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Pharmacology > Pharm Final Exam - From Review Session > Flashcards

Pharm Final Exam - From Review Session Flashcards

1
Q

3 concerns with decreasing acid (with PPIS, etc)

A

decrease gastric emptying time, decrease drug absorption, increase in gastric ph can allow bacterial growth

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2
Q

why use antacids w/ caution in HF and HTN patients

A

all contain a lot Na+

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3
Q

which drug creates a sticky gel that provides a barrier over ulcer

A

sucrafalte

last 6 hours

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4
Q

which drug is Direct replacement for NSAIDS that inhibit PG

A

misoprostol

don’t give in pregnancy!

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5
Q

bulk forming laxative example and MOA

A

Psyllium
Act like dietary fiber
Absorb water→ soften and enlarge fecal mass → promotes peristalsis

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6
Q

surfactant laxative

A

Factilates water penetration
Secretion of H2O/ e-lytes into intestine
Lowers surface tension of stool = facilitation of H2O entry

ex: docusate

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7
Q

stimulant laxatives

A

Stimulates peristalsis
Secretion of H2O/ e-lytes into intestine

ex: Bisacodyl, Senna, Castor oil*

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8
Q

Castor oil

A

only laxative that works in small intestine (very rapid and powerful)
type 1, very rapid

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9
Q

osmotic laxative

A

retains water in the intestinal lumen & thereby soften & enlarges feces → promotes peristalsis

ex:
Mag hydroxide*
Mag sulfate*
Mag citrate*
Polyethylene glycol*
Lactulose*
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10
Q

methylnatrexone

A

Blocks mu receptors on GI tract → increases peristalsis

Selective mu antagonists

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11
Q

two pathways for anti-emetics

A

Drugs either alter receptor agonizing in CTZ

OR neuronal transmission from inner ear to vomiting center

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12
Q

anti-emetics that block CTZ

A

serotonin antagonists
substance P/NK 1 antagonists
dopamine antagonists
benzos

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13
Q

antiemetics that work on inner ear

A

anti-cholinergics (scopolamine)

antihistamines (meclizine)

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14
Q

AE of ondansetron

A

HA, dizziness
diarrhea
QT prolongation

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15
Q

AE of aprepitant

A

can increase metabolism of warfarin and OCs

-teach pt to use alternative form of BC

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16
Q

AEs of butyrophenones (dopamine antagonists)

A

hypotension, sedation, resp depression, EPS
-contraindicated in <2 years
-tissue injury w/ extravasation!
QT prolongation

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17
Q

AEs of scopolamine

A 
Dry mouth
Blurred vision
Drowsiness/sedation
Less common
Urinary retention
Constipation
Disorientation
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18
Q

when is scopolamine most effective

A

prophylatically

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19
Q

what is midazolam used for

A

Sedation, suppression of anticipatory emesis

More used for patients that get nausea after chemo

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20
Q

which glucocorticoid can be used for N/V

A

dexmethasone
short term, low dose therapy
can lead to hyperglycemia
IV!

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21
Q

which drug do you use for IBS in women

A

Alosetron

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22
Q

MOA of alosetron

A

5-HT3 specific block→ ↓ abdominal pain, increased colonic transit time, increase absorption of water and sodium

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23
Q

MOA of sulfasalazine (5-aminosalicylates)

A

Metabolized by intestinal bacteria → to 5-ASA and sulfapyridine = suppression of PG synthesis and migration of inflammatory cells

5ASA - suppression of PG synthesis and local inflammation
Sulfapyridine = leads to AE

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24
Q

AE of sulfasalazine*

A

-N/V, rash, arthralgia

Rare: agranulocytosis, hemolytic anemia

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25
Q

what does metoclopramide do and what is it used for

A

Increase tone and motility of GI tract
DA & 5HT receptor block in CTZ
Increases upper GI motility via ACh enhancing

Used for N/V

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26
Q

when don’t we give antibiotics

A

Viral infection
Fever of unknown origin
Before we know enough information and not life threatening
w/o surgically draining abscesses (abx will have limited efficacy)

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27
Q

bacteriostatic drugs

A

Tetracyclines
Macrolides
Clindamycin
Linezolid

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28
Q

bactericidal drugs

A 
Penicillins (PCNs)
Cephalosporins
Vancomycin
Lipoglycoproteins
Daptomycin
Imipenem
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29
Q

The function of penicillin binding proteins (PBPs)

