Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

1 > Pharm 2 > Flashcards

Pharm 2 Flashcards

1
Q

ACC/AHA 2017 Guidelines

A

Normal BP <120
Goal for all patients <130/80

Stage 1 HTN: 130-139/80-89
Stage 2 HTN: > 140/90

When to start treatment:
IF CVD/ASCVD 10 year risk: >130/80
IF NO CVD/risk: >140/90

Consider 2 agents if >20/10 over goal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

HTN agent s/p MI for all ages and races

A

B-blocker + ACE-I
(Aldosterone antagonist if HF present)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

HTN agent for recurrent stroke prevention (all ages/races)

A

Thiazide + ACE-I

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

HTN agent in HF for all ages/races

A

B-blocker + ACE-I

Diuretics for fluid retention
Aldosterone antagonists
Hydralazine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

1st line HTN

A

Thiazide
CCB
ACEI
ARB

(2nd line = combo of above choices)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Thiazides

A

Diuretic
Inhibit active exchange of Na and Cl (in equal amounts) in distal convoluted tubules

Indication:
-HTN (HCTZ, Chlorthiazide)
-Edema (Metolazone)

Interactions: digoxin, lithium, electrolyte based drugs, caution in sulfa allergy

*Not useful in anuric renal failure

ADE:
-Decrease K, Na, Cl, PO4, Mag
-Increase glucose, Ca, uric acid, lipids
-Photosensitivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Loops

A

Diuretic *greatest diuretic effect of all classes

Inhibit exchange of Na/K/Cl on thick segment of ascending Loop of Henle

Indication:
-Better in HF than HTN
-HTN, edema, ascites, renal disease

*More useful than thiazides in pt w/ chronic renal insufficiency (GFR <30)

ADE:
-Decrease K, Na, Mag, Phos, Ca
-Increase glucose, uric acid, lipids
-Rash
-Photosensitivity
-Ototoxicity

Interactions
-Lithium
-Digoxin
-Ototoxic drugs
-K sparing diuretics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

K-sparing

A

Diuretic *Modest diuretic effect, usually used in combo w/ others
Inhibit reabsorption of Na in distal convoluted tubule and collecting ducts (blocks aldosterone)
Main function=antagonize aldosterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

ACEI

A

Blocks conversion of angiotensin-1 to
angiotensin-2, halting vasoconstriction.
Also inhibits degradation of bradykinin

Renoprotective agent in cases where renal afferent arteriolar pressure is increased: lowers both afferent/efferent pressure. NOT helpful in already low afferent pressures

Indications: HTN/HF/post MI

HD effects
-vasodilation
-reduced preload and afterload
-increased CO
-increased Na/water excretion

ADE: rash, ACE cough, 1st dose hypotension, hyperK, angioedema, neutropenia, teratogenicity, renal insufficiency

Interactions: K supplements, diuretics, ASA

Contraindications: renal artery stenosis, pregnancy, Hx angioedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

ARB

A

block angiotensin II receptors on cell membranes

Indications: HTN, CHF

Interactions: K sparing diuretics/supplements, NSAIDS

ADE: Teratogenicity, cough, angioedema,

Contraindications: Renal artery stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

CCB

A

Blocks inward movement of calcium into muscle by binding to calcium channels in the heart and SM of the coronary and peripheral vasculature
DHP: dilatory properties
non-DHP: conduction disorders
Indications: HTN, angina, dysrhythmias, HF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

non-DHP CCBS

A

Verapamil, Diltiazem
Decreases HR and contractility, slows cardiac conduction, dilates SM of coronary and peripheral arteriolar vasculature

ADES: Constipation (verapamil), dizziness, HA, nausea, LE edema

Interactions: Digoxin, beta blockers
Caution: heart block, decomp HF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

DHP CCBs

A

Nifedipine, nicardipine, amlodipine
Effects on smooth muscle causes vasodilation, little effect on conduction
Indication: HTN, prinzmetal’s angina, HF
ADE: peripheral edema, HA, gingival hyperplasia
Interactions: Beta blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

B-blockes

A

Competitively inhibit beta adrenergic receptors
Selective (B1): atenolol, metoprolol
vs
Nonselective (B1 and B2): propranolol, timolol

Decrease CO, sympathetic outlfow from CNS, inhibit renin release

Indication: HTN, HF, MI, angina
Caution: COPD, asthma, decompensated HF, DM, PVD, block
ADE: hypotension, bradycardia, CNS effects, impotence, hyperlipidema, hypoglycemia masking

