BECOM Exam #2 Flashcards
(161 cards)
1
Q
Sympathetic Branch: Stimulation
A
Pupil dilation (mydriasis) Dry mouth Sweat production Increased heart rate & force of contraction Bronchiole dilation Fuel mobilization (glucose, lipolysis) Blood vessel constriction Increase blood pressure Exercise increased metabolism in skeletal muscle which over-rides this effect and dilates to allow blood flow to increase Gut constrict Coagulation Ejaculation/orgasm
2
Q
Parasympathetic Branch: Actions
A
Constricts pupils and bronchioles
Slows heart rate & force of contraction
Stimulates
Digestion
Salivation
Insulin release
Urination
Erections (arousal)
S.L.U.D.G.E.(M) ->extreme parasympathetic stimulation
Organophosphate poisoning
Salivation, lacrimation, urination, defecation, gastrointestinal, emesis, muscle spasm/miosis (pinpoint pupil)
3
Q
Intracrine
A
signals are produced by the target cell that stay within the target cell. Example: secondary messengers
4
Q
Autocrine
A
signals are produced by the target cell, are secreted, and affect the target cell itself or a near by cell of the same type via a receptor. An example of this are immune cells.
5
Q
Paracrine
A
signals target cells in the vicinity of the emitting cell. E.g. neurotransmitters.
6
Q
Endocrine
A
signals target distant cells. Endocrine cells produce hormones that travel through bloodstream to reach all parts of the body. E.g. hormones
7
Q
Juxtacrine
A
signals target adjacent (touching) cells. These signals are transmitted along cell membranes via protein or lipid components integral to the membrane and are capable of affecting either the emitting cell or cells immediately adjacent. E.g. gap (tight junctions, notch signaling, etc).
8
Q
Receptor Tyrosine Kinases Regulate what?
A
Cell proliferation, growth, differentiation, migration
9
Q
GEF
A
GDP –> GTP
10
Q
GAP
A
speed up GTP hydrolysis
11
Q
Adenylyl Cyclase
A
ATP makes 5’-AMP -> cAMP
12
Q
phosphodiesterase
A
cAMP –> 5’-AMP
13
Q
What occurs when GDP goes to GTP (amino acids)
A
Thr and Gly residues are pulled to the third phosphate making a conformational change
14
Q
Ras MAP Kinase Pathway causes
A
cell proliferation
15
Q
Signaling issues that promote cancer
A
- RTK: becomes dimerized and phosphorylated with out ligand bound
- Overexpression: large amount of kinases in the membrane
- Activating mutation: produce a product that mimics phosphorylation or conformational change of kinase
16
Q
HER2
A
RTK that are over expressed that cause cell proliferation. antibody bind to HER2 receptor causing no dimerization
17
Q
NF-kB
A
- TNF activates NF-kB
- alphaB is phosphorylated and disassociates with NF-kB allowing NF-kB to translocate into the nucleus and act as a transcription factor
- leads to pro-inflammatory signals
- rheumatory arthritis
18
Q
Humira
A
- is a monoclonal antibody that binds to TNFalpha not allowing it to bind to TNFR (RTK)
- lowers immune response
19
Q
Enbrel
A
receptor that binds to TNFalpha with no signal (essentially an inhibitor to the cascade)
20
Q
Philadephia Protein
A
- translocation of chromosome 9 and 22
- chromosome 22 shorter than normal
- Bcr-Abl protein
21
Q
Graded Potential
A
- starts above threshold at is initiation point but decreases in strength as it travels through the cell body
- if not a threshold at trigger point -> no action potential
- summation
22
Q
Action Potential
A
- A regenerating depolarization of membrane potential that propagates along an excitable membrane
- at trigger zone (all or nothing)
- only uses K+/Na+ channels
- no summation
23
Q
speed of transmission depends on
A
- fiber size
- myelinated
- resistance
24
Q
refractory period
A
is defined from the time the activation/inactivation gates begin moving, until they are “re-set” (activation gate closed / inactivation gate open) to their original configuration at resting membrane potential
25
Absolute refractory period
AP will not fire, irrespective of stimulus intensity.
