Pharm Seizure, Migrain, Thyroid, Diabetes

Front 1

Elevates GABA levels by Ca++
Partial, GTC
Not protein bound OR metabolized
Clearance reduced by: Cimetidine, Antacids
Peripheral neuropathies

Back 1

Gabapentin

Front 2

Blocks Na+
Inhibits glutamate
Induced by: Phenytoin, Primidone, Carbamazepine
Prolonged by Valproic Acid due to glucoronidation
Side effect: Steven Johnson

Back 2

Lamotrigine

Front 3

Inhbits GABA transaminase
Partial Seizures
Reduces Primodone (unknown mech)
Side effct: Psychosis, Visual Degradation

Back 3

Vigabatrin

Front 4

Blocks Na+
Inhibits glutamate
Enhances GABA

Back 4

Topiramate

Front 5

Blocks Na+
Partial, GTC, Status epilepticus
Non-linear absorption **stored in fat
Side effects: hirsutism, gingival hyperplasia, CNS depression, balance disturbance, cardiac arrhythmias, teratogen

Back 5

Phenytoin

Front 6

Blocks Na+
2 metabolites: Phenoarb, PEM
Partial, GTC
Side effects: drowsy, nystagmus, ataxia, teratogen

Back 6

Primadone

Front 7

Blocks Na+
Potentiates GABA
TCA antidepressant
Trigeminal neuralgia
Partial, GTC
Active metabolite
Side effects: ataxia, diplopia, nystagmus, dizzy, APLASTIC ANEMIA, STEVEN JOHNSON
Toxicity increased by: Cimetidine, Propoxyphene, Diliazem, Erythro, INH, Verapamil

Back 7

Carbamazepine

Front 8

Ca++ T-type
Absense, Myoclonic
Microsomal metab
Side effects: GI pain, nausea, vomit

Back 8

Ethosuximide

Front 9

Valproic Acid

Back 9

Block Na+
Ca++ T-type
GABA metab inhibited
Absence seizures
Blood levels don't correlate
Side effects: HEPATOTOXIC, GI, nausea, LITTLE SEDATION

Front 10

Diazepam

Back 10

GABAa affinity increased
Status Epilepticus
Tonic Clonic, Myoclonic
Microsomal metab

Front 11

Seizure drugs: microsomal metab

Back 11

Phenytoin --> inactive metab
Carbamazepine --> active metab
Primidone --> active metab
Valproic Acid
Ethosuximide
Diazepam

Front 12

Seizure drugs that do not block Na+

Back 12

Ethosuximide = Ca++ T-type
Diazepam = GABAa
Gabapentin = Ca++
Vigabatrin = GABA transaminase

Front 13

GTC drugs

Back 13

Phenytoin
Carbamazepine
Valproic Acid
Lamotrigine
Gababpentin

Front 14

Partial Seizures

Back 14

Phenytoin
Carbamazepine
Lamotrigine
Gabapentin

Front 15

Absence Seizures

Back 15

Ethosuximide
Valproic Acid
Lamotrigine

Front 16

Seizure drugs causing Steven Johnson

Back 16

Carbomazepine
Lamotrigine

Front 17

Seizure drugs causing Blood dyscrasia

Back 17

Carbomazepine
Lamotrigine

Front 18

Seizure drug causing Hepatoxicity

Back 18

Valproic Acid

Front 19

Seizure drug causing Psychosis

Back 19

Vigabatrin

Front 20

Seizure drug causing Little Sedation

Back 20

Valproic Acid

Front 21

Seizure drug causing Cardiac Arrhythmias

Back 21

Phenytoin

Front 22

Seizure drug causing hirsutism

Back 22

Phenytoin

Front 23

Seizure drug causing gingival hyperplasia

Back 23

Phenytoin

Front 24

Seizure drug causing nystagmus

Back 24

Carbamazepine
Primadone

Front 25

Seizure drug causing ataxia

Back 25

Carbamazepine
Primadone

Front 26

Seizure drug used to treat Peripheral Neuropathy

Back 26

Gabapentin

Front 27

Seizure drug used to treat Trigeminal Neuralgia

Back 27

Carbamazepine

Front 28

Seizure drug that is a tricyclic antidepressant

Back 28

Carbamazepine

Front 29

a. Vasoconstrictor!
b. Ergot
c. High efficacy
d. Side effects:
i. GI
ii. Vasoconstriction: vascular fibrosis, spasm, occlusion
iii. Inflammatory fibrosis (endocardial, retroperitoneal) potentially serious and increased risk over time **used less because of this!

