Exam 1 Flashcards
1
Q
Adeno
A
granular
2
Q
Lei
A
smooth
3
Q
Rhabdo
A
skeletal
4
Q
Anaplasia
A
lack of differentiation
5
Q
Dysplasia
A
disordered growth
- reversible
- increased mitotic figures
6
Q
Malignancy- 6 requirements
A
- acquire self growth signals & turn off inhibitory signals
- evade apoptosis
- deficits in DNA repair
- unlimited dividing
- promote angiogenesis
- invade surrounding tissue
7
Q
Inhibitors and Promoters
A
Inhibitors- damage and mutate
Promotors- increase cell number by cell cycle
8
Q
Protooncogenes and oncogenes
&
Mechanism (TAPO)
A
Protooncogenes= normal cell growth by division
When ON= bad:
Oncogenes= further divide bad cells= produce neoplasm
T- translocation
A- amplification
P- point mutation
O- overexpression
9
Q
Tumor suppressor genes
A
When OFF= bad (uncontrolled growth)
slow down cell growth
10
Q
Cytokines
A
Produced by tumor
Leads to Cachexia= loss of body fat and muscle
signaling and communication
11
Q
Paraneoplastic syndromes
PASE
A
“Stop” this is not what I am !
side effect not usually associated with cell type tumor
Parathyroid- hypercalcemia
ACTH- Cushing’s syndrome- hypercortisolism
SIADH
Erythropoietin
12
Q
Tumor markers
A
CEA- colon & pancreatic AFP- liver B-HCG- chorio CA-125- ovarian S-100- melanoma Alkaline- bony
13
Q
Grade
A
differentiation
14
Q
Stage
A
size and how far it has spread
0= in situ 4= spread
15
Q
TNM scale
A
Used in staging
16
Q
Ecto
A
epidermis epithelium eyes mouth nails nose
(outer)
17
Q
Epithelium
A
covers surfaces of any organ- ecto, meso or endo origin
18
Q
Meso
A
connective tissue muscle bone fat cardiovascular lymph system
(middle)
19
Q
Endo
A
GI
Respiratory
(outer)
20
Q
Embryonic stem cells
A
blastocytes
21
Q
Adult stem cells
A
various tissues
22
Q
Stroma
A
supportive tissue
23
Q
Parenchyma
A
functional tissue
24
Q
Connective tissue
A
meso
dense= ligaments, fascia, tendons loose= areolar- swelling
25
N in TNM
N w a= no metastasis
| N w b= met
26
Fibrosis
excess fibrous connective tissue
27
Degeneration
reversible
28
Fatty degeneration
steatosis
29
Atrophy
```
not immediately lethal
Symmetric- old age, reduced blood supply
Asymmetric-
decreased workload
nutritional deficiencies
low level injury
neuro endocrine
```
30
Necrosis
follows irreversible cell and tissue injuries (coagulation of intracellular proteins)
Coagulative- normal protein
Liquefaction- poor protein
31
Inflammation
vasodilation &
Histamine and NO released= increased hydrostatic pressure by decreased blood flow
increased permeability
Histamine and Leukotrines released
Fluid crosses tissue- increased protein in tissue- increased osmatic pressure in tissue= decreased osmatic pressure in blood
= WBCs accumulation at the site (chemotaxis)
32
Acute inflammation
exudative fluid and protein
| neutrophils= main cell
33
Acute cell mechanisms
1. Endothelial contraction- short lived, immediate
2. Endo... retraction- long lived, rearrangement of cytoskeleton
3. Direct injury- all vessels- necrosis
4. Delayed prolonged
5. Leukocyte- increased bacterial- damage vessel wall permeability
34
Transmigration of WBC movement
platelet cell mediated
35
Leukocytes
= opsonin, IgG, C3b, collectins
36
Killing done by
Decreased NADPH oxidase--> hydrogen peroxide
(bacteria)
Myeloperoxide--> HOCL
(lipid and protein peroxidation)
37
Chronic inflammation
proliferation of new capillaries and fibroblasts (produce collagen and scarring)
lymphohistiolytic infiltration w increasing fibroblasts= granulation tissue
If t cell dominant= granuloma (collection of macrophages)
ex Tb
38
Chronic inflammation
Lymphocytes and macrophages
lymphoytes- collagen and scarring
| macrophages- proteases- try to eliminate invader
39
Regeneration
no scar- regeneration
40
Healing
scar- replacement of damage tissue
41
Replacement by scar time frame
3-5 days granulation tissue
week 2- collagen deposition continues
1 month- collagen starts to strengthen
42
Steps of repair
```
inflammation
