Neuro1

Front 1

what is the Monoamine hypothesis of depression?

Back 1

too little serotonin and epi lead to depression

Front 2

what is the Neurotrophic hypothesis of depression?

Back 2

BDNF regulate neural
plasticity,survival and and neurogenesis.

Depression decreases BDNF and antidepressants
increase BDNF.

Front 3

What type of depression is this:

Loss (Adverse life events). Physical illness (myocardial infarct, cancer). Drugs (antihypertensives, alcohol, hormones). Other psychiatric disorders (senility).

Back 3

Reactive

Front 4

What type of depression is this:

Precipitating life event not adequate for degree of depression. Autonomous (unresponsive to changes in life). May occur at any age (childhood to old age). Biologically determined (family history)

Back 4

Endogenous

this is where the neurotrophic hypothesis comes into play (that you have neuronal issue)

Will see more PHYSICAL symptoms

Front 5

What type of depression is this:

Characterized by episodes of mania. Cyclic: mania alone, rare; depression alone, occasional; mania-depression, usual

Back 5

Manic-depressive

Front 6

What kind of drug is Fluoxetine? used to treat?

Back 6

Specific serotonin reuptake inhibitors (SSRIs)

These are a relatively new class of antidepressants and have become drugs of first choice

Front 7

What kind of drug is Paroxetine? used to treat?

Back 7

Specific serotonin reuptake inhibitors (SSRIs)

These are a relatively new class of antidepressants and have become drugs of first choice

Front 8

What effects do SSRIs have on the ANS and CNS?

Back 8

Nothing significant!

This makes them safe, OD won't likely kill you

Front 9

what is the half life like for Paroxetine and Sertraline? What is important about this?

Back 9

Short as compareted to Fluoxetine (1 day vs 3 days)

so you have to make sure to wean them off it slowly or you can cause depression pretty quick

these are all SSRIs

Front 10

what do SSRIs do to the metabolism of other drugs?

Back 10

inhibit the metabolism of other drugs

Front 11

What is the major side effect of SSRIs? why

****TEST

Back 11

Nausea, headache, diarrhea are most common (stimulation of 5HT3 receptors)

note: another reason people may discontinue the drug is due to sexual dysfunction

Front 12

pt comes in on an SSRI with anxiety and motor restlessness, what drug(s) could have caused this?

Back 12

Fluoxetine, and to a lesser extent, sertraline

Front 13

Which SSRI ) may induce birth defects. Use during 3rd trimester may cause persistent pulmonary hypertension in newborns or withdrawal syndrome.

Back 13

paroxetine

Front 14

what do you have to worry about with kids taking SSRIs

Back 14

high risk of suicide

Front 15

What must you be careful of when you give an SSRI with SNRIs,TCA, MAOI, meperidine, or triptans?

****TEST

Back 15

SEROTONIN SYNDROME

mental status changes,(confusion to coma) disorders of motor activity (hyperreflexia, rigidity), and autonomic disturbances ( hyperthermia, hypertens.) All SSRIs)

more dangerous with fluvoxetine (long acting)

Front 16

PMDD, generalized anxiety disorder, panic, OCD, and bulimia can all be treated with what? (general)

Back 16

SSRIs

Front 17

Venlafaxine is what kind of drug?

Back 17

Serotonin and norephinephrine Reuptake Inhibitors (SNRI)

Front 18

duloxetine is what kind of drug?

Back 18

Serotonin and norephinephrine Reuptake Inhibitors (SNRI)

Front 19

which Serotonin and norephinephrine Reuptake Inhibitors (SNRI) should you avoid in pts with liver disease?

Back 19

Duloxetine – liver damage (rare) – avoid in pts with chronic liver disease or hepatic insufficiency

Front 20

Duloxetine does what to P450s?

Back 20

Duloxetine has greater potential than venlafaxine because it inhibits CYP2D6 and may increase drug levels of TCAs, Type 1C antiarrhythmics (e.g., flecainide) and phenothiazines.

INHIBITS METABOLISM

SNRI

Front 21

2 drug classes that can treat diabetic peripheral neuropathy?

Back 21

SNRIs and Tricyclics

Front 22

milnacipran is what kind of drug? Used to treat?

Back 22

SNRI

Fibromyalgia

note: all SNRIs can tx fibromyalgia, but milnacipran is used ONLY for fibromyalgia, not depression

Front 23

Trazodone MOA? Use?

Back 23

blocking 5HT2A receptors.

Most common use of trazodone is as hypnotic.
Side effects – arrhythmias and priapism

Front 24

Bupropion MOA? Use? Risk of causing?

Back 24

causes presynaptic release of DA and NE and blocks their reuptake.

Depression (used after SSRI)

Risk of seizures

note:Less sexual dysfunction, wt gain or sedation than other antidepressants.

Front 25

Mirtazapine MOA? Use? why it is liked?

Back 25

blocks H1 receptors, presynaptic a2-adrenergic receptors, increases NE and 5HT release and blocks 5HT2 and 5HT3 receptors

depression

liked: Less sexual dysfunction; more wt gain and sedation.

Front 26

Doxipen
Maprotiline
Amoxapine

are what kind of drugs

Back 26

second generation Tricyclic Antidepressants

Front 27

Imipramine
Desipramine
Amitriptyline

are what kind of drugs?

Back 27

first generation Tricyclic Antidepressants

Front 28

MOA of tricyclic antidepressant

Back 28

block the reuptake of NE and serotonin in the CNS, thereby potentiating transmitter action. This may be an early event in the mechanism of antidepressant action.

Front 29

which tricyclic has the strongest anticholinergic action?

Back 29

Amitriptyline

Front 30

What are the 3 ways you have adverse effects with Tricyclic antidepressants

Back 30

Antimuscarinic – e.g., dry mouth, constipation, blurred vision, Intensity varies with different drugs (amitriptyline strongest).

CNS – sedation, weakness, fatigue; may switch depressed patient to manic phase; tremor; seizures

Cardiovascular – orthostatic hypotension (a1 block), tachycardia, myocardial infarction, congestive heart failure, arrhythmias. May be less likely or less severe with 2nd generation drugs

Front 31

what can happen with acute poisoning of tricyclics? tx?

Back 31

Acute poisoning – life threatening; excitement and restlessness

Convulsions → coma → death. Must support vital functions. Physostigmine can reverse antimuscarinic, cardiotoxic, and neurotoxic effects.

Front 32

these drugs in addition to treating depression can be used to treat neuropathic pain, nocturnal enuresis, and fibromyalgia

Back 32

Tricyclics

nocturnal enuresis (imipramine), fibromyalgia (amitriptyline, doxipen).

Front 33

Tranylcypromine MOA? Use?

Back 33

Block metabolism of naturally occurring monoamines, e.g., NE, 5HT. Are used in the treatment of depression when tricyclics are not effective and ECT refused.

MAOi

Front 34

Phenelzine MOA? Use?

Back 34

Block metabolism of naturally occurring monoamines, e.g., NE, 5HT. Are used in the treatment of depression when tricyclics are not effective and ECT refused.

MAOi

Front 35

Isocarboxazid MOA? Use?

Back 35

Block metabolism of naturally occurring monoamines, e.g., NE, 5HT. Are used in the treatment of depression when tricyclics are not effective and ECT refused.

MAOi

Front 36

2 main reasons we don't use MAOi?

***TEST

Back 36

Potentiate sympathomimetic amines

*****Dangerous interaction with tyramine (found in food)-->causes release of NE-->Hypertensive crisis

(MAO knocks out Tyramine, without it, it gets into the system and causes the release of NE, leads to hypertensive crisis)

Front 37

How does St. John's Wort help with depression? What are the problems associated with it?

Back 37

Contains compounds that inhibit MAO and block 5HT reuptake

Drug interactions are a problem. Hyperforin, a P450 inducer found in St. J. W., increases metabolism of drugs used to treat AIDS and suppress transplant rejection.

Front 38

MOA of Lithium Carbonate? Use?

Back 38

interferes with second messenger system, can't remake PIP2, SLOWS DOWN NEURONAL ACTIVITY

stabilize mood in bipolar pts

Front 39

A bipolar pt comes in complaining that they are constantly thirsty and peeing all the time...what drug is causing this? how?

***

Back 39

Lithium- Antagonizes ADH

leads to excessive thirst and urination

Front 40

Primary drug of choice for mood stabilization (bipolar)?

Back 40

VALPROATE (remember this is also an anti-epileptic!)

others that can be used: carbamazepine (na channel block), lamotrigine (na channel block)

Front 41

2 drugs that are first choice for depression?

Back 41

SSRIs or venlafaxine (SNRI)

Front 42

when is Electroconvulsive therapy (ECT) indicated

Back 42

when a person is a serious threat to kill themselves when depressed

Front 43

What are the first line choice drugs for bipolar

Back 43

Mood stabilizers are mainstays of treatment – Lithium, valproate or lamotrigine are first choice.

Carbamazepine also used.

Front 44

this is an antidepressant that can be added for severe depression, but don’t use alone. Can be used first line

Back 44

lamotrigine (another antiepileptic).

An antidepressant can be added for severe depression, but don’t use alone. Certain antidepressants may not be effective.

Front 45

for a manic episode, what drugs can be added to mood stabilizers?

Back 45

olanzapine or risperidone (atypical antipsychotics)

added to mood stabilizer (Lithium, valproate or lamotrigine).

Front 46

what is the Monoamine hypothesis of depression?

Back 46

too little serotonin and epi lead to depression

Front 47

what is the Neurotrophic hypothesis of depression?

Back 47

BDNF regulate neural
plasticity,survival and and neurogenesis.

Depression decreases BDNF and antidepressants
increase BDNF.

Front 48

What type of depression is this:

Loss (Adverse life events). Physical illness (myocardial infarct, cancer). Drugs (antihypertensives, alcohol, hormones). Other psychiatric disorders (senility).

Back 48

Reactive

Front 49

What type of depression is this:

Precipitating life event not adequate for degree of depression. Autonomous (unresponsive to changes in life). May occur at any age (childhood to old age). Biologically determined (family history)

Back 49

Endogenous

this is where the neurotrophic hypothesis comes into play (that you have neuronal issue)

Will see more PHYSICAL symptoms

Front 50

What type of depression is this:

Characterized by episodes of mania. Cyclic: mania alone, rare; depression alone, occasional; mania-depression, usual

Back 50

Manic-depressive

Front 51

All anti-psychotics share what mechanism in common?

Back 51

block D2 receptors

(both typical and atypical)

but the importance of this in relation to other receptor actions varies from drug to drug

Front 52

What kind of drug is Paroxetine? used to treat?

Back 52

Specific serotonin reuptake inhibitors (SSRIs)

These are a relatively new class of antidepressants and have become drugs of first choice

Front 53

What kind of drug is Fluoxetine? used to treat?

Back 53

Specific serotonin reuptake inhibitors (SSRIs)

These are a relatively new class of antidepressants and have become drugs of first choice

Front 54

what is the half life like for Paroxetine and Sertraline? What is important about this?

Back 54

Short as compareted to Fluoxetine (1 day vs 3 days)

so you have to make sure to wean them off it slowly or you can cause depression pretty quick

these are all SSRIs

Front 55

what do SSRIs do to the metabolism of other drugs?

Back 55

inhibit the metabolism of other drugs

Front 56

What effects do SSRIs have on the ANS and CNS?

Back 56

Nothing significant!

This makes them safe, OD won't likely kill you

Front 57

pt comes in on an SSRI with anxiety and motor restlessness, what drug(s) could have caused this?

Back 57

Fluoxetine, and to a lesser extent, sertraline

Front 58

Which SSRI ) may induce birth defects. Use during 3rd trimester may cause persistent pulmonary hypertension in newborns or withdrawal syndrome.

Back 58

paroxetine

Front 59

what do you have to worry about with kids taking SSRIs

Back 59

high risk of suicide

Front 60

for a manic episode, what drugs can be added to mood stabilizers?

Back 60

olanzapine or risperidone (atypical antipsychotics)

added to mood stabilizer (Lithium, valproate or lamotrigine).

Front 61

this is an antidepressant that can be added for severe depression, but don’t use alone. Can be used first line

Back 61

lamotrigine (another antiepileptic).

An antidepressant can be added for severe depression, but don’t use alone. Certain antidepressants may not be effective.

Front 62

What are the first line choice drugs for bipolar

Back 62

Mood stabilizers are mainstays of treatment – Lithium, valproate or lamotrigine are first choice.

Carbamazepine also used.

Front 63

when is Electroconvulsive therapy (ECT) indicated

Back 63

when a person is a serious threat to kill themselves when depressed

Front 64

2 drugs that are first choice for depression?

Back 64

SSRIs or venlafaxine (SNRI)

Front 65

Primary drug of choice for mood stabilization (bipolar)?

Back 65

VALPROATE (remember this is also an anti-epileptic!)

others that can be used: carbamazepine (na channel block), lamotrigine (na channel block)

Front 66

A bipolar pt comes in complaining that they are constantly thirsty and peeing all the time...what drug is causing this? how?

***

Back 66

Lithium- Antagonizes ADH

leads to excessive thirst and urination

Front 67

MOA of Lithium Carbonate? Use?

Back 67

interferes with second messenger system, can't remake PIP2, SLOWS DOWN NEURONAL ACTIVITY

stabilize mood in bipolar pts

Front 68

How does St. John's Wort help with depression? What are the problems associated with it?

Back 68

Contains compounds that inhibit MAO and block 5HT reuptake

Drug interactions are a problem. Hyperforin, a P450 inducer found in St. J. W., increases metabolism of drugs used to treat AIDS and suppress transplant rejection.

Front 69

2 main reasons we don't use MAOi?

***TEST

Back 69

Potentiate sympathomimetic amines

*****Dangerous interaction with tyramine (found in food)-->causes release of NE-->Hypertensive crisis

(MAO knocks out Tyramine, without it, it gets into the system and causes the release of NE, leads to hypertensive crisis)

Front 70

Isocarboxazid MOA? Use?

Back 70

Block metabolism of naturally occurring monoamines, e.g., NE, 5HT. Are used in the treatment of depression when tricyclics are not effective and ECT refused.

MAOi

Front 71

Phenelzine MOA? Use?

Back 71

Block metabolism of naturally occurring monoamines, e.g., NE, 5HT. Are used in the treatment of depression when tricyclics are not effective and ECT refused.

MAOi

Front 72

Tranylcypromine MOA? Use?

Back 72

Block metabolism of naturally occurring monoamines, e.g., NE, 5HT. Are used in the treatment of depression when tricyclics are not effective and ECT refused.

MAOi

Front 73

these drugs in addition to treating depression can be used to treat neuropathic pain, nocturnal enuresis, and fibromyalgia

Back 73

Tricyclics

nocturnal enuresis (imipramine), fibromyalgia (amitriptyline, doxipen).

Front 74

what can happen with acute poisoning of tricyclics? tx?

Back 74

Acute poisoning – life threatening; excitement and restlessness

Convulsions → coma → death. Must support vital functions. Physostigmine can reverse antimuscarinic, cardiotoxic, and neurotoxic effects.

Front 75

What are the 3 ways you have adverse effects with Tricyclic antidepressants

Back 75

Antimuscarinic – e.g., dry mouth, constipation, blurred vision, Intensity varies with different drugs (amitriptyline strongest).

CNS – sedation, weakness, fatigue; may switch depressed patient to manic phase; tremor; seizures

Cardiovascular – orthostatic hypotension (a1 block), tachycardia, myocardial infarction, congestive heart failure, arrhythmias. May be less likely or less severe with 2nd generation drugs

Front 76

which tricyclic has the strongest anticholinergic action?

Back 76

Amitriptyline

Front 77

MOA of tricyclic antidepressant

Back 77

block the reuptake of NE and serotonin in the CNS, thereby potentiating transmitter action. This may be an early event in the mechanism of antidepressant action.

Front 78

Imipramine
Desipramine
Amitriptyline

are what kind of drugs?

Back 78

first generation Tricyclic Antidepressants

Front 79

Doxipen
Maprotiline
Amoxapine

are what kind of drugs

Back 79

second generation Tricyclic Antidepressants

Front 80

Mirtazapine MOA? Use? why it is liked?

