Neoplasms Flashcards
(143 cards)
1
Q
neoplasm
A
new tissue, tumor, mainly cancers
2
Q
neoplasia
A
new growth
3
Q
cancer
A
malignant tumor
4
Q
where do neoplasms come from?
A
normal tissue that can proliferate
5
Q
how many mutations have to occur in a cell for a change to occur?
A
two
6
Q
fibroma
A
from fibroblasts
7
Q
lipoma
A
adipose
8
Q
adenoma
A
exhibits gland patterns or from adrenal glands
9
Q
chondroma
A
cartilaginous
10
Q
leiomyoma
A
smooth muscle
11
Q
myoma
A
regular skeletal muscle
12
Q
papilloma
A
epithelial growth on surface, finger like fronds
13
Q
how are benign neoplasms named?
A
beginning of word tells you where its coming from, and always ends in ‘oma’
14
Q
sarcomas, carcinomas, adenocarcinomas, teratoma, melanoma, hematopoietic invade adjacent tissue metastasize wide range of differentiation kills host not encapsulated goes from one tissue to another does not look like the tissue that is supposed to be there
A
malignant neoplasms
15
Q
from mesenchymal tissue (liposarcoma, fibrosarcoma, osteosarcoma); mesoderm (middle layer)
A
sarcomas
16
Q
from epithelial cells; ectoderm (surface)
A
carcinomas
17
Q
glandular growth/gland association
A
adenocarcinomas
18
Q
made of cells from more than one germ layer; come from the stem cells and can grow into anything
A
teratoma
19
Q
coming from melanocytes (cells in your skin that give color or freckles) start to grow out of control and end up with patchy tumors
A
melanoma
20
Q
blood cells; leukemia
A
hematopoietic
21
Q
remain localized, don't metastasize grows as a cohesive unit tend to become encapsulated well differentiated not deadly looks like the tissue cell that is supposed to be there
A
benign neoplasms
22
Q
we have this wide arrange of differentiation or no differentiation at all
A
anaplasia
23
Q
increase in size but not in number
still the correct type of cell
ex: pregnant, cardiovascular disease
A
hyperplasia
24
Q
replacement of one cell type with another
better adapted to altered environment
ex. ppl w acid reflux
A
metaplasia
25
```
disordered growth
loss of uniformity
loss of architectural orientation
metastasize
many different cells type show up
```
dysplasia
26
any sort of chemical that can cause cancer
can be called mutagen
but not all of _____ are mutagen and vice versa
carcinogen
27
what must happen for cancer to occur?
mutate DNA twice
28
what two types of cancers are associated with viruses?
cervical carcinomas (HPV) and hepatomas (liver cancers, hep C)
29
any sort of gene that's in the DNA that will lead to the development of a cancer
oncogene
30
how do tumor viruses cause cancer?
by the interaction between carcinogen and endogenous viruses
31
```
#1 on the outside, you have this extracellular domain and that's where the signal binds
#2 domain that goes through the membrane - transmembrane domain
#3 on the inside, there's kinase
```
growth factors - start of the signal cascade
32
enzyme that phosphorylates and activates the protein and changes its shape
kinase
33
what happens to mutated receptors?
changes kinase domain of growth factor so it no longer needs the signal and can activate itself
34
how many cells produce and stimulate growth factors and how are they related?
```
two cells (epithelian and mesenchymal)
one will produce some of the growth factors and go to the other cell to be activated and/or vice versa
```
35
what happens to these cells in a cancer cell?
a cancer cell that produces the signal will also produce the receptor thus it can activate itself
36
autocrine signaling
self signaling
37
what is G1 preparing for?
S phase
38
S phase
synthesizes (makes two copies of) DNA
39
after S phase
G2
40
what is G2 preparing for?
mitosis (inphase)
41
how much time in G1?
12-15 hrs
42
how much time in S phase?
6-8 hrs
43
how much time in G2?
3-5 hrs
44
how much time inphase (Mitosis)?
1 hour for cell to divide into two
45
how long does it take for a cell to divide?
