Term
| What is the 1st line drug family in treatment of panic disorder and obsessive compulsive disorder? |
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Definition
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Term
| How long does it take for SSRI to start working |
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Definition
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Term
| Whats the theory for why SSRI don't work well? |
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Definition
| body initially compensates and down regulates which means less receptors. |
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Term
| does SSRI and SNRI work on the presynapse or post synapse? |
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Definition
| they both work on the presynapse by blocking the reuptake so that there is an INCREASE AMT OF NE and 5HT3. |
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Term
| which antidepressant may cause HTN? |
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Definition
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Term
| Whats the most common reason for noncompliance of antidepressant? |
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Definition
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Term
| List 5x side effect sx of antidepressants |
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Definition
1. insomnia
2. agitation
3. headache
4. nausea
5. diarrhea |
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Term
| what risk of SSRI/SNRI is important for our profession |
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Definition
| can inhibit plat aggregation and cause bleeding. |
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Term
| which antidepressants had anticholinergic, antiadrenergic and antihistamine effects |
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Definition
| tricyclic antidepressants |
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Term
| which drugs can augment serotonergic activity and worsen serotonin sydrome |
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Definition
1. fentanyl
2. cocaine
3. zofran
4. St John's Wart |
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Term
| What do people take St. John's Wart for? What considerations should you have for someone on this? |
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Definition
| It is a natural antidepressant that is similar in nature to tricyclic antidepressants. It increases cytochrome P450 so you can have increase metabolism of drugs. |
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Term
| What population is most frequently on an anti depressant? |
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Definition
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Term
| Which anti dep can cause platelet aggregation? |
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Definition
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Term
| Which antidepressants have a narrow therapeutic range? |
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Definition
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Term
| Which drugs need to be tapered off to prevent discontinuation syndrome |
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Definition
1. SSRI
2. SNRI
3. Tricyclic
4. MAOI |
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Term
| low doses of this antidepressant can treat chronic pain |
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Definition
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Term
| CNS toxicity of tricyclics will show the following Sx |
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Definition
1. seizures
2. coma
3. hyperthermia |
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Term
| which antidepressant lowers the seizure threshold |
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Definition
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Term
| if a patient is on a tricyclic for > 6 weeks do you want to treat hypotension with a direct or indirect acting sympathomimetic |
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Definition
| either can work. Decrease the dose to see if there is an enhanced effect. |
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Term
| If a patient is newly placed on a tricyclic antidep <6 weeks what kind of sympathomimetic would you give..direct or indirect |
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Definition
| avoid indirect like ephedrine. Give direct such as phenyl. |
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Term
| describe serotonin syndrome |
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Definition
| serotonin syndrome occurs whenver there is excess serotonin in the brain. Anything which leads to excess serotonin can cause this. Rapid onset of sx. Mild symptoms may consist of increased heart rate, shivering, sweating, dilated pupils, myoclonus (intermittent tremor or twitching), as well as overresponsive reflexes.Moderate intoxication includes additional abnormalities such as hyperactive bowel sounds, high blood pressure and hyperthermia; a temperature as high as 40 °C (104 °F) is common in moderate intoxication Mental changes include hypervigilance or insomnia and agitation.[1] Severe symptoms include severe increases in heart rate and blood pressure that may lead to shock. Temperature may rise to above 41.1 °C (106.0 °F) in life-threatening cases. Other abnormalities include metabolic acidosis, rhabdomyolysis, seizures, renal failure, and disseminated intravascular coagulation; these effects usually arising as a consequence of hyperthermia |
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Term
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Definition
The symptoms are often described as a clinical triad of abnormalities:
Cognitive effects: headache, agitation, hypomania, mental confusion, hallucinations, coma
Autonomic effects: shivering, sweating, hyperthermia, vasoconstriction, tachycardia, nausea, diarrhea.
Somatic effects: myoclonus (muscle twitching), hyperreflexia (manifested by clonus), tremor. |
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Term
| Name some meds which can cause serotonin syndrome |
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Definition
1. st johns wart
2. fentanyl
3. tramadol
4. SSRI, SNRI, MAOIs, TCAs
5. trazadone
6. Ritalin
7. cocaine
8. zofran
9. Reglan |
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Term
| which MAO enzyme in noreadrenergic and dopamine neurons? |
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Definition
| A is found in both noreadrenergic and dopamine. So MAOa enzymes located there. They deactivate serotonin, epi, norepi, melatonin. |
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Term
| which anti depressant causes an increase norepinephrine release from CNS neurons? |
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Definition
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Term
| most common and serious side effect of MAOI are? |
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Definition
| orthostatic hypotension and precipitous HTN. |
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Term
| This Antidepressant adversely interacts with opiooids |
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Definition
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Term
| Describe the two opioid induced interactions with patients on MAOI |
|
Definition
excitatory phase (type 1)from excess serotonin.
- agitation, headache, skeletal muscle rigidity, hyperpyrexia
Depresisve Response (Type 2)from delayed breakdown of opioid from liver ezymes not working as well.
- hypotension, depression of ventilation and coma. |
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Term
| first line of treatment for acute mania is? |
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Definition
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Term
| which antidepressant is known to reset circadian rhythms |
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Definition
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Term
| Which antidepressant antagonizes serotonin receptors |
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Definition
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Term
| Which antidepressant lowers seizure threshold |
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Definition
|
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Term
| what is the difference between MAOa and MAOb |
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Definition
| MAOa found in dopaminergic and noradrenergic neurons while MAOb found in serotonergic neurons. |
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Term
| which MAO enzyme is found in the platelets? |
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Definition
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Term
| first line of treatment for acute mania? |
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Definition
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Term
| how does Na levels can potentially cause lithium toxicity? Explain the physiology |
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Definition
| Lithium competes with Na at the proximal tubule for reabsorption. So low levels of Na means less competition for lithium at the proximal tubules.. So more lithium will be absorbed and therefore higher lithium will be in the blood. |
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Term
| what is the difference between first and second generation antipychotics? |
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Definition
| 1st generation drugs were not selective and targeted all dopamine receptors and muscarinic, histamine, alpha and serotonin which meant more side effects. |
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Term
| Which receptor is most often the culprit for dystonia and is also responsible for effects on this ____ pathway? |
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Definition
| D2 recpetors the culprit for extrapyramidal side effects and act on the nigrostriatal pathway. |
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Term
| Motor restlessness where pt performs continuous patterns of complex motor activity |
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Definition
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Term
| A complication that devleops late in 1st generation treatment with chronic use, most common features are oral and facial dyskinesia. Irreversible |
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Definition
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Term
| Whats the biggest worry for heart rhythm realted to 1st generation antipsychotic |
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Definition
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Term
| What is the drug used to reverse dopamine blockade |
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Definition
|
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Term
| what is the downside to 2nd generation antipyschotics |
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Definition
| agranulocytosis develops in the first 3 months. |
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Term
| The 2nd generation side effects of drowsiness is from what receptor blockade |
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Definition
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Term
| Antiepileptic drugs can be challenging to use with anesthetics because they may decrease the effects of anesthesia..why? |
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Definition
| antiepileptics increases effects of CYP enzymes and leads to increased metabolism of neuromuscular blocking agents. |
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