Exam 1 Flashcards
(141 cards)
1
Q
Components of the Cell
A
- plasma membrane
- cytoplasm & organelles
- endoplasmic reticulum
- golgi apparatus
- lysosomes
- mitochondria
- nucleus
- cytoskeleton
- cilia
2
Q
Endoplasmic Reticulum
A
extension of nucleus
- rough: contains ribosomes
- smooth: participates in metabolism of carbs, lipids,
- sarcoplasmic reticulum: Ca storage which is needed for muscle contraction
3
Q
Golgi Apparatus
A
packages molecules in vesicles and transports
4
Q
Lysosomes
A
packed w/ enzymes that break down damaged products
5
Q
Mitochondria
A
produces energy
6
Q
Nucleic Acids
A
DNA & RNA
7
Q
DNA
A
made up of nucleotides (3 phosphates, a sugar, and 1 of 4 bases)
- T-A, C-G - held together by H bonds
- essential for life
- replication happens during mitosis
- sequencing: determing base pair
- codon: 3 nucleotides code for amino acid
8
Q
RNA
A
mRNA: copies DNA & transported to cytoplasm - ribosome
*template for protein
*1 strand of mRNA = 1 gene = 1 protein
tRNA: transfers amino acids to ribosome
*contains anticodon- matches w/ codon on mRNA
9
Q
rRNA
A
together w/ protein makes ribosomes
10
Q
Central Dogma
A
DNA -transcription-> RNA -translation-> protein
11
Q
Cellular Functions
A
- transport
- Ingestion (endocytosis) & Secretion (exocytosis)
- respiration
12
Q
Diffusion
A
movement of solutes from high concentration to low concentration
passive
13
Q
Osmosis
A
movement of h2o from decreased pressure to high pressure
* cell will expand due to increase in water and rupture * passive
14
Q
Facilitated Diffusion
A
uses transport proteins to get solutes from high concentration to low concentration
passive
15
Q
Active Transport
A
uses transport proteins to move molecules from low to high concentration
* ex. sodium/potassium pump - needed for creating membrane potential - maintaining osmotic balance & stabilizing cell volume - failure results in cell death
16
Q
Respiration
A
energy production through oxidation of fuel molecules (carbs and lipids)
*glucose oxidation- 1st source of energy used by
bodies
-anaerobic glycolysis
-aerobic glycolysis
*lipid fatty acid oxidation
-beta oxidation
*protein metabolism
17
Q
Anaerobic glycolysis
A
- happens in cytoplasm
- 1 molecule of glucose = 2 molecules ATP
- end product- pyruvic acid –> lactic acid (decreases pH)
- LDH
18
Q
LDH
A
- enzyme that catalyzes pyruvic acid to lactic acid
- only found inside the cell, if present in blood- cells have ruptured
- can tell what tissue is damaged based of markers in LDH
19
Q
Aerobic glycolysis
A
- happens in mitochondria
- krebs cycle
- oxidative phosphorylation in ETC
- 1 molecule of glucose = 34 molecules ATP
- more efficient than anaerobic and faster than beta oxidation
20
Q
Cyanide poisioning
A
cyanide binds to an enzyme in ETC which disrupts cell respiration
no energy- cells die
21
Q
Lipid (fatty acid) respiration
A
- stored in adipocytes as triglycerides
- lipolysis: breakdown of triglycerides into fatty acids and glycerol
- Circulation: adipocytes - blood bound to albumin - mitochondria
- beta oxidation
22
Q
Beta oxidation
A
- 2 carbon fragments are released in repeated cycles to form acetyl CoA
- acetyl CoA enters citric acid cycle - oxidative phosphorylation
- 1 molecule of palmitate - 106 ATP
23
Q
Protein Metabolism
A
- composed of amino acids
- digested in GI tract and broken down into amino acids
- turnover of endogenous proteins
- nitrogen waste from proteins breakdown (ammonia) is removed as ureas
- produced to bind N from amino acid break down
24
Q
Glycogenesis
A
glucose –> glycogen (stored in m and liver)
25
Glycogenolysis
glycogen --> glucose
26
Gluconeogenesis
proteins, fat --> glucose
27
Cell Communication
* receptors
* channels
* adhesion molecules
* signal transduction
28
Receptors
proteins outside the membrane that respond to signals coming from different molecules (hormones, growth factors, chemical transmitters, drugs)
29
Channels
proteins embedded in membrane that help ions go through
30
Signal Transduction
process by which a cell converts one kind of signal or stimulus (extracellular) into another (cellular response)
31
Classes of surface cell receptors
* g-protein coupled receptors
* enzyme linked receptors
* ion channel receptors
32
Ligand
primary messenger
33
Receptor
all have a chain of amino acids that span the membrane 7 times - domain
34
Intracellular signaling molecules
* g-proteins
* effector proteins - produce 2nd messengers
* 2nd messenger proteins: stay in the membrane
- catalyze and change molecules so signal can be read
* target proteins
35
2nd messenger proteins
cyclic AMP, cAMP and cyclic GMP
calcium ion
IP3
DAG
36
Cholera
protein that modifies G-protein so its activation is disrupted- constantly being stimulated to produce 2nd messenger.
