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Pharm Exam 5 > L 13-15 Analgesic, Antipyretic, NSAID, Antirheumatic > Flashcards

L 13-15 Analgesic, Antipyretic, NSAID, Antirheumatic Flashcards

1
Q

Effects of Histamine on blood vessels

A

Histamine causes vasodilation and contraction on endothelial cells. This is what allows blood contents to leak into the interstitial tissue.

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2
Q

What are the mediators of acute inflammation?

A 
Histamine
Serotonin
Bradykinin
Prostaglandins
Leukotrienes
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3
Q

Effects of Bradykinin in inflammation

A

Vasodilation

Pain

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4
Q

Effects of Prostaglandins in inflammation

A

Vasodilation
Chemotaxis
Pain

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5
Q

Effects of Leukotrienes in inflammation

A

Vascular permeability

Chemotaxis!

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6
Q

Where do Prostaglandins come from?

A

Produced from the breakdown of membranes by Phospholipase A2 to form Arachidonic Acid. AA is then converted into PGs and TXs by COX. AA can also be converted into LTs by Lipoxygenase pathways.

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7
Q

What are glucocorticoids

A

Glucose metabolism regulating molecules that are steroids which come from the adrenal cortex
They are a feedback mechanism for the immune system and function to reduce the actions of Phospholipase A2 and thereby reduce the production of prostaglandins and reduce inflammation

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8
Q

Difference between COX-1 and 2 and the PGs that they produce

A

COX-1 is constitutive and its function is dependent on genetics. The PGs it produces are more house keeping in function. Thromboxane

COX-2 is more inducible and the PGs it produces are more pro-inflammatory. Prostacyclin
Therefore, a more COX-2 specific drug will have less side-effects

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9
Q

Effects of Gs and Gq receptors on intracellular calcium

A

Gs: causes an increase in cAMP => inc protein kinase => phosphorylated outward Ca pumps => dec intracellular Ca

Gq: inc IP3 => inc intracellular free Ca

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10
Q

Effects of Prostacyclin and TXane on vasodilation and platelet aggregation

A

Prostacyclin: great at vasodilation and prevents platelet aggregation

Thromboxane: Very Good at vasoconstriction and platelet aggregation

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11
Q

Effects of PG’s and TX on GI tract

A

All cause diarrhea from increased contractility of the bowels
Some PG’s reduce HCl secretion

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12
Q

Effects of PG’s on pregnant women

A

Work like Oxytocin in that they cause uterine contractions even early in pregnancy–used for abortion

Also ripens/softens cervix for delivery

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13
Q

What happens when the GFR goes down?

A

Decreased GFR to the kidney => inc Renin => increased ANG II => Vasoconstriction throughout the body except in the coronaries, brain, lungs

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14
Q

Effects of PG’s on the kidneys

A

The kidneys produce their own PG’s and they are used for vasodilation to increase GFR.
Loop diuretics work by inducing COX function to produce PG’s
Use of COX inhibitors can diminish effects of loop diuretics by reducing PG synthesis.
Reducing PG in the kidney can also cause a decrease in GFR and the kidney will quickly be damaged by lack of O2

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15
Q

Common adverse effects of prostaglandins

A

Vomiting, Diarrhea, fever, bronchoconstriction, hyper/hypo tension, syncope, dizziness

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16
Q

Thromboxane and PG’s in terms of coagulation come from what cells?

A

Platelets produce TXA2 and the endothelial cells produce PGI2

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17
Q

Which PG is most useful in protecting the gastric mucosa?

A

PGE1

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18
Q

What is PGE2 (dinoprostone) used for?

A

Abortion
Causing Labor
Treating dysmenorrhea

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19
Q

What is PGE1 (alprostadil) used for?

A

Injected in penis to cause erection

Also used in pediatrics to keep ductus arteriosus open

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20
Q

What is prostacyclin (epoprostenol) used for?

A

Used to produce vasodilation in primary pulmonary HTN

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21
Q

Latanoprost (Xalatan)

A

Analog of PGF2alpha
Increases resorption of aqueous humor (Used for Glaucoma)
Administered topically
Can change the color of the iris to a darker color

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22
Q

What drug can cause reddish tears?

A

Rifampin

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23
Q

What drug causes irreversible retinal deposits? Reversible corneal deposits?

A

Thioridazine

Amiodarone

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24
Q

Lubiprostone (Amitiza)

A

Activates Chloride channels in the bowels which leads to softer stool to treat constipation

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25
Q

What PG derivative drugs can be used for asthma?

A

Zileuton (lipoxygenase inhibitor) and

Zafirlukast & Montelukast (leukotriene receptor inhibitors)

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26
Q

Misoprostol

A

PGE1 analog

Reduces gastric acid secretion in ulcers

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27
Q

Why is low dose aspirin useful as prophylactic treatment of MI?

A

Aspirin inhibits production of TXA2 by platelets and thereby prevents platelet aggregation and thrombosis

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28
Q

How can aspirin be used for dysmenorrhea?

A

Dysmenorrhea is painful menstruation from cramping. Uterine contraction is caused by PG’s. Aspiring is a non-selective Cox inhibitor that will reduce PG synthesis and thereby reduce cramping.

