Pharm Final Part Four

Front 1

How do epilepsy drugs work?

Back 1

They prolong the state of inactivation of Na channels or block Ca channels, or interact w/ GABA receptors

Front 2

Name the epilepsy drugs.

Back 2

phenytoin
valproate
carbamazepine
ethosuxamide
baclofen

Front 3

Phenytoin

Back 3

1. DOC for generalized tonic-clonic seizures

2. Treatment of status epilepticus (diazepam is DOC),

3. Tx of episodic clonic movements following severe head injury

4. Non-linear kinetics at large doses, i.e., at large doses elimination not first order

Front 4

Phenytoin S/E’s?

Back 4

1. gingival hyperplasia

2. ataxia, nystagmus, diplopia

3. psychological disturbances

4. megaloblastic anemia (interferes w/ folate metabolism)

5. osteomalacia (responds to vitamin D)

6. teratogenic (cleft lip/palate)

not much sedation

Front 5

Carbamazepine MOA?

Back 5

prolong the state of inactivation of the Na channels
-- no impulse propagation

Front 6

Carbamazepine therapeutic use?

Back 6

1. Tx of temporal lobe seizures

2. DOC for trigeminal neuralgia

Front 7

Carbamazepine S/E’s?

Back 7

1. Monitor LFTs, espec in young pts or pts treated w/ valproate + other seizure meds

2. can cause ↑ release of AVP and potentiate the antidiuretic effects of AVP
-- result is dilutional hyponatremia

Front 8

Phenytoin and phenobarbitol?

Back 8

Causes osteomalacia

MOA: induction of CYP450 which increases the metabolism of vit D and vit K (vit K a cofactor for the synthesis of osteocalcin)

Decreased vit D lowers the GI absorption of Ca++.

In order to maintain plasma [Ca++], bone is resorbed.

Front 9

Primidone?

Back 9

metabolized to Phenobarbital
-- probably acts directly on Na channels like phenytoin

Front 10

Ethosuxamide MOA?

Back 10

blocks T-type Ca channels in thalamus

Front 11

Ethosuxamide therapeutic use?

Back 11

DOC for absence seizures
-- blank stare
-- eyelids flutter
-- 3-sec spike wave rhythms from thalamus

Front 12

Baclofen MOA?

Back 12

Interacts w/ GABA-B receptors linked to K channels
-- enhanced K conductance hyperpolarizes cells presynpatic membrane of glutaminergic neurons in spinal cord to prevent the release of glutamate onto alpha-motor neurons
-- ↓ efferent excitation of spastic skeletal muscle

Front 13

Baclofen therapeutic use?

Back 13

Tx of spasticity from spinal cord injury, CP, and MS

Front 14

Dantrolene MOA?

Back 14

Inhibits release of “trigger” Ca++ from SR in skeletal muscle

Front 15

Dantrolene therapeutic use?

Back 15

1. spasticity from spinal cord injury

2. malignant hyperthermia

3. neuroleptic malignant syndrome

Front 16

Dantrolene S/E’s?

Back 16

generalized muscle weakness

Front 17

Therapeutic effect of TCAs does not correlate with…?

Back 17

blockade of uptake of any of the biogenic amines

Front 18

Explain the specificity for amine transporters and antidepressants.

Back 18

NE reuptake blocked
-- desipramine
-- secondary amine

5-HT reuptake blocked
-- SSRI’s
-- fluoxetine, paroxetine, citalopram, fluvoxamine

BOTH NE and 5-HT reuptake blocked
-- imipramine (tertiary amine)
-- clomipramine
-- venlafaxine

Front 19

Tyramine-containing foods and MAOIs?

Back 19

Phenelzine or Tranylcypromine

Tyramine contraindicated in these pts can cause “cheese reaction”

Front 20

Antidepressant S/E’s?

Back 20

1. confusion in elderly patients
2. postural hypotension (-blockade)
3. sedation (central antimuscarinic effect)
4. urinary retention
5. tachycardia (atropine-like effect),
6. fine tremor
7. AV block (direct toxic effect)

Front 21

MAO inhibitor MOA?

Back 21

inhibit MAO-A which degrades NE and 5-HT

(MAO-B degrades DA)

Front 22

CLINICAL: Schizophrenic patient w/ depression?

