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BECOM 1 > BECOM Exam #2 > Flashcards

BECOM Exam #2 Flashcards

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
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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)

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3
Q

Intracrine

A

signals are produced by the target cell that stay within the target cell. Example: secondary messengers

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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.

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5
Q

Paracrine

A

signals target cells in the vicinity of the emitting cell. E.g. neurotransmitters.

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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

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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).

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8
Q

Receptor Tyrosine Kinases Regulate what?

A

Cell proliferation, growth, differentiation, migration

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9
Q

GEF

A

GDP –> GTP

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10
Q

GAP

A

speed up GTP hydrolysis

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11
Q

Adenylyl Cyclase

A

ATP makes 5’-AMP -> cAMP

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12
Q

phosphodiesterase

A

cAMP –> 5’-AMP

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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

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14
Q

Ras MAP Kinase Pathway causes

A

cell proliferation

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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
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16
Q

HER2

A

RTK that are over expressed that cause cell proliferation. antibody bind to HER2 receptor causing no dimerization

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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
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18
Q

Humira

A
  • is a monoclonal antibody that binds to TNFalpha not allowing it to bind to TNFR (RTK)
  • lowers immune response
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19
Q

Enbrel

A

receptor that binds to TNFalpha with no signal (essentially an inhibitor to the cascade)

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20
Q

Philadephia Protein

A
  • translocation of chromosome 9 and 22
  • chromosome 22 shorter than normal
  • Bcr-Abl protein
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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
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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
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23
Q

speed of transmission depends on

A
  • fiber size
  • myelinated
  • resistance
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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

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25
Q

Absolute refractory period

A

AP will not fire, irrespective of stimulus intensity.

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26
Q

Relative refractory period

A
  • 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
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27
Q

greater than normal stimulus effect on amplitude of AP

A
  • 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
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28
Q

Postsynaptic receptor proteins bind to receptors (binding component) and then either

A
  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
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29
Q

Postsynaptic receptor proteins activate 2nd messenger systems

A
  • Open specific ion channels on the postsynaptic membrane
  • Activation of cAMP or cGMP
  • Activation of one or more intracellular enzymes
  • Activation of gene transcription
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30
Q

Neurotransmitter inhibitors

A
  • g-aminobutyric Acid (GABA)
  • Glycine

-hyperpolarize the cell

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31
Q

Tyrosine Hydroxylase (TH)

A

tyrosine -> L-Dopa -> Dopamine

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32
Q

Dopamine B hydroxylase (DBH)

A

Dopamine -> Norepinephrine

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33
Q

phenylthanolamine-N-methyltransferase (PNMT)

A

Norepinephrine -> Epinephrine

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34
Q

VMA

A

Breakdown of norepinephrine and epinephrine

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35
Q

HMA

A

breakdown of dopamine

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36
Q

Monoamine Oxidase (MAO)

A

breaks down 5HT in serotonin synapse

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37
Q

Monoamine Oxidase (MAO)

A
  • breaks down 5HT in serotonin synapse

- Norepinephrine

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38
Q

Inactivation of Neurotransmitters

A

glial cells
blood vessels
enzymes

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39
Q

Choline acetyltransferase

A

catalyzes the transfer of an acetyl group from the coenzyme acetyl-CoA to choline, yielding acetylcholine

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40
Q

Post-synaptic cholinergic receptors

A
  • Muscarinic

- Nicotinic

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41
Q

acetylecholine esterase

A

acetylcholine -> acetate + choline

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42
Q

Spatial Summation

A

total surface area that inputs are taking up on a neuron

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43
Q

Temporal Summation

A

The net sum of inputs per unit of time on the presynaptic neuron determine the level of excitability

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44
Q

Presynaptic vs postsynaptic inhibition

A

Presynaptic: 2/3 synapses release neurotransmitter
Postsynaptic: 0/3 synapses release neurotransmitter

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45
Q

Synaptic Transmission Fatigue

A
  • 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)
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46
Q

Synaptic Transmission Fatigue

A
  • 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)
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47
Q

Acidosis effect on excitability/inhibition

A

H+ accumulates extracellularly -> Less Na+ in (exchanged for H+) -> tends to hyperpolarize and depress excitability.

