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Immunopharm - Antihistamines and Migraines Flashcards

1
Q

A migraine is a ___ headache. The inflammatory response spreads along the ___ system and arrives in the ___ ___ ___ and other areas to convey pain.

A

A migraine is a neurovascular headache. The inflammatory response spreads along the trigeminovascular system and arrives in the trigeminal nucleus caudalis and other areas to convey pain

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2
Q

Histamine:

Derived from ___ of ___, catalyzed by L-___ ____. Once formed it is stored or inactivated by ___-N-____ (in the CNS) or diamine oxidase (resulting in ____)

A

Histamine:

Derived from decarboxylation of histidine catalyzed by L-_histidine decarboxylase_. Once formed, it is stored or inactivated by histamine-N-_methyltransferase_ (in the CNS) or diamine oxidase (resulting in deamination)

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3
Q

Histamine:

  1. Where is it stored? Speed of turnover?
  2. Where does it have rapid turnover?
A

Histamine:

  1. Stored in mast cells and basophils with slow turnover
  2. Rapid turnover in neurons and enterochromaffin-like cells in the gastric mucosa
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4
Q

Histamine:

The allergen stimulates __ cells to produce ___ antibodies that then bind to ___ receptors on mast cells and basophils. This causes _____ and further allergen binding causes ___ of __/___ receptors producing degranulation (____ release)

A

Histamine:

The allergen stimulates B cells to produce IgE antibodies that then bind to Fc receptors on mast cells and basophils. This causes sensitization and further allergen binding causes crosslinking of IgE/Fc receptors producing degranulation (histamine release)

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5
Q

Function of Histamine:

  1. ____ responses: rhinitis and ___ (hives)
  2. 4 cardiovascular effects?
  3. What does it do to the airways?
A

Function of Histamine:

  1. Allergic response: rhinitis and urticaria
  2. CV: vasodilation, increased vascular permeability, injection produces a triple response (red spot/flare/wheal), and increase force of contraction of the heart
  3. Causes bronchoconstriction
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6
Q

Function of Histamine:

  1. Increases ___ ___ secretion
  2. Causes itch and potential ____ (severe hypotension, bronchoconstriction, and ____ swelling)
A

Function of Histamine:

  1. Increases gastric acid secretion
  2. Causes itch and potential anaphylaxis (severe hypotension, bronchoconstriction, and epiglottal swelling)
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7
Q

Histamine receptors:

H1:

  1. Distribution?
  2. Function?
A

Function of Histamine:

H1:

  1. In smooth muscle, vascular endothelium, and brain
  2. Bronchoconstriction, separation of endothelial cells (hives), pain, and itching
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8
Q

Histamine Receptors:

H2:

  1. Distribution?
  2. Function?
A

Histamine Receptors:

H2:

  1. Gastric mucosa, cardiac muscle, and brain
  2. vasodilation and stimulation of gastric acid secretion
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9
Q

Histamine Receptors:

H3:

  1. Distribution?
  2. Function?
A

Histamine Receptors:

H3:

  1. CNS and some PNS (autoreceptor in the PNS)
  2. Decreases NT release: histamine, ACh, NE, 5-HT
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10
Q

Histamine Receptors:

  1. All receptor subtyptes are ___ ____ ___.
  2. H1 receptors activate __ ___ that convert ____ to IP3 and ___ and are primarily involved in ___ and ___.
A

Histamine Receptors:

  1. All receptor subtypes are G protein couples
  2. H1 receptors activate G proteins that convert phosphatidylinositol to IP3 and DAG and are primarily involved in inflammation and allergy
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11
Q

Histamine Receptors:

  1. H2 receptors linked through G proteins to increase ___ with its primary function to regulate ___ ___ ___.
  2. H3 receptors function as ____ ____ in the CNS and PNS
A

Histamine Receptors:

  1. H2 increase cAMP and regulate gastric acid secretion
  2. Function as feedback inhibitors
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12
Q

3 strategies to inhibit histamine’s actions?