Back 22

SSRI like fluoxetine

Front 23

CLINICAL: Depressed pt w/ hypotension?

Back 23

SSRI like fluoxetine

Front 24

CLINICAL: Depressed pt being treated w/ antidepressant suffers from sedation and hypotension. Which antidepressant is the likely cause?

Back 24

Could be MAOI or TCA since both cause sleepiness and hypotension, but pick TCA b/c TC’s cause greater orthostatic hypotension than do MAOIs

Front 25

CLINICAL: Small child w/ nocturnal enuresis?

Back 25

Treat w/ TCA for atropine-like effect in urinary bladder

Front 26

CLINICAL: Which NT is involved in OCD?

Back 26

5-HT

Treatment for OCD – clomipramine or SSRI

Front 27

CLINICAL: Depressed pt w/ CHF being treated w/ digoxin is given TCA…what happens?

Back 27

Inverts or flattens T-wave

Slows conduction in fast fibers so QRS increased

Front 28

CLINICAL: OD w/ imipramine?

Back 28

Imipramine (tertiary amine which blocks 5-HT and NE uptake1)
-- converted to desipramine (secondary amine which blocks NE uptake1)

If OD – usual affects are:
-- ↓BP from alpha blockade
-- ↑HR from ↓BP and anticholinergic effects
-- decreased AV conduction w/ ↑ QT interval

Front 29

What causes serotonin syndrome?

Back 29

results from excessive stimulation of central 5-HT receptors
-- ↑ BP, HR & respiration
-- increased muscle activity (muscle twitching, shivering, myoclonus) causing hyperthermia and sweating
-- pupillary dilation
-- confusion, agitation, hallucinations

Caused by
-- SSRI (ex: fluoxetine) OR
-- TCA which blocks both NE and 5-HT uptake (ex: imipramine)
-- especially in pts taking MAOI --> prevents degradation of 5-HT in CNS and accum of 5-HT in the cytoplasm of central 5-HT neurons

Front 30

What are the antipsychotic drugs?

Back 30

haloperidol
clozapine
chlorpromazine
Lithium

Front 31

MOA of antipsychotic drugs?

Back 31

blocks D2 receptors in the mesolimbic DA pathway

Front 32

Haloperidol?

Back 32

least sedating

greatest likelihood of ESP

DOC for Tourette’s syndrome (vocal and motor tics, copralalia)

Front 33

Clozapine?

Back 33

Effective in treatment of negative symptoms
-- measure CBC weekly w/ clozapine

Front 34

Chlorpromazine?

Back 34

prevets emetic effects of D2 receptor stimulation at CTZ

Front 35

S/E’s of antipsychotic drugs?

Back 35

ALPHA BLOCK
-- dizziness
-- orthostatic hypotension
-- ↑ HR
-- nasal stuffiness
-- impotence

MUSCARINIC BLOCK
-- dry skin and mouth
-- mydriasis
-- ↑HR
-- urinary retention
-- sedation

CENTRAL D2 BLOCKADE
-- fine tremor
-- muscular rigidity
-- EPS
-- tardive dyskinesis
-- hyperprolactinemia
-- galactorrhea
-- amenorrhea
-- neuroleptic malignant syndrome

Front 36

Li MOA?

Back 36

inhibits enzymes important in recycling phosphoinositides, so PIP2 is depleted

Front 37

HCTA and furosemide and Li?

Back 37

Both enhance the reabsorption of Li in the PT causing toxicity

Front 38

Li S/E’s?

Back 38

1. tremor

2. motor and psychiatric disturbances

3. causes nephrogenic DI by inhibiting adenylase coupled to V2-ADH receptors in CD

Front 39

Li in a female pt w/ bipolar disease?

Back 39

Must discontinue Li treatment during first trimester to prevent teratogenesis

Ebstein’s anomaly
-- leaflets of mitral valve displaced downward into right ventricle
-- tricuspid regurgitation
-- right ventricular dysfxn

Front 40

Which drugs can cause Parkinsonian-like side effects?

Back 40

D2 receptor antagonists such as
-- haloperidol
-- chlorpromazine
-- trifluperazine

Front 41

Drugs used to treat PD?