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48
Q

Alkalosis effect on excitability/inhibition

A

less H+ extracellularly -> drives exchange -> more Na+ in -> increases excitability through depolarization effect.

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49
Q

hypoxia effect on excitability/inhibition

A
  • Initial (very short) excitation

- Reduced O2 availability prolonged  No ATP for pumps

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50
Q

Post-tetanic facilitation

A
  • 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.
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51
Q

Synaptic delay

A

-0.5 ms in mammals

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52
Q

Sympathetic

A

“Fight or flight”
Energetic action
Mobilization of energy to fight or flee

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53
Q

Parasympathetic

A

“Rest and digest”
Restore body function
Decreased metabolism, favors energy storage

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54
Q

Medulla controls

A
  • Respiration

- Cardiac, vascular, visceral

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55
Q

Pons

A

Respiration, urinary

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56
Q

Hypothalamus

A

Body fulid balance, temperature, and hunger

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57
Q

Sympathetic Innervation Only (non-dually innervated

A
  • Arteriolar smooth muscle – blood pressure
  • Kidney – body fluid balance and blood pressure
  • Sweat glands
  • Adipose (lipolysis)
  • Clotting
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58
Q

Somatic neural pathway

A

motorneuron -> Nicotinic 2 on skeletal muscle

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59
Q

Autonomic Neuron Structure & Synapse

A
  • Varicosities
  • large area, slow acting
  • no synaptic cleft
  • released into extracellular fluid
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60
Q

Alpha 1

A
  • Smooth muscle contraction

- NE>EPI

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61
Q

Alpha 2

A
  • Also presynaptic inhibition of NE release

- NE>EPI

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62
Q

Beta 1

A
  • Cardiac, renin release from kidney, lipolysis

- NE=EPI

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63
Q

Beta 2

A
  • Smooth muscle relaxation

- EPI»NE

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64
Q

Beta 3

A
  • Thermogenesis from brown adipose tissue

- NE>EPI

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65
Q

Sympathetic Branch Inhibition

A 
Increased digestion
Pancreas secretion
Urination
Slow heart rate
Reduce blood pressure
66
Q

Sympathetic spinal seg

A

thoracolumbar (T1-L3)

67
Q

Parasympathetic spinal seg

A

cranial and sacral divisions

68
Q

Sympathetic neural pathway

A
  • 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
Q

Parasympathetic neural pathway

A
  • preganglionic (ACh) -> Nicotinic 2 receptor on postganglionic (ACh) -> Muscarinic
  • smooth muscle, glands, cardiac muscle
70
Q

Adrenal Medulla neural pathway

A

-preganglionic (ACh) -> Nicotinic 2 receptor on adrenal medulla -> to circulation (80% EPI, 20% NORE)

71
Q

Parasympathetic Branch Inhibition

A

Inhibit digestion
Reduces secretory functions (dry mouth)
Increases heart rate

72
Q

Vagus nerve stimulates

A
  • parasympathetic
  • Heart
  • Lungs
  • Intestines
  • Stomach
73
Q

bradycardia

A

slow HR

74
Q

diaphoresis

A

sweaty

75
Q

hypertension

A

high blood pressure

76
Q

blood pressure is mainly controlled by

A

sympathetic nerves system

77
Q

Low dose EPI

A

blood pressure decreases

78
Q

High dose EPI

A

blood pressure increases

79
Q

Heart Beta stimulation

A

Increased HR

80
Q

Bronchiole smooth muscle Beta stimulation

A

bronchodilation

81
Q

Apla 1 signaling cascade

A

IP3, increase intracellular Ca2+

82
Q

Apla 2 signaling cascade

A

inhibit adenylyl cyclase, decrease cAMP

83
Q

Beta 1 signaling cascade

A

stimulate adenylyl cyclase, increase cAMP

84
Q

Beta 2 signaling cascade

A

stimulate adenylyl cyclase, increase cAMP

85
Q

Nicotinic signaling cascade

A

Opening Na+ and K+ channels, depolarization

86
Q

Muscarinic signaling cascade

A
  • IP3, increase intracellular Ca2+

- inhibit adenylyl cyclase, decrease cAMP

87
Q

Alpha 1 target tissue

A

vascular smooth muscle
skin
gastric tract
bladder

88
Q

Alpha 2 target tissue

A

gastrointestinal tract

89
Q

beta 1 target tissue

A

heart
salivary glands
adipose tissue
kidney

90
Q

beta 2 target tissue

A

vascular smooth muscle of skeletal muscle
gastrointestinal tract
bladder
bronchioles

