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MSK Part 2 > Pharmacology MSK > Flashcards

Pharmacology MSK Flashcards

1
Q

Explain Neuromuscular Blockers (NMB’s)

A

Used during surgery to induce paralysis.

Peripherally acting agents. Don’t cross the blood-brain barrier and act at the motor end-plate.

They target Nicotinic cholinergic receptors.

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2
Q

What was the first NMB?

A

d-tubocurarine

No analgesic or sedating effects

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3
Q

What are the kinds of ACh receptors?

A

Nm for Nicotinic muscles
Nn for Nicotinic neuronal
M for muscarinic (parasympathetics and sweat glands)

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4
Q

Generally describe the 2 kinds of NMB’s

A

Depolarizing agents: agonists of Nicotinic acetylcholine receptors

Non-depolarizing agents: Antagonists of Nicotinic acetylcholine receptors.

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5
Q

How does Succinylcholine function?

A

It binds to gates causing the receptor gate to keep the channel open.

Widespread fasciculation
Flaccid Paralysis

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6
Q

What are the two phases of succinylcholine paralysis?

A

Phase 1 block: open Nicotinic channels, Na+ channels are effectively inactivated, new AP cannot be achieved.

Phase 2 block: Nicotinic receptors become desensitized and are less responsive to additional agonist

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7
Q

Explain the pharmacokinetics of Succinylcholine

A

Rapid onset 1-2 min, short duration of 5-10 min
(Good to be used in endotracheal intubation, administered by IV or IM)

Metabolized in the plasma by plasma cholinesterase.

1 of 25 of European descent are deficient in a AChase allele and have prolonged drug action.

There is no antidote

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8
Q

What are the ADR and contraindication of Succinylcholine

A

ADR: Myalgia, jaw rigidity, rhabdomyolysis with acute renal failure. Increased intraocular pressure.

Off-target agonism bradycardia, arrhythmia, cardiac arrest. Pretreat with antihistamine

Contraindications: If they have Duchenne Muscular Dystrophy.
Patients has burn, crush, or denervation that increase hyperkalemic reaction risk.

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9
Q

What is Malignant Hyperthermia (MH)

A

Life-threatening complication of Succinylcholine.

Autosomal dominant genetic disorder or RyR1 that results in massive Ca release from SR.

Will lead to muscle rigidity, rise in body temp, and high arterial CO2.

Those taking SSRIs and Neuroleptics are at higher risk.

Take Dantrolene as antidote.

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10
Q

What is Dantrolene?

A

Antidote for Malignant Hyperthermia. Blocks power stroke of myosin/actin.

Will cause Diarrhea and Black box warning for hepatotoxicity.

Worth giving because it has low affinity at heart and smooth muscle and mortality rates go from 80 to 10%

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11
Q

What are Succinylcholine drug-drug interactions?

A

Acetylcholinesterase inhibitors may prolong effects.

Several antibiotics may enhance:
-Aminoglycosides, Bacitracin, cyclosporine, polymixin B, Tetracyclines, Vancomycin

Other: inhalation aesthetics, antidepressants (SSRI’s), neuroleptics (antipsychotics

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12
Q

Are non-depolarizing NMB’s competitive inhibitors?

Why could this be important?

A

Yes they are, and they can be out competed by Acetylcholinesterase inhibitors to speed rate of recovery.

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13
Q

Generally explain Non-depolarizing NMB’s

A

Prevent Muscle cell action potentials

Cause flaccid paralysis

Are competitive inhibits of the Nicotinic acetylcholine receptors

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14
Q

Which nondepolarizing NMBs are short-acting, longer-acting, and the exceptions. Where are they eliminated?

A

Short acting are eliminated in the liver

  • Rocuronium
  • Vecuronium

Longer-acting agents are renally eliminated

  • Pancuronium
  • Pipecuronium
  • Tubocurarine

Exceptions degrade spontaneously in the blood

  • Atracurium
  • Cisatracurium
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15
Q

Which is better to take: atracurium or cisatracurium

A

Cisatracurium because it forms less laudanosine which can cross the BB barrier and cause seizures.