A

a. Administer drugs to counter pathology (Ep for aniphylaxis)
b. Prevent mast cell degeneration - cromolyn
c. Use Histamine receptor antagonists

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13
Q

H1 receptor antagonists:

  1. All agents are ___, ___, inhibitors.
  2. They all ___ the effects at H1 receptors and thus are useful in treating?
  3. What are the NOT effective in treating?
A

H1 receptor antagonists:

  1. All agents are reversible, competitive, inhibitors
  2. They all attenuate the effects at H1 and are good for allergic reactions, rhinitis, urticaria, itch, and flare
  3. DRUGS NOT EFFECTIVE FOR BRONCHOCONSTRICTION
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14
Q

H1 receptor antagonists:

First vs. Second generation Antagonists:

  1. First generation are highly ___ soluble and distribute to the ___ whereas second do not.
  2. First generation drugs produce ___ and ___ and exhibit some anti-_____ activity. Second generation in comparison?
A

H1 receptor antagonists:

First vs. Second generation Antagonists:

  1. First generation are highly lipid soluble and distribute to the CNS whereas second do not
  2. First generation drugs produce drowsiness and sedation and exhibit some anti-_muscarinic_ activity. Second generation has no anti-muscarinic activity and much less drowsiness/sedation
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15
Q

H1 receptor antagonists:

First vs. Second generation Antagonists:

  1. Why dont second generation drugs readily penetrate the CNS?
  2. Example of a girst generation drug with anti-muscarinic activity? Uses?
A

H1 receptor antagonists:

First vs. Second generation Antagonists:

  1. Dont penetrate because they are ionized at pH=7.4 and they are highly bound to albumin
  2. 1st generation: meclozine –> antiemetic or some antiparkinsons
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16
Q

First generation H1 receptor Antagonists:

  1. 5 drugs?
  2. Absorption? Distribution? Metabolization?
A

First generation H1 receptor Antagonists:

  1. Diphenhydramine, chorphenamine, dimenhydrinate, hydroxyzine, and promethazine
  2. Well absorbed, widely distributed (even to CNS), and extensively metabolized
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17
Q

First generation H1 receptor Antagonists:

  1. The major side effect? Which drug thus is best and why?
  2. What are the anticholinergic SE?
  3. Other SE?
A

First generation H1 receptor Antagonists:

  1. Major SE: sedation - chlorphenamin is best because its the least sedating
  2. Anticholinergic SE: dry mouth, cough, urinary retention, and blurred vision
  3. Other SE: loss of appetitie, N/V, dizziness, fatigue, tremor, hypersensitivity reactions
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18
Q

First generation H1 receptor Antagonists:

Dimenhydrinate and diphenhydramine have a ___ therapeutic index and often are used ____ as OTC ____.

A

First generation H1 receptor Antagonists:

Dimenhydrinate and diphenhydramine have a low therapeutic index and are often used recreationally as OTC hallucinogens

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19
Q

Second Generation H1 Receptor Antagonists:

  1. Drugs?
  2. Absorption? Distribution? Metabolism?
  3. SE?
A

Second Generation H1 Receptor Antagonists:

  1. Cetirizine, loratedine, desloratadine, and fexofenadine
  2. Well absorbed; no distribution to CNS; CYP450
  3. Minimal SE: sedation/drowsiness –> no anticholinergic effects
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20
Q

Therapeutic Actions of Antihistamines:

  1. Acute ____ reactions
  2. Reduce ___
  3. Diminish symptoms of ___ and ___
  4. What first generation drugs are used for prophylaxis and treatment of motion sickness?
A

Therapeutic Actions of Antihistamines:

  1. Acute allergic reactions
  2. Reduce itching
  3. Diminish symptoms of cold and flu
  4. Motion sickness: diphenhydramine and promethazine
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21
Q

