Pharmacology Test 3 Flashcards
(500 cards)
1
Q
Cause of hypopituitarism
A
deficiency in any hormones
2
Q
Anterior Pituitary hypopituitarism
A
deficiency in GH = dwarfism
3
Q
Tx for dwarfism
A
replace GH with synthetic form somatropin
4
Q
MOA of somatropin
A
increase bone, skeletal and organ growth, RBC mass, transport of water, electrolytes and fluid
5
Q
AE of somatropin
A
- fluid retention/edema 2. muscle and joint pain
6
Q
Posterior pituitary hypopituitarism
A
decreased ADH = Diabetes Insipidus
7
Q
what is ADH also called?
A
Vasopressin
8
Q
What does ADH normally do?
A
decrease water excretion by increasing urine concentration
9
Q
Tx of Diabetes Insipidus
A
Desmopressin (DDAVP)
10
Q
what is desmopressin?
A
synthetic form of Vasopressin (ADH)
11
Q
administration route for Desmopressin?
A
1). subcut. 2). PO 3). intranasal
12
Q
MOA of desmopressin
A
increase water reabsorption @ kidney by increasing aquaporin 2 channel permeability
13
Q
other indications for Desmopressin?
A
nocturia
14
Q
Desmopressin AE
A
1). dry mouth 2). hyponatremia
15
Q
What hormones does the Anterior Pituitary normally secrete?
A
1). GH 2). LH and FSH 3). TSH 4). ACTH 5). Pr
16
Q
What hormones do the posterior pituitary normally secrete?
A
1). oxytocin 2). ADH
17
Q
Hyperpituitarism
A
excessive production of hormones from pituitary (typically anterior)
18
Q
Hyperpituitarism results in which disease(s)?
A
1). Gigantism 2). Acromegaly
19
Q
T/F: Gigantism occurs in children not adults
A
TRUE
20
Q
what is gigantism in adults called?
A
Acromegaly
21
Q
What causes acromegaly?
A
excessive GH
22
Q
physiologic effects of acromegaly
A
1). affects bone and soft tissue growth 2). hyperglycemia 3). cardiomeglia (increase risk for HTN and arrhythmias)
23
Q
T/F: individuals with acromegaly have an increased risk for HTN and arrhythmias?
A
TRUE
24
Q
TX for acromegaly
A
1). surgery is 1st line - typically remove a tumor that is the cause 2). medications follow surgery
25
Medications used in Tx of acromegaly
1). somatostatin analogue 2). GH receptor anatagonist
26
Therapeutic Concerns with Hypopituitarism Tx
1). easy to over treat 2). watch for AE of increased hormone levels 3). communicate with endocrinologist any changes 4). decreased GH = decreased BMD
27
T/F: there is an increased risk of bone fractures in individuals with dwarfism?
TRUE
28
what is slipped capital femoral epiphyses and who is at greater risk for it?
essentially a hip condition that causes hip dislocations. Hypopituitarism has increased risk for it
29
Suffix for synthetic GHs
-trope/tropin
30
Various brand names for synthetic GHs
1). Humatrope 2). Genotropin 3). Norditropin
31
Hyperthyroidism disease
Graves disease
32
S/sx of Graves disease
goiter, expothalmos, increased metabolism, nervousness, weight loss despite increased appetite
33
T/F: graves disease can result in thyroid storm
TRUE
34
what is thyroid storm
fatal symptoms of dehydration, tachycardia, delirium and fever
35
TX for graves disease
1). anti-thyroid meds 2). Radioactive Iodine 3). Thyroidectomy
36
Antithyroid meds
1). Methimazole 2). Propylthirouracil (PTU)
37
Which antithryoid med is the preferred option?
Methimazole - smaller dose needed and no black box warning
38
PTU black box warning
heptatoxicity
39
MOA of antithyroid meds
blocks formation of T4 to T3 by inhibiting iodine oxidation
40
When are antithyroid meds used?
1). mild cases 2). older 3). avoid radioactive iodine
41
AE of antithyroid meds
1). rash 2). GI upset 3). arthralgia
42
how often is methimazole dosed?
one or 2x daily
43
how often is propylthirouracil dosed?
initially dosed 4x/day
44
T/F: methimazole can cause birth defects in 1st trimester of pregnancy?
TRUE
45
When is PTU preferred over methimazole
1). during 1st trimester of pregnancy 2). while breastfeeding
46
Rare AE of antithyroid meds
1). agrunulocytosis 2). heptotoxicity
47
s/sxs of agrunlocytosis
1). fever 2). sore throat 3). mouth ulcers
48
what is radioactive iodine?
radioactive destruction of thyroid
49
AE for radioactive iodine?
hypothyroidism (will require life long treatment)
50
What other med can be used in trx of hyperthyroidism?
Propanolol \>\> used to trx symptoms
51
Types of Hypothyroidism
1). primary 2). secondary
52
What is primary hypothryoidism?
autoimmune destruction of thyroid gland
53
What is secondary hypothryoidism?
1). reduced secretion of TRH (hypothalamus) 2). reduced secretion of TSH (pituitary)
54
S/Sxs of hypothyroidism (8)
1). bradycardia 2). anemia 3). lethargy 4). wt gain 5). cold intolerance 6). menstrual irregularities 7). general muscle weakness 8). Goiter is possible
55
Tx for hypothyroidism
Levothyroxine (Synthroid)
56
What is levothyroxine
synthetic T4 \> it is the DOC for hypothyroidism b/c it is cheap
57
MOA of Levothyroxine
synthetic T4 is converted to T3
58
T/F: Levothyroxine is an NTI drug?
TRUE \>\> requires monitoring and dose adjustments
59
AE of Levothyroxine (Synthroid)?
overall well tolerated unless overtreated: 1). sweating 2). heat intolerance 3). tachycardia 4). diarrhea 5). nervousness 6). menstrual irregularities 7). increased BMR
60
Special considerations for Levothyroxine (2)
1). take on empty stomach 2). don't take along with Fe, Ca, Mg, Al containing products
61
T/F: chronic hypothyroidism can increase your risk of CV disease?
TRUE
62
Types of hyperparathyroidism
1). primary 2). seconday
63
Cause of primary hyperparathyroidism
1). parathyroid adenoma 2). hyperplasia or carcinoma
64
Causes of secondary hyperparathyroidism
underlying conditions such as chronic kidney disease \> Ca lvls become low triggering release of PTH
65
TX options of primary hyperparathyroidism
1). surgery 2). medications
66
Medications used to trx hyperparathyroidism
1). Calcimimetics 2). Bisphosphonates
67
MOA of calcimimetics
competitive antagonist of Ca receptors \>\> decreases PTH secretion
68
AE of calcimimetics
1). most common: N/V 2). monitor for hypocalcemia
69
TX options for secondary hyperparathyroidism
treat underlying condition
70
Causes of Hypoparathyroidism
All result in hypocalcemia1). injury during surgery 2). autoimmune disease 3). congenital defect
71
TX for hypoparathyoidism
1). Calcium 1-3 grams/day 2). Vitamin D
72
Over treatment of hypoparathyroidism can cause \_\_\_\_\_\_\_\_\_
1). hypercalcemia 2). hypercalciuria \>\> leading to nephrolithiasis
73
The adrenal glands secrete from what regions?