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16
Q

What can be used to reverse rocuronium and vecuronium?

A

Sugammadex
IV injection

Reverse the clinical blockade in 3 minutes vs 19 minutes with neostigmine

No activity in the cholinergic system

Exctreted Renally, but is very expensive.

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17
Q

Tubocurarine

A

Duration of Action: More than 50 min

Effects at Nn: weak block***

Effects at M: none

Histamine Release: moderate***

Relative Potency: 1

Time to Onset: 6 min

Non-selective blockade (antagonism) of Nn.
Stimulate histamine causing hypotension and bronchospasm

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18
Q

Cisatracurium

A

Duration of Action: 25-44 min

Effects at Nn: none

Effects at M: none

Histamine Release: none

Relative Potency: 1.5

Time to Onset: 2-8 min

Best self-degrading Non-depolarizing NMB

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19
Q

Pancuronium

A

Duration of Action: more than 35 min

Effects at Nn: none

Effects at M: moderate heart block

Histamine Release: none

Relative Potency: 6

Time to Onset: 3-4 min

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20
Q

Atracurium

A

Duration of Action: 20-35 min

Effects at Nn: none

Effects at M: none

Histamine Release: slight

Relative Potency: 1.5

Time to Onset: 3

Can cause allergic reaction through histamine

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21
Q

Rocuronium

A

Duration of Action: 20-35 min

Effects at Nn: none

Effects at M: Slight heart block**

Histamine Release: none

Relative Potency: .8

Time to Onset: .5 -2 min

QUICK ONSET

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22
Q

Vecuronium

A

Duration of Action: 20-35 min

Effects at Nn: none

Effects at M: none

Histamine Release: none

Relative Potency: 6

Time to onset: 2-3 min

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23
Q

Succinylcholine: Depolarizing

A

Duration of Action: Less than 8 min

Effects at Nn: stimulation

Effects at M: stimulation

Histamine Release: slight

Relative Potency: .4

Time to Onset: .8-1.4 min

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24
Q

What can be given to avoid stimulation of cardiac M receptors before surgery?

A

Atropine: reverses the nondepolarizing NMB

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25
Q

What are spasms?’

Spasticity?

A

Painful, involuntary muscle contractions treated with antispasmodic agents

Involuntary contraction of skeletal muscle causes stiffness that interferes with mobility and speech. Treated with spasmolytic agents

Ex: Spasticity: MS, ALS, cerebral palsy, spinal injury.

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26
Q

Spasticity

A

Deficit in upper motor neuron. Signaling leaves lower motor neurons hyperexcitable.

Deficit due to spinal cord injury or neurodegeneration. Ex: Cerebral palsy, MS, stroke.

Dysregluation of the stretch reflex causes contraction response in the absence of stretch stimulus.

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27
Q

What do pharmacological agents target for spasticity?

A

Lower motor neurons
Interneurons in the reflex arc
Skeletal muscle directly (Dantrolene)

CNS active spasmolytics decrease alpha motor neuron activity by

  1. Reducing activity of the excitatory interneurons
  2. Enhancing activity of the inhibitory interneurons.
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28
Q

What do excitatory interneurons release?

A

Glutamine

Target AMPA receptors on the motor neuron and trigger an AP

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29
Q

What do inhibitory interneurons release, and what do they target?

A

They use GABA to target the excitatory interneurons and the motor neuron.

They decrease cAMP and close Ca channels by targeting a2-adrenergic receptors and GABAb receptors.

They inhibitors can upregulate GABAa Cl- channels or down regulate GABAb proteins.

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30
Q

What drugs affect GABA receptor ligands?

A

Baclofen

Diazepam

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31
Q

What are a2-adrenergic receptor agonists?

A

Tizanidine

32
Q

What is a centrally-acting agent?