A

bind antbiotic and drug disrupts cell wall

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30
Q

pencillin binding proteins

A

expressed by bacteria during growth and division

have to be present for pencillins to work

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31
Q

beta lactam ring

A

essential for antibacterial property of antibiotic

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32
Q

major concern with pencillin

A 
allergic reactions (10% mortality)
watch for 30 mins after
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33
Q

MOA of pencillins

A
  • bactericidal
  • bind penicillin binding proteins (PBPs) on bacterial cell
  • Weaken bacterial cell wall → H2O is absorbed d/t high intracellular osmotic pressure → cell bursts
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34
Q

AE of cephalosporins

A

1% cross sensitivity w/ PCN

Cefotetan, ceftriaxone, cefazolin: Can interfere with vit K. metabolism → Can increase bleeding time (w/ prolonged tx), caution with other drugs that cause bleeding
Cefazolin, cefotetan: Disulfiram like reaction → avoid alcohol

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35
Q

MOA of carbapenem

A

MOA: same as PCN but
Resistance to beta lactamase
Gram - penetration ability
Reserved for resistant to mixed type infections

ex: imipenem

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36
Q

MRSA

A

staph aureus infection that is resistance to all beta lactam antibiotics
Production of a PBP that has a low affinity for antibiotics

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37
Q

vancomycin MOA

A

no beta lactam ring
Inhibits cell wall synthesis
Doesn’t PBPS
Only gram +!

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38
Q

how to give vanco

A

IV/PO

GIVE SLOWLY MAX 1G/HR

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39
Q

AE of vanco

A
  • dose related renal failure
  • ototoxicity
  • rapid infusion leads to histamine release —> hypotension
  • red man syndrome = anaphylactoid rxn
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40
Q

daptomycin MOA

A

Insert self into bacterial cell membrane → form channels to allow for K+ efflux → inhibition of DNA/RNA/proteins → cell death

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41
Q

Aminoglycosides MOA

A

Bactericidal
Binds 30S subunit = inhibition of protein synthesis + production of abnormal proteins

Gram - aerobic

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42
Q

AEs of aminoglycosides

A

Ototoxicity - drug accumulation occurs in inner ears
Make sure trough levels are low enough so drug diffuses out
First sign = tinnitus or HA
Irreversible

Nephrotoxicity - drug is taken up by tubular cells
Correlates with high trough levels also
s/s = ATN, proteinuria, casts, dilute UOP, BUN/cr elevation
Risks: elderly, CKD, other nephrotoxic drugs
Usually reversible

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43
Q

tetracycline MOA

A

Gram + and gram - = broad spectrum

Binds 30S subunit of ribosome → tRNA to mRNA cannot occur → amino acids cannot be added

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44
Q

AEs of tetracyclines

A

GI irritation
Bind Ca++ in developing teeth → discoloration –> Avoid > 4th month gestation to 8 yr old**
Superinfection (d/t broad spectrum)
C. diff
Hepatotoxicity d/t fatty infiltration of liver
Biggest risk with preg/postpartum and CKD
Renal toxicity (caution w/ CKD)
Photosensitivity

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45
Q

macroslides MOA

A

Bind 50S ribosomal subunit → block addition of new amino acids to peptide chain → proteins can’t be synthesized

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46
Q

can you give macroslides during pregnancy

A

yes

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47
Q

fluoroquinolones MOA

A

Inhibits 2 enzymes (DNA gyrase & topoisomerase IV)

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48
Q

AE of Fluoroquinolones

A

GI effects
CNS effects - seizures
Phototoxicity
Tendon rupture - black box warning!

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49
Q

how to avoid development of resistance w/ TB

A

Always treat 2+ (up to 7) drugs

Treat x6-24 months (longer for HIV patients)

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50
Q

TB drugs (4)

A

isoniazid*
Rifampin*
pyrazinamide*
ethambutol*

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51
Q

AEs of isoniazid, rifampin, pyrazinamide

A

hepatotoxicity

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52
Q

Major AE of ethambutol

A

Optic neuritis (most sig)
s/s = blurred vision, change in virtual field and color
Usually resolves, not always
Assess pre-tx and monthly, educate pts

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53
Q

Amphotericin B MOA

A

Binds fungal cell membrane → increased permeability & leakage of electrolytes → cell death

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54
Q

how long an amphotericin B be detected in body for

A

up to 1 year

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55
Q

AEs of amphotericin B

A 
Infusion reactions (fever, chills, rigors)
Phlebitis
Nephrotoxicity (dose related)
hypoK+ (d/t kidney damage) 
Bone marrow suppression
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56
Q

what drug to use for malaria

A

Chloroquine - use for erythocytic phase

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57
Q

can malaria be cured?

