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Pharm II - Chamberlain > Exam I > Flashcards

Exam I Flashcards

1
Q

What are the three layers of the adrenal cortex and what do they secrete?

A

outermost to inner

  • zona glomerulosa - mineralcorticoids (Aldosterone)
  • zona fasiculata - glucocorcoids (cortisol)
  • zona reticularis - sex steroids (P, E, T, DHEA)
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2
Q

This is the precursor of all steroid hormones..

A

progesterone

- produced in zona fasiculata

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3
Q

what is the name for cortisol when it’s used as a medication?

A

hydrocortisone

- can cause mild inc. in BP

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4
Q

What increases with glucocorticoids?

A
  • glucose (gluconeogenesis, glycogenolysis)

- neutrophils

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5
Q

what decreases with glucocorticoids? leading to what significant SE of these medications?

A
  • circulating lymphocytes
  • decreased production of prostaglandins/leukotrienes
  • decreased ability to fight off infection**
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6
Q

what are the two primary effects of glucocorticoid use?

A
  • anti-inflammatory

- immunosuppressive (useful in organ transplant)

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7
Q

Compare steroid potencies of cortisone, hydrocortisone, prednisone, flumethasone, dexamethasone and betamethasone. Which are long (>48hr), intermediate (12-36), or short (<12) acting?

A 
cortisone - 0.8, short
hydrocortisone - 1.0, short
prednisone - 4.0, intermed. 
flumethasone - 15.0, long
dexamethasone -30, long
betamethasone - 35, long
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8
Q

when considering topical steroids - which compounds are best for which skin types and what is a common SE of topical steroids?

A

dry - ointment, paste (50% pts)
oily - cream, lotion, drying gel

SE - skin thinning (increased with increase potency)

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9
Q

this, is a rapid decrease in the response to a drug over a relatively short time period - how is it avoided?

A

tachyphylaxis

- avoid by rx’ing use to one week on, one week off

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10
Q

what are the 6 mechanisms of tolerance?

A
  • change in receptors
  • loss of receptors
  • exhaustion of mediators
  • increased metabolic degradation
  • physiological adaptation
  • active extrusion of drug from cells
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11
Q

this product works as an effective vasoconstrictor - what is it? and what is it’s active ingredient?

A

Preparation H

- phenylephrine

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12
Q

when considering ocular glucocorticoids - what must be ruled out?

A

any infectious process

- ocular herpes esp, could cause complete corneal ulceration

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13
Q

this important drug class works by inhibiting phospholipase A2, blocking the release of arachadonic acid, which is the precursor to what?

A

glucocorticoids
- sones

inhibits

  • prostaglandins
  • leukotrienes
  • suppresses histamine release and kinin activity
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14
Q

this drug class commonly causes SE of weight gain from salt and water retention, if used topically, it can cause skin atrophy - which drug class is this?

A

glucocorticoids

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15
Q

chronic glucocorticoid use can create redistribution of body fat, rounding of the face, appearance of striae, telangiectrasias, acne, and increase body hair growth - otherwise known as?

A

cushing-like appearance

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16
Q

This is generally due to glucocorticoid OVER-USE until proven otherwise, what is it?

A

bilateral avascular necrosis

cellular bone death due to interrupted blood supply

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17
Q

the stronger the corticosteroid effect, the ______ the mineral corticoid effect?

A

WEAKER

and visa versa

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18
Q

abrupt withdrawal of glucocorticoids can lead to (2)?

A
  • ACUTE ADRENAL INSUFFICIENCY SYNDROME (ie - Addisonian crisis - LETHAL - fatigue, mm weakness, loss of appetite, weight loss, N/V, LOW BP*)
  • exacerbation of the underlying disease
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19
Q

Hyperpigmentation can occur in what but not, what?

A

Hyperpigmentation occurs in:
PRIMARY Addison’s disease
NOT SECONDARY

  • often in skin folds, mucus membranes
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20
Q

this drug is the preferred drug for cortisol replacement therapy, it works by affecting gene transcription either by up or down-regulating protein production - what is it and what’s it duration of action?