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29
Q

Explain the relationship between aspirin and asthma

A

Arachidonic acid can be used by either COX to produce PG’s and TXA or by Lipoxygenase to produce leukotrienes.
If given ASA, COX pathway will be blocked and AA will be more available to produce leukotrienes. Leukotrienes are very good at bronchospasm and therefore, ASA can cause asthma symptoms.

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30
Q

What are the effects of ASA?

A

Analgesic
Antipyretic
Anti-inflammatory
Platelet effects

31
Q

Compare pain relief from NSAID’s and Opioids

A

NSAID’s are good at relieving pain that is mild and from integumentary or inflammatory sources and not from hollow viscera
Opioids are best at relieving sharp pain that can be more neurogenic

32
Q

Aspirin and antipyretic effects

A

Aspirin only lowers body temperature in febrile patients. It resets the temperature gauge in the hypothalamus. It will not cool the normal body.
It is not effective in hyperthermic situations like: malignant hyperthermia, serotonin syndrome, neuroleptic malignant syndrome

33
Q

Where will aspirin be absorbed and why?

A

Aspirin is a simple organic acid with a pKa=3.5, Therefor it will absorb best in the stomach where the pH is low and it will be in an un-ionized or neutral form.

34
Q

Why is aspirin so bad for the stomach?

A

Aspirin reaches concentration levels 20 times that of the blood and therefore has a huge affect on inhibiting PG synthesis. PG in the stomach is how the stomach protects itself from acid overproduction.

35
Q

How does aspirin interact with other drugs?

A

Being an acid, aspirin is excreted by the kidney by a common transporter used for many other acids. It is the OAT (organic acid transporter). Has effects on uric acid transport and many other components by competing for this transporter.
Competes for plasma protein binding.

36
Q

Zero vs first order kinetics

A

Zero order kinetics are a constant rate regardless of dose i.e. 10 mg/hr
First order is dose dependent

37
Q

How long does aspirin anti-platelet effects last?

A

8-10 days
This is because it irreversibly inhibits COX function in platelets and because platelets have no nuclei, they cannot re-synthesize the enzymes. Takes 8-10 days to make new platelets.

38
Q

Effects of aspirin on blood pH and respirations at high and low doses

A

At low doses, aspirin (as an acid) will act like CO2 in the respiratory cells and increase respiration to blow off the extra acid leading to alkalosis

At higher doses, it will have the opposite effect and inhibit respirations and lead to acidosis

39
Q

How is bleeding stopped after the placenta is removed from the uterus?

A

Bleeding is stopped not by coagulation, but by the contraction of the smooth muscles in the uterus.

40
Q

Explain effects of aspirin on excretion of uric acid

A

Remember that uric acid is 100% filtered at the glomerulus, but then 99% is reabsorbed immediately. About 50% is secreted later in the tubules and of that 80% is reabsorbed so the majority of the uric acid that is excreted is from the secreted portion.

At low doses, aspirin competes for the secretion and lowers the amount of uric acid that is ultimately excreted. At higher levels, it also blocks the re-uptake of uric acid from tubules and therefore causes a uricosuric effect where more uric acid is secreted than before

41
Q

Adverse effects of Aspirin

A

GI upset, gastritis, ulcer, bleeding

Kidney failure from the prevention of PG synthesis => prolonged vasoconstriction in the kidney and O2 starvation

42
Q

Should Aspirin be given to kids?

A

Aspirin is not given to kids because if they have a viral infection it is believed that ASA can cause cerebral edema (situation called Reye’s Syndrome)
This is why Acetaminophen is the DOC for fevers in children

43
Q

Diflunisal

A

A salicylic acid derivative but it is unique in that it is not metabolized back into salicylic acid

44
Q

Celecoxib (Celebrex)

A

Selective Reversible cyclooxygenase-2 inhibitor
Because it blocks COX-2, COX-1 will actually be increased which may increase the action platelets and aggregation => CV effects
Better for the GI than drugs that block COX-1 as well
May cause GI ulceration and bleeding, increased risk of CV disease

45
Q

Different functions/Effects of COX-1 vs COX-2

A

COX-1: small effect on inflammation (remember it is more involved in daily maintenance activities), Huge influence on protecting the stomach by producing PGE1, huge role is platelets producing TXA2 => aggregation and vasoconstriction

COX-2: Huge effect in inflammation, small effect on stomach protection, Large effect on vasoconstriction and platelet aggregation–this is the primary mechanism that opposes the actions of TXA2

46
Q

General actions and effects of a COX-2 specific inhibitor

A

Large effect on preventing inflammation, small adverse effects on the stomach, significant increase in TXA2 actions

47
Q

What kind of drug is ibuprofen?