Back 41

levodopa

carbidopa

benztropine

bromocriptine

amantadine

selegiline

bromocriptine

Front 42

Levodopa MOA?

Back 42

Dopa precursor which is pumped into brain via the aromatic amino acid pump

Front 43

What can interfere w/ levodopa treatment?

Back 43

Treatment w/ vitamin B6 interferes w/ therapeutic action of levodopa
-- B6 increases the peripheral decarboxylation of levodopa to Dopa

Front 44

Carbidopa MOA?

Back 44

inhibits DOPA (L-aromatic amino acid) decarboxylase outside brain to enhance the amount of DOPA taken up by the brain and converted to DA

Front 45

Benztropine MOA?

Back 45

central muscarinic receptor blockade

Front 46

Bromocriptine MOA?

Back 46

central D2-dopamine receptor agonist

Front 47

Amantadine MOA?

Back 47

antiviral drug which release DA centrally

Front 48

Selegiline MOA?

Back 48

selective MAO-B inhibitor, blocks breakdown of DA in CNS

Front 49

Centrally acting anticholinergic drugs and levodopa?

Back 49

Enhance central actions of levodopa in PD

Front 50

Carbidopa + levodopa?

Back 50

1. can reduce dose of Dopa

2. prevents decarboxylation of Dopa outside CNS

3. carbidopa does not enter CNS

4. carbidopa does not attenuate the orthostatic hypotension caused by levodopa

Front 51

Levodopa and schizophrenics?

Back 51

Can cause reappearance of psychotic symptoms in a schizophrenic pt w/ PD caused by atypical antipsychotic drugs (ex: haloperidol)

Front 52

Which drugs can increase plasma prolactin?

Back 52

D2 dopamine receptor blockers
Haloperidol
Reserpine
Metoclopramide
alpha-methyldopa

Hyperprolactinemia causes galactorrhea, amenorrhea, anovulatory cycles, and infertility in women; causes decreased libido and impotence in men

Front 53

Bromocriptine MOA?

Back 53

a D2-dopamine receptor agonist

Used to treat PD and inhibit prolactin release in hyperprolactinemia

Reverses infertility caused by hyperprolactinemia

Front 54

Ethanol metabolism?

Back 54

Oxidized to acetaldehyde by alcohol dehydrogenase

Acetadehyde degraded to water and CO2 by acetaldehyde dehydrogenase

Front 55

Ethanol kinetics?

Back 55

Alcohol dehydrogenase easily saturated at low concentrations of ethanol
-- so ethanol removed by zero-order kinetics = constant amount of drug/h metabolized

Front 56

What inhibits acetaldehyde dehydrogenase?

Back 56

Inhibited by disulfiram & metronidazole

Build up causes
-- peripheral vasodilation (red skin)
-- n/v
-- pulsating headache
-- sweating
-- chest pain
-- vertigo
-- syncope
-- blurred vision
-- confusion

Front 57

How does EtOH enhance loss of body heat?

Back 57

peripheral vasodilation

Front 58

CLINICAL: Patient is being treated w/ Giardia + some other infection (bacterial) and develops n/v and headache after drinking a beer. What drug causes this?

Back 58

Metronidazole

Front 59

Alcoholism causes…?

Back 59

1. hyperlipidemia and fatty infiltration of the liver

2. cardiomyopathy, portal hypertension, gastric ulceration, esophageal varices

3. Wernicke-Korsakoff syndrome - assoc w/ thiamine deficiency - get paralysis of external eye muscles, altered mentation and ataxia

Front 60

Fetal alcohol syndrome?

Back 60

flattened face, short nose, short palpebral fissures = underdevelopment of mid-facial region, microcephaly with low IQ, retarded growth

Front 61

Describe methanol toxicity.

Back 61

severe visual disturbance (“like being in a snow storm”) with relatively clear sensorium

headache

dyspnea

cold digits

GI pain

breath smells of formaldehyde.

Front 62

Treatment of methanol toxicity?

Back 62

treat w ethanol to saturate enzymes which degrade EtOH and MeOH
-- because toxic product of MeOH appears to be a formate compound produced by the sequential actions of alcohol and acetaldehyde dehydrogenases

Front 63

What occurs when someone ingests ethylene glycol from antifreeze?