Why is this concept important?

A

Agents that cross the blood-brain-barrier (BBB) to affect the brain and spinal cord.

So agonism of inhibitory receptors in the spinal cord to slow signals will also sedate the brain. This is common with spasmolytics and centrally active antispasmodics

33
Q

What are Benzodiazepines?

How are they administered and explain the properties?

A

Well known for their use as CNS-active sedatives and anxiolytics.

They are positive allosteric modulator of GABAa receptors.
-GABAa receptor has enhanced permeability to CL- which hyperpolarizes the neuron.

This DOESN’T

Administered orally and are nearly completely absorbed.
Plasma protein bound!
They can be short, intermediate or long acting

34
Q

What is the best drug for spasticity?

A

Diazepam: it is a long acting BZD.

35
Q

Explain Diaszepam

A

Long-acting BZD.

It has interactions with CYP3A4 substrates that increase apparent dose. (Ketoconazole, grapfruit juice, ritonavair)

Interactions with CYP3A4 inducers decrease apparent dose (st. John’s wort, anticonvulsant)

Adverse drug response:
Will cause sedation
-daytime drowsiness
-Rebound insomnia/anxiety
-Anterograde amnesia
-Coma and respiratory depression when used with CNS depressants like ALCOHOL
36
Q

What can be used to treat BZD overdose?

A

Flumazenil

It is a benzodiazepine-binding site antagonist, not effective against barbiturates or alcohol.

IV, rapid onset and short acting. (Needs to be readministered if large amount of BZD is consumed because it is plasma bound.)
-side effects are agitation, confusion, dizziness, nausea.

37
Q

What is Baclofen’s function?

A

It agonizes GABAb Receptor

Often first choice for muscle spasticity due to MS or spinal cord injuries, if tolerated
-Less sedation than diazepam.

Short acting GABA analog and again agonizes GABAb and causes hyperpolarization.

Reduces release of excitatory transmitters in the brain and spinal cord.

38
Q

What is the DMPK and ADR to Baclofen?

A

Rapid and complete oral absorption.

T1/2: 3-4 hours. And most of the drug is eliminated renally and through biliary excretion.

Nitrate also catheter of baclofen can control severe spasticity and muscle pain that is unresponsive to medication by other routes of administration. (Can be more dangerous by injecting it like this because it can’t cross the BBB to get out and can cause overdose.)

ADR:
Not tolerated well in all patients.
-Can cause seizures in epileptic patients, can cause respiratory depression and coma.

Abrupt discontinuation may cause seizures.

Caution in pregnant women: animal studies suggest birth defects.

39
Q

What is Gabapentin?

A

(Neurontin)

Made to target GABA, but it doesn’t target GABA. It targets Ca channels at the presynaptic nerve terminal that trigger synaptic vesicles release. Treats shingles

Causes less activation of post-synaptic GABA receptors. And reduces Gluatmetergic activity.

Eliminated unchanged from the body.
T1/2: 6 hrs.

Well tolerated with adverse effects of sedation, somnolence, ataxia, fatigue.

40
Q

What is Tizanidine?

A

(Zanaflex)

A2-adrenergic agonist

Agonism of a2-adrenergic receptors reduces firing rate of the presynaptic neuron.
Inhibitory GPCR

Not fully understood

Used to treat spasms cause by MS, ALS, spastic diplegia, back pain, or other CNS injuries.

Clinical trials with oral tizanidine report efficacy in relieving muscle spasm. As effective as baclofen, diazepam, and dantrolene.

ADR:
CNS-related: drowsiness, dizziness, Athenians

A2-adrenergic receptors are expressend in ANS: hypotension, dry mouth.
-CONTRAINDICATED for those with orthostatic hypotension.

Can cause hepatotoxicity and acute liver failure.
-Dosage must be adjusted in patients with renal and liver impairments.

CYP1A2 inhibition raises the apparent dose.

Induction of CYP1A2 by smoking will lower apparent dose!

