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
aldosterone, released from the zona glomerulosa - is responsible for what? in which disease is it decreased?
regulating - intravascular volume - BP retains Na, HCO3- excretes K decreased in Addison's disease patients
26
Aldosterone levels increase in patients with this, and treated with this aldosterone antagonist.
Aldosterone increases in - Conn's Syndrome TX'd with spironolactone
27
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?
fludrocotisone | - NOT indicated as ANTI-INFLAMMATORY
28
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?
Dehydroepiandrosterone (DHEA) | - although, thought to help with bone development post-menopausal
29
this is a nerve response resulting from injury to, or inflammation of tissue - what is it? How is it treated?
nociception - the perception of pain - subjective, can arise without physical stimulus - treated with AIs or analgesic medications
30
Does the brain have nociception?
no - pain insensitive the meninges however, do.
31
this type of pain, is generally chronic, described as burning, sharp, shooting or aching - may be associated with tingling, numbness
peripheral neuropathy | - treated with medications that act on neurotransmitters and AIs
32
these are pain killers, while these cause delirium and drowsiness - what does both and what are they called?
analgesics - pain killers narcotics - delerium and drowsiness opiates do both - narcotic analgesics
33
what are the narcotic analgesics?
``` 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 ```
34
this 18th and 19th century camphorated tincture, made from powdered opium, was widely used to calm fretful children
paregoric - schedule II - anti-tussive - anti-D
35
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
landanum
36
at present, this has no accepted medical use and therefore carries a DEA designation of schedule I
heroin | - lipid soluble, rapidly crosses BBB
37
this drug is 2-3 times more potent than morphine
heroin
38
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?
opiate analgesics mimic OPIOPEPTINS* - endorphines - enkephalins
39
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?
opiate analgesics | - also inhibit release of substance P at presynaptic cleft
40
the analgesic properties of the opiates are primarily mediated by what receptor?
mu others: - kappa - sigma (hallucinations) - delta (enkepalins peripherally) - epsilon
41
which receptor may be responsible for hallucinations and dysphoria associated with opiate use?
sigma
42
These, since 2014 have been reclassified as schedule II substances and have tighter restrictions - what are they and what are they a product of
hydrocone combination products (HCPs) - vicodin - lorcet - lortab - norco can only be prescribed for one month at a time.
43
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?
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
44
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!
Morphine / MS Contin
45
What is the DEA and pregnancy category for Morphine?
Schedule II | Pregnancy Categ. C
46
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?
Fentanyl / Duragesic - SE - respiratory depression - HIGHLY ADDICTIVE Schedule II Category C
47
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?
fentanyl / duragesic
48
this is a semi-synthetic opioid used to treat opioid addiction
buprenorphine | - butrans (transdermal for chronic pain)
49
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
codeine
50
Differentiate Tylenol #3 and #4 - what are they combined with and what are the relative potencies - what category?
codeine and acetaminophine ``` #3: 30mg codeine phosphate, 300 mg acetaminophine ``` #4 60mg codeine 300 mg acetaminophine ``` schedule II, V (dose dependent) category C (preg) ```
51
what should not be prescribed for pain following tonsillectomy and or adenoidectomy - due to what genetic variant?
codeine - ultra-rapid metabolizers (CYP2D6) - faster and more complete conversion of codeine to morphine - obstructive sleep apnea syndrome - OD, death
52
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?
tramadol / ultram SE - N/V, memory loss, sweating, constipation weaning too quickly can cause withdrawal
53
this acetaminophen containing narcotic is no longer indicated for elderly due to increased risk of falls
darvocet | propoxyphene / acetaminophin
54
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
methadone
55
this opioid receptor antagonist is primarily used in management of ALCOHOL and OPIOID dependence
Naltrexone
56
This is primarily used for emergent treatment of narcotic overdose - what other drug is similar and used for the same thing?
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
this opioid antagonist is used to reverse the coma and respiratory depression of opioid overdose - what is it's onset of action?
naloxone | - works in 30 mins
58
this is an isomer of codeine - it's an effective anti-tussive and commonly used in OTC cough meds
dextromethorphan
59
prostaglandins call in the immune system, there are 4 of them, what enzyme makes which ones and what do they do?
COX-1 (physiologically important) - PG1 - secretes mucus for stomach - PG2 - platelet stickiness COX-2 (inflammatory) - PG3 - PAIN - PG4 - inflammation
60
this class of drug acts by inhibiting the synthesis of prostaglandins
NSAIDS (non-steroidal anti-inflammatory drugs) - COX enzymes play important role in cyclooxygenase pathway
61
This medication is a COX 1/2 inhibitor also used to treat GOUT
indomethacin / indocin
62
what are the COX2 inhibitors?
Celecoxib / celebrex | Refecoxib / Vioxx
63
This NSAID binds IRREVERSIBLY to COX 1 and 2 enzymes - diminishing pain, inflammation, fever
Aspirin / acetylsalicyclic acid (ASA) SE: GI irritation, increased risk of REYEs syndrome (don't admin unless >15-18yrs), PUD, good shit - TINNITUS*
64
This NSAID reversibly binds COX1 and 2, but does not have increased risk for Reye's syndrome
Ibuprofen / Motrin, Advil
65
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?