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Nonselective beta blockers

A

Inhibit B1 and B2 adrenergic receptors
Propranolol, timolol, nadolol, penbutolol
Can cause bronchoconstriction (special caution in asthma/COPD)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Selective beta blockers

A

Inhibit B1
Atenolol, metoprolo, acebutolol, betaxolol, esmolol
Preferred w/ PVD, DM, and reactive airway disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Alpha/beta adrenergic blockers

A

Carvedilol, labetalol

Inhibit alpha 1, beta 1, beta 2

No effect on lipid and CHO metabolism

ADE: orthostatic hypotension, dizziness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Alpha-1 Adrenergic blockers

A

Prazosin, terazosin

Relaxation of arterial and venous smooth muscle, decreased PVR
Minimal changes in CO, renal blood flow, GFR
Indication: HTN, BPH
ADE: palpitations, postural hypotension, syncope

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Alpha 2 agonist

A

Clonidine, methyldopa
Indication: HTN, pain management
ADE: rebound HTN, drowsiness, dizziness, constipation

*Methyldopa-useful in HTN in pregnancy
ADE: SLE, sedation, orthostatic hypotension, hemolytic anemia, increased LFTs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Hydralazine

A

Arterial vasodilator: decreases PVR
but
increases CO and causes reflex tachycardia

Indications: HTN, HTN crisis

ADE: HA, nausea, angina, lupus like syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Digoxin

A

Cardiac glycoside
+inotropic action, – neurohormonal activation, sensitizes cardiac baroreceptors

Indication: improve symptoms and quality of life in HF, no affect on mortality

Caution: electrolyte disorders, renal insufficiency, thyroid disorders, hypermetabolic state

ADE=digitalis intoxication (N/V, dizziness, visual disturbances), hyperkalemia, conduction abnormalities
VERY NARROW TI
Goal drug level: 08
Keep K+ 4.0, Mg 2.0

Drugs that increase levels: amiodarone, CCB, diuretics, macrolides
Drugs that decrease levels: St. John’s wort, antacids, reglan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Statin benefiting groups

A
  1. ASCVD
  2. LDL >190
  3. LDL 70-190, age 40-75 w/ DM and no ASCVD
  4. Estimated 10 year risk >7.5 for individuals 40-75 w/ LDL 70-190 and no DM
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Statins

A

Inhibit HMG-CoA-Reductase (important step in cholesterol synthesis)

Rosuvastatin, atorvastatin, Simvastatin, Pravastatin

Issues: liver abnormalities, myalgia/myopathy which can elevate CPK and lead to rhabdo, many drug/food interactions (metabolized by CYP3A4)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Fibrates

A

Promotes fat removal from plasma via enzyme
activation (LPL, Reduces hepatic secretion of LDL
Primarily triglyceride lowering agent

ADE: GI, flu-like, rash, photosensitivity, myopathy, pancreatitis, gallbladder disease

Interactions: statin, warfarin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Bile acid sequestrants (resins)

A

Cholestyramine
Reduces LDL; may increase HDL
Prevents bile acids from being absorbed and
returned to liver, leading to fecal elimination
Side effect profile discourages use

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Nicotinic acid (niacin)

A

Available OTC, Rx
Lowers VLDL, which ↓ production of LDL
May also increase HDL
ADE: flushing, tingling, itching, Hepatic toxicities reported
interactions: statins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Beta 2 agonists

A

Bronchodilators
SABA: albuterol/levalbuterol (rescue, onset ~15 min)
LABA: formeterol/salmeterol (maintenance), used in conjunction w corticosteroids

ADE: tachycardia, tremor, hyperglycemia, hypokalemia

Indications: sympathomimetics, MAOI

More effective to use corticosteroid + Beta 2 agonist than higher doses of corticosteroids alone

Can see tolerance develop over time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Methylxanthines (Theophylline)

A

MOA: SM relaxation from PDE inhibition, preventing breakdown of cAMP

ADE: convulsions, arrhythmias, CNS stimulation, N/V
insomina, aggravation of reflux/ulcers
VERY NARROW TI (5-15)
Decreased metabolism: erythromycin, cimetidine, liver failure, heart failure, elderly
Increased metabolism: smokers, oral contraceptives, phenytoin