Back 63

converted to aldehydes, acids and oxalate
-- oxalate causes acute renal failure

Front 64

Describe amphetamine toxicity

Back 64

nervousness, restlessness, insomnia, hypertension, tachycardia, hyperthermia, toxic psychosis = paranoid schizophrenia, weight loss, formication, tonic-clonic seizures.

EARLY USE get pupillary dilation from the release of NE in the radial muscle

PROLONGED USE can get miosis due to depletion of NE from radial muscle

Front 65

Amphetamine withdrawal?

Back 65

DOES NOT cause delirium tremens (DTs)

Front 66

Methylphenidate use?

Back 66

Treatment of ADD and ADHD in children

CAN CAUSE: depression, insomnia, loss of appetite, weight loss, slowed growth rate

Front 67

Theophylline, aminophylline and caffeine therapeutic use?

Back 67

normalize breathing in neonatal apnea

Front 68

Phentermine therapeutic use?

Back 68

suppresses appetite via release of NE in the hypothalamus

Front 69

What is MDMA?

Back 69

“Ectasy”
-- can cause degen of central 5-HT neurons

Front 70

ALL sedative hypnotics cause…?

Back 70

dependence, shortened sleep latency, suppression of REM sleep, tolerance, rebound insomnia, respiratory depression.

They are NOT analgesic.

(barbiturates, BZs, choral hydrate, glutethimide)

Front 71

General effect of barbiturates?

Back 71

general CNS depressants w/ low therapeutic index

Front 72

Barbituate MOA?

Back 72

enhance GABA-A receptor-mediated increase in Cl conductance to hyperpolarize neurons
-- enhances duration of channel opening

Front 73

What predicts which barbiturate will have the most rapid onset of action?

Back 73

oil:water partition coefficient predicts most rapid onset

Front 74

Barbituate S/E’s?

Back 74

-- can cause paradoxical excitation in older patients

-- decrease sleep latency, but decrease REM and slow-wave sleep

Front 75

Phenobarbital?

Back 75

active when given p.o. and is the least sedating

Front 76

Thiopental?

Back 76

Poor analgesic activity
-- used for induction of anesthesia
-- short duration of action due to redistribution (blood-brain/viscera --> skeletal muscle --> fat
-- transient ↓ in BP with reflex ↑ in HR and dP/dT, so CO not depressed

Front 77

BZ MOA?

Back 77

enhance GABAA receptor-mediated increase in Cl- conductance to hyperpolarize neurons
-- enhances rate of channel opening

Front 78

BZs and older patients?

Back 78

-- older patients exhibit ↑ half-life due to ↓ Cl
-- ↑ free plasma concentration from ↓ plasma protein binding

-- ↑ receptor sensitivity to BZ’s = ↑ risk of falls and hip fracture

Front 79

Several BZs are converted to active metabolites…

Back 79

Diazepam converted to
-- desmethydiazepam
-- oxazepam
-- temezepam

Front 80

Which BZs are preferred for older pts?

Back 80

lorazepam

oxazepam

-- cleared by glucuronidation rather than CYP450
-- rate of glucuronidation does not ↓ w/ age

Front 81

Triazolam?

Back 81

BZ w/ the shortest half-life

Used to tx insomnia

Greatest risk of rebound insomnia

Front 82

Describe the BZ withdrawal syndrome.

Back 82

anxiety, dysphoria, agitation, insomnia, vomiting, sweating, muscle and abdominal cramps, myoclonic jerks, convulsions.

No CV effects!

Front 83

What is the BZ receptor antagonist?

Back 83

flumazenil

Front 84

Flumazenil therapeutic use?

Back 84

Used to treat OD w/ BZs

Also precipitate BZ w/d syndrome in pts addicted to BZs

Front 85

Zolpidem?

Back 85

NON-BZ hypnotic drug
-- acts to increase Cl conductance

Front 86

Buspirone MOA?

Back 86

a partial agonist at 5-HT1A receptors linked to K channel
-- causes hyperpolarization to suppress neuronal activity

Anxiolytic but NOT addictive

Front 87

Buspirone vs BZs?