A

hydrocortisone

- short duration (8-12hrs)

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21
Q

this is the most used PO glucocorticoid in medicine and preferred in reactive airway diseases. it affects gene transcription by up or down-regulating protein production - it’s also important for leukemia reaction - what is it and what’s it’s DOA?

A

prednisone
- intermed. (12-36hrs)

  • must be tapered*
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22
Q

this potent fluorinated corticosteroid is used IV for intracranial pressure reduction - affects gene transcription of proteins (up or down-reg), and it has minimal mineralcorticoid effect - drug and DOA?

A

dexamethasone

- long acting (>48hrs)

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23
Q

this corticosteroid is indicated for asthma maintenance, NOT ACUTE, it works by diminishing inflammation of the bronchial wall, what is it?

A

triamcinolone

- SE: thrush, sore throat, nosebleed, increased coughing, HA, runny nose

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24
Q

this pro-drug of corticosteroid is used for asthma prophylaxis, can be used to treat unusually severe aphthous ulcers

A

beclomethasone (QVAR)

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25
Q

aldosterone, released from the zona glomerulosa - is responsible for what? in which disease is it decreased?

A

regulating

  • intravascular volume
  • BP

retains Na, HCO3-
excretes K

decreased in Addison’s disease patients

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26
Q

Aldosterone levels increase in patients with this, and treated with this aldosterone antagonist.

A

Aldosterone increases in
- Conn’s Syndrome

TX’d with spironolactone

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27
Q

this halogenated glucocorticoid/mineralcorticoid agonist is used as a mineralcorticoid replacement for Addisons - it works by retaining sodium - what is it?
Even though it’s a glucocorticoid, it’s not indicated for what?

A

fludrocotisone

- NOT indicated as ANTI-INFLAMMATORY

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28
Q

this steroid, produced in the zona reticularis - has been proposed as an anti-aging drug, but can cause the adverse effect of acne or hirsuitism and is contraindicated in patients with a history of sex hormone responsive cancer - what is it?

A

Dehydroepiandrosterone (DHEA)

- although, thought to help with bone development post-menopausal

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29
Q

this is a nerve response resulting from injury to, or inflammation of tissue - what is it? How is it treated?

A

nociception

  • the perception of pain
  • subjective, can arise without physical stimulus
  • treated with AIs or analgesic medications
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30
Q

Does the brain have nociception?

A

no - pain insensitive

the meninges however, do.

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31
Q

this type of pain, is generally chronic, described as burning, sharp, shooting or aching - may be associated with tingling, numbness

A

peripheral neuropathy

- treated with medications that act on neurotransmitters and AIs

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32
Q

these are pain killers, while these cause delirium and drowsiness - what does both and what are they called?

A

analgesics - pain killers
narcotics - delerium and drowsiness

opiates do both
- narcotic analgesics

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33
Q

what are the narcotic analgesics?

A 
heroin - Sch. I
methadone - Sch. II
morphine - Sch. II, Categ. C
fentanyl - Sch. II, Categ. C
codeine - Sch. II
Tylenol #4 - Sch. II, Categ. C
Tylenol #3 - Sch. III, Categ. C
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34
Q

this 18th and 19th century camphorated tincture, made from powdered opium, was widely used to calm fretful children

A

paregoric - schedule II

  • anti-tussive
  • anti-D
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35
Q

this tincture of opium has a history for anti-D, and anti-tussive, analgesic activity, but is now used almost exclusively for anti-D, but also off-label for treating neonatal withdrawal syndrome, schedule II narcotic

A

landanum

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36
Q

at present, this has no accepted medical use and therefore carries a DEA designation of schedule I

A

heroin

- lipid soluble, rapidly crosses BBB

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37
Q

this drug is 2-3 times more potent than morphine

A

heroin

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38
Q

this category of drug is used primarily to relieve pain and anxiety from pain, it mimics a specific type of neurotransmitter - what is it and what’s the neurotransmitter?