Back 80

blocks H1 receptors, presynaptic a2-adrenergic receptors, increases NE and 5HT release and blocks 5HT2 and 5HT3 receptors

depression

liked: Less sexual dysfunction; more wt gain and sedation.

Front 81

Bupropion MOA? Use? Risk of causing?

Back 81

causes presynaptic release of DA and NE and blocks their reuptake.

Depression (used after SSRI)

Risk of seizures

note:Less sexual dysfunction, wt gain or sedation than other antidepressants.

Front 82

Trazodone MOA? Use?

Back 82

blocking 5HT2A receptors.

Most common use of trazodone is as hypnotic.
Side effects – arrhythmias and priapism

Front 83

milnacipran is what kind of drug? Used to treat?

Back 83

SNRI

Fibromyalgia

note: all SNRIs can tx fibromyalgia, but milnacipran is used ONLY for fibromyalgia, not depression

Front 84

2 drug classes that can treat diabetic peripheral neuropathy?

Back 84

SNRIs and Tricyclics

Front 85

Duloxetine does what to P450s?

Back 85

Duloxetine has greater potential than venlafaxine because it inhibits CYP2D6 and may increase drug levels of TCAs, Type 1C antiarrhythmics (e.g., flecainide) and phenothiazines.

INHIBITS METABOLISM

SNRI

Front 86

which Serotonin and norephinephrine Reuptake Inhibitors (SNRI) should you avoid in pts with liver disease?

Back 86

Duloxetine – liver damage (rare) – avoid in pts with chronic liver disease or hepatic insufficiency

Front 87

duloxetine is what kind of drug?

Back 87

Serotonin and norephinephrine Reuptake Inhibitors (SNRI)

Front 88

Venlafaxine is what kind of drug?

Back 88

Serotonin and norephinephrine Reuptake Inhibitors (SNRI)

Front 89

PMDD, generalized anxiety disorder, panic, OCD, and bulimia can all be treated with what? (general)

Back 89

SSRIs

Front 90

What must you be careful of when you give an SSRI with SNRIs,TCA, MAOI, meperidine, or triptans?

****TEST

Back 90

SEROTONIN SYNDROME

mental status changes,(confusion to coma) disorders of motor activity (hyperreflexia, rigidity), and autonomic disturbances ( hyperthermia, hypertens.) All SSRIs)

more dangerous with fluvoxetine (long acting)

Front 91

What is the major side effect of SSRIs? why

****TEST

Back 91

Nausea, headache, diarrhea are most common (stimulation of 5HT3 receptors)

note: another reason people may discontinue the drug is due to sexual dysfunction

Front 92

Please compare the difference in typical and atypical's tendency to bind to different receptors

Back 92

“Atypical” antipsychotics have different receptor binding profiles, but they all tend to be less potent at D2 receptors than chlorpromazine or halperidol and more potent at 5HT2 and D4 receptors.

Front 93

how does blocking D2 receptors help with Schizophrenia?

Back 93

alleviates positive symptoms of schizophrenia (tension, hostility, hyperactivity, combativeness, hallucinations, delusions, insomnia, and anorexia.

Front 94

Betaseron is what kind of drug?

Back 94

interferon beta-1b

Mechanism of action – uncertain but beneficial effects may be due to immunomodulatory actions. One thought is that INFs decrease antigen presentation in the CNS, which appears to limit immune attack on myelin

Front 95

which is more likely to make you want to eat more, typical or atypical antipsychotics?

Back 95

Atypical

Front 96

how do anti-psychotic drugs affect the ANS?

Back 96

peripheral cholinergic block, a-adrenergic block

Front 97

most important side effects of anti-psychotic drugs

Back 97

– CV, endocrine, central and autonomic are most important. Other dangerous effects include seizures, agranulocytosis and pigmentary degeneration of retina

Front 98

Halloperidol is more likely to cause what serious side effect? is this a typical or atypical anti-psychotic?

**

Back 98

Tardive dyskinesia

Typical

Front 99

how does blocking D4 and 5HT2 receptors help with SZ?

Back 99

Blocking D4 and 5HT2 receptors may alleviate negative symptoms (apathy, withdrawal, unresponsiveness).

Front 100

what 2 antipsychotic drugs cause QT prolongation

Back 100

thioridazine, ziprasidone

Front 101

clozapine is likely to cause what side effect?

Back 101

Seizures

Front 102

what 2 anti-psychotic drugs are likely to cause weight gain?

Back 102

clozapine and olanzapine

Front 103

Most serious adverse affect of Clozapine? When would you use it?

Back 103

mild leukocytosis, leukopenia, and eosinophilia. Bone marrow suppression or agranulocytosis with clozapine

Last resort drug

anti-psychotic

Front 104

Phenothiazines is also known as?

Back 104

Chlorpromazine

or

Fluphenazine

Front 105

in elderly pts on risperidone what do you have to worry about?

what is another drug that can cause this?

Back 105

STROKE

Olanzapine

(these are anti-psychotics)

Front 106

Butyrophenone is what drug?

Back 106

Haloperidol

Front 107

2 side effects of Atypicals in general?

Back 107

weight gain and diabetes

Front 108

what type of treatment will lead to low number of re-hospitalizations of schizophrenic patients?

Back 108

Drug therapy + social therapy

Front 109

Chlorpromazine (Thorazine)
Thioridazine (Mellaril)
Fluphenazine (Prolixin)
Perphenazine (Trilafon)
Thiothixene (Navane)
Haloperidol (Haldol)
Loxapine (Loxitane)

Back 109

Typical Anti-psychotics

Front 110

Clozapine (Clozaril)
Risperidone (Risperdal) Paliperidone (Invega)
Olanzapine (Zyprexa)
Quetiapine (Seroquel)
Ziprasidone (Geodon)
Aripiprazole (Abilify)
Asenapine (Safris)
Iloperidone (Fanapt)

Back 110

Atypical Anti-psychotics

Front 111

All agents improve positive symptoms, which improve negative sx?

Back 111

Atypicals

Front 112

Avonex and Rebif are is what kind of drugs?

Back 112

interferon beta-1a

Mechanism of action – uncertain but beneficial effects may be due to immunomodulatory actions. One thought is that INFs decrease antigen presentation in the CNS, which appears to limit immune attack on myelin

Front 113

reteplase (r-PA)

Back 113

Retavase

Hint 113

fibrinolytic - direct plasminogen activator
is altered t-PA for duration
fibrin specific
inactivated by PAI-1

Front 114

use of the interferon drugs?

Back 114

Used to decrease the frequency and severity of exacerbations in patients with relapsing forms of MS. Uncertain whether they actually slow the progression of the disease.

Front 115

Mitoxantrone is what kind of drug? MOA?

what is important about this drug?

Back 115

a cancer chemotherapeutic agent recently approved to treat advanced MS

Acts by suppressing immune attack on myelin

important thing to remember: THERE IS A TIME LIMIT TO HOW LONG YOU CAN USE IT (2-3 year)--> will cause problems with cardiac conduction

Front 116

Natalizumab is what kind of drug? How does it work?

Back 116

A recombinant humanized MAB

Binds to a specific site on an adhesion molecule on activated lymphocytes and monocytes. This blocks adhesion and prevents leukocyte entry into CNS, therby decreasing immune attack on myelin.

Front 117

major side effect of Natalizumab?

Back 117

Progressive multifocal leukoencephalopathy-->FATAL

Binds to a specific site on an adhesion molecule on activated lymphocytes and monocytes. This blocks adhesion and prevents leukocyte entry into CNS, therby decreasing immune attack on myelin.

Front 118

Fingolimod MOA?

important thing about it?

Back 118

Mechanism – inhibits migration of T cells out of lymph nodes

The first oral specific therapy for MS!!

Front 119

MOA of Levodopa?

Back 119

immediate precursor of dopamine which will cross the blood brain barrier

conversion of l-dopa to dopamine in CNS, thus increasing dopamine in the basal ganglia

Front 120

adverse effects of Fingolimod

Back 120

bradycardia and increased infections

Mechanism – inhibits migration of T cells out of lymph nodes

Front 121

Riluzole major adverse effect?

Back 121

Hepatotox

MOA: voltage-gated sodium channel blocker which is thought to act by inhibiting glutamate release

Front 122

What is Riluzole used for? MOA?

Back 122

is the first (and, so far, only) drug approved for the specific treatment of ALS

voltage-gated sodium channel blocker which is thought to act by inhibiting glutamate release

Front 123

Galantamine is what kind of drug?

Used to tx?

Back 123

Acetylcholinesterase inhibitors

Drug treatment Alzheimer’s Disease

– the cognitive deficits of the disease are thought to be related, in part, to degeneration of cholinergic neurons in the cortex and hippocampus resulting in deficient cholinergic neurotransmission.

Front 124

Donepezil is what kind of drug?

Used to tx?

Back 124

Acetylcholinesterase inhibitors

Drug treatment Alzheimer’s Disease

– the cognitive deficits of the disease are thought to be related, in part, to degeneration of cholinergic neurons in the cortex and hippocampus resulting in deficient cholinergic neurotransmission.

Front 125

Alteplase (t-PA)

Back 125

Cathlo Activase, Activase

Hint 125

Fibrinolytics - direct plasminogen activator
fibrin specific
inactivated by PAI-1
bleed risk only at high doses

Front 126

Memantine is what kind of drug?

used to tx?

Back 126

"use-dependent” (only kicks in when there are high lvls of activity) NMDA receptor antagonist. The theory behind its action in Alzheimer’s is that it blocks glutaminergic overstimulation of NMDA receptors, which can be toxic to neurons which are important in learning and memory, but allows low levels of receptor activation.

Drug treatment Alzheimer’s Disease

Front 127

what effect might gingko have on AZ? Estrogen?

Back 127

Gingko has been shown to modestly improve memory in some Alzheimer’s patients.

Estrogen may increase risk.

Front 128

what kind of drug is Glatiramer? used to treat? MOA

Back 128

a synthetic compound which resembles a component of myelin

Mechanism of action
Since drug resembles a component of myelin, it’s thought that it may protect myelin by acting as a “decoy” attracting immune cells away from myelin

tx: MS

Front 129

what MS drug has the adverse effects of Flushing, chest tightness or pain, shortness of breath (within 15 min)

Back 129

Glatiramer

Front 130

Tacrine is what kind of drug?

Used to tx?

Back 130

Acetylcholinesterase inhibitors

Drug treatment Alzheimer’s Disease

– the cognitive deficits of the disease are thought to be related, in part, to degeneration of cholinergic neurons in the cortex and hippocampus resulting in deficient cholinergic neurotransmission.

Front 131

what limits the use of levodopa?

Back 131

need to have dopamine neurons to convert L dopa to dopamine

over time these neurons are dying

Front 132

what are the changes you will see in pts who take in levodopa?

Back 132

Bradykinesia and rigidity are reversed quickly; reversal of tremor requires continued therapy

Changes in mood associated with PD are reversed; patients more alert and interested in environment. Dementia may not reverse

Front 133

what are the cardiovascular and endocrine effects of L-dopa

(not sure how important this is but here you go anyways)

Back 133

Cardiovascular
Asymptomatic (usually) orthostatic hypotension
Dopamine stimulates both alpha and beta receptors
Cardiac stimulation

Endocrine
Dopamine important in regulation of anterior pituitary function
Prolactin secretion inhibited
Little change in growth hormone secretion

Front 134

what are the short and long term side effects of L-Dopa?

Back 134

Early side effects
Dose dependent; tolerance may develop
GI – nausea, vomiting (80%)
CVS – orthostatic hypotension (30%), cardiac arrhythmias

Long term effects – severity correlates with the degree of clinical improvement, duration of therapy and dose. No tolerance develops.

***Abnormal involuntary movements (dyskinesia)*** (80% after 1 year). Reduction in dosage required

Psychiatric and behavioral disturbances (15%)

***“On-Off” syndrome – oscillations in performance involving rapid changes from akinesia to dyskinesia (different from “end of dose”). **

Front 135

antipsychotic drugs have what effect on L-dopa?

Back 135

Typical” antipsychotic drugs are dopaminergic antagonists and thus counteract the effects of dopa

Front 136

MAOi interact how with L-dopa?

Back 136

MAO inhibitors increase the effects of dopa, may lead to hypertensive crises

note: Tricyclic antidepressants – may aggravate hypotensive symptoms

Front 137

Carbidopa MOA?

Back 137

prevents PERIPHERAL conversion of Dopa to Dopamine

allows more L-dopa to get to the brain to be converted

allows for lower dose of L-dopa to be used

decreases peripheral side effects of L-dopa (less CV, NV)

Front 138

what are the side effects of Carbidopa?

Back 138

remember, it decreases L-dopa side effect peripherally BUT

increased central side effects of dopa
Early development of long term side effects possible
Activation of COMT pathway
--so in a way it may progress the disease more quickly

Front 139

What kind of drug is Tolcapone?

Back 139

COMT inhibitor

thereby increasing the duration of action of l-dopa and dopamine (COMT inactivates l-dopa and dopamine).

Works in CNS and periphery

Front 140

MOA of Levodopa?

Back 140

immediate precursor of dopamine which will cross the blood brain barrier

conversion of l-dopa to dopamine in CNS, thus increasing dopamine in the basal ganglia

Front 141

major tox of tolcapone? is this a problem in entacapone?

Back 141

Hepatotox

NO

Front 142

Ropinirole is what kind of drug?

Back 142

non-ergot DA agonists

Direct stimulation of DA receptors in striatum

Front 143

pramipexole is what kind of drug?

Back 143

non-ergot DA agonists

Direct stimulation of DA receptors in striatum

Front 144

what is one of the few drugs that may slow the progression of Parkinsons?

Back 144

pramipexole

Front 145

impulse control problems is a side effect of what drugs?

Back 145

Non-ergot DA agonists

pramipexole/Ropinirole

Front 146

what is a unique side effect of pramipexole?

Back 146

Pramipexole can cause sudden onset of sleep with no warning

MOA:Non-ergot DA agonist

Front 147

Use for Apomorphine?

Back 147

non-ergot DA agonist recently approved for rescue treatment of PD patients with “off” episodes (freezing).

Adverse effects include vomiting, orthostatic hypotension and syncope.

Front 148

How is Amantadine used in Parkinson's?

Back 148

An antiviral agent found to be effective against PD
.
Apparently acts by increasing dopamine release from intact dopaminergic neurons. Also blocks NMDA receptors.

Is effective quickly but for short time (6-8 weeks). Also used to control dyskinesias occurring with l-dopa therapy late in progression of disease.

Front 149

Hallucinations, confusion, and nightmares
Insomnia, dizziness, lethergy, slurred speech
Long term use may result in livido reticularis (net like discoloration of the skin)

are adverse rxns of what drug?

Back 149

Amantadine

Apparently acts by increasing dopamine release from intact dopaminergic neurons. Also blocks NMDA receptors.

Front 150

Trihexyphenidyl is what kind of drug? how does it help with PD?

Back 150

Anticholinergic drugs - used as adjunct to l-dopa therapy

Decrease tremor
Little effect on rigidity and bradykinesia
Generally have little peripheral effect, but may reduce some autonomic symptoms

Front 151

benztropine is what kind of drug? how does it help with PD?

Back 151

Anticholinergic drugs - used as adjunct to l-dopa therapy

Decrease tremor
Little effect on rigidity and bradykinesia
Generally have little peripheral effect, but may reduce some autonomic symptoms

Front 152

adverse effects of anticholinergic drugs used for PD?

Back 152

CNS – confusion, delerium, somnolence, hallucinations (try to avoid them in old people)

Peripheral – may produce cycloplegia, constipation, and urinary retention in certain patients

Front 153

MOA of Selegiline?

Back 153

MAO B Inhibitors

MAO B metabolizes dopamine--prevents this

Front 154

MOA of Rasagiline?

Back 154

MAO B Inhibitors

MAO B metabolizes dopamine--prevents this

Front 155

Pt has Parkinson's, what should you use first? second? third?

Back 155

Selagilline for neuroprotection

Dopamine Agonists

Levodopa

COMT inhibitor

All others

Front 156

Tetrabenazine is used to treat what?