Not recommended for exacerbations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Anticholinergics (muscarinics)

A

MOA: prevents increase of cGMP and antagonizes
action of Ach, resulting in bronchial SM relaxation
SAMA=ipratropium
LAMA=tiotropium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Corticosteroids

A

oral: prednisone, methylprednisolone. Short term, gain control of inadeuately controlled persistent asthma (3-10 days)

inhaled: beclomethasone, flunisolide. Long term for prevention

MOA: antiinflammatory, reduces airway hyperresponsiveness. inhibits cytokine production, inflamm cell migration and
activation

1st line Tx starting at step 2 but not for acute attacks

ADE: candidiasis, cough, dysophonia, HA, reversible glucose increases, fluid retention, peptic ulcer
*adrenal axis suppression @ high doses

Growth issues in long term use? If concern replace w/ mast cell stabilizers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Mast cell stabilizers (Cromolyn sodium)

A

MOA: anti-inflammatory; stabilizes mast cell
membranes, inhibiting activation and release of
mediators from eosinophils and epithelial cells

Indication: most useful in younger, allergic asthmatics with mild persistent asthma, also useful in exercise induced asthma

May take some time to see effects. Weak drug compared to corticosteroids

ADE: (Rare) cough, congestion

No risk growth suppression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Leukotriene modifiers (montelukast)

A

MOA: Block leukotriene receptors on inflammatory cells and SM (montelukast),
Stop synth of leukotrienes via lipoxygenase inhibition

Well tolerated, minimal ADE, less effective than corticosteroids

Enzyme inhibition of CYP450: decrease metabolism of warfarin and theophylline
Watch LFTs

33
Q

Monoclonal Antibody (IgE binder) Omalizumab

A

MOA: Forms complexes with IgE and prevents binding to
receptors limiting inflammatory mediator release
Indication: >12 y/o moderate-severe asthma and failed traditional agents

34
Q

Opioid actions

A

CNS: analgesia, sedation, euphoria, resp/cough suppression, N/V, pupil constriction

GI: delayed gastric emptying, increased intrabiliary pressure, constipation

Other: histamine release from mast cells, immune suppression, hypotension/bradycardia, osteoporosis, hyperalgesia

35
Q

Morphine

A

MOA: Activation of m, k, and d opioid receptors, activation of Gi –> K+ channels hyperpolarize and depress neuron function

Metabolism: Primarily in gut wall and hepatocyte, conversion to M6G (active) and M3G (neurotoxic). ~10% excreted unchanged (renal)

ADE: resp depression, sedation, N/V, mental clouding, urinary retention, constipation, pruritis, hypotension

Contraindications: (relative) liver/heart failure, resp failure, asthma, hypotension

36
Q

Codeine

A

Weak opioid, analgesic properties related to conversion to morphine by CYP2D6 (watch polymorphisms)

37
Q

Hydromorphone

A

Low levels of active metabolites, so preferred in renal failure
ADE: CP

38
Q

Oxymorphone

A

Low propensity to release histamine

39
Q

Meperidine

A

Phenylpiperidine opioid w/ relatively short half life

Less constipating than morphine

ADE: CNS excitation (tremors, muscle twitches, seizures)

Not for Tx of chronic pain d/t metabolite toxicity, not to be taken w/ MAOI, not for pt w tachycardia

40
Q

Fentanyl

A

Highly lipophilic, highly potent opioid that can be given transdermal/transmucosal

Very short half life, no active metabolites (preferred in renal insufficiency)
TD fentanyl is less constipating than morphine

Not for opioid naive pt, not for acute, intermittent, mild pain

41
Q

Methadone

A

Long acting u, k, d opioid agonist and NMDA antagonist
Half life: 20-35 hours (4-10 days to reach Css). Metabolism highly variable btwn individuals (portion of drug that is free vs. protein bound and metabolic activity towards CYPS)

No active metabolites
Primarily metabolized by CYP3A4, induces CYP3A4

QTc prolongation

Less prone to developing tolerance, best opioid for tx neuropathic pain

42
Q

Tolerance

A

Progressive loss of effect with sustained administration of an opioid receptor agonist
Progressive decrease in drug efficacy
Increased dosing decreases pain
May develop adverse effects with increased dosing

43
Q

Opioid induced hyperalgesia

A

Paradoxical increase in sensitivity to painful stimuli
Increased dosing increases pain
Same pain or different pain
Increased sensitivity to pain

