Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharm > Heme/Onc > Flashcards

Heme/Onc Flashcards

1
Q

Purine Degradation

A

-Purine -> Xanthine or hypoxanthine –> uric acid (xanthine oxidase)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Urate in the Kidney

A
  • Urate is filter, secreted, and reabsorbed
  • reabsorption predominates
  • URAT-1 (OAT)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Causes of Hyperuricemia

A
  • Under excretion due to renal impairment, HTN, low dose aspirin
  • Urate overproduction from purine rich diet, tumor lysis syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

TX of asymptomatic Hyperuricemia

A

-Diet modification and weight loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

TX of symptomatic Hyperuricemia

A
  • Diet modification

- Drug therapy to lower risks of recurrent attack, relieve symptoms of acute attack, and reduce serum urate levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Drug Classes

A
  • Uricostatic agents: reduce formation of uric acid
  • Enzymes: metabolize uric acid
  • Uricosuric Agents: Increase excretion of uric acid by the kidney
  • Anti-inflammatory agents: relieve acute attacks of gout
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Allopurinol

A
  • Analog of hypoxanthine acts as competitive inhibitor of xanthine oxidase
  • XO turns allopurinol into oxypurinol which is a non competitive XO inhibitor (longer half life)
  • Dissolution of tophi by lowering serum levels of urate
  • Decreases risk of nephropathy
  • Increase risk of acute attacks due to tissue mobilization of urate (Colchicine given before therapy is started)
  • Probenecid increases clearance of oxypurinol which requires incr. dose, but allopurinol increases the half life of probenecid requires lower dose
  • Mercaptopurine and azathioprine require dose reduction due to inhibition of XO
  • Hypersensitivity RXN (rash fever malaise and myalgias)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Feboxostat

A
  • Non-purine, non-competitive inhibitor of oxidized and reduced form of XO
  • Used as an alternative to allopurinol approved for hyperuricemia with gout attacks
  • Abnormal liver functions, nausea, joint pain and rash
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Pegloticase

A
  • Urate oxidase that converts rate to inactive and soluble allantoin
  • Peds tumor lysis syndrome in cases of leukemia, NOT CHRONIC GOUT
  • pegylation increases half life and reduces antigenicity
  • Blood samples for urate levels must be chilled to prevent enzymatic degradation
  • Hemolytic anemia in G6P, anaphylaxis, metheglobinemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Probenecid

A
  • Decreases reabsorption of urate by inhibiting URAT-1
  • Liberal H20 intake to prevent stones and keep urine pH above 6
  • DONT USE: nephrolithiasis, over production of urate and patients with renal insufficiency
  • Combine with Colchicine to prevent acute attacks
  • GI irritation use caution with patients who have ulcers
  • Salicylates reduce efficacy:
    • Low dose blocks proximal tubule secretion of urate -> hyperuricemia
    • High doses: block secretion and reabsorption w/ increase risk of stones
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Losartan

A

-moderate uricosuric option for patients w/ HTN who are intolerant to probenecid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Anti-inflammatory Drugs

A
  • NSAIDS: within 24 hrs of onset for 3-4 days and then taper for 7-10 (aspirin contraindicated)
  • Glucocorticoids: Use if NSAIDs don’t work, intra articular administration effective if 1-2 joints affected
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Colchicine

A
  • Anti-inflammatory
  • prevents activation, degranulation, and migration of neutrophils that mediate gout symptoms
  • Enterohepatic recirc, dose reduction in liver and renal insufficiency
  • Uses acute gout, and fixed dose combo with probenecid
  • GI effects are frequent
  • myelosuppression, leucopenia, granulocytopenia, thrombopenia, aplastic anemia
  • Don’t use with 3A4 and P-glycoprotein inhibitors
  • minimum of 3 days between treatments
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Indomethacin

A
  • nonselective COX-inhibitor
  • 30-50% experience adverse effects
  • GI effects can be fatal
  • severe frontal headaches
  • Seizures, depression, psychosis, hallucinations, and suicide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Amino Esters

A

Benzocaine cocaine Tetracain Procaine

Ester linkage between lipophilic and hydrophilic ends

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Amino Amide

A

Lidocaine, Prilocaine, Meprivacine, Bupivacaine

-Amide linkage between lipophilic and hydrophilic ends

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Mechanisms of action for local anesthetics

A
  • Block Na channels along Axons when the channel is open in a voltage and time dependent manner.
  • No loss of consciousness
  • Reversible
  • Ionized form has a higher affinity for the receptor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Local anesthetics crossing the membrane and blocking the receptor

