• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/92

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

92 Cards in this Set

  • Front
  • Back
  • 3rd side (hint)
avonex
beta-INF 1a: 30 mg IM q wk,

delay progression
Rebif
high-dose Beta IFN 1a: 22 or 44 microg SC QOD -

dose related benefit, much higher rate of neutralizing antibodies
Betaseron
Beta-IFN 1b
8 MIU IU SC QOD

may delay progression in active relapsing-remitting or secondary progressive MS
glatiramer
copaxone

fragments of myelin basic protein 20 micro gm SC qd
mitoxantrone
approves for active relapsing-remitting secondary progressive MS

- inhibits topoisomerase II; interferes with RNA and crosslinks breaks DNA proliferating and nonproliferating cells

has a lifetime dose limit
cyclophosphamide
cytoxan

controversial

for aggressive progressive MS
MS attack
high dose : methylprenisolone IV 1000mg x 3 days, with/without taper
fatigue from MS treat with?
modafinil 100-2000 mg in AM and at noon

pharmacology of modafinil is?
to increase the levels of various monoamines,
- dopamine in the striatum and nucleus accumbens
- noradrenaline in the hypothalamus and ventrolateral preoptic nucleus,
- serotonin in the amygdala and frontal cortex
treatment for transverse myelitits
1 g methylprednisolone IV or 100 mg dexamethasone IV for at least 3 days

consider IVIg
McDonald Criteria for MS Dx (5)
1. 2+ attacks and 2+lessions

2. 2+ attacks and 1 lesion, with dissemination in space by MRI or 2+ MRI lesions plus CSF or 2nd clinical attack in different site

3. 1attack, 2+ lesions, dissemination in time by MRI, or 2nd clinical attack

4. 1 attack and 1 lesion disseminated in space by MRI or 2+ MRI lesions plus CSF

5. Insidious neurological progression - one year of progression and 2 of the following 3: MRI lesions or 4 - T2 lesions with VEP, spinal cord 2 lesions; + CSF
Treatment for GBS includes?
plasmapharesis - ANS instability is a relative contraindication

IVIG - equally effective
treatment of CIDP or multifocal motor neuropathy includes?
long term IVIG, plasma exchange and steroids DO NOT WORK!
What are two possible treatments for chronic aggitation-delerium?
respiridone - less sedating

quetiapine - less risk of movement disorder
What treatment can you give Lewy Body disease?
can try low-dose Levodopa or a dopamine agonists

in combination with : an atypical neuroleptic - quetiapine
What is the treatment for acute cluster headaches?
Ergot
100% O2


What is the treatment for prevention of cluster headaches?
Calcium channel blockers or lithium
What mechanism of action are the triptans?
5-HT1 serotonin receptor agonists

What is a major contraindication of taking triptans?
if you have taken an Ergot withint the previous 24 hours, also CAD could be a contraindication
How do we administer Dihydroergotamine?
put patient on cardiac monitor for first DHE dose,

- give metoclopramide 10 mg IV 10 min beforehand

- then give 1 mg DHE

-repeat in 1 hour prn, then q6h prn if it works
When do we start prophylactically treating migraines?
if the patient is having them 3+ /month
What is the treatment for prevention of migraine's?
Amitriptyline - proven efficacy

- propranolol - start 10-20 bid

- 5-HT antagonists - methysergide (need test dose, danger of retroperitoneal fibrosis)

- CCB - verapamil (cardiac selective, but will minimally vasodilate)
What drugs do we use to treat a brain abscess assumingly from ear or from an unknown source?
Ceftriaxone 2g IV q12h
and
Metronidazole 500 mg IV q6h
What drugs do we use to treat a brain abscess in a post head truama or surgery patient?
Staph aureus is more highly suspected

treat with vancomycin 1 g IV q 12 hours
and
ceftrazidime 2 g IV q8h or cefepime 2g IV q 12 hour (both have pseudomonas coverage, weaker Gm+, but Van will cover gm +)
What is the treatment for neuropathy associated with lyme disease?
doxycycline 100mg BID x 21-28 d
or
amoxicillin 500 mg TID x 21-28 days

What is the treatment for Lyme disease meningitis?
Ceftriaxone 2 g IV q12 hours x 2-6 weeks
Patient presents with viral like symptoms, then rapidly progresses to having abnormal behavior, amnesia, seizures, hemiplegia, and could have altered level of consciousness, suspected diagnosis?
Herpes simplex encephalitis
What is a good drug for vasospasm control?
Nimodipine 60 mg q4h PO after 30mg q2h to a total dose of 180mg/d as tolerated.
What is Milrinone?
Milrinone is a phosphodiesterase-3 inhibitor,

This drug inhibits the action of phosphodiesterase-3 and thus prevents degradation of cAMP. With increase cAMP levels there is an increase activation of PKA.