91
Q

tachycardia

A

increase HR

92
Q

glycogenolysis

A

break down of glycogen

93
Q

GLUT 2

A
  • 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
Q

GLUT 3

A

Brain

95
Q

GLUT 4

A
  • skeletal muscles and adipose

- insulin response and exercise

96
Q

Leptin

A

stops hunger when glucose level are sufficient

97
Q

S.L.U.D.G.E.(M)

Organophosphate poisoning

A

Salivation, lacrimation, urination, defecation, gastrointestinal, emesis, muscle spasm/miosis (pinpoint pupil)

98
Q

Acetyl CoA carboxylase in fed and fasting state

A

unphosphorylated (active) in fed state

phosphorylated (inactive) in fasting state

99
Q

TCA cycle occurs in the

A

mitochondrial matrix

100
Q

Acetyl CoA comes from

A

Glycolysis, fatty acid b-oxidation (ketone bodies), amino acid breakdown

101
Q

B3 (nicotinamide) makes up

A

NAD

102
Q

NADH is produced where and used where

A

produced through TCA and used in Oxidative phosphorylation

103
Q

Complex I reduces

A

NADH

104
Q

Complex IV reduces O2

A

with 4 H+ to make H2O

105
Q

Coenzyme Q (Ubiquinone) job

A

Small molecule electron shuttle in the mitochondrial

inner membrane

106
Q

complex I is inhibited by

A

rotenone
barbituantes
MPP+

107
Q

complex II is inhibited by

A

nitropropionic acid

malonate

108
Q

complex III is inhibited by

A

antimycin A

109
Q

complex IV is inhibited by

A

CN-, N3-, H2S, CO

110
Q

Complex II oxidizes

A

succinate to fumarate

111
Q

Most reactive ROS

A

.OH hydroxyl radical

112
Q

ROS pathway

A

O2.- -> H2O2 -> OH- + OH. -> H2O

113
Q

Fenton and Haber-Weiss reaction

A

Fe2+ and Cu1+ react with hydrogen peroxide and superoxide to form hydroxyl radicals

114
Q

NOX 1

A

neutrophils releases H2O2 from its cell to affect bacteria

115
Q

NOX 2

A
  • neutrophils will release HOCl and OH- in the phagosome membrane to break down bacteria
  • granulomas can form when this is defective
116
Q

Nitric Oxide synthase constitutive form job

A

-iNOS1
-NO normally involved in vasorelaxation via
soluble guanylate cyclase
-make small “bursts” of ●NO in response to Ca2+ transients

117
Q

Process of Nitric oxide formation form macrophage

A

202 + NADPH (enzyme NOS2) -> NO

118
Q

How do ROS effect us?

A
  • oxidize fatty acids

- oxidized fatty acid can diffuse out of cell and attack other parts

119
Q

Antioxidants include

A

-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
Q

How do Tocopherols (vitamin E) act

A

takes radical from hydroperoxal radical and allows to have the radical taken up

121
Q

GSH as cellular reductant

A
  • Acts with enzymes like glutathione peroxidase to remove peroxides ROOH
  • comes from
122
Q

what are antioxidant gene regulated by

A

Nrf2 disassociates from Keap

123
Q

Cori Cycle

A

Heart & liver convert lactate back to pyruvate, liver converts pyruvate back to glucose (gluconeogenesis) or oxidizes it.

