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Pharmacology (MPAS) > Lecture 5: Migraines and NSAIDS > Flashcards

Lecture 5: Migraines and NSAIDS Flashcards

1
Q

Common causes of headaches

A

Neck and jaw tension

Nasal pressure

Lack of sleep

Caffeine withdrawal

Eye strain

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2
Q

What are the pharmacological effects of NSAIDS? How are they mediated?

A

Non-steroidal anti-inflammatory drugs

Analgesic (anti-pain)

Antipyretic (anti-fever)

Anti-inflammatory (except acetaminophen)

All seem to be mediated by common mechanism: inhibition of prostaglandin

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3
Q

Synthesis of prostaglandins

A

See figure

NSAIDS act on COX enzymes

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4
Q

Cyclo-oxygenase isoforms

A

COX-1: non inducible, found in many cell types, has critical functions such as maintaining stomach lining

COX-2: induced in immune cells, responsible for pain inflammation and fever

COX-3: highest content in brain and heart, splice variant of COX-1

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5
Q

What is inflammation caused by?

A

infectious agents

ischemia

antigen/antibody reaction

thermal and other damage

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6
Q

Three phases of inflammation

A

1) Acute transient phase: local vasodilation, increased capillary permeability (where NSAIDS can control)
2) Delayed subacute phase: infiltration of leukocytes and phagocytes
3) Chronic proliferative phase: tissue degeneration and fibrosis

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7
Q

What does injection of PGs cause?

A

local inflammation

increased blood flow

Severe pain

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8
Q

Uses of PGs and PG inhibitors on uterus

A

PGs cause uterine cramping

PGs used in abortions

inhibitors used in dysmenorrhea and to delay delivery

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9
Q

What is temperature set point regulated by?

A

Hyopthalamus

Delicate balance between heat loss and heat production

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10
Q

How do PGs induce pain?

A

Stimulating local pain fibres

Inflammation induces hyperalgesia (increased pain sensitivity)

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11
Q

What are other effects of PGs other than pain?

A

Critical for platelet aggregation (formation of clots) - Aspirin (ASA) used for this reason

Modulate stomach acidity and mucous lining

Important for uterine contraction

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12
Q

How aspirin inhibits COX-1

A

Aspirin is the only NSAID that permanently blocking COX-1 (destroys enzyme)

Body secretes more COX-1

Exception: Aspirin gets to the platelets via the portal vein. Platelets do not make more COX-1, they are permanently unable to make PGs.

Aspirin is more effective than ibuprofen (advil) when it comes to platelets

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13
Q

How does aspirin work?

A

Irreversibly acetylates COX enzymes

Effect lasts as long as it takes to replace the COX enzyme

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14
Q

What does caffeine do to analgesic drugs

A

Increases analgesic effect of all non-opioid analgesic drugs

Cause of effect is unknown, may be cortical vasoconstriction

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15
Q

Required dose of caffeine for coanalgesic effect

A

60-120 mg

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16
Q

What should you take to cure a headache?

A 
NSAID 
\+
Tylenol
\+
Coffee
\+
ice water (causes contents of stomach to dump into intestine)
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17
Q

In what population is salicylate overdose common?

A

Children

Acetominophen is most common

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18
Q

Drugs that are known to cause salicylate overdose

A

Pepto-bismol (bismuth salicylate)

Methylsaliculate (oil of wintergreen)

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19
Q

Why shouldn’t you take pesto bismol if you have a aspirin-induced stomach ache?

A

It is a salicylate and will make your stomach ache worse

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20
Q

Signs and symptoms of salicylate overdose

A

Tinnitus (typical of elderly using enteric coating)

Marked increase in metabolic rate (SA overdose interferes with oxidative metabolism)

21
Q

What happens when there is an increase in metabolic rate

A

Initial hyperventilation: due to futile cycle burning of oxygen, overproduction of CO2

Metabolic acidosis (too much CO2)

Severe hypoglycaemia: futile cycle uses up glucose

22
Q

Treatment of salicylate overdose

A

Immediate danger = hyperthermia, dehydration, hypoglycaemia

Parenteral fluids and glucose

parenteral sodium bicarbonate (caution: K+ depletion)

acetazolamide if parenteral bicarbonate does not alkalinize the urine (want urine pH to be above 7)

Activated charcoal (only effective within 2 hours of overdose)

Polyelectrolyte lavage solution

Hemodyalysis (severe overdose)

23
Q

NSAID classes

A

Salicylates (methylsalicylate, bismuth salicylate, aspirin)

Proprionic acid (Ibuprofen/Advil, Naproxen/Aleve)

Diclofenac

Indomethacin

24
Q

Effects of Ibuprofen

A

Propionic acid

Similar effects to other non-selective COX inhibitors

Less GI effects (but still major problem)

25
Q

Dosing of Naproxen (aleve)

A

Has half life of 12-18 hours

Can be dosed only twice a day

26
Q

Indomethacin

A

Used for gout pain and swelling

Less common for chronic conditions than diclofenac

27
Q

What is the primary problem with non-selective COX inhibitors?

