Week 28 Headache Flashcards

Question

Non-selective NSAIDs

Answer 1

Inhibit both COX 1 & COX 2. All non-selective NSAIDS [EXCEPT ASPIRIN] act as reversible COX inhibitors. As opposed to COX 2 selective NSAIDs.

Answer 2

Irreversibly binds to COX enzyme and modifies the configuration. Since platelets have no nucleus, they are unable to make more enzymes therefor are not able to create PGH2 which is then made into Thromboxane A -> no platelet aggregation. Cells with nucleus are able to synthesize new COX enzymes to replace the ones aspirin bound to.

Answer 3

Phospholipid bilayer + Phospholipase A2 -> Arachidonic acid Arachidonic acid + COX 1 (in all tissues, esp GI tract) -> Thromboxane + Prostaglandins.

Answer 4

Phopholipid bilater + Phospholipase A2 -> Arachidonic acid Arachidonic acid + COX 2 (from inflam stimuli, hormones, growth factors) (in Kidney, GI tract, CNS, endothelium) -> Prostaglandins that promote vasodil, pain.

Answer 5

Great anti-platelet activity. Terrible analgesic activity.

Answer 6

Ketorolac causes the most GI ulcers and bleeds. Add aspirin and this increases the risk of ulcers/bleeds in GI tract.

Answer 7

Selective COX 2.

Answer 8

SAH, sentinal bleed RCVS (reversible cerebral vasospasm) ICH Ischemic stroke Arterial dissection Cerebral venous thrombosis Pituitary hemorrhage/Sheehan's syndrome Retroclimal hematoma

Answer 9

Meningitis Spontaneous CSF leak Posterior reversible leukoencephalopathy/hypertensive encephalopathy 3rd ventricle colloid cyst

Answer 10

**Diagnosis of exclusion** Primary cough headache Primary exercise headache Primary headache associated with sexual activity Primary thunderclap headache Primary stabbing headache - not thunderclap severity, aka Ice-pick headaches.

Answer 11

SNOOP4 S Systemic symptoms N Neuro-deficit O Onset O Older than 55 P Pregnancy P Previous headache change P Positional change P Precipitated by valsalva, cough, exertion (Increased ICP)

Answer 12

Labwork Imaging: CTA - shows aneurysm CT non-contrast - shows blood and location [ARCH TO VERTEX STAT] MRI Angiography Lumbar puncture

Answer 13

Age Vision changes Hurts to chew Muscles ache Weight loss Low energy Hurts to wash hair Previous, current, or later presentation of polymylagia rheumatica

Answer 14

Vitals Eyes: Acuity, pupils, visual fields Palpate temoral artery

Answer 15

RAPD Optic disc: swollen, blurred margins Thin artery Cotton wool spots Simultaneous presence of Anterior ischemic optic neuropathy (AION) and retinal artery occlusion = high suspicion for GCA.

Answer 16

CBC & platelets Inflammatory markers (CRP +/- ESF) Opthalmology referral Temporal artery ultrasound: halo sign/compression sign Temporal artery biopsy: intimal wall thickening, multinucleated giant cells, disruption of internal elastic lamina.

Answer 17

Normal vitals. Normal acuity/pupils Neuro exam abnormal Fundoscopy: Optic nerve head swelling, blurred margins, disc hemorrhages, cotton wool spots. RULE OUT ICP/PAPILLEDEMA

Answer 18

Headache worse in a.m. Nausea/vomitting. Ptosis Double vision: Monocular or binocular? Pupils unequal Eye movements abnormal RAPD RULE OUT COMPRESSIVE/ANEURYSMAL 3RD NERVE

Answer 19

SEND TO EMERGENCY NEURO-IMAGING: if incomplete palsy, if pupil involved, if not isolated. CTA to detect aneurysm >4mm MR angiography if CTA contraindicated

Answer 20

First line modality in trauma Used as a screening tool Can be combined with IV contrast to image vessels

Answer 21

Excellent further characterization of abnormalities detected on CT Not as good as CT with contrast for assessing vessels.

Answer 22

IV contrast for venous system. Angiogram for arterial system.

Answer 23

CT head w/out contrast

Answer 24

CT temporal bone

Answer 25

CT head w/contrast

Answer 26

CTA head/neck

Answer 27

CT venogram head

Answer 28

Use appropriateness criteria. Decision is based on clinical exam, labs, and patient hx. Don't do imaging on uncomplicated headaches unless red flags are present. Unstable patients need imaging urgently.

Answer 29

Right lateral ventricle

Answer 30

Left lateral ventricle

Answer 31

White matter in right frontal lobe

Answer 32

Gray matter in the left frontal lobe

Answer 33

Falx cerebri

Answer 34

Depression

Answer 35

TCAs Duloxetine (SNRI) Gabapentin/pregabalin

Answer 36

Amitriptyline Divalproex Topiramate

Answer 37

High prominence of pain and pain-related diseases.