A

Ibuprofen is a nonspecific, reversible inhibitor of COX-1 and COX-2
Has the best side effect profile of all such drugs

48
Q

Indomethacin (indocin)

A

40 times more potent than Aspirin or Acetaminophen, 10 times more potent than Ibuprofen
Very potent Nonselective COX1/2 inhibitor, also inhibits phospholipase Ahigh incidence of side-effects
Used for patent ductus arteriosus

49
Q

Diclofenac (Voltaren)

A

Potent COX inhibitor
Mostly GI side-effects
Combine with misoprostol to decrease GI effects

50
Q

Ketorolac (Toradol)

A

Cox inhibitor (100 times strength of acetaminophen)
Used mainly as analgesic in post-surgical pain
Can be combined with opioids
After 5 days use frequent GI symptoms

51
Q

Ibuprofen (Motrin)

A

DOC for NSAID’s
lowest side effects
combination with ASA decreases the platelet effects of ASA by competing to binding and ASA is quickly metabolized
Half-life 2-4 hours, liver metabolism

52
Q

Naproxen (Naprosyn)

A

NSAID similar to aspirin or ibuprofen
Known for long half life of 13 hours
Extensively bound to plasma proteins
Leans more to COX-2 inhibition and therefore can cause some CV issues with coagulation

53
Q

Piroxicam (Feldene)

A

COX inhibitor
Long half life
Many GI side effects

54
Q

Nabumetone (Relafen)

A

COX inhibitor
Prodrug–requires activation
Long half-life

55
Q

Phenylbutazone

A

COX inhibitor
Very potent
Serious side effects
Not marketed in USA

56
Q

How is acetaminophen thought to work?

A

It is thought to be a CNS COX inhibitor that allows it to have antipyretic and analgesic properties without the GI effects of classical NSAID’s

57
Q

Why is acetaminophen preferred to aspirin in many situations, but what must be remembered?

A

Acetaminophen is better tolerated by patients, doesn’t cause ulcers, has not clotting effects, doesn’t cause acid base balance

Must remember that can cause FATAL hepatic toxicity in higher doses. Produces free radicals that are taken care of by glutathione. When that runs out, it causes hepatic toxicity. Alcohol increases toxicity.

Has no antiinflammatory action

58
Q

Treatment of acetaminophen toxicity

A

Specific antidote is

N-acetylcysteine (Mucomyst)

59
Q

Use of NSAID’s and PUD

A

No history of PUD: can use any NSAID

PUD in history, but not active: use celecoxib w/ or w/o antacids, or can use some NSAID’s w/ misoprostol or “-prazols” (PPI’s)

Active PUD: no NSAID’s! use acetaminophen or opioids like codeine

60
Q

Penicillamine (Cuprimine)

A

Used for rheumatoid arthrits
chelating agent, overall mechanism unknown
High incidence of adverse reactions

61
Q

Hydroxychloroquine (Plaquenil)

A

Used for chronic inflammation like RA
Inhibits PG synthesis
Inhibits response to chemotactic stimuli
Toxicity: hemolysis => Hb in urine, retinopathy

62
Q

Sulfasalazine (Azulfidine)

A

RA treatment

As effective as Penicillamine, but less toxic

63
Q

Infliximab (Remicade)

A

Monoclonal antibody against TNF-alpha partially mouse and part human
Used for Crohn’s and RA
Combined with Methotrexate
Contraindications: pregnancy, breast feeding, children, infections (this is because these situations can’t really be tested so we don’t know)
Overall, inhibits the immune system => higher chance of infections, cancer, TB emergence…

64
Q

Adalimumab (Humira)

A

Like Infliximab, except all human components and therefore less immune reaction to the antibody
Against TNF-alpha
Used for RA

65
Q

Certrolizumab pegal (Cimiza)

A

TNF-alpha binding antibody

Used against RA

66
Q

Golimumab (Simponi)

A

TNF-alpha binding antibody

Used against RA

67
Q

Etanercept (Enbrel)

A

Fake TNF-alpha receptors that bind TNF and prevent it from having its action

68
Q

Rituximab (Rituxan)

A

Binds CD-20 cells and prevents their differentiation and activation. This includes T and B cells
Used for RA and chronic inflammation

69
Q

Abatacept (Orencia)

A

Inhibits T-cell activation

Treats RA

70
Q

Leflunomide (Arava)

A

For activation of cellular immunity, there must be reproduction of cells to produce antibodies etc.
Leflunomide blocks a step that is needed for the production of pyrimidines in mitochondria of leukocytes. Leukocytes make de novo most of their nucleic acids for replication whereas normal cells get 90% of their nucleic acids from a recycled pathway.
Also inhibits the induction of cyclooxygenase-2 and actions of cytokines and growth factors on tyrosine kinase receptors.
Used for chronic inflammation like RA

71
Q

Mycophenolate mofetil (cellcept)

A

Prodrug, immunosuppressant

Inhibits lymphocyte purine synthesis for replication

72
Q

Anakinra (Kineret)

A

IL-1 receptor antagonist

Treats RA

73
Q

Tocilizumab (Actemra)

A

IL-6 receptor inhibiting antibody

Treats RA

74
Q

Tofacitinib (Xeljanz)

A

Inhibits JAK-1 and 3 and partially 2
For adults with active RA who have intolerance to methotrexate
So good, may lead to serious infections or malignancy

Pharm Exam 5 (6 decks)

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