Pharm Exam 4 Part 2

Front 1

What is a benefit for giving histamine?

Back 1

To diagnose an allergic response.

Front 2

What is histamine in the brain?

Back 2

Neuropathic or psychogenic

Front 3

How does histamine work in the periphery?

Back 3

Released locally and acts locally in the connective tissue.

Front 4

What is the autocoid group?

Back 4

Histamine, serotonin, prostaglandins, leukotrienes. They are mediators of allergic and inflammatory process.

Front 5

How is histamine stored? Where is it stored?

Back 5

It is stored rapidly in the mast cells. They can also be in the brain as a neurotransmitter and in the stomach to increase the release of HCl.

Front 6

What releases antibodies?

Back 6

Plasma cells

Front 7

What meds can produce histamine-like responses?

Back 7

Morphine and tubocurarine

Front 8

Where is H1 and H2?

Back 8

Mostly in the periphery

Front 9

Where is H3 and H4?

Back 9

Both are in the the CNS, but H4 is involved with immune cells and their effects. H1 is also here.

Front 10

What does H1 do?

Back 10

contracts causing leakiness and increases IP3 and DAG.

Front 11

What does H3 do?

Back 11

Decreases cAMP and prevents additional release of histamine

Front 12

What does H2 do?

Back 12

Increase cAMP

Front 13

What do histamine receptors do in the nervous system?

Back 13

Stimulates pain and itching

Front 14

What does histamine do to the cardiovascular system?

Back 14

Vasodilates, which can lead to anaphylaxis. It's only around for a short time, too, so not good for medications.

Increase HR

Front 15

What does histamine do to the GI system?

Back 15

In the stomach, it increases the secretion of HCl

In the GI smooth muscle, it increases the fluid secretion, which is not significant unless there is tons of histamine.

Front 16

What does histamine do to the lungs?

Back 16

causes bronchoconstriction

Front 17

What is the wheal and flare?

Back 17

It is a triple response in an allergy test that looks for redness, swelling, and itching. It is place subepidermally.

Front 18

What are some histamine antagonists?

Back 18

Physiologic reversal of effects

-Epinephrine

Release of inhibitors

-cromolyn

Receptor Antagonists

Front 19

What is the issue with 1st generation anti-histmines?

Back 19

They have a sedative effects because they are lipid soluble and go into the brain. They can be ANS blocking. (on both sides)

Front 20

What did 2nd generation anti-histamines do?

Back 20

They took away the sedative effects because they are not as lipid soluble.

Front 21

What are the pharmacokinetics of H1 antagonists?

Back 21

A: Very good

D: Goes into CNS(1st gen)

Doesn't go to CNS(2nd gen)

M: liver

Front 22

What does the H1 Antagonist do at the receptor?

Back 22

Can have competitive antagonism or inverse antagonism.

Doesn't work as much at the H2 and H3 receptor

Mild effects at other receptors(muscarinic, alpha adrenoreceptor, serotonin, local anesthetic sites)

Front 23

What can we use the 1st generation H1 antagonist for other than allergies?

Back 23

Sedation

-resemble the antimuscarinic drugs

-children may have reverse effects(hyper)

Anti-nausea/emetic

-motion sickness

Antiparkinsonism

-only treats tremors(not for those with parkinson's)

Inhibits mast cell release

Front 24

If a patient is allergic to local anesthetics, then what can we use as a local anesthetic?

Back 24

1st generation H1 antagonist

Front 25

What symptoms do we use H1 antagonist for?

Back 25

Allergic rhinitis

Urticaria

Front 26

Where does the H1 receptor antagonist have to go in order to help in motion sickness? What generation is it?

Back 26

Needs to get to the limbic system, so it needs to be the 1st generation.

Front 27

What are some concerns with using 1st gen H1 receptor antagonist for morning sickness?

Back 27

Some teratogen birth defects, but the larger study showed no effects.

Front 28

What are some signs of H1 receptor antagonist toxicity?

Back 28

Sedation

anti-muscarinic effects(1st gen more)

Less common (excitation, convulsions, postural hypotension)

Front 29

What are H2 receptor antagonists used for?

Back 29

These are OTC and help decrease the HCl release in the body.

Front 30

Where is the most serotonin? What body part is serotonin most associated with?

Back 30

In the Enterochromaffin cells.

The brain

Front 31

What is another name for Serotonin?

Back 31

5-hydroxytryptamine

Front 32

Where is serotonin stored?

Back 32

It is rapidly stored in platelets

Front 33

Where does serotonin work?

Back 33

Clotting/vasoconstriction(platelets)

Important neurotransmitter

Gut

Migraines

Brain(feel good in pineal gland for mood elevation)

Front 34

When enterochromaffin cells become tumors, what are they called? What do they release? What do they do? How do we find it?