A

GI side effects

PGE2 and PGI2 (products of COX-1) ae made by gastric mucosa. These PGs suppress acid production, increase gastric blood flow, increase secretion of mucin

Inhibition of COX-1: increases acid production, decreases mucous protection

28
Q

Adverse effects and drug interactions of NSAIDS

A

Reye’s syndrome (fatal hepatic encephalopathy in children with viral infection (chicken pox, influenza) *only children with mitochondrial diseases

Hypertension, Angina (increase in circulating volume)

Bleeding disorders (inhibition of COX, alcohol, warfarin and rofecoxib)

29
Q

Distinguishing features of Acetominophen

A

Tylenol

Analgesic

Acts centrally, no ceiling effect (NSAIDS have ceiling effect)

Anti-pyretic

Not anti-inflammatory

Works in the brain

30
Q

Acetominophen overdose mechanism

A

Minor clearance pathway for highly reactive metabolite of acetaminophen at low doses: Glutathione (GSH) in lover

GSH is crucial antioxidant

At high doses of acetaminophen, the reactive metabolite depletes GSH

Causes oxidative damage to liver cells from loss of anti-oxidant and direct damage to liver cells from the highly reactive intermediate

31
Q

Signs and symptoms of acetominophen overdose

A

No obvious signs or symptoms

Severely elevated serum transaminase levels (AST, ALT)

Hepatic encephalopathy

Jaundice

32
Q

Prevalence of migraine headache

A

18% women, 6% men (more common in boys than girls, reverses after puberty)

33
Q

Symptoms of migraines

A

Unilateral or bilateral

Throbbing

Nausea

Often preceded by an aura (usually visual)

Variable duration (hours-days)

Variable incidence (few per year to a few per month)

34
Q

Triggers for migraines

A

Weather

Missing a meal

Stress

Alcohol

Food

Menses

Crying

35
Q

Migraine attack steps

A

Prodrome

Aura

Headache

Postdrome (exhaustion)

See figure

36
Q

Management of acute headache

A

Non-opioid analgesics (NSAIDS) will be effective, should be tried first

Combination of acetaminophen, acetylsalicylic acid and caffeine (excedrin)

Opioid drugs may be used as a last resort

37
Q

Mechanism of action of ergot alkaloids, ergotamine and dihydroergotamine, side effects

A

Nonspecific serotonin agonists

Arteriolar vasoconstriction

38
Q

Caution with ergot alkaloids

A

Liver disease

Rebound headache with frequent use

Cardiovascular disease - arteriolar vasoconstriction

Poor peripheral circulation

39
Q

What is Raynaud’s?

A

Poor peripheral circulation

40
Q

St Anthony’s Fire

A

People overdosed on Ergot, vasoconstriction of limbs which caused limbs to rot

Also, ergot made people crazy so there were basically zombies walking around

41
Q

What we actually use to control acute headache

A

Triptans

Sumatriptan, naratriptan, risatriptan, zolmitriptan

Available as pill, nasal spray, sublingual (fast and effective)

Relieve nausea and headache

42
Q

Mechanism of action of triptans

A

Agonist at 5HT1-1B and 1D (serotonin) receptor agonists

43
Q

Side effect of Triptans

A

Simliar to ergot alkaloids

44
Q

Disadvantage of triptans

A

Expensive

45
Q

Caution with triptans

A

Do not use with MAOI or SSRI antidepressants

Could cause serotonin syndrome

Restlessness, muscle twitches, myoclonus, hyperreflexia, sweating, shivering, tremor -> possible seizures and coma

46
Q

Prevention of migraines

A

Propanolol (and other beta blockers) - regulate blood flow, reduce BP

Amytriptyline (and other TCAs) - lower dose than depression

Gabapentin - anticonvulsant, possible modulates GABA receptors

Candesartan - angiotensin II receptor antagonist, reduces BP

Dietary supplements (Riboflaxin, coenzyme Q10, magnesium, citrate)

47
Q

Side effects of propanolol

A

Tiredness, dizzyness, decreased libido, dream effects, exacerbate asthma

48
Q

Side effects of amitriptyline

A

dry mouth and eyes, drowsiness

Pharmacology (MPAS) (19 decks)

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