Back 156

approved for treatment of chorea associated with Huntington's Dz

Front 157

What kind of drug is Entacapone?

Back 157

COMT inhibitor

thereby increasing the duration of action of l-dopa and dopamine (COMT inactivates l-dopa and dopamine).

only works in the periphery

Front 158

what limits the use of levodopa?

Back 158

need to have dopamine neurons to convert L dopa to dopamine

over time these neurons are dying

Front 159

what are the changes you will see in pts who take in levodopa?

Back 159

Bradykinesia and rigidity are reversed quickly; reversal of tremor requires continued therapy

Changes in mood associated with PD are reversed; patients more alert and interested in environment. Dementia may not reverse

Front 160

what are the cardiovascular and endocrine effects of L-dopa

(not sure how important this is but here you go anyways)

Back 160

Cardiovascular
Asymptomatic (usually) orthostatic hypotension
Dopamine stimulates both alpha and beta receptors
Cardiac stimulation

Endocrine
Dopamine important in regulation of anterior pituitary function
Prolactin secretion inhibited
Little change in growth hormone secretion

Front 161

what are the short and long term side effects of L-Dopa?

Back 161

Early side effects
Dose dependent; tolerance may develop
GI – nausea, vomiting (80%)
CVS – orthostatic hypotension (30%), cardiac arrhythmias

Long term effects – severity correlates with the degree of clinical improvement, duration of therapy and dose. No tolerance develops.

***Abnormal involuntary movements (dyskinesia)*** (80% after 1 year). Reduction in dosage required

Psychiatric and behavioral disturbances (15%)

***“On-Off” syndrome – oscillations in performance involving rapid changes from akinesia to dyskinesia (different from “end of dose”). **

Front 162

antipsychotic drugs have what effect on L-dopa?

Back 162

Typical” antipsychotic drugs are dopaminergic antagonists and thus counteract the effects of dopa

Front 163

MAOi interact how with L-dopa?

Back 163

MAO inhibitors increase the effects of dopa, may lead to hypertensive crises

note: Tricyclic antidepressants – may aggravate hypotensive symptoms

Front 164

Carbidopa MOA?

Back 164

prevents PERIPHERAL conversion of Dopa to Dopamine

allows more L-dopa to get to the brain to be converted

allows for lower dose of L-dopa to be used

decreases peripheral side effects of L-dopa (less CV, NV)

Front 165

what are the side effects of Carbidopa?

Back 165

remember, it decreases L-dopa side effect peripherally BUT

increased central side effects of dopa
Early development of long term side effects possible
Activation of COMT pathway
--so in a way it may progress the disease more quickly

Front 166

What kind of drug is Tolcapone?

Back 166

COMT inhibitor

thereby increasing the duration of action of l-dopa and dopamine (COMT inactivates l-dopa and dopamine).

Works in CNS and periphery

Front 167

What kind of drug is Entacapone?

Back 167

COMT inhibitor

thereby increasing the duration of action of l-dopa and dopamine (COMT inactivates l-dopa and dopamine).

only works in the periphery

Front 168

major tox of tolcapone? is this a problem in entacapone?

Back 168

Hepatotox

NO

Front 169

Ropinirole is what kind of drug?

Back 169

non-ergot DA agonists

Direct stimulation of DA receptors in striatum

Front 170

pramipexole is what kind of drug?

Back 170

non-ergot DA agonists

Direct stimulation of DA receptors in striatum

Front 171

what is one of the few drugs that may slow the progression of Parkinsons?

Back 171

pramipexole

Front 172

impulse control problems is a side effect of what drugs?

Back 172

Non-ergot DA agonists

pramipexole/Ropinirole

Front 173

what is a unique side effect of pramipexole?

Back 173

Pramipexole can cause sudden onset of sleep with no warning

MOA:Non-ergot DA agonist

Front 174

Use for Apomorphine?

Back 174

non-ergot DA agonist recently approved for rescue treatment of PD patients with “off” episodes (freezing).

Adverse effects include vomiting, orthostatic hypotension and syncope.

Front 175

Tetrabenazine is used to treat what?

Back 175

approved for treatment of chorea associated with Huntington's Dz

Front 176

Pt has Parkinson's, what should you use first? second? third?

Back 176

Selagilline for neuroprotection

Dopamine Agonists

Levodopa

COMT inhibitor

All others

Front 177

MOA of Rasagiline?

Back 177

MAO B Inhibitors

MAO B metabolizes dopamine--prevents this

Front 178

MOA of Selegiline?

Back 178

MAO B Inhibitors

MAO B metabolizes dopamine--prevents this

Front 179

adverse effects of anticholinergic drugs used for PD?

Back 179

CNS – confusion, delerium, somnolence, hallucinations (try to avoid them in old people)

Peripheral – may produce cycloplegia, constipation, and urinary retention in certain patients

Front 180

benztropine is what kind of drug? how does it help with PD?

Back 180

Anticholinergic drugs - used as adjunct to l-dopa therapy

Decrease tremor
Little effect on rigidity and bradykinesia
Generally have little peripheral effect, but may reduce some autonomic symptoms

Front 181

Trihexyphenidyl is what kind of drug? how does it help with PD?

Back 181

Anticholinergic drugs - used as adjunct to l-dopa therapy

Decrease tremor
Little effect on rigidity and bradykinesia
Generally have little peripheral effect, but may reduce some autonomic symptoms

Front 182

Hallucinations, confusion, and nightmares
Insomnia, dizziness, lethergy, slurred speech
Long term use may result in livido reticularis (net like discoloration of the skin)

are adverse rxns of what drug?

Back 182

Amantadine

Apparently acts by increasing dopamine release from intact dopaminergic neurons. Also blocks NMDA receptors.

Front 183

How is Amantadine used in Parkinson's?

Back 183

An antiviral agent found to be effective against PD
.
Apparently acts by increasing dopamine release from intact dopaminergic neurons. Also blocks NMDA receptors.

Is effective quickly but for short time (6-8 weeks). Also used to control dyskinesias occurring with l-dopa therapy late in progression of disease.

Front 184

MOA of Levodopa?

Back 184

immediate precursor of dopamine which will cross the blood brain barrier

conversion of l-dopa to dopamine in CNS, thus increasing dopamine in the basal ganglia

Front 185

what limits the use of levodopa?

Back 185

need to have dopamine neurons to convert L dopa to dopamine

over time these neurons are dying

Front 186

Tetrabenazine is used to treat what?

Back 186

approved for treatment of chorea associated with Huntington's Dz

Front 187

what are the changes you will see in pts who take in levodopa?

Back 187

Bradykinesia and rigidity are reversed quickly; reversal of tremor requires continued therapy

Changes in mood associated with PD are reversed; patients more alert and interested in environment. Dementia may not reverse

Front 188

Pt has Parkinson's, what should you use first? second? third?

Back 188

Selagilline for neuroprotection

Dopamine Agonists

Levodopa

COMT inhibitor

All others

Front 189

what are the cardiovascular and endocrine effects of L-dopa

(not sure how important this is but here you go anyways)

Back 189

Cardiovascular
Asymptomatic (usually) orthostatic hypotension
Dopamine stimulates both alpha and beta receptors
Cardiac stimulation

Endocrine
Dopamine important in regulation of anterior pituitary function
Prolactin secretion inhibited
Little change in growth hormone secretion

Front 190

MOA of Rasagiline?

Back 190

MAO B Inhibitors

MAO B metabolizes dopamine--prevents this

Front 191

what are the short and long term side effects of L-Dopa?

Back 191

Early side effects
Dose dependent; tolerance may develop
GI – nausea, vomiting (80%)
CVS – orthostatic hypotension (30%), cardiac arrhythmias

Long term effects – severity correlates with the degree of clinical improvement, duration of therapy and dose. No tolerance develops.

***Abnormal involuntary movements (dyskinesia)*** (80% after 1 year). Reduction in dosage required

Psychiatric and behavioral disturbances (15%)

***“On-Off” syndrome – oscillations in performance involving rapid changes from akinesia to dyskinesia (different from “end of dose”). **

Front 192

MOA of Selegiline?

Back 192

MAO B Inhibitors

MAO B metabolizes dopamine--prevents this

Front 193

adverse effects of anticholinergic drugs used for PD?

Back 193

CNS – confusion, delerium, somnolence, hallucinations (try to avoid them in old people)

Peripheral – may produce cycloplegia, constipation, and urinary retention in certain patients

Front 194

benztropine is what kind of drug? how does it help with PD?

Back 194

Anticholinergic drugs - used as adjunct to l-dopa therapy

Decrease tremor
Little effect on rigidity and bradykinesia
Generally have little peripheral effect, but may reduce some autonomic symptoms

Front 195

Trihexyphenidyl is what kind of drug? how does it help with PD?

Back 195

Anticholinergic drugs - used as adjunct to l-dopa therapy

Decrease tremor
Little effect on rigidity and bradykinesia
Generally have little peripheral effect, but may reduce some autonomic symptoms

Front 196

Hallucinations, confusion, and nightmares
Insomnia, dizziness, lethergy, slurred speech
Long term use may result in livido reticularis (net like discoloration of the skin)

are adverse rxns of what drug?

Back 196

Amantadine

Apparently acts by increasing dopamine release from intact dopaminergic neurons. Also blocks NMDA receptors.

Front 197

How is Amantadine used in Parkinson's?

Back 197

An antiviral agent found to be effective against PD
.
Apparently acts by increasing dopamine release from intact dopaminergic neurons. Also blocks NMDA receptors.

Is effective quickly but for short time (6-8 weeks). Also used to control dyskinesias occurring with l-dopa therapy late in progression of disease.

Front 198

Use for Apomorphine?

Back 198

non-ergot DA agonist recently approved for rescue treatment of PD patients with “off” episodes (freezing).

Adverse effects include vomiting, orthostatic hypotension and syncope.

Front 199

what is a unique side effect of pramipexole?

Back 199

Pramipexole can cause sudden onset of sleep with no warning

MOA:Non-ergot DA agonist

Front 200

what is one of the few drugs that may slow the progression of Parkinsons?

Back 200

pramipexole

Front 201

impulse control problems is a side effect of what drugs?

Back 201

Non-ergot DA agonists

pramipexole/Ropinirole

Front 202

pramipexole is what kind of drug?

Back 202

non-ergot DA agonists

Direct stimulation of DA receptors in striatum

Front 203

[ʒ]

Back 203

Voiced Palato-Alveolar Fricative
azure [æʒər]

Front 204

major tox of tolcapone? is this a problem in entacapone?

Back 204

Hepatotox

NO

Front 205

What kind of drug is Entacapone?

Back 205

COMT inhibitor

thereby increasing the duration of action of l-dopa and dopamine (COMT inactivates l-dopa and dopamine).

only works in the periphery

Front 206

[n]

Back 206

Voiced Alveolar Nasal
note [nowt]

Front 207

what are the side effects of Carbidopa?

Back 207

remember, it decreases L-dopa side effect peripherally BUT

increased central side effects of dopa
Early development of long term side effects possible
Activation of COMT pathway
--so in a way it may progress the disease more quickly

Front 208

Carbidopa MOA?

Back 208

prevents PERIPHERAL conversion of Dopa to Dopamine

allows more L-dopa to get to the brain to be converted

allows for lower dose of L-dopa to be used

decreases peripheral side effects of L-dopa (less CV, NV)

Front 209

MAOi interact how with L-dopa?

Back 209

MAO inhibitors increase the effects of dopa, may lead to hypertensive crises

note: Tricyclic antidepressants – may aggravate hypotensive symptoms

Front 210

antipsychotic drugs have what effect on L-dopa?

Back 210

Typical” antipsychotic drugs are dopaminergic antagonists and thus counteract the effects of dopa

Front 211

What is a left shift?

Back 211

Neutrophils are present

(right shift is more lymphocytes than neutrophils)

Front 212

what is the lymphatic system of the CNS like?

Back 212

there isn't one!

Front 213

what will produce a ring enhancement on imaging?

Back 213

an abscess

has to do with central necrosis and capsule formation

Front 214

which form of meningitis will have a large number of neutrophils?

what will glucose levels be like in the CSF in this type of infection?

Back 214

Bacterial

Decrease--using up the glucose

Front 215

in viral and fungal meningitis what type of cells will be elevated in the CSF

Back 215

Lymphocytes

Front 216

which type of meningitis will be self-limited and has a low mortality

Back 216

Viral

Front 217

1. Purulent leptomeningeal inflammation, cloudy CSF, vascular engorgement, may extend to cortex

2. Mild leptomeningeal inflammation, brain swelling

which is bacterial and which is viral/

Back 217

(1-bacterial; 2-viral)

Front 218

What is a left shift?

Back 218

Neutrophils are present

(right shift is more lymphocytes than neutrophils)

Front 219

what are some of the predisposing conditions for focal suppurative infections of the brain (abscess)?

Back 219

Acute bacterial endocarditis, right to left shunts, chronic pulmonary sepsis
Mastoiditis, paranasal sinusitis, acute otitis, open fracture, previous neurosurgery

Front 220

what physiologically leads to hydrocephalus? 2

Back 220

Hydrocephalus can be due to lack of absorption of CSF or due to an obstruction to flow of CSF

Front 221

what is the therapy of choice for a brain abscess? (reduces mortality to less than 10%)

Back 221

Surgery and antibiotic therapy can reduce mortality to less than 10%

Front 222

Hydrocephalus, leptomeningeal fibrosis (may cause cranial nerve impairment) is a result of what type of meningitis?

Back 222

Bacterial

Front 223

what are 3 causes of chronic bacterial meningoencephalitis?

Back 223

Tuberculosis (mycobacterium tuberculosis)

Neurosyphilis (treponema pallidum)

Lyme Disease (borrelia burgdorferi)

Front 224

pt presents with a headache, maliaise, mental confusion and vomiting. A micro finding is caseating granuloma...

Back 224

TB

Front 225

perivascular inflammatory infiltrate of plasma cells and lymphocytes is a micro finding of what?

Back 225

Neurosyphilis

Chronic Bacterial Meningoencephalitis

Front 226

what 2 types of pts are likely to get fungal (candida) caused meningitis?

**

Back 226

HIV and Diabetic pts

immunocompromised

Front 227

causes of diffuse parenchymal meningoencephalitis? 2

*

Back 227

Candida, Criptococcus

Front 228

if you see meningitis associated with vasculitis, what are 2 of your possible causes?

*

Back 228

Mucor, Aspergillus

Front 229

if a pt has histoplasmosis in the lung, what is there potential for?

*

Back 229

abscess in the brain

Front 230

Chronic memningitis with aids is normally caused by?


**

Back 230

Toxoplasmosis

Front 231

necrosis of the temporal lobe is associated with what type of meningoenchepalitis?

how bout Rabies-Negri bodies in hippocampal and Purkinje neurons

and microglial nodules and multinucleated giant cells

*

Back 231

Herpes-temporal lobe necrosis

Rabies-Negri bodies in hippocampal and Purkinje neurons

HIV-microglial nodules and multinucleated giant cells

Front 232

what is the lymphatic system of the CNS like?

Back 232

there isn't one!

Front 233

what will produce a ring enhancement on imaging?

Back 233

an abscess

has to do with central necrosis and capsule formation

Front 234

which form of meningitis will have a large number of neutrophils?

what will glucose levels be like in the CSF in this type of infection?

Back 234

Bacterial

Decrease--using up the glucose

Front 235

moa of the -triptan drugs?

Back 235

5HT1 Receptor Agonists

Mechanism and pharmacological effects – 5HT1D/5HT1B receptor agonists which constrict large cranial blood vessels, decrease inflammation around sensory nerves, and inhibit trigeminal neuronal discharge. These actions relieve pain and other symptoms of migraine

Front 236

which type of meningitis will be self-limited and has a low mortality

Back 236

Viral

Front 237

1. Purulent leptomeningeal inflammation, cloudy CSF, vascular engorgement, may extend to cortex

2. Mild leptomeningeal inflammation, brain swelling

which is bacterial and which is viral/

Back 237

(1-bacterial; 2-viral)

Front 238

in viral and fungal meningitis what type of cells will be elevated in the CSF

Back 238

Lymphocytes

Front 239

what are some of the predisposing conditions for focal suppurative infections of the brain (abscess)?