activates NA channels to open- water flows into cell
causes diarrhea
37
G-protein coupled receptor (GPCR) - components of signal transduction
* ligand
* receptor
* intracellular signaling molecules
- g-proteins
- effector proteins
- 2nd messengers
- target proteins
38
Growth factor receptor (enzyme linked receptor)
* 1 transmembrane domain
* ligand binds outside & changes the shape of the receptor (2 come together and modify each other)
* protein inside cell gets phosphorylated then phosphorylates another protien etc
* phosphorylated proteins look for target protein inside nucleus (through nucleopore)
* target protein gets together with another protein, together the form a transcription factor and bind to the promoter
* old proteins must be deactivated by enzymes in cell
39
Insulin Resistance
* receptor or downstream components are unresponsive- insulin cant act on cells
* insulins role is to promote glucose mvmt
* only way glucose gets into cell is through facilitated diffusion
* glucose transporters found in cytoplasm migrate to membrane and form channel where glucose comes in after activation of insulin receptor
40
Receptor Channels
ligand binds to receptor causing the channel to be opened and ions can move through
41
Reproduction
* cell growth controlled by growth factors
* excessive growth prevented by cell cycle inhibitors inside the cell
* cell cycle
* terminally differentiated cells
42
Cell cycle
* cell grows, dna replication starts
* goes through mitosis
* stops dividing when telomere gets too short
43
Telomere
determines how many times a cell will divide
* piece of DNA at end of chromosome
* each time cell divides a piece is lost
44
Terminally differentiated cells
cells that dont go through cell cycle
* for specific function
* cant divide, once they die, can't be regenerated
* neurons, cardiomyocytes
45
Proliferation
increasing number of cells
46
Differentiation
each cell type differentiates (becomes specialized) to carry out a particular function
47
Mitosis
cell division
48
Mutation
if Dna in parent cell is altered and passed on, offspring cells will carry the mutation
49
Stressors
- oxygen
- temp
- electrolytes
- molecular toxins
50
Reversible changes
* ceases once the stressor is removed
* no damage done to cell
* physiological hypertrophy of heart - athletes
51
Irreversible changes
eventually results in cell death
* damage done and cant be reversed
* pathological hypertrophy of hear - high BP
52
Atrophy
* decrease in cell size
* results in reduced tissue mass
* reduced use
* malnutrition
* decreased hormonal stimulation
* aging
53
Hypertrophy
* increase in cell size
* results in enlarged tissue mass
* training: cardiac and skeletal muscles
* hypertension
* increased hormonal stimulation - acromegaly
54
Hyperplasia
* increased number of cells
* may be accompanied by hypertrophy
* resulting in an enlarged tissue mass
* hormonal changes in puberty
* liver regeneration after partial hepatoectomy
* exposure to high altitudes
55
Metaplasia
* mature cell type is replaced by a different cell type
* occurs in response to chronic irritation
* chronic smokers: ciliated columnar epithelium is substitutes with stratified squamous epithelium
56
Dysplasia
* cells vary in size and shape within a tissue
* occurs in response to chronic irritation (infection)
* DNA mutations
* may be precancerous
57
Anaplasia
* undifferentiated cells with variable nuclear and cell structures
* characteristic of cancer
58
Neoplasm
new growth - tumor
59
Hypoxia
* due to reduced oxygen of breathed air (altitude)
| * low oxygen saturation in blood
60
Ischemia
* most common injury to cell
* due to lack/reduction of blood supply
* oxygenation deprivation to a tissue
- respiratory problems & circulatory problems
* lack of oxygen interferes w/ energy production - oxygen not present, metabolism shifts to anaerobic, decreases pH
* energy production decreases, Na/K pump stops working, Na goes into cell bringing water - dies