A

yes

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58
Q

drug for cytomegalovirus

A

ganciclovir

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59
Q

ganciclovir MOA

A

Converted to active form inside infected cells
Suppresses replication of viral DNA - inhibits DNA polymerase
Incorporates into viral DNA chain → chain termination

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60
Q

Ganciclovir AEs

A

Teratogenic
Bone marrow suppression (thrombocytopenia, granulocytopenia)
Usually reversible
Monitor blood counts (hold for ANC < 500 and plts < 25k)

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61
Q

general principles of drugs for HIV (4)

A
  1. high/nearly universal rate of relapse if medications are stopped
  2. Drug resistance is common due to rapid viral replication
  3. Most components of ART/HAART are cyp450 inhibitors, increasing chance of drug-drug interactions
  4. Expensive
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62
Q

3 drugs for Hep C.

A

PEG Interferon A
ribavirin
sofosbuvir

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63
Q

is ribavirin effective alone

A

No - need to take with PEG IFA

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64
Q

PEG IFA MOA

A

Binds to host receptors blocks viral entry into cells

Blocks viral synthesis of mRNA and proteins

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65
Q

administration of PEG IFA

A

SQ weekly

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66
Q

AE of PEG IFA

A
  • Flulike sx in 50% (decreases over time)
  • Neuropsych effects (depression, SI)
  • Organ dysfunction: thyroid, heart, bone marrow
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67
Q

MOA of sofosbuvir

A
  • Nucleotide analog inhibitor
  • Direct antiviral activity - blocks transcription of HCV RNA
  • Effective against resistance - can be used with other agents if needed
  • Can cure HCV in 12 weeks but expensive
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68
Q

methotrexate MOA (DMARD)

A

Folate antagonist

Results in ↓ B and T cell production

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69
Q

AEs of methotrexate

A

Hepatic fibrosis
Bone marrow suppression
GI ulceration
Pneumonitis

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70
Q

when is methotrexate contraindicated

A

blood dyscrasias, immunodeficiency, liver disease, pregnancy

*Vaccine risks - decreased efficacy, infection risk w/ live vaccines

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71
Q

how to treat RA

A

NSAIDs - do not alter disease progression!
glucocorticoids
DMARDS

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72
Q

tx for gout

A

NSAIDs: to treat symptoms
Glucocorticoids: PO or IM in those who can’t use NSAIDs
Colchicine: anti inflammatory agent specific for gout

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73
Q

what is long term therapy for gout?

A
  1. Inhibit uric acid formation (xanthine oxidase inhibitors)
  2. Accelerate uric acid excretion (probenecid)
  3. Convert uric acid to metabolite allantoin - renally excreted (pegloticase and rasburicase)

*all are not anti-inflammatory

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74
Q

MOA of xanthine oxidase inhibitors

A

Inhibition of XO (enzyme required for uric acid formation) → decreased uric acid levels, prevention of tophi formation

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75
Q

when can you use colchicine?

A

Short term use for gout flare up OR long term use to prevent attacks

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76
Q

MOA of colchicine

A

Unknown - might inhibit WBC infiltration via disruption of cellular microtubules

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77
Q

MOA of bisphosphonates

A

Structural analogs of pyrophosphate (normal constituent of bone)
Drugs is incorporated into bone and remains active for years
Decreases osteoclast activity → decreased bone resorption

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78
Q

Bisphosphonates: AE

A

Esophagitis - Avoid by taking w/ fully glass of water and remain upright x30-60 mins

Serious AE:
Ocular inflammation
Osteonecrosis of jaw
Atypical femur fractures
New onset a fibrillation
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79
Q

AE calcium salts (IV)

A 
Highly irritating (avoid extravasation)
Give slowly, severe HTN w/ rapid injection
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80
Q

AEs of traditional chemo

A 
Bone marrow suppression
GI tract damage
N/V
Alopecia
Infertility, teratogenic effects
Urinary stones (uric acid crystals)
Extravasation: local injury- worry about IV moving out of vein --Refers to escape of a chemotherapy drug into extravascular space - leakage from a vessel or by direct infiltration
promo of secondary cancer
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81
Q

Anthracyclines (doxorubicin) AE

A

-Cardiac toxicity: may be more sensitive to cardiac depressive side effects of medications even if normal resting echo
free radical production causes myocardial damage
-bone marrow suppression
-red/orange color urine and sweat