Back 34

Carcinoid tumors, release massive amounts of serotonin, increase GI motility(diarrhea), find 5-HIAA in the feces for serotonin or the pathways.

Front 35

Where is serotonin produced in the brain?

Back 35

Raphe magnum nuclei by chromaffin cells

Front 36

What is the origin of serotonin?

What happens when serotonin is broken down?

Back 36

Tryptophan

5-HIAA

Front 37

How many families of receptors are in Serotonin?

Back 37

7 (6 are GPCRs and 1 is a Na+ Ion channel)

Front 38

What is melatonin and where does it come from?

Back 38

Some effect on sleep wake cycles.

Made from serotonin

Front 39

What does serotonin do in the nervous system?

Back 39

Vomiting

pain and itch

chemoreceptor reflex

(bradycardia and hypotension)

Front 40

What does serotonin do in the respiratory system?

Back 40

Facilitate ACh release-constriction

Hyperventilation

Front 41

What does serotonin do in the cardiovascular system?

Back 41

contraction of the SM, which provides an overall increase in BP

encourages platelet aggregation.

Front 42

What does serotonin do in the GI system?

Back 42

Increases tone

peristalsis

an overproduction can cause Diarrhea

Front 43

What is Buspirone?

Back 43

5-HT1A Agonist, Non-benzodiazapine anxiolytic (GAD, OCD, PTSD) -less sleepiness

Front 44

What is Sumatriptan?

Back 44

5-HT1D/1B Agonist, mainly works at the blood vessel to dilate the prevent the stretch on nerve endings. Not prophylactic.

Given SQ, oral, nasal.

Onset is 1.5 hrs, 1/2 life is 2 hours, dose is 5-10 mg

Toxicity: Recurrence of migraine, coronary vasospasm, serotonin symdrome

Front 45

What is a migraine?

Back 45

It is a chronic disorder (CGRP, Substance P, trigeminal nerves)

SEVERE HA, N/V, photophobia, Phonophobia, speech abnormalities.

-See some zig-zagging in an aura

Front 46

Serotonin syndrome

Back 46

Triptan and MAOI/SSRI(something increasing the lvls of serotonin) Hyperthermic syndrome.

Treated with Benzodiazepines with intubation and ventilation.

Front 47

Neuroleptic Malignant Syndrome

Back 47

D2 block anti-psychotics.(haloperidol) Hyperthermic syndrome.

Treat with Diphenhydramine and cooling

Front 48

Malignant hyperthermia

Back 48

Hyperthermic syndrome

Set off by volatile gases and sux

Treat with dantrolene and cooling

Front 49

What are some serotonin antagonists? What are they used for?

Back 49

phenoxybenzamine and cyproheptadine and zofran

Carcinoid tumors before they are surgically removed. (phenoxybenzamine and cyproheptadine)

Zofran is an anti-emetic

Front 50

Where does phenoxybenzamine attach to?

Back 50

5-HT2

Front 51

Where does zofran bind?

Back 51

5-HT3

Good for SX and CA chemotherapy

Front 52

What happens in depression?

Back 52

lack of serotonin

Front 53

What are the 3 major classes of anti-depressants? What do they all do?

Back 53

MAOIs, TCAs, SSRIs

They all increase the amount of serotonin at the synapse.

Front 54

What is the 1st line in depression?

Back 54

SSRI

Front 55

What do SSRIs do?

Back 55

They inhibit SERT, so serotonin stays in the synapse for longer. It might inhibit NET.

Sertraline (Zoloft), Fluoxetine (Prozac)

Front 56

What do SRNIs do?

Back 56

They are used if SSRIs don't work. They have more SE.

They inhibit SERT and NET.

Cymbalta and pristique

Front 57

What do TCAs do?

Back 57

Inhibit SERT, NET, and have some anti-cholinergic effects. Not popular due to SE. Can be useful in seizures.

Amitriptyline (Elavil)

Front 58

What do MAOIs do?

Back 58

Target MAO-B/MAO-A for refractory depression that doesn't respond to any other medications. Can have lethal drug interactions.

Front 59

What are the general pharmakokinetics of antidepressants?

Back 59

-Good oral bioavailability(binds to plasma)

-Peak lvls in 2-3 hours(will take weeks to see results)

-Hepatic metabolism and renal clearance

Front 60

What are some other uses for anti-depressants?

Back 60

SSRI and SNRI-Anxiety disorder

TCA and SNRI-Pain disorder

Smoking cessation

Eating disorders

Front 61

What are the Adverse effects of anti-depressants?

Back 61

-Black box warning: increase suicidal tendencies

drug interactions

-N/V/D

-Gi upset

-Sexual dysfunction

Front 62

How many of the world's population has seizures?

Back 62

Approximately 1%

Front 63

What is the difference between epilepsy and seizures?

Back 63

Epilepsy is a condition that has seizures, whereas seizures occur as a symptom in many countries.

Front 64

What are some of the causes of seizures?