* when cell swells, decreases integrity of membrane - lets in ions (Ca) which stimulate proteolytic enzymes that digest internal components and apoptotic enzymes - cause cell death
61
Infarction
cell/tissue death due to oxygen deprivation due to absence of blood supply
62
Cell damage
* drugs: anticancer; immunosuppressants'acetaminophen
* microorganisms: bacteria, viruses
* abnormal metabolites: genetic disorders (inborn errors) & altered metabolism
* nutritional deficits
* imbalance of fluids of electrolytes
* extreme temps
* chemical agents (exogenous & endogenous)
63
High temps
* inactivation of temp sensitive enzymes
* protein misfolding
* protein coagulation
* damage to organelles
* disrupting cell membrane
64
Low temps
* increase vasoconstriction
* reduced oxygen supply
* ice crystal formation
65
Exogenous
* from environment
| * carbon monoxide, tobacco smoke, carbon tetrachloride
66
Endogenous
* from inside body
* reactive oxygen species or free radicals (can damage proteins, lipids, irreversible)
* from oxidative phosphorylation
* role of vitamine E- fat soluble compound incorporates itself into the membrane and when free radicals present, sequesters and neutralizes them
67
Apoptosis
* programmed cell death
* controlled by genetic elements
* may increase in development and aging
* occurs when cell number is excessive or cells are injured
* cells self destruct
* tumor cells lack apoptotic mechanisms
68
Necrosis
* disrupted cell metabolism
* lack energy
* inflammation
* Ca flux activates lysosomal enzymes - cell swells & ruptures- inflammation to neighboring cells- cell components leak in blood
* specific enzymes can be measure by diagnostic tests to identify the dype of damaged cells
69
Growth and differentiation changes
* atrophy
* hypertrophy
* hyperplasia
* metaplasia
* dysplasia
* anaplasia
* neoplasia
70
First line of defense- mechanical barriers
* Physical barriers: unbroken skin, mucous membranes, nasal hair, blood clot
* fluids: saliva, tears, gastric juices, seat glands
71
Second line of Defense
*Phagocytosis
neutrophils & macrophages engulf and destroy
*inflammation: limits effects of invading agents - destroy foreign bodies, clean space from debris, prepare site for healing
72
Third Line of Defense
* antibodies
| * Cell-mediated immunity
73
Inflammation
response to vascular tissue to injury
| localize, neutralize and remove harmful agents and remove dead tissues
74
Granulocytes
WBC
* neutrophils: phagocytosis
* basophils: release histamine
* eosiniophils: combat histamine
75
Agranulocytes
wbc
* monocytes: enter tissue become macrophages
* lymphocytes: produce cytokines
76
Mast cells
located in tissues
release chemicals from granules in response to injury
histamine
bradykinin
77
Macrophages
monocytes that entered tissues
| act as phagocytes
78
Cytokines
made by lymphocytes & macrophages
small proteins that affect cell behavior
include: interleukins, lymphkines & chemokines
79
Interferons
made by leukocytes
produced to prevent virus replication in cells
stimulate immune system
80
Histamine
vasodilation
| increase capillary permeability
81
Bradykinin
vasodilation
increase capillary permeability
pain
chemotaxis
82
Leukotrines
released by damaged cells
vasodilation
increase capillary permeability
chemotaxis
83
Prostaglandins
released by damaged cells
vasodilation
increased capillary permeability
pain
84
Increased Vascular Permeability
epithelial cells stick together tightly
inflammatory mediators increase size- contents less tightly packed
creates gap junctions- allow larger molecules in
immunoglobulins (antibodies) migrate to extracellular space
fibrinogen repair vessel or block infectious agent
85
4 Cardinal Signs of Inflammation (local effects)
```
redness
warmth
swelling
pain
loss of function
```
86
Systemic Effects
```
mild fever
malaise
fatigue
headache
loss of appetite
```
87
Inflammation Protection
removes harmful agents
removes dead tissues
enables tissue to heal
88
Inflammation Harmful
too much- becomes chronic
misdirected- infectious agent contiained by healing process to keep occurring