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82
Q

anthracyclines (doxorubicin) AE: acute cardiac toxicity

A

acute (10%): tachycardia, arrhythmia, transient and rare
ECG changes and acute EF reduction
usually lasts < 1-2 months

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83
Q

anthracyclines (doxorubicin): AE: chronic cardiac toxicity

A

(2% w/ 60% fatality): severe cardiomyopathy/CHF
related to cumulative dose

protective therapies: dexrazoxane (prevents free radical formation), ACE inhibitors

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84
Q

non-anthracyclines (bleomycin) AE

A
  • pulmonary toxicity
  • -skin reactions
  • hypersensitivity in lymphoma pts → fever, chlls, confusion, hypotension and wheezing (use test dose first)
  • myelosuppression rarely seen
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85
Q

nonanthracyclines (belomycine) pulmonary toxicity AE

A

Lungs take up high concentrations of drug and lack hydrolase enzyme to inactivate bleomycin
↑ risk / ↑ cumulative dosing, age, chest radiation, pulmonary co-morbidity, o2 exposure, other chemo drugs, genetics

*d/c w/ signs of dry cough, dyspnea, tachypnea, and infiltrates on CXR
*Can lead to pulmonary fibrosis → severe fibrosis → death
↓ diffusion capacity
*Keep FIO2 concentrations at or below 30% during anesthesia if possible

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86
Q

vincristine AE

A

little bone marrow suppression!
Peripheral neuropathy via damage to neurotubules in almost 100% of patients (sensory loss, weakness, autonomic dysfunction)
fatal if given intrathecally

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87
Q

chemo handling/admin guidelines

A

Drugs are mutagenic, carcinogenic and teratogenic
Protect yourself!
Handle with gloves
Do not break, crush or chew
Patient should use an effective form of birth control and shouldn’t breastfeed

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88
Q

methotrexate AE (cancer)

A
  • pulmonary fibrosis (8%) and/or noncardiogenic pulmonary edema
  • neutropenia and thrombocytopenia
  • mucositis & GI ulceration
  • renal toxicity (10%) - tx:alkalinize urine and hydrate
  • Hepatic toxicity
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89
Q

coenzyme Q10 AE

A

AE: GI upset, elevated LFTs
No safe dose in pregnancy
May antagonize warfarin

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90
Q

what is coenzyme Q10 used for

A

Correct of deficiency
Mitochondrial disease
To decrease statin related myopathy (theoretical)

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91
Q

what is flaxseed used for

A
  • Constipation
  • high cholesterol: can ↓ LDL and total cholesterol; no effects on HDL or triglycerides
  • menopausal sx
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92
Q

AE of flaxseed

A

GI effects

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93
Q

what are glucosamine and chondroitin used for

A

osteoarthritis (w/ mixed results)

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94
Q

AE.of glucosamine and chondroitin

A

Nausea
Heartburn
Possible increased bleeding risk

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95
Q

what is saw palmetto used for

A

Symptom relief with BPH (does not decrease size of prostate or affect PSA)

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96
Q

when to use saw palmetto w/ caution

A

with antiplatelets and anticoagulants due to antiplatelet effects and increased bleeding risk

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97
Q

which vitamins are fat soluble

A

A, D, E, K

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98
Q

What is minimum effective concentration?

A

How much dose is needed for drug to work

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99
Q

What electrolyte should be monitored when giving digoxin?

A

Calcium

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100
Q

What is unique about the therapeutic index of digoxin and lithium?

A

Narrow therapeutic index

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101
Q

Opioid agonists have a stronger (efficacy/potency) than opioid agonist-antagonist.

A

Efficacy

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102
Q

How is the starting dose for new medications determined?

A

ED50

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103
Q

What is the definition of a black box warning?

A

Strongest safety warning available

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104
Q

Which anti-seizure drug should not be given during pregnancy?

A

Valproate

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105
Q

What are characteristics of a molecule that can pass through the BBB?

A

small, lipid-soluble, transport system, nonpolar

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106
Q

What characteristics of neonates affect their medication dosing?

A

Neonates have immature BBB, kidneys, and CYP450 systems

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107
Q

What receptor is located at the neuromuscular junction of the somatic nervous system?

A

Nm (N1)

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108
Q

What receptor is located at all autonomic ganglion (PSNS and SNS)?

A

Nn (N2)

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109
Q

What receptor does epinephrine agonize that norepinephrine does not?