1). Cortex 2). medulla
74
What is secreted from the medulla of the adrenal glands?
1). NE 2). epinephrine
75
What is secreted from the cortex of the adrenal glands?
1). mineralocorticoids 2). glucorticooids 3). some sex steroid
76
What is an example of a mineralocorticoid?
Aldosterone
77
What do mineralocorticoids do?
effects electrolyte/water balance
78
What do glucocorticoids do?
effect carb/fat metabolism
79
What are some examples of glucocorticoids?
1). hydrocortisone 2). cortisol
80
A deficiency of mineralocorticoids is called \_\_\_\_\_
Hypoaldosteronism
81
What disease is primarily associated with hypoaldosteronism?
Addison's Disease
82
What causes Addison's disease?
1). general adrenocoticoid insufficiency \>\> autoimmune system destroys adrenal cortex (main cause)2). defective aldosterone producing enzyme (rare)
83
TX for Addison's disease
Fludrocortisone (synthetic aldosterone)
84
What is excessive production of aldosterone called?
hyperaldosteronism
85
causes of Hyperaldosteronism?
1). Adrenal tumor (Conn's syndrome) 2). Adrenal hyperplasia
86
Tx for Conn's syndrome
Surgery
87
Tx for adrenal hyperplasia
1). Spironolactone 2). Eplerenone
88
why are diuretics used to treat hyperaldosteronism
they are aldosterone receptor antagonists
89
which diuretic tx for hyperaldosteronism have less AE?
Eplerenon (selective for aldosterone receptors, Spironolactone is nonselective)
90
S/Sxs of Hyperaldosteronism (7)
1). muscle weakness 2). fatigue 3). paresthesias 4). headache 5). polydipsia 6). nocturnal polyuria 7). HTN
91
What is excessive production of glucocorticoids called?
1). Cushing's syndrome
92
What is Cushing's syndrome due to?
Hypercortisolism
93
what can lead to hypercortisolism?
1). take too much 2). make too much 3). tumor on pancreas/thyroid telling adrenal gland to make too much
94
TX options for Cushing's syndrome?
1). surgery (1st line)2). meds surrounding surgery
95
Medications used as adjunct TX in Cushing's syndrome?
1). Steroidogenesis inhibitors 2). Glucocorticoid-antagonist
96
Glucocortioid deficiency types
1). primary adrenal insufficiency 2). secondary adrenal insufficiency
97
What is primary adrenal insufficiency?
Addison's Disease \>\> autoimmune destruction of adrenal cortex
98
Primary adrenal insufficiency results in what \_\_\_\_\_\_?
deficiency of both mineralcorticoids and glucocorticoids
99
What causes secondary adrenal insufficiency?
Too much exogenous corticosteroid admin \>\> suppresses hypothalamic-pituitary-adrenal axis \>\> decreased ACTH release
100
What does secondary adrenal insufficiency tell us about steroid dosages?
It is important to taper off of steroids
101
TX for primary and secondary adrenal insufficiency
1). Both = replace glucocorticoids (hydrocortisone, prednisone, cortisone) 2). primary = fludrocortisone as well (replace aldosterone)
102
Short term AE of primary/secondary adrenal insufficiency TX
1). increased blood glucose 2). mood changes 3). fluid retention
103
Long term AE of primary/secondary adrenal insufficiency TX
1). osteoporosis (increased fracture risk) 2). thin skin 3). muscle wasting 4). poor wound healing 5). Adrenal suppresion 6). Cushing's syndrome 7). increased risk of infection
104
T/F: exercise and increased stress will require higher med dosing for glucocortioid deficiencies?
TRUE
105
Therapeutic Concerns of Adrenal Steroids
1). lots of pts w/dif disorder use them (RA, lupus, bursitis, etc.)2). catabolic effect on supporting tissue \>\> fall risk ! do not overload 3). can cause HTN 4). immunosupressive = increase infection risk 5). drug toxicity \>\> mood changes, psychoses
106
Stimulation cascade for sex hormones
Hypothalamus releases GnRH --\> Ant. pituitary gland releases LH and FSH --\> stimulates gonads to release sex hormones
107
Effects of testosterone (6)
1). masculinizing effects 2). development of male genitals in embryo 3). increase muscle/bone size 4). stimulates synthesis of clotting factors in liver 5). stimulates production of erythropietin in kidneys 6). regulates LH production from ant pituitary
108
Types of testosterone deficiency
1). primary 2). secondary
109
what causes primary testosterone deficiency?
testicular failure
110
what cause secondary testosterone deficiency?
decreased GnRh
111
S/Sxs of testosterone deficiency? (8)
1). delay in puberty 2). low energy 3). decreased libido 4). ED 5). decreased pubic hair6). anemia 7). osteoporosis 8). muscle atrophy
112
TX for testosterone deficiency
exogenous admin of testosterone (IM or topical)
113
T/F: perfectly safe to administer testosterone PO?
FALSE \>\> risk of heptatoxicity
114
IM admin of testosterone considerations
1). variable symptom relief (cycle between high to low)2). mood changes 3). can cause hepatic adenomas
115
topical admin of testosterone considerations
keep it covered so no contact
116
Risks/AE with testosterone administration
1). increased risk of MI, stroke, CV death 2). hepatotoxicity (long-term) 3). large doses may cause infertility
117
AE of testosterone in Athletic populations (11)
1). acne 2). MI, CV death, VTE3). PE 4). Cancer (testicular or prostate) 5). injection site infections 6). feminization 7). menstrual irregularities (in women) 8). tendon/ligament rupture 9). insomnia 10) mood disorder 11). aggressiveness
118
Therapeutic concerns with testosterone TX
1). monitor BP 2). athletic use of androgens
119
Role of estrogen (4)
1). develops female genitals in embryo 2). causes puberty and female specific changes 3). deposition of subcutaneous fat stores 4). widens pelvic girdle
120
What is the menstrual cycle?
28 day cycle. regulated by interaction between pituitary and ovarian hormones
121
Positive feedback loop in Menstrual cycle
1). low estrogen levels increase LH release 2). LH release further increases estrogen
122
Negative feedback loop in Menstrual cycle
LH and FSH are inhibited during second half of cycle from high estrogen and progesterone levels
123
What does the altering normal control between pituitary and ovarian hormones provide?
contraceptive control
124
Estrogen and Progesterone Medical uses
1). Contraceptives 2). Post-menopausal hormone replacement therapy (HRT)
125
Types of Contraceptives
1). Combination Oral contraceptive (COC)2). Long-acting intrauterine device (IUD)
126
common COC AEs (6)
1). increased BO2). N/V 3). weight gain 4). acne 5). depression 6). topical rxn
127
Rare COC AEs (3)
1). DVT/PE 2). Stroke 3). MI
128
T/F: the risk for MI from contraceptive use increases after 35 years of age?
TRUE, also if uncontrolled smoker and diabetic
129
T/F: AE of N/V from COC generally improve after 2-3 cycles?
TRUE
130
Complications from IUDs?
pelvic inflammatory disease
131
Goals of HRT?