may be accompanied by loss of function
89
Acute Inflammation
```
Early reaction
short duration
neutrophils
followed by repair
vasodilation
increased capillary permeability
migration of inflammatory cells (neutrophils) to the site of injury
```
90
Chronic Inflammation
slow onset; may follow acute
longer duration
lymphocytes, macrophages & fibroblasts
simultaneous inflammation and repair
less swelling and exudate
collagen produced- fibrous scar tissue
granuloma- small mass of cells w/ necrotic center and covered by connective tissue
91
Complications of Inflammation
Infection
Deep ulcers
skeletal muscle spasm
local complications (obstruction, loss of sensation, decreased cell function)
92
Treatments
```
Acetylsalicylic acid - aspirin
acetaminophen - tylenol
glucocorticoids
ibprofen
COX inhibitors
```
93
Anti inflammatory Effects of Glucocorticoids
made in adrenal cortex gland
decrease capillary permeability
enhance effectiveness of epinephrine and norepinephrine (vasoconstrictors)
reduce number of leukocytes and mast cells
reduce immune response - immunosuppressants (side effect)
94
Adverse effects of glucocorticoids
atrophy of lymphoid tissue; reduce production of WBC
catabolic effects: increase tissue breakdown; decrease protein synthesis (affects healing)
delay healing
delay growth in children
retention of Na and H2O- lead to high BP and edema
95
Resolution
minimal tissue damage
| sun burn
96
Regeneration
damaged tissue replaced with cells that are functional
cell must be able to divide
new cells laid down on extracellular matrix
growth factors stimulate local cells to divide
*endothelial cells proliferate
-fill the wound cavity
-promote angiogenesis
*granulation tissue appears- extensive network of capillaries
-highly vascular
- fragile
-need as precursor for blood supply
97
Replacement
functional tissue replaced by scar or fibrous tissue
loss of function
no new cell proliferation OR injury to where cells don't divide
98
Humoral Immunity
antibodies produced to neutralize foreign antigen
99
Cell-Mediated Immunity
lymphoctyes programmed to attack non-self cells
100
Antigen
something that elicits an immune response
101
Major histocompatibility complex (MHC)
cell surface proteins that allow immune system to recognize self
every cell in body has same MHCs
changed when cell membrane is altered- not self anymore
102
MHC Class I
in all nucleated cells
process and present antigens INSIDE the cell
*proteins produced w/in cell broken down into fragments (antigens) --> rough ER and combine w/ MHC --> transported to golgi--> plasma membrane - t-cells activated and destroy cell
103
MHC Class II
present on macrophages & other immune cells
process & present on exogenous antigen
*phagocyte ingests foreign particles & breaks into particles w/ in vesicle - combines w/ MHC vesicle and combines - complex transported to cell membrane - immune cells respond
104
Lymphoid Structures
```
lymph nodes
spleen
thymus
intestinal lymphoid tissue
lymphatic circulation
```
105
Tissues where immune cells develop
bone marrow - origination & maturation of immune cells
| thymus- maturation of t-lymphocytes
106
Macrophages
```
produced when monocytes move into tissue
MHC class II
secrete interleukins- activate lymphocytes
```
107
Lymphocytes
```
primary cells in immune response
WBC
mature lymphocytes- immunocompetent cells
t- lymphocytes
b- lymphocytes
natural killer cells
```
108
T-lymphocytes
derive from bone marrow
differentiate in thymus
participate in cell-mediated immunity
cytotoxic, helper, suppressor, memory
109
Cytotoxic T-cells
bind to the antigen, release enzymes and chemicals and destroy the cell
CD8+
110
Helper T-cells
facilitate immune response by secreting cytokines
| activate and regulate all cells in the immune system
111
Regulatory T-cells
suppress immune response
| protect against auto immune response
112
Memory T-cells
after being exposed, remembers antigen for quicker response next time
113
Cluster of Differentiation
cell surface molecules
Each CD is 1 molecule