A

-Non-ionized form diffuses across the nerve membranes while the ionized form (with H+ ion) blocks the receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Effects of Na+ blockage on nerve conduction

A
  • Threshold for excitation increases
  • Impulse conduction slows
  • Action potential amplitude decreases
  • Eventually ability to generate action potential is completely abolished
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Fibers affected by Local anesthetics

A
  • Local anesthetics are more efficacious on nerves that are rapidly firing or chronically depolarized
  • C and B (pain)fibers are blocked first followed by A fibers
  • A-alpha are blocked last (motor and proprioception)
  • Recovery occurs in the reverse order
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Potency and Duration of Local anesthetics

A

-Increases in lipophilicity –> increases in duration and potency.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Vasoconstrictors with Local Anesthetics

A

-Used to reduce rate of systemic absorption and prolong duration of action

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Most potent and longest lasting amino ester

A

-Tetracaine (procaine shortest and weakest)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Most potent and longest lasting amino amide

A

-Bupivacaine (mepivacaine the worst)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Metabolism of Esters and amides

A
  • Esters: Metabolized in plasma by plasma cholinesterases

- Amides: Metabolized in the liver by cytochrome P450 enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Toxicity of local anesthetics

A
  • Degradation: Hypersensitivity due to formation of benzoic acids and derivatives -> allergic rxns
  • CNS: sedation, visual and auditory disturbances, tongue numbness and metallic taste, Nystagmus and muscular twitching –> tonic-clonic convulsions (depression of inhibitory pathways)
  • Cardio: cardiac conduction and function effects (Bupivacaine)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Transient Nuerological Symptoms

A

-Syndrome of transient pain or dysethesia from spinal or epidural administration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

General anesthesia

A

-Reversible CNS state loss of response to and perception of stimuli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Dissociative Sedation

A

-Trance like cataleptic state in which the patient experiences analgesia and amnesia but retains reflexes and CV stability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Inhalation

A

-Continuous inhalation of gas or volatile liquid which rate depth and duration of anesthesia are under control. Recovery occurs when gas is turned off and anesthetic is eliminated by exhalation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Intravenous

A

-Lipophilic and injected, rapid onset, but depth and duration are not well controlled, duration depends on rate of metabolism.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Stages of Anesthesia

A
  1. Conscious but drowsy with variable degrees of analgesia
  2. Excitement and delirum –> unconscious reflex response to pain (during recovery)
  3. Surgical anesthesia regular respiration
  4. medullary depression with loss of respiration and vasomotor control -> death

-Now defined as induction, maintenance and emergence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

CV effects of general anesthesia

A

-Decrease mean arterial blood pressure by

vasodil, myo suppression, blunted baroreceptor reflex and decreased sympathetic tone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Respir effects of General anesthesia

A
  • Reduced or eliminated vent. drive
  • Lose gag and cough reflex
  • reduced LES tone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Emergence

A
  • Naseau and vomiting due to tim of CTZ (treat with 5HT3 agonist)
  • Return of sympathetic tone –> Tachy and HTN
  • Shivering treated with meperidine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Mechanism of Action

A

-Reversibly interact with hydrophobic sites of specific membrane receptors (enhance inhibit GABA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Pharmacokinetics of Inhaled Anesthetics

A

-Achieve equilibrium between alveolar gas and brain tissue: exhaled gas = inhaled gas
which is affected by blood solubility, alveolar blood pressure and partial pressure
-Concentration is expressed as partial pressure (more H2O soluble = lower partial pressure)
-Blood solubility: Lower solubility = higher partial pressure = faster rate of induction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Nitrous Oxide

A
  • Use in dental procedures or in combo to reduce dose of other inhalation agents
  • Advantages: good analgesia and amnesia, minimal CV effects, Reduced side effects of other inhalation agents
  • Disadvantages: Not complete anesthetic, rigidty, Diffusion hypoxia, Pneumothorax, inhibits b12 dependent enzymes so don’t use chronically
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Halothane

A
  • Induction/maintenance of anesthesia, still used in US for induction of peds (side effects less pungent)
  • advantages: rapid induction and recovery, muscle relaxant/bronchodilator
  • Disadvantages: Poor analgesic (hangover), significant cardiac depression (decrease MAP and sensitizes heart to epi tachy), Increase ICP, hepatitis
40
Q

Isoflurane

A
  • Use for maintenance at 1-2%
  • Advanatages: good CV profile
  • Disadvantages: pungent
41
Q