Back 87

Slow onset compared to BZs

No sedation or EtOH interaction

No hypnotic, anticonvulsant or muscle relaxant effects

Front 88

Describe the drug schedule.

Back 88

CLASS 1
-- heroin, LSD, marijuana, mescaline, PCP, psilocybin, MDA, DMT, DET, bufotenine
-- no med uses

CLASS 2
-- opiates (meperidine, methadone, fentanyl, oxycodone)
-- amphetamines (methylphenidate, etc)
-- cocaine
-- some barbiturates (amo, pento, seco), dronabinol
-- NO tel scripts/ refills

CLASS 3
-- codeine, opium, some barbiturates
-- rewrite script after 6 mos or 5 refills

CLASS 4
-- BZs, pentazocine, propoxyphene, phenobarbital
-- rewrite script after 6 mos or 5 refills

CLASS 5
-- diphenoxylate

Front 89

Opiates: beta-endorphin and enkephalins

Back 89

agonists at certain opiate receptors
-- found in adenohypophysis and certain nerve cells
-- suppress spinal nociceptive pathways

effects blocked by naloxone

Front 90

Clinically useful opiates are relatively selective for which receptors?

Back 90

Mu receptors

Larger doses affect all receptors

Front 91

Mu receptor natural agonists?

Back 91

beta-endorphins
enkephalins
morphine

Front 92

Mu receptor analgesia?

Back 92

supraspinal Mu1 (predominant effect)

spinal Mu2 receptors

Front 93

Effects at Mu2 receptor?

Back 93

respiratory depression

decreased GI motility

Front 94

Other effects of Mu receptor stimulation?

Back 94

miosis
-- increases PSNS activity from E-W nucleus to sphincter muscle of iris

-- euphoria

-- physical dependence

Front 95

Kappa receptors?

Back 95

Natural agonists
-- dynorphin A and K1

Analgesia
-- supraspinal kapp3
-- spinal kappa1

Dysphoria and sedation

Front 96

Delta receptors?

Back 96

Natural agonists
-- enkephalins

Spinal and supraspinal analgesia
-- spinal is most important

Front 97

Where does the supraspinal effect occur?

Back 97

1. GABA neuron normally inhibits pain-inhibiting neurons (PIN)

2. Opiates inhibit GABA neuron, so no GABA released onto PIN = no inhibition of PIN = central descending inhibition of pain pathways
-- inhibitory effect on GABA neurons can explain seizures caused by some opiates like meperidine

Front 98

Where does the spinal effect occur?

Back 98

Opiates block nociceptive stimuli in ascending spinothalamic pathways

1. mu2, delta2 & kappa1 stimulation decreases NT release (probaby glutamate) from presynaptic terminal of nociceptive primary afferent

2. mu receptor stimulation creates IPSP (hyperpolarization) in secondary ascending pain transmission neuron

Front 99

Mu, kappa, and delta receptors are coupled to…?

Back 99

G-proteins
-- mu & delta = increased K conductance = hyperpolarization

-- kappa = decreased Ca conductance

Front 100

Actions of opiates?

Back 100

-- analgesia
-- respiratory depression - MOA: increase in the threshold [CO2] which activates the medullary respiratory center
-- constipation = no tolerance; increases smooth muscle tone but decreases GI motility
-- miosis - no tolerance (NB: meperidine causes mydriais via atropine-like effect)
-- sedation, euphoria, physical dependence
-- sedation, dysphoria, psychotomimesis
-- cough suppression (act on cough pathways in the brainstem) - MOA of dextromethorphan & codeine does not involve opiate receptors!

Front 101

Actions of opiates (cont)?

Back 101

-- truncal rigidity - a spinal mechanism
-- emesis - via stimulation of CTZ
-- not much effect on BP or HR in a supine patient , but i.v. morphine can induce histamine release which can decrease BP and cause cutaneous dilation and itching (hives)
-- morphine acts centrally to decreases peripheral sympathetic nerve acivity; can cause orthostatic hypotension
-- smooth muscle contraction in biliary tract and GU tract

Front 102

Toxicity triad of opiates?