A

opiate analgesics
mimic OPIOPEPTINS*
- endorphines
- enkephalins

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39
Q

these work to inhibit neuronal activity by binding to G-coupled receptors and inhibiting adenylate cyclase. They also - hyperpolarize the postsynaptic cleft and reduce influx of Ca pre-synaptically - what are they?

A

opiate analgesics

- also inhibit release of substance P at presynaptic cleft

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40
Q

the analgesic properties of the opiates are primarily mediated by what receptor?

A

mu

others:

  • kappa
  • sigma (hallucinations)
  • delta (enkepalins peripherally)
  • epsilon
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41
Q

which receptor may be responsible for hallucinations and dysphoria associated with opiate use?

A

sigma

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42
Q

These, since 2014 have been reclassified as schedule II substances and have tighter restrictions - what are they and what are they a product of

A

hydrocone combination products (HCPs)

  • vicodin
  • lorcet
  • lortab
  • norco

can only be prescribed for one month at a time.

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43
Q

this is a potent opiod agonist, with high affinity for mu receptors. it relieves pain in the CNS by raising pain threshold in the brain stem, thalamic and spinal cord - while also altering brain’s perception of pain. It works in acute MI as a peripheral vasodilator. How is tolerance achieved?

A

morphine / MS contin

  • acts directly on CNS to relieve pain
  • perception of actual sensation of pain, blocked

tolerance by

  • up-reg of CYP450 system (sig first pass metab)
  • down-reg of mu receptor sites
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44
Q

respiratory depression is a serious side effect of this drug and the most common cause of death due to it’s use. Itching, due to increased histamine release is an annoying additional SE too!

A

Morphine / MS Contin

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45
Q

What is the DEA and pregnancy category for Morphine?

A

Schedule II

Pregnancy Categ. C

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46
Q

This drug works similarly to morphine (acting on CNS to decrease pain perception) but is 80x more potent - what is it and what side effect do we need to be aware of?

A

Fentanyl / Duragesic

  • SE - respiratory depression
  • HIGHLY ADDICTIVE

Schedule II
Category C

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47
Q

concurrent consumption of ethanol while using this drug can increase CNS depression, likewise, grapefruit can increase it’s concentration in the blood. while St. John’s wort works to decrease blood levels - what drug is it?

A

fentanyl / duragesic

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48
Q

this is a semi-synthetic opioid used to treat opioid addiction

A

buprenorphine

- butrans (transdermal for chronic pain)

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49
Q

this opioid agoist converts to morphine in the body, but is a much weaker analgesic comparatively. It has a lower abuse potential and is an effective antitussive

A

codeine

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50
Q

Differentiate Tylenol #3 and #4 - what are they combined with and what are the relative potencies
- what category?

A

4

codeine and acetaminophine

#3:
30mg codeine phosphate, 300 mg acetaminophine

60mg codeine
300 mg acetaminophine

schedule II, V (dose dependent)
category C (preg)
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51
Q

what should not be prescribed for pain following tonsillectomy and or adenoidectomy - due to what genetic variant?

A

codeine

  • ultra-rapid metabolizers (CYP2D6) - faster and more complete conversion of codeine to morphine
  • obstructive sleep apnea syndrome
  • OD, death
52
Q

this centrally-acting analgesic is used to treat pain, it mildly agonizes the mu-receptor while also affecting reuptake of NE and serotonin, what is it?

A

tramadol / ultram

SE - N/V, memory loss, sweating, constipation

weaning too quickly can cause withdrawal

53
Q

this acetaminophen containing narcotic is no longer indicated for elderly due to increased risk of falls

A

darvocet

propoxyphene / acetaminophin

54
Q

this synthetic, orally effective opiod is used to control withdrawal of heroin and morphine, it has a potency equal to morphine, but less euphoria - longer DOA

A

methadone

55
Q

this opioid receptor antagonist is primarily used in management of ALCOHOL and OPIOID dependence

A

Naltrexone

56
Q

This is primarily used for emergent treatment of narcotic overdose - what other drug is similar and used for the same thing?

