1. What this is psychobiology behind thought disorders/psychotic symp- toms?:
1. due to elevated dopamine levels in the basal ganglia
2. possible
... [Show More] structural abnormalities
3. change greatest in the mesolimbic and mesocortical circuits
4. decreased serotonin receptor activity may also contribute to negative symptoms
2. What is the psychobiology behind mood disorders/depressive symp- toms?:
1. Depression may be due to decreased levels of serotonin and/ or nor- epinephrine in the brain. The most involved circuit is the Locus coeruleus. Involved areas of the brain includes the prefrontal cortex, Basal forebrain, striatum, new- cleus accumbens, thalamus, hypothalamus, amygdala, hippocampus, brainstem, spinal cord,, and cerebellum.
2. bipolar disorder may be due to interactions between norepinephrine, dopamine, serotonin, acetylcholine, gabba, and peptides.
3. What is this psychobiology behind anxiety disorders?:
1. elevated levels of 5ht and NE, and decreased levels of GABA
2. Raphe nucleus is the most involved circuit.
4. What is the psychobiology behind cognitive disorders?:
1. ADHD- circuits involve the anterior cingulate cortex, dorsal lateral prefrontal cortex, and orbital frontal cortex
2. dysregulation involves DA, NE, and other neurotransmitters
5. What is the role of the dopamine?:
-it's an excitatory neurotransmitter impor- tant in controlling thoughts and emotions, and for the cortex, meso- cortical track and are involved in attention focus and depression
-dopamine also helps control complex movement in the nigrostriatal dopamine pathway
-in the mesolimbic dopamine pathway that projects to the nucleus accumbens, a part of limbic system involved with pleasurable behaviors; elevated dopamine levels in this pathway or associate it with psychosis
-influences the tuberoinfundibulnar pathway that influences prolactin excretions- blockade in this pathway increase gynecomastia and prolactin
- D2 receptor is stimulated by dopaminergic agonist for Parkinson's treatment and blocked by dopamine antagonist such as antipsychotics
6. What is the role of norepinephrine?: - located primarily int he locus coeruleus (in brainstem)
- projections from LC to frontal cortex regulate mood (beta 1 receptors)
- frontal cortex projections influence attention, concentration, (alpha 2 receptors)
- projections in to the limbic cortex influence emotions and energy
- brain stem projections affect blood pressure and innervate the heart via beta 1 receptors
- innervation of the urinary treat via the sympathetic neurons effects bladder emptying, causing urinary retentions via alpha one receptors
- excitatory NT that helps elevate mood, modulate attention, and fatigue
- may contribute to anxiety d/o
7. What is the role of 5HT?: -5HT1A (somatodendritic) and 5HT1 D( terminal autoreceptor) are presynaptic
- located primarily in the raphe nucleus
- Projects from raphe nucleus to: frontal lobe, basal ganglia (esp 5HT2A which con- trol movements/obsessions/compulsions), limbic area, (esp 5HT2A and 5HT2C, related to anxiety and panic), hypothalamus (5HT3- reg appetite and sleep), brainstem, spinal cord, peripheral (5HT3 and 4.) regulate appetite and GI motility.
8. What is the role of 5HT 2A?: in basal ganglia 5HT2A controls movements/ob- sessions/compulsion
limbic system - related to anxiety and panic
9. What is the role of 5HT2C ?: in limbic system, related to anxiety and panic
10. What is the role of 5HT3?: Regulate appetite and sleep in hypothalamus
in gut, with 5HT4, helps regulate appetite and GI motility
11. What is the role of GABA?: inhibitory NT - works to sedate and calm
12. What is the role of acetylcholine?: Plays a role in cognition and memory Held imbalance with dopamine in the substantia nigra
13. What is the role of glutamate?: It is an excitatory neurotransmitter
14. What does the pituitary gland hormones stimulate?: Thyroid Adrenals
Gonads
Other tissues and organs
15. Where is CRH (corticotropin releasing hormone) released from? When is it released?: from the hypothalamus/during times of stress and as a part of normal diurnal rhythms
16. What does CRH stimulate the release of?: adrenocorticotropic hormone form the anterior pituitary
17. What does Adrenocorticotropic hormone stimulate the release of?: corti- sol from the adrenals
18. What is the role of cortisol?: normally elevates blood glucose and fats helps elevate blood pressure
suppresses the immune response
19. Describe the HPA axis: hypothalamus releases CRH
CRH stimulates the release of adrenocorticotropic hormone form the anterior pituitary
Adrenocorticotropic hormone stimulates the release of cortisol from the adrenals
20. Which individuals may have and abnormal HPA axis?: Individuals with disorders of:
circadian rhythm stress disorders depression
comorbidity such as diabetes and hyperlipidemia
21. Describe the HPT (hypothalamus-pituitary-thyroid axis): Hypothalamus re- leases thyrotropin releasing hormone (TRH)
TRH acts on anterior pituitary to secrete TSH
TSH stimulates the thyroid to synthesize and secrete the hormone T4- T4 is converted to T3 by hepatic pathways
22. What is the role of T3?: primary regulators of basal metabolic rate important for normal neurological function
23. Deficiencies in the HPT may lead to what?: wt gain depression
slow mentation
mental retardation when it occurs at birth
24. Excessive activity in the HPT can lead to what?: anxiety stress
hypermetabolic state
25. Describe the HPG Axis: Hypothalamus releases GnRH (gonadotropin releas- ing hormone)- GnRH acts on the pituitary to secrete FSH and LH- LH stimulates the secretion of estrogen and progesterone in females and testosterone in males. FSH stimulates sperm production in males and estrogen and ovarian follicle development in female.