Back 102

1. miosis

2. coma

3. depressed respiration

Front 103

What affect of morphine do we NOT develop tolerance to?

Back 103

miosis

constipation

Front 104

Pentazocine, butorphanol, nalbuphine, & buprenorphine?

Back 104

Partial opiate agonist

1. less depression of respiration

2. causes w/d symptoms in pts addicted to morphine/heroin and pts on methadone maintenance for addiction

Front 105

Symptoms of opiate withdrawal?

Back 105

1. rhinorrhea, lacrimation, chills

2. n/v, diarrhea, hyperthermia

3. sweating and piloerection (“goose flesh”)

4. myalgia, tremor, urticaria,

5. mydriasis, anxiety, hostility

Front 106

methadone?

Back 106

1. active p.o.

2. longest duration of action (15-30h)
-- impt to keep addicts off morphine

Front 107

Which opiate inhibits respiration the greatest?

Back 107

morphine

Front 108

Which opiate has the least potential for addiction?

Back 108

diphenoxylate
-- used to treat diarrhea

Front 109

CLINICAL: Morphine is DOC for…?

Back 109

1. pain & pulmonary edema caused by acute MI
-- acts in CNS to decrease SNS activity
-- decreased preload and afterload

Front 110

CLINICAL: Tx of female w/ acute pain from gallstones w/ morphine causes greater pain. Why?

Back 110

Morphine contracts smooth muscle of gall bladder

Front 111

CLINICAL: female on methadone has emergent surgery and is tx w butorphanol; patient experiences S/S of opiate withdrawal. Why?

Back 111

Butorphanol is a partial agonist at mu receptors.
-- partial agonists pentazocine, nalbuphine and buprenorphine can also cause S/S of opiate withdrawal in a patient taking methadone.

Front 112

CLINICAL: Which opiate does not cause a dose-related inhibition of respiration?

Back 112

partial agonists

Pentazocine
Butorphanol
Nalbuphine

Front 113

CLINICAL: If mom receives opiate during labor…?

Back 113

Newborn baby may have respiratory depression

Front 114

CLINICAL: Why do we treat MI pt w/ morphine?

Back 114

Chest & arm pain  the activity of the sympathetic nervous system which constricts arterioles and venules to increase preload and afterload.

The damaged heart cannot pump the increased venous return, especially in the face of an increase in afterload.

Morphine acts centrally to decrease pain and to decrease
sympathetic outflow.
-- Decreased activity of the SNS decreases preload and afterload and improves CO.

The analgesic effects of morphine also make the patient more comfortable.

Front 115

General anesthesia and partition coefficients?

Back 115

Partition coefficients have actual clinical significance.

The minimum alveolar concentration (MAC) is the concentration of gas in the inspired air (in percent) which is required to cause a surgical plane of anesthesia in 50% of patients.
-- The MAC is a measure of anesthetic potency and is inversely related to the oil/gas partition coefficient.

High oil/gas partition coefficient = high lipid solubility = low MAC = high potency

Front 116

Nitrous oxide and anesthesia?

Back 116

Cannot be used for anesthesia b/c its MAC is >100%
-- even if N2O had MAC of 90%, it could still not be used for anesthesia b/c the pt has to breathe at least 20% oxygen to prevent hypoxia

Front 117

Which drugs lower the MAC dose of volatile anesthetic agents?

Back 117

nitrous oxide

BZs

ketamine

Barbituates

EtOH

NOT NMB agents!!

Front 118

General anesthesia and blood/gas coefficients?

Back 118

The blood/gas partition coefficient determines the rate of onset (induction)/offset of anesthesia.
-- Agents that are poorly soluble in blood have a rapid onset/offset b/c the blood (including the RBC’s) must be saturated with gas before the gas will move from the blood into the brain.

After the volatile anesthetic agents are d/c, the partial pressures of the gases will fall in exactly the same order that they rose
-- nitrous oxide drops rapidly
-- halothane drops more slowly
-- methoxyflurane drops very slowly.

***If vapor pressures are given in the question, ignore them. They will not help you answer the Q.

Front 119

CLINICAL: If there is a question regarding the potency of MAC…?