44
Q

Pain transmission

A

Nociceptor stimulation in injured tissue causes release of bradykinin, 5HT, K+, histamine, prostaglandins, Substance P that further sensitize/activate other nociceptors (decreasing pain threshold)

Nociceptor activation produces action potentials that are transmitted to the spinal cord along myelinated A-delta fibers (sharp, fast) and unmyelinated C-fibers (slow, dull, burning)

Pain signals transmitted via spinal cord to thalamus and project to cortical regions where pain is received

Modulation of pain through: endogenous opioids (endorphins), descending pain pathway (5HT, NE @ dorsal horn)

45
Q

Cyclooxygenase inhibitors

A

Effects: antiinflammatory, analgesic, antipyretic

Most are highly protein bound

ADE: bleeding, gastric ulceration, renal impairment

COX 1 inhibition:
Gastric ulceration/bleeding/renal impairmnt
MI/CVA protection

COX 2 inhibition:
Decrease pain/fever/inflammation
MI/CVA risk

46
Q

Acetaminophen

A

COX-inhibitor w/ no anti-inflammatory action

Indication: mild-moderate nociceptive pain (lacks efficacy in neuropathic/functional pain)

Very little protein bound (unlike other NSAIDS)

Metabolism: extensive liver metabolism through conjugation w/ glucoronic acid, small portion CYP mediated

47
Q

Acetaminophen metabolism

A

Liver: extensive through conjugation with glucuronic acid (60%), sulfuric acid (35%), and cysteine (3%). A small proportion undergoes CYP-mediated N-hydroxylation (CYP2E1).

Major metabolism pathway–> nontoxic metabolites

Minor pathway (mediated by CYP450) –>Toxic metabolite (NAPQI) —> glutathione –> nontoxic metabolite

P450 induced by alcohol

Glutathione inhibited by alcohol AND tylenol OD

48
Q

Aspirin

A

Irreversible COX1 and COX2 inhibitor

Indication: inflammatory disorders mild-moderate pain, menorrhagia

Vd: highly protein bound

Metabolism: Plasma esterase to yield salicylate which is 90% eliminated through hepatic metabolism
Half life of ASA very short, but salicylate 2-3 hr (and up to 30 hr if hepatic mechanisms become saturated)

49
Q

tNSAIDS

A

Reversible inhibitors of COX 1 and COX 2

Risk of MI/CVA d/t TXA2/PGI1 imbalance
Inhibit TXA2 (COX1) vasoconstrictor/promote plt agg

Inhibit PGI2 (COX2) vasodilator/inhibit plt agg

Nonselective COX inhibitors have bias towards COX2 inhibition

50
Q

COXIBS

A

Selective COX 2 inhibitors

Just as effective as traditional NSAIDs in suppressing inflammation and pain
Somewhat lower risk for GI side effects
Can impair renal function and cause hypertension and edema
Increased risk of MI and stroke

51
Q

PGE2

A

In GI mucosa
Protective @ stomach lining (increase mucous production, bicarb, mucosal blood flow)

Inhibiting=peptic ulcers and GI bleeding

52
Q

Carbamazepine

A

Indications: epilepsy (1st line for partial and tonic clonic), trigeminal neuralgia, bipolar mania

Action @ voltage gated Na channels (stabilize in inactive state)

Advantages: less sedating than other AEDs, mood stabilizing effects, no cognitive deficits

High (75-90% protein bound)

Metabolized by CYP3A4, induces CYP1A2, 2CP, 3A4.
Initially high half life, decreases w/ multiple doses because it induces its own metabolism
*also decreases concentration of other CYP mediated AEDs

ADE: acute intox, resp depression, ataxia, drowsiness, blurred vision
BBW for severe hemolytic anemia and derm rxns (HLH allele)

Preg category D

53
Q

Phenytoin

A

Indication: partial and tonic clonic seizures, during and after NSGY

MOA: Stabilizes inactive state of volt-gated Na channels

High variability in oral bioavailability (20-90%)
High protein binding, low Vd
*drug interactions mainly related to protein binding

Metabolism via CYP2C9, induces other CYP enzymes

Zero order kinetics: elimination rate increases with higher concentrations (saturable)

ADE: ataxia, diplopia, drowsiness/sedation, gingival hyperplasia, anemia, lymphadenopathy, osteoporosis