Phosphorylation of calcium channels permits an increase in calcium influx into the cell.
Name the receptors activated and effects of this activation for each medication:

1. Dopamine:
2. Norepinephrine
3. Phenylephrine
4. Isoproterenol
5. Epinephrine
1. Dopamine: D1, D2 and then non-selective mostly, mildly increased renal perfusion, but overall very non-selective

2. Norepinephrine: alpha slightly more than beta,

3. Phenylephrine: alpha1 only

4. Isoproterenol: beta only,

5. Epinephrine: non-selective
What is the mannitol dosing for elevated ICP?
1g/kg (usually 50-100g) IV bolus

then 25 mg q6h for:
- osm < 310
- Serum Na < 160
- osmolal gap < 10
How do we reverse anticoagulation if patient was on coumadin?
give 2-4 units of FFP and IV Vit K 10mg x 1, until INR < 1.3
If patient is on coumadin (warfarin) and asprin, how do we reverse the anticoagulation?
for coumadin: 2-4 units of FFP and IV Vit K 10mg x 1

For asprin: give 6 units of platelets
What do we treat a patient with who has poor CSF resorption?
acetazolamide - decreases CSF production

osmolar agent, and/or shunt
What are the antihypertensives we should avoid when we have a high ICP?
nitroprusside
nitroglycerine
hydralazine
Ca channel blockers other than Nicardipine

These all raise ICP via vasodilation and therefore decrease cerebral blood flow
What chelating agent can we use to treat arsenic, lead, or mecury?
penicillamine 250 mg PO qid
What is the purpose of benzatropine?
Benzatropine is an anticholinergic drug used in patients to reduce the side effects of antipsychotic treatment, such as pseudoparkinsonism and dystonia.
How does Haloperidol work in treatment of choreoathetosis?
Haloperidol is a typical neuroleptic that has D2 receptor antagonism, this will block the excess DA actions, and treat symptoms
What is the function of entacapone?
Entacapone is a COMT inhibitor, which COMT (catechol-O-methyl transferase) is an enzyme used to degrade dopamine, this will decrease level of degradation of DA and is used to treat parkinson's disease
What is the function of pramipexole?
This is a dopamine agonist, more sedative and causes hallucinations but longer half-life and less link to dyskinesias than levodopa
What do drugs like selegiline and rasagiline do?
They are both Monamine oxidase B irreversible inhibitors: which MAOB prefers to metabolize Dopamine (DA) specifically, whereas MAO-A: prefers to metabolize norepinephrine (NE), serotonin (5-HT), and Dopamine (DA) and are used in the treatment of depression
How does amantadine work?
a weak antagonist of the NMDA type glutamate receptor, increases dopamine release and blocks dopamine reuptake
How does trihexyphenidyl (artane) work?
It binds to the M1 muscarinic receptor[1] and possibly the dopamine receptor

The exact mechanism of action in parkinsonian syndromes is not precisely understood, but it is known that trihexyphenidyl blocks efferent impulses in parasympathetically innervated structures like smooth muscles (spasmolytic activity), salivary glands, and eyes (mydriasis)
What is promethazine?
aka phenegran
- a first-generation antihistamine, drug has anti-motion sickness, antiemetic, and anticholinergic effects, as well as a strong sedative effect
What is ondansetron?
aka Zofran:
- is a serotonin 5-HT3 receptor antagonist used mainly as an antiemetic (to treat nausea and vomiting), often following chemotherapy
How does clonidine work?
Clonidine treats high blood pressure by stimulating α2 receptors in the brain, which decreases cardiac output and peripheral vascular resistance, lowering blood pressure.

It has specificity towards the presynaptic α2 receptors in the vasomotor center in the brainstem. This binding decreases presynaptic calcium levels, and inhibits the release of norepinephrine (NE). The net effect is a decrease in sympathetic tone.
What is riluzole?
Riluzole preferentially blocks TTX-sensitive sodium channels, which are associated with damaged neurons.[1] This reduces influx of calcium ions and indirectly prevents stimulation of glutamate receptors.