Back 64

Infection

Neoplasm

Head Injury

Heredity

Toxic Effects

Metabolic disorder

Front 65

What are some previous seizure treatments?

Back 65

Trephining

Cupping

Herbal remedies

Animal extracts

Front 66

What types of seizures does phenytoin treat?

Back 66

Single partial Seizures

Complex Partial Seizures

Partial Seizures secondarily generalized

Generalized tonic clonic grand mal seizures

Front 67

How do seizure medications work?

Back 67

modification of ion conductance

Na+

K+

Ca++

Front 68

Inhibiting neurotransmitter

Back 68

GABA

Front 69

Simple Partial Seizure

Back 69

In a specific part of the brain, affects one part of the body. There is minimal spread of discharge. Does not affect the pt's consciousness. EEG may show normal discharge.

Front 70

Complex Partial Seizure

Back 70

Does affect the consciousness and may become unresponsive or lose consciousness. Many of these arise from the temporal lobe.

Front 71

What are some automatisms?

Which type of seizures have them?

Back 71

lip smacking

swallowing

fumbling

scratching

walking about

Complex Partial Seizures

Front 72

Partial Seizures Secondarily Generalized

Back 72

They begin as simple or complex, but then spread to the rest of the brain.

Will look like generalized tonic clonic seizures

Front 73

Generalized Seizures

Back 73

Begin over the entire surface of the brain.

Grand mal - person falls to the ground, entire body stiffens, muscles jerk or spasm, tongue or cheek may be bitten, urinary incontinence.

Post-ictal - weak, unresponsive

Front 74

How can dogs help seizures?

Back 74

They can get help and support the patient. They can detect when they are about to have seizure, too.

Front 75

What is the TONIC and CLONIC part of the seizure?

Back 75

Tonic: Stiffening of the muscles

Clonic: Relaxation of the muscles

Front 76

Absent (petite mal) Seizure

Back 76

Generalized Seizure

Stare into space, and wake up with no notice of seizure. Can have some automatism.

Front 77

Atonic Seizure

Back 77

Sudden loss of muscle tone

Patient falls over w/o warning

a drop attack

Front 78

Tonic Seizure

Back 78

Muscles suddenly contract and stiffen

Causes pt to fall

Another form of drop attack

Front 79

Clonic and myoclonic Seizure

Back 79

looks like body is jerking

Front 80

Infantile Spasms (West's syndrome)

Back 80

Developmental type of Seizure

Affect head, torso, and limbs

Usually begins before 6 months

Looks like a jerky motion

Front 81

What is the oldest anti-seizure drug that we use today?

Back 81

Phenobarbital(status elepiticus)

-35 analogs

Front 82

What are the different Mechanisms of Action for anti-seizure medications?

Back 82

Modification of ion channels - Na+,K+, Ca++

Enhancing Inhibition- GABA

Inhibiting Excitation - Glutamate

Front 83

Phenytoin

Back 83

Oldest non-sedative anti-seizure drug. MOA: ALL Used for Partial and tonic-clonic seizures. Dose: 10-20 mcg/ml Toxic: 30-50 Lethal: >100

A: variable 3-12 hrs to peak

D: Highly protein bound, accumulate in ER of brain, liver muscle and fat. (other highly plasma bound drugs can displace)

M: Liver 1/2 life(12-36 hrs) Malnourished has more problems.

E: Dose Dependent

Toxicity: (dose related)nystagmus, loss of extraocular movement, diplopia, ataxia, sedation, gingival hyperplasia, hirsuitism, coarsening facial features.

Front 84

GABA

Back 84

Major inhibitory neurtransmitter in the CNS

Front 85

Carbamazepine

Back 85

TCA: Na+ channel blocker at therapeutic lvl and K+ and Ca+ at higher lvls. Used for partial seizures, trigeminal neuralgia, and bipolar disorder. Synergistic with phenytoin.

A: usually complete 6-8 hrs

D: slow 70% plasma bound (no displacement)

M: induces hepatic enzymes 1/2 life 1 dose: 36 hrs continuous: 20 hrs

Drug interaction due to P450 inducement can be a problem.

(Phenytoin, phenobarbital, ethosuxemide, valproic acid, clonazepam)

Front 86

Phenobarbital

Back 86

Oldest and safest anti-seizure drug. Drug of choice in infants. Sedative effects. MOA is unknown(may suppress abnormal neurons).

Useful: Partial seizures, generalized tonic-clonic

Worsens: absence, atonic, infantile spasms

Toxicity: hepatic enzyme inducer, sedation, OD(unsteady gait, slurred speech, confusion, respiratory depression, coma)

Front 87

What is lamotrigine(Lamictal)?

Back 87

for partial seizures

Developed in the 1990s

Front 88

What is pregabalin(Lyrica)?

Back 88

GABA analog, adjunct, neuralgia

Developed in the 1990s