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IP-10 Final Exam > HA and HTN review > Flashcards

HA and HTN review Flashcards

1
Q

What is the difference between a primary and secondary HA disorder?

A

Primary is a disorder in which the HA is the disorder itself and secondary HA is caused by a different underlying disorder.

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2
Q

Explain the typical patient type, clinical presentation, duration, pain severity and frequency for migraines

A

Typical patient type: Can occur at any age but peaks in early-mid adolescents and rarely occurs after age 50. Equal in males and females during adolescents but more common in females in the adult population.
Pain and symptoms: Unilateral, pulsating, throbbing, often accompanies by N/V, photo/phonophobia. With or without aura
Duration: 4-72 hours
Pain severity: Mild-severe
Frequency: Often related to triggers, Can be intermittent, episodic or chronic.

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3
Q

Explain the clinical presentation, duration, pain severity and frequency for tension HA

A

Patient type: All ages, more common in women
Pain and symptoms: Bilateral, tightening “band-like” sensation
Duration: 30 mins- 7 days
Severity: Mild-moderate
Frequency: intermittent, episodic, chronic

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4
Q

Explain the clinical presentation, duration, pain severity and frequency for cluster HA

A

Patient type: Most common age 30-50, but present at any age > 10. Males more affected
Pain and symptoms: Unilateral, usually involves areas around the eye and temple. Described as “burning” or “stabbing” pain. May observe tear formation, nasal drainage, lip drooping and papillary changes.
Duration: 15 mins-3 hours
Frequency: Cyclical, (up to 8 times per day for a period of weeks/months)

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5
Q

What is the trigeminovascular system?

A

A complex of nerves and blood vessels around the brain. Because the brain tissue has no sensation, the pain experienced during a HA involved the trigeminovascular system

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6
Q

Explain the cortical spreading depression pathophysiology of migraines

A

The CSD is most often triggered in the Visual cortex but it can also occur in the cerebral cortex, cerebellum and hippocampus.
A migraine is initiated by slow moving wave of neuronal excitement followed by inhibition (CSD).
Intracellular calcium levels rise and a wave of depolarization moves across cerebral cortex (arachidonic acid, H+ and K+ are released extracellularly).
CSD leads to vasoconstriction and reduced cerebral blood flow. Reduced blood flow activated the trigeminovascular system.

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7
Q

What happens after the CSD activated the trigeminovascular system? Including sterile neurogenic inflammation and peripheral sensitization

A

Neurons of the system release neuropeptides (CGRP, substance P and neurokinin A). These peptides dilate the blood vessels and become inflamed and plasma protein extravasation occurs (sterile neurogenic inflammation). First order neurons are activated and carry pain signals centrally (peripheral sensitization). These pain signals travel to the various brain regions and results in symptoms associated with migraines.

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8
Q

Explain the pathophysiology associated with an untreated migraine

A

If the migraine left untreated, second and third order neurons may be activated (central sensitization). This leads to release of excitatory NT (glutamate and NO) which further increase pain sensation.

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9
Q

Explain the relevance of serotonin in migraines

A

Normally serotonin acts at 5-HT1B to cause cranial vasoconstriction and at 5-HT1D to inhibit neuropeptide release. If normal levels of serotonin are present, neuropeptide release is inhibited and there is minimal vasodilation.

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10
Q

Explain serotonin concentrations at the start of a migraine attack and what effect this has

A

At the start of a migraine, serotonin levels decrease and levels of the metabolite (5-HIAA) rise. Low levels of serotonin lead to increased neuropeptide release and vasodilation.

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11
Q

Which 2 mechanisms associated with low levels of serotonin are the major pathophysiological mechanisms of a migraine

A

Increased neuropeptide release

Vasodilation

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12
Q

What is the role of COX enzymes in the synthesis of prostaglandins

A

Arachidonic acid metabolism leads to products called eicosanoids which are cyclized and take up oxygen. They cause vasodilation and subsequent release of neuropeptides involved in pain. COX and LOX are the pathways by which arachidonic acid metabolism occurs. COX pathways produces prostaglandins and thromboxanes.

