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2-Spring18-PharmII > Block 5 > Flashcards

Block 5 Flashcards

1
Q

What are the 3 general anesthetic inhalants?

A

Nitrous oxide (gas)
Halothane
Enflurane

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2
Q

What is the MOA of nitrous oxide (gas)?

A

It inhibits the NMDA receptor

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3
Q

What are the side effects of Halotahne?

A

Halothane hepatitis

Not used in the US anymore

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4
Q

What is the use and side effects of Enflurane?

A

It’s an inhalant used for maintenance - it is a better muscle relaxant than halothane

Side effects are depressed myocardial force of contraction and may induce seizures

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5
Q

What are the drugs used for IV general anesthetic?

A

Propofol
Ketamine
Fentanyl

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6
Q

What is the MOA , use, and side effects of propofol?

A

GABAa to open Cl- channels

Used for induction and maintenance

Side effects are hypothension and respiratory depression

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7
Q

What is the MOA, use, and side effects of ketamine?

A

It’s dissociative anesthesia
MOA - NMDA receptor agonist
Used for induction
Side effects are hallucinations and cardiac stimulation

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8
Q

What is use for fentanyl?

A

Pain relief - its an opioid - neurolept analgesic

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9
Q

How does lipid solubility affect general anesthesia?

A

More lipid soluble, means lower MAC and higher potency

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10
Q

What is MAC?

A

Minimum alveolar concentration

It’s the minimum amount that works in 50% of patients

MAC values are lower in children and elderly

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11
Q

How is partial pressure related to concentrations and solubility?

A

Partial pressure is directly proportional to concentration

Partial pressure is invertely proportional to solubility

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12
Q

What is the MOA of local anesthetics?

A

They cross the membrane and block the Na+ channels to stop the action potential

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13
Q

Why are LAs less effected when injected into acidic tissue?

A

B/c more acidity means the drug is more in the charged form

More charged means it can’t cross the membrane as easily - this causes less of an effect

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14
Q

Higher solubility means what as far as LAs?

A

More solubility means the drug can easily cross the membrane, which leads to longer duration and more potency - also means increased toxicity

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15
Q

LA drugs have a preference to which binding state?

A

Active and inactive states

They do not bind well to resting state

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16
Q

Which nerve fibers are more easily blocked by LA?

A

Miller and more myelinated nerve fibers

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17
Q

Which drug is often combined with a local anesthetic to delay absorption and prolong the action of the drug?

A

Epinephrine - it vasoconstricts

*remember don’t need a vasoconstrictor with cocaine but it vasoconstricts all by itself

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18
Q

What is the toxicity of LAs?

A 
CNS - sedation, respiratory & cardiovascular depression (depresses myocardial contractility) 
Also vasodilates (except cocaine) 
superificial Punctate keratitis - LAs soften the corneal epithelium if overdosed
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19
Q

What are the 2 groups of drugs for LAs?

A

Esters

Amides

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20
Q

What are the LA drugs categorized as an ester?

A

Tetracaine

Cocaine

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21
Q

Where are esters metabolized?

A

Locally in the plasma by esterase

Shorter duration and mostly topical use

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22
Q

What is the metabolite formed by esters?

A

PABA - an allergen!

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23
Q

When is cocaine contraindicated?

A

When taking another adrenergic agonist
Hypertension
Angle closure glaucoma

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24
Q

What are the LA drugs categorized as amides?

A

Bupivacaine

Lidocaine

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25
Q

How are amides metabolized?

A

In the liver by the P450 system
Therefore liver dysfunction increases toxicity

Amides are usually longer lasting and usually injected

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26
Q

What are the side effects of bupivacaine?

A

Severe cardiovascular toxicity including arrhythmias

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27
Q

What is the use for lidocaine?

A

Most commonly used due to potency, rapid onset, moderate duration, and versatility

Used as an antiarrhythmic agent

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28
Q

What are the nociceptors?

A

Pain receptors

Have 2 types: A-delta or C fibers

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29
Q

What are the A-delta nociceptors?

A

Large diameter, sparsely myelinated fibers that carry sharp, well localized pain (somatic pain)

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30
Q

What are the C nociceptors?

A

Small diameter, unmyelinated fibers that carry aching, poorly localized pain (visceral pain)

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31
Q

What receptors do the peptide enkephalins bind to?