1). decrease menopausal symptoms 2). increase BMD 3). decrease fracture risk
132
TX for HRT
1). estrogen only (if no uterus) 2). estrogen + progestogens
133
Route of admin for estrogen (4)
1). PO 2). transdermal patch/spray 3). topical gel/solution 4). vaginal ring/cream
134
Estrogen AE (4)
1). nausea 2). HA 3). breast tenderness 4). vaginal bleeding
135
Progestogens admin
1). PO 2). patch
136
Progestogens AE (4)
1). bloating 2). headache 3). weight gain 4). irritability
137
Known risks with HRT TXs
1). DVT 2). PE 3). gallbladder disease 4). breast cancer (with combo) 5). endometrial cancer (with estrogen alone)
138
General Men's health disorder
Benign prostatic hypertrophy (BPH)
139
TX options for BPH
1). Alpha-adrenergic antagonists 2). 5a-reductase inhibitors 3). anticholinergic agents 4). B3-adrenergic agonsit
140
Alpha-adrenergic antagonist used for BPH
Tamsulosin
141
MOA of tamsulosin
relax smooth muscle in prostate and bladder neck
142
5a-reductase inhibitor used for BPH
finasteride
143
MOA of finasteride
interfere with stimulatory effects of testosterone
144
AE of tamsulosin and finasteride
Hypotension
145
Anticholinergic agents used to treat BPH
oxybutynin
146
MOA of oxybutynin
antispasmodic effect on smooth muscle \>\> blocks acetylcholine on smooth muscle
147
AE of oxybutynin
ABCDs
148
B3-adrenergic agonist used to treat BPH
mirabegron (Myrbetriq)
149
MOA of mirabegron (Myrbetriq)
relaxes detrusor muscle to decrease voiding symptoms
150
AE of mirabegron (Myrbetriq)
may increase BP
151
Other indication for mirabegron (Myrbetriq)
OAB
152
Male to Female gender transition meds
1). Estrogen and Progesterone 2). Spironolactone (testosterone blocker) 3). Finasteride (testosterone blocker)
153
Female to Male gender transition meds
testosterone
154
T/F: sex at birth still defines some risks for individuals undergoing gender transition?
TRUE
155
What causes Osteoporosis?
decreased osteoblast function
156
T/F: osteoporosis is more common in post-menopausal women?
TRUE
157
Types of Osteoporosis
1). primary 2). seconday
158
What causes primary osteoporosis?
1). idiopathic (unknown 2). increased age
159
what causes secondary osteoporosis?
1). underlying diseases2). medications
160
Clinical manifestations for osteoporosis
1). sudden back pain (compression fx of vertebral body) 2). increased kyphosis of T spine 3). decreased height
161
Risk factors for developing osteoporosis (9)
1). decreased bone mass after 35 years old 2). female hormone changes 3). genetics 4). Caucasian 5). low physical activity 6). tobacco/alcohol use 7). medications 8). depression 9). diet/nutrition deficits
162
TX for osteoporosis?
1). calcium and Vitamin D2). Bisphosphonates (most common tx) 3). Denosumab 4). Sclerostin Inhibitor 5). Teriparatide
163
AEs of calcium?
Consitipation
164
suffix for Bisphosphonates
-dronate
165
MOA of Bisphosphonates
binds key enzyme to inhibit natural bone turnover pathway \>\> increases osteoclast apoptosis which decreases bone turnover
166
Bisphosphoantes considerations
1). stay upright 2). take w/water 30-60 minutes before food
167
Bisphosphonates common AE
GI issues (increased if not upright)
168
Rare Bisphosphoantes AE
1). atypical femur fx 2). osteonecrosis of jaw (ONJ) - from IV use or long-term trx
169
Bisphosphonates contraindications
1). hypocalcemia 2). esophageal abnormalities 3). inability to remain upright
170
what type of drug is denosumab (Prolia)
Anti-RANKL
171
denosumab (Prolia) AEs
same as bisphospnates
172
denosumab (Prolia) considerations
administered in provider's office
173
Sclerostin inhibitors MOA
increase bone formation
174
Sclerostin inhibitors common AE
arthraligia
175
Sclerostin inhibitors rare AEs
1). hypocalcemia (atypical) 2). femur fx3). ONJ 4). increased risk of MI, stroke, or CV death
176
Synthetic PTH MOA
1). stimulate osteoblast function 2). increases GI calcium absorption 3). increase renal calcium absorption all this increases BMD
177
Synthetic PTH AEs
transient OH within 4 hours of dose
178
Drug name for Synthetic PTH
Teriparatide (Forteo)
179
Osteoporosis medication considerations
also given to pts with longterm steroid use and men receiving androgen deprivation therapy
180
Osteoporosis meds Therapeutic Concerns
1). excessive doses of Ca supplements can cause arrhythmias 2). utilize weight bearing activities to promote bone growth 3). avoid high impact activities for pts with osteroporosis
181
Types of Diabetes
Type 1Type 2
182
Pathophysiology T1DM
selective beta cell destruction in the pancreas \>\> can't produce insulin
183
what causes T1DM?
Autoimmune dysfunction, genetic, viral infections
184
What is T2DM?
1). moderate beta cell destruction that can become more severe 2). Insulin resistance
185
Which type of diabetes is more prevalent in youth?
T1DM
186
what is LADA?
latent autoimmune diabetes in adults (Type 1.5 \>\> requires insulin)
187
What type of diabetes can only be treated with insulin?
T1DM
188
Pathophysiology of T2DM?
Egregious Eleven
189
what is the overall result of the egregious eleven?
Hyperglycemia
190
TX options for T2DM?
1). diet 2). exercise 3). non-insulin meds 4). insulin
191
what are non-insulin meds that treat T2DM also called?
Antihyperglycemic Drug
192
List the classes of Antihyperglycemic Drugs (6)
1). Biguanide 2). Sulfonylureas 3). Thiazolidinedione (TZDs) 4). DPP-4 inhibitor 5). SGLT2 Inhibitor 6). GLP1 Receptor agonist
193
MOA for Biguanide
unclear, but it stops: 1). production of glucose 2). intestinal absorption of glucose also 3). increases insulin sensitivity in muscle and fat
194
AE of Biguanide
1). GI (N/V/cramps) 2). Vitamin B12 deficiency
195
how is vitamin B12 deficiency from Biguanide important?
it can be misdiagnosed as peripheral neuropathy
196
Biguanide boxed warnings
lactic acidosis
197
Sulfonylureas MOA
increase insulin release
198
Sulfonylureas AE
1). hypoglycemia 2). weight gain
199
AE from Sulfonylureas are increased in which populations?
1). elderly 2). individuals with renal dysfunction
200
T/F: some Sulfonylureas are on the Beer's List?
TRUE
201
Thiazolidinedione (TZDs) MOA
increase insulin sensitivity in muscle and fat
202
Thiazolidinedione (TZDs) AE
1). edema 2). long-term increased risk of bone fractures
203
Thiazolidinedione (TZDs) boxed warnings
HF
204
What does DPP-4 inhibitor stand for?