Desflurane

A

Widely used for maintenance during outpatient due to fast onset and recovery

  • Advantages: very rapid induction and emgerence, similar CV effects to isoflurane
  • Disadvantages: Pungent -> bronchial irritation cough and salivation
42
Q

Sevoflurane

A
  • Wide use for induction and maintenance in kids

- Advantages: low pungency and good CV profile

43
Q

Malignant hypothermia

A
  • Genetically susceptible patients exposed to halogenated inhalation anesthetics and/or succinylcholine
  • Post-op Hypercatabolic state: (hypercapnia, muscle rigidity, tachycardia, hyperthermia, hyperkalemia, Frequently fatal)
  • Mutation in skeletal muscle dihydropyridine or ryanodine receptors -> excessive intracellular Ca accumulation (severe contractions)
  • Tx: stop trigger, pure O2, skeletal muscle relaxant, and treat hyperkalemia and it’s related effects
44
Q

IV anesthetics

A
  • Used for induction
  • Benzodiazepines used prior to sedation anxiolysis
  • Given IV bolus or by constant infusion
  • Barbituates: Methohexital, thiopental
  • Non-Barbiturates: Propofol, Ketamine, etomidate
45
Q

Methohexital:

A
  • Short acting barbiturates
  • Activates barbiturate binding site on GABA-A receptors
  • Duration 10 min
  • Induction of anesthesia and procedural sedation
46
Q

Propofol

A
  • Most commonly used IV agent in the US
  • GABA-A agonist: sedative and amnestic, non analgesic
  • Duration 6 min
  • General anesthesia induction and maintenance
  • procedural sedation
  • Pst-Op anti emetic
  • Hypotension, respiratory depression, pain at induction site, potential for hypertriglyceridemia (fosopropofol no side effects)
47
Q

Ketamine

A
  • NMDA receptro antagonist (blocks glutamate) -> dissociative sedation, significant analgesia and bronchodilation and minimal CV side effects
  • Unpleasant emergence phenomenon, less prevalent in kids
  • Can be used for procedural analgesia/sedation for brief painful procedures
  • CNS pyschotomimetic: Vivid dreams, hallucinations, distorted visual and auditory sensitivity during emergence associated with fear and confusion, but may also produce euphoria can be counteracted with benzos
48
Q

Causes of muscle spams

A
  • Over stretching of muscle
  • Repetitive strain of Muscle
  • Wrenching of a joint
  • Tearing of tendon or ligament
49
Q

Spasm pain spasm

A
  • Muscle overuse activates nociceptors in muscle which have synaptic connections with alpha and gamma motor neurons
  • increased activity of neurons and increased muscle contraction
  • Force of muscle contractions may compress blood vessels leading to ischemic contraction which excite nociceptors
50
Q

Spasmolytics

A
  • Chlorzoxazone, cyclobenzaprine, methocarbamol, orphenadrine
  • All spasmolytic drugs alleviate the Sx of localized muscle spasms and no one is better than the other while all are equally effective as NSAIDS
  • The difference amongst pain meds is onset and duration of action
51
Q

Onset and duration of Spasmolytics

A

-Carisoprodol and methocarbamol are the quickest while cyclobenzaprine is the longest acting.

52
Q

Mechanism of actions of the spasmolytics

A
  • Depresses polysynaptic reflexes in the spinal cord (over monosynaptic)
  • Cyclobenzaprine reduces tonic somatic motor activity influencing both alpha and gamma motor neurons
  • Orphenadrine is an anticholinergic used to treat spasms of various etiologies ( i.e. lumbargo and sciatica
53
Q

Cyclobenzaprine

A
  • Related to tricyclics
  • Serotonergic and noradrenergic
  • Used for short term treatment of spasticity, not effective for treatment of spasticity
  • Drowsiness, loss of coordination, anticholinergic, dizziness, physical dependence,
  • At high doses: areflexia, flaccid paralysis, respiratory depression, tachycardia, hypotension
54
Q

Methocarbamol

A
  • Related to tricyclics
  • Short term treatment of skeletal muscle spasms, but not effective for treatment of spasticity
  • Drowsiness, loss of physical coordination, light headedness, dizziness, discoloration of urine
  • After parenteral administration: syncope, hypotension, bradycardia, ataxia and vertigo, seizures, hemolysis
  • Addicition and physical dependence
  • CNS and respiratory depressions
55
Q