26. What can stress activate?: stress can activate the HPA axis can suppress the immune response
can cause epinephrine release
27. What percent of Caucasians are poor metabolizers of CYP 450 2D6?: 5 to 10%
28. What is the relationships between CYP 450, 2C19 and Asians? Cau- casians?: 20% of asians have reduced activity of 2C19. 5% of Caucasians have reduced activity of 2C19
29. What is CYP 450 1A2 inhibited by?: - SSRI fluvoxamine, therefor it can increased levels of theophylline.
30. What is CYP 450 1A2 induced by?: cigarette smoking, increases the elimi- nation of olanzapine
31. CYP 450 2D6 is inhibited by which drugs?: fluoxetine paroxetine
bupropion
These will affect the metabolism of hydrocodone, morphine, and tramadol- will affect pain control
32. Which drugs inhibit CYP 450 34A?: nefazodone some SSRI - prozac
grapefruit juice
EES- carbamazepine levels with be affected
will cause some bento levels to rise, such as xanax when given with prozac
33. What drugs induce CYP 450 34A?: carbamazepine (effects oral contracep- tives)
34A induction affects methadone, so certain HIV meds will induce methadone requiring adjustment of dose.
34A is induced by St. Johns Wart, which decreases cyclosporin levels
34. Discuss the relationship between oral contraceptives and lamotrigine.: - exogenous estrogen in the form of oral contraceptives in combo with lamotrigine will induce the production of 1A4, increasing the metabolism of lamotrigine up to 50%
35. Discuss the relationship between lithium and Ibuprofen.: lithium levels increase with inhibitions prostaglandins, she common nsaids such as ibuprofen will effect levels. expeptions are ASA, sulindac and tylenol
36. How do atypical antipsychotics work?: By blocking D2 receptors in the mesolithic and mesocortical tract
37. What are the side effects of typical antipsychotics and the d2 receptor blockade?: - sedation/wt gain from Histamine (H1) blockade
- orthostatic hypotension and drowsiness from alpha 1 adrenergic receptor block- ade
- increased prolactin from the d2 blockade tubinfundivular tract
- anticholinergic effects from M1 blockade
-EPS form d2 blockade in the nigrostriatal tract
38. what are some tx for EPS?: - change in med
- lower dose
- benztropine
39. What are long term s/e of typical antipsychotics?: permanent effects on movement
- tardive dyskinesia
- potential NMS
40. List some examples typical antipsychotics.: Thorazine (chlorpromazine) mellaril (thioridazine)
Stelazine (Trifluoperazine) Trilafon (perphenazine) Haldol (haloperidol) Navene (thiothexene) Taractan (chlorprothixene)
41. What is the MOA of atypical antipsychotics?: blocks d2 and 5ht (specifically 5ht2a) receptors in the brain
5HT2A blockade helps decrease eps and get relief of negative symptoms of psychosis which is not seen with typical antispsychotics
42. What are some side effects of atypical antipsychotics?: orthostatic hy- potension
dizziness wt gain tachycardia
sleep disturbances constipation
NMS
43. What is unique to clozapine?: may cause agranulocytosis at increased risk for sz
rigorous monitoring of ANC, weekly for 6 months, biweekly for 6 months, then
monthly for year
if WBC less than 2, or ANC les than 1, stop and monitor daily
if WBC less than 3 or ANC 1.0 to 1.5, hold and get daily levels until ANC rises IF WBC less than 3.5 or ANC 1.5 to 2, repeat CBC and get biweekly until levels rise
44. What is unique to Risperdal?: may cause sz contraindicated in pregnancy
increase prolactin
45. Which antipsychotics come in a depot?: fluphenazine deconate Risperidone
paliperidone palmitate olanzapine aripiprazole
46. What is NMS?: -Neuroleptic Malignant syndrome
-life threatening complication of antipsychotic med (also seen with abrupt withdraw- al of levodopa)
- usually develops within the first 2 weeks of antipsychotic med (90%)
47. What are the classic signs and symptoms of NMS?: classic triad (HOT, STIFF, OUT OF IT)
-Extreme mental status change/confusion
-Extreme muscle rigidity/dystonia
- extreme autonomic instability/hyperthermia
48. What are some associated symptoms of NMS?: mutism akinesia
hyperthermia diaphoresis hypertension tachycardia catatonia
altered mental status irregular pulse
ELEVATED CREATINE KINASE ELEVATED MYOGLOBIN