Answer 38

health related quality of life Work Increased risk of other medical illness

Answer 39

Increased healthcare utilization Lost productivity

Answer 40

Decrease (not eliminate) pain Goal directed therapy Multidisciplinary approach Function-centered life Minimize harm

Answer 41

Physical therapies Psychological therapies Pharmacotherapies interventional Procedures

Answer 42

CBT Operant-behavioural therapy Mindfulness-based stress reduction Acceptance and commitment therapy

Answer 43

First line agents: Gabapentenoids/TCAs/SNRIs Second line agents: Tramadol/Opioid analgesics Third line agents: Cannabinoids then Fourth line agents

Answer 44

Consider screening high risk presentations; ODs, recurrent skin and soft tissue infections, infective endocarditis. Adults: NIDA Quick Screeen In the past year: EtOH 5+M/4+W, Tobacco, Rx drugs for non-medical reasons, Illegal drugs. Pediatric: CRAFFT

Answer 45

Larger amounts or longer period than intended. Persistent desire/unsuccessful attempts to cut down/control. Time spent obtaining, using, recovering. Craving. Recurrent use -> obligations at work, school, home. Continued use despite negative effects. Loss of activities d/t use. Use in physically hazards situations. Continued use despite knowledge of physical/psych prob d/t use. Tolerance. Withdrawal. 2 = OUD 2-3 = mild 4-5 = moderate 6+ = severe

Answer 46

Located in medulla Decreased sensitivity of chemoreceptors to hypercapnia. Decreased ventilation response to hypoxia. -> No stimulus to breath (apnea) Suppression of cough centre (no airway protection) *Can develop tolerance to loss of hypercapnic drive. *Onset for heroin = 20-30 minutes, fentanyl = 2 minutes

Answer 47

Mental status: euphoric, sedated, coma Vitals: depressed RR & HR Head/neck: Miosis, cyanosis Skin: May see track marks

Answer 48

Opioid antagonist, high affinity for mu receptor. IV, IM, nasal. Not sublingual d/t significant first pass metabolism. Onset = 2 minutes Short duration of effect 2min-2 hours. May be shorter than opioids. Indications: Evidence of opioid toxicity on exam. CNS depression. RR < 8 or O2 sat <90% Consider alternative diagnosis after 10-15 mg given. Target dose to avoid withdrawal.

Answer 49

Initial: 0.1mg IV, 0.4 mg IM Q3min PRNx2 Escalating doses: 0.4mg -> 0.4mg -> 2mg -> 4mg -> 10 mg

Answer 50

Irritability/aggitation GI: nausea, vomiting, diarrhea Muscle and joint pain Piloerection Dilated pupils Diaphoresis Anxiety

Answer 51

In acute care: Increased rates of leaving AMA Increased risk of mortality and morbidity Increased self treatment Decreased tolerance and increased overdose risk

Answer 52

Improve therapeutic relationship. Unmasks underlying illness.

Answer 53

OAT Inpatient: morphine/hydromorphone

Answer 54

Approaches such as rapid OAT taper, supportive management alone (Clonidine), and abrupt cessation of any opioids. Strong recommendation against this strategy: High rates of relapse, High risk of OD, Increased risk of transmission of infection.

Answer 55

Decrease all cause mortality Decrease risk of HIV/HCV Increase retention to treatment Increase rates of abstinence

Answer 56

Discuss patient goals and preferences Offer harm reduction. If wanting clinical management: First line OAT is buprenorphine or methadone Second line is slow release oral morphine. Slow taper for any reductions. If not wanting clinical management: Discuss withdrawal management: risks of withdrawal alone, suggest slower OAT taper that is individualized and monitored. Discuss psychosocial interventions and treatments.

Answer 57

First line Mu partial agonist: low receptor activity, high receptor affinity, long duration of action. Metabolized: hepatic Better safety profile, flexibility for take home doses, quicker to achieve therapeutic effects, fewer drug interactions. Initiation can be a barrier for some, potential for higher drop out based on prior literature (? lower doses)

Answer 58

First line Mu full agonist Metabolized: hepatic CYP3A4 Better retention, strong base of evidence for treatment of OUd. Requires daily witnessed ingestion at pharmacy (DWI) until stability criteria met, higher risk for OD, greater side effects, greater drug interactions, potential for QT prolongation.

Answer 59

Second line Mu full agonist Metabolized: hepatic with renal clearance. No QT prolongation, equal effectiveness to methadone, maybe fewer side effects than methadone, fewer drug interactions. Consider off-label (not widely available), requires DWI until stability criteria met, CI in renal impairment, caution with sedatives, less body of evidence.