Back 119

Most potent drug has the smallest MAC gas with lowest MAC (most potent) = gas with the highest oil/gas partition coefficient.

gas with the highest MAC (least potent) = gas with lowest oil/gas coefficient

Front 120

What is the second gas effect?

Back 120

A rapidly absorbed gas ↑ the rate of uptake of a second gas

Give 70% nitrous oxide + 0.78% halothane + 29% oxygen, and the rapid uptake of nitrous oxide pulls the halothane along with it.

The arterial tension (partial pressure) of halothane rises more rapidly when given with nitrous oxide (N2O). Net effect is 2-fold:
1. 0.78% halothane +70% N2O --> the steady-state alveolar concentration of halothane is increased (2.00%)
2. the MAC of halothane is decreased (normal MAC = 0.78%; w N2O, MAC = 0.29%)

Front 121

Describe diffusion hypoxia.

Back 121

Nitrous oxide is very insoluble in blood. When its administration is discontinued, large volumes of N2O pour out of the blood into the lungs.

This large volume of N2O dilutes the oxygen, and the patient becomes hypoxic.

Occurs during first 10 min after D/C of N2O

Tx patient w/ 100% oxygen

Front 122

N2O and air-filled cavities…?

Back 122

N2O easily leaves the blood to enter any air-filled cavity in the body.

If N2O enters a compliant air-filled cavity (e.g., intestinal gas, pneumothorax, air bubbles)
-- the gas space expands.

If the air-filled cavity is non-compliant (e.g., sinuses, middle ear and cerebral ventricles)
-- intracavity pressure increases
-- Increased middle ear pressure can rupture the tympanic membrane or cause n/v after surgery

Front 123

What are the factors controlling rate of INDUCTION of anesthesia?

Back 123

1. alveolar ventilation rate

2. blood/gas partition coefficient

3. partial pressure of gas in lungs

4. - cardiac output

5. increase in FI (concentration of gas in inspired air) = concentration effect =  dose

6. cerebral blood flow

7. NOT potency (MAC)

Front 124

What are the factors controlling rate of OFFSET of anesthesia?

Back 124

1. blood/gas partition coefficient

2. hyperventilation

3. cardiac output

4. drug metabolism by the liver

Front 125

What are the CV effects of halothane, isoflurane, enflurane?

Back 125

ALL volatile agents decrease MAP by decreasing either CO or TPR
-- but effect to decrease BP is attenuated in the presence of N2O which tends to increase sympathetic activity

**isoflurane has little effect on CO

Front 126

Volatile agents directly…?

Back 126

relax skeletal muscle and potentiate the effects of the NMB’s

Front 127

Methoxyflurane S/Es?

Back 127

causes renal failure after surgery via release of fluoride ions

Front 128

Ketamine MOA?

Back 128

blocks NMDA glutamate receptor coupled to Ca channel

(NB: glutamate is an excitatory NT in the CNS)

Front 129

Ketamine effects?

Back 129

produces a dissociative state of consciousness, analgesia and postanesthetic hallucinations

least likely to supppress respiration (all opiates, barbiturates, BZ’s and gaseous anesthetics suppress respiration)

MAP via ↑ CO (↑LV-EDP, dp/dt, HR). Little effect on TPR

Front 130

Etomidate MOA?

Back 130

enhances GABAA-mediated chloride conductance to hyperpolarize neurons

Front 131

Etomidate effects?

Back 131

minimal effect on BP or respiration

causes myoclonic movements (not epilepsy) which can be prevented by pre-tx w BZ’s

can cause adrenal suppression w decrease in plasma cortisol

Front 132

CLINICAL: Which of the following drugs decreases BP and respiration when given i.v.?
-- opiate
-- ketamine
-- etomidate
-- thiopental

Back 132

OPIATE
-- nc BP
-- ↓ respiration

KETAMINE
-- ↑BP
-- nc respiration

ETOMIDATE
-- nc BP
-- nc respiration

THIOPENTAL
-- ↓BP
-- ↓ respiration

Front 133

Halothane predisposes to…

Back 133

Epi induced cardiac arrhythmias

Tx w/ β-blockers

Front 134

N2O produces…

Back 134

analgesia, amnesia, and mental confusion

DOES NOT cause anesthesia!!!