Identify cell type
Identify stage of differentiation - each stage has different
change as cell matures and differentiates
recognized by antibodies- used to label & identify CD
114
B lymphocytes
made and mature in bone marrow
proceed to spleen and lymphoid tissue
humoral immunity
*become antibody producing plasma cells after exposure to antigen w/ help from t-helper
*b-memory: clone plasma cell so already have genetic material for antibody
115
Natural Killer Cells
destroy tumor cells and virus infected cells
| cell mediated immunity
116
IgG
```
most common in blood (75%)
primary and secondary immune response
antibacterial, antiviral, antitoxin, antibody
activate complement
cross placenta
```
117
IgM
early immune response
| natural antibodies- involved in ABO incompatibility reaction
118
IgA
in secretions
| protection for newborns
119
IgE
allergic reaction
| bind to mast cells- release histamine
120
IgD
attached to B cells
| needed for cell maturation
121
Complement System
activated by antigen-antibody complex
complex binds to C1 - cascade activation
complement gets incorporated into membrane of bact. making pore-cell dies
triggers release of mast or basophils - inflammatory response
makes neutrophils/macrophages release lysosomal enzymes - cell damage tissue destruction
122
Titer
diagnostic test
| measures levels of serum immunoglobins
123
Determining specific antibody
enzyme linked immunosorbent assay (ELISA)- detects HIV virus
124
MHC typing
tissue matching before transplant
125
Primary Response
first exposure to antigen
antigen processed and presented (develop antibody, sensitized t cells)
1-2 weeks antibody titer to reach efficacy
126
Secondary Response
repeat exposure to same antigen
| more rapid response with efficacy in 1-3 days due to memory b cells
127
Innate Immunity
nonspecific
always present
attacks non self antigens
128
Active natural immunity
natural exposure to antigen- making antibody, producing sensitized t- cells
flu, cold
129
Active artificial immunity
antigen purposefully introduced to body to have memory cells built up
immunizations
130
passive natural immunity
protection of infant for first few months
IgG transfer through placenta
IgM transferred through breast milk
131
Passive artificial immunity
injection of antibodies for short term protection - when body can't produce enough antibodies
someone w/ no immune system
132
Immunosuppression
reduction of immune response to prevent transplanted tissue rejection
133
Type I Hypersensitivity (Immediate)
allergic reactions
exposed to allergen, produce IgE
Mast cells sensitzed by binding to IgEs
second exposure- already have complex, allergen binds to antibodies- mast cells release histamine - inflammation
134
Anaphylaxis
```
decreased blood pressure (vasodilation)
edema (increased vessel permeability)
airway obstruction
severe hypoxia
treates w/ eminephrine, glucocorticoids, antihistamines, oxygen
```
135
Type II (antibody mediated cytotoxic)
antigen present on membrane
circulating IgGs react w/ antigen
complement activated
antigen carrying cells are destroyed by phagocytosis
response to incompatible blood transfusion
136
Type III (immune complex mediated)
antigen combines w antibody forming immune complexes - deposited in tissue - complement activated
stays in tissues and activates neutrophils - destroy tissue
137
Type IV (cell-mediated or delayed)
no antibodies present
delayed response by sensitized t cells
release of lymphokines (attract immune cells)
inflammatory response
lyse and destroy antigen bearing cell, destroy normal tissue
138
Primary immune deficiencies
basic development failure somewhere
139
Secondary or acquired immune deficiencies
loss of immune response due to specific causes
140
AIDS
caused by HIV
destroys CD4+ helper t cells
loss of immune response
increased susceptibility to secondary infections
prolonged latent period
development may be suppressed by antiviral agents
141
HIV positive
virus is known to be in the body
| no evidence of immune suppression - no symptoms