Its used to treat ALS, delays the onset of ventilator-dependence or tracheostomy in selected patients and may increase survival by approximately 3–5 months
What is the effects of botulism?
toxin blocks acetylcholine ACh release from NMJ.
How does edrophonium work?
is a short-acting cholinesterase inhibitor, used in the tensilon test, should alleviate symptoms in myasthenia gravis patient
How does prostigmine (neostigmine) work ?
as a reversible acetylcholinesterase inhibitor.
How does ipratropium bromide work?
an anticholinergic drug used for the treatment of chronic obstructive pulmonary disease and acute asthma. It blocks the muscarinic acetylcholine receptors in the smooth muscles of the bronchi in the lungs, opening the bronchi
What medication do we treat active seizures with, or status epilepticus?
diazepam
What is the treatment of choice for patient with partial or secondary generalized seizures?
Levetiracetam (keppra), carbamazepine (tegretol) are first line more than valproate
What is the treatment of choice for a patient that suffers from primary generalized seizures?
valproate and carbamazepine (tegretol) are first line

*avoid ethosuximide, can make seizures worse
What is the treatment of choice for patient with absence (petit mal) seizures?
ethosuximide or valproate,


*avoid: phenytoin can make seizures worse
What is the treatment of choice for myoclonic seizures?
valproic acid or clonazepam

*avoid: phenytoin or carbamazepine
What is a good first line treatment for seizures in a young woman?
lamotrigine (lamictal) or carbamazepine (tegretol)

*avoid: phenytoin - teratogenic
What are the first line treatments for patients with liver disease?
levetiracetam (keppra) and lamotrigine (lamictal)
Zolpidem (ambien) - mechanism of action and good time to use it:
- nonbenzodiazepine GABA receptor drug, very good for anxiety and sleep disorder in the elderly, very little addiction associated and short half-life
What is Ramelteon and how does it work?
Ramelteon is in a class of medications called melatonin receptor agonists.

- Specifically used for patients who have sleep onset insomnia, effects last for roughly 8 hours
How does Trazadone work and when do we use it?
Trazadone is an inhibitor of: adrenergic receptors, histamine receptors, and some serotonin receptors, but is a partial agonists of 5-HT1A.

Its overall affects are mild anti-depression and anti-anxiety, with additional effects of a sleep aid due to the adrenergic inhibition.

Used to treat insomnia with/without depression/anxiety
How does doxepin work and what do we use it for?
Doxepin inhibits the reuptake of serotonin and norepinephrine. Doxepin also has antagonistic effects at a variety of receptors:
Extremely strong: H1, H2
Strong: 5-HT2, α1-adrenergic, mACh
Moderate: 5-HT1, local anesthetic action.


Doxepin is used to treat depression, anxiety disorders, insomnia and as a second line treatment of chronic idiopathic urticaria.[
How does methylphenidate work and what do we use it for?
increases the levels of dopamine and norepinephrine in the brain through reuptake inhibition of the respective monoamine transporters.


Methylphenidate (Ritalin) is a psychostimulant drug approved for treatment of ADHD or attention-deficit hyperactivity disorder,
How does modafinil work and what do we use it for?
The exact mechanism of action of Modafinil is unclear, although numerous studies have shown it to increase the levels of various monoamines, namely; dopamine in the striatum and nucleus accumbens, noradrenaline in the hypothalamus and ventrolateral preoptic nucleus, and serotonin in the amygdala and frontal cortex.

treatment of narcolepsy, shift work sleep disorder, and excessive daytime sleepiness associated with obstructive sleep apnea. Also has been shown to help in ADHD and concentration.
What do we use to treat cataplexy?
TCAs: imipramine 25 mg TID
What do alpha-receptor agonists control?
vasoconstriction
intestinal relaxation and sphincter constriction
increased heart contractile force
arrhythmias
dilated pupils

What is a selective alpha-agonists and what is an alpha-antagonists?
Alpha-agonist: phenyephrine

Alpha-antagonists: prazosin
What do Beta-1 receptor agonists do and what do Beta-2 receptor agonists do?
Beta-1: cardioselective - increased heart contractile force, increased heart rate, AV conduction, renin secretion,