Answer 60

3rd line exception Opioid antagonist - can cause precipitated withdrawal. Can reduce cravings, OD risk if used consistently. High risk for OD d/t loss of tolerance if not adhered to. Only used in exceptional circumstances: those declining OAT, those without tolerance.

Answer 61

Outpatient Intensive outpatient programs: Daytox, VAMP Inpatient Offered as adjuct to treatments, not mandatory to receive OAT

Answer 62

Taper over a long period 12-52 weeks. Plan dose reductions to occur bi-weekly or monthly as opposed to more or less frequently.

Answer 63

SNOOP4 S Systemic N Neurologic O Onset O Older age P Pregnancy P Previous headaches P Positional P Precipitated by valsalva, cough: ICP

Answer 64

Meningitis Encephalitis Thunderclap headache: SAH - LOC, nausea, vomiting, meningismus, sentinal headache ICH - Headache, vomiting, decreased LOC, slurred/incomprehensible speech, facial droop, hemiplegia/hemiparesis, not always maximal at onset Cervical artery dissection - Focal neurological, hx of trauma, hx of hyperextension, neck pain Acute angle-closure glaucoma: red eye, visual acuity, >40 years old, visual disturbances, halos, nausea, vomiting, fixed dilated pupil, blindness. Temporal arteritis ICP

Answer 65

POUND P Pulsatile O hOurs 4-72 duration U Unilateral N Nausea D Disabling

Answer 66

Bilateral Dull, pressing, non-throbbing Mild-moderate intensity Not aggravated by physical activity No nausea/vomiting Episodic Chronic Easily confused with migraine

Answer 67

Diary to identify triggers. CBT, biofeedback, relaxation training. Exercise. PT/acupuncture.

Answer 68

Acetaminophen Ibuprofen Naproxen

Answer 69

Combination analgesics containing caffeine

Answer 70

MM relaxants. Opioids. Triptans

Answer 71

TCAs: Amitriptyline, Nortriptyline

Answer 72

Consider if pt has >15 headache days/month and uses NSAID or acetaminophen >15 days/month. May develop insidiously (acetaminophen Used to work and didnt realize they were using more) Comorbid with depression and anxiety. May have poor coping skills/self efficacy. Use headache diary to help diagnose and manage. Stop offending medication. Consider prophylaxis. Encourage non pharm management techniques

Answer 73

Influenza, Covid, Sinusitis. Systemic and upper resp S&S. Ddx: meningitis & encephalitis Flu: sudden onset, fever at onset, headache at onset, cough. Management: Hydration Rest Acetaminophen Ibuprofen Antiviral therapy within 48 hrs of onset.

Answer 74

Social and psychological history important. Exacerbation by anxiety, depression, stress, sleep, substance use. Some cultures localize stress/anxiety as pain/tension in the head. Use FIFE Consider: environment change, life control, social stressor/supports, languange and literacy, cultural explanatory models for illness.

Answer 75

Structures, innervation to meninges, scalp, skull, sinuses, blood vessels. No pain receptors in the brain parenchyma.

Answer 76

History: Onset, timing, location, quality, severity, exacerbating/alleviating, associated symptoms, red flags. Prior headaches. Context (fhx, shx, meds, mhx, occupation) Red flags: SNOOP4 Exam: fundoscopy, focal neuro. Imaging LP

Answer 77

TIA/stroke: Older age, vascular risk factors, Abrupt onset, maximal at onset, no spreading, negative symptoms, minutes to days, may have headache. Migraine aura: Younger age, no vascular risk factors, gradual onset, spreading quality, positive symptoms, 5-60 minutes, followed by headache (usually). Focal seizure: Variable age, no vascular risk factors, variable onset, variable spreading, positive symptoms, <5 minutes, post ictal headache or other symptoms.

Answer 78

SAH Get CThead CTA head and neck. +/- LP

Answer 79

Lifestyle Acute tx: TCAs, GPANTs, acetimenophen, NSAIDS. Preventative tx

Answer 80

Shorter duration headaches with prominent cranial autonomic features. Ipsilateral lacrimation/conjuctival injection Ipsilateral nasal congestions/rhinorrhea Eyelid edema Forehead/facial sweating Miosis/ptosis Restlessness/agitation

Answer 81

Idiopathic Intracranial Hypertension Headache and visual disorder caused by high intracranial pressure, without secondary cause. Positional (worse supine) Pulsatile tinnitus Visual disturbances Risks: Female, weight, younger age, certain medications.

Answer 82

Most common type. Mild-moderate intensity. 30 min - 7 days. Bilateral, pressing/tightening. No aggravated by usual physical activity. No nausea, none or 1 of light/sound sensitivity.