Back 29

Methysergide
5-HT2 blockers

Front 30

has 2 major effects for anti-emesis and enhanced gastric emptying. Not analgesic.
1. 5-HT3 blocker helps with emesis
2. D2 blocker helps with nausea
3. Common adjuvant

Back 30

Metoclopramide

Front 31

1. Mechanism uncertain
a. Cerebral vasoconstrictors
b. Non-selective 5-HT agonist at trigeminal nerve

Back 31

Ergotamine

Front 32

7. Side effects (dirty drug):
a. Nausea, cramps, vertigo, cold, gangrene, diarrhea
b. Dependence rebound headaches “ergotamine dependence”
c. CI in pregnancy due to uterine constriction

Back 32

Ergotamine

Front 33

This ergot has fewer reports of nausea and dependence.
a. Weaker vasoconstrictor
b. Parenteral administration (parenteral, nasal)

Back 33

Dihydroergotamine

Front 34

are selective agonists at 5-HT1B/1D

Back 34

Sumatriptan

Front 35

7. Side effects (better profile because selective):
a. Coronary artery disease due to vasoconstriction
b. Avoid MAOIs

Back 35

Sumatriptan

Front 36

d. Side effects:
i. GI
ii. Vasoconstriction: vascular fibrosis, spasm, occlusion
iii. Inflammatory fibrosis (endocardial, retroperitoneal) potentially serious and increased risk over time **used less because of this!

Back 36

Methysergide

Front 37

5-HT blockers are used how?

Back 37

non-selective 5-HT agonist at trigeminal - Ergotamine, Dihydroergotamine (acute, severe)

5-HT1B/1D agonist - Sumatriptan (acute, severe)

5-HT2 antagonist - Methysergide (prophylactic)

5-HT3 antagonist - Metoclopramide (acute, mild, adjuvant)

Front 38

MOA of Glipizide

Back 38

Inhibits ATP sensitive K+ channel to enhance release of insulin from beta-cells.

Front 39

MOA of`Repaglinide

Back 39

Action like sulfonylureas: enhanced insulin secretion

Front 40

MOA of Acarbose

Back 40

Inhibit brush-border enzyme in gut: interferes w/ starch hydrolysis & carb absorption; blunts post-prandial rise in blood glucose

Front 41

MOA of Metformin

Back 41

Inhibits gluconeogenesis -Activates liver enzyme AMPK; AMPK inhibits TORC2 which would otherwise stimulate gluconeogenesis

Front 42

MOA of Rosiglitazone

Back 42

Not hypoglycemic
-Act at target tissues to: ↓ insulin resistance, improve glucose metabolism
-Binds to & activates PPARγ, alters gene expression (mainly in adipocytes)
-↑ glucose transporters↑ in FFA transporters↑ in lipid metabolic enzymes↓ in resistin (which is normally released from adipocytes & contributes to insulin resistance)

Front 43

MOA of Sitagliptin

Back 43

Inhibits DPP-4, which deactivates GLP-1-Enhances endogenous GLP-1

Front 44

Net effect: enhanced insulin sensitivity
-↑ uptake of glucose & FFAs
-↑ utilization of glucose & FFAs
-↓ gluconeogenesis
-↓ insulinemia-improved fasting & postprandial hyperglycemia
-demonstrated anti-inflammatory effects (cytokines?)
-improved lipid profile; anti
-atherosclerotic effects?

Back 44

Rosiglitazone

Front 45

-GI common: abdominal pain, diarrhea, metallic taste
-Avoid EtOH, conditions that may yield lactic acidosis
-Avoid in renal or liver disease, cardiac failure

Back 45

Metformin

Front 46

-Does NOT stimulate insulin release; not hypoglycemic
-No weight gain
-Demonstrated to inhibit microvascular complications

Back 46

Metformin

Front 47

Possibly cross-allergenic w/ sulfonamides

Back 47

Glipizide

Front 48

Drug Interactions:
-Hypoglycemia risk ↑ when combined w/: NSAIDS, salicylates, dicumarol, EtOH, MAOI, β blockers (can mask symptoms)
-Hyperglycemia when combined w/: P450 inducers (rifampin, barbiturates)

Back 48

Glipizide

Front 49

Insulin
glucose update
glycogen storage
gluconeogenesis
glycogen breakdown

Back 49

-↑ glucose update
-↑ glycogen storage
-↓ gluconeogenesis
-↓ glycogen breakdown

Front 50

-Major problem: hypoglycemia; esp. w/ elderly, hepatic or renal insufficiaincy
-Weight gain-Minor incidence: GI (N/V); jaundice, transient leukopenia

Back 50

Glipizide

Front 51

↓ in resistin (which is normally released from adipocytes & contributes to insulin resistance)

Back 51

Rosiglitazone