Dipeptidyl peptidase 4 inhibitor
205
DPP-4 inhibitor MOA
inhibit breakdown of incretin =\> 1). increases insulin sensitivity and release 2). decreases glucagon secretion 3). decreases liver glucose production
206
DPP-4 inhibitor AE
very well tolerated
207
rare AE of DPP-4 inhibitor
1). arthraliga 2). increased risk of HF
208
SGLT-2 Inhibitor MOA
blocks glucose reabsorption in kidneys =\> increases urinary glucose excretion
209
SGLT2 inhibitor AE
1). volume depletion related 2). genitourinary infections 3). renal insufficiency
210
Rare SGLT2 inhibitors AE
euglycemic diabetic ketoacidosis
211
SGLT2 inhibitor boxed warnings
increased risk of bone fractures and lower limb amputations
212
GLP1 receptor agonist MOA
1). increase insulin secretion 2). decrease glucagon secretion 3). decrease gastric emptying (incretin hormones)
213
GLP1 receptor agonist AE
GI (nausea, bloating, diarrhea)
214
Sulfonylureas suffix
-ide
215
DPP-4 inhibitor suffix
-gliptin
216
SGLT2 inhibitor suffix
-flozin
217
GLP1 receptor agonist suffix
-tide
218
What are the symptoms of Diabetes? (10)
1). tired 2). always hungry 3). frequent urination 4). always thirsty 5). blurry vision 6). numb/tingling hands or feet 7). sexual problems 8). sudden weight loss 9). wounds that won't heal 10). vaginal infections
219
MOA of Insulin
1). increase glucose uptake 2). inhibit glucose production
220
Types of Insulin
1). basal 2). bolus 3). Other
221
What are the "Other" types of insulin?
1). intermediate (NPH) 2). mixed 3). concentrated 4). U-500 5). inhaled regular insulin (afrezza)
222
how often is basal insulin injected?
normally only once daily, sometimes twice
223
types of bolus insulin
1). rapid 2). regular
224
onset for rapid bolus insulin
10-30 minlasts for 3-5 hours
225
onset for regular bolus insulin
~30 minlasts 4-12 hours
226
what type of insulin can be given as correction insulin?
rapid bolus insulin
227
Therapeutic considerations for DM?
1). exercise = good 2). monitor blood glucose 3). avoid heat/massage @ injection site 4). need good footwear 5). exercise after meals
228
if blood glucose is \<100 mg/dL then \_\_\_\_\_\_\_
eat a snak
229
if blood glucose is \>300 mg/dL then \_\_\_\_\_\_\_-
No PT
230
what are the signs of hypoglycemia?
1). shaky 2). sweaty 3). dizzy 4). confusion 5). difficulty speaking 6). weak/tired 7). HA 8). nervous/upset
231
\_\_\_\_\_\_\_ masks all the symptoms of hypoglycemia except \_\_\_\_\_\_
1). Beta blockers 2). sweating
232
Which Antihyperglycemic Drugs reduce the risk for hypoglycemia?
1). Biguanide 2). Thiazolidinedione (TZDs) 3). DPP-4 inhibitors
233
what is ADHD?
a series of behavioral disorders
234
what are the subtypes of ADHD?
1). inattentive 2). hyperactive-impulsive 3). combined
235
what is the etiology of ADHD?
multi-factorial: environmental, genetic and biological factors
236
what increases the risk of developing ADHD?
pre/perinatal expsoure to cigarettes/alcohol
237
TX options of ADHD?
1). stimulants 2). Atomoxetine (Strattera) 3). Other
238
How do stimulants work?
block NE and dopamine reuptake
239
boxed warnings with stimulants?
1). increase CV risk 2). abuse potential
240
common AE for stimulants?
1). decreased appetite/weight loss 2). stomach ache 3). insomnia 4). HA 5). irritability/jitteriness
241
Rare/uncommon AE for stimulants?
1). dysphoria 2). "spacey"/zombie-like state 3). tics/abnormal movements 4). HTN, HR fluctuations 5). hallucinations 6). discolorations from patch
242
Atomoxetine (strattera) MOA
selective NE re-uptake inhibitor (SNRI)
243
Pro/Con of Atomoxetine (Strattera)?
less effective than stimulants but also less abuse potential
244
AE of Atomoxetine (Strattera)
more fatigue, sedation and dizziness than stimulants
245
boxed warnings for Atomoxetine (Strattera)
increased risk of suicide
246
Other ADHD drugs
1). alpha-2 adrenergic agonists 2). Bupropion 3). Lithium 4). Anti-psychotics
247
What is epilespy?
a chronic condition characterized by recurrent seizures
248
what is a seizure?
a finite event resulting from excessive discharge of cerebral neurons causing transient impairments or loss of consciousness
249
what can cause a seizure?
1). too little GABA 2). too much Glutamate 3). CNS inflammation
250
what is GABA?
main CNS inhibitory neurotransmitter \> normally inhibits depolarization
251
what is Glutamate?
an excitatory neurotransmitter
252
What are the types of seizures?
1). partial 2). generalized
253
what occurs in a partial seizure?
one cerebral hemisphere with no loss of consciousness
254
what is a a generalized seizure?
effects both hemispheres and results in loss of consciousness
255
Types of generalized seizures?
1). Tonic/Clonic 2). only Tonic 3). only Clonic
256
What is the most common type of generalized seizure?
Tonic/Clonic
257
how long does an only tonic seizure last?
a few seconds
258
how long does an only clonic seizure last?
a few seconds
259
What occurs during a tonic/clonic seizure?
1). rigid extensor spasm 1st 10-30 seconds 2). rhythmic flexor spasm 2-4 minutes
260
during the rigid extensor spasm what can happen?
stopped respiration, poop, pee and salivate
261
during the rhythmic flexor spasm what can happen?
continued loss of consciousness \>\> alertness will slowly return after
262
what are the two types of epilepsy?
1). Primary 2). Seconday
263
What causes primary epilepsy?
it is idiopathic and accounts of 50% of cases
264
what causes secondary epilepsy?
1). in children: injury @ birth or metabolic disease 2). in adults: TBI
265
TX for epilepsy
excitatory or inhibitory:1). antiepileptic drug (AED) 2). antiseizure drug (SD) 3). anti-convulsant
266
drug TX for epilepsy depends on \_\_\_\_
1). patient specific factors 2). type of seizure 3). response to previous meds
267
goals for epilepsy TX
1). eliminate seizures 2). experience no AEs 3). improve QOL
268
AE of Epileptic drugs
1). rash (Steven Johnson's Syndrome)2). neurotoxicity 3). hypothyroidism
269
At risk populations for Epilepsy
1). Women 2). pregnant women 3). children 4). elderly
270
Therapeutic considerations for Epilepsy
1). some drugs are NTI 2). watch for sedation, dizziness and ataxia 3). rashes 4). bone marrow depression 5). vitamin K deficiency 6). ask about seizure activity 7). know how to respond appropriately to a seizure
271
therapeutic considerations for women and AEDs
1). decreased ovarian function 2). infertility 3). PCOD 4). weight gain
272
what is PCOD?
polycystic ovarian disease
273
what is multiple sclerosis (MS)?
a chronic, progressive disease of CNS - axonal damage and demyelination
274
what is the etiology of MS
1. autoimmune process
2. genetic predisposition
3. environmental exposure
275
what are the clinical symptoms of MS?