49. What are the lab findings with NMS?: WBC elevated CPK elevated (creation phosphokinase)
myoglobin elevated
iron deficiency in 95% of cases
wide spread fasciculations/diffuse increase in muscle fibers
50. What is the progression of NMS?: rapid, death form cardiac, respiratory or renal failure
51. What is the incidence of NMS?: 0.2 to 2.4%
52. What is the pathophysiology of NMS?: abnormalities in 3 systems:
- central dopamine system
-muscle membrane dysfunction
- sympathetic nervous system
53. What drugs are at increased risk of causing NMS?: high potency neurolep- tics
54. What is the mortality of NMS?: 10-20%
55. What are some complications of NMS?: rhabdomyolysis renal failure
DIC
aspiration pneumonia pulmonary emboli cardiorespiratory arrest
peripheral nerve and muscle damage
56. What is the tx or NMS?: 1. d/c neuroleptics
2. blood pressure, hydration
3. oxygen
4. cooling blankets
5. Dantrolene (bromocriptine) to relieve rigidity
57. What are the side effects of TCAs and tetracyclic drugs?: sedating anticholinergic effects
cognitive impairment memory loss
wt gain
58. What are the side effects of MAOIs?: dizziness vertigo
headache insomina
memory impairment
hypertensive crisis with foods containing tyramine MAOIs metabolize anesthetics
59. Where are some common side effects of SRIs and SSRIs?: nervousness insomnia
sedating- paxil headache sweating
dry mouth
sexual dysfunction nausea, wt gain
60. What is Serotonin syndrome?: rare but potentially fatal side effect of sero- tonergic drugs
- caused by increased levels of serotonin
-s/s are tachycardia, fever, anxiety, muscle rigidity
61. What are the risk factors for serotonin syndrome?: use of more than one SSRI
use of st johns wart with an SSI
use of another antidepressant and an SRRI
62. What is the tx of serotonin syndrome?: d/c SSRI stabilize temp
Benzos for muscle relaxation beta blocker for tachycardia
63. What is the MOA of lithium?: exact mechanism unclear and complex may work by affecting NE and DA release in central nerves
can ease both mania and depression in Bipolar
64. What are the common side effects of lithium?: Muscle weakness Tiredness
Slurred speech Fine hand tremor Thirst
Nausea
Diarrhea vomiting
Side effects correlate with blood levels, esp over 1.2 meq/l
PROBLEMS WITH KIDNEY AND THYROID- MONITOR TSH AND KIDNEY FUNCTION
65. When should you check your blood levels for lithium?: Check serum levels 12 hours after the last dose, and after five days steady dosing
For chronic treatment blood levels every two months and every six months
long-term
For acute treatment check blood levels twice a week
66. What are cautions with lithium?: -aspirin or acetaminophen for over-the-counter analgesic is recommended
-Ibuprofen can increase their levels of lithium
-calcium channel blockers are contraindicated
-use diuretics with caution
67. What is the mechanism of action anticonvulsants?: Mechanisms of action that involves either:
-decreasing the firing of CNS nerves
-potentiating the effects of gap but in certain parts of the brain, reducing the numbers of action potentials
68. What are the adverse effects of anticonvulsants?: Sedation Fatigue
Dizziness
G.I. upset
Phenobarbital: induction of liver enzymes Phenytoin: gingival hyperplasia Carbamazepine: hepatitis and liver failure Lamotrigine: serious skin rash
69. What are contraindications for use of anticonvulsants?: Pregnancy Hepatic impairments
No hypersensitive
70. What what are the side effects associated with anxiolytic drugs?: Lethar- gy
Sedation Depression Dizziness
Anticholinergic effects Addiction
71. What are some withdrawal symptoms of benzos?: Irritability Anxiety
Insomnia Depression Seizures
72. What are examples of ADHD medications?: 1. Methylphenidate (Ritalin)
-Concerta (methylphenidate ER)
- metadate ER
-focalin (dexmethylphenidate)
2. dextroamphetamine sulfate Dextroamphetamine (Dexedrine)
Lisdexamfetamine (Vyvanse)- chemically similare to dextramphetamine) Combined Dextroamphetamine/ amphetamine salts (Adderall) Dextrostat
3. Atomoxetine (Strattera)
73. What are side effects of stimulants?: Weight loss Hypertension
Insomnia Irritability Nervousness Palpitations Tachycardia
74. What are contraindications to using stimulants?: Glaucoma Motor tics
Tourette's
Caution should be use your disorders [Show Less]