Spasticity

A
  • Increase in tonic stretch reflexes and flexor muscle spasms with muscle weakness
  • Usually associated with brain or spinal cord injuries (loss of supra spinal inhibitory influence on alpha motor neurons
  • Contractions are velocity dependent, greater resistance with faster stretches
56
Q

Treatment of spasticity

A
  • Reduce pain, frequency of spasms or irritating stimuli
  • Improve gait, hygiene, and ADLs
  • Multi-disciplinary approach
57
Q

Baclofen

A
  • Oral: Decrease spasticity due to multiple sclerosis and SC injury, can also be used for trigeminal neuralgia
  • Intrathecal: Takes a lower dose and has fewer side effects. Used for Cerebral palsy, anoxic brain injury, MS, stroke, SC injury, AV malformation
  • MOA: Binds presynaptic GABA B receptors which decreases Ca influx in presynaptic terminals which depresses the release of glutamate, aspartate, and reduces substance P release from nociceptive afferent nerve terminal
58
Q

Depolarizing NMBD agents

A
  • Agonists at nACh Receptors
  • Depolarize end plates
  • Produce fasciculations
59
Q

Non-Depolarizing NMBD agents

A
  • Competitive antagonists for nACh receptors, can also block pore of channel
  • induce flaccid paralysis
  • Do not depolarize end plate
  • No fasciculation
60
Q

NMDB structure

A

related to acetylcholine

61
Q

Sensitivity to block by NMBDs

A

-Rapidly moving muscles > limbs > trunk> diaphragm

62
Q

Succinylcholine

A
  • Only brief relaxation required
  • Rapid short action hydrolyzed by cholinesterase
  • No crossing BBB
  • Phase 1 Succinyl binds to nAChR and causes depolarization, not metabolized by ACh esterases leads to membrane remaining depolarized –> flaccid paralysis
  • Phase II: Membrane may become repolarized but can’t be depolarized again (desensitized)
  • BLOCKAGE CANT BE REVERSED BY ACh ESTERASE INHIBITORS
63
Q

Succinylcholine metabolism

A
  • Plasma cholinesterases hydrolyze in liver
  • Only small fraction of drug reaches NMJ
  • Block terminated by diffusion
  • Side effects: Malignant hyperthermia, stimulate autonomic ganglia, hyperkalemia (release of K+) , myoglobinuria,
64
Q

Blockage due to non-depolarizing blocker

A

-Can be reversed by ACh esterase inhibitor (edrophonium and neostigmine) allow ACh to build up and compete with NMDB

65
Q

ND NMDB PK

A
  • Dont cross BBB
  • Rapid distribution followed by slower elimination
  • Eliminated by plasma cholinesterases, excreted by kidney, metabolized by liver, spontaneous breakdown
66
Q

Atracurium

A
  • Slower onset of action with intermediate duration
  • Organ-independent metabolism
  • Laudanosine is a non-active metabolite (convulsions)
  • Dose dependent histamine release
  • Hemodynamic instability and bronchospasms
67
Q

Cisatracurium

A
  • Slow onset with intermediate duration
  • Organ-independent metabolism
  • Less laudanosine is produced (appropriate for infusion)
  • Much less histamine is released compared to atracurium
68
Q

Methotrexate: USES, Structure, and PK

A
  • Used in early RA, RA w/ poor prognosis, generally first choice
  • Orally or subq (bioavailability and fewer side effects) once/week (hepatoxicity) may take 4-6 weeks for effects
  • Folic acid analog used for chemo, enter cells via folate transporter and is polyglutamated (traps and increases half-life)
69
Q

Methotrexate: MOA

A
  • Mech 1: inhibit purine synthesis by inhibiting dihydrofolate reductase and tetrahydrofolate formation (anti-cancer)
  • Mech 2: Inhibits AICAR –> increase in adenosine –> resolution of inflammation (maybe major benefit in RA)
  • Mech 3: Inhibits thymidylate synthetase –> reduction in thymidine levels –> inhibition of inflamm cell proliferation
70
Q

Methotrexate: Side effects

A
  • Rare hepatotoxicity with high doses, reason for once/week dosing, NO ETOH, Elevation of liver enzymes, Don’t use with liver failure
  • NO RENAL INSUFFICIENCY
  • NO PREGNANCY
  • PULMONARY TOXICITY
  • INCREASE INFX
  • GIVE FOLATE 24 hrs. after administration to counteract side effects
71
Q