A

Naloxone

“get them out of the red zone, with naloxone” (I just made that up, whatever)

nalorphine

  • structurally similar to naloxone
  • acts on mu (agonist) and kappa (antagonist)
57
Q

this opioid antagonist is used to reverse the coma and respiratory depression of opioid overdose - what is it’s onset of action?

A

naloxone

- works in 30 mins

58
Q

this is an isomer of codeine - it’s an effective anti-tussive and commonly used in OTC cough meds

A

dextromethorphan

59
Q

prostaglandins call in the immune system, there are 4 of them, what enzyme makes which ones and what do they do?

A

COX-1 (physiologically important)

  • PG1 - secretes mucus for stomach
  • PG2 - platelet stickiness

COX-2 (inflammatory)

  • PG3 - PAIN
  • PG4 - inflammation
60
Q

this class of drug acts by inhibiting the synthesis of prostaglandins

A

NSAIDS (non-steroidal anti-inflammatory drugs)

  • COX enzymes play important role in cyclooxygenase pathway
61
Q

This medication is a COX 1/2 inhibitor also used to treat GOUT

A

indomethacin / indocin

62
Q

what are the COX2 inhibitors?

A

Celecoxib / celebrex

Refecoxib / Vioxx

63
Q

This NSAID binds IRREVERSIBLY to COX 1 and 2 enzymes - diminishing pain, inflammation, fever

A

Aspirin / acetylsalicyclic acid (ASA)

SE: GI irritation, increased risk of REYEs syndrome (don’t admin unless >15-18yrs), PUD, good shit
- TINNITUS*

64
Q

This NSAID reversibly binds COX1 and 2, but does not have increased risk for Reye’s syndrome

A

Ibuprofen / Motrin, Advil

65
Q

This NSAId is a selective COX2 inhibitor and therefore has minimal effects on GI tract, with fewer reports of bleeding, so what are it’s SE?

A

Celecoxib / Celebrex

- SE may be increased risk of CVD

66
Q

This NSAID weakly blocks peripheral prostaglandin synthesis, with strock blockade of prostaglandin synthesis in the hypothalamus, decreasing fever and pain

A

acetaminophen / tylenol

- may be a selective COX3 inhibitor, only found in Brain and SC

67
Q

So acetaminophen has some shit wrong with it - it has an overdose amount you should not exceed in 24 hours, and what should never be mixed with it - both, to avoid what?

A

OVERDOSE: 7gm/24hrs
NEVER mix with ethanol

  • can lead to severe hepatic necrosis - liver failure - coma - death.

Preg. Categ. B

68
Q

acetaminophen is oxidatively metabolized in the liver, made into this toxic metabolite, to prevent the side effects of acetaminophen toxicity, what should be administered?

A

N-acetyl-p-benzoquinone-imine (NAPQI)

  • XS causes hepatocellular death and liver necrosis

Antidote: N-acetyl cysteine (NAC)

69
Q

What are the 4 stages of acetaminophen toxicity?

A

1 (12-24hrs) - N/V
2 (24-48hrs) - LFTs increase (ALT, AST), increased bilirubin
3 (72-96hrs) - PEAK HEPATOTOXICITY
4 (>96hrs) - recover, await transplant

70
Q

this is a precursor to glutathione and increases glutathione availability to bind NAPQI
- used mainly as a mucolytic agent

A

NAC

- most effective if administered within 8 hours ingestion

71
Q

This agent was used as a “narcotic” drug in the ER until the drug seekers found out what the docs were doing

A

Ketorolac
- first injectable NSAID

PO = increased GI issues

72
Q

Gout is a disorder of

A

purine metabolism

  • uric acid crystalizes to monosodium urate
  • precipitate in joints and tissue
73
Q

this enzyme breaks down uric acid in humans, but seems to be struggling to survive an evolutionary loss - what is it?