1. weakness, poor endurance
2. sensory impairments
3. balance impairments
4. ataxia
5. UMN signs
6. blurred vision, nystagmus
7. dysarthria
8. autonomic dysfunction
276
what are UMN signs in MS?
1. spasticity
2. hyperreflexia
277
What are some outcome measures used to determine trx effectiveness in MS?
1. MRI - visualize lesion
2. relapse rate
3. expanded disability severity scale (EDSS)
278
how is the Kurtzke EDSS scored?
0-10 (0 = normal, 10 = death)
279
what are the major aspects of MS treatment?
1. Disease modifying therapies
2. symptom management
280
what do DMTs lessen?
1. # of new lesions that form/keep existing from getting larger
2. lessen # of relapses
281
name 5 DMT drugs
1. Interferon B
2. Glatiramer acetate
3. Sphingosine 1-Phosphate Receptor Modulator
4. Dimethyl fumarate
5. Monoclonal antibodies
282
MOA for Interferon-B
exact MOA is unknown. Impacts immune function
283
Administration route for Interferon-B
subcut or IM
284
Indications for Interferon-B
1. relapsing MS 2. decrease exacerbations and delay accumulation of physical disability
285
AE for \>50% Interferon-B
1. flu-like symptoms
2. HA
3. injection site rxn
286
AE for \>20% Interferon-B
1. fatigue
2. depression
3. pain
4. abdominal pain
5. nausea
6. leukopenia
7. increase LFTs
8. myalgia
9. back pain
10. weakness, fever
287
\*monitor Interferon-B for \_\_\_\_\_\_\_\_\_\_
1. Neuropsychiatric changes
2. drug-induced hypothyroidism
3. worsening cardiac function in HF
288
MOA of Glatiramer acetate
reduce autoimmune response to myelin by reducing T-cell response against myelin
289
Administration route for Glatiramer acetate
subcut or IM
290
Indication for Glatiramer acetate
relapsing MS, decreasing exacerbation and lesion on MRI
291
Most common AE for Glatiramer acetate
injection site rxs
292
other common AE for Glatiramer acetate
1. rash
2. VD
3. dyspnea
4. chest pain
293
what drug is a S1P receptor modulator?
Fingolimod
294
Fingolimod MOA
coverts to active metabolite which blocks release of lymphocytes into CNS = decrease in inflammation
295
Fingolimod use
PO daily to decrease exacerbation and overall disease severity
296
Fingolimod \>15% AE
headache, increased LFTs
297
Rare Fingolimod AEs
1. macular edema (report vision changes immediately),
2. infection
298
What AE warrants an immediate referral for somone on an S1P receptor modulator?
vision changes
299
Dimethyl fumarate Use
PO 2x/day to decrease exacerbations and disease severity
300
MOA of dimethyl fumarate
unknown in MS; may have anti-inflammatory properties
301
AEs of dimethyl fumarate
1. GI (N/V/D, abdominal pain in 12-18%)
2. flushing (up to 40%)
302
Rare AE for dimethyl fumarate
hepatoxicity
303
Monoclonal Antibodies drugs suffix
-mab
304
general MOA for monoclonal antibodies
decrease inflammation in CNS and autoantibody formation
305
Use of Monoclonal antibodies
1. may decrease exacerbations
2. decrease lesions on MRI and slow progression
306
Common AEs for monoclonal antibodies
1. infusion related rxns
2. HA
3. fatigue
4. arthralgia
307
What is PML?
Progressive Multifocal Leukoencephalopathy
demyelinating CNS disorder caused by reactivation of JCV
308
Patients on which meds are at a higher risk of developing PML?
1. Monoclonal Antibodies
2. Dimethyl Fumarate
3. SP1 receptor modulators
309
Signs and Symptoms of PML?
1. altered mental status (AMS)
2. aphasia
3. ataxia
4. hemiparesis
5. hemiplegia
6. visual field disturbances (double vision, partial blindness)
7. seizures
310
Off-label trxs for relapsing/progressive MS
1. Azathioprine
2. Methotrexate
311
Symptom trx for MS
1. **Spasticity -- baclofen**
2. ambulation and mobility impairments -- dalfampridine
3. **Upper extremity tremor -- botulinum toxin type A**
4. **Central neuropathic pain -- gabapentin**
5. Psudobulbar dysfunction -- combo dextromethorphan/quinidine sulfate
6. Urinary symptoms -- oxybutynin
7. depression/anxiety -- antidepressants
312
Drug Concerns for MS patients
1. Fatigue
2. Corticosteroid drug treatment
3. DMT drugs can have substantial AEs influcing flu-like symptpoms to immunosuppression
313
Key features of Alzheimer's Disease
1. Progressive neurodegenerative disease
2. Gradual loss of memory and function leading to total dependence on caregivers
3. Eventual inability to recognize family/friends/self
314
What neurotransmitters are depleted in AD?
1. Acetylcholine
2. serotonin
3. somatostatin
4. NE
315
General trx approach for AD
1. Mild case
1. cholinesterase inhibitor
2. Moderate case
1. cholinesterase inhibitor + memantine (delays progression)
2. address behavioral and pyschological symptoms
3. Severe case
1. consider if meds will be beneficial
2. may continue cholinesterase inhibitor
316
Cholinesterase Inhibitor Drug
Donepezil (Aricept)
317
Cholinesterase Inhibitors pros
modest improvements in cognition and ADLs
benefits last ~3-24 months
318
Cholinesterase Inhibitors MOA
inhibit acetylcholinesterase from breaking down acetylcholine =
increased ACh helps correct ACh deficiency in AD
319
Primary AEs for Cholinesterase Inhibitors
SLUDGE
DUMBELLS
320
T/F: Cholinesterase Inhibitors can exacerbate UTOs, asthma, and COPD
TRUE
321
T/F: Cholinesterase Inhibitors are on the Beers List?
TRUE
322
what class of drug is Memantine (namenda)
NMDA antagonist
323
NMDA antagonist MOA
antagonise NMDA receptor = stops excessive receptor activation by glutamate = decreases excitation and neuronal death
324
When are NMDA antagonists used?
1. monotherapy for moderate cases
2. in conjunction with cholinesterase inhibitor in moderate cases
3. Not FDA approved for mild cases
325
NMDA Antagonists AE
1. usually well tolerated
2. monitor for falls
326
Individuals with AD should not be taking what?
1. Anticholinergic Drugs
2. OTC antihistamines (Benadryl)
327
AD drug concerns
1. Cholinergic meds: GI issues (NVD) most common
2. Memantine may cause dizziness, watch for falls
3. Communicate behavioral issues to healthcare providers
328
What should be taken into consideration when scheduling PT for patients with AD?