41
Q

What are drugs that act on the skeletal muscle directly?

A

Dantrolene and Botulinum Toxin

42
Q

Describe Botulinum Toxin Type A

A

Botox

Produced by clostridium botulinum.

LD: 1.3-2.1 ng/kg intravenously or IM

BTX enxymatically cleaves the SNARE proteins involved in vesicular release.
-chemodenervation and local paralysis.

Incontinence due to overactive bladder and chronic migraine.

43
Q

What is Cyclobenzaprine?

What group is it in?

A

An antispasmodic (Flexeril)

Cyclobenzaprine:
Centrally active agents that react peripheral muscle spasms by targeting the brain stem.

Major interactions with other CNS-depressant drugs.

-Strong antimuscarinic side effects, significant sedation, confusion and transient visual hallucinations, seizures, tachycardia, hypotension.

Carisprodol is another that is metabolized to meprobamate, a schedule IV drug with sedative action and abuse liability.

44
Q

What are prostaglandins, and what are some examples?

A

Mediators of inflammation

Histamine, bradykinin, serotonin, eicosanoids

45
Q

What are three effects that NSAIDS have on prostaglandins?

A

They can relieve pain, reduce inflammation, and reduce fever which are both exasperated by prostaglandin.

46
Q

What are presentations of Osteoarthritis?

A

Loss of articular cartilage and presents asymmetrically.

It is related to weather, and duration of pain is less than 30 minutes.

Pain is resolved with motion and recurs with rest.

Only effects hands with Herberden nodes and Bouchard’s nodes, the knee, hips and spine.

47
Q

What are some non-pharmacological management of OA?

A

Weight Management
Physical Activity
Insoles, and assistive devices

Patient Education is crucial!!!!!!

48
Q

What are the general classes of NSAIDS?

A

Non-selective

  • Salicylates (aspirin)
  • Propionic Acid derivatives (ibuprofen)
  • Oxicam derivatives (piroxicam)
  • Acetaminopehn is not an NSAID, but has antipyretic and analgesic activity

Selective: COX-2 inhibitors (Celecoxib, and Rofecoxib** not on the market.)

49
Q

What are Cyclooxygenase (COX) enzymes?

A

Catalyze arachadonic acid to Prostaglandin

COX-1 is housekeeping
-maintains gut integrity, vascular tone, platelet aggregation, kidney function.

COX-2 is induced by pro-inflammatory signals like cytokines
-Cause inflammation, pain, regulate temp control, inhibit platelet aggregation

50
Q

Explain Non-selective NSAIDs

A

They inhibit both COX-1 and COX-2

Most are competitive, non-competitive or mixed reversible inhibitors.

51
Q

Which MSAID is irreversible? And explain it

A

Salicylate (Aspirin)
-Inhibitor of COX1 and COX2. Inhibits prostaglandins and synthesis and platelet aggregation.

1/2 is 30 minutes
Hydrolyze to salicylic acid.

Indications: OA, RA, fever, pain, prophylaxis of stroke and MI.

Salicylic acid is excreted in the breast milk and is category D in 3rd trimester

Reduces TxA2 which reduces clotting.

ADR: GI disturbance, can have allergic reactions.

52
Q

What are Propionic Acid Derivatives?

A

Reversible non-selective inhibitor of COX1 and 2
(Ibuprofen, Naproxen, Ketoprofen, Flurbiprofen)

Ibuprofen is ok while breastfeeding, long 1/2 life of naproxen should be avoided.

Black Box Warning: Increased risk of serious cardiovascular thrombotic event. Increased risk of serious GI event

53
Q

What are Acetic acid derivatives? Explain them and what are they better for?

A

Reversible inhibitors of COX 1 and 2.

They have longer 1/2 lives which is better for more long term use.

Ketorolac remains valuable alternative when opioid use is not an option.

Not for fever treatment!!!

Black Box Warning: Increase CV and GI event risk.