A

uricase

74
Q

These are pathognomonic for gout disease, whereas radiographically, this is typically seen

A

tophi - pathognomonic

rat bite lesion - radiograph

75
Q

definitive dx of gout is based upon identification of?

A

monosodium urate crystals

  • needle like morphology
  • strong negative birefringence
76
Q

what condition is most important to differentiate from gout?

A

septic arthritis
- synovial fluid gram stain and culture should be performed.

  • other similar conditions
  • pseudogout
  • RA
77
Q

which joint is mc affected in gout? in pseudogout? - which crystals are seen?

A

gout - 1st MTP
needle-like monosodium urate crystals)
pseudogout - knee
rhomboid shaped calcium pyrophosphate dihydrate crystals

78
Q

what common drink can increase you chance of developing gout - why?

A

Beer
full of purines
- go for wine.

often gout is associated with DM, HTN, obesity

79
Q

These have been associated with gout attacks, but low-dose of this particular one, does not seem to increase the risk of gout. Which drug class, what’s the exception and what other two medications increase risk of gout?

A

diuretics
- except Hydrochlorothiazide

other meds:

  • niacin
  • aspirin
80
Q

Which two drug classes are associated with lower risk of gout?

A

CCBs

losartan

81
Q

half of all gout cases occur where

A

MTP-1, big toe.

- lower body temperature can precipitate, gen occurs during evening

82
Q

what are first line tx for gout?

A

NSAIDS (x1-2 weeks)

- Indomethacin, however SE of HA is common.

83
Q

When combined with NSAIDS this can exacerbate ulcer and these can be cytoprotective

A

H2, exacerbates ulcers

PPI - cytoprotective

84
Q

Acute treatments for Gout

A

NSAIDs
Steroids
Colchicine

85
Q

Chronic treatments for Gout

A

Colchicine
Allopurinol
Probenecid

86
Q

This NSAID inhibits COX 1 and 2, treats acute gout - what is it? What’s a common SE and should nursing mothers use it?

A

Indomethacin / indocin

SE - HA**

  • excretes in breast milk, CI for breastfeeding
87
Q

Sampter’s Triad

A
  • nasal polyps
  • allergy to aspirin/NSAIDs
  • asthma
88
Q

This drug amazingly has the ability to close patent ductus arteriosus in neonates, whaaaaat?

A

indomethacin / indocin

  • can worsen parkinson’s sx though
  • be careful with K sparing diuretics
89
Q

this injection is given short-term to relieve pain and swelling from joints, tendons, etc. Can also treat anaphylaxis. It does this by decreasing inflammation and inhibiting inflammatory proteins - but it comes with its SE

A

cortisone injection

SE:
HYPERGLYCEMIA
insulin resistance
DM
osteoporosis
anxiety/depression, 
cataracts, glaucoma
90
Q

glucocorticoids primarily mediated through what? which does what?

A

lipocortin-1

- suppresses phospholipase A2, blocks eicosanoid production and therefore PG and leukotriene synth.

91
Q

this mitotic inhibitor is indicated for acute gout or prophylaxis - it inhibits microtubule polymerization - essential for the mitosis.

A

colchicine

  • AI effects linked to it’s ability to bind with TUBULIN, main microtubule constituent
  • also inhibits motility of neutrophils
92
Q

colchicine seems awesome, but what SE should we be aware of?

A

peripheral neuropathy
neutropenia
hair loss

OD (like arsenic poisoning)- N/V, acute renal failure

93
Q

This purine analog inhibits xanthine oxidase, an enzyme important in conversion of purine to uric acid, what is this drug? what side effect is it commonly known to cause

A

Allopurinol / Zyloprim

  • SE: SJS* common SE
  • N/V, Skin rash
94
Q

these are sustances that increase the excretion of uric acid and reduce plasma concentration - however with the ability to contribute to these suckers?