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13
Q

What is the difference between COX 1 and 2

A

COX-1 is mostly expressed in the GI mucosa, platelets, vascular endothelium and the kidneys.
COX-2 is mostly expressed in activated macrophages and monocytes. COX-2 mostly produces the pro-inflammatory mediators involved in pain.

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14
Q

Mechanism of action for NSAIDs?

A

Inhibition of COX enzymes leads to reduction in prostaglandin synthesis. Pain relief and reduction of tissue inflammation.

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15
Q

Mechanism of action for Triptans? 3 mechanisms

A

Serotonin 1B/1D agonists.
Activation of presynaptic 1D receptors blocks the release of peptides that dilate blood vessels and reduce inflammation.
Stimulation of 1B receptors leads to constriction of blood vessels, thus receiving intracranial dilation.
Triptans might decrease neuronal signaling through all 3 5-HT receptor subtypes, reducing pain.

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16
Q

Mechanism of action for ergots?

A

They structurally resemble various neurotransmitters involved in the pain signaling process. They have affinity for a-adrenergic receptors, and dopaminergic and serotinergic systems. They relieve HA symptoms mostly due to vasoconstriction in the CNS and block release of CGRP and substance P.

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17
Q

Explain the common features of the triptan family of drugs as it relates to structure

A

They contain moiety that looks identical to serotonin. This structure is referred to as an INDOLE.

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18
Q

Common adverse effects for NSAIDs, triptans, and ergots

A

NSAIDs: Gastric ulcer formation, kidney adverse effects, and increased risk of cardiovascular side effects
Triptans: Tingling, warm feeling, muscle weakness, dizzy, neck pain (CAD and angina are contraindicated)
Ergot: GI stuff, N/V/D, weakness, fatigue, muscle pain. (Severe: prolonged vasospasm that may cause gangrene and amputation)(contraindications: Pregnancy, CAD and angina)

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19
Q

Explain the mechanism by which ergots can cause peripheral ischemia

A

Life threatening peripheral ischemia can be observed when dihydro ergot mixed with 3A4 inhibitors. This combination of drugs is contraindicated.

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20
Q

Explain the mechanisms by which NSAIDs can cause GI irritation

A

By inhibiting the prostaglandins that protect the GI mucosa, NSAIDs promote formation of gastric ulcers and potentially GI bleeding.

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21
Q

List the available formulations for triptans and ergotamine

A

Triptans: Sumatriptan comes as intranasal and as SQ. Zolmitriptan comes as sublingual and intranasal. Good for patients who want faster onset or who have N/V that accompany their HA.
Ergotamine: SL rapid absorption and avoids first pass.
Dihydroergotamine: IV, IM, SQ, intranasal

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22
Q

How are the 2 different ergots metabolized? How are the 2 main triptans metabolized?

A

Ergotamine: Unknown
Dihydroergotamine: CYP3A4
Sumatriptan: MAO via oxidative deamination
Zolmitriptan: N-dealkylation via several CYP enzymes to the active metabolite (Prodrug)

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23
Q

4 classes of drugs used for migraine prevention

A

Anticonvulsants, B-blockers, antidepressants, ACE/ARBs

24
Q

5 phases of migraine HA and symptoms associated with each

A

Phase 1: Premonitory:
Neurologic: Central pain sensitization (allodynia), phonophobia, photophobia, hyperosmia and difficulty concentrating.
Psychological: Anxiety, depression, restlessness
Autonomic: Diarrhea, constipation
Constitutional: Yawning, thirst, food cravings, anorexia
Phase 2: Aura: Visual, sensory or language abnormalities.
Phase 3/4: Early and late HAL Unilateral, throbbing HA pain usually with N/V and photo/phonophobia
Phase 5: Resolution: fatigue, irritability, impaired concentration, scalp tenderness or mood changes. Some patients feel depressed, some feel relieved or euphoric.