1. lots of structure to help reduce behavioral issues
2. reduce behavioral issues related to sundowning
3. utilize time of day when pateint most alert
329
Characterizations of Parkinson's Disease
1. Akinesia
2. Bradykinesia
3. Postrual instability
4. Rigidity (freezing episode)
5. Tremor (pill-roll)
330
Pathophysiology of PD
1. progressive death of dopamine-producing neurons in basal gangali
2. reduced communication with Thalamus
3. results in loss of voluntary movement, especially automatic movements
331
Etiology of basal ganglia neurotransmitter imbalance
Overall unknown, possible impact of
1. genetics
2. environmental factors
332
Medical management of PD
1. Dopamine replacement
2. Dopamine agonist therapy
3. Anticholinergic therapy
333
Overall goal of pharmacologic treatment Parkinson's Disease
Restore neurochemical balance
334
Name of Parkinson's Disease Scales
1. Unified Parkinson's Disease Rating Scale (UPDRS)
2. Hoehn & Yahr Scale
335
PD, dopamine replacement therapy drugs
Levodopa-carbidopa (L-dopa)
MAO-B inhibitors
COMT Inhibitor
Amantadine (both agonist and replacement therapy)
336
PD, dopamine agonist therapy
Amantadine
Ropinirole (Requip)
337
Anticholinergic Therapy Drugs for PD
1. Benztropine (Cogentin)
2. Trihexyphenidyl
338
benefits of Levodopa-carbidopa
1. improves movement velocity
2. may reduce tremor
3. reduce rigidity
4. improves force production & coordination of anticipatory postural task
339
What are the long-term effects of dopamine replacement therapy
1. Movement-related complications
2. Dyskinesia
3. Motor Fluctuations
340
how does dopamine impact cholinergic response?
without dopamine the cholinergic response is uninhibited
341
what is the 1st line trx and most effective treatment for PD patients?
Levodopa-carbidopa (Sinemet)
342
carbidopa MOA (why is it combined with l-dopa)?
stops breakdown of l-dopa to dopamine in periphery so more l-dopa crosses BBB
343
AE of Levodopa-carbidopa (Sinemet)
1. End of dose "wearing of"
2. "Delayed on" or "no on"
3. Freezing
4. "on" period dyskinesia
344
MOA for MAO-B inhibitors
inhibit monoamine oxidase (MAO) B which breaks down dopamine = increased dopamine levels in CNS
345
what PD treatment has a risk for serotonin syndrome?
Selegiline (a type of MAO-B inhibitor) when combined with serotonergic meds
346
MOA of COMT inhibitors
Inhibit COMT which in turn decreases breakdown of l-dopa
347
when are COMT inhibitors used?
Adjunct
used to reduce end of dose wearing off with l-dopa
348
AE of COMT Inhibitors
\>10% = involuntary movements, nausea
349
what has Amantadine been used to treat in the past?
Influenze
350
MOA of Amantidine
Unknown
possibly increases dopamine release
351
Amantadine AE
1. confusion
2. hallucinations
3. dizziness
4. dry mouth
5. constipation
6. livedo retiularis
352
T/F: Dopamine agonists can be a 1st line option for trx PD?
TRUE
353
Dopamine Agonist Drug
ropinirole (Requip)
354
ropinirole (Requip) AE
1. nausea
2. drowsinee
3. dizziness
4. syncope
355
what to monitor for on a pt on ropinirole?
1. light-headedness
2. postural hypotension
3. hallucinations
4. lower-extremity edema
356
less common AE of ropinirole
1. impulsive behavior
2. sleep attacks
357
when might ropinirole be used?
as a monotherapy
adjunt therapy to reduce end of dose wearing off with l-dopa
358
Anticholinergic Therapy for PD MOA
antagonzie muscarinc receptors to prevent acetylcholine binding
359
PD Drug concerns
1. Timing of PT session with delivery of meds
2. Effects of exercsie on med absorption, utilization, and motor effects
3. Long-term meds use and disease progression
360
What is spasticity?
caused by a lesion on the spine or brain which leads to reduced neural innervation and increased tone
361
Spasticity is synonymous with \_\_\_\_\_\_\_\_\_
hypertonicity
362
What is muscle tone?
continuous tension in muscle
* normal tone enables motor function
* low tone = flaccid
* high tone = excessive muscle tension
363
spasticity is ___________ resistance to ________ stretch
velocity-dependent
passive
364
What scale measures spasticity?
Ashworth Scale (0-4)
365
Hypertonicity can lead to impairment with:
1. ROM
2. coordination
3. skin hygiene
4. pain
5. functional mobility
6. ADLs
366
What are muscle spasms?
increased muscle tension following musculoskeletal injury and inflammation
no damage to brain or spinal cord
367
What overall drug class is used to treat spasticity and muscle spasms?
Muscle Relaxants
and
Antispasticity meds
368
Drug list for treating muscle spasms and spasticity
1. Tizanadine
2. Cyclobenzaprine (Flexaril)
3. Diazepam (Valium)
4. Botox (botulinum toxin)
5. Baclofen (Lioresal)
6. ITB pump (intrathecal baclofen)
369
What type of drug is tizandine?
alpha-2 agonist
370
MOA of tizanadine
bind to alpha-2 receptors to decrease excitatory NTs which decrease excitability to post synaptic neurons
371
tizanadine instructions for use
2-3x/day
PO at night
must tritate to find correct dosage
372
tizanadine AEs
1. drowsiness
2. dizziness
3. asthenia
4. sedation (within 30 min, peaks 1.5 hrs after dose)
5. hypotension (within 1 hr, peaks 2-3 hrs after dose)
373
what type of drug is cyclobenzaprine (Flexaril ) and diazepam (Valium)?
Centrally acting antispasmodic
374
MOA of centrally acting antispasmodics
Unknown
might inhibit polysnaptic reflex in spinal cord
possible GABA and serotonin effects
375
instructions for use of cyclobenzaprine (Flexaril)
onset: 1 hr
peak: 3-8 hrs
duration: 12-24 hr
376
AEs of cyclobenzaprine (Flexaril)
1. sedation
2. dizziness
3. \*\*on the Beers list
377
Note on Benzodiazepines (aka Valium)
Schedule IV drug
Sedation and respiratory depression when used with opiods
378
how does botox work?
works at the neuromuscular junction to block the release of ACh
379
T/F: botox has decreased efficacy with longterm use
TRUE
380
instructions for Botox use
onset: 1-3 days
duration 3-6 months
381
Botox (botulinum toxin) AEs
Boxed warnings!
may spread to distal tissues causing issues = distant paralysis
382
what type of drug is Baclofen (Lioresal)?
Ethyl Alcohol and Phenol Direct Acting Agent
383
Baclofen MOA
inhibits excitatory neurons = decreased NT release and K+ influx to increase inhibition
384
Use of Baclofen (Lioresal)
PO
intrathecal pump (ITB)
385
baclofen (Lioresal) AEs
1. CNS depression
2. muscle weakness
3. memory and cognitive impairments in adults with TBI
386
why would someone use an ITB?
better results with less AEs
generally need smaller doses
387
PT notes for post-implantation of ITB?
1. assess changes in motor skills due to muscle tone changes
2. equipment modifications
3. no modalities near pump site
4. refill is needed every 3 months
5. battery must be replaced every 4-5 years
388
Complications of an ITB pump
1. infection
2. dislodgement
3. kinking and blocking
4. failure
5. observe for signs of withdrawl or overdose
389
Boxed warnings for ITB
abruptly stopping meds can cause:
1. fever
2. altered mental status (AMS)
3. exaggerated rebound spasticity/rigidity
4. in extreme cases
1. rhabdomyolysis
2. organ failure
390
Therapeutic concerns for pts on muscle relaxants and antispastic meds
1. sedation and weakness are biggest AEs
1. can result in limited participation in PT
2. requires intensive PT to develop new motor patterns and functional abilities
3. must assess equipment
4. be aware of ITB pump malfunctions
391
what is depression?
mood disorder described as having the presence of 2 or more symptoms effecting:
1. energy level
2. sleep
3. appetite
4. self-esteem
5. concentration
6. decision-making
392
what are the 2 major categories of depression?