A

Beta 2

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110
Q

What effect does baroreceptors have on the heart rate during severe vasoconstriction?

A

reflex bradycardia

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111
Q

What drug is an A1 receptor agonist that causes reflex bradycardia?

A

Phenylephrine

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112
Q

Are A2 agonist drugs catecholamines?

A

No. They are NOT catecholamines, so they CAN cross the BBB, causing decreased CNS effects.

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113
Q

What are alpha antagonists primarily used for?

A

BPH and HTN

Phenoxybenzamine (noncompetitive, causes reflex tachy and congestion)

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114
Q

What class of drug is isoproterenol?

A

B agonist, nonselective

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115
Q

What is the role of isoproterenol?

A

Chemical pacemaker

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116
Q

What are major AEs of alpha blockers?

A

orthostatic hypotension, reflex tachycardia

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117
Q

What are common AEs of beta blockers?

A

bradycardia, decrease contractility

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118
Q

What are contraindications for beta blockers?

A

heart block, severe asthma

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119
Q

What are the effects of atropine?

A

increased HR, decrease secretions, decreased peristalsis, tachycardia
will promote SNS

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120
Q

What class of drug is neostigmine?

A

Acetylcholinesterase inhibitor

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121
Q

What are contraindications for using acetylcholinesterase inhibitors?

A

obstructions, bradycardia
i.e. neostigmine
will cause increase in Ach build up –> increase GI motility

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122
Q

Where is erythropoietin produced?

A

Kidneys

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123
Q

What population do you NOT want to give erythropoietin to?

A

Ppl with HTN

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124
Q

What clotting factor affects Hemophilia A?

A 
Factor VIII (8)
Use Desmopressin
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125
Q

High dose use of glucocorticoids to prevent transplant rejection can cause what?

A

neoplasms, high risk for infections

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126
Q

Is the onset and duration of action of glucocorticoids long or short?

A

long

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127
Q

Long term use of glucocorticoids have what AEs?

A

osteroporosis, hyperglycemia

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128
Q

Which class of histamine receptors can cross the BBB?

A

1st Gen.

2nd Gen does not cross BBB, does not cause sedation

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129
Q

What should histamine receptor drugs not be taken with?

A

CNS depressants (i.e. alcohol)

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130
Q

What is the lifespan of a platelet?

A

8 days

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131
Q

Which COX inhibitor has a black box warning?

A

Celecoxib, d/t increase in CV events

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132
Q

What drug class does Celecoxib fall under?

A

COX2 selective inhibitor

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133
Q

What is the antidote for Tylenol overdose?

A

acetylcysteine

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134
Q

Does Tylenol cause suppress platelet aggregation?

A

No silly. Tylenol does not suppress platelet aggregation.

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135
Q

What are the effects of long-term, high dose use of COX inhibitors?

A

ulcers, bleeding

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136
Q

What is the drug for T4?

A

Levothyroxine

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137
Q

What are the signs of hypothyroidism?

A

sensitive to cold, bradycardia, fatigue, weight gain

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138
Q

What are the signs of hyperthyroidism?

A

sensitive to heat, tachycardia

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139
Q

If TSH is high, what changes must be made to the medication dose?

A

TSH is high, T4/T3 is low –> need to give higher dose

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140
Q

If you have hyperthyroidism, what medication would you give?

A

PTU

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141
Q

If you have hypothyroidism, what medication would you give?

A

T4

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142
Q

What is the difference between vasopressin and desmopressin?

A

Vasopressin causes vasoconstriction. Desmopressin also used for Hemophilia A.

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143
Q

When would you prescribe progestin only OCs?

A

If pt has high risk of thromboembolic events, if pt is breastfeeding

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144
Q

What are CI for OCs?

A 
Acute liver disease
Hypertension 
CVA 
PE 
MI
Uterine bleeding with unknown cause
Breast/endometrial cancer
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145
Q

What are drugs to halt labor?

A

Terbutaline
Indomethacin
Nifedipine
Magnesium sulfate

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146
Q

What drug is used to develop fetal lung maturity?

A

Betamethasone

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147
Q

What drug is used for cervical ripening?

A

Prostaglandins

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148
Q

What conditions need to be met before giving pitocin?

A

Cervical ripening is complete, and baby’s lungs have to be mature

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149
Q

What drugs are given for PP hemorrhage?