Hydroxychloroquine

A
  • Antimalaria drug thought to act by altering intracellular pH
  • Orally effective with slow onset and LONG half-life
  • Frequently used with MTX and/or sulfasalazine
  • RETINAL DAMAGE (eye exams) more common with renal insufficiency
  • hypoglycemia in diabetics (possible reduction in incidence of T2DM)
  • Safe in pregnancy
  • DONT USE WITH PSORIASIS OR PORPHYRIA
  • Caution with neurological, hepatic, or hematologic disorders and alcoholism
72
Q

Sulfasalazine

A
  • Immune suppressive drug frequently used with hydroxycholorquine and MTX
  • Orally effective –> salicylate and sulfapyridine (both poorly absorbed by affect GI immune system
  • Skin reactions (urticaria, rash, and pruritus)
  • Blood dycrasias in first 3-6 months
  • Reduction in folate absorption so supplement
  • DONT USE W/ SULFA or CELEBREX allergies
73
Q

Triple Drug therapy

A
  • Methotrexate weekly
  • Try Hydroxychloroquine plus sulfasalazine daily
  • try all three in combo
  • Can add prednisone or NSAID
  • Multiple drugs with synergist actions –> less side effects than any one drug by itself
  • Goal: markedly slow or stop disease progression, ideally disease remission not just to relieve symptoms
74
Q

Leflunomide

A
  • Immunosuppressive agent which inhibits dihydro orotate (pyrimidine synth) and tyrosine kinase at higher doses.
  • Inhibits T-Cell proliferation and reduces auto-antibody formation
  • Orally daily –> teriflunomide (active agent)
  • Extremely long half-life due to enterohepatic recirc.
  • Cholestyramine to clear drug from body
  • Inhibits CYP P450s
  • Teratogenic and carcinogenic
  • ABSOLUTELY CONTRAINDICATED DURING PREGNANCY need 2 negative tests two weeks apart
75
Q

MInocycline

A
  • Tetracycline antibiotic which inhibits metalloproteinases and collagenases
  • Inhibits collagen degradation component of RA
  • Effective one or twice daily in seropositive RA
  • No real side effects
76
Q

Biological response modifiers

A
  • Peptides or proteins
  • advances in making and suing peptides as drugs
  • Target individual specific mediators early in inflame signaling cascade
  • Start when tDMARDS fail as add on agent. More effective in combo with MTX
  • Increased risk of info (TB, URI, herpes zoster, fungal)
  • Blood dyscrasias
  • Increased cancer incidence
77
Q

ANTI-TNF

A
  • Etanercept, Infliximab, Adalimumab
  • Cytokine central to immune and inflammation, upstream regulator of many other immune/inflammatory cytokines
  • Promotes inflammation and Joint destruction
78
Q

Etanercept

A
  • 2 Soluble p75 subunit of TNF receptor linked the the Fc domain of IgG1
  • Binds TNF and prevents binding to cellular receptors inhibiting all steps down stream
  • Protein, SC weekly, shortest duration
  • Possible PML (rare viral infection of CNS
  • Cancer risks similar to methotrexate
79
Q

Infliximab

A
  • Monoclonal antibody against TNF, not part of TNF receptor (mouse-human chimera)
  • Administered IV 4-8 weeks always combined with MTX and other DMARDs
  • Hypotension
80
Q

Adalimumab

A
  • Anti-TNF antibodies like infliximab (not part of TNF receptor just antibody against
  • Fully humanized
  • Injected SC every 2 weeks
  • Approved for juvenile idiopathic arthritis
  • Causes demyelination so contraindicated in patients with demyelinating disease like MS
81
Q

CTLA-4, CD-80, and CD-28

A

CD-28 = T-Cell surface protein that recognizes activated APCS
CD-80 = on APCs is the CD-28 receptor
CD-80 and CD-28 binding activates the T-Cell
CTLA-4 is an antagonist for CD-80 that keeps CD-28 from binding there

82
Q

Abatacept

A
  • CTLA-4 Analog
  • CD 28 receptor antagonist (binds CD-80)
  • T-Cell activation inhibitor
  • IgG1 and CTLA-4 binding domain fusion protein
  • Injected SC weekly or IV monthly
  • Severe RA not responsive to other DMARDS
  • Serious INFX
  • Infusion reactions (bronchospasm, angioedema, hypotension
  • NOT COMBINED WITH TNF INHIBITORS (increased risk of INFX)
  • NOT WITH PEOPLE WHO HAVE COPD
83
Q

Rituximab

A
  • Anti-CD20 monoclonal antibody and therefore and B cell inhibitor
  • IV two injections two weeks apart
  • Used w/ MTX
  • Dont Use with anti-TNF
84
Q

Concentration gradient and second gas effect

A

-Bulk uptake of one gas increases apparent concentration of second gas causing increase absorption of 2nd gas.

