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The BIG Test > Cell Physiology & Muscle Relaxants > Flashcards

Cell Physiology & Muscle Relaxants Flashcards

1
Q

What is the most abundant component of the cell membrane on the basis of # of molecules?

A

Phospholipids

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2
Q

What is the most abundant component of the cell membrane on the basis of weight?

A

Proteins

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3
Q

Nonpolar Molecules

A 
Nonpolar: 
Uniformly distributed charge 
NO net charge 
Lipophilic/hydrophobic 
Ex: O2, N2, inhalational/IV agents
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4
Q

Polar Molecules

A 
Polar: 
Clustered charge
\+/- poles repelled by lipid bilayer
NO net charge
Hydrophilic/lipophobic 
Ex: glucose, H2O, CO2
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5
Q

Who crosses the lipid bilayer?

A

Hydrophobic: O2, N2, IV anesthetics, inhalational agents

Small Polar: H20, CO2, urea, glycerol

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6
Q

Who can’t cross the lipid bilayer?

A

Large Polar: glucose, sucrose

Ions!

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7
Q

2 Types of Endocytosis

A
  1. Pinocytosis aka cell drinking - NO digestion (how proteins are reabsorbed from the PCT of the kidney)
  2. Phagocytosis (how macrophages eat bacteria)
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8
Q

Describe the type of receptor at the NMJ.

A

Ligand gated channels

Ach binds to nicotinic receptor, channel opens - Na + Ca diffuse IN, K diffuse OUT

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9
Q

Receptors are found on the outside surface of the lipid bilayer. Enzymes are found on the inside surface of the lipid bilayer. What is the exception?

A

At the NMJ, acetylcholinesterase projects outward into the synaptic cleft

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10
Q

A membrane receptor either operates a _________ OR controls an __________.

A

Receptor

Enzyme

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11
Q

What proteins are the best known for relaying messages from receptors to enzymes?

A

G proteins

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12
Q

What is the result of increased cAMP in the heart?

In the lung?

A

Heart - increased contractility (increased Ca) - Beta 1 agonists
Lung - bronchodilation (decreased Ca) - Beta 2 agonists

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13
Q

Na-K Pump

A

3 Na OUT

2 K IN

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14
Q

Insulin stimulates the _________ and opens ________ channels.

A

Na-K pump

Glucose

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15
Q

What 2 things stimulate the Na-K pump?

A
  1. Insulin

2. Beta 2 agonists (Ritodrine, Terbutaline)

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16
Q

Examples of 2nd messengers.

A 
cAMP
cGMP
IP3
Calcium
Calmodulin
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17
Q

Intracellular vs. Extracellular Ionic Gradients

A

Intracellular: K, PO4, Mg
Extracellular: Na, Cl, HCO3, Cl

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18
Q

In the resting cell, what lines the outside membrane? Is it positive or negative? What lines the inside membrane? Is it positive or negative?

A

Outside - K - positive charge

Inside - proteins - negative charge

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19
Q

What is the resting membrane potential? This is mostly determined by________.

A

70 mV

K

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20
Q

What happens to the resting membrane potential in the presence of hyperkalemia?

A

Decreased diffusion gradient through the leak K channels
Decreased K leaving the cell
RMP changes from -70 to -60
Cells depolarize

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21
Q

What happens to the resting membrane potential in the presence of hypokalemia?

A

Increased diffusion gradient through the leak K channels
Increased K leaving the cell
RMP changes from -70 to -80
Cells hyperpolarize

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22
Q

Describe the 4 stages of action potentials.

A
  1. Resting: (- 70 mV)
  2. Depolarization: Na channel opens, Na moves IN, (+ 30 mV)
  3. Repolarization: Na channel now in inactivated state, K channel opens, K moves OUT
  4. Restore Ionic Balance: the job of the Na-K pump
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23
Q

When is the absolute refractory period?

A

When the Na channel is in the inactivated state

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24
Q

Name 3 examples of the absolute refractory period…when the Na channel is in the inactivated state

A
  1. Cardioplegia
  2. Sux
  3. LA
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25
Q

In the neuron, where are the Na channels found?

A

On the axon

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26
Q

Diffusion of ____ ions INTO the cell is responsible for depolarization of the axon.

A

Na

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27
Q

Diffusion of _____ ions OUT of the cell is responsible for repolarization of the axon.

A

K

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28
Q

What is found embedded in the lipid bilayer of the presynaptic nerve terminal?