1. major depressive disoder
2. dysthymic disorder
393
what is major depression disorder?
symptoms for 2+ weeks
classified as mild, moderate, or severe
394
what is dysthymic disorder?
mild chronic depression
symptoms for 2+ months
can still have major depressive episodes
395
what are the symptoms typically for dysthymic disoder?
more cognitive features (low self-esteem)
affective (low mood)
social dysfuncction (social withdrawal)
396
what are the overall symptoms of depression?
1. low mood
2. lost of interest
3. loss of motivation
4. loss of libio
5. feelings of helplessness, hopelessness
6. sleep distrubances
7. suicidal thoughts
8. eating disturbance
9. pessimism
397
Depression can increase your risk for what other diseases?
1. reduced cardiovascular health (MI)
2. osteoporosis, PUD, DM
3. increased cortisol levels
398
Pathophysiology of Depression
exact pathogenesis not completely understood
Possible factors:
1. Monoamine hypothesis
2. receptor downregulation and changes in sensitivity
3. Neuroplasticity hypothesis
399
what is the monoamine hypothesis?
deficiency or imbalance of monoamines leading to receptor downregulation and changes in sensitivity
400
what is neuroplasticity hypothesis?
neurohistological changes lead to changes in the hardwiring of the brain
Antidepressants reverse these changes
401
General MOA of antidepressants
inhibit reuptake of monoamines (5-HT or NE)
desensitizationof autoreceptors
enhance NE release
402
What is a risk in treatment of depression?
Serotonin Syndrom
403
Individuals undergoing Antidepressant therapy should be monitored for what?
1. DDIs (cyp enzymes)
2. BP/HR
3. worsening depression (\*\*red flag statement)
4. serotonin syndrome
5. boxed warnings
* increased suicidal thoughts
404
What is Serotonin Syndrome?
accumulation of high levels of serotonin
classified as mild, moderate, severe, and life threatening
405
what are the symptoms of mild Serotonin Syndrome?
1. HTN
2. tachycardia
3. tremor
406
what are the symptoms of moderate Serotonin Syndrome?
same as mild in addition to:
1. hyperthermia (1040)
2. hyperactive bowels
3. mild agitation
407
what are the symptoms of severe Serotonin Syndrome?
all of the mild/moderate symptoms
hyperthermia (106 degrees)
408
what medication puts you at the highest risk of Serotonin Syndrome?
MAO Inhbitors
409
treatment for Serotonin Syndrome?
1. Benzodiazepines
2. Serotonin antagonist
3. discontinuing serotonergic agents
4. cardiac monitoring
410
what is the goal of Antidepressant Therapy (treating depression)?
1. reduce acute symptoms
2. return to baseline level of function
3. prevent further episodes
4. prevent suicide attempts
411
how long does it take after starting meds to see improvements in physical symptoms of depression ?
usually 2 weeks
412
how long does it take after starting meds to see improvements in emotional symptoms of depression?
usually 6-8 weeks
413
Drug Classes for Depression
1. Selective Serotonin Reuptake Inhibitors (SSRI)
2. Seretonin/NE Reuptake Inhibitors (SNRI)
3. Atypical agents
4. Tricyclic Antidepressants
5. MAO Inhibitors
6. Other
414
SSRI suffix
-pram
415
SSRI Drugs
1. citalopram (Celexa)
2. escitalopram (Lexapro)
416
SSRI MOA
selectively inhibit 5-HT reuptake
417
SSRI AE
1. HA
2. N/V/D
3. insomnia
4. sexual side effects
\*Rare = hyponatremia, bleeding
418
SSRI Indications
1. Depression
2. eating disorders
3. PTSD
4. anxiety
5. OCD
6. bipolar disorder
7. vasomotor menopausal symptoms
419
SNRI suffix
-ine
420
SNRI drugs
1. venlafaxine (Effexor)
2. duloxetine (Cymbalta)
421
SNRI MOA
inhibits 5-HT and NE reuptake
422
SNRI AE
1. HA
2. nausea
3. dry mouth
4. sweating
5. sexual dysfunction
6. insomnia
423
SNRI indications
1. depression
2. anxiety
3. OCD
4. panic disorder
5. PTSD
6. vasomotor menopausal symptoms
7. fibromyalgia
8. neuropathic pain
424
Atypical Agents used to treat Depression
Buproprion (Wellbutrin)
425
what is buproprion (Wellbutrin) used to treat in depression?
used as adjunct therapy to reduce sexual dysfunction
426
buproprion (Wellbutrin) MOA
inhibits reuptake of DA and NE
427
buproprion (Wellbutrin) AE
1. HA
2. nausea
3. insomnia
4. tremor
5. dry mouth
6. decreased appetite
\*\*risks of seizures
428
buproprion (Wellbutrin) Indications
1. depression
2. ADHD
3. smoking cessation
4. weight loss
429
T/F: Tricyclic Antidepressants are cholinergic?
FALSE -\> they are anticholinergic
430
Tricyclic Antidepressants MOA
inhibits reuptake of 5-HT and NE. Creates receptor blockades for other NTs
431
Tricyclic Antidepressants AE
1. weight gain
2. sexual dysfunction
3. sedation
4. anticholinergic effects (ABCDs)
\*\*risks = overdose (cardiac)
432
Tricyclic Antidepressants Indications
1. Depression
2. Neuropathic pain
3. migraine prevention
4. insomnia
433
MAO Inhibitors MOA
inhibits MAO enzyme = more monoamines
434
MAO Inhibitors AEs
1. OH
2. weight gain
3. sexual dysfunction
435
MAO Inhibitors Risks
Serotonin Sydrome
Hypertenisve crisis
436
someone on an MAO Inhibitor should avoid what things to reduce their risk of hypertensive crisis?
1. tyramine containing foods (wine, beer, cheese)
2. sympathomimetic agents
437
MAO Inhibitors Indications
1. depression
2. Parkinson's Disease
438
Other agents used to treat depression?
1. alpha 2 antagonists
2. 2nd generation antipsychotics
3. Katamine (for highly trx resistant depression)
* admin in providers office
4. Trazodone
5. Nefazodone
439
What medication is 1st line in treating depression?
SSRI
due to efficacy and tolerability
440
what drug is 1st line for fibromyalgia and neuropathic pain?
SNRIs
441
Therapeutic Concerns for Antidepressant therapy
1. intermittent tx may diminish drug efficacy
2. monitor BP/HR
3. tremor and sedation will impact participation in PT
442
what is anxiety?
an appropriate response that becomes pathologic when out of proportionto the siutation
443
Somatic symptoms of anxiety?