Back 239

Acute bacterial endocarditis, right to left shunts, chronic pulmonary sepsis
Mastoiditis, paranasal sinusitis, acute otitis, open fracture, previous neurosurgery

Front 240

Hydrocephalus, leptomeningeal fibrosis (may cause cranial nerve impairment) is a result of what type of meningitis?

Back 240

Bacterial

Front 241

what physiologically leads to hydrocephalus? 2

Back 241

Hydrocephalus can be due to lack of absorption of CSF or due to an obstruction to flow of CSF

Front 242

what are 3 causes of chronic bacterial meningoencephalitis?

Back 242

Tuberculosis (mycobacterium tuberculosis)

Neurosyphilis (treponema pallidum)

Lyme Disease (borrelia burgdorferi)

Front 243

pt presents with a headache, maliaise, mental confusion and vomiting. A micro finding is caseating granuloma...

Back 243

TB

Front 244

perivascular inflammatory infiltrate of plasma cells and lymphocytes is a micro finding of what?

Back 244

Neurosyphilis

Chronic Bacterial Meningoencephalitis

Front 245

causes of diffuse parenchymal meningoencephalitis? 2

*

Back 245

Candida, Criptococcus

Front 246

if you see meningitis associated with vasculitis, what are 2 of your possible causes?

*

Back 246

Mucor, Aspergillus

Front 247

Chronic memningitis with aids is normally caused by?


**

Back 247

Toxoplasmosis

Front 248

what 2 types of pts are likely to get fungal (candida) caused meningitis?

**

Back 248

HIV and Diabetic pts

immunocompromised

Front 249

if a pt has histoplasmosis in the lung, what is there potential for?

*

Back 249

abscess in the brain

Front 250

necrosis of the temporal lobe is associated with what type of meningoenchepalitis?

how bout Rabies-Negri bodies in hippocampal and Purkinje neurons

and microglial nodules and multinucleated giant cells

*

Back 250

Herpes-temporal lobe necrosis

Rabies-Negri bodies in hippocampal and Purkinje neurons

HIV-microglial nodules and multinucleated giant cells

Front 251

what is the therapy of choice for a brain abscess? (reduces mortality to less than 10%)

Back 251

Surgery and antibiotic therapy can reduce mortality to less than 10%

Front 252

what are the long acting -triptan drugs?

Back 252

frovatriptan

naratriptan

-good for outlasting long headaches

note: these also take longer to start working

Front 253

most common side effect of the triptans? Who are they contraindicated in?

Back 253

Nausea and vomiting most common after oral administration.

Pain and redness at injection site plus tingling, dizziness, burning sensations,

tightness and pressure in the chest. Contraindicated in patients with coronary artery disease and angina. (will hit 5HT2 receptors on coronary vasculature)

Front 254

why should triptans be avoided in pts on SSRIs?

Back 254

triptains affect serotonin

Possibility of serotonin syndrome in patients also taking SSRIs

Front 255

what is the MOA of Ergotamine and Dihydroergotamine?

how does this help with migranes?

how is it different from the triptans

Back 255

Ergotamine binds to all subtypes of 5HT1, and 5HT2 receptors as well as adrenergic and dopaminergic receptors. Agonist activity at 5HT1B and/or 5HT1D receptors on cerebral blood vessels probably responsible for anti-migraine activity.

SIDE EFFECTS are really bad-Nausea vomiting, muscle weakness, numbness/tingling in fingers and toes, allergic rxn, chest pain

note: caffeine can help with absorption

Front 256

What is the major drug interaction of benzodiapepines?

Back 256

Potentiation of CNS depressant effects of antipsychotics, tricyclic antidepressants, sedative hypnotics, alcohol

Front 257

which b-blockers can be effective for tx of migraine?

Back 257

propranolol

timolol

Front 258

what antiepileptic drug can be good to treat migraine?

Back 258

Valproate

Front 259

Amitriptyline can be used to treat?

Back 259

Migraine

Front 260

SSRI is a good treatment for what type of headache?

Back 260

menstrual migraine

Front 261

Cafergot plus CYP3A4 inhibitor (macrolides, protease inhibitors) may do what?

Back 261

fatal ischemia

cafergot--Ergotamine+Caffeine

Front 262

pt has:
Occasional throbbing headachesNo major impairment of functioning

stage of migraine?

Therapies?

Back 262

stage of migraine: Mild

Therapies:
Mild analgesics (NSAID)Combination analgesicsAntiemetics, depending on severity

Front 263

pt has:
Moderate or severe headachesSome impairment of functioningNausea common


stage of migraine?

Therapies?

Back 263

stage of migraine: Moderate

Therapies:
Combination analgesicsTriptan or Ergot alkaloidAntiemetics

Front 264

pt has:
More than 3 severe headaches a monthSignificant functional impairmentMarked nausea and/or vomiting


stage of migraine?

Therapies?

Back 264

stage of migraine: Severe

Therapies:
Triptan or Ergot alkaloid (+/- NSAIDS) Prophylactic medicationsAntiemetics

Front 265

first line treatment for acute cluster headache?

Back 265

Fast acting triptan (nasal or SC) or oxygen are the first choices

Front 266

how can montelukast be used to tx migraine?

Back 266

decrease frequency by decreasing inflammation

Front 267

prevention tx for verapamil?

Back 267

Verapamil is drug of choice; melatonin may be effective

Front 268

Felbamate (Felbatol) – was approved for use in....? What is a stipulation of its use?

Back 268

adults with partial seizures and in children with seizures associated with Lennox-Gastaut Syndrome

can only be gotten for pts who this is the ONLY DRUG THAT WILL WORK...people have to sign a waiver to use it because it causes high incidence of aplastic anemia, and liver failure

Front 269

MOA of Vigabatrin?

side effects?

use?

Back 269

Inhibits GABA degradation (GABA transaminase) and reuptake

Adverse rxns – **vision loss in 30% of pts**. Also headache, somnolence, fatigue, dizziness.
Used as last resort for infantile spasms.

Also for refractory complex partial seizures

Front 270

MOA of Rufinamide (Benzel)?

tox?

use?

Back 270

Action on sodium channels

Adverse rxns – somnolence, vomiting

Used to treat Lennox-Gastaut syndrome

Front 271

lamotrigene use?

MOA?

**

Back 271

Adjunct drugs for partial seizures
approved add-on drug

acts by slowing recovery in Na+ channels, inhibiting voltage gated Ca channels, and perhaps by inhibiting glutamate release

also:probably block L-type calcium channels to some extent

Front 272

gabapentin use?

Back 272

Adjunct drugs for partial seizures
approved add-on drug

act at a subunit of voltage-gated calcium channels to decrease depolarization-induced calcium influx, which decreases release of excitatory neurotransmitters (glutamate).

also:probably block L-type calcium channels to some extent

Front 273

topiramate use?

Back 273

Adjunct drugs for partial seizures; approved add-on drug; treats TREMORS and prevents migraines

mechanism may involve block of sodium channels and AMPA/Kainate receptors. Other possible uses include treatment of tremors and prevention of migraine.

Front 274

Gabapentin use?

Back 274

effective in treatment of neuropathic pain and fibromyalgia

Front 275

pregabalin use?

Back 275

effective in treatment of neuropathic pain and fibromyalgia

Front 276

Side effects of Lamotrigene? what was the use of this again?

Back 276

Most common – weakness, diplopia, ataxia, nausea, irritability, life-threatening rash, Stevens-Johnson syndrome. Also inhibits carbarmazepine metabolism. Increased risk of cleft lip/palate(?)

Adjunct drugs for partial seizures
approved add-on drug

act at a subunit of voltage-gated calcium channels to decrease depolarization-induced calcium influx, which decreases release of excitatory neurotransmitters (glutamate).

Front 277

Common side effects of Topiramate?

Back 277

. Slight increase in incidence of kidney stones

Front 278

What is the major drug interaction of benzodiapepines?

Back 278

Potentiation of CNS depressant effects of antipsychotics, tricyclic antidepressants, sedative hypnotics, alcohol

Front 279

Zonisamide should be avoided in what kind of pts?

Back 279

Avoid in patients allergic to sulfonamides

Front 280

What is status epilepticus?

some causes?

Back 280

A state of continuous seizure activity without recovery of consciousness. Generalized tonic-clonic type is life-threatening (10% fatal)

Some causes – sudden withdrawal of CNS depressants or antiepileptic agents, or drug poisoning

Front 281

drug therapy tx for status epilepticus?

Back 281

IV diazepam or lorazepam followed by maintenance therapy of slow IV infusion of phenytoin (fosphenytoin) or phenobarbital

Front 282

What are the Drugs of Choice for a Primary Generalized Tonic-Clonic (Grand Mal)

**

Back 282

Valproate
Carbamazepine
Phenytoin

Front 283

What are the Drugs of Choice for Partial Including Secondarily Generalized seizures?

Back 283

Carbamazepine
Penytoin
Valproate

Front 284

What are the Drugs of Choice for Absence (Petit Mal) seizures?

Back 284

Ethosuximide
Valproate

Front 285

What are the Drugs of Choice for Atypical Absence, Myoclonic, Atonic seizures?

Back 285

Valproate

Front 286

important side effect of Tiagabine?

***

Back 286

Off-label use in patients without epilepsy may cause seizures.

Front 287

what is always found as a symptom of epilepsy? if epilepsy is untreated what 2 things might this lead to?

Back 287

Abnormal and excessive EEG discharges (always) – if untreated, may lead to anoxic brain damage. Also danger of “excitotoxicity”. (will just keep happening over and over)

Front 288

Spread of epileptic activity to affect both hemispheres
Loss of consciousness
Motor pattern similar to “generalized seizures”

type of seizure?

Back 288

Partial seizures secondarily generalized

will start as a localized partial seizure, then it will become a generalized tonic clonic

Front 289

Consciousness preserved
Localized EEG spikes
Various manifestations of motor or sensory disturbances related to specific cortical area affected

type of seizure?

Back 289

simple partial

Front 290

Disturbed consciousness
Focal EEG spikes originate from temporal lobe
Confused behavior, automatisms, sensory, emotional distortions

type of seizure?

Back 290

Complex partial

Front 291

Major convulsion typified by tonic contraction, conic jerking, and a prolonged post-seizure (postictal) depression of CNS activity
Loss of consciousness
Generalized high voltage EEG spikes

type of seizure?

Back 291

Generalized seizures
Convulsive type:

Tonic-clonic (Grand Mal)

Front 292

this is a disease in which you have mental retardation, and a mirage of seizure types (tonic clonic, absence, etc)

Back 292

Lennox-Gastaut Syndrome

Front 293

What is status epilepticus?

Back 293

repeated seizures

one seizure leads to another

medical emergency

Front 294

3 mechanisms of antieplieptic drugs?

Back 294

Limit sustained repetitive firing of neurons by slowing rate of recovery in Na+ - channels

Enhancing GABA-mediated synaptic inhibition

Limit activation of CA++ - channels

Front 295

this drug Prevents seizures without producing general CNS depression, by reducing the rate at which Na channels recover from inactivation, thus slowing firing

Back 295

Phenytoin

Front 296

Brief, abrupt loss of consciousness
With or without clonic motor activity
Generalized 3 per second spike and wave EEG activity

type of seizure?

Back 296

Generalized
Nonconvulsive type

Absence

Front 297

MOA of phenytoin?

Back 297

reduce rate at which Na+ channels recover from inactivation, thereby slowing firing.

note: Prevent seizures without producing general CNS depression

Front 298

describe how phenytoin is metabolized.

Also, how is 90% of it found in the body? what does this imply?

Back 298

98% metabolized by liver microsomal enzymes; zero order (no matter the dose it can only be cleared at a certain rate) elimination kinetic at therapeutic concentration (1st order at low doses)

90% plasma protein bound--if displaced you will have loads of side effects

Front 299

what is an important tox of Phenytoin assoc with administration of the drug?

Back 299

Acute toxicity after rapid IV administration – cardiovascular collapse and/or CNS depression

note: Fosphenytoin (a soluble pro-drug of phenytoin) decreases, but does not eliminate, this problem.

Front 300

chronic side effect of Phenytoin? (2 key)

Back 300

behavioral changes,
***gingival hyperplasia, peripheral neuropathy,
osteomalacia***
GI-disturbances,
megaloblastic anemia (decreased vitamin B12), hirsutism, depression of serum folate and vitamin K level.

Front 301

What drug class is Phenytoin?

Back 301

D

It can be used if you have no choice, but it is teratogenic

Front 302

what happens with sudden withdrawal of Phenytoin

Back 302

STATUS EPILEPTICUS

causes tons of seizures!!

make sure if you need to change the drug that you SLOWLY take them off phenytoin

Front 303

Chloramphenicol, dicumerol, cimetidine, and sulfonamides have what effect on Phenytoin?

Back 303

Inhibit its metabolism

What were those drugs again? There were 4 of them..yeah slack ass, flip it over for the answer, and if you didn't remember, mark that shit wrong.

Front 304

what effect will Phenytoin have on the CYP system?

Back 304

Induces hepatic drug metabolizing enzymes (CYP1A2, CYP2C9, CYP2C19, CYP2D6, CYP3A4)

Front 305

Dicumerol, salicylates, BZDs have what effect on phenytoin?

Back 305

displace from protein binding sites to increase plasma level

Front 306

Acutely, what effect do phenobarbital and ethanol have on phenytoin?

Chronically?

Back 306

compete for the same metabolic sites leading to an INCREASE in plasma phenytoin (inhibit metabolism)

Chronically, phenobarbital is a classic inducer of drug metabolizing enzymes. So chronically, both phenobarbital and ethanol increase metabolism of Phenytoin

Front 307

what effect does phenytoin have on OCP? why is this especially important

Back 307

it will decrease their effectiveness

this is important because it is also a teratogen, so if you get pregnant while on it, you are harming the baby

Front 308

therapeutic use of Phenytoin?

Back 308

Effective for all types of seizures except absence
Tonic-clonic-seizures in adults or older children
Used in status epilepticus
Wound healing

Front 309

what effect does Carbamazepine have on phenytoin

Back 309

enhances phenytoin metabolism, decreasing plasma levels

Front 310

what effect does phenobarbital have on drug metabolizing enzymes?

Back 310

induces drug metabolizing enzymes

Front 311

what 2 pts (think demographics) would you want to avoid phenobarbital in? why?

Back 311

hyperactivity (children)

confusion in elderly patients, decreased cognitive ability

Front 312

what drug can Precipitate acute intermittent porphyria

Back 312

Phenobarbital

penetrate the brain and cause death of neurons

Front 313

what category drug is phenobarbital?

Back 313

Potentially teratogenic (Pregnancy Category D)

Front 314

MOA of Phenobarbital?

Back 314

Potentiates GABA inhibitory transmission and decreases glutamate excitation

note: can cause sedation, but can be used at low doses so its not a big deal

Front 315

MOA of Primidone

Back 315

Structurally similar to phenobarbital
Also has similar pharmacology but less potent-prevents Na channel recovery-->inhibition

Front 316

aplastic anemia, agranulocytosis can be a side effect of what anti-seizure drug?

Back 316

Carbamazepine

Front 317

if you are Asian, and you need to go on Carbamazepine, what should you have done? why?

Back 317

FDA recommends genetic testing before starting therapy in patients of Asian descent.

Hypersensitivity reactions (SJS) in Asians with HLA-B* 1502 gene

Front 318

Oxcarbazepine works like Carbamazepine (how was this agian?)...what is different about it?

Back 318

slows recovery of voltage-sensitive Na+ channels (also like phenytoin)

less likely to cause SJS and agranulocytosis

Front 319

Carbamazepine MOA?

Back 319

Anticonvulsant effects resemble phenytoin (slows recovery of voltage-sensitive Na+ channels).

note: Structurally related to tricyclic antidepressants--so it takes a while to start working

Front 320

what anti-seizure drug can cause Parkinsonism?

Back 320

Ethosuximide

Front 321

MOA of Valproic acid?