25
Q

What does POUND mean and how many symptoms are predictive and highly predictive?

A 
P=Pulsatile quality
O=One-day duration
U=Unilateral location
N=N/V
D=Disability intensity
3/5 criteria is predictive of migraine
4/5 is highly predictive
26
Q

How does the international headache society classify the criteria for migraine without aura

A

at least 5 attacks the meet

  1. HA length 4-72 hours
  2. HA has 2 of the following 4 characteristics (Unilateral, pulsatile quality, mod-severe pain, aggravation causing avoidance of routine physical activity.
  3. During HA at least 1 of the following (N/V, photo or phonophobia)
  4. Not better attributed to another disorder
27
Q

How does the international HA society classify the criteria for migraine with aura

A

At least 2 attacks fulfilling the following criteria:

  1. Visual/sensory/speech symptoms each fully reversible
  2. 2 of the following 4 characteristics (at least 1 aura symptom spreads gradually over > 5 mins, and/or 2 or more symptoms occur in succession, each individiual aura lasts 5-60 minutes, at least 1 aura symptoms is unilateral, aura is accompanied by a HA within 60 minutes
  3. Not attributed to another disorder
28
Q

Identify HA features that are suggestive of serious, secondary cause of HA

A

New onset after age 50, sudden explosive nosey of HA with rapid progression over seconds to minutes, worst HA of life

29
Q

Treatment goals for management of acute migraines

A

Treat rapidly and consistently without recurrence, restore patients ability to function, minimize use of backup medications, optimize self-care, be cost effective, cause minimal to no side effects

30
Q

Which medications are migraine specific and non-specific

A

Migraine specific medications: Effective for migraine symptoms by acting directly on the pathophysiology underlying HA (Triptans and ergots)
Non-specific: Treat migraines by modulating pain, inflammatory and ancillary pathways and also alleviate other disorders (OTC analgesics, NSAIDs, antiemetics, corticosteroids, opioids)

31
Q

Explain the stratified care approach to managing migraines

A

Initial therapy should be based on severity of symptoms and the associated functional disability rather than the old “step care” which recommended non-specific agents before escalating to migraine specific medications. This step care has largely been replaced.

32
Q

Which medications can be used effectively in mild-mod severity HA

A

Simple analgesics (APAP, Excedrin, NSAIDs). They are effective and less costly and less likely to cause side effects. Should be taken at first sign of migraine onset including during aura

33
Q

Which medications should be used for a moderate or severe HA

A

Migraine specific medications including triptans and ergots. Triptans are first line because better tolerability and less adverse effects.

34
Q

Why should treatment with triptans be reserved for severe HA?

A

They can cause really bad medication overuse HA which are harder to treat than the original condition.

35
Q

Drug interactions with triptans

A

Use with pro-serotinergic medications can increase the risk of serotonin syndrome

36
Q

Contraindications for triptans

A

CAD and angina because they can cause coronary spasm. They are also contraindicated in ischemic vascular disorder and in rare migraines called (Hemiplegic and basilar migraines). Also within 24 hours of ergots.

37
Q

What is the only triptan available as a combo? What is it called?

A

Treximet: Sumatriptan and naproxen combo

38
Q

Given the fact that all triptans are equally effective in terminating HA, what other factors should be taken into consideration when choosing a triptan for a patient

A

Half-life, minimum interval between dosing, cost, and maximum dose per day

39
Q

How is treatment failure with triptan defined? What should be done if a patient fails a triptan?

A

Patient should trial a single triptan for 3 migraines before saying they failed that medication. If they do fail, try another triptan

40
Q

Compare and contrast the half-lives of available triptans

A

With the exception of frovatriptan most of the triptans have a half life of 2-6 hours. Frovatriptan has a half life of 26 hours, next is naratriptan at 6 hours and the shorted half life is suma/riza at approx 2-2.5 hours.

41
Q

Describe safety and efficacy of butalibital

A

Effective for treating tension HA (no studies in acute migraine). It is a barbiturate and is associated with causing chronic HA, analgesic rebound, intoxication, withdrawal symptoms, tolerance and dependence.