Preg category D

54
Q

Gabapentin

A

Indication: partial seizures, postherpetic neuralgia **no efficacy for tonic-clonic seizures

MOA: likely inhibits Ca channel activity

Insignificant protein binding, excreted unchanged in urine/no hepatic enzymes (fewer drug interactions)

ADE: somnolence, dizziness, ataxia, fatigue, HA, tremor (generally well tolerated)

Pregnancy category C–safer than other AEDs

55
Q

Pregabalin (Lyrica)

A

Reduces glutamate, NE, and Substance P levels (analgesic properties, neuropathic pain management)
*abuse liability

56
Q

Phenobarbital

A

Indication: Epilepsy, sedation

MOA: barbiturate, action @ GABA receptors

Drug of choice for infant/neonatal seizures

ADE: resp depression, sedation, physical dependence, hyperactivity, cognitive impairment

57
Q

Levetiracetam (Keppra)

A

Indication: partial, tonic-clonic seizures

Can exacerbate neuropsych disorders and aggression

58
Q

Valproate

A

Indication: generalized seizures (beyond just tonic clonic), BPD, migraine prophylaxis

MOA: Na channel inactivation, reduction in T type Ca currents, increase GABA signaling

90% protein bound

Metabolism via CYP2C9, inhibits 2C9 and UGT

ADE: A/N/V, sedation, ataxia, tremor, rash, alopecia, weight gain
Rare risk of fulminant hepatitis which may be fatal

BBW for hepatic toxicity and teratogenicity

Preg Category D *worst AED

Interactions: inhibits metabolism of CYP2C9 substrates (phenytoin, phenobarbital, ethosuximide)

59
Q

Lamotrigine

A

Indication: Partial, tonic clonic seizures, BPD

MOA: Na channel inactivation

Insignificant protein binding

Extensive hepatic metabolism, induces UGT

Half life reduced by phenytoin, carbamazepine, phenobarbital. Increased by valproate

Toxicity: weight gain, ataxia, nervousness, dizziness, blurred vision
Risk of SJS and DIC (more common in peds)

60
Q

Ethosuximide

A

Indication: absence seizures

MOA: Decreases low threshold Ca currents in thalamic neurons

Insignificant protein binding

75% hepatic metabolism via CYP3A4, no enzyme induction

ADE: N/V/A, drowsiness/lethargy/dizziness, urticaria, SLE, eosiniphilia

Preg category D

61
Q

SSRI

A

Citalopram, escitalopram, fluoxetine, paroxetine, sertraline

MOA: highly specific in inhibiting SERT, efficacy attributed to subsequent actions of elevated 5-HT at postsynaptic 5-HT1A receptors

ADE: nausea (5-HT3), agitation, insomnia, sexual dysfunction (5-HT2), serotonin syndrome= tremor, hyperthermia, CV collapse

Inhibit CYP enzymes (esp Paroxetine and fluoxetine inhibit 2D6 and should not be used w TCAs)

Highly protein bound

Fluoxetine and sertraline have active metabolites with long half lives. Need washout period before starting TCA

Mostly category C in pregnancy (Paroxetine category D)

62
Q

Serotonin syndrome

A

Risk when SSRIs/SNRIs used in combo w/ TCAs or OD of TCA

Tremor, hyperthermia, CV collapse

63
Q

SNRI

A

Venlafaxine, Desvenlafaxine, Duloxetine

MOA: Inhibit SERT and NET

ADE: Similar to SSRIs + b-adrenergic effects (HTN, tachy, CNS activation)

Low risk OD but must not use with MAOIs

No CYP metabolism (elimination by conjugation) so no high profile drug interactions

Lower protein binding (exception = duloxetine is highly protein bound)

Overall shorter T1/2 than SSRIs

Also for anxiety disorders and pain

64
Q

TCAs

A

Amitryptiline, imipramine

MOA: Inhibit both 5-HT and NE reuptake, major metabolites also have activity (antagonism at muscarinic Ach, H1, alpha-adrenergic receptors)

ADE:
muscarinic- dry mouth, blurred vision, constipation, urinary retention, delayed gastric emptying
H1: sedation
alpha-adrenergic: postural hypotension

Risk of overdose: ventricular arrhythmias, confusion, mania (narrow TI)

Interactions: CYP substrates, SSRI/SNRIs, potentiate alcohol/anesthetic agents, anti-HTNs