Ketorolac Black Box Warning: Should be used for no more than 5 to 7 days to avoid renal and GI damage.

54
Q

What are Oxicams? Explain the differences?

A

Non-selective reversible COX-1 and 2 inhibitor.

57 hour 1/2 life for piroxicam, and 20 hours for meloxicam.

Much longer half life.

Same Black box Warning of CV and GI events

Oxicam analgesic is better than aspirin.

55
Q

Explain Analgesic and Antipyretic Acetaminophen

Why is it not an NSAID?

A

Centrally acting analgesic and antipyretic with minimal anti-inflammatory properties.

Mechanism in reducing pain is the reversible inhibition of of the peroxidase site of COX1 and 2.

Not anti-inflammatory!

Black Box: Liver failure and acute hepatic damage needing transplant.****

56
Q

What is the connection of NSAIDs and GI bleeds?

A

COX1 is cytoprotective in gastric cells.

Inhibition of COX-1 reduces both protective Prostaglandins and TxA2 that can lead to ulcers. TxA2 activates platelets so the inhibition of TxA2 will lead to bleeding ulcers.

To stop this you can use combo therapy with omeprazole (20mg/once per day) protects upper GI

57
Q

Explain COX and cardiovascular events.

A

COX2 products regulate blood pressure and inhibit hemostasis (clotting)

Selective COX2 inhibition decreases PGI2 (inhibits platelet aggregation)

This increases total aggregation due to imbalance between TxA2.

58
Q

Explain Celecoxib

A

COX-2 selective inhibitor NSAID

1/2 life of 11 hrs.

Uses for pain, OA, and RA

Causes HTN, GI disturbance (not GI bleeds, it is nausea/vomiting), headache

Avoid for patients with heart failure or those taking ACE inhibitors. (Diuretic)

BLACK BOX for increased risk of CV thrombotic event.

59
Q

Should NSAIDs be used in elderly patients?

A

They are recommend not to use NSAIDs. Proton pump inhibitors should be used in conjunction when they need to be given.

60
Q

What are the Pros of NSAID use?

A

Alternative analgesic to opioids that have addiction potential.

61
Q

What is a DMARD?

A

Disease-Modifying Antirheumatic Drugs

Most common for RA
Goal is to control inflammation

62
Q

How can you tell arthritis is Rheumatoid?

A

Inflamed synovium, symmetrical, extra-articular involvement, morning stiffness that lasts more than 30 minutes.

Autoimmune disease

No hip and back involvements.

63
Q

What are used to manage RA?

A

PT, exercise, and rest

NSAIDs for pain relief, but don’t slow the process.

DMARDs will modify the disease immune response.

64
Q

How do DMARDs help with RA?

A

Slows the deterioration of tissue destructions

Does not repair damage already done.

Early diagnosis is needed.

65
Q

What are the two classes of DMARDs?

A

Traditional

  • Antimetabolites
  • Corticosteroids
  • Aminoquinoline
  • 5-Aminosalicylate
  • Dihydroorotate Dehydrogenase inhibitor

Biological

  • Tyrosine Kinase Inhibitor
  • TNFa inhibitor
  • IL-1 inhibitor
  • CD80/86 inhibitor
66
Q

Explain Corticosteroids for RA

A

Prednisone, Methylprednisolone, triamcinolone

Not a mono therapy usually.

Inhibit numerous steps in the inflammatory response such as inhibition of antigen presentation to T cell, prostaglandin and leuktriene synthesis, and neutrophil and monocytes radical generation.

1/2 Prednisone 2-3 hrs
- Others 18-36 hrs.

ADR: Hypothalamic-pituitary-adrenal suppresion (Has to be tapered down).

  • Can lead to osteoporosis.
  • Glucose intolerance
  • Increased susceptibility to infections.
67
Q

What are the two Antimetabolite drugs for RA?

A

Methotrexate: Folate analogue that inhibits DHFR. This inhibits cytokines production, purine biosynthesis, and may stimulate adenosine release.