124
Q

catapleurosis

A
  • removal of intermediates from the Kreb cycle

- OAA -> asparagine/aspartate

125
Q

anapleurosis

A
  • replacement of kreb cycle intermediate “fill up”

- asparagine/aspartate -> OAA

126
Q

Methyl malonic aciduria (MMA):

A
  • Genetic deficiency of methyl malonyl CoA mutase or low B12

- methyl malonyl CoA -> succinyl CoA for TCA Cycle

127
Q

pyruvate carboxylase

A

Pyruvate -> oxaloacetate

128
Q

Pantothenic acid = Vitamin B5

A

CoA

129
Q

carboxylase enzymes need

A

biotin (B7)

130
Q

Thiamine (B1)

A
  • pyruvate dehydrogenase and oxoglutarate dehydrogenase (also called α-ketoglutarate dehydrogenase)
  • alc can damage uptake of thiamine
131
Q

Lipoic acid

A

Cofactor of PDH and aKGDH

132
Q

Riboflavin (vitamin B2)

A
  • Bound cofactor of succinate dehydrogenase
  • used by complex II of ETC
  • part of FAD
133
Q

Pyridoxal phosphate (vitamin B6)

A
  • PLP enzyme

- B6 and B12 deficiencies in older individuals

134
Q

beriberi and wernicke-korsakoff

A

thiamine deficiency

135
Q

pelagra

A

niacin deficiency

136
Q

Pyruvate kinase

A
  • Brain, muscle, RBCs contain no allosteric site
  • Liver: inhibited (ATP, alanine) activation (F 1,6 bisP)
  • inactive when phosphorylated (high glucagon levels)
137
Q

Conversion of glucose to 2 lactate generates how many ATP via?

A

2 ATP from substrate-level phosphorylation

138
Q

Malate-OAA shuttle

A

malate (reduced carrier) -> OAA (oxidized carrier)

139
Q

Glucokinase vs hexokinase

A

Glucokinase has higher km than hexokinase and is localized in the liver

140
Q

Pyruvate dehydrogenase

A
  • pyruvate -> acetyl CoA
  • links glycolysis and TCA cycle
  • Turned off when the energy level of the cell is high or oxygen is lacking
141
Q

Cofactors of Pyruvate Dehydrogenase Complex

A

thiamine pyrophosphate (TPP) (B1)

lipoate (lipoamide) (octanoic acid)

flavin adenine dinucleotide (FAD) (B2)

nicotinamide adenine dinucleotide (NAD+) (B3)

coenzyme A (CoA) (B5)

142
Q

Enzymes that regulate glycolysis

A

hexokinase
Phosphofuctokinas 1
pyruvate kinase (regulated only in liver)

143
Q

PFK-2 vs. FBPase

A 
-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
Q

whats the point of gluconeogenesis

A

make glucose in the liver so that it can be excreted and raise low glucose levels

145
Q

What effects will high and low Acetyl CoA levels have on Pyruvate dehydrogenase and pyruvate carboxylase

A
  • 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
Q

alc effect on gluconeogenesis

A
  • increases the amount of NADH
  • inc NADH causes pyruvate to lactate
  • because lost of pyruvate gluconeogenesis can’t occur
147
Q

glycogenesis

A

the buildup of glycogen

148
Q

glycogen phosphorylase

A

breaks down glycogen by inserting phosphate to break alpha 1,4 chain

149
Q

Von Gierke Disease

A
  • deficiency in glucose 6-phosphatase

- glycogen storage disease, can’t break down glycogen

150
Q

Alpha receptor prefers

A

NE>EPI

151
Q

Beta receptor prefers

A

EPI>NE

152
Q

Beta receptor signaling pathway

A

cAMP inc

153
Q

Alpha receptor signaling pathway

A

DAG + PIP2

154
Q

Tumor in adrenal medulla secretes large amounts of

A

epinephrine

155
Q

2nd Messenger Postsynaptic Effects

A
  • 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
Q

muscarinic vs beta 1 receptors

A
  • heart rate
  • muscarinic: inhibit AC, open K+ channels (hyperpolarization)
  • beta 1: activates AC -> inc cAMP, open Na+ channels (depolarization)
157
Q

major cellular reducing agent

A

NADH, NADPH, and GSH

158
Q

Nitric Oxide synthase Inducible isoform

A
  • 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
Q

mydriasis

A

dilation of pupils

160
Q

normal glucose levels

A

70-80

161
Q

C peptide

A
  • used in the synthesis of insulin

- if individual doesn’t produce insulin then C peptide level will be low

BECOM 1 (4 decks)

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