42
Q

Why do we use antiemetics in the treatment of migraines?

A

Adjunctive antiemetic therapy useful for treating N/V that is associated with migraine or medication used to treat the migraine. A single dose of metoclopramide, chlorpromazine or prochlorperazine 15-30 minutes before migraine medication is best.

43
Q

Whens should rescue medications be used and what medications should we use?

A

Rescue therapy describes treatment that is unresponsive to standard acute migraine medications including triptans. Opiates or analgesics either PO or IV. If symptoms continue after one triptan dose, another dose 2-4 hours later. This repeat triptan dose is not a rescue medication.

44
Q

Indications for preventative therapy

A

HA >2 days per week or >8days/month, HA disability persists despite aggressive treatment, recurring migraines that interfere with daily routines, presence of prolonged or complex aura or migraine induced stroke, medication use > 2 days per week, contraindications or adverse effects to acute therapies, patient desire to reduce HA frequency

45
Q

Which medications have the greatest evidence in migraine prevention

A

All level A evidence: VPA, topirimate, metoprolol, propranolol, timolol and frovatriptan (only for menstrual related)
Level B: SSRI, SNRI, other B-blockers and other triptans

46
Q

When do people typically see a response to migraine preventative therapy?

A

Maintenance meds should start low and be increased slowly. Some patients may see response in 1 month but typically is it 2-3 months.

47
Q

How long should preventative treatment continue after initial response is seen?

A

6-12 months then gradual taper should occur.

48
Q

What is the preferred treatment regimen for tension HA

A

Self care with OTC analgesics with ow without caffeine (APAP or NSAIDs)

49
Q

Differentiate medication overuse HA from other HA types

A

MOH occurs from excessive use of acute HA medications which can increase HA frequency and drug consumption. Also called rebound HA. In MOH, HA resolved upon medication administration. In medication induced HA, the HA occurs upon medication administration.

50
Q

ALL HA therapies should be limited to how many days per month?

A

< 10 days per month.

51
Q

What do we use to treat acute cluster HA? What about prevention?

A

Acute therapy: Oxygen, SQ sumatriptan or intranasal ZOMIG.
Preventative therapy: CCB, lithium carbonate, steroids.
Nonpharm: Avoid triggers, alcohol or changes in sleep habit.

52
Q

Consequences of elevated BP?

A

Stroke, cardiovascular events and kidney failure

53
Q

What is the blood pressure goals for those under the age of 80 and those over the age of 80?

A

Under 80 goal is <140/90

Over 80 goal is<150/90

54
Q

Non-pharm recommendations for reducing BP

A

Weight loss, salt reduction, exercise, drink booze (cardioprotective), stop smoking

55
Q

When HTN is the only condition what is first line therapy depending on patient population?

A

Black population: CCB or thiazide
White and other non-black < 60 YO: ACE/ARB
White and other non-black >60 YO: CCB or thiazide (ACE/ARB considered equal)

56
Q

When HTN is associated with diabetes, CKD, CAD, stroke, HF recommend appropriate first line anti-HTN

A

Diabetes: ACE/ARB (CCB or thiazide in blacks)
CKD: ACE/ARB everyone
CAD: B-blocker + ACE/ARB
Stroke: ACE/ARB
HF: ACE/ARB + B-blocker + spironolcatone regardless of BP. (Add dihydro CCB if further control is needed)

57
Q

Adverse effects for each anti-HTN drug class and appropriate monitoring parameters

A

ACE: Cough, angioedema, increased SCr, hyperkalemia, hypotension, avoid in preg
ARB: Increased SCr, avoid in preg
Thiazide: Hypokalemia, hyperglycemia, hyperuricemia
CCB: Peripheral edema, avoid non-dihydro in HF
B-blockers: Impaired glucose metabolism, reduced sexual function, reduced exercise tolerance
A-blockers: Beneficial effects on blood glucose and lipid levels

IP-10 Final Exam (5 decks)

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