1. muscle ache
2. GI issues
3. fatigue
4. restlessness
444
Psychological symptoms of anxiety
1. sleep disturbances
2. excessive worrying
3. poor concentration
445
Pathophysiology of anxiety
impacts the following regions of the brain
1. periaqueductal gray matter (PAG)
2. locus coeruleus
3. hypothalamus
4. limbic system
* amygdala
* hippocampus
446
what does stimulation of the PAG cause?
vascular effects of anxiety
447
what does stimulation of the locus coeruleus cause?
anxious behavior and panic
448
how is the hypothalamus involved in anxiety?
central to anxiety response (hypothalmus-pituitary-adrenal axis)
secretes hormones involved in stress reaction
449
describe the limbic system's role in anxiety
1. amygdala is connected to area involved in anxiety
2. chronic stress (cortisol) reduces hippocampal volume
450
Neurochemistry of Anxiety
1. Monoamines = alpha 2 decrease sympathetic outflow to decrease anxiety
2. serotonergic system = releases serotonin
3. GABAergic system = inhibits release of GABA
451
drugs used to treat anxiety act where?
1. Serotonergic system
2. GABAergic system
452
Treatment of Anxiety
1. SSRIs
2. SNRI
3. Tricyclic Antidepressants
4. MAO Inhibitors
5. Propranolol
6. Benzodiazepines
7. buspirone (Buspar)
453
what is the 1st line treatment for anxiety?
SSRIs and SNRIs
454
what is used in maintenace treatment for anxiety?
Tricyclic antidepressants and MAO inhibitors
455
what is used for long-term treatment of anxiety?
propranolol = for panic attacks
456
how are benzodiazepine used to treat anxiety?
only for acute treatment
457
how is buspirone used to treat anxiety?
maintenance in generalized anxiety
458
Benzodiazepines drug
alprazolam (Xanax)
459
alprazolam (Xanax) MOA
binds BZD receptors ot enhance GABA inhibitory effects
460
alprazolam (Xanax) AEs
1. sedation
2. ataxia
3. memory problems
\*\*high abuse potential
461
alprazolam (Xanax) Indications
1. spasticity
2. muscle spasms
3. acute anxiety
4. serotonin syndrome
462
buspirone (Buspar) MOA
unknown
binds to 5-HT and DA receptors
463
buspirone (Buspar) AEs
1. dizziness
2. paradoxical anxiety (potentially)
464
buspirone (Buspar) indications
1. anxiety
2. panic disorders (less useful)
465
what are the advantages to using buspirone (Buspar)?
1. no abuse risk
2. no dependence
3. no withdrawal
466
what are the disadvantages of using buspirone (Buspar)?
1. DDIs (cyp enzymes)
2. onset = 3 weeks
467
Therapeutic concerns with drugs that treat anxiety
1. caution in elderly -\> BZDs increase fall risk
2. BZDs can interfere with sleep cycle (REM)
3. overall sedation will
* limit PT participation
* increase fall risk
468
what is Schizophrenia?
psychotic illness w/periods of psychosis
chronic dysfunction of mood, cognition, and social behavior
469
Etiology of Schizophrenia
Unknown
possible genetic disposition and birth complications
470
Possible pathophysiology of Schizophrenia
Possible cause
reduced prefrontal blood flow during cognitive tasks along with dopamin "dysregulation" (imbalance with overactivity and underactivity in various brain regions)
471
what are the types of symptoms (categories) that Schizophrenic patients can have?
1. Positive - presence of behaviors
2. Negative - diminished/absent behaviors
3. Cognitive - impaired behaviors
472
what are some positive symptoms of schizophrenia?
1. hallucinations
2. disturbed reality
3. abnormal motor behaviors
473
What are some negative symptoms of schizophrenia?
1. diminished speech
2. flattened emotions
3. social withdrawal
474
what are some cognitive symptoms of schizophrenia?
1. reduced attention
2. decreased executive function
475
what is the overall goal for treatment in schizophrenia?
reduce symptoms and mediate AE while improving function and QOL
476
what schizophrenic symptoms are easier/harder to treat?
easier = positive symptoms
harder = negative symptoms
477
what types of medications are typically used to treat schizophrenia?
antipsychotics
at a min takes 4-6 weeks to observe changes
478
what are the classifications of antipsychotics?
1. First generation (FGA) = older, more AE
2. Second generation (SGA) = newer, less EPS and TD AEs
479
what is the 1st line trx for schizophrenia and why?
SGA = there are less extrapyramidal symptoms and tardive dyskinesia
480
what are extrapyramidal symptoms?
collection of symptoms that are drug induced movement disorders. include:
1. actue dystonia
2. akathesia
3. delayed tardive dyskinesia
4. acute parkinsonism
481
what is tardive dyskinesia?
repetitive and involuntary movements such as grimicing and eye blinking
\*orofacial dyskinesia
482
T/F: tardive dyskinesia can be irreversible if left untreated and unnoticed?
TRUE
483
what is acute dystonia?
spasm of muscles of tongue, face, neck and back
484
what is akathesia?
restlessness and inability to stay still, manifests with finger-tapping, pacing
485
MOA of first generation antipsychotics?
block dopamine receptors in mesolimbic tract where excess dopamine may contribute to postive symptoms
486
SGA drugs on our list
quetiapine (Seroquel)
487
quetiapine (Seroquel) MOA
block D2 receptors but less than FGA; more affinity for 5-HT receptors
\*variable effect on histamine, muscarinic and alpha receptors = more variable AE
488
SGA binding to D2 receptors AEs
1. Motor = bradykinesia, and possible EPS
2. Endocrine (higher risk for metabolic syndromes)
3. Neuroleptic malignant syndrome
489
if SGAs bind to other receptors what possible AEs can occur?
1. H1 receptors
* sedation and wt gain
2. Muscarinic receptors
1. ABCDs
3. a1 receptors
1. hypotension, dizziness
490
Rehab concerns for FGAs
1. CV risks
2. caution with UV exposure
3. imapired thermoregulation = caution with overexertion
4. monitor for EPS
491
Rehab concerns for SGAs
1. wt gain, hyperglycemia, and lipid abnormalities
2. CV abnormalities risk
3. risk for heat intolerance
492
what are the types of Bipolar Disorder?
1. Bipolar I disorder
2. Bipolar II disoder
493
what is Bipolar I disorder (aka manic-depression illness)
one manic episode accompanied by history of one or more major depressive episodes
494
what is Bipolar II disoder?
major depressive disorder accompanied by at least one hypomanic or milder manic phases
495
what is hypomania?
at least 4 days of elevated/irritable mood combined with over-activity
496
Pathogenesis of Bipolar Disoder?
Unknown
appears to be dysregulation in dopamine and serotonin systems
497
what regions of the brain are altered in Bipolar disoder and how?
1. limbic-cortical dysfunction
* hippocampus and prefrontal cortex have diminished acitivty w/smaller volumes
* amygdala is hyperactivity leading to emotional sensitivity
498
how is Bipolar disorder treated?
1. acute depressive episode = SSRI, bupropion
2. acute manic episode = lithium
3. maintenance trx = lithium
499
what is the role of Lithium in treatment of Bipolar Disorder?
1. Management of acute manic or hypomanic episode
2. prevention of further manic and depressive episodes
500
If lithium is so effective in lots of patients what is the drawback?
Lots of AEs