Beta-2 : vasodilation, bronchodilation, intestinal relaxation

Name some beta-receptor agonists and a general beta-receptor antagonist
Beta-receptor agonists: isoproterenol

with beta-1 agonists: dobutamine

with beta-2 agonists: albuterol and terbutaline

beta- general antagonists: propranolol
beta-1 selective antagonists: metoprolol
What receptor activity do Norepinephrine and epinephrine have?
NE and Epi have equal binding to alpha receptors, and both have binding activity to both beta receptors, but Epi has an increased affinity to binding to beta-2 receptors than NE

What does this mean when choosing a pressor?
If we need both beta and alpha affects, then one of these two drugs should be chosen, if the patient has any COPD or asthmatic component of their decomposition, then Epi would be first line.
What receptors does DA activate and in what concentration dependency?
At very low dosee: 0.5-2 micro/kg/min selectively only activates D1, D2 receptors

At mid-range dosese 2-10 micro/kg/min will activate both Beta receptors and both Dopamine receptors

At high doese >10mico/kg/min will activate both alpha receptors, both beta, and both dopamine receptors
What do alpha-2 receptor agonists do?
cause platalet aggregation, lower insulin secretion, lower NE and acetylcholine release (can be used to increased cardiac output while vasodilating mildly),

What is an example of a alpha-2 agonists and an alpha-2 antagonist?
Alpha-2 agonist: clonidine, dexmedetomide

alpha-2 antagonists: yohimbine
Which out of the adrenergic receptors, alpha, beta, or dopamine, has the greatest effect on the heart?
Beta-1 receptors: AV node, contractile forces, heart rate
What are the longest acting opiates?
MS contin,
methadone
levorhanol
fentanyl patch
What is the side-effect profile of a patient who is going through withdrawal from opiod use?
muscle aches, lacrimation or rhinorrhea, pupillary dilation, sweating, diarrhea, yawning, fever, insomnia
If prescribing an opiod, what should you also prescribe at the same time?
2 senna tabs TID
metoclopramide 10 mg TID (only in patient with low risk for movement disorder)
colace 100 mg TID
lactulose or poylethylene glycol (miralax)

Ileus: oral narcan give 2-3 amp PO or as enema q4hours until bowel movement
Name the trade name associated with each Opiod drug listed below:
1. Meperidine
2. Hydromorphone
1. Meperidine - Demerol
2. Hydromorphone - Dilaudid
What are the neurologic side effects of each of the following drugs:
1. acyclovir
2. Aminoglycodie
3. Amphotericin B
4. HIV drugs
5. Isoniazid
6. Metronidazole
7. Penicillin derivatives
8. Tetracyclines
9. Vancomycin
10. Zidovudine
1. Acyclovir: encephalopathy is associated with renal failure, methotrexate, or interferon
2. Amingolycosides: vestibular and ototoxicity, neuromuscular blockade especially in myasthenia
3. Amphotericin B: rare headache, tremor, confusion, akindetic mutism
4. HIV: distal symmetrical polyneuropathy
5. Isoniazide: seizures, altered mental status, optic neuritis
6. metronidazole: distal exonopathy, psychosis, hallucinations
7. Penicillin derivatves: rare myoclonus, asterixis, and coma
8. Tetracyclines: rare pseudotumor cerebri in infants
9. Vancomycin: ototoxicity
10. Zidoviudine: HA, insomina, sometimes confusion, seizures, myopathy
What is the goal INR for A-fib?
2-3
How do we monitor coumadin (warfarin), heparin, and enoxaparin (lovenox) respectively?
warfarin (coumadin) - PT/INR

Heparin: PTT, therapeutic range is 60-80

Enoxaparin (lovenox): Factor Xa
What type of medicine can we use for anticoagulation if a patient has a history of heparin induced thrombocytopenia?
heparinoids: danaparoid, fondaparinux (arixtara), danaparoid (orgaran) these are synthetic heparin-like polysaccharides, they bind antihrombin III and thus inhibit factor Xa

Direct THrombin inhibitors: lepirudin, hirudin, argatroban, ximelagatran *these are hard to monitor and have no specific antidotes
How do we reverse Warfarin (coumadin)?
Vit K 1mg IV/SQ to lower PT a little, 10mg qd x 3 d to normalize, but makes anticoagulation hard for the next week

If active bleding, consider fresh frozen plasma or DDAVP to bolost platelets
How do we reverse heparin?
protamine 10-50 mg IV over 5 mins,

1 mg reverses approximately 100 U of heparin

Again if active bleeding can give FF Plasma and DDAVP to boost plateletes
What do we need to check before we start somenoe on Carbamazepine?
CBC - can cause leukopenia,

LFTs - can cause hepatitis

BMP - can cause low Na

Iron - do not start if iron > 15% micrograms, because it autoinduces its metabolism

What additional side effects are of concern with carbamazepine?
RASH!!