Celecoxib / Celebrex | - SE may be increased risk of CVD
66
This NSAID weakly blocks peripheral prostaglandin synthesis, with strock blockade of prostaglandin synthesis in the hypothalamus, decreasing fever and pain
acetaminophen / tylenol | - may be a selective COX3 inhibitor, only found in Brain and SC
67
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?
OVERDOSE: 7gm/24hrs NEVER mix with ethanol - can lead to severe hepatic necrosis - liver failure - coma - death. Preg. Categ. B
68
acetaminophen is oxidatively metabolized in the liver, made into this toxic metabolite, to prevent the side effects of acetaminophen toxicity, what should be administered?
N-acetyl-p-benzoquinone-imine (NAPQI) - XS causes hepatocellular death and liver necrosis Antidote: N-acetyl cysteine (NAC)
69
What are the 4 stages of acetaminophen toxicity?
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
this is a precursor to glutathione and increases glutathione availability to bind NAPQI - used mainly as a mucolytic agent
NAC | - most effective if administered within 8 hours ingestion
71
This agent was used as a "narcotic" drug in the ER until the drug seekers found out what the docs were doing
Ketorolac - first injectable NSAID PO = increased GI issues
72
Gout is a disorder of
purine metabolism - uric acid crystalizes to monosodium urate - precipitate in joints and tissue
73
this enzyme breaks down uric acid in humans, but seems to be struggling to survive an evolutionary loss - what is it?
uricase
74
These are pathognomonic for gout disease, whereas radiographically, this is typically seen
tophi - pathognomonic | rat bite lesion - radiograph
75
definitive dx of gout is based upon identification of?
monosodium urate crystals - needle like morphology - strong negative birefringence
76
what condition is most important to differentiate from gout?
septic arthritis - synovial fluid gram stain and culture should be performed. - other similar conditions - pseudogout - RA
77
which joint is mc affected in gout? in pseudogout? - which crystals are seen?
gout - 1st MTP needle-like monosodium urate crystals) pseudogout - knee rhomboid shaped calcium pyrophosphate dihydrate crystals
78
what common drink can increase you chance of developing gout - why?
Beer full of purines - go for wine. often gout is associated with DM, HTN, obesity
79
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?
diuretics - except Hydrochlorothiazide other meds: - niacin - aspirin
80
Which two drug classes are associated with lower risk of gout?
CCBs | losartan
81
half of all gout cases occur where
MTP-1, big toe. | - lower body temperature can precipitate, gen occurs during evening
82
what are first line tx for gout?
NSAIDS (x1-2 weeks) | - Indomethacin, however SE of HA is common.
83
When combined with NSAIDS this can exacerbate ulcer and these can be cytoprotective
H2, exacerbates ulcers PPI - cytoprotective
84
Acute treatments for Gout
NSAIDs Steroids Colchicine
85
Chronic treatments for Gout
Colchicine Allopurinol Probenecid
86
This NSAID inhibits COX 1 and 2, treats acute gout - what is it? What's a common SE and should nursing mothers use it?
Indomethacin / indocin SE - HA** - excretes in breast milk, CI for breastfeeding
87
Sampter's Triad
- nasal polyps - allergy to aspirin/NSAIDs - asthma
88
This drug amazingly has the ability to close patent ductus arteriosus in neonates, whaaaaat?
indomethacin / indocin - can worsen parkinson's sx though - be careful with K sparing diuretics
89
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
cortisone injection ``` SE: HYPERGLYCEMIA insulin resistance DM osteoporosis anxiety/depression, cataracts, glaucoma ```
90
glucocorticoids primarily mediated through what? which does what?
lipocortin-1 | - suppresses phospholipase A2, blocks eicosanoid production and therefore PG and leukotriene synth.
91
this mitotic inhibitor is indicated for acute gout or prophylaxis - it inhibits microtubule polymerization - essential for the mitosis.
colchicine - AI effects linked to it's ability to bind with TUBULIN, main microtubule constituent - also inhibits motility of neutrophils
92
colchicine seems awesome, but what SE should we be aware of?
peripheral neuropathy neutropenia hair loss OD (like arsenic poisoning)- N/V, acute renal failure
93
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
Allopurinol / Zyloprim - SE: SJS* common SE - N/V, Skin rash
94
these are sustances that increase the excretion of uric acid and reduce plasma concentration - however with the ability to contribute to these suckers?
uricosurics | - increasing uric acid in urine can cause renal lithiasis
95
this uricosuric works by interfering with kidney's organic anion transporter - by stopping it's reclamation of uric acid back to the blood
Probenecid / probalan C/I with aspirin, works against probenecid SE - SJS Anemia in G6PD deficiency leukopenia -URIC ACID RENAL STONE POTENTIAL
96
This drug can double concentrations of antivirals and penicillin..
probenecid
97
This drug can cause exacerbation of gout even though it's a treatment for it
probenecid | - switch to colchicine
98
what is happening to the vasculature during prodrome and actual headache? Which receptors are involved in these stages?
vasoconstriction - prodrome - serotonin 1 receptor (vasoconstricts) vasodilation - actual HA - serotonin 2 receptor (vasodilates)
99
Which drugs are used in the prodromal phase and which are used during actual HA?
prodromal: - triptans actual HA - analgesics - anti-emetics
100
Migraine prophylaxis can include (3)?
