Headaches in Pregnancy

Question 1

list the different types of headaches

Answer 1

acute: tension, migraine, cluster
chronic: brain tumour, migraine, cluster, med overuse

Question 2

compare non-migraine headaches

Answer 2

tension: most freq, improves with exercise & NSAID
Cluster: rare, usually short but severe, hemiplegic, tx with triptan and 100% O2

Question 3

list usual tx for headaches

Answer 3

NSAIDS, paracetamol, opioids

Question 4

describe PG as a pain mediator

Answer 4

PG made in a pathway that can be blocked by corticosteroids or NSAIDS, arachidonic acid is a precursor for PG which mediate pain, inflam, fever, COX1/2 are needed to transform AA into PG and thromboxane

Question 5

describe NSAID MOA in pain mediation

Answer 5

block PG synthesis by inhibiting COX1/2 -> anti-inflam, anti-pyretic and analgesic

Question 6

describe IL1 effect on temperature

Answer 6

IL1 causes PG to reset temp set point to higher level -> shivering, sweating

Question 7

what is thought to be the main source of production of inflammatory PGs?

Answer 7

COX2: pain sensed by nociceptors, temp increases, inflam cells recruited through vasodilation = oedema, redness, inflam

Question 8

describe aspirin MOA

Answer 8

irreversibly inhibits COX1/2 through COX acetylation, blocks PG ability to change temp set point, inhibits platelet thromboxane and irreversibly binds to platelets stopping aggregation

Question 9

describe ibuprofen MOA

Answer 9

reversible inhibitor of COX1/2, anti-inflam/pyretic

Question 10

describe SE of NSAIDS on pregnancy

Answer 10

affect mat platelet function -> increased risk PPH, may cause prem closure of ductus arteriosus, delay labour/birth, oligohydramnios and fetal renal dysfunction, stop at 32K

Question 11

describe paracetamol MOA

Answer 11

may inhibit COX3 in CNS, reduces pain and fever

Question 12

describe codeine

Answer 12

metabolised to morph in liver, cough suppressant, can make migraines worse

Question 13

list common causes of headaches

Answer 13

hormonal changes, increased blood vol, stress, lack of sleep, dehydration, depression/anxiety

Question 14

describe the two theories of migraine pathophysiology

Answer 14

vascular: vasoconstriction during aura, vasodilation during headache
sensory nerve: activation of trigeminal nerve terminals leads to pain and inflam

Question 15

describe triptane MOA

Answer 15

binds to presynaptic serotonin nerve endings to inhibit release of CGRP and binds to postsynaptic serotonin R on blood vessels to cause vasoconstriction