Therapeutic Actions of Antihistamines:

  1. What can diphenhydramine reduce?
  2. What can promethazine treat?
  3. First generation drugs are used for ___ and occassionally for ___ but routine use is not recommended.
A

Therapeutic Actions of Antihistamines:

  1. Diphenhydramine can reduce Parkinson’s symptoms
  2. Promethazine can treat nausea and vomitting
  3. 1st generation: somnolence and occasionally insomnia but shouldnt be used long term
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22
Q

H2 receptor antagonists:

  1. Drugs?
  2. Function?
A

H2 receptor antagonists:

  1. Cimetidine, famotidine, ranitidine, and nizatidine
  2. Inhibits stomach acid production
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23
Q

H2 receptor antagonists:

  1. Indicatons?
  2. Why is cimetidine no longer recommended?
A

Therapeutic Actions of Antihistamines:

  1. Indications: GERD, peptic ulcer disease, and heartburn
  2. Cimetidine: no longer recommended because it is used as a suicide substrate for CYP 3A4 and potential toxicity of concurrently ingested drugs that are metabolized by this CYP isoform
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24
Q

5-Hydroxytryptamine (serotonin):

  1. Mainly found where?
  2. 80% is in what cells?
  3. Mainly metabolized to ____ by the ___. This is used to determine 5HT levels in the body via urine analysis.
A

5-Hydroxytryptamine (serotonin):