A

Pitocin
Hemabate (not to someone with asthma)
Methergine (not for ppl with HTN)
Cytotec (given PR)

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150
Q

What drug is PDE5 contraindicated with?

A

Nitroglycerin

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151
Q

What route of testosterone replacement therapy are hepatotoxic?

A

PO

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152
Q

What are the ultrashort acting insulin drugs?

A

apart, lispro, glulisine

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153
Q

What are the routes of administration for insulin?

A

SQ, IV

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154
Q

What is the name of the short acting insulin?

A

Regular insulin

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155
Q

Which insulin has a DOA of 4 hours and is considered intermediate acting?

A

NPH

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156
Q

Which insulin has no peak and lasts for 24 hours?

A

Glargine

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157
Q

Which oral anti-diabetic drugs have hypoglycemic risks?

A

Sulfonylureas (three Gs) and meglitinides

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158
Q

What are the AEs of HMG-CoA inhibitors?

A

rhabdo, myopathies

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159
Q

What is the best time to take HMG-CoA inhibitors?

A

At night

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160
Q

What lab values should be monitored when taking statins?

A

Creatinine kinase serum

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161
Q

What drug class lowers VLDLs rather than LDLs?

A

Fibrates

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162
Q

What clotting factors does Vitamin K affect?

A

2, 7, 9, 10

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163
Q

What lab value needs to be monitored when giving warfarin?

A

PT-INR

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164
Q

What are AEs caused by heparin infusions?

A

Bleed risk, heparin induced thrombocytopenia (watch for drop in platelets)

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165
Q

What are the four types of diuretics?

A

osmotic, loop, thiazides, potassium-sparing

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166
Q

What type of diuretic is mannitol?

A

Osmotic, usually for volume overload

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167
Q

What are the AEs of loop diuretics?

A

Hypokalemia, hyponatremia (all goes down), ototoxicity, HTN, dehydration

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168
Q

In the event of edema, what type of fluid would be infused?

A

hypertonic

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169
Q

In the event of ketoacidosis or hyperglycemia, what type of fluid would you infuse?

A

hypotonic

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170
Q

Out of all the RAAS drugs, which has the greatest amount of mortality/morbidity improvement?

A

ACE inhibitors

171
Q

What kind of drugs are the “prils?”

A

ACE inhibitors

172
Q

What kind of drugs are the “sartans?”

A

ARBs

173
Q

If your patient develops a dry cough with ACE inhibitors, what do you do?

A

prescribe them ARBs instead

174
Q

What are AEs of ACE inhibitors?

A

dry cough, angioedema, hyperkalemia

175
Q

What are standard practices when taking nitroglycerin daily?

A

Change site
Wash hands immediately
Drug free time (take it off at night)
Don’t take with PDE5

176
Q

Absorption

A

drug’s movement from site of administration into the blood

177
Q

What factors affect absorption?

A 
Rate of dissolution
Surface area (i.e. how big a transdermal patch is)
Lipid solubility
Route Administration
Blood flow
178
Q

what impacts PO meds

A

Increased or slower motility time
Gastric acids
Other foods, medications, empty stomach

179
Q

Small vd

A

drug is mostly in vasculature → it is not widely distributed!

180
Q

Large vd

A

drug is distributed outside of the vasculature

181
Q

what impacts vd?

A 
CO
Perfusion of tissues
Capillary system
Polarity of drug molecules - can they move through membranes
Protein binding
182
Q

BBB

A

can make it hard to treat CNS pathologies
Made up of tight junctions and PGP
Drugs need to be Lipid soluble, non polar, has transport system
Catecholamines can’t cross
PGP works against us

183
Q

If protein levels are too low…

A

it can lead to drug toxicity

184
Q

cyp450 Inducers

A

increase enzyme concentration → increase drug metabolism → decrease therapeutic response of all drugs in the body

185
Q

cyp450 inhibitors

A

decrease enzyme concentration → decrease drug metabolism → increases drug effects, risk for toxicity
I.e. grapefruit juice

186
Q

Zero order kinetics

A

same amount of drug will be metabolized/hour no matter how much drug is present
*similar to alcohol

187
Q

First order kinetics

A

% of drug metabolized depends on the dose - a larger dose will have a larger amount metabolized
*most drugs

188
Q

older adults have…

A

increased body fat, decreased skeletal muscle mass, decreased renal blood flow

189
Q

MEC

A

plasma drug level below which therapeutic effects will not occur
First dose is usually here