Most are long acting w/ active metabolites, highly protein bound

65
Q

Monoamine receptor antagonists

A

Mirtazapine, trazadone

Fewer sexual side effects than SSRI/SNRIs

Very sedating

66
Q

MAOIs

A

Inhibits MAO mediated degradation of monoamines (irreversible inhibition of MAO-A and MAO-B)

Risk of triggering HTN crisis if pt eats food rich in tyramine

ADE: CNS stimulation, orthostatic hypotension

67
Q

Atypical antidepressant: Buproprion (Wellbutrin)

A

Stimulant

Also for smoking cessation, appetite suppression

Inhibits NE/DA reuptake

Lowers seizure threshold

68
Q

Ketamine

A

NMDA receptor antagonist: increases glutamate levels in the brain and produces rapid antidepressant effect (10-15 min), normally for seizures/sedation/analgesia

At high doses, may cause sedation and out of body experiences
ADE: sedation, inattention, dissociation, abuse potential, SI

69
Q

Brexanolone

A

Allopregnalone=neuroactive metabolite of progesterone, peaks during 3rd trimester and falls after delivery
(+allosteric modulator of GABA channels)

Cont. infusion over 60 hours approved for tx of postpartum depression

ADE: sedation–> LOC, HA, dizziness, dry mouth, hot flashes

70
Q

Benzodiazepines

A

Anxiolytic-GABA receptor actions

alpha 1 subunit: sedation
alpha 2/3: anxiolysis

anticonvulsant, hypnosis, anterograde amnesia

Advantages: high TI, rapid onset of action, little induction of liver enzymes

ADE: rebound anxiety, withdrawal

71
Q

Buspirone

A

MOA: blockade of 5-HT1A autoreceptors but stimulation of 5-HT1A postsynaptic receptors (partial agonist)

Anxiolytic w/ lower abuse potential than Benzos

Time to onset similar to SSRIss, slower and less effective than benzos

72
Q

Parkinson’s symptoms

A

Tremor
Rigidity
Akinesia/bradykinesia
Postural instability/abnormal gait

Sleep disturbances
Other (N/V, pain, fatigue)
Autonomic (urinary, sweating, orthostasis)
Psych (depression, anxiety, cognition)

73
Q

MAO-B Inhibitors

A

Rasagaline, seligiline

increase DA levels in the striatum
For mld cases or as adjunct during Levodopa off periods
Benefits rapidly decline

ADE: nausea, hallucinations, confusion, depression, insomnia, orthostatic hypotension, HTN

74
Q

Centrally acting anticholinergics

A

Benzotropine

Partially block cholinergic receptors to help balance cholinergic & DA activity
Ind: mild disease
< 60 years old without cognitive impairment

75
Q

Amantadine

A

Promotes release of DA from terminals in dorsal striatum. May increase DA @ receptors by releasing intact striatal DA stores, may block neuronal DA reuptake

Monotherapy for tremor or combo w/ Levodopa/Carbidopa to reduce Levodopa induced dyskinesia

Need dose adjustment for renal insufficiency

Decreases efficacy after few months (drug holiday can restore)

76
Q

DA agonists (non-ergot)

A

1st line for Parkinsons. Direct activation of DA2 R in striatum. Less effective than levodopa, but less likely to cause dyskinesias

All can cause impulse control disorders d/t DA activation @ PFC

Pramipaxole: sleep attacks unique, renal excretion
Ropinirole: nausea more common, liver metabolism
Rotigotine: TD (extensive 1st pass metabolism), for early/mild Sx
Apomorphine: SQ. D2 and alpha 1/2 adrenergic receptors; increases NE. QT prolongation

77
Q

Levodopa/Carbidopa

A

Most effective therapy for Parkinson’s but takes several months of tx before seeing full response
Dyskinesia=most troubling ADE

Off periods and weaning off occur

Levodopa–increases DA synth in striatum and helps restore proper balance btwn DA and AcH=h
Carbidopa–enhances effects of Levodopa by inhibition of decarboxylation in peripheral tissues

78
Q

COMT inhibitors

A

Selective, reversible inhibitor of COMT –> decreased peripheral levodopa metabolism, prolonging T1/2 and duration of levodopa.

Increases duration of on phase, reduces weaning off phenomenon

ADE: dyskinesia, N/D, hallucinations, ortho hypo, urine discoloration

1 (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions