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Pharmacology > Ch 36: Non-Steroidal Anti-Inflammatory Drugs > Flashcards

Ch 36: Non-Steroidal Anti-Inflammatory Drugs Flashcards

1
Q

what are some examples of eicosanoids?

A

prostaglandins, thromboxanes, leukotrienes

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2
Q

what are eicosanoids?

A
  • hormones & molecules that activate receptors (PLA2)

- formed from membrane phospholipids

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3
Q

what does phospholipase A2 cleave?

A

an essential fatty acid (arachidonic acid)

  • which then cleaves to form lipoxogenase & cyclooxogenase
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4
Q

Lipoxygenase

A
  • forms leukotrienes

* * released in an autocrine & paracrine fashion

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5
Q

Zileuton

A

lipoxygenase inhibitor

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6
Q

Montelukast & Zaphirlukast

A

leukotriene receptor blocker

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7
Q

What are the effects of LOX

A

LTC4 & LTD4 = bronchoconstrictors

- can lead to anaphylaxis

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8
Q

COX

A
  • activated by hormones & biomolecules when acting at receptors
  • forms PGG2, converts to PGH2, then to various prostaglandins & thromboxanes
  • consists of 2 isoforms
    • COX-1 & COX-2
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9
Q

COX-1

A
  • produced in tissues for normal tissue function

- (produces prostaglandins & activates platelets and protect the stomach & intestinal lining)

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10
Q

COX-2

A

-induced by inflammatory cells

used to treat inflammation, pain & fever
(release IL-6, IL-1B, and TNF-a)

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11
Q

What parts of the body does COX products play key roles?

A 
Smooth muscle
Platelets
Kidneys
CNS
Inflammation
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12
Q

smooth muscle

A

Vascular:
- can be constrictor (TXA2 & PGF2a) or dilator (PGI2 & PGE2)

GI:
- mostly constrictors

Airways:
- PGI2 & PGE2 relax, and others constrict

Reproductive:

  • PGF2a + oxytocin = parturition
  • PGE2 & PGI2 = relax
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13
Q

platelets

A
  • aggregation that’s mostly inhibited by PG’s

- TXA2 can be released which can lead to aggregation

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14
Q

Kidney

A
  • TXA2 lead to renal vasoconstriction
  • elevated renal inflammation
  • PGI2 & PGE2 help w/ renal blood flow & function
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15
Q

Inflammation

A
  • PGE2 & PGI2 (prominent) inflam. agents

* * increase B.F. = edema & leukocyte infiltration

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16
Q

CNS

A
  • can lead to fever (PGE2)
  • sleep (PGD1)
  • regulation of neurotransmission
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17
Q

prostaglandins & thromboxanes cause?

A

pain (sensitize pain receptors to bradykinin…)
inflammation (increased vascular permeability)
fever (hypothalamic effect)
thrombus formation (clotting)

– vasoconstriction, vasodilation, dysmenorrhea, etc

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18
Q

what are some NSAID effects?

A

analgesia –> mild-mod pain
anti-inflammation –> corticosteroids
anti-pyretic –> reducing temperature in fever
anti-coagulant –> platelet aggregation

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19
Q

some NSAIDS

A 
aspirin
indomethacin
naproxen
oxaprocin
etodolac
flurbiprofen
ibuprofen
diflunisal
celecoxib
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20
Q

NSAID adverse effects

A 
CNS -- headaches, tinnitus, dizziness
CV -- fluid retention, edema
GI -- pain, nausea, vomiting, ulceration
Hematologic -- rare (thrombocytopenia)
Hepatic -- abnormal liver function
Pulmonary -- asthma
Rash -- pruritus
Renal -- insufficiency to even failure
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21
Q

aspirin

A
  • acetylsalicylic acid
  • cheap/ inexpensive
  • irreversible inhibitor of COX1 & COX2 (esp. on platelets)
  • effective due to COX2 action
  • side effects due to COX1 activity
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22
Q

Aspirin side effects

A

GI
(irritates upper GI)
— so take w/ meals. PG’s = mucous formation

CNS
(tinnitus, vertigo)
– possible kidney/ liver damage

Reye’s Syndrome
- children & teens
- after influenza/ chicken pox
(high fever, vomit, liver dysfunction, unresponsive, delirium, convulsions, coma, death)

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23
Q

Ibuprofen

A
  • similar to aspirin
  • less GI side effects
  • more potent
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24
Q

Side effects on ibuprofen

A
  • GI
  • Rash, pruritis, tinnitis
  • nephrotoxic
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25
Q

What area of the body is affected due to the toxicity of Ibuprofen

A

Stomach
Kidneys

why?

  • less stomach protection (mucous production)
  • less renal B.F. (nephrotoxicity)
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26
Q

symptoms of Ibuprofen toxicity

A 
vomiting (w/ or w/o blood)
abdominal pain
diarrhea
black/tarry stool
loss of appetite
increased drinking
increased urination
lethargy
dehydration
seizures
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27
Q

Naproxen

A

similar to ibuprofen ( but long lasting)

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28
Q

sulindac

A

less toxicity for kidneys

has greater GI affects than aspirin & ibuprofen

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29
Q

oxaprozin

A

50 hr half life

- take once a day

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30
Q

acetaminophen

A
  • inhibits cox enzymes
  • anti-pyretic & analgesic (NOT a NSAID)
  • less anti-coagulant * anti-inflammatory
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31
Q

side effects of acetaminophen

A

hepatotoxic at high doses (can be fatal)

- no GI effects & nor Reye’s

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32
Q

indomethacin

A
  • reduce pre-term labor (under 32 weeks)

- manage patent ductus arteriosus

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33
Q

COX-2 meds

A

celecoxib (Celebrex)
Rofecoxib (Vioxx)
** but removed due to strokes and MI

(for arthritis, dysmenorrhea)

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34
Q

COX-2 inhibitors

A
  • reduce GI side effects (ulceration)

- increased thrombosis, MI, and stroke which lead to retraction of VIOXX

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35
Q

Rheumatoid Arthritis

A
  • chronic, systemic disorder
  • synovitis, joint destruction
  • morning stiffness
  • arthritis in 3+ areas
  • affects about 1% of population
  • most often women (20-40 yrs)
  • auto-immune
    * * initiated from previous. infections
    * * (IL’s PG’s LK’s cause synovial proliferation, cartilage & bone destruction)
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36
Q

Treating Rheumatoid Arthritis

A

NSAIDS (treat inflammatory)
Corticosteroids (treat inflammatory)
DMARDS (slow disease)

37
Q

What are some goals for Rheumatoid Arthritis

A
  1. decrease joint inflammation

2. arrest disease progression

38
Q

Glucocorticoids

A
  • naturally cortisol (hydrocortisone) produced in adrenal cortex
  • bind to receptors in cytosol (orphan receptors)
  • bound to heat shock proteins

NOTE:
- once steroid binds to receptors, HSP releases receptors, it dimerizes, then moves into the nucleus

  • while in nucleus, receptor/ steroid complex acts like a txn factor to initiate mRNA txn
  • leads to lipocortin-1 inhibits PLA2 activity
39
Q

corticosteroid effects

A 
physiologic
metabolic
catabolic
stimulate acid & pepsin in stomach
anti-inflammatory/immunosuppressive
better than NSAIDS (inhibit leukotrienes)
efficacious
limiting side effects
40
Q

when are corticosteroids used?

A

ONLY when NSAIDS are no longer effective

41
Q

side effects of corticosteroids

A

peptic ulcer formation
muscle wasting
osteoporosis

42
Q

Name some corticosteroids

A

Betamethasone
cortisol (hydrocortisone)
prednisolone
triamcinolone

43
Q

DMARDS

A

disease modifying anti-rheumatic drugs

  • takes 6 weeks to 6 months to work
44
Q

methotrexate

A

immunosuppressive
one that’s most effective
best for toxicity ratio

45
Q

side effects to methotrexate

A

hepatotoxicity
GI
pulmonary effects
hair loss

46
Q

what does methotrexate inhibit?

A

thymidylate synthetase

47
Q

chloroquine, hydroxychloroquine

A

anti-malaria drugs

  • takes 12-24 wks to work
  • used when NSAIDS stop working
48
Q

side effects to chloroquine, hydroxychloroquine

A

safest DMARDS
ocular damage
headaches

49
Q

gold therapy (auranofin)

A
  • given orally w/ less side effects
  • given early on (don’t reverse previous. damage)
  • accumulates in lysosomes of synovial tissue (decrease lysosome & macrophages)
50
Q

side effects of gold therapy

A

GI
oral irritation
common rashes, pruritis
blood disorders

51
Q

Azathioprine

A
  • immunosuppressant to prevent tissue damage
  • FOR SEVERE CASES (cases that prevent other treat.)
  • anti-metabolyte
  • TOXIC & NOT well tolerated
    • ** fever, sore throat, fatigue, vomiting
52
Q

Penicillamine

A
  • chelates heavy metals
  • used for lead poisoning
  • used for arthritis incase GOLDS don’t work
  • immunosuppressant (reduce T cell function)
53
Q

side effects of Penicillamine

A

moderately toxic (fever, joint pain, pruritis)

54
Q

Leflunomide

A
  • NEW
  • well tolerated
  • works within first month
    blocks RNA synthesis in lymphocytes to reduce their activity
55
Q

side effects of Leflunomide

A

GI
allergy
hair loss
hepatotoxic (need monitoring)

56
Q

Etanercept

A
  • new & effective (binds/blocks TNF binding action)
  • successful to patients unresponsive to DMARDS
  • given by sub-cutaneous injection (2x weekly)
57
Q

side effects of etanercept

A

risk of infections (TNF = key part of immune system)

58
Q

osteoarthritis

A
  • Increase viscosity of synovial fluid
    1. Hyaluronan: polysaccharides injected into joints for long lasting relief
  • Joint tissue precursors
    1. glucosamine & chondroitin sulfate: used to reverse damage by providing precursors
59
Q

Autonomic Pharmacology

A

CNS

  • brain
  • spinal cord

PNS

  • somatic (skeletal muscle function)
  • autonomic (body functions) –> HR, rest rate, etc
    • sympathetic (thoracolumbar)
    • parasympathetic (cranial sacral)
60
Q

sympathetic division

A

1st thoracic to 3rd lumbar

pre-ganglionic neuron–> cord (ventral root) to ganglia

post-ganglionic neuron–> ganglion (dendrite & cell body) to organ

61
Q

parasympathetic inervation

A 
from brainstem (3,4,9,10 & vagus) to sacral cord
Two neurons reach the end of the organ 
- ganglia found in end organ or tissue
- longer pre-gang & shorter post-gang
- 1:1 ratio of pre- to post-

Both pre and post neurons release ACh onto smooth muscle, cardiac muscle or glands

62
Q

What are some ways that drugs can interfere?

A 
block synthesis
block uptake
block storage
displace transmitter
prevent exocytosis
agonist mimetic
block receptor
inhibit breakdown
63
Q

cholinergic receptor

A

nicotinic receptors

Nn–> neuronal

  • post-ganglionic neurons
  • pre synaptic cholinergic terminals
  • open Na+ or K+ channels

Nm–> muscle

  • skeletal muscle neuromuscular junction
  • open Na+ or K+ channels
64
Q

muscarinic receptors

A

from a mushroom (amanita muscarina)

G protein coupled receptors
- activate ion channels, adenyl cyclase, PLC

at least 4 subtypes

  • agonist: muscarine
  • antagonist: atropine

(location: sm muscle, glands, heart, brain)

65
Q

muscarinic receptors & locations

A 
M1
M2
M3
M4
M5
66
Q

M1

A

CNS & Symp. post-gang neurons

67
Q

M2

A

heart & smooth muscle

68
Q

M3

A

glands, smooth muscle

69
Q

M4

A

glands, smooth muscle

70
Q

M5

A

?? (cloned?? )

71
Q

Muscarinic effects

A
  • depolarization of ganglia
  • decreased chronotropic & inotropic response
  • smooth muscle contraction & glandular secretions
72
Q

cholinergic stimulants

A

A. Direct-Acting: active receptors

  1. choline esters: similar to ACh
    - Bethanechol
    - Pilocarpine
    - Methacholine
  2. Alkaloids: from plants
    - muscarine
    - nicotine
    - pilocarpine
73
Q

what are the effects of direct acting cholinergics

A

eye:
pupil constriction, accommodation, increased lacrimation & decreased intraoccqular pressure

CV system:
bradycardia, decreased contractility, relax peripheral vessels

Respiratory System:
airway constriction, increased secretions

GI- increased motility
CNS- hypothermia, tremors, convulsions
Bladder- stim detrussor, relax trigone (urination)

74
Q

SLUD

A 
poisoning by cholinergics
salivation
lacrimation
urination
defecation
75
Q

indirect- acting cholinergics

A

inhibit AchE
similar effects as direct acting

Reversible:
edrophpnium, neostigmine, physostigmine

Irreversible:
insecticides (malathion, parathion)
nerve gases

76
Q

what are cholinergics used for?

A

glaucoma
GI and bladder
Heart
Atropine intoxication

77
Q

Glaucoma

A

pilocarpine, physostigmine

- to reduce intraocular pressure

78
Q

GI and bladder

A

bethanechil, neostig

- for post-op atony

79
Q

Heart

A

edrophorium

- for tachycardia

80
Q

Atropine intoxication

A

physostigmine

81
Q

side effects/ toxicity of cholinergics

A

contraindications
- asthma, peptic ulcer, bradycardia, hypotension

SLUD

Cholinesterase inhibitor poisoning

  • give heroic doses of atropine
  • for organphosphatases, use 2-PAM
82
Q

muscarinic receptor blockers effect:

A

heart:
tachycardia by clocking vagal input

resp. system:
bronchodilator & less secret

eye:
dilate & accomodate

Urinary & GI:
reduce activity/motility

CNS:
sedative, then excitement

83
Q

muscarinic blocker uses

A

respiratory: Ipratropium (Atrovent)
- for asthma & pre- anesthesia

eye: Cyclopentylate
- for mydriasis & Cyclopegia

urinary/GI: Dicyclomine
- for incontinence or irritable bowel

motion sickness: Scopolamine

heart: Atropine
- for bradycardia

others: mushroom poisoning

84
Q

muscarinic blockers are contraindicated for

A

glaucoma patients
prostate hypertrophy patients
anti-depressant patients

85
Q

Ganglionic blockers

A

autonomic selective inhibitors

pirenzepine

86
Q

pirenzepine

A
  • for peptic user
    • specific for muscarinic gang.
    • have less side effects
87
Q

autonomic selective inhibitors

A
  • Hexamethonium, trimethaphan: used in hypersensitive emergencies
88
Q

what does autonomic selective inhibitors cause?

A

tachycardia, mydriasis, constipation, urinary retention, decreased sweat & saliva

Pharmacology (17 decks)

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