A

uricosurics

- increasing uric acid in urine can cause renal lithiasis

95
Q

this uricosuric works by interfering with kidney’s organic anion transporter - by stopping it’s reclamation of uric acid back to the blood

A

Probenecid / probalan
C/I with aspirin, works against probenecid

SE - SJS
Anemia in G6PD deficiency
leukopenia

-URIC ACID RENAL STONE POTENTIAL

96
Q

This drug can double concentrations of antivirals and penicillin..

A

probenecid

97
Q

This drug can cause exacerbation of gout even though it’s a treatment for it

A

probenecid

- switch to colchicine

98
Q

what is happening to the vasculature during prodrome and actual headache? Which receptors are involved in these stages?

A

vasoconstriction - prodrome
- serotonin 1 receptor (vasoconstricts)

vasodilation - actual HA
- serotonin 2 receptor (vasodilates)

99
Q

Which drugs are used in the prodromal phase and which are used during actual HA?

A

prodromal:
- triptans

actual HA

  • analgesics
  • anti-emetics
100
Q

Migraine prophylaxis can include (3)?

A

BB - propranolol
CCBs - verapamil
Tricyclic antidpressants - Amitriptyline

101
Q

This non-selective BB blocks adrenergic stimulation which decreases HR, also decreases renin release - SE is?

A

propranolol / inderal

SE - bronchoconstriction (impotence, hypoTN, fatigue)

102
Q

this tricyclic antidepressant modulates both serotonin and NE at the CNS - what is it and what should be avoided while taking?

A

amitriptyline / elavil

SE - anticholinergic - dry mouth, constipation

DO NOT USE WITH MAOIs

103
Q

this prophylaxis drug for migraine, is an anti-convulsnt that blocks voltage-dependent sodium channels in the CNS, augmenting GABA activity

A

Topiramate / topamax

104
Q

this ergot derivative is a serotonin 2 (vasodilatory) receptor antagonist - used prophylactically for migraine

do not use within 24 hours of what? why?

why isn’t this drug preferred?

A

methysergide / sansert

not to be used within 24 hours of triptan
increases risk of vasoconstrictive spasm

MULTIPLE SE
pulmonary fibrosis
heart valve thickening

105
Q

This serotonin agonist to 5-Ht 1D and 1B receptors reducing vascular inflammation - what drug is it? what are common SE?

A

Sumatriptan / Imitrex

SE - MYOCARDIAL INFARCTION

  • dizziness, tingling, facial flushing, HTN, arrhythmias
  • Categ. C
106
Q

What is an uncommon, but potential side effect of the triptans?

A

Serotonin syndrome

  • agitation
  • tremor
  • ataxia
  • fever
  • chills, D
107
Q

This opioid analgesic is indicated for migraine HA refractory to triptans - it works as a mixed agonist-antagonist of opioid receptors

A

Butorphanol / Stadol

108
Q

These anti-emetics block serotonin receptors in the CNS and GI tract. They can be used to tx post-operative and cytotoxic drug N/V. They can however cause constipation, diarrhea, dry mouth and fatigue

A

5-HT Receptor Antagonists

109
Q

this neuroleptic works as an H1-histamine receptor, D2 dopaminergic receptor, and alpha-adrenergic receptor ANTAGONIST

A

prochlorperazine / compazine

  • anti-emetic for migraines/vertigo
  • DEFECTS SEEN IN PREGNANCY - spina bifida
110
Q

this is characterized by repetitive involuntary, purposeless movements such as grimacing, tongue protrusion, lip smacking, puckering and pursing of the lips with rapid eye blinking

A

tardive dyskinesia

- seen with high doses of prochlorperazine

111
Q

this anti-emetic blocks serotnin 5HT3 receptors signs and significantly reduces nausea

A

ondansetron / zofran

112
Q

what is the major risk involved with DMARD use?

A

increased vulnerability to:
infection
malignancy

113
Q

what is the corticosteroid MC used for immunosuppression of organ transplant?

A

prednisone

SE: hyperglycemia, increase risk osteoporosis, cushing syndrome, adrenal suppression, poor wound healing

114
Q

which non-steroidal immunosuppressive drugs are cytotoxic (4)?