A

Nicotinic receptor (increases synthesis and release of Ach, this is a positive feedback loop)

Ca channel (Ca IN, NT OUT)

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29
Q

What is found postsynaptically in the membrane of the motor end-plate?

A

Nicotinic receptor

Acetylcholinesterase

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30
Q

What happens when BOTH alpha subunits of the nicotinic receptor are occupied by Ach?

A

Channel opens
Na + Ca diffuse INTO cell
K diffuse OUT of cell
Depolarization

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31
Q

Describe the termination of Ach.

A

Acetylcholinesterase aka “True” cholinesterase

Ach is broken down into choline (recycled) and acetate

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32
Q

What is associated with a DECREASE in the amount of NT released?

A

Decreased calcium

Increased magnesium

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33
Q

What is associated with an INCREASE in the amount of NT released?

A

Increased calcium

Decreased magnesium

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34
Q

How many Ach molecules are needed to open each nicotinic receptor?

A

2

40K, alpha subunits

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35
Q

How do NDMR work?

A

Competitive inhibitors
Inhibit Ach from attaching to the 2 alpha subunits of the nicotinic receptor
Channel remains closed

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36
Q

How does Sux work?

A

Sux mimics Ach
Opens the channel by binding to the nicotinic receptor
Channel stays open
Na channels remain in the inactivated state

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37
Q

Sux is composed of 2 ______ molecules.

A

Ach

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38
Q

How is Sux metabolized?

A

Plasma cholinesterase/Pseudocholinesterase

As metabolized, gradient develops - Sux diffuses away from the motor end-plate

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39
Q

The nicotinic receptor found presynaptically increases the synthesis and release of Ach - positive feedback.
Does Sux do this?

A

Yes - presynaptic action of Sux enhances its postsynaptic action
Augments the release of Ach

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40
Q

MR: Short DOA

A

Sux

Mivacurium

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41
Q

MR: Intermediate DOA

A

Atracurium
Cisatracurium
Vecuronium
Rocuronium

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42
Q

MR: Long DOA

A 
d-Tubocurarine
Metocurine
Pancuronium
Gallamine
Pipecuronium
Doxacurium
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43
Q

Structure of Quaternary Ammonium Compounds

A

Nitrogen surrounded by 3CH3 and 1CH2-R

44
Q

Are MR ionized? Protein bound? Do they cross the BBB/placenta?

A

Yes - 100% ionized at physiologic pH
Yes - very protein bound
NO - do NOT cross the BBB/placenta

45
Q

What 2 MR are eliminated primarily by biliary excretion?

A
  1. Vec

2. Roc

46
Q

What 4 MR are eliminated primarily by metabolism?

A
  1. Sux - plasma cholinesterase
  2. Mivacurium - plasma cholinesterase
  3. Atracurium - Ester hydrolysis (nonspecific esterases) + Hofmann
  4. Cisatracurium - Hofmann
47
Q

All other MR are primarily eliminated by…

A

Renal excretion

*All MRs can be excreted by the kidney (trapped d/t ionization)

48
Q

Hofmann elimination depends on what…

A

pH
Temp
Increase rate with increase in pH + increase in temp

49
Q

What MR stimulates the autonomic ganglia?

A

Sux

50
Q

What 2 MRs produce autonomic ganglionic blockade?

A
  1. d-Tubocurarine - mod
  2. Metocurine - mild
    * Block nicotinic receptors at the autonomic ganglia
51
Q

What 2 MRs are vagolytic or have an antimuscarinic effect?

A
  1. Pancuronium

2. Gallamine

52
Q

What MR causes bradycardia?

A

Sux

*Directly stimulates muscarinic receptors of the SA node

53
Q

What 3 MRs lead to decreased BP?

A
  1. Sux
  2. d-Tubocurarine
  3. Metocurine
54
Q

What 2 MRs lead to increased BP?

A
  1. Pancuonium - mild

2. Gallamine - mod

55
Q

Which MR can increase HR in children but not in adults?

A

Roc

56
Q

Name 5 MRs that release histamine.

A
  1. Sux
  2. Mivacurium
  3. Atracurium
  4. d-Tubocurarine
  5. Metocurine
57
Q

Name 5 MRs that cause tachycardia.

A
  1. Atracurium - reflex
  2. d-Tubocurarine - reflex
  3. Metocurine - reflex
  4. Pancuronium - mod
  5. Gallamine - marked
58
Q

Name adverse effects of Sux.