A

Delta receptors

32
Q

What receptor do the endorphins bind to?

A

Mu receptors

33
Q

What receptors do the dynorphins bind to?

A

Kappa receptors

34
Q

Which protein are the opioid peptides coupled to?

A

Gi (inhibitory)

35
Q

Which 2 opioid receptors cause sedation?

A

Delta and mu

Kappa just causes slowed GI tract

36
Q

What is the MOA of Opioid drugs?

A

Gi inhibits adenylyl cyclase to decrease cAMP
Presynaptically Ca+ channels are closed to inhibit neurotransmitter release
Postsynaptically K+ channels are opened to cause membrane hyperpolarization

37
Q

Where are opioids metabolized?

A

In the liver by the P450 enzymes

So opioids don’t eliminate as quickly in patients with liver disease

Active metabolites are formed: morphine-6-glucuronide, morphine-3-glucuronide, and morphine (from codeine)

If the patients lacks P450 enzymes they will receive less pain relief
Also if patient drinks alcohol (P450 inducer) their serum levels of opioids will be higher

38
Q

What are the side effects of opioids?

A

Constipation, pinpoint pupils, respiratory depression, urinary retention

Toxicity = coma

39
Q

What do we treat opioid overdose with?

A

Naloxone (given intravenously)

40
Q

What are the withdrawal symptoms of opioids?

A

Mydriasis, chills, hyperventilation, diarrhea, anxiety

41
Q

Wha do we treat an heroin addiction with?

A

Methadone (agonist) plus Natrexone (antagonist)

42
Q

What are drug interactions with opioids?

A

Don’t use with sedative-hypnotics, ethanol, anesthetics, MAO inhibitors, or antipsychotic tranquilizers

43
Q

What are the opioid full agonists?

A

Morphine
Methadone
Codeine
Oxycodone

All Mu receptors

44
Q

What are the partial agonist opioids?

A

Buprenorphine

Partially binds to mu

45
Q

What are the mixed agonist-antagonist opioids?

A

Pentazocine

Kappa agonist, mu antagonist

46
Q

What are the full antagonist opioids?

A

Naloxone

Mu antagonist

You can combine naloxone with Buprenorphine for abuse but naloxone only works if injected

47
Q

What are prostaglandins?

A

They are act locally (not found circulating in blood) and synthesized quickly by the COX-1 and COX-2 pathways

48
Q

What is the MOA of aspirin?

A

Irreversibly blocks both COX 1 & 2 to stop prostaglandin synthesis

Low dose - antiplatelet aggregation
Med dose - fever and pain relief
High dose - anti inflammatory

49
Q

What are side effects of aspirin?

A

GI irritation and ulcers (b/c prostaglandins form protective mucus in stomach), respiratory depression, tinnitus, prolonged bleeding, and Reye Syndrome

50
Q

What is Reye syndrome?

A

Hepatitis with cerebral edema

Never give small children aspirin

51
Q

What is the MOA of ibuprofen

A

Reversibly blocks COX 1 & 2

Watch out for cardioeffects and GI upset

52
Q

What are the uses and side effects of Diclofenac?

A

Blocks COX 1&2
Combined with misoprostol which is a prostaglandin analog to decrease the GI ulcers and irritation but still causes cardio risks

Used in post-op eye inflammation

53
Q

What is the MOA of Celecoxib?

A

Inhibits COX-2 only!
Still cardio risks, but reduced risk of GI effects such as ulcers and bleeding

It does contain sulfonamide so don’t use with sulfa allergies

Does NOT inhibit platelet aggregation b/c has no effect on COX 1

54
Q

What is acetaminophen?

A

NO anti inflammatory effect - only relieves pain and fever

It inhibits PGE in the CNS but not in the periphery

55
Q

What is a metabolite of Acetaminophen?

A

Conjugated by glucuronidation and sulfation to form NAPQI - very dangerous
At normal doses it reacts with glutathione to form a nontoxic substance

It causes hepatic necrosis and liver failure

No effect on platelets or uric acid. No Reye syndrome

56
Q

What is the antidote for NAPQI toxicity from acetaminophen?

A

Acetylcysteine

57
Q

What is the role of H1 receptors in histamine release?

A

They are coupled to Gq
Activates phospholipase C to IP3 & DAG which increases Ca+. This increases smooth muscle contraction, capillary permeability, and vasodilation

This is what causes pain and itching, allergic rhinitis and motion sickness

Vasodilation causes a decrease in BP
Capillary permeability causes increased lymph flow and edema

58
Q

What is the the MAO of H1 receptor antihistamines?

A

They compete for the binding site with histamine

59
Q

What do the first generation H1 antihistamines do?

A

Cause sedation!
Very lipid soluble so easily cross BBB
Short duration
Used for motion sickness
Cause constipation, dry mouth, and orthostatic hypotension
*don’t use these with other sedative, P450 inhibitors, or MAO inhibitors

60
Q

What are the 1st gen antihistamine drugs?

A

(-mine and -zine)
Diphenhydramine
Chloropheniramine
Promethazine - for motion sickness and focal anesthetics

61
Q

What do the 2nd generation antihistamines do?

A

NO sedating
Longer duration and not very lipid soluble
So no BBB crossing, no anti motion sickness effects, no anticholinergic side effects and no drug interactions

62
Q

What are the 2nd gen antihistamine drugs?

A

(-dine)
Loratadine
Fexofenadine

63
Q

What is the initial treatment for rheumatoid arthritis?

A

NSAIDs at high doses

*this is only for acute treatment, this does NOT slow the progression of the disease

64
Q

What is the treatment to slow the disease progression of Rheumatoid arthritis?

A

DMARDs

65
Q

What are the DMARD drugs?

A 
Slow disease progression of RA
Methotrexate
Hydrochloroquin (Plaquenil) 
Sulfasalazine
Tofacitinib 
Infliximab 
Adallimumab (Humera)
66
Q

What is the MOA and side effects of Methotrexate?

A

Inhibits dihydrofolate reductase - can’t make DNA so immune cells stop proliferating

Side effects - hepatotoxicity with long term use

67
Q

What are the side effects of Hydrochloroquin (Plaquenil)

A

Ringing in ears, nausea, vomiting, vision changes!

68
Q

What is the MOA and side effects of Sulfasalazine?

A

It’s a prodrug activated by the colon
-colon breaks it into 2 drugs - 5-ASA for Crohn’s disease and Sulfapyradine for RA

Side effects - very bad - nausea, vomiting, diarrhea, sulfa allergies, urine and skin turn yellow-orange

69
Q

When are Tofacitinib and Infliximab/Adalimumab used?

A

Only for severe RA, they suppress the immune system

Only when methotrexate has failed

70
Q

What is the MOA and side effects of Tofacitinib?

A

JAK-STAT inhibitor to stop inflammatory cytokine activity

Side effects - infection, lymphomas

Always test for TB before use

71
Q

What is the MOA and side effects of Infliximab and Adalimumab (Humera)?

A

They are monoclonal antibodies for anti-TNFalpha

Side effects are increased risk of infection

Always test for TB

72
Q

What is the goal for treatment of gout?

A

Decrease uric acid production
Stop reabsorption of uric acid
Increase metabolic breakdown of uric acid

73
Q

What is the treatment of acute pain and swelling from gout?

A

NSAIDs (indomethacin or naproxen)
Corticosteroids injected directly into joint
Colchicine - binds to tubulin to stop polymerization and mitosis
-side effects are nausea, vomiting, and diarrhea

74
Q

What are the drugs taken long term for prevention of gout?

A

Allopurinal
Probenecid
Pegloticase

75
Q

What does Allopurinal do?

A

Decreases uric acid production by stopping Xanthine oxidase

Side effects - increased toxicity with 6-MP if high doses

76
Q

What does Probenecid do?

A

Stops reabsorption of uric acid in the PCT (improves elimination of uric acid)

Side effects - may cause renal stones b/c more uric acid is in the urine

77
Q

What does Pegloticase do?

A

Enzyme that increases metabolic breakdown of uric acid by converting it to Allantoin (easily excreted)

Side effects - must be given IV very slowly (over 2 hrs) otherwise it will trigger a histamine release

  • pretreat with antihistamines or corticosteroids
  • similar to vancomycin

2-Spring18-PharmII (1 decks)

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