clean up
new blood vessels
collagen
tissue remodeling
wound contracture
increase wound strength
```
43
mediators of repair
platelets- smooth m
| transforming- inside out wound healing
44
IgA
mucosa
45
IgE
allergic
46
IgM and IgD
on B cells
47
Cells involved in immunology
lymphocytes and macrophages- "flags" for T cell recognition (opsonization)
48
Ab binds to __ of Ag
epitope
49
Anamnestic response (humoral)
memory
| efficiency
50
Humoral
Ag activates B cells
| non self recognition activation
51
Complement
= proteins circulating
makes APC
activated by Ag-Ab binding to RBC or bacteria
52
Classic vs alternative
classic- ab
| alternative- no ab
53
Complement C3
promotes phagocytosis, cell lysis and inflammation
inserts MAC membrane attack complex- cannot eject Ca= lysis
calls macrophage for phagocytosis and opsonization
54
Natural killer cells
from stem cells
no receptors like other lymphocytic cells
cytokine production
55
Interferon
Innate
nonspecific and spontaneous
attract macrophages and natural killer cells
56
T helper (cd4)
primed by APC
lymphokines released- attract neutrophils'
cytokines
57
Activation cell mediated
T cell binds Ag presenting MHC
58
MCH1 and 2
1- all cells except blood, self- cytotoxic activated
| 2- each other in immune system- helped activated
59
HLA
all except RBCs and trophoblasts
60
HLA B27
ankylosing spondylitis
61
ELISA
Ab testing
| using known- if binding = +
62
Immunoelectro.
Ig identification
| M spike- multiple myeloma and mgus
63
Mono
IgM
64
immunophenotyping/cytogenetics
flow cytometry
| quantitate cell
65
ana
autoimmunity
66
Ig overproduction
Multiple myeloma- increased plasma, decreased Ab
Bence-jones proteins
MGUS
67
HIV
advantage of decreased CD4s and increased viral load
68
RA
MHC 2 or HLA
| macrophage produces tumor necrosis factor- fill joint spaces
69
Lupus
IgG, IgM- kidney filtration, skin manifestation (clog)
ANA (-)
Anti dsDNA
70
Myasthenia gravis
self reactive ab binds to ach receptor
= muscle weakness and paralysis
Gillian barre down- up
clostrodium up- down
71
hypersensitivity
1. Immediate, IgE, increased vas perm- edema & smooth muscle contraction
2. Ab, IgM, IgG cascade- destruction of cell w ag
3. Immune complex- deposit in organs= damage
4. Delayed- T lymph, transplant rejection
72
Cytokine storm
excessive cytokines (proinflammatory)
73
graft and host disease
body attacks cells from a transplant
74
Types of cytokines
interleukins (il1 and il6)
chemokines- leukocyte recruitment
colony stimulating- cell proliferation
tumor necrosis factor- activates cytotoxic t cells
75
il1 and il6
il1- acute phase reactants- dendritic cells
il6- acute... and Ig synthesis- T cells, endothelial
76
Storm pathology
inflammation
edema- extravascular pressure increases, decrease tissue perfusion
ali (acute lung infection)
release of TNF and il1 --> more sustained il6 level
77
Storm symptoms
hypotension
| tachycardia
78
ARDS
increased permeability tissue edema
increased cytokines-
direct 1 injury to lung epithelium
direct to pulmonary capillary
79
ARDS cause
aveolar epithelial barrier damage= fluid leakage into lungs --> dysregulated response and aveolar macrophages
il1, il6, TNF, il8 into lungs and further proinflammatory effect-- neutrophils & monocytes -- more leakage of barrier = fluid filled lungs= no O2
80
ARDS symtoms
tachypenea (breathing out more CO2 than O2 going in)- decrease drive to breath due to decrease CO2
cyanosis (decreased O2 profusion)
81
Covid 19 drugs
Remdisivir- protease inhibitor
slows replications, decrease viral load
Dexamethasone-
decrease inflammation response
82
Jak1 and Jak2
Janus kinase inhibitors
block inflammation used for autoimmune conditions
with remdisivir= improved outcomes if high O2 required and no vent
83
Il6 inhibitors
Actemra
Kevzara
used to regulate storm (downgrade)
84
Il1 inhibitors
Kineret (receptor anatgonist) inhibits il1- decreased need for ventilation and decrease mortality