1/2: 3-10 hrs.

Don’t use when pregnant!!!
Can be used for cancer at higher doses.

DMARD of choice for initial therapy. Results may be seen in 2-3 weeks and you can stay for 5-7 years.

BLACK Box are bone marrow suppression and will cause fetal death or toxicity.

Azothioprine:
Imidazolyl derivative is an immunosuppressive antimetabolite that suppresses cell-mediated hypersensitivites and amuses alterations in antibody production

1/2 life: 5 hrs

Serious: Leukopenia, hepatotoxicity.
BLACK BOX: Chronic immunosuppression

ADIVES PEOPLE to wear sunscreen!!!!!!

68
Q

What are aminoquinoline drugs for RA?

A

Hydroxychloroquine:
Immunosuppressant, interferes with antigen presentation.

1/2: 172 hrs to 50 days

Considered safe during pregnancy and breastfeeding.

Can cause retinal disorders, hypoglycemia, and torsades de pointes

May cause vision changes.

69
Q

What are 5-Aminosalicylate drugs for RA?

A

Sulfasalazine:
Prodrug that is cleaved in the terminal lieu and colon that inhibits inflammation due to blockage of cyclooxygenase and prostaglandin synthesis in the colon.

Inhibits IL-1 and TFNa production. Also Natural killer cells, and macrophages.

1/2: 7-14 hrs.

Serious side effects due to sulfapyridine moiety. 40% of patients can’t tolerate it.****

Antibiotics reduce availability of active moiety
And also may cause yellow-orange urine or skin

70
Q

What are Dihydroorotate Dehydrogenase Inhibitors for RA?

A

Leflunomide:
Pyrimidine synthase inhibitor

1/2 life 14-16 days with loading dose.

Teratogenic: May need Wash Out period before trying to conceive.

Serious complication are Stevens-Johnson syndrome.

Can cause liver toxicity by it is has efficacy similar to methotrexate.****

Avoid live vaccines during therapy!

71
Q

Explain Tyrosine Kinase Inhibitor for RA

A

Tofacitinib:

JAK inhibitor. JAK is a tyrosine kinase protein that facilitiates STAT protein for expression of inflammatory genes.

1/2: 3-6 hrs

Will Increase LDL and HDL levels***

BLACK box warning: serious infections leading to hospitalization or death. TB, viral

Cholesterol should be monitored
Don’t give with live vaccinations.

72
Q

What are TNFa inhibitors for RA

A

Biological
Infliximab, etanercept, Adalimumab, golimumab, certolizumab.

Monoclonal antibody with specific activity for TNFa

1/2 life is 14 days for all but etanercept which is 102 hrs.

Increase risk of Hep B and cancer. Can get Autoimmune hepatitis.

Don’t give with live vaccines

Etanercept is less selective for TNFa also hits TNFb

73
Q

What are IL-1 inhibitors for RA?

A

Biological DMARD

Anakinra:
Competitive inhibitor of IL-1 binding
Helps stop cartilage degradation

1/2: 4-6 hrs

Can cause neutropenia

Don’t give live vaccinations

74
Q

What are IL-6 receptors inhibitors for RA?

A

Biological DMARD

Tocilizumab:
IL-6 receptor inhibitor that binds to IL-6 receptor to mediate signaling

1/2: 11-13 days

Increased ALT/AST levels**

ADR: Neutropenia BLACK box of increased infection risk.

Don’t give live vaccinations.

More effective than adalimunab montherapy who can’t tolerate methotrexate.

75
Q

What are CD/86 inhibitors for RA?

A

Biological DMARD

Abatacept:
Downregulates T cell activation by binding to CD80/86 on the antigen presenting cell and prevents them from binding to CD28

1/2: 13-14 days

Increases risk of infection. Can cause upper respiratory infection.

Considerations: False high glucose readings may occur cause maltose is in the drug solution. May worsen COPD

MSK Part 2 (8 decks)

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