1 day
46
why do we need checkpoints?
stops cell from going through cycles and makes sure we have all the enzymes and proteins to go through with
47
what does the check point in S phase used for?
it checks for DNA damage and stops everything and causes cell to kill itself if damaged
48
what does the check point in G2 used for?
it makes sure that the DNA is replicated
49
what is the R point?
restrictive point will determine whether cell cycle will go all the way through or not
50
what do CDKs depend on?
presence of kinase
51
why are cyclins important and how many are there?
this is how the cell knows it should be in a specific cycle; 4 (DEAB)
52
around G1 then it goes away
D
53
at the end of G1 and beginning of S phase after that it goes away
E
54
middle of S phase and goes away towards beginning of G2
A
55
is around in G2
B
56
CDK 4/6
D and G1
57
CDK 2
E
58
CDK 1
A and B
59
where is the R point?
at the end of CDK 4/6 and D and this is the point that will determine whether the DNA will be synthesized
60
what is the protein that controls the R point?
retinoblastoma, Rb
61
what does Rb do?
it causes CDK 4/6 to go away and process continues
62
guardian of the genome - makes sure that there are no other mutations in the DNA
initiates cell death
p53
63
a cell that is cancerous we say that the cell has been ______
transformed
64
```
contact inhibition loss
foci development
altered shape
ability to grow in low serum
immortal
anchorage independence
tumorigenicity
```
transformed characteristics
65
how can cancer make new blood vessels form?
through angiogenesis)
66
first line of defense
second line of defense
defenses against any pathogen
not specific
innate immunity
67
third line of defense
immunity or resistance to a specific pathogen
specific response --> going to be a lot stronger
has memory
slower to respond
adaptive immunity
68
intact skin
mucous membranes and their secretions
normal microbiota
first line of defense
69
phagocytes (neutrophils, eosinophils, dendritic cells, macrophages)
inflammation
fever
antimicrobial substances
second line of defense
70
specialized lymphocytes: T cells and B cells
| antibodies
third line of defense
71
ability to ward off disease
immunity
72
keratinized epidermis (consists of tightly packed cells)
replaced every 4-5 days
dry environment
no blood vessels
skin
73
sebum (oil)
sweat (viscous)
organic acids (lowers pH)
glands
74
transports microbes trapped in mucus away from lungs
ciliary escalator
75
washes eye
lacrimal apparatus
76
dilutes and washes microbes off
saliva
77
flows out
urine
78
flow out and low pH
vaginal secretions
79
in perspiration, tears, saliva, and urine
| an enzyme that breaks down bacterial cell wall
lysozyme
80
microbial competition (competing w pathogens)
normal microbiota
81
```
one organism (microbe) benefits, the other (host) is unharmed
may be opportunistic pathogens
```
commensal microbiota
82
part of the immune system, a series of proteins made to fight bacteria/infections
complement system
83
increased in numbers at start of infection, most abundant
neutrophils
84
present in all tissues, important in presenting antigen to adaptive immune
dendritic cells
85
10-15% of lymphocytes in peripheral blood
lack antigen specific receptors
attack whatever but kill tumor cells and virally infected cells
natural killer cell
86
10-15% of lymphocytes in peripheral blood
lack antigen specific receptors
attack whatever but kill tumor cells and virally infected cells
natural killer cell
87
redness, swelling, pain, heat, loss of function
inflammation
88
1. destroy injurious/infecting agent, remove it and its products - vasodilation
2. limit the effect of agent by confining - not letting it spread - phagocytose
3. repair or replace damage tissue - start the repair process - repair
inflammation steps
89
in fever, which endotoxin does gram negative bacteria cause phagocytes to release ?
IL-1 and TNF a ; they instruct the hypothalamus to increase internal temperature
90
what does the hypothalamus release that resets the hypothalamus to a high temperature
prostaglandins
91
increases transferrin
increases IL1
produces interferon
advantages of fever
92
tachycardia
acidosis (pH of blood goes down)
dehydration
106 dg C
disadvantages of fever
93
cause cell to produce antiviral proteins that inhibit viral replication
IFNa and IFN b
94
causes neutrophils and macrophages to phagocytize bacteria; puts a little tag on bacteria
IFNy
95
IFNa IFNb IFNy
interferons
96
binds iron
transferrin
97
inhibits microbial growth by inhibiting cell wall, forms pores in membranes and destroys DNA and RNA
non-antibody proteins that attack and destroy bacteria
antimicrobial peptides (pt of complement system)
98
what are the two complement proteins?