Back 321

acts via several mechanisms. Blocks recovery in Na+ channels, hyperpolarizes cell via an action on K+ channels and perhaps an action on GABA systems (inhibition)

Front 322

Valproic acid is used for what kind of seizures?

Back 322

approved for absence and complex partial seizures in U.S. May also be useful in treatment of grand mal, myoclonic and febrile seizures. Also used in patients who don’t respond to any drug, regardless of seizure type

pretty much all of them!
It is the Amiodarone of seizure drugs

Front 323

biggest potential tox assoc with Valproic Acid?

which population is this risk highest in?

Back 323

Hepatotoxicity

especially in kids under 2

Front 324

Ethosuximide MOA?

Back 324

Increases neuronal refractory period by decreasing conductance in Ca++ channels (T current).

T currents in thalamic neurons important in generation of absence seizures

Front 325

why are Benzodiazepines typically not used for tx of seizures?

MOA

Back 325

tolerance builds up quick

Suppression of seizure spread in the cortex, thalamus, and limbic structures
May facilitate GABA mediated pre- and post-synaptic inhibition

Front 326

what is the difference btw a bizarre and non-bizarre delusion?

Back 326

Delusion-erroneous beliefs that usually involve a misinterpretation of perceptions or experiences

Bizarre-clearly implausible, not understandable, and not derived from ordinary life experiences (guy thinks someone took all his organs while he slept even though he has no scars)

Non bizarre- involve situations that can conceivably occur in real life

Front 327

Felbamate (Felbatol) – was approved for use in....? What is a stipulation of its use?

Back 327

adults with partial seizures and in children with seizures associated with Lennox-Gastaut Syndrome

can only be gotten for pts who this is the ONLY DRUG THAT WILL WORK...people have to sign a waiver to use it because it causes high incidence of aplastic anemia, and liver failure

Front 328

MOA of Vigabatrin?

side effects?

use?

Back 328

Inhibits GABA degradation (GABA transaminase) and reuptake

Adverse rxns – **vision loss in 30% of pts**. Also headache, somnolence, fatigue, dizziness.
Used as last resort for infantile spasms.

Also for refractory complex partial seizures

Front 329

MOA of Rufinamide (Benzel)?

tox?

use?

Back 329

Action on sodium channels

Adverse rxns – somnolence, vomiting

Used to treat Lennox-Gastaut syndrome

Front 330

lamotrigene use?

MOA?

**

Back 330

Adjunct drugs for partial seizures
approved add-on drug

acts by slowing recovery in Na+ channels, inhibiting voltage gated Ca channels, and perhaps by inhibiting glutamate release

also:probably block L-type calcium channels to some extent

Front 331

gabapentin use?

Back 331

Adjunct drugs for partial seizures
approved add-on drug

act at a subunit of voltage-gated calcium channels to decrease depolarization-induced calcium influx, which decreases release of excitatory neurotransmitters (glutamate).

also:probably block L-type calcium channels to some extent

Front 332

topiramate use?

Back 332

Adjunct drugs for partial seizures; approved add-on drug; treats TREMORS and prevents migraines

mechanism may involve block of sodium channels and AMPA/Kainate receptors. Other possible uses include treatment of tremors and prevention of migraine.

Front 333

Gabapentin use?

Back 333

effective in treatment of neuropathic pain and fibromyalgia

Front 334

pregabalin use?

Back 334

effective in treatment of neuropathic pain and fibromyalgia

Front 335

Side effects of Lamotrigene? what was the use of this again?

Back 335

Most common – weakness, diplopia, ataxia, nausea, irritability, life-threatening rash, Stevens-Johnson syndrome. Also inhibits carbarmazepine metabolism. Increased risk of cleft lip/palate(?)

Adjunct drugs for partial seizures
approved add-on drug

act at a subunit of voltage-gated calcium channels to decrease depolarization-induced calcium influx, which decreases release of excitatory neurotransmitters (glutamate).

Front 336

Common side effects of Topiramate?

Back 336

. Slight increase in incidence of kidney stones

Front 337

Zonisamide should be avoided in what kind of pts?

Back 337

Avoid in patients allergic to sulfonamides

Front 338

What is status epilepticus?

some causes?

Back 338

A state of continuous seizure activity without recovery of consciousness. Generalized tonic-clonic type is life-threatening (10% fatal)

Some causes – sudden withdrawal of CNS depressants or antiepileptic agents, or drug poisoning

Front 339

important side effect of Tiagabine?

***

Back 339

Off-label use in patients without epilepsy may cause seizures.

Front 340

drug therapy tx for status epilepticus?

Back 340

IV diazepam or lorazepam followed by maintenance therapy of slow IV infusion of phenytoin (fosphenytoin) or phenobarbital

Front 341

What are the Drugs of Choice for Partial Including Secondarily Generalized seizures?

Back 341

Carbamazepine
Penytoin
Valproate

Front 342

What are the Drugs of Choice for Atypical Absence, Myoclonic, Atonic seizures?

Back 342

Valproate

Front 343

What are the Drugs of Choice for Absence (Petit Mal) seizures?

Back 343

Ethosuximide
Valproate

Front 344

What are the Drugs of Choice for a Primary Generalized Tonic-Clonic (Grand Mal)

**

Back 344

Valproate
Carbamazepine
Phenytoin

Front 345

what is always found as a symptom of epilepsy? if epilepsy is untreated what 2 things might this lead to?

Back 345

Abnormal and excessive EEG discharges (always) – if untreated, may lead to anoxic brain damage. Also danger of “excitotoxicity”. (will just keep happening over and over)

Front 346

Disturbed consciousness
Focal EEG spikes originate from temporal lobe
Confused behavior, automatisms, sensory, emotional distortions

type of seizure?

Back 346

Complex partial

Front 347

Consciousness preserved
Localized EEG spikes
Various manifestations of motor or sensory disturbances related to specific cortical area affected

type of seizure?

Back 347

simple partial

Front 348

Spread of epileptic activity to affect both hemispheres
Loss of consciousness
Motor pattern similar to “generalized seizures”

type of seizure?

Back 348

Partial seizures secondarily generalized

will start as a localized partial seizure, then it will become a generalized tonic clonic

Front 349

Brief, abrupt loss of consciousness
With or without clonic motor activity
Generalized 3 per second spike and wave EEG activity

type of seizure?

Back 349

Generalized
Nonconvulsive type

Absence

Front 350

Major convulsion typified by tonic contraction, conic jerking, and a prolonged post-seizure (postictal) depression of CNS activity
Loss of consciousness
Generalized high voltage EEG spikes

type of seizure?

Back 350

Generalized seizures
Convulsive type:

Tonic-clonic (Grand Mal)

Front 351

this is a disease in which you have mental retardation, and a mirage of seizure types (tonic clonic, absence, etc)

Back 351

Lennox-Gastaut Syndrome

Front 352

What is status epilepticus?

Back 352

repeated seizures

one seizure leads to another

medical emergency

Front 353

3 mechanisms of antieplieptic drugs?

Back 353

Limit sustained repetitive firing of neurons by slowing rate of recovery in Na+ - channels

Enhancing GABA-mediated synaptic inhibition

Limit activation of CA++ - channels

Front 354

MOA of phenytoin?

Back 354

reduce rate at which Na+ channels recover from inactivation, thereby slowing firing.

note: Prevent seizures without producing general CNS depression

Front 355

describe how phenytoin is metabolized.

Also, how is 90% of it found in the body? what does this imply?

Back 355

98% metabolized by liver microsomal enzymes; zero order (no matter the dose it can only be cleared at a certain rate) elimination kinetic at therapeutic concentration (1st order at low doses)

90% plasma protein bound--if displaced you will have loads of side effects

Front 356

this drug Prevents seizures without producing general CNS depression, by reducing the rate at which Na channels recover from inactivation, thus slowing firing

Back 356

Phenytoin

Front 357

what effect will Phenytoin have on the CYP system?

Back 357

Induces hepatic drug metabolizing enzymes (CYP1A2, CYP2C9, CYP2C19, CYP2D6, CYP3A4)

Front 358

what is an important tox of Phenytoin assoc with administration of the drug?

Back 358

Acute toxicity after rapid IV administration – cardiovascular collapse and/or CNS depression

note: Fosphenytoin (a soluble pro-drug of phenytoin) decreases, but does not eliminate, this problem.

Front 359

chronic side effect of Phenytoin? (2 key)

Back 359

behavioral changes,
***gingival hyperplasia, peripheral neuropathy,
osteomalacia***
GI-disturbances,
megaloblastic anemia (decreased vitamin B12), hirsutism, depression of serum folate and vitamin K level.

Front 360

what happens with sudden withdrawal of Phenytoin

Back 360

STATUS EPILEPTICUS

causes tons of seizures!!

make sure if you need to change the drug that you SLOWLY take them off phenytoin

Front 361

What drug class is Phenytoin?

Back 361

D

It can be used if you have no choice, but it is teratogenic

Front 362

Acutely, what effect do phenobarbital and ethanol have on phenytoin?

Chronically?

Back 362

compete for the same metabolic sites leading to an INCREASE in plasma phenytoin (inhibit metabolism)

Chronically, phenobarbital is a classic inducer of drug metabolizing enzymes. So chronically, both phenobarbital and ethanol increase metabolism of Phenytoin

Front 363

Dicumerol, salicylates, BZDs have what effect on phenytoin?

Back 363

displace from protein binding sites to increase plasma level

Front 364

Chloramphenicol, dicumerol, cimetidine, and sulfonamides have what effect on Phenytoin?

Back 364

Inhibit its metabolism

What were those drugs again? There were 4 of them..yeah slack ass, flip it over for the answer, and if you didn't remember, mark that shit wrong.

Front 365

what effect does Carbamazepine have on phenytoin

Back 365

enhances phenytoin metabolism, decreasing plasma levels

Front 366

what effect does phenytoin have on OCP? why is this especially important

Back 366

it will decrease their effectiveness

this is important because it is also a teratogen, so if you get pregnant while on it, you are harming the baby

Front 367

why are Benzodiazepines typically not used for tx of seizures?

MOA

Back 367

tolerance builds up quick

Suppression of seizure spread in the cortex, thalamus, and limbic structures
May facilitate GABA mediated pre- and post-synaptic inhibition

Front 368

biggest potential tox assoc with Valproic Acid?

which population is this risk highest in?

Back 368

Hepatotoxicity

especially in kids under 2

Front 369

Valproic acid is used for what kind of seizures?

Back 369

approved for absence and complex partial seizures in U.S. May also be useful in treatment of grand mal, myoclonic and febrile seizures. Also used in patients who don’t respond to any drug, regardless of seizure type

pretty much all of them!
It is the Amiodarone of seizure drugs

Front 370

MOA of Valproic acid?

Back 370

acts via several mechanisms. Blocks recovery in Na+ channels, hyperpolarizes cell via an action on K+ channels and perhaps an action on GABA systems (inhibition)

Front 371

what anti-seizure drug can cause Parkinsonism?

Back 371

Ethosuximide

Front 372

Ethosuximide MOA?

Back 372

Increases neuronal refractory period by decreasing conductance in Ca++ channels (T current).

T currents in thalamic neurons important in generation of absence seizures

Front 373

Oxcarbazepine works like Carbamazepine (how was this agian?)...what is different about it?

Back 373

slows recovery of voltage-sensitive Na+ channels (also like phenytoin)

less likely to cause SJS and agranulocytosis

Front 374

if you are Asian, and you need to go on Carbamazepine, what should you have done? why?

Back 374

FDA recommends genetic testing before starting therapy in patients of Asian descent.

Hypersensitivity reactions (SJS) in Asians with HLA-B* 1502 gene

Front 375

aplastic anemia, agranulocytosis can be a side effect of what anti-seizure drug?

Back 375

Carbamazepine

Front 376

Carbamazepine MOA?

Back 376

Anticonvulsant effects resemble phenytoin (slows recovery of voltage-sensitive Na+ channels).

note: Structurally related to tricyclic antidepressants--so it takes a while to start working

Front 377

MOA of Primidone

Back 377

Structurally similar to phenobarbital
Also has similar pharmacology but less potent-prevents Na channel recovery-->inhibition

Front 378

what drug can Precipitate acute intermittent porphyria

Back 378

Phenobarbital

penetrate the brain and cause death of neurons

Front 379

what category drug is phenobarbital?

Back 379

Potentially teratogenic (Pregnancy Category D)

Front 380

what 2 pts (think demographics) would you want to avoid phenobarbital in? why?

Back 380

hyperactivity (children)

confusion in elderly patients, decreased cognitive ability

Front 381

what effect does phenobarbital have on drug metabolizing enzymes?

Back 381

induces drug metabolizing enzymes

Front 382

MOA of Phenobarbital?

Back 382

Potentiates GABA inhibitory transmission and decreases glutamate excitation

note: can cause sedation, but can be used at low doses so its not a big deal

Front 383

therapeutic use of Phenytoin?

Back 383

Effective for all types of seizures except absence
Tonic-clonic-seizures in adults or older children
Used in status epilepticus
Wound healing

Front 384

PT comes in with headache or other acute neuro findings in the ER

What is the first imaging study you want to use?

******

Back 384

NON CONTRAST CT

Front 385

in Schizophrenia, you need to have 2 or more of the following symptoms for at least 1 month...what are these sx? (5)

Back 385

Delusions
Hallucinations
Disorganized speech
Disorganized or catatonic behavior
Negative symptoms (e.g., flat affect, avolition)

Front 386

what is the difference btw positive and negative symptoms?

examples?

Back 386

Positive=Present and shouldn’t be
Delusions
Hallucinations
Disorganized Speech
Disorganized Behavior

Negative=
Missing and should be there
Flattened Affect
Alogia-impoverished speech
Avolition- can’t initiate or persist in goal-directed activities
Anhedonia- loss of interest or pleasure

Front 387

Delusions
Hallucinations
Disorganized speech
Disorganized or catatonic behavior
Negative symptoms (e.g., flat affect, avolition)

describes what kind of Schizophrenia?

Back 387

Paranoid

Front 388

Disorganized Speech
Disorganized Behavior
Flat/Inappropriate Affect
Active, but aimless
Little contact w/reality
Does not meet criteria for Catatonic type.

describes what kind of Schizophrenia?

Back 388

Disorganized

Front 389

Motoric immobility
Excessive motor activity
Extreme negativism or mutism
Peculiarities of voluntary movement as evidenced by posturing
Echolalia or Echopraxia

describes what kind of Schizophrenia?

Back 389

Catatonic

Front 390

What is one of the worst prognostic factors in Schizophrenia?

Back 390

Assaultiveness

Front 391

Acute onset, later age of onset, mood symptoms present, and no psychiatric history are what type of prognostic factors for Schizophrenia?

Back 391

Good prognostic factor

Front 392

How is Schizophreniform different from Schizophrenia?

***TEST

Back 392

Schizophreniform:

Essential features are identical to those of Schizophrenia except for two differences:
Total duration of illness is at least 1 month but less than 6 months.
Impaired social or occupational functioning is not required

Front 393

What is a delusional disorder?

Back 393

Nonbizarre delusions-1 month
Criterion A for Schizophrenia never been met
Functioning is not markedly impaired
Behavior is not obviously odd or bizarre
If mood episodes have occurred concurrently with delusions, their total duration has been brief relative to the duration of the delusional periods.

example: Erotomanic- think someone of high stature in love with you

Grandiose: you have a connection with god

Front 394

What is Shared Psychotic Disorder (Folie à Deux)

Back 394

A delusion develops in an individual in the context of a close relationship with another person, who has an already-established delusion.
The delusion is similar in content to that of the person who already has the established delusion.

seen in dependent child parent relationship

Front 395

Prominent hallucinations or delusions
Evidence (hx, physical exam, lab findings) that the disturbance is the direct physiological consequence of a GMC.
Not better accounted for by another mental disorder.
Does not occur exclusively during a delirium.

Back 395

Psychotic Disorder Due to a General Medical Condition

Front 396

Substance-Induced Psychotic Disorder

define it (pretty simple)

Back 396

Prominent hallucinations or delusions. Note: Do not include hallucinations if the person has insight that they are substance induced.
There is evidence (hx, physical exam, lab findings) that
The symptoms developed during, or within a month of, Substance Intoxication or Withdrawal
Medication use is etiologically related to the disturbance
Not better accounted for by a psychotic disorder that is not substance induced.
Does not occur exclusively during a delirium.