A 
Increased IOP, ICP, IGP
Hyperkalemia 
(normal 0.5 mEq/L, burn/trauma/HI 5-10 mEq/L) 
Bradycardia, AV block 
Mus pain - fasiculations 
Myoglobinuria 
Atypical plasma cholinesterase
MH
59
Q

What makes Sux-induced hyperkalemia worse?

A

Proliferation of extrajunctional post-synaptic cholinergic nicotinic receptors…up regulation
Nicotinic receptor sitmulation - channel opens - K exits
BURNS, PARA/HEMIPLEGIA, TRAUMA, UMN INJURY
(HI, CVA, Parkinson’s), MUSCULAR DYSTROPHY

60
Q

The patient has right sided hemiplegia…twitch monitor should be placed on the right or the left?

A

Left

Right will be exaggerated (upregulation)

61
Q

Malignant Hyperthermia

A

Sarcoplasmic reticulum fails to sequester Ca - sustained contraction - increased metabolism - hypercarbia
Increased ETCO2 = earliest, most sensitive
SNS stimulation - increased HR, RR
Trismus 50%, whole body rigidity 75%
Increased: H, K, Ca, CO2
Decreased: O2, pH
Tx: d/c causative agents, hyperventilate, Dantrolene, cool, treat hyperK

62
Q

What are the 2 agents that trigger MH?

A
  1. Sux

2. Volatile inhalational agents

63
Q

What increases the block of NDMR?

A

Abx (mycin), LA, volatile agent, HYPOkalemia, HYPERmag, acidosis, HYPOthermia, increased age, lithium, diuretics, CCB, antiarrhythmias, renal disease, hepatic disease, MG

64
Q

What decreases the block of NDMR?

A
  1. Anticonvulsants

2. Burn injury

65
Q

What increases the block of Sux?

A

Abx (mycin), LA (ester), anticholinesterase agents, HYPERkalemia, HYPERmag, lithium, CCB

66
Q

What increase the block of NDMR, but does NOT affect the block of Sux?

A

Volatile agent

67
Q

At this % of receptors blocked you have no twitches in TOF BUT the diaphragm moves?

A

95%

68
Q

This % of receptors blocked is adequate for intra-abdominal procedures?

A

1/4 twitches

90%

69
Q

TV returns to normal when what % of receptors are blocked?

A

75-80%

*Not an indicator of recovery

70
Q

What % of receptors are blocked when you have no palpable fade in TOF? And you have sustained tetanus 50 Hz for 5 seconds?

A

70-75%

71
Q

What % of receptors are blocked when you have no palpable fade in DBS?

A

60-70%

72
Q

What % of receptors are blocked with head lift for 5 sec, sustained handgrip, and sustained bite?

A

50%

73
Q

What % of receptors should be blocked for intubation?

A

> 95%

74
Q

When monitoring Sux on a peripheral nerve stimulator know that…

A

Twitches will be reduced in amplitude
NO fade in TOF, DBS, or tetany
NO post-tetanic facilitation
*Block is antagonized by NDMR

75
Q

Define phase I block.

A

Motor end-plate is depolarized

Ion channels are open

76
Q

Define phase II block aka desensitization.

A

Result of increased doses of Sux or prolonged exposure
Ion channels close, motor end plate repolarizes
Looks like a NDMR block on a peripheral nerve stimulator

77
Q

Name the enzyme that breaks down cAMP to 5’AMP.

A

Phosphodiesterase

78
Q

Describe the pathway of nitric oxide, starting with the amino acid that is the immediate precursor of nitric oxide.

A

L-arginine - NOS - nitric oxide - guanylate cyclase - cGMP - PKG - decrease Ca in cytoplasm

79
Q

What is the name of the specific type of enzyme-linked insulin receptor?

A

Tyrosine kinase receptor

80
Q

What is the most common excitatory NT in the CNS?

A

Glutamate

81
Q

Name 6 ligand binding sites of the GABA receptor.

A
  1. GABA
  2. Barbiturates
  3. Benzos
  4. Propofol
  5. Steroids
  6. Anesthetics/alcohol
82
Q

How fast does temp increase with MH?

A

1-2 deg C Q5 min

83
Q

Dantrolene
Works of what receptor?
What is the dose?
What does a vial of Dantrolene contain?

A

Ryanodine receptor
2.5 mg/kg Q 5min Max 10-20 mg/kg
20 mg of Dantrolene + 3 G of Mannitol - mix with 50 mL of sterile water

84
Q

What is the best method for decreasing temp in the case of MH?

A

Gastric lavage

STOP cooling at 38 deg C

85
Q

What syndrome can mimmic MH?