A

cyclophosphamide
chlorambucil
methotrexate
azathiopine

115
Q

these immunosuppressive drugs inhibit proliferation or function of lymphocytes, targeting calcineurin and therby inhibiting interleukin-2 production via T-lymphocytes (2)

A

Cyclosporine

Tacrolimus

116
Q

this anti-folate, anti-metabolite is immunosuppressive and a chemotherapeutic, it has been shown that when used in combination with other cytotoxic drugs, its efficacy increases, what is it? is it safe in pregnancy?

A

methotrexate / MTX

SE: N, abd. pain, fatigue, fever, dizziness, ULCER, low WBC ct

CATEGORY X

117
Q

the use of what during methotrexate treatment for cancer is contraindicated? is this the case when it’s used for AI disorders?

A

the use of FOLATE during cancer TX is CI

Not the case when used for RA, SLE, etc

118
Q

This purine anti-metabolite’s breakdown products act to inhibit purine synthesis which blocks protein synthesis, esp in rapid turnover cells. Safe in pregnancy?

A

Azathioprine / Imuran
- can cause pancreatitis
SE: hair loss, BM suppression, GI toxicity, leuko- thrombocyto-penia

NOT SAFE IN PREG.

119
Q

this immunosuppressant drug derived from soil fungus inhibits T cells and blocks production of IL-1,-2,-3,-4 and IFN gamma - what is it and what is a common increased risk?

A

Cyclosporine / Sandimmune

  • as with all immunosuppressives, increased risk for infection leading to sepsis
120
Q

blood levels of these immunosuppressants are increased when patients drink grapefruit juice

A

cyclosporine / sandimmune

tacrolimus / prograf

121
Q

This immunosuppressant is related to the macrolide class of antibiotics (soil microorganism) - inhibits T cells and acts similarly to cyclosporine

A

tacrolimus / prograf

122
Q

this is a cytokine produced by monocytes and macrophages - with two receptor types, what is it and what do it’s receptors do?

A

TNF-alpha

  • receptors in WBCs, respond to TNF by releasing cytokines
  • soluble receptors which deactivate TNF and blunt immune response

on all nucleated cells - RBCs, non-nucleated, do not contain

123
Q

This DMARD, recombinant DNA, is the most widely used anti-TNF biologic in rheumatology - it mimics the effects of naturally occurring soluble TNF receptors and reduces inflammatory response - anti-TNF therapy - what is it? How is it made?

A

Etanercept / Enbrel

combines TNF receptor to Fc human immunoglobulin and stops transport of WBCs to site of inflammation
- does NOT cause cell death

EXPENSIVE

124
Q

This DMARD, recombinant DNA drug neutralizes biological activity of TNFalpha by binding soluble receptors and trans-membrane receptors therefore preventing binding

A

Infliximab / Remicade (IV)

  • causes programmed cell death of TNFalpha expressing Tcells
  • when all FDA approvided indications are considered, this is the most used anti-TNF biologic (take out UC and Crohn’s and it’s enbrel)
125
Q

which is more efficacious in Crohn’s and US, Infliximab or Etanercept?

A

Infliximab is more effective due to it’s ability to kill the cell
Etanercept has shown NO efficacy in treating these

126
Q

this anti-malarial drug is useful in treating RA, SLE and Sjogrens as well as post-Lyme arthritis, it increases lysosomal pH in APCs and blocks TLRs on pasmacytoid dnedritic cells - therefore decreasing TLR 9 signaling which would otherwise increase IFN in response to immune complexes found in AI disease - anti-spirochete, anti-inflammatory activity

A

Hydroxycholorquine / Plaquenil

  • can have effect on cornea and macula - yearly dilated eye exams recommended
127
Q

this medication, sometimes used in kiddos who are unresponsive to NSAIDS, methotrexate and DMARDs - use this anti-mitochondrial drug - what is it?

A

gold salts

Pharm II - Chamberlain (5 decks)

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