Front 397

What is the key to Schizoaffective disorder

Back 397

An uninterrupted period of illness during which, at some time, there is either a Major Depressive Episode, a Manic Episode, or a Mixed Episode concurrent with symptoms that meet criteria A for Schizophrenia

**During the same period of illness there have been delusions or hallucinations for at least 2 weeks in the absence of prominent mood symptoms.**

Front 398

What is one key reason why CT is better than MRI?

***

Back 398

it is good for quick evaluation of acute bleeding: Excellent for acute intracranial hemorrhage


(also, MRI might require pre-approval for access)

Front 399

where do epidural bleeds most commonly occur

Back 399

fronto-temporal area

Front 400

What is this? Where is it occuring

Back 400

Epidural bleed

frontal lobe

Front 401

what are the Hounsfield units for:
water
bone
air
blood
Fat

Back 401

0 = water density
+ 1000 = bone
-1000 = air
+ 60 – +80 = blood
- 5 to –12 = fat

Front 402

T1 vs T2 on MRI?

Back 402

T1 = the “anatomic” sequence
T2 = the “pathology” sequence


On T1 water is dark black
On T2 water is bright white

Front 403

T1 or T2?
What 4 things are black on this type of image?

Back 403

T1

Cortical bone
Bone
Moving blood
Fluid

Front 404

T1 or T2

Back 404

T2

Front 405

Which study, MRI or CT can detect ischemic injusry 24-36 hours earlier than CT?

Back 405

MRI

Front 406

This imaging study has no bone artifact (especially in the posterior fossa), and is better at assessment of tumors, white matter, and disease/early edema?

Back 406

MRI

Front 407

Which imaging study (CT or MRI) has unchanged multi-planar capability?

**

Back 407

MRI

Front 408

A 26 y/o patient presents to the ED after being struck by a softball bat. You want to rule our intracranial hemorrhage. You order:
A. CT
B. MRI

Back 408

CT (no contrast)

Cranial bone will be white

Front 409

Which modality is best for evaluating white matter disease?
A. CT
B. MRI

Back 409

MRI

Front 410

CT or MRI?

Back 410

MRI

Front 411

type of image? Path?

Back 411

Front 412

what normally causes an epidural hematoma?

Subdural?

Back 412

epi: skull fracture

sub: direct blow to the head w change in lvl of conciousness

Front 413

What happens in shear injuries?

Back 413

diffuse axonal injury

can be due to rotational injury (not necessarily blow to a head)

Front 414

path?

will it cross sutural lines?

what blood vessel causes it?

Back 414

epidural hematoma

DOESN'T CROSS SUTURAL LINES

assoc with skull fracture

due to arterial tear (middle meningeal artery)

Front 415

epidural hematoma vs subdural hematoma

which crosses suture lines?

Back 415

epidural hematoma :DOESN'T CROSS SUTURAL LINES

Sub: does

Front 416

for an epidural hematoma, at what amount of bleeding do you have to consider operative tx?

Back 416

less than 5mm: NON OPERATIVE

greater than 5mm: drain

Front 417

Back 417

epidural hematoma in kid

Front 418

describe some of the characteristics of subdural hematomas (shape, blood source, who it happens to)

Back 418

crecentic,
bridging veins,
old people who fall

Front 419

SDH more common with ____ while

EDH more common with _____

(cause of injury)

Back 419

SDH more common with falls
EDH more common with MVA

Front 420

Back 420

Subdural Hematoma

Front 421

this type of bleed is Spread over a larger area, limited by the falx and the tentorium

Back 421

Subdural Hematoma

Front 422

there are 3 densities seen on CT with a SDH..what are they and what are the time frames assoc with them

Back 422

Acute 0 to 3-4 days hyperdense

Subacute 3 to 20 days isodense

Chronic > 20 days hypodense

Front 423

Back 423

SDH

Front 424

Back 424

epidural hematoma

Front 425

this type of injury Occur with rapid acceleration/deceleration
Usually involves large WM tracts: corpus callosum, brainstem and deep white matter
Occurs at gray-white matter interface due to slight differences in mass
Minor differences in tissue inertia

Back 425

Shear Injuries

Front 426

Back 426

Intraparenchymal hemorrhage from shear injuries

Front 427

Back 427

MRI showing
intra parenchymal
hemorrrhage

Front 428

Left Middle Cerebral Artery Infarction with midline shift:

what is the most useful landmark for measuring midline shift?

Back 428

Most useful landmark for measuring midline shift: Septum Pellucidum

note:This type of edema is called cytotoxic edema


cytotoxic edema visible on CT and MRI

Front 429

what is key to remember about cytotoxic edema?

Back 429

Affects both gray and white matter

Front 430

History: stroke symptoms

Back 430

cytotoxic edema

Front 431

44 y/o female
New onset seizures
Fell, hit head

hemorrhage or tumor?

Back 431

This is an enhancing
tumor with edema
confined to the
white matter (vasogenic
edema)

Front 432

vasogenic edema is found where?

cytogenic?

causes?
***

Back 432

vasogenic edema: CONFINED TO WHITE MATTER (tumor or infection)

where cytogenic could be in white or gray (infarct or stroke)

Front 433

SUMMARY SLIDE

CT is 1st in the emergent setting to rule out hemorrhage.
MRI is more sensitive for edema, tumors, infections and white matter disease.
Be able to distinguish SDH from EDH.

Be able to distinguish cytotoxic (stroke) from vasogenic (tumor or infection)

Back 433

CT is 1st in the emergent setting to rule out hemorrhage.--FAST

MRI is more sensitive for edema, tumors, infections and white matter disease.--CONTRAST MAKES IT EVEN MORE SENSITIVE

Be able to distinguish SDH from EDH.--SDH more cresentic, covers further distance, not confined by sutures

Be able to distinguish cytotoxic (stroke-effects both grey and white matter) from vasogenic (tumor or infection--just in white matter)

Front 434

Define the purpose of the Mental Status Exam

(o)

Back 434

Examination of neuropsychiatric functioning

Comprehensive description of a patient’s appearance, behavior, thinking, feeling, etc.

Meaningful only in the context of other baseline data (e.g., history, physical / neurologic exam)

Ex. Tearful patient may be reacting to stress or pain, be depressed, have neurological disease, or other cause

The MSE ≠ MMSE

Front 435

Explain how the Mental Status Exam is performed

(o)

Back 435

By observation
i.e., many areas assessed while obtaining the history
e.g., speech, behavior, affect

By asking relevant questions to elicit symptoms that usually cannot be observed
e.g., hallucinations, paranoid ideation, mood

By performing cognitive screening tests
e.g., MMSE, other bedside tests

Front 436

Identify the major components of the Mental Status Exam

(o)

Back 436

General appearance, attitude (toward the examiner), and behavior

Motor activity (overactivity, underactivity, abnormal movements, catatonia)

Speech

Mood and affect

Thought process (form) and content

Perception

Cognitive function

Insight and judgment

Front 437

What is the difference btw catatonia, catalepsy, and cataplexy?

***

Back 437

Catatonia: motor symptom: Dx by any two of the following: a. motor immobility, b. motor excitement, c. negativism or mutism, d. posturing, stereotypies or mannerism, e. echolalia (parroting) or echopraxia (miming)

Catalepsy: feature of catatonia, waxy flexibility (muscular rigidity and fixity of posture regardless of external stimuli, as well as decreased sensitivity to pain.)

Cataplexy: sudden loss of muscle tone leading to collapse, related to narcolepsy

Front 438

describe the following mood/affects

Constricted/Restricted (flat)
Labile
Expansive

Back 438

Front 439

define the following disturbances in thought process:

Circumstantiality
Tangentiality
Looseness of associations
Verbigeration
“Word Salad”
Neologisms
Clang associations

Back 439

Circumstantiality (excessive detail but gets to point)
Tangentiality (never gets to point of message)
Looseness of associations (ideas loosely connected)
Verbigeration (meaningless repetition of words/phrases)
“Word Salad” (incoherent collection of words/phrases)
Neologisms (creation of new words)
Clang associations (rhyming/punning; no logical connection)

Front 440

describe circumstantial thought

*board fodder

Back 440

Front 441

Describe Tangential thought

*

Back 441

Front 442

Describe flight of ideas

*****

Back 442

Front 443

what is the difference between hypnagogic and hypnopompic hallucinations? are these pathological or non pathological?

***

Back 443

Nonpathological: hypnagogic (when you go to sleep), hypnopompic (when you wake up)

Pathological: Auditory, visual, tactile, olfactory, gustatory, somatic

Front 444

what are
Perceptual disturbances? (4)

****

Back 444

include:
hallucinations,
derealization (where I am at doesn't feel real, i am floating in the space I am in),
depresonalization (feel like you are floating outside of yourself),
déjà vu

Front 445

What are illusions (with respect to perceptual disturbances?)

**

Back 445

misinterpretation of real stimuli

Front 446

on the MMSE what score points to cognitive problems?

Back 446

less than 20

Front 447

Recognize the difference between the Folstein MMSE and the mental status examination

(o)

note: answer extrapolated from Wiki

Back 447

The mini–mental state examination (MMSE) or Folstein test is a brief 30-point questionnaire test that is used to screen for cognitive impairment. It is commonly used in medicine to screen for dementia. It is also used to estimate the severity of cognitive impairment at a given point in time and to follow the course of cognitive changes in an individual over time, thus making it an effective way to document an individual's response to treatment.

Mental status is way more in depth

Front 448

One-half of all lifetime cases of mental illness begin by age...

Back 448

14

three-quarters by age 24.

Front 449

Define psychiatric illness

(o)

Back 449

Any of various conditions characterized by impairment of an individual's normal cognitive, emotional, or behavioral functioning, and caused by social, psychological, biochemical, genetic, or other factors, such as infection or head trauma.

Also called emotional illness, mental illness, mental disorder.

Front 450

what is the difference btw primary and secondary psychiatric disorders?

Back 450

Primary psychiatric disorders
No underlying medical disorder to account for the diagnosis
Not caused by medication
Not caused by substance abuse or withdrawal

Secondary psychiatric disorders
Due to a medical condition
Due to a medication(s)
Due to substance abuse or withdrawal

Front 451

Identify the domains of psychiatric illness (6)

(o)

Back 451

Some People Can Eat Bad Eggs

Front 452

Identify the classification systems used to diagnose psychiatric illness

(o)

Back 452

Diagnostic and Statistical Manual of Mental Disorders, 4th Edition, Text Revision (DSM-IV-TR)
Published by the American Psychiatric Association (2000)
Most recent update of criteria: DSM-IV (1994)
Current DSM bases diagnostic codes on ICD-9-CM

International Classification of Diseases, 9th Revision, Clinical Modification (ICD-9-CM)
Published by the US government in 1979
Official coding system in the US for all diseases (Ch.5 Mental Dis)
Revises codes annually but has not kept up with diagnostic changes in the DSM

Front 453

What is an important thing to remember about the DSM IV and diagnosis it gives

****

Back 453

Contains a listing of psychiatric disorders, diagnostic codes, and criteria for each disorder

Also contains text with information about the disorder (e.g., associated features, prevalence, course, familial patterns, age-,culture- and gender-specific features, differential diagnosis)

***Does NOT contain information about presumed etiology or treatment****

Front 454

Describe the DSM-IV-TR multiaxial diagnostic system

(o)

Back 454

Axis I: Clinical Disorders (psychiatric)

Axis II: Personality disorders and traits, mental retardation, prominent defense mechanisms

Axis III: General Medical Conditions

Axis IV: Psychosocial and environmental problems (stressors)

Axis V: Global Assessment of Functioning (1-100 scale)


EXAMPLE
Axis I 296.22 Major Depressive Disorder, single episode, moderate
305.00 Alcohol Abuse

Axis II 301.6 Dependent Personality Disorder

Axis III Hepatitis B

Axis IV Threat of job loss

Axis V GAF = 45 (current)

Front 455

Almost all psychiatric diagnoses are made...

Back 455

CLINICALLY

Front 456

Identify the components of a psychiatric evaluation

(o)

Back 456

History (Identifying Data/Reason for admission or evaluation, Past Psychiatric History, Substance History, Mental Status Exam)




Exam (neuro/mental)

Radiological and lab

Front 457

SUMMARY SLIDE FOR LECTURE 2 OF PSYCH

Back 457

Psychiatric symptoms can be seen in many conditions

The etiology of most primary psychiatric disorders is not known

Diagnosis is based primarily on history and mental status exam

Physical exam, neurologic exam, lab, and other studies are performed to rule out possible non-psychiatric causes of psychiatric symptoms

The DSM-IV-TR increases reliability of diagnosis

Front 458

explain why most mechanisms of action given the neuropharmacologic drugs are approximations.

(o)

Back 458

Entire mechanism is generally unknown. Approximations of

CNS mechanism made from information regarding effects of drugs in isolated systems.
CNS as a “Black Box”
Extrapolation from biochemical events to behavior is difficult.

Front 459

define what is meant by specific mechanism of action.

(o)

Back 459

A specific drug action affects a recognized protein target, i.e., a receptor, an ion channel, an enzyme, or a transporter.

Front 460

describe the various events in synaptic transmission which might be altered by drugs

(o)

Back 460

Front 461

describe the various events in synaptic transmission which might be altered by drugs

(o)

Front 462

describe the various events in synaptic transmission which might be altered by drugs

(o)

Front 463

what is the difference between a neurotransmitter and a neuromodulator?

(o)

Back 463

Neurotransmitter – a substance which is released locally and causes a change in post-synaptic potential.

Neuromodulator – a substance which acts to modify the response of the synapse to a neurotransmitter. (make a stimulus stronger or weaker)

Front 464

describe the various events in synaptic transmission which might be altered by drugs

(o)

Back 464

Front 465

recognize the substances which have been proposed to act as CNS neurotransmitters

(o)

Back 465

Acetylcholine
Amino acids
Biogenic amines
Peptides
Purines (ATP, adenosine)
Nitric acid
Endocannabinoids

Front 466

differentiate between ionotropic and metabotrophic receptors.

(o)

Back 466

Ionotropic receptors (also known as ligand-gated ion channels) are associated with ion channels, and change ionic conductance.
Mediate fast, short effects.

Metabotropic receptors are coupled with enzymes via G-proteins and other intermediates.
Mediate slow, long effects.

Front 467

describe the blood brain barrier and its implications in drug therapy (what are the characteristics that regulate diffusion of substance through capillaries)

(o)

Back 467

A term used to describe diffusional barriers retarding the passage of substances from the central circulation to nerve cells.

Characteristics which regulate diffusion of substances through capillaries are:

Molecular weight
Lipid solubility
Ionization at physiological pH (ionized drugs are not lipid soluble)

Front 468

define epilepsy...

incidence?

Back 468

2 or more unprovoked seizures

incidence is highest in kids and old folk

Front 469

in-between epileptic seizures, what is a common finding on EEG?

Back 469

Spikes

Front 470

What happens in an absence seizure? clinically and EEG

(o)

Back 470

Clinic: pt suddenly stops responding/no eye contact for about 7 seconds and then just resumes back to normal (full recovery)

EEG: sudden spiking in all leads, quick onset, quick ending

Front 471

What happens in a tonic-clonic seizure? clinically and EEG

(o)

Back 471

Clinic: abrupt onset with no warning, pt starts arching back (tonic) and then clonic (shaking all over), NO IMMEDIATE RECOVERY, pt might have pissed themselves, bit their tongue, want to go to bed--this is what you classically think of as a seizure

EEG: sudden rapid hashy spiking (tonic) in all leads, followed by spike then pause, spike then pause (in all leads) leading to the jerkiness (clonic). When the seizure ends, the EEG is not completely normal (shows the disorientation when it ends)

Front 472

What happens in a Partial Simple Seizure? clinically and EEG

(o)

Back 472

specific to what brain area is affected

for example, a pt could have a left motor seizure causing a right arm tremor. Pt is wide awake, aware of the symptoms, but can't stop them

EEG: Will only see irregular activity in certain leads (that correspond to one side of the brain, thus focal)

Front 473

What happens in a Partial Complex Seizure? clinically and EEG

(o)

Back 473

occurs in the Temporal lobe

usually clouding of consciousness

EEG: Will only see irregular activity in certain leads (that correspond to one side of the brain, thus focal)
Can occur in 4 places:
anterior-deja vu/psychic symptoms
Sylvian- Epigastric sensation, movement of mouth and face
Mid-temporal - auditory hallucinations, depersonalization
posterior temporal-Complex visual hallucinations

Front 474

a pt says every now and then I keep seeing a pack of wild dogs that nobody else can see...what is this?