26
Relative refractory period
- stronger than normal stimulus may elicit an AP.
- Note: As relative refractory period progresses, the level of excitability increases.
- action potential will take more time because not as many fast Na+ channels in ready state
27
greater than normal stimulus effect on amplitude of AP
- no effect on amplitude but will have a greater than normal frequency of AP firing
- rate of frequency is how AP is graded
- greater release of neurotransmitter
28
Postsynaptic receptor proteins bind to receptors (binding component) and then either
1. Alter chemically gated ion channel (open or close)
- EPSP (excitatory)
- IPSP (inhibitory)
2. Activate 2nd messenger systems
- Open specific ion channels on the postsynaptic membrane
- Activation of cAMP or cGMP
- Activation of one or more intracellular enzymes
- Activation of gene transcription
29
Postsynaptic receptor proteins activate 2nd messenger systems
- Open specific ion channels on the postsynaptic membrane
- Activation of cAMP or cGMP
- Activation of one or more intracellular enzymes
- Activation of gene transcription
30
Neurotransmitter inhibitors
- g-aminobutyric Acid (GABA)
- Glycine
-hyperpolarize the cell
31
Tyrosine Hydroxylase (TH)
tyrosine -> L-Dopa -> Dopamine
32
Dopamine B hydroxylase (DBH)
Dopamine -> Norepinephrine
33
phenylthanolamine-N-methyltransferase (PNMT)
Norepinephrine -> Epinephrine
34
VMA
Breakdown of norepinephrine and epinephrine
35
HMA
breakdown of dopamine
36
Monoamine Oxidase (MAO)
breaks down 5HT in serotonin synapse
37
Monoamine Oxidase (MAO)
- breaks down 5HT in serotonin synapse
| - Norepinephrine
38
Inactivation of Neurotransmitters
glial cells
blood vessels
enzymes
39
Choline acetyltransferase
catalyzes the transfer of an acetyl group from the coenzyme acetyl-CoA to choline, yielding acetylcholine
40
Post-synaptic cholinergic receptors
- Muscarinic
| - Nicotinic
41
acetylecholine esterase
acetylcholine -> acetate + choline
42
Spatial Summation
total surface area that inputs are taking up on a neuron
43
Temporal Summation
The net sum of inputs per unit of time on the presynaptic neuron determine the level of excitability
44
Presynaptic vs postsynaptic inhibition
Presynaptic: 2/3 synapses release neurotransmitter
Postsynaptic: 0/3 synapses release neurotransmitter
45
Synaptic Transmission Fatigue
- exhaustion of the stores of transmitter in synaptic terminals
- excitatory synapses are repetitively stimulated at a rapid rate until rate of postsynaptic discharge becomes progressively less.
- development of fatigue is a protective mechanism against excessive neuronal activity (seizures)
46
Synaptic Transmission Fatigue
- exhaustion of the stores of transmitter in synaptic terminals
- excitatory synapses are repetitively stimulated at a rapid rate until rate of postsynaptic discharge becomes progressively less.
- development of fatigue is a protective mechanism against excessive neuronal activity (seizures)
47
Acidosis effect on excitability/inhibition
H+ accumulates extracellularly -> Less Na+ in (exchanged for H+) -> tends to hyperpolarize and depress excitability.
48
Alkalosis effect on excitability/inhibition
less H+ extracellularly -> drives exchange -> more Na+ in -> increases excitability through depolarization effect.
49
hypoxia effect on excitability/inhibition
- Initial (very short) excitation
| - Reduced O2 availability prolonged No ATP for pumps
50
Post-tetanic facilitation
- enhanced responsiveness following repetitive stimulation.
- mechanism thought to be build-up of calcium ions in the presynaptic terminals.
- build-up of calcium causes more vesicular release of transmitter.