C3 and C5
99
what causes pores to be formed in the membrane, part of the flagging mechanism so that macrophages and neutrophils find the offending agent
C3B
100
activates other sorts of neutrophils and WBC to hunt down microbes present in the area; need to be cut in half
C3
101
is activated via C3 in order to bring those macrophages and neutrophils to kill offending agent
C5
102
coats microbes for phagocytosis and complement activation
elevated plasma levels
beginning of an infection
tagging mechanism
c-reactive proteins
103
releases antibodies in order to do something; pathogens outside of the cell
humoral; B cells
104
specifically use cells to attack things with antibodies; trying to control antibodies by attacking cell; pathogens inside the cell
cellular; T cells
105
where do B and T cells mature?
B in bone marrow, T in thymus
106
a substance that causes the body to produce specific antibodies or sensitized T cells
antigen
107
what do antibodies interact with?
epitopes
108
globular proteins called immunoglobulins
| number of antigen-binding sites determines valence (how many epitopes present)
nature of antibodies
109
protein with 2 heavy chains and 2 light chains
constant region
variable region
antibody structure
110
how many immunoglobulins are there?
5 )GAMED)
111
```
monomer
2 epitope binding site
80% of serum antibodies
neutralize toxins
23 days
```
IgG
112
```
dimer
4 epitope binding sites
10-15% of serum antibodies
secretions, mucosal protection
6 days
```
IgA
113
```
pentamer
10 epitope binding sites
5-10% of serum antibodies
agglutinate microbes
5 days
first to show up in adaptive immune response
```
IgM
114
```
monomer
2 epitope binding site
0.2% of serum antibodies
B cells, innate immune response
3 days
```
IgD
115
monomer
0.002% of serum antibodies
allergic rxn, lysis of parasitic worms
2 days
IgE
116
where are B cells sitting?
lymph nodes
117
antigen presented Th cell
| Th cell produces cytokines
T dependent antigens
118
stimulate the B cell to make antibodies
| antigen/epitope randomly bumps into a cell and causes activation to occur
T independent antigens
119
what do B cells differentiate into?
plasma cells and memory cells
120
what eliminates harmful B cells?
clonal deletion
121
what do B cells do?
```
agglutination
opsonization
activation of complement
neutralization
antibody dependent cell mediated cytotoxicity
```
122
macrophages, Tc Cells, natural killer cells
T Helper (1) cell
123
eosinophils, IgM and IgE
T helper (2) cell
124
destroys target cell on contact
cytotoxic T lymphocyte
125
regulates immune response and helps maintain tolerance
T regulatory cell
126
attacks cancer cells
activated macrophage
127
destroys target cells (virus infected, tumor cells)
participates in antibody dependence
cell mediated cytotoxicity
granular leukocytes destroy cells that don't express MHC I
natural killer cells
128
what are the three antigen presenting cells ?
dendritic
macrophage
B cell
129
viral pathogens and allergens; all throughout the body
dendritic
130
intracellular and extracellular pathogens; mainly bacteria
macrophage
131
recognize viruses and pathogens
B cell
132
what is the pedestal where the bacteria is presented?
MHC II
133
CD4+
TCR recognize antigens and MHC II
produce cytokines and differentiate
T Helper Cells
134
CD8+
endogenous antigens
releases perforin and granzymes
carry their own antigens
T cytotoxic cells
135
stops autoimmune responses
T regulatory cells
136
situation where we have a foreign thing inside of us that is too big to be phagocytosed - coat it with antibodies
antibody dependent cell mediated cytotoxicity (ADCC)
137
amount of antibody in the serum
antibody titre
138
occurs after initial contact with the antigen
primary response
139
occurs after second exposure
secondary (memory or anamnestic) response
140
adaptive immunity resulting from infection
naturally acquired active immunity
141
adaptive immunity resulting from transplacental or via colostrum
naturally acquired passive immunity
142
adaptive immunity resulting from injection of antigen (vaccination) itself
artificially acquired active immunity
143
adaptive immunity resulting from injection of antibody to take care of something
artificially acquired passive immunity