A

Neuroleptic malignant syndrome (NMS) - antipsychotic agents, dopamine depletion
MH has an acute onset, NMS develops over 24-72 hrs

86
Q

Duchenne’s Muscular Dystrophy
Males or females?
Diagnosis at the age of?
Concerns?

A

X-linked recessive disorder - affecting males
Diagnosed at 3-5 years
Concerns - Myocardial dysfunction, hyperK with Sux, MH

87
Q 
Myasthenia Gravis 
Cause? 
Most common onset? 
Tx?
Major concern?
A

Autoimmune destruction of nicotinic receptors at the NMJ
Ocular - ptosis and diplopia
Tx: anticholinesterase drugs
Major concern - postop respiratory failure
*Sensitive to NDMR and sensitive or resistant to Sux

88
Q 
Cholinergic Crisis 
S/S?
Drugs that could be possible causes? 
Diagnosis?
Tx?
A

Accumulation of Ach
Excessive muscarinic receptor stimulation - weakness, diarrhea, salivation, miosis, bradycardia
Anticholinesterase drugs, organophosphates, insecticides, pesticides
Diagnosis - give edrophonium- if they get better then it is a myasthenic crisis - if they get worse then cholinergic crisis
Tx? Atropine + Pralidoxime (reactivates acetylcholinesterase)

89
Q 
Lambert-Eaton Myasthenic Syndrome 
Cause? 
S/S? 
Associated with? 
Does weakness improve with repeated stimulation?
A

Antibodies attack Ca channel
Proximal skeletal mus weakness that typically affects the LE
Associated with small-cell carcinoma of the lung
Yes - weakness improves with repeated stimulation
*Sensitive to both NDMR and Sux

90
Q

Does Sux have an active metabolite?

A

Yes - succinylmonocholine

91
Q

Sux is contraindicated for patients taking what eye drop medication?

A

Echothiophate

92
Q

Benzylisoquinolines

A

NDMR with “curium”

*Steroid derivatives have “curONium”

93
Q

Name the metabolite of ester hydrolysis of Atracurium.

A

Laudanosine - CNS stimulant

94
Q

Which 3 MRs have active metabolites?

A
  1. Sux
  2. Vec
  3. Pancuronium
95
Q

How does a pretreatment dose of NDMR affect Sux?

A

Sux is less potent and has a shorter DOA

96
Q

What happens to the potency of a NDMR given after Sux?

A

Potency is enhanced

97
Q

Name 4 anticholinergic/antimuscarinic drugs.

A
  1. Atropine
  2. Glyco
  3. Scopolamine
  4. Ipratropium
98
Q

Which antimuscarinic has the greatest…
antisialagogue effect?
sedative and amnesic effect?
heart rate effect?

A

Scopolamine
Scopolamine
Atropine

99
Q

How do antimuscarinics interfere with sweating?

A

Large doses of atropine increase body temp by preventing sweating
Sweat glands contain antimuscarinic receptors (Ach is released by sympathetic postganglionic neurons)

100
Q

Antimuscarinics have what effect on the lower esophageal sphincter?

A

Decrease the tone of the lower esophageal sphincter

101
Q

Anticholinergic Syndrome
What 2 drugs are responsible?
Central and peripheral S/S?
Tx?

A
  1. Scopolamine
  2. Atropine
    S/S: Confusion to coma, BUDCAT
    Tx: Physostigmine
102
Q

What would you consider if your patient with myasthenia gravis exhibits excessive salivation?

A

Muscarinic side effects
Excessive anticholinesterase drug effects
If muscle weakness, consider cholinergic crisis

103
Q

What 3 drugs should be avoided in a patient with atypical pseudocholinesterase?

A
  1. Sux
  2. Mivacurium
  3. Ester-type local anesthetics
104
Q

Describe the dibucaine test.

What is normal?

A

Dibucaine depresses the activity of pseudocholinesterase
Normal - dibucaine will depress the activity of pseudocholinesterase by 70-85% - 70-85
Heterozygotes - 30-70
Homozygotes - 20
*The dibucaine # does NOT reflect the quantity or concentration of the enzyme

105
Q

List the 4 anticholinesterase agents/cholinesterase inhibitors.

A
  1. Edrophonium - quaternary amine (charged)
  2. Neostigmine - quaternary amine (charged)
  3. Pyridostigmine - quaternary amine (charged)
  4. Physostigmine - tertiary amine (uncharged) - crosses the BBB

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