51
Synaptic delay
-0.5 ms in mammals
52
Sympathetic
“Fight or flight”
Energetic action
Mobilization of energy to fight or flee
53
Parasympathetic
“Rest and digest”
Restore body function
Decreased metabolism, favors energy storage
54
Medulla controls
- Respiration
| - Cardiac, vascular, visceral
55
Pons
Respiration, urinary
56
Hypothalamus
Body fulid balance, temperature, and hunger
57
Sympathetic Innervation Only (non-dually innervated
- Arteriolar smooth muscle – blood pressure
- Kidney – body fluid balance and blood pressure
- Sweat glands
- Adipose (lipolysis)
- Clotting
58
Somatic neural pathway
motorneuron -> Nicotinic 2 on skeletal muscle
59
Autonomic Neuron Structure & Synapse
- Varicosities
- large area, slow acting
- no synaptic cleft
- released into extracellular fluid
60
Alpha 1
- Smooth muscle contraction
| - NE>EPI
61
Alpha 2
- Also presynaptic inhibition of NE release
| - NE>EPI
62
Beta 1
- Cardiac, renin release from kidney, lipolysis
| - NE=EPI
63
Beta 2
- Smooth muscle relaxation
| - EPI>>NE
64
Beta 3
- Thermogenesis from brown adipose tissue
| - NE>EPI
65
Sympathetic Branch Inhibition
```
Increased digestion
Pancreas secretion
Urination
Slow heart rate
Reduce blood pressure
```
66
Sympathetic spinal seg
thoracolumbar (T1-L3)
67
Parasympathetic spinal seg
cranial and sacral divisions
68
Sympathetic neural pathway
- preganglionic (ACh) -> Nicotinic 2 receptor on postganglionic (NE) -> alpha 1/2, beta 1,2,3
- smooth muscle, glands, cardiac muscle
- postganglionic (ACh) -> Muscarinic
- sweat glands
69
Parasympathetic neural pathway
- preganglionic (ACh) -> Nicotinic 2 receptor on postganglionic (ACh) -> Muscarinic
- smooth muscle, glands, cardiac muscle
70
Adrenal Medulla neural pathway
-preganglionic (ACh) -> Nicotinic 2 receptor on adrenal medulla -> to circulation (80% EPI, 20% NORE)
71
Parasympathetic Branch Inhibition
Inhibit digestion
Reduces secretory functions (dry mouth)
Increases heart rate
72
Vagus nerve stimulates
- parasympathetic
- Heart
- Lungs
- Intestines
- Stomach
73
bradycardia
slow HR
74
diaphoresis
sweaty
75
hypertension
high blood pressure
76
blood pressure is mainly controlled by
sympathetic nerves system
77
Low dose EPI
blood pressure decreases
78
High dose EPI
blood pressure increases
79
Heart Beta stimulation
Increased HR
80
Bronchiole smooth muscle Beta stimulation
bronchodilation
81
Apla 1 signaling cascade
IP3, increase intracellular Ca2+
82
Apla 2 signaling cascade
inhibit adenylyl cyclase, decrease cAMP
83
Beta 1 signaling cascade
stimulate adenylyl cyclase, increase cAMP
84
Beta 2 signaling cascade
stimulate adenylyl cyclase, increase cAMP
85
Nicotinic signaling cascade
Opening Na+ and K+ channels, depolarization
86
Muscarinic signaling cascade
- IP3, increase intracellular Ca2+
| - inhibit adenylyl cyclase, decrease cAMP
87
Alpha 1 target tissue
vascular smooth muscle
skin
gastric tract
bladder
88
Alpha 2 target tissue
gastrointestinal tract
89
beta 1 target tissue
heart
salivary glands
adipose tissue
kidney
90
beta 2 target tissue
vascular smooth muscle of skeletal muscle
gastrointestinal tract
bladder
bronchioles
91
tachycardia
increase HR
92
glycogenolysis
break down of glycogen
93
GLUT 2
- Liver and Pancreatic Beta cells
- will take in glucose for storage as glycogen when level of glucose are high
- high km for glucose
- Pancreatic Beta cells: when high glucose excretes insulin
94
GLUT 3
Brain
95
GLUT 4
- skeletal muscles and adipose
| - insulin response and exercise
96
Leptin
stops hunger when glucose level are sufficient
97
S.L.U.D.G.E.(M)
| Organophosphate poisoning