Back 474

Partial-Complex Seizure

Front 475

what is common and similar in Absence and Partial Complex Seizures
Consider:
brain involvement
Age of pt
Duration
Sx recalled by pt
Movements or behaviors
After-effects
EEG pattern
Underlying Cause
Effective Tx

TEST!!!!!!!!!!!!!!!!!!!!!!!!!

Back 475

ONLY THING SHARED: STARING AND DECREASED RESPONSIVENESS

Front 476

The student will be able to correlate the age of onset of first seizure with likely underlying causes.
Consider:
Idiopathic
Febrile
Birth Injury
Metabolic
Infection
Trauma
Tumor
Stroke

(o)

Back 476

Front 477

The student will be able to describe the means and rationale for investigation of a new seizure disorder by history, examination and ancillary testing.-JUST READ

(o)

Back 477

CBC—is there an elevated white count to imply infection?
Chemistries—especially glucose, sodium, calcium, renal function tests and liver function tests.
Brain imaging to look for macroscopic focal disease, such as tumor, stroke, arteriovenous malformation or developmental anomaly.
An MRI scan including coronal sections through the medial temporal lobes is ideal, but there are circumstances in which a CT is substituted, e.g. when the patient is restless, claustrophobic or has a pacemaker.
An EEG, preferably sleep-deprived to increase sensitivity. Does the EEG show abnormalities, especially spikes, highly associated with seizures? If so, are they focal or generalized?

Front 478

The student will be able to explain and account for differences in brain-injury patterns caused by high- and low-velocity missiles.

(o)

Back 478

k.e.= ½ m v2

so the faster the traveling bullet (military weapon) will be more likely to kill you than a slow moving bullet (civilian weapon)

Front 479

please define a concussion

(o)

Back 479

Diffuse, physiological and microscopic insult, with or without diffuse axonal injury

Usually defined as involving a period of confusion or unconsciousness, even if just brief

Numerous common associated symptoms, e.g. headache, dizziness, irritability, emotionality, poor concentration

Front 480

highschool football player gets hit on the head in the second half of the game and dies. Why did this happen? this is an example of?

*

Back 480

You look back and see that the kid got hit on the head in the 1st half but it was dismissed or not realized

the SECOND IMPACT SYNDROME says that the brain is waaayyyy more vulnerable to a 2nd injury

this is more common in younger ppl

Front 481

Little Johnny gets hit in the head during a game and gets knocked out. Mom and Dad bring him to you and ask if he can play the next game in 2 days. What do you tell them

Back 481

have to be at least a week of no symptoms before they can resume play

Front 482

pleas define a brain contusion..where do they tend to occur?

(o)

Back 482

Focal hemorrhages within brain tissue
Big enough to see with naked eye in a pathology specimen or as an area of intensity (whiteness) on a CT scan
Tend to occur around edges of brain, particularly at base of cerebrum and in anterior temporal lobes

Front 483

describe a subdural hematoma including the location, and appearance on CT initially and chronically

(o)

Back 483

Traumatic hemorrhage from veins inside dura but outside brain

This behaves like an actual space, so, acutely, blood runs from anterior to posterior pole

The hematomas appear initially white (X-ray dense) on CT

Over time, the hematomas get diluted and resorbed, and become less X-ray dense

Front 484

describe an epidural hematoma including the location, and appearance on CT initially and chronically...what is the cause?

(o)

Back 484

Traumatic hemorrhage from meningeal arteries inside skull but outside dura

This is a potential space through which the fresh blood dissects from edge to edge, creating a lens-shaped hematoma that does not extend from pole to pole (the subdural does)

The hematomas appear white (X-ray dense) on CTs acutely, but become less dense as they dilute and resorb

Front 485

please describe the Glasgow Coma scale, including the 3 aspects, and scoring ranges

Back 485

Front 486

pt presents with multiple cognitive deficits including memory impairment, aphasia, apraxia (arm won't do what you tell it to), agnosia (trouble remembering what objects are), or trouble in executive functioning (have trouble cooking). What do they have?

(o)

Back 486

Alzheimer's Dz

note: the shrinking effect on the brain is bigger due to age than Alzheimers (like an 80 year old with AD would have a larger brain than a normal 90 year old)

Front 487

on a PET scan, what will be a difference seen in a pt with Alzheimer's dz?

Back 487

less activity posteriorly

Front 488

amyloid plaques are commonly seen on silver stain in what? what is another pathological finding of this problem?

Back 488

Alzheimer's Dz

Neurofibrillary Tangles (used to be neurotubules, will be in the cells)

Front 489

What are 2 pharmacological tx for AD?

Back 489

Acetylcholinesterase Inhibitors [Examples: Donepezil (Aricept) Galantamine (Reminyl, Razadyne)
Rivastigmine (Exelon)] --used in mild to moderate disease

NMDA (Glutamate) Receptor Blocker (Memantine (Namenda))-- Moderate level of disease

Front 490

Progressive dementia clinically similar to Alzheimer’s disease

Early, prominent involvement of frontal and temporal lobes (“frontotemporal dementia”)

(o)

Back 490

Pick's Disease

will find Pick Bodies intracellularly

note: PET scan will show less activity in the frontal and temporal lobes (who'da thought)

Front 491

Hypokinesia/akinesia
Bradykinesia
Rigidity (not to be confused with spasticity or paratonia)
Stooped posture
Small-stepped gait
“Rest” tremor, typically unilateral or asymmetric

area all seen in what?

Back 491

Parkinsonism

Front 492

associated with degeneration of substantia nigra cells containing intracellular Lewy bodies

(o)

Back 492

Parkinson's Disease

Front 493

Usual fluctuations in cognitive function, involving alertness and attention
Visual hallucinations are common
Will also have movement problems
Pathologically, intracellular Lewy bodies appear diffusely in the cerebral cortex

(o)

Back 493

Dementia with Lewy Bodies

Clinically resembles a blend between Alzheimer’s and Parkinson’s diseases

note: in Parkinson's, the Lewy Bodies are mostly in the Substantia Nigra

Front 494

flip for a comparison of dementia with Lewy Bodies, Alzheimer's Disease, Parkinson's

Back 494

Front 495

flip for a comparison of dementia with Lewy Bodies, Alzheimer's Disease, Parkinson's

Back 495

Front 496

pt presents to your office due to changes in mood. Upon walking you notice that they seem to flick their hand, or kind of dance around. What is this? Genetics?

(o)

Back 496

Huntington’s Disease

Autosomal dominant with high penetrance
Abnormal gene on chromosome 4

note: the dancing/flicking movement is known as CHOREA

Front 497

What change in the brain would you see in a pt with Huntington's disease?

Back 497

Absence of the Caudate Nucleus

Front 498

A rapidly progressive, fatal dementia involving prominent motor symptoms, such as rigidity, clumsiness, and myoclonic jerks
A transmissible “spongiform” encephalopathy involving abnormal proteins called prions
Diagnosed with certainty only by brain biopsy

(o)

Back 498

Creutzfeldt-Jakob Disease

Front 499

What are the 3 categories of Creutzfeldt-Jakob Disease? Which are we most concerned about?

Back 499

Sporadic CJD appearing without known risk factors accounts for 85% of cases.

Hereditary CJD involves positive family history or positive testing for a genetic mutation. 5-10% of U.S cases.

Acquired CJD involves transmission by exposure to brain or nervous system tissue. 1% of cases. (****transmission from open wounds, retina transplant, etc)

Front 500

Increased levels of CSF protein 14-3-3 would give you the diagnosis of?

Back 500

Creutzfeldt-Jakob Disease

Front 501

inflammatory demyelinating plaques in the central nervous system is the hallmark of what?

(o)

Back 501

Multiple Sclerosis (MS)

has to do with OLIGODENDROCYTES (not Schwann--peripheral)

Front 502

T1 “Black Holes” and brain atrophy can be seen in what?

Back 502

Multiple Sclerosis

note: Gilenya ™ - Fingolimod is the first oral pill tx for MS

Front 503

(o)

Back 503

Front 504

2. The student will be able to correlate brain tumors and their usual anatomic compartments.

3. The student will be able to provide examples of brain tumors that are more or less common in younger and older patients.

(o)

Back 504

Front 505

midline tumors and tumors of cerebellar lobes are more common in adults or kids?

Back 505

kids

Front 506

this is the Fastest-growing and most lethal brain tumor in astrocytoma series
Infiltrates and spreads widely within brain, so surgery cannot entirely remove
Surgery still warranted for biopsy, with or without de-bulking and insertion of Gliadel wafer
Radiation therapy usually applied

*

Back 506

Glioblastoma Multiforme

Front 507

this brain tumor is chiefly in adults 30-50, has Intermediate growth rates depending on grade, can sit dormant for years with no effect. Radiation therapy can be applied, but is usually reserved for when the tumor is perceived as growing because there is a lifetime limit to how much can be given.

Back 507

Cerebral Astrocytomas

Front 508

Usually the slowest growing brain tumors, but can eventually crowd the brain.
Often discovered as an incidental finding on a scan done for another reason
Are usually calcified and are therefore very recognizable on CT scans.

Back 508

Meningiomas

Front 509

please give an example that fits each of the following:
A fast-growing intracranial tumor displaces brain.

A slow-growing intracranial tumor replaces brain

Back 509

A fast-growing intracranial tumor displaces brain. (Examples: glioblastoma multiforme, metastases.)

A slow-growing intracranial tumor replaces brain. (Example: typical meningioma.)

Front 510

Most frequent incidence between ages of 30 and 50
Also calcify and usually show this on CT scans.
Intermediate growth rate, and is usually "managed" (surgery, RT) rather than cured
Glial cell in origin

Back 510

Oligodendrogliomas

Front 511

Can be hormonally active or disruptive
Can compress optic chiasm from below and produce visual field losses
Often removed surgically through the nose and sphenoid sinus

Back 511

Pituitary Adenomas

Front 512

Usually arise from the 8th cranial nerve as Schwannomas
Auditory symptoms (unilateral hearing loss and tinnitus) are prominent
Meningiomas and other tumors can also appear in this location

Back 512

Cerebellopontine Angle Tumors

Front 513

Comprise about 1/3 of childhood posterior fossa tumors
Predilection for cerebellar vermis
Though malignant, they are highly radio-sensitive

Back 513

Medulloblastomas

Front 514

posterior fossa tumor of childhood
Often encapsulated
Complete surgical extirpation often possible

Back 514

Cerebellar Astrocytoma

Front 515

2 of the most common primary cancers in existence are what? so what can this lead to?

(o)

Back 515

breast and Lung

can lead to brain (intermediate tenancy to go to the brain)

Front 516

The student will be able to describe more and less common sources of metastatic brain tumors.

aka what are the most and least likely to go to the brain***

(o)

Back 516

Prostate: DOES NOT go to brain

Melanoma: GOES TO BRAIN (very high propensity)

Front 517

The student will be able to describe treatments for tumors of the nervous system as well as their optimum applications and limitations. What are the options (4)

(o)

Back 517

High-dose corticosteroids
Surgery
Radiation therapy
Chemotherapy

Front 518

How do high dose corticosteroids help treat brain tumors?

(o)

Back 518

Buys time by shrinking the edema around the tumor deposit, rather than affecting the tumor itself.
Effective against extracellular edema, but not intracellular edema, such as that seen in ischemia.
A typical starting dose is dexamethasone 10 mg, followed by 4 mg q.i.d

Front 519

how does radiation therapy help treat CNS tumors?

(o)

Back 519

RT is usually palliative--to shrink but not eliminate tumor deposits
For brain metastases, RT is sufficiently effective that the patient usually dies of non-CNS complications before CNS complications.
The treatment itself can damage the CNS.

Front 520

When do you often see chemotherapy for CNS tumor treatment?

(o)

Back 520

Usually reserved for glioblastoma multiforme (Fastest-growing and most lethal brain tumor in astrocytoma series
Infiltrates and spreads widely within brain, so surgery cannot entirely remove)


IV administration is complicated by intact blood-brain barrier blocking entry into CNS.
BCNU (carmustine) given IV probably crosses BBB to some extent.
Gliadel® wafers (also carmustine) can be implanted within the tumor bed.

Front 521

what are some of the important areas that can be damaged by occluding the middle cerebral arteries?

Back 521

Broca/Wiernicke's

Motor/Sensory cortex

Frontal eyelid

Optic radiation... others

Front 522

anterior cerebral artery blockage can lead to problems where

Back 522

leg and foot of motor and sensory

Front 523

Posterior cerebral artery occlusion will give you what major problem?

Back 523

visual deficits

Front 524

non-traumatic Subarachnoid Hemorrhage is normally due to what?

Back 524

aneurysm

Front 525

where do aneurysms typically occur? (berry)

Back 525

close to the circle of willis

most in Anterior communicating (like in marfans)

Front 526

besides trauma, what are the 2 major causes of intraparenchymal hemorrhage?

(o)

Back 526

Hypertension-associated

Arterio-venous malformation (AVM)

note: this is literally bleeding into brain tissue

Front 527

where do Charcot-Bouchard microaneursyms occur? how are these different from Berry aneurysms

*

Back 527

on penetrating arteries (deep in the brain, leading to areas like the basal ganglia)--assoc with intraparenchymal hemorrhage

different from saccular (Berry) aneurysms occurring near the circle of Willis. assoc with subarachnoid hemorrhage

Front 528

large wedge shaped damage vs small pockets of damage...

please list what type of vessels were damaged

(o)

Back 528

Wedges: large vessels

small pockets/lacunae: small (will be in penetrating arteries

Front 529

what is the difference between an embolism and thrombosis

(o)

Back 529

embolism: some garbage from upstream got dislodged, then it gets stuck in the brain

thrombosis: clot...can lead to breaking off and causing an embolism

so: embolism arises from somewhere else, thrombus occurs from the site

Front 530

what is most commonly going to cause an embolism?

Back 530

Atrial fibrillation

(irregularly irregular)

Front 531

what is the concept of ischemic penumbra?

*

Back 531

There is a central core of forever-lost brain cells that no treatment can revive surrounded by a larger zone of sick brain cells that may or may not recover – depending on acute management.

Front 532

in stroke, what effect can blood sugar have on acute stoke management?

Back 532

Too high can be damaging!!

Front 533

what are some of the modifiable atherosclerotic risk factors? 4 (+1 non-modifiable)

(o)

Back 533

Blood pressure
Blood sugar
Lipids (statin drug)
Smoking


note: Family History

Front 534

shortly after stroke it is important to monitor BP. If it is really high what should you do? Should you let a pt walk right away?

Back 534

we lost autoregulation, so be careful not to drop BP too aggressively-->can extend the stoke

so if their BP is high, don't worry about it for the immediate time being

also, don't let them walk, they may have an unsafe drop in BP

Front 535

if you are going to give a drug for acute treatment of thrombotic stroke, which of the following would you use?

t-PA
heparin
aspirin

Back 535

ASPIRIN has small benefit acutely

note: heparin would be good to prevent DVT from bed rest

Front 536

what commonly causes stroke for old and young folks?

(o)

Back 536

old folks: atherosclerosis or emboli from heart

young folks: congenital heart/great vessel defects; hypercoaguable states, migraine with aura + smoking + contraceptives

Front 537

Giant Cell Arteritis
Tumor
Subarachnoid Hemorrhage
Subdural Hematoma
Epidural Hematoma
Medication Overuse Headaches

are examples of what type of headache?

(o)

Back 537

Secondary Headaches

Front 538

a pt shows up with really bad headaches and insists they have a tumor that is causing it. You respond..