85
Q

Elimination of Anesthetic

A
  • Reverse process -> exhalation
  • More blood soluble agent -> hangover
  • Diffusion back in to the lungs can result in hypoxia b/c partial pressure increases -> decreased partial pressure of O2
  • Currently used agents are only minimally metabolized b/c metabolites are toxic
86
Q

Potency of inhalation anesthetics

A
  • Minimum concentration of agent required to induce anesthesia
  • MAC = minimum partial pressure that prevents movement in 50% of adult patients
  • MAC ISN’T related to induction time.
87
Q

Calcineurin Inhibitors (Cyclosporine): MOA

A
  • Interferes with T-Cells by binding to cyclophilin to for a calcineurin inhibitory complex
  • Calcineurin activates NFAT which leads to IL-2 transcription
  • IL-2 activates T-Cells
88
Q

Calcineurin Inhibitors (Cyclosporine): PK, and Therapeutic uses

A

-PK: Poor oral, CYP 3A4 (grapefruit juice), individual dosing and blood level monitoring
Uses: Prevent rejection of allogenic kidney, liver, lung, and heart, usually given with glucocorticoids
-DOESNT REVERSE ACUTE EPISODES OF ESTABLISHED REJECTION
-Psoriasis, and rheumatoid arthritis
-Dry eyes

89
Q

Calcineurin Inhibitors (Cyclosporine): adverse effects

A
  • CsA ISNT MYELOTOXIC!
  • Nephrotoxicity: does dependent and reversible, reduction in RBF due to fibrosis
  • HTN: renal vasoconstriction and Na retention
  • Tremor, hirsutism, gingival hyperplasia
90
Q

Calcineurin Inhibitors (Tacrolimus): MOA and Uses

A

-Similar to CsA (not in structure)
-Binds to FKBP-12 and forms a complex that inhibits calcineurin
-More potent and better efficacy than CsA
USES:
-Prevent rejection of kidney, liver, lung and heart with glucocorticoids
-Psoriasis and rheumatoid arth
-Topical for atopic dermatitis, and oral for ulcerative colitis

91
Q

Calcineurin Inhibitors (Tacrolimus): PK and Adverse effects

A
  • CYP3A4
  • nephrotoxicity
  • Neuro: seizures and tremors
  • Hyperglycemia and diabetes
  • HTN
92
Q

mTOR Inhibitors (Sirolimus): MOA and Uses

A

MOA:
-Binds and complexes with FKBP-12 that then binds to and inhibits the MTOR complex 1
-MTOR complex 1 is a serine threonine kinase and inhibition arrests T-Cell division in G1 phase
USES:
-Kidney transplant rejection in combo with CsA B/C lower risk of kidney toxicity
-Steroid refractory acute and chronic GVHD
-CAD

93
Q

mTOR Inhibitors (Sirolimus): PK and Adverse effects

A 
PK: 
-60 hr T1/2 
-CYP3A4 and P-glycoprotein elimination
Adverse:
-Profound myelosuppression
-Poor wound healing
-Incr. serum cholesterol and triglycerides (STATIN)
-NOT FOR LIVER OR LUNG TRANSPLANT
94
Q

Cytotoxic (Antiproliferative) Agents (Azathioprine): MOA, Uses, and Adverse effects

A 
MOA: 
-Prodrug of 6-Mercaptopurine
-Direct antiproliferative (s-phase) effects on activated T-cells and reduces B-Cell activation but less effects on antibody production
USES:
-Adjunct with other agents to prevent rejection
-RA in NON-PREGNANT PATIENTS
AE:
-Myelosuppression
-Mutagenic and teratogenic
-Dose reduction w/ pts on Allopurinol
95
Q

Cytotoxic (Antiproliferative) Agents (Mycophenolate Mofetil): MOA, Uses, AE, and PK

A

MOA:
-Prodrug of mycophenolate
-Highly specific for T and B lymphocytes due to heavy reliance on de novo pathway for purine synthesis
-Reversible non-comp inhibit of lymphocyte inosine monophosphate dehydrogenase
Uses:
-Heart, liver, kidney transplants,
Adverse effects:
-GI effects, myelosuppression, infections
PK:
-converted by plasma esterases to MPA

Pharm (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions