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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
How are amides metabolized?
In the liver by the P450 system Therefore liver dysfunction increases toxicity Amides are usually longer lasting and usually injected
26
What are the side effects of bupivacaine?
Severe cardiovascular toxicity including arrhythmias
27
What is the use for lidocaine?
Most commonly used due to potency, rapid onset, moderate duration, and versatility Used as an antiarrhythmic agent
28
What are the nociceptors?
Pain receptors Have 2 types: A-delta or C fibers
29
What are the A-delta nociceptors?
Large diameter, sparsely myelinated fibers that carry sharp, well localized pain (somatic pain)
30
What are the C nociceptors?
Small diameter, unmyelinated fibers that carry aching, poorly localized pain (visceral pain)
31
What receptors do the peptide enkephalins bind to?
Delta receptors
32
What receptor do the endorphins bind to?
Mu receptors
33
What receptors do the dynorphins bind to?
Kappa receptors
34
Which protein are the opioid peptides coupled to?
Gi (inhibitory)
35
Which 2 opioid receptors cause sedation?
Delta and mu Kappa just causes slowed GI tract
36
What is the MOA of Opioid drugs?
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
Where are opioids metabolized?
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
What are the side effects of opioids?
Constipation, pinpoint pupils, respiratory depression, urinary retention Toxicity = coma
39
What do we treat opioid overdose with?
Naloxone (given intravenously)
40
What are the withdrawal symptoms of opioids?
Mydriasis, chills, hyperventilation, diarrhea, anxiety
41
Wha do we treat an heroin addiction with?
Methadone (agonist) plus Natrexone (antagonist)
42
What are drug interactions with opioids?
Don’t use with sedative-hypnotics, ethanol, anesthetics, MAO inhibitors, or antipsychotic tranquilizers
43
What are the opioid full agonists?
Morphine Methadone Codeine Oxycodone All Mu receptors
44
What are the partial agonist opioids?
Buprenorphine Partially binds to mu
45
What are the mixed agonist-antagonist opioids?
Pentazocine Kappa agonist, mu antagonist
46
What are the full antagonist opioids?
Naloxone Mu antagonist You can combine naloxone with Buprenorphine for abuse but naloxone only works if injected
47
What are prostaglandins?
They are act locally (not found circulating in blood) and synthesized quickly by the COX-1 and COX-2 pathways
48
What is the MOA of aspirin?
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
What are side effects of aspirin?
GI irritation and ulcers (b/c prostaglandins form protective mucus in stomach), respiratory depression, tinnitus, prolonged bleeding, and Reye Syndrome
50
What is Reye syndrome?
Hepatitis with cerebral edema Never give small children aspirin
51
What is the MOA of ibuprofen
Reversibly blocks COX 1 & 2 Watch out for cardioeffects and GI upset
52
What are the uses and side effects of Diclofenac?
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
What is the MOA of Celecoxib?
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
What is acetaminophen?
NO anti inflammatory effect - only relieves pain and fever | It inhibits PGE in the CNS but not in the periphery
55
What is a metabolite of Acetaminophen?
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
What is the antidote for NAPQI toxicity from acetaminophen?
Acetylcysteine
57
What is the role of H1 receptors in histamine release?
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
What is the the MAO of H1 receptor antihistamines?
They compete for the binding site with histamine
59
What do the first generation H1 antihistamines do?
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
What are the 1st gen antihistamine drugs?
(-mine and -zine) Diphenhydramine Chloropheniramine Promethazine - for motion sickness and focal anesthetics
61
What do the 2nd generation antihistamines do?
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
What are the 2nd gen antihistamine drugs?
(-dine) Loratadine Fexofenadine
63
What is the initial treatment for rheumatoid arthritis?
NSAIDs at high doses *this is only for acute treatment, this does NOT slow the progression of the disease
64
What is the treatment to slow the disease progression of Rheumatoid arthritis?
DMARDs
65
What are the DMARD drugs?
``` Slow disease progression of RA Methotrexate Hydrochloroquin (Plaquenil) Sulfasalazine Tofacitinib Infliximab Adallimumab (Humera) ```
66
What is the MOA and side effects of Methotrexate?
Inhibits dihydrofolate reductase - can’t make DNA so immune cells stop proliferating Side effects - hepatotoxicity with long term use
67
What are the side effects of Hydrochloroquin (Plaquenil)
Ringing in ears, nausea, vomiting, vision changes!
68
What is the MOA and side effects of Sulfasalazine?
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
When are Tofacitinib and Infliximab/Adalimumab used?
Only for severe RA, they suppress the immune system Only when methotrexate has failed
70
What is the MOA and side effects of Tofacitinib?
JAK-STAT inhibitor to stop inflammatory cytokine activity Side effects - infection, lymphomas Always test for TB before use
71
What is the MOA and side effects of Infliximab and Adalimumab (Humera)?
They are monoclonal antibodies for anti-TNFalpha Side effects are increased risk of infection Always test for TB
72
What is the goal for treatment of gout?
Decrease uric acid production Stop reabsorption of uric acid Increase metabolic breakdown of uric acid
73
What is the treatment of acute pain and swelling from gout?
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
What are the drugs taken long term for prevention of gout?
Allopurinal Probenecid Pegloticase
75
What does Allopurinal do?
Decreases uric acid production by stopping Xanthine oxidase Side effects - increased toxicity with 6-MP if high doses
76
What does Probenecid do?
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
What does Pegloticase do?
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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