BB - propranolol CCBs - verapamil Tricyclic antidpressants - Amitriptyline
101
This non-selective BB blocks adrenergic stimulation which decreases HR, also decreases renin release - SE is?
propranolol / inderal | SE - bronchoconstriction (impotence, hypoTN, fatigue)
102
this tricyclic antidepressant modulates both serotonin and NE at the CNS - what is it and what should be avoided while taking?
amitriptyline / elavil SE - anticholinergic - dry mouth, constipation DO NOT USE WITH MAOIs
103
this prophylaxis drug for migraine, is an anti-convulsnt that blocks voltage-dependent sodium channels in the CNS, augmenting GABA activity
Topiramate / topamax
104
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?
methysergide / sansert not to be used within 24 hours of triptan increases risk of vasoconstrictive spasm MULTIPLE SE pulmonary fibrosis heart valve thickening
105
This serotonin agonist to 5-Ht 1D and 1B receptors reducing vascular inflammation - what drug is it? what are common SE?
Sumatriptan / Imitrex SE - MYOCARDIAL INFARCTION - dizziness, tingling, facial flushing, HTN, arrhythmias - Categ. C
106
What is an uncommon, but potential side effect of the triptans?
Serotonin syndrome - agitation - tremor - ataxia - fever - chills, D
107
This opioid analgesic is indicated for migraine HA refractory to triptans - it works as a mixed agonist-antagonist of opioid receptors
Butorphanol / Stadol
108
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
5-HT Receptor Antagonists
109
this neuroleptic works as an H1-histamine receptor, D2 dopaminergic receptor, and alpha-adrenergic receptor ANTAGONIST
prochlorperazine / compazine - anti-emetic for migraines/vertigo - DEFECTS SEEN IN PREGNANCY - spina bifida
110
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
tardive dyskinesia | - seen with high doses of prochlorperazine
111
this anti-emetic blocks serotnin 5HT3 receptors signs and significantly reduces nausea
ondansetron / zofran
112
what is the major risk involved with DMARD use?
increased vulnerability to: infection malignancy
113
what is the corticosteroid MC used for immunosuppression of organ transplant?
prednisone SE: hyperglycemia, increase risk osteoporosis, cushing syndrome, adrenal suppression, poor wound healing
114
which non-steroidal immunosuppressive drugs are cytotoxic (4)?
cyclophosphamide chlorambucil methotrexate azathiopine
115
these immunosuppressive drugs inhibit proliferation or function of lymphocytes, targeting calcineurin and therby inhibiting interleukin-2 production via T-lymphocytes (2)
Cyclosporine | Tacrolimus
116
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?
methotrexate / MTX SE: N, abd. pain, fatigue, fever, dizziness, ULCER, low WBC ct CATEGORY X
117
the use of what during methotrexate treatment for cancer is contraindicated? is this the case when it's used for AI disorders?
the use of FOLATE during cancer TX is CI Not the case when used for RA, SLE, etc
118
This purine anti-metabolite's breakdown products act to inhibit purine synthesis which blocks protein synthesis, esp in rapid turnover cells. Safe in pregnancy?
Azathioprine / Imuran - can cause pancreatitis SE: hair loss, BM suppression, GI toxicity, leuko- thrombocyto-penia NOT SAFE IN PREG.
119
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?
Cyclosporine / Sandimmune - as with all immunosuppressives, increased risk for infection leading to sepsis
120
blood levels of these immunosuppressants are increased when patients drink grapefruit juice
cyclosporine / sandimmune | tacrolimus / prograf
121
This immunosuppressant is related to the macrolide class of antibiotics (soil microorganism) - inhibits T cells and acts similarly to cyclosporine
tacrolimus / prograf
122
this is a cytokine produced by monocytes and macrophages - with two receptor types, what is it and what do it's receptors do?
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
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?
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
This DMARD, recombinant DNA drug neutralizes biological activity of TNFalpha by binding soluble receptors and trans-membrane receptors therefore preventing binding
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
which is more efficacious in Crohn's and US, Infliximab or Etanercept?
Infliximab is more effective due to it's ability to kill the cell Etanercept has shown NO efficacy in treating these
126
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
Hydroxycholorquine / Plaquenil - can have effect on cornea and macula - yearly dilated eye exams recommended
127
this medication, sometimes used in kiddos who are unresponsive to NSAIDS, methotrexate and DMARDs - use this anti-mitochondrial drug - what is it?
gold salts