  1. Found in gut, platelets, and CNS
  2. 80% in enterochromaffin cells in the gut
  3. Mainly metabolized to 5-HIAA by the liver
25
5-Hydroxytryptamine (serotonin): Has three fates after synthesis, what are these?
5-Hydroxytryptamine (serotonin): a. Storage (gut) b. Rapid inactivation by MAO c. Precursor for melatonin in pineal gland
26
5-Hydroxytryptamine (serotonin) receptors: 1. 5HT1A/1B: thought to be ____ receptors in the ___ nuclei and \_\_\_\_\_. 2. 5HT2A: contributes to ____ aggregation in the \_\_\_, \_\_\_, blood vessels, GI, and ____ muscle 3. 5HT1D: produces ___ in the \_\_\_
5-Hydroxytryptamine (serotonin) receptors: 1. 5HT1A/1B: thought to be _auto_-receptors in the _raphe_ nuclei and _hippocampus_ 2. 5HT2A: contributes to _platelet aggregation_ in the _CNS, PNS,_ blood vessels, GI, and _smooth_ muscle 3. 5HT1D: produces _vasoconstriction_ in the _brain_
27
5-Hydroxytryptamine (serotonin) receptors: 1. 5HT2A/3/4: is involved in ___ excitation in the \_\_\_, \_\_\_, and \_\_\_ 2. 5HT2A/2B: ____ smooth muscle in the \_\_\_, PNS, ___ \_\_\_, and GI
5-Hydroxytryptamine (serotonin) receptors: 1. 5HT2A/3/4: is involved in _neuronal_ excitation in the _CNS_, _PNS_, and _GI_ 2. 5HT2A/2B: _contracts_ smooth muscle in the _CNS_, PNS, _blood vessels_, and GI
28
5-Hydroxytryptamine (serotonin) receptors: 1. All of the roles of 5HT2A? 2. Which receptor produces vasoconstriction in the brain? 3. Which receptors are auto-receptors?
5-Hydroxytryptamine (serotonin) receptors: 1. 5HT2A: platelet aggregation, neuronal excitation, and contraction of the smooth muscle 2. 5HT1D - vasoconstriction in brain 3. 5HT1A/1B - autoreceptors (raphe nuclei and hippocampus)
29
5-Hydroxytryptamine (serotonin) receptors: 1. Which receptors produce neuronal excitation? 2. Which receptors contracts smooth muscle?
5-Hydroxytryptamine (serotonin) receptors: 1. 5HT2A/3/4 - neuronal excitation 2. 5HT2A/2B - contracts smooth muscle
30
Actions of Serotonin: 1. ___ aggregation 2. Contraction of vascular smooth muscle where? 3. Function on the heart?
Actions of Serotonin: 1. _Platelet_ aggregation 2. Contraction of vascular smooth muscle in splanchnic, renal, pulmonary, and cerebral vasculatures 3. Acts as a positive inotrope (increases strength) and positive chronotrope (increases HR) on the heart
31
Actions of Serotonin: 1. Stimulaes what part of the GI? Inhibits what part? 2. Sensitizes small diameter ___ neruons 3. What "cerebral" functions does it effect?
Actions of Serotonin: 1. Stimulates SI motility, inhibits stomach smooth muscle 2. Sensitizes _sensory_ neurons 3. Affects sleep, cognition, temperature regulation, and motor activity
32
Actions of Serotonin: 1. Drugs that block 5HT2C are associated with? 2. Migraine = complex _____ disorder. Key features are ___ (often ____ and throbbing) and associated with \_\_\_, as well as sensitivity to \_\_, \_\_\_, and exacerbation with head movements
Actions of Serotonin: 1. Block 5HT2C: wt gain because generally serotonin inhibits stomach smooth muscle and decreases appetite. By blocking this inhibition - stimulating appetite 2. Migraine = complex _neurobiological_ disorder. Key features are _HA_ (often _unilateral_ and throbbing) and associated with _nausea_ as well as sensitivity to _light_, _sound_, and exacerbations of heat movements
33
Overview of migraines: 1. In about 20-30% of subjects, headache is preceeded by ___ ( visual, \_\_\_, or ___ deficits). There is often a strong ___ component. 2. The key pathway for the pain is the \_\_-\_\_\_\_\_ input from the ___ vessels. These nerves pass through the ___ ganglion and synapses, and project though the _____ tract and form synapses in the \_\_\_.
Overview of migraines: 1. Preceeded by _aura_ (visual, _motor, or speech_ deficits). There is often a strong _genetic_ component 2. The key pathway for the pain is the _tri-geminovascular_ input from the _meningeal_ vessels. These nerves pass through the _trigeminal_ ganglion and synapses, and project through the _quintothalamic_ tract and form synapses in the _thalamus_
34
Phases of a migraine attack: What are the 5 phases? Many dont have which?
Phases: a. Prodrome b. Aura phase c. Migraine headache d. Resolution phase e. Migraine hangover -- Many dont have prodrome or postdromes
35
Phases of a migraine attack: 1. Prodrome: vague ___ or ___ symptoms as much as ___ (time) prior 2. Aura - what does this involve? Length of time?
Phases of a migraine attack: 1. Prodrome: vague _vegetative_ or _affective_ symptoms as much as _24 hours_ prior 2. Aura: focal neurological symptoms - up to one hour long preceeding the migraine headache
36
Phases of a migraine attack: 1. Migraine headache: within _ \_\_ (time) of resolution of the aura, typical migraine (often with \_\_\_) occurs for up to ___ hours 2. Resolution phase is characterized by ___ \_\_\_ 3. Migraine hangover: duration? What does it involve?
Phases of a migraine attack: 1. Migraine headache: within _1 hour_ of resolution the aura, typical migraine (often with _throbbing_) occurs for up to _72_ hours 2. Resolution phase is characterized by _deep sleep_ 3. Migraine hangover: up to 24 hours after with fatigue, maliase, and transient return of pain following cough/sudden head movement
37
CSD: 1. What does CSD stand for? 2. What is it the cause of?
CSD: 1. Cortical Spreading Depression 2. The cause of _migraine aura_
38
Cortical Spreading Depression: 1. Wave of ___ - lasting electrophysiological ____ followed by a wave of ___ \_\_\_ of neuronal activity usually in the cerebral \_\_\_\_. 2. CSD upregulates a variety of genes coding for? 3. Increased metalloproteinases leads to ___ of BBB allowing \_\_\_, \_\_\_, and ___ to reach the dural perivascular ___ afferents.
Cortical Spreading Depression: 1. Wave of _short_ lasting electrophysiological _hyperactivity_ followed by a wave of _prolonged inhibition_ of activity in the _cortex_ 2. Upregulates genes for: COX-2, TNF, IL-1, galanin, or metalloproteinases 3. Leads to _leakage_ of BBB allowing _K+, NO, and adenosine_ to reach perivascular _trigeminal_ afferents
39
Migraine: 1. The aura phase is a primarily ____ phenomenon as it may activate the ____ fibers through the \_\_\_. 2. Nonspecific treatment of acute attack migraine? 3. Specific treatment of acute attack migraine? 4. What is the first choice combination as analgesic and antipyretic?
Migraine: 1. The aura phase is a primarily _cortical_ phenomenon as it may activate the _trigeminal_ fibers through the _dura_. 2. Nonspecific: NSAIDs, anti-emetics, opioids, corticosteroids, and dopamine antagonists 3. Specific: ergotamine, DHE, and triptans 4. Aspirin, acetaminophen, and caffiene
40
Triptans: 1. Act at what receptor? Subtypes? 2. Drug examples?
Triptans: 1. Act at 5HT1 --\> 5HT1B and 5HT1D 2. Sumatripan and zolmitriptan
41
Triptans: Two proposed MOA: a. Direct ____ action on ______ blood vessels by binding \_\_\_. b. _____ inhibition on ___ neurons by blocking ____ gene regulated peptide. This is a _____ NT
Triptans: Two MOA: a. Direct _vasoconstrictive_ action on _intracrania_ blood vessels by binding _5HT1_ b. _Presynaptic_ inhibition on _sensory_ neurons by blocking _calcitonin gene regulated peptide_. This is a _proinflammatory_ NT
42
Triptans: 1. Indications? Not useful for? 2. Administration? 3. SE?
Triptans: 1. _DRUG OF CHOICE_ for acute treatment of migraine; not for long term or prophylaxis 2. Subcutaneous injection, orally, or nasal spray 3. SE: nausea, malaise, dizziness, weakness, dry mouth, paresthesia, pain at injection site
43
Triptans: 1. Rare SE? 2. Who should be screened prior to administration of sumatriptan/zolmitriptan?
Triptans: 1. Rare: coronary artery spasm, ischemia, and arrhythmias 2. Screened: those at _risk_ for coronary heart disease, diabetes, obesity, severe uncontrolled hypertension, or hypercholesterolemia
44
Triptans: Contraindications: 1. History of? 2. Those with what vascular diseases? 3. Uncontrolled \_\_\_\_ 4. Taking \_\_\_\_. 5. Naratriptan is not for patients with severe ___ or ___ disease