Salivation, lacrimation, urination, defecation, gastrointestinal, emesis, muscle spasm/miosis (pinpoint pupil)
98
Acetyl CoA carboxylase in fed and fasting state
unphosphorylated (active) in fed state
| phosphorylated (inactive) in fasting state
99
TCA cycle occurs in the
mitochondrial matrix
100
Acetyl CoA comes from
Glycolysis, fatty acid b-oxidation (ketone bodies), amino acid breakdown
101
B3 (nicotinamide) makes up
NAD
102
NADH is produced where and used where
produced through TCA and used in Oxidative phosphorylation
103
Complex I reduces
NADH
104
Complex IV reduces O2
with 4 H+ to make H2O
105
Coenzyme Q (Ubiquinone) job
Small molecule electron shuttle in the mitochondrial
| inner membrane
106
complex I is inhibited by
rotenone
barbituantes
MPP+
107
complex II is inhibited by
nitropropionic acid
| malonate
108
complex III is inhibited by
antimycin A
109
complex IV is inhibited by
CN-, N3-, H2S, CO
110
Complex II oxidizes
succinate to fumarate
111
Most reactive ROS
.OH hydroxyl radical
112
ROS pathway
O2.- -> H2O2 -> OH- + OH. -> H2O
113
Fenton and Haber-Weiss reaction
Fe2+ and Cu1+ react with hydrogen peroxide and superoxide to form hydroxyl radicals
114
NOX 1
neutrophils releases H2O2 from its cell to affect bacteria
115
NOX 2
- neutrophils will release HOCl and OH- in the phagosome membrane to break down bacteria
- granulomas can form when this is defective
116
Nitric Oxide synthase constitutive form job
-iNOS1
-NO normally involved in vasorelaxation via
soluble guanylate cyclase
-make small “bursts” of ●NO in response to Ca2+ transients
117
Process of Nitric oxide formation form macrophage
202 + NADPH (enzyme NOS2) -> NO
118
How do ROS effect us?
- oxidize fatty acids
| - oxidized fatty acid can diffuse out of cell and attack other parts
119
Antioxidants include
-Superoxide dismutase (SOD) accelerate O2•- ->H2O2
-Catalase (CAT, a Mn-containing enzyme) finishes detoxing H2O2
2 H2O2 O2 + 2 H2O
-Glutathione Peroxidase (GPx, Se dependent & independent)
GSH + H2O2 -> GSSG + H2O
120
How do Tocopherols (vitamin E) act
takes radical from hydroperoxal radical and allows to have the radical taken up
121
GSH as cellular reductant
- Acts with enzymes like glutathione peroxidase to remove peroxides ROOH
- comes from
122
what are antioxidant gene regulated by
Nrf2 disassociates from Keap
123
Cori Cycle
Heart & liver convert lactate back to pyruvate, liver converts pyruvate back to glucose (gluconeogenesis) or oxidizes it.
124
catapleurosis
- removal of intermediates from the Kreb cycle
| - OAA -> asparagine/aspartate
125
anapleurosis
- replacement of kreb cycle intermediate "fill up"
| - asparagine/aspartate -> OAA
126
Methyl malonic aciduria (MMA):
- Genetic deficiency of methyl malonyl CoA mutase or low B12
| - methyl malonyl CoA -> succinyl CoA for TCA Cycle
127
pyruvate carboxylase
Pyruvate -> oxaloacetate
128
Pantothenic acid = Vitamin B5
CoA
129
carboxylase enzymes need
biotin (B7)
130
Thiamine (B1)
- pyruvate dehydrogenase and oxoglutarate dehydrogenase (also called α-ketoglutarate dehydrogenase)
- alc can damage uptake of thiamine
131
Lipoic acid
Cofactor of PDH and aKGDH
132
Riboflavin (vitamin B2)
- Bound cofactor of succinate dehydrogenase
- used by complex II of ETC
- part of FAD
133
Pyridoxal phosphate (vitamin B6)
- PLP enzyme
| - B6 and B12 deficiencies in older individuals
134
beriberi and wernicke-korsakoff
thiamine deficiency
135
pelagra
niacin deficiency
136
Pyruvate kinase
- Brain, muscle, RBCs contain no allosteric site
- Liver: inhibited (ATP, alanine) activation (F 1,6 bisP)
- inactive when phosphorylated (high glucagon levels)
137
Conversion of glucose to 2 lactate generates how many ATP via?