HA, nausea, ataxia. and need to increase oral contraceptive dose
What is the major side effect to be aware of with lamotrigine (lamictal)?
rash

What is the biggest side efefct to be aware of with use of levetiracetam (keppra)?
rash
What are the contraindications for phenytoin use?
secondary or complete AV block
bradycardia
hypotension
low ejection fraction
pregnancy

What are the side effects of phenytoin?
sedation, nystagmus, ataxia, transient dystonias, ophthalmoplegia, and rash

chronic: coarse features, gingival hyperplasia, ataxia, cerebellar atrophy
What is the therapeutic dose for phenytoin?
10-20 microgram/ ML or free level of 1-2 microgram/mL
If given the measued dilantin level in the blood how do we calculate the free phenytoin level?
free level = measured level / [ (0.2 x albumin) + 0.1]

* this also works if a person has a low albumin and the free might be different based on more free relative to bound

How do we calculate the free phenytoin level in a person with renal failure (CrCl < 20)?
adjusted level = measured level / [ (0.1 x albumin) + 0.1]
What are the pharmacokinectics of phenytoin near its theraputic level in the body?
kinetics change from first order to saturation near therapeutic dose

What does this mean when we are dosing a level initially < 8 vs a level > 8 but subtherapeutic because its still less than 10-20?
<8 : can increase dose by 100 mg qd

>8 : can increase the dose by no more than 50 mg
What are the side effects of Valproate (Depakote)?
liver toxicity (check LFTs)
Nausea
weight gain
thin hair
teratogenic
polycystic ovarian syndrome
pancreatitis
hepatitis
How does mirtazapine (remeron) work?
Mirtazapine (remeron) work as an antagonists at adrenergic, seretonin, histamine, and muscarinic receptors

- Good to treat insomnia, tremor, anxiety, and cachexia
How do selegiline and rasagiline work?
MAO-B inhibitors:
- MAO-B metabolizes dopamine and phenylethylamine. Selegiline exhibits little therapeutic benefit when used independently, but enhances and prolongs the anti-Parkinson effects of levodopa.

Rasagiline - also an MAO-B inhibitor
What does an MAO-A inhibitor do?
It preferentially deaminates norepinephrine (noradrenaline), epinephrine (adrenaline), serotonin, and dopamine (dopamine is equally deaminated by MAO-A and MAO-B).


It is inhibited by clorgiline and befloxatone
How do tricyclic antidepressants work?
antagonists of adrenergic, cholinergic, and histamine.

before starting a person on TCA what should we check?
EKG: this is a Na+ channel blocker and can prolong AV node depolarization --> prolonged PR, QRS, and QT
What are the metabolic profiles of the following?

1. alprazolam (Xanax(
2. clonazepam (klonopin)
3. Chlordiazepoxide (librium)
4. Diazepam (valium)
5. Lorazepam (ativan)
6. Oxazepam (serax)
1. Alprazolam (xanax) - fast metabolism
2. clonazepam (klonopin) - slow metabolism
3. chlordizepoxide (librium) - slow metabolism
4. diazepam (valium) - slow
5. lorazepam (ativan) - fast metabolism
6. oxazepam (serax) - fast metabolism
Calcium channel blockers: Diltiazem, verapamil, and nifedipine.

List with regards to blood pressure effects from most lower to least

List with regards to cardiac affects from most nodal blockade to least.
Lowers blood pressure: nifedipine > diltiazem > verapamil

Cardiac: Verapamil > diltiazem >>>> nifedipine
What are the side effects of digoxin toxicity?
vomiting, diarrhea, diplopia, yellow-haloed vision, confusion, long PR interval, heart block, junctional tachy, V Tach, and V fib
How does Nacardipine work?
Nacardipine - mechanism of action and clinical effects closely resemble those of nifedipine and the other dihydropyridines (amlodipine, felodipine), except that nicardipine is more selective for cerebral and coronary blood vessels.