Triptans: Contraindications: 1. History of coronary artery disease 2. Those with cerebrovascular or peripheral vascular disease 3. Uncontrolled hypertension 4. Taking MAOIs 5. Naratriptan: not for _hepatic_ or _renal_ disease
45
Ergot Alkaloids: 1. Drug examples? 2. Mechanism is attributed to ___ action at \_\_\_.
Ergot Alkaloids: 1. Ergotamine and dihydroergotamine 2. Mechanism is attributed to _agonist_ action at _5HT1_
46
Ergot Alkaloids: 1. What are these for? Not for? 2. Administration of ergotamine? 3. Administration of DHE?
Ergot Alkaloids: 1. For moderate to severe migraine; not for prophylaxis 2. Ergotamine: oral, IV, or IM 3. DHE: IV
47
Ergot Alkaloids: 1. What increases rate/extension of absorption? 2. This is best when given in ___ phase. 3. Major SE?
Ergot Alkaloids: 1. Caffiene increases rate of absorption 2. Best in _prodromal_ phase 3. Major SE: nausea, vasoconstriction with ischemia/leg weakness/muscle pain
48
Ergot Alkaloids: Contraindications? (7)
Ergot Alkaloids: Contraindications a. Pregnancy: stimulate uterus and restric uterine BF b. Coronary/peripheral artery disease c. Liver/renal disease d. stroke e. Severe hypertension
49
Prophylactic Agents: Name some categories.
Prophylactic agents: a. Beta blockers b. Antidepressants c. Ca++ antagonists d. Anticonvulstants e. NSAIDs f. Methysergide g. 5HT antagonists
50
Amitriptyline: 1. Class of drug? 2. MOA? 3. SE?
Amitriptyline: 1. TCA 2. 5HT/NE reuptake inhibitor and antagonist at some 5HT/histamine receptors 3. SE: sleepy, dry mouth, and can induce hepatotoxicity
51
Propranalol 1. Class? 2. Used for treatment of \_\_\_, anxiety, panic, ___ \_\_\_, and cluster HA prophylaxis 3. MOA: blocks action of ___ and ___ on what receptors?
Propranalol 1. Non-selective beta blocker 2. Used for treatment of _hypertension_, anxiety, panic, _migraine prophylaxis_, and cluster HA prophylaxis 3. MOA: blocks action of _epinepherine_ and _NE_ on both _beta1 and beta2 receptors_
52
Topiramate: 1. Class of drug? 2. Used for wt loss in combination with \_\_\_, treatment of ____ in kids/adults, and most frequently prescribed for ___ \_\_\_. 3. SE?
Topiramate: 1. Anticonvulsant 2. Wt loss in combo with _phentermine_, treatment of _epilepsy_ in kids/adults, but most frequently for _migraine prophylaxis_ 3. SE: parasthesia, upper RTI, diarrhea, and nausea
53
Methysergide: 1. Class? 2. Antagonist at ____ receptor. Prevents or decreases __ and \_\_\_. Inhibits release of ___ from ___ cells. Antagonist at ___ alters patients feeling of satiety. 3. Metabolism?
Methysergide: 1. Ergot Alkaloid 2. Antagonist at _5HT2B_ receptor. Prevents or decreases _pain_ and _frequency_. Inhibits release of _histamine_ from _mast_ cells. Antagonist at _5HT2C_ alters feelings of satiety 3. Metabolised by CYP450 3A4
54
Methysergide: 1. Short term SE? 2. Long term SE:
Methysergide: 1. Short: nausea, vasoconstriction with ischemia/leg weakness/muscle pain 2. Long: _retroperitoneal, heart, or lung fibrosis_
55
Methysergide: Contraindications?
Methysergide: Pregnancy, coronary artery disease (may cause MI), peripheral vascular disease, hypertension, hepatic or renal impairment
56
Cyproheptadine: 1. Acts at what receptors? 2. For ___ reactions, nightmares, ____ syndrome, management of ______ from ___ producting carcinoid tumor.
Cyproheptadine: 1. Acts at H1, 5HT2A/2B/2C 2. For _allergic_ reactions, nightmares, _serotonin_ syndrome, management of _hyperseritonemia_ from _serotonin_ producing carcinoid tumor
57
Ondansetron: 1. Acts at what receptor? 2. Indication?
Ondansetron: 1. Acts at 5HT3 receptor (antagonist) 2. For nausea following chemotherapy/post operative as well as vomitting: acts as antiemetic
58
Ondansetron: 1. MOA: decreases activity of the ___ which deactivates ___ center in medulla oblongotta and ___ receptor in ___ receptor trigger zone 2. SE? 3. Metabolism?
Ondansetron: 1. MOA: decreases activity of the _vagus_ which deactivates _vomitting_ center in the medulla oblongotta and _serotonin_ receptor in the _chemo_-receptor trigger zone 2. SE: HA, dizziness, constipation 3. Metabolism: CYP450

Pharmacology (24 decks)

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