2 ATP from substrate-level phosphorylation
138
Malate-OAA shuttle
malate (reduced carrier) -> OAA (oxidized carrier)
139
Glucokinase vs hexokinase
Glucokinase has higher km than hexokinase and is localized in the liver
140
Pyruvate dehydrogenase
- pyruvate -> acetyl CoA
- links glycolysis and TCA cycle
- Turned off when the energy level of the cell is high or oxygen is lacking
141
Cofactors of Pyruvate Dehydrogenase Complex
thiamine pyrophosphate (TPP) (B1)
lipoate (lipoamide) (octanoic acid)
flavin adenine dinucleotide (FAD) (B2)
nicotinamide adenine dinucleotide (NAD+) (B3)
coenzyme A (CoA) (B5)
142
Enzymes that regulate glycolysis
hexokinase
Phosphofuctokinas 1
pyruvate kinase (regulated only in liver)
143
PFK-2 vs. FBPase
```
-PFK-2: fructose 6-P -> fructose 2,6 bisphosphate
high insulin (high blood glucose)
```
```
-FBPase: fructose 2,6 bisphosphate -> fructose 6-P
high glucagon (low blood glucose)
```
144
whats the point of gluconeogenesis
make glucose in the liver so that it can be excreted and raise low glucose levels
145
What effects will high and low Acetyl CoA levels have on Pyruvate dehydrogenase and pyruvate carboxylase
- high Acetyl CoA with inhibit PDH and activate PC so that glucose can be made for glycogen storage
- high acetyl CoA because a FAs so oxaloacetate can be used to make glucose
146
alc effect on gluconeogenesis
- increases the amount of NADH
- inc NADH causes pyruvate to lactate
- because lost of pyruvate gluconeogenesis can't occur
147
glycogenesis
the buildup of glycogen
148
glycogen phosphorylase
breaks down glycogen by inserting phosphate to break alpha 1,4 chain
149
Von Gierke Disease
- deficiency in glucose 6-phosphatase
| - glycogen storage disease, can't break down glycogen
150
Alpha receptor prefers
NE>EPI
151
Beta receptor prefers
EPI>NE
152
Beta receptor signaling pathway
cAMP inc
153
Alpha receptor signaling pathway
DAG + PIP2
154
Tumor in adrenal medulla secretes large amounts of
epinephrine
155
2nd Messenger Postsynaptic Effects
- Open specific ion channels on the postsynaptic membrane
- Activation of cAMP or cGMP
- Activation of one or more intracellular enzymes
- Activation of gene transcription
156
muscarinic vs beta 1 receptors
- heart rate
- muscarinic: inhibit AC, open K+ channels (hyperpolarization)
- beta 1: activates AC -> inc cAMP, open Na+ channels (depolarization)
157
major cellular reducing agent
NADH, NADPH, and GSH
158
Nitric Oxide synthase Inducible isoform
- NOS2
- in macrophages and microglia (brain macrophages)
- iNOS is upregulated in response to inflammogens, makes ●NO constantly so long as the protein and its cofactors (esp. tetrahydro-biopterin) are present and functional
159
mydriasis
dilation of pupils
160
normal glucose levels
70-80
161
C peptide
- used in the synthesis of insulin
| - if individual doesn't produce insulin then C peptide level will be low