Back 538

they are extremely rare, and not likely the cause of your headache

Front 539

What is a medication overuse headache?

(o)

Back 539

person needed to take medicine for a headache

they took it too often for a long enough time

you transform it into a 2ndary headache that is more difficult to treat

headaches will occur everyday, present throughout the whole day, and is mild to moderate. It worsens when the medication is discontinued

Front 540

an elderly female presents to your office with a unilateral headache, jaw claudication and impaired vision. What does this pt have? is this a primary or secondary headache? FIRST AID REVIEW: What is the tx??

(o)

Back 540

Giant cell arteritis

secondary

High dose steroids

Front 541

Migraine without Aura
Migraine with Aura
Tension-Type Headaches
Cluster Headaches

are what kind of headaches?

(o)

Back 541

Primary

Front 542

pt presents with a unilateral headache that feels like it is "pulsing". They say it is aggravated with activity and they have some nausea. They say they only have light sensitivity some of the times when this occurs...what is it?

Back 542

Migraine without aura

Front 543

what are some of the common triggers for migraines?

Back 543

Hormonal – menstruation, ovulation, OCP, HRT
Dietary – alcohol, nitrite-laden meat, MSG, aspartame, chocolate, aged cheese, missing a meal
Psychological – stress, post-stress let-down, anxiety, worry, depression
Physical/Environmental – glare, flashing lights, visual stimulation, fluorescent lighting, odors, weather changes, high altitudes
Sleep-related – lack of sleep, excessive sleep
Miscellaneous – head trauma, physical exertion, fatigue
Drugs – NTG, histamine, reserpine, hydralazine, ranitidine, estrogen

Front 544

what is the most common aura in migraines with aura? some examples?

Back 544

VISUAL

scotomas (blind spots), photopsia (unformed flashes of light), fortification spectra (scintillating zig-zag lines), distortions in shape and size. In “retinal migraine,” these occur unilaterally instead of bilaterally.

Front 545

what are the 5 types of migraine auras?

Back 545

Visual: scotomas (blind spots), photopsia (unformed flashes of light), fortification spectra (scintillating zig-zag lines), distortions in shape and size. In “retinal migraine,” these occur unilaterally instead of bilaterally.

Somatosensory: unilateral paresthesias (spontaneous sensations) or hypesthesia (decreased perception of applied stimuli).

Motor: hemiparesis.

Language: aphasia (impairment of language comprehension or expression).

Brainstem: loss or change in level of consciousness, diplopia, tinnitus or hearing loss, vertigo, dysarthria, ataxia, bilateral sensory or motor symptoms.

Front 546

pt comes in with a mild/moderate pressing headache that is bilateral. It does not get worse with activity and there is no nausea associated with it...what is this?

(o)

Back 546

Tension type headache

THE ANTI MIGRAINE (pretty much the opposite: no light sensitivity, no nausea, doesn't get worse with activity)

Front 547

what does the "cluster" refer to in cluster headache?

Back 547

The "cluster" means clustering in time (not location)

Front 548

pt presents with recurrent headaches occurring around the the eye lasting for about 15 minutes to 2 hours. He says the pain is intense but then goes away. What is this?

(o)

Back 548

Cluster headache

Front 549

Clumsiness in greater proportion than loss of power
Babinski sign present (immediate)
Spasticity (delayed)
Increased tendon reflexes (delayed)
Little if any atrophy

what type of lesion?

(o)

Back 549

Upper motor neuron lesion

Front 550

what is Spasticity...what is it associated with (upper or lower mn)

(o)

Back 550

A unidirectional increase in muscular tone

Involves increased tone in “anti-gravity” muscles

In the upper extremities, resistance to stretching out biceps, but not triceps
In the lower extremities, resistance to stretching out quadriceps but not hamstrings

seen in upper motor neuron

Front 551

What is Rigidity? what is it seen in?

(o)

Back 551

Seen in Parkinson’s disease and other extrapyramidal disorders

A bi-directional increase in tone to passive range of motion

The resistance to passive range of motion is relatively independent of degree of force or rate of speed

Front 552

What is Paratonia? commonly seen in?

(o)

Back 552

feels like the pt is trying to stop you from moving the limb

Commonly seen in dementia

Also known as gegenhalten (to hold against)

A bidirectional resistance to passive range of motion that increases with force and rate of movement, as if voluntary

Front 553

Loss of power in greater proportion than clumsiness
Hypotonia
Muscle atrophy
Muscle fasciculations

what type of lesion?

(o)

Back 553

Lower Motoneuron

Front 554

Compare Duchenne, Facioscapulohumeral, and Limb girdle Muscular dystrophies for the following characteristics:
Age of onset
Sex
Pseudohypertorphy
Initial distribution
Involvement of the face
Rate of progression
Contractures and deformity
Inheritance

(o)

Back 554

Front 555

what is the genetic defect in duchenne muscular dystrophy?

Back 555

Dystrophin gene on short arm of X chromosome codes for dystrophin protein, which is a cytoskeletal structural protein.

this is damaged

Front 556

a boy presents to your office and on physical exam you note that their calves are pretty toned. Mom says that when the boy is on the ground he does this strange thing where he arches his back and climbs his way off the ground...what is this called? sign of?

Back 556

Gower's sign

in Duchenne

Front 557

you are in your neuro office and examining a young lady patient who has issues with smiling. You ask her to smile and she physically can't. Her forehead is unwrinkeld and the corners of her mouth do not curl. On physical exam, you note winging of the scapula. What does this pt have?

Back 557

Facioscapulohumeral Muscular Dystrophy

One key gene is on the long arm of chromosome 4. The function of the gene product is as yet unknown.

Front 558

a man presents to you with a seemingly triangular face. On a hunch, you hit their hypothenar eminence with your reflex hammer and it causes their thumb to move towards their pinky. To confirm what you think, you have the pt squeeze your hand and tell them to open it as soon as you tell them. When you say go, their hand stays in a grip...what do they have? What is the genetics going on?

Back 558

Myotonic Dystrophy
A gene near the centromere of chromosome 19 codes for myotonic dystrophy protein kinase. In M.D. dozens to hundreds of “CTG” repeats occur in the gene. The transcribed mRNA gets trapped within the cell’s nucleus.

Front 559

what happens in Myasthenia gravis physiologically?

(o)

Back 559

antibodies to the AChR

Front 560

pt presents to your office with muscle weakness. They say they are fine in the morning, but by the end of the day they have drooping eyelids, jaw drop, and drooling...what do they likely have?

Back 560

MG

Front 561

what are some of the associated dz with MG? what is the most important one?

Back 561

THYMOMA (malignant mediastinal tumor)

thyroid disease

widespread immune complex disease

Front 562

what is a polyneuropathy

(o)

Back 562

Bilaterally symmetric
Distinct from mononeuropathy and multiple mononeuropathies

so the key is that you have to have the deficit on the same spot on both sides

mulitple mononeuorpathies would be like radial on one side, ulnar on the other

poly is like whole left and right hand (stocking and glove is a common characteristic of polyneuopathy)

Front 563

Distal-greater-than-proximal weakness
Distal-greater-than-proximal numbness
A “stocking-glove” pattern of weakness, numbness or both
“Length-dependent” neuropathy
Disrupts DTRs more than other forms of lower-motoneuron weakness

this describes?

(o)

Back 563

Polyneuropathy

the longer the axon the worse it is affected

Front 564

Werdnig-Hoffman is a motoneuron disease affecting what population?

*

Back 564

NEONATES

you will see characteristic FROG LEG position and floppy baby
(other thing that causes floppy baby? Botulin toxin)

BABIES WILL NOT HAVE REFLEXES

Front 565

a 60 year old man presents to your office and says that he cannot do routine tasks such as going up steps, getting out of a chair, or swallowing. You note widespread atrophy. What do you suspect...

Back 565

Amyotrophic Lateral Sclerosis

ALS

Front 566

Back 566

Front 567

of the following, which will have a MARKEDLY increase CK level?

Myopathy
MG
Polyneuropathy
Motorneuron disease

Back 567

Myopathy

(think duchenne's muscular dystrophy)

Front 568

what is a pathologic finding of babinski's sign?

Back 568

dorsiflexion of the big toe

Front 569

. The student will be able to measure and record visual acuity according to generally agreed upon conventions

Back 569

Eye chart for visual acuity testing. Standard distances are 20 feet for a wall chart and 14 inches for a hand-held card.

Read down to the smallest characters possible or until reaching the 20/20 line, whichever comes first. The acuity is the last line correctly read.

say they read like all of the letters but miss 1 or 2 you say 20/20 minus (assuming they read at the 20 20 line)

Front 570

a cut at the optic nerve would cause what visual problem?

Back 570

Front 571

a cut at the optic chiasm would cause what visual problem?

Back 571

Front 572

a cut at the optic tract would cause what visual problem?

Back 572

left homonomous hemianopia

Front 573

right temporal damage could cause what visual damage?

Back 573

4

Front 574

what system is responsible for constricting the pupil?

Back 574

PNS

Front 575

please diagram the light reflex pathway...is this PNS or SNS?

Back 575

CN II

pretectal nucleus

Edinger Westphal nucleus

ciliary ganglion

contract pupil

(This is PNS)

Front 576

please diagram out the sympathetic pathway for pupilary dilation

Back 576

ipsilateral hypothalamus

synapse at T1 (IML)

travel up the sympathetic chain and to the apex of the lung (look out for horners)

goes to carotid bifurcation but then sends to the pupil for dilation

Front 577

how can a tumor of the apex of the lung lead to pupil issues?

Back 577

this is horner's syndrome due to a pancoast tumor

you will see a constricted pupil because the sympathetics (which would normally dilate the pupil) stop at the apex of the lung and are disrupted by the tumor

Front 578

pt presents with a droopy eyelid and constricted pupil...

Back 578

ipsilateral sympathetic chain issue--HORNERS

miosis-small pupil

ptosis- droppy eyelid

Front 579

please list the primary and secondary action of the extraocular muscles. consider what would happen with a lesion

Back 579

Front 580

What do CN 6 and 4 do?

Back 580

LR6SO4

LR (lateral rectus) connected to CN 6
SO (superior oblique) connected to CN 4
Remaining EOMs and levator palpebrae connected to CN 3

Front 581

right lower face is weak, upper face is fine

is this an upper or lower motor neuron problem

(o)

Back 581

UPPER

Front 582

right lower face is weak, upper face is also weak

is this an upper or lower motor neuron problem

(o)

Back 582

LOWER

Front 583

The student will be able to grade muscular strength according to the MRC (Medical Research Council) scale.

(o)

Back 583

Front 584

afferent vs efferent

Back 584

afferent: carry nerve impulses from receptors or sense organs towards the central nervous system

efferent: from CNS to target

Front 585

what makes up the brainstem?

Back 585

the midbrain (sup/inf colliculus)

pons

medulla

Front 586

Back 586

Front 587

4 lobes of the brain? major functions?

Back 587

frontal: high order processing, planning, etc

parietal: somatosensory

temporal: sound

Occipital: vision

Front 588

where is broca's area located? (what lobe)

where is Weirnikes area?

Back 588

B: Frontal lobe

W: Temporal

Front 589

post central gyrus=?

pre=?

Back 589

post central=somatosensory

pre= motor

Front 590

cerebellum function?

Back 590

compare planned motor behavior with actual movement

checks/balances

Front 591

functions of the insular lobe

Back 591

emotions, drives, drug addiction etc

Front 592

function of the calcarine fissure

Back 592

primary visual processing area

Front 593

difference btw gray and white matter?

Back 593

gray: cell bodies (and some axons)

white: axons

Front 594

what makes up the basal ganglia?

Back 594

Caudate Nucleus

Putamen

Globus Pallidus

Front 595

just list the cranial nerves and their functions

Back 595

* I-Olfactory nerve,
* II-Optic nerve,
* III-Oculomotor nerve,
* IV-Trochlear nerve/pathic nerve,
* V-Trigeminal nerve/dentist nerve
* VI-Abducens nerve,
* VII-Facial nerve,
* VIII-Vestibulocochlear nerve/Auditory nerve,
* IX-Glossopharyngeal nerve,
* X-Vagus nerve,
* XI-Accessory nerve/Spinal accessory nerve and
* XII-Hypoglossal nerve.

Front 596

Dorsal horn is associated with what?

Ventral?

Back 596

Dorsal: Sensory

Ventral Motor

Front 597

consider the locations of white and gray matter in the spinal cord and brain (which is deep and which is superficial in each)

Back 597

spinal cord: gray matter deep

brain: gray matter superficial

Front 598

what divides the gracile and cuneate fasciculi?

Back 598

posterior intermediate sulcus

Front 599

what is the difference btw the gracile and cuneate fasiculate

Back 599

Gracile: carries axons from lower extremities

cuneate: upper (t6 and up)

REMEMBER: Feet in the grass

Part of the DCML pathway for sensory info (pressure, vibration, fine touch)

Front 600

what type of information is carried by the Dorsal column/ medial lemniscus pathway

Back 600

fine touch
proprioception,
vibration.

Front 601

lateral corticospinal tract does what?

Back 601

somatomotor

Front 602

does a 1st, 2nd, or 3rd order neuron cross?

Back 602

2nd will cross

such as the second order neurons from the nucleus cuneatus crossing as internal arcuate fibers in the medulla

Front 603

what does the anterolateral system (ALS) do?

Back 603

pain
temperature
touch (crude)

Front 604

please diagram out the DCML pathway...what info does this carry?

Back 604

Front 605

please diagram out the Anterior Lateral System, and list what it carries

Back 605

Front 606

Please diagram out fine touch and vibration of the face

Back 606

Front 607

please diagram orofacial pain and temp

Back 607

Front 608

The left optic tract carries info from what visual field?

Back 608

right visual field

Front 609

What is the job of the Lateral Geniculate Nucleus (LGN)?

Back 609

visual processing

receives synapse from eyes

Front 610

where will superior visual field info end up?

Back 610

inferior calcarine fissure

(remember they also travel inferior in the meyers loop)

Front 611

a pituitary tumor causes pressure on the optic chiasm...what will this lead to?


****TEST

Back 611

Bitemporal hemianopia

Will only be able to see info from medial visual fields (peripheral vision lost-->tunnel vision)

Front 612

Back 612

Front 613

pt falls off their bike and was not wearing a helmet. They now say that they have lost vision just in the very center of each eye...what is going on?

Back 613

Central scotomas

Front 614

diagram out the corticospinal and corticobulbar tracts

Back 614

Front 615

pt has flaccid paralysis...what is the problem

Back 615

lower motor neuron

Front 616

pt has spastic paralysis...what is the problem?

Back 616

upper motor neuron

Front 617

middle cerebral artery damage will lead to issues in what structure

Back 617

face

comes out of sylvian fissure and branches like a tree

Front 618

anterior cerebral artery damage will lead to issues in what structure

Back 618

legs and feet

Front 619

describe the role of the Direct pathway and the indirect pathway in the basal ganglia

**TEST

Back 619

Direct pathway: starting movement

indirect pathway: stopping movement

Front 620

which pathway (direct or indirect) encourages GPm activity...what does this do?

Back 620

INDIRECT

GPm has tonic inhibition of the thalamus (which is always wanting to activate movement...it's like GO GO GO)

thus the indirect by activating GPm will stop movement (this is the key thing to remember)

note: in the direct pathway, you inhibit GPm so inhibiting the inhibition leads to activity

Front 621

FIRST AID REVIEW QUESTION

abdominal pain radiating to the back, weight loss, migratory thrombophlebitis and obstructive jaundice should make you think what?

Back 621

Pancreatic adenocarcinoma

more common in pancreatic head

aggressive (prognosis is 6 months or less)

CEA and CA19-9 tumor markers

assoc with Cigarettes and chronic pancreatitis but not EtOH

Front 622

FIRST AID REVIEW QUESTION

What are some of the causes of aplastic anemia?

Back 622

Radiatoin and drugs (Benzene, chloramphenicol, alkylating agents, antimetabolites)

Viral agents (B19 parvo, EBV, HIV, HCV)

Fanconi's anemia

Idiopathic