190
Q

toxic concentration

A

plasma levels at which toxic effects begin

191
Q

TI

A

b/w MEC and toxic concentration
Usually takes 4 half lives to get here
If we don’t have time → bolus dose

192
Q

Affinity (potency)

A

how much drug must be administered to elicit a desired response

193
Q

Intrinsic activity (efficacy)

A

intensity of effect that the drug produces

194
Q

criteria to cross placenta

A 
Lipid soluble 
Unionized
Not protein bound
Non polar
small
195
Q

how to dose for pediatrics

A

by weight
Peds have greater variability in response
In very young - immature organ system

196
Q

neonates and infants: BBB

A

is not fully developed

Less Exclusion of drugs from CNS by BBB → risk of CNS effects

197
Q

neonates and infants: hepatic drug metabolism

A

immature CYP450 → decreased metabolism→ increased drug accumulation

198
Q

neonates and infants: renal drug excretion

A

low renal blood flow, GFR and active tubular secretion → reduced excretion

199
Q

most common cause of ADRs in older adults?

A

Decreased renal blood flow, decreased GFR, decreased tubular section, decreased # of nephrons

200
Q

what receptor does NE not agonize

A

B2 so NE won’t cause hyperglycemia (d/t no glycogenolysis) and doesn’t cause calcium release from muscles

201
Q

baroreceptor reflex: when BP falls…

A

vasoconstriction and increase CO

202
Q

baroreceptor reflex: when BP is too high

A

vasodilation + decreased CO

203
Q

phenylephrine

A

a1 agonist

leads to severe vasoconstriction

204
Q

indirect agonists

A

drug doesn’t do it itself

examples: increases NT concentration release from presynaptic, Blocks NE reuptake, Block NE breakdown (MAO)

205
Q

which receptors does epi agonize

A

A1, a2, b1, b2

206
Q

epi effects

A
  • increased HR, contractility, AV node conduction rate (b1)
  • vasoconstriction (a1) + vasodilation (a2, b2) → leads to increase in systolic BP
  • other fight or flight effects!
207
Q

indications for epi

A
  • Anaphylactic shock
  • bronchoconstriction from asthma
  • cardiac arrest
208
Q

cautions for epi

A
  • Hypertensive crisis → dramatic increase in BP because of vasoconstriction
  • Dysrhythmias
  • Angina pectoris
  • Necrosis after extravasation
  • Hyperglycemia
209
Q

AE of norepi

A
  • Tachydysrhythmias - reflex brady and then increased HR so it doesn’t go too out of wack
  • Angina
  • Hypertension
  • Local necrosis upon extravasation
  • metabolic acidosis
210
Q

what are the effects of agonizing alpha 2 receptors

A
  • Suppresses firing of sympathetic nerves to the heart → can cause bradycardia and a decrease in CO
  • Promotes vasodilation
  • Decrease BP
211
Q

effects of alpha antagonists

A

vascular vasodilation

212
Q

AE of alpha antagonists

A 
orthostatic hypotension
Reflex tachycardia
Nasal congestion
Inhibition of ejaculation
Decreased renal blood flow
213
Q

what type of drug is phenoxybenzamine

A

alpha antagonist

214
Q

phenoxybenzamine effect and indications

A

very long acting - permanently bindings

indicated for: Long term HTN crisis - pheochromocytoma, BPH

215
Q

location and effects of beta 1 receptors

A

Heart → contractility, increased HR, increased AV node conduction velocity
*does not vasodilate or constrict
Kidneys → stimulation of renin release

216
Q

beta 2 receptors location and effects

A

Smooth muscle in the uterus, bronchioles, GI, GU, vascular system
Bronchodilation
Decreased uterine contractions
Vasodilation of the coronary arteries
GI/GU motility
Skeletal muscle → increased contraction, speed, glycogenolysis, tremor, increased K+uptake
Liver → glycogenolysis

217
Q

beta agonists

A

isoproterenol
dobutamine
terbutaline
albuterol

218
Q

isorproterenol effect

A

“Chemical pacemaker”

  • increased HR
  • increased contractility
  • bronchodilation
219
Q

beta antagonists effects

A 
Cardiac - decrease HR/contractility
Bronchospasm
Vasoconstriction in skeletal muscles
Decreased renin release → decreases BP
Decreases K+ uptake → hyperkalemia = risk
Decreased glycogenolysis
220
Q

CIs for beta blockers

A 
Preexisting AV block or cardiac failure
Severe asthma
Reactive airway disease
Uncontrolled diabetes
Hypovolemia
221
Q

when to use atropine?

A
  • bradycardia
  • reduce frequency of bowel movements
  • reverse muscarinic poisoning
  • can treat peptic ulcer disease
  • asthma (rarely used because it could dry and thicken secretions)
222
Q

effects of atropine

A
  • increased HR
  • decreased secretions
  • bronchodilation
  • mydriasis
  • cycloplegia (paralysis of ciliary muscle)
223
Q

when is pyridostigmine indicated

A
  • glaucoma
  • myasthenia gravis
  • NMB reversal
224
Q

pyridostigmine MOA

A

Pyridostigmine binds to cholinesterase → takes a while → less available to break down Ach → more Ach is available

225
Q

how do you treat hemophilia A pts?

A

desmopressin –> Releases stored factor VIII from vascular endothelium

226
Q

what is epoetin alfa and how is it administered?

A

EPO

administered IV or SQ

227
Q

glucocorticoid MOA

A

Diffuse into the cell → bind to receptor steroid complexes in the cytoplasm → migrates to nucleus and binds to to DNA → results in alteration of mRNA transcription → modulate production of regulatory proteins
*this is a slower process → DOA is long too

228
Q

short acting glucocorticoids

A

8-12 hours

cortisone, hydrocortisone

229
Q

medium acting glucocorticoids

A

18-36 hours

prednisone, triamcinolone

230
Q

long acting glucocorticoids

A

36-54 hours

dexamethasone (no sodium retaining potency!)

231
Q

when do adverse effects of glucocorticoids happen

A

at higher pharmacologic doses

232
Q

AEs of glucocorticoids at higher doses

A 
anti inflammatory --> risk for infection
adrenal insufficiency
osteoporosis
hyperglycemia
growth delay in children
fluid/electrolyte disturbances (mineralcorticoids)
neoplasms w/ really high doses
233
Q

stress dosing

A

adrenal cortex can’t muster up necessary extra glucocorticoid secretion d/t long term suppression
Might need extra dose with trauma, surgery and other stressors on the body

234
Q

risks associated with immunosuppressants

A

infection and neoplasms

235
Q

which H1 antagonists cross the BBB

A

first generation = small and highly lipid soluble

236
Q

H1 antagonists

A

Diphenhydramine (benadryl)

Promethazine (phenergan)

237
Q

second generation H1 antagonists

A

large, polar

Fexofenadine (allegra)

238
Q

harmful effects of inhibiting Cox 1

A

Gastric erosion and ulceration - decreased prostaglandins → decreased vasodilation
Bleeding tendencies (decreases platelet aggregation)
Renal impairment - decreased prostaglandins → decreased vasodilation → decreased RBF

239
Q

beneficial effects of cox1 inhibition

A

Protection against MI and stroke secondary to reduced platelet aggregation

240
Q

beneficial effects of inhibiting cox 2

A

Suppression of inflammation
Alleviation of pain
Reduction of fever
Protection against colorectal cancer

241
Q

harmful effects of inhibiting cox 2

A

Promotion of MI and stroke secondary to suppressing vasodilation
Renal impairment

242
Q

nonselective COX inhibitor prototype

A

aspirin

243
Q

second generation cox 2 selective inhibitor

A

celecoxib

244
Q

AE of celecoxib

A

*does not inhibit cox 1 platelet aggregation → does not provide CV benefits like aspirin does → black box warning
GI ulceration - should be low b/c cox 1 produces protective gastric mucosa
Renal impairment

245
Q

acetaminophen

A

cox 2 inhibitor

246
Q

what effects does acetaminophen have

A

not anti-inflammatory
Inhibition is limited to the CNS - cox 2
Reduces prostaglandin in the CNS to reduce fever and pain

247
Q

antidote to acetaminophen?

A

acetylcysteine

100% effective if given within 8-10 hours of overdose

248
Q

hypothyroidism: TSH and T3 T4 levels

A

TSH↑

T3T4↓

249
Q

hyperthyroidism: TSH and T3T4 levels

A

TSH ↓

T3t4↑

250
Q

MOA of levothyroxine

A

synthetic T4

long 1/2 life - can take 1 month to plateau

251
Q

which hyperthryoidism drug is preferred in the first trimester

A

Propylthiouracil (PTU) (thioamide)

less placental crossing

252
Q

absolute CIs for hormone therapy or OCs (7)

A 
Pregnancy
Breast or endometrial CA
Acute liver disease
Uncontrolled HTN
Thrombosis
Undiagnosed