and proliferation/migration
73
what do MMPs do
degrade the ECM to help manage disorganized ECM production
74
what GF do the opposite of MMPs
TGF-beta
PDGF
TIMPS (inhibit MMPs)
75
define organization
fibrosis in tissue filled with inflammatory exudate
76
defin keloid
excess collagen deposition in scarring/healing
77
what are the new cytokines in chronic inflammation
IL-4,5,13,17, and IFN-gamma
78
what does IL-1 and IL-13 do in scar healing
collagen synthesis and proliferation
79
what does TGF-B do in scar healing
make collagen
80
what does PDGF do in scar healing
migration and proliferation of fibroblasts
81
what does FGF-2 do in scar healing
proliferation of endothelial cells
82
IL-2 does what?????
Clonal Expansion of B-cells and T-cells
83
what are the cytokines involved in adaptive immunity
IL-2, 4, 6, 10, IFN-gamma (all stimulate differentiation into APC's for B cells)
84
what are the cytokines involved in hematopoiesis
GM-CSF, G-CSF, M-CSF, IL-3
85
explain mechanism for Azathioprine drug
inhibits cell division of Th cells and CTL's
86
explain mechanism for Cyclosporin A drug
inhibits CTL clonal expansion
87
explain mechanism for Tacrolimus drug
Makes T helper cells = silent
88
explain mechanism for Rapamycin
interfers with IL-2 = no clonal expansion
89
explain mechanism for Biologics
antibodies produced against T helper cells
90
IL-4, IL-6, IL-10, and IFN - gamma all do what
stimulate differentiation into antibody-producing cells
91
define central tolerance
self reactive B and T cells are deleted early on = apoptosis
92
define peripheral tolerance
self reactive T cells that escape the thymus are stopped by:
Anergy = pull in receptors
Suppression
Apoptosis
93
what are the 4 mechanisms of developing autoimmunity
loss of seclusion
alteration of tissue antigens (injury)
exposure to similar antigens with bacteria
impaired T cell regulatoin
94
autoimmune diseases are more common in who
women
95
what is the genetic predisposition of SLE
HLA DR2, DR3
96
what are the 3 primary immune deficiencies mentioned in class
SCID
DiGeorge syndrome
Bruton
97
define SCIDs
no antibodies and no Tc response
ADA deficiency = build up of A and dATP = kills lymphocytes
Common gamma chain defect = defective cytokine receptor = no communication or proliferation
98
define DiGeorge syndrome
lack of thymus development
Deletion in C22
99
define Brutons Disease
X-linked ammaglobulinemia = no antibodies
pre-b cells fail to mature and get to blood
100
what is the one secondary immune deficiency talked about
AIDS
101
what does serological testing look for
antibody/antigen interactions between donor and recipient
102
Graft vs host disease, what attacks what
donor attacks recipient
103
platelets stick to endothelium through what
von willebrand factor
104
platelets stick together through what receptor
Gplb
105
thrombin activates what that cleaves what
PAR that cleaves fibrinogen to fibrin = clot
106
the Gplb receptor causes what disorder
Bernard-syndrome
107
the Gpllb-IIa receptor causes what syndrome
glanzmann thrombasthenia
108
name the 3 anticoagulation systems
antithrombin, protein C and protein S, TFPO
109
what are the two common inherited disorders with a risk of thrombosis
Factor V-leiden mutation
Prothrombin mutation
110
rate inherited disorders with risk of thrombosis
antithrombin III
protein C deficiency/resistance
fibrinolytic pathway disorders
111
name the risks factors for thrombosis
taking oral contraceptives = estrogen causes liver to produce more clotting factors
increase in Vitamin K
malignancy
112
define HIT syndrome
patients are treated with heparin for anticoagulation, they end up making autoantibodies that bind heparin and platelet membranes = chronic inflammation
113
define Antiphospholipid antibody syndrome
autoantibodies that cause endothelial injury
114
pulmonary embolism starts as what
DVT = in knee pit
115
what is the most common systemic emboli
thromboembolism, source is left side of the heart
they lodge in other areas
116
define stable angina
pain upon effort
117
define unstable angina
pain upon rest
118
response to injury hypothesis is describing what
atherosclerosis
119
define arteriosclerosis
hardening of arteries
120
define atherosclerosis
occurs in large arteries
thickening of the innermost layer of arteries
121
steps of arteriosclerosis
fatty streaks
atherosclerosis
122
what is in the fibrous cap of vessels
smooth muscle cells, collagen, elastin, proteoglycans
123
what is in the necrotic center of atherosclerosis
cell debris, foam cells, calcium
124
atherosclerotic core contains
foam cells, collage, Ca2+ deposits
125
describe what is happening in foam cells
The macrophages take up the LDL through a process called phagocytosis, but because they can't process the excess lipids efficiently, the cholesterol accumulates inside the cell, making it appear foamy or filled with lipid material.
126
what are the steps of response to injury hypothesis
1) chronic endothelial injury
2) accumulation of lipoproteins - oxidized LDL build up
3) platelet adhesion - attracted to the damage
4) monocytes get involved and migrate to the intima
5) lipid accumulation in macrophage (foam cells)
- causes release of cytokines and crease of ROS = more LDL oxidation
6) smooth muscle recruitment from media
- building the cap
127
is atherosclerosis more common in males or females
males
128
HDL decreases what, and LDL increases it
risk for atherosclerosis
129
familiall hypercholesterolemia has a loss of function in what
ApoB which helps LDL bind to the receptor
130
What two cell surface proteins are necessary for HIV to enter a cell?
CD4 and chemokine receptor
131
what are the translocations cancers
Burkitts lymphoma
Follicular B cell lymphoma
CML
132
burkitts lymphoma has a translocation with what gene
MYC
133
Follicular B cell lymphoma has a translocation with what gene
BCL2
134
CML is causes by what translocation and what is the name for the chromosome and what chromosomes
chromosome 9 and 22
creates BCR-ABL mutant
philadelphia chromosome
135
what are the gene amplification cancers
NMYC neuroblastoma
ERBB2 breast cancer
136
within epigenetics methylation occurs where specifically
histones and DNA
137
Burkitt's lymphoma does what with B cells
attaches them through CD21 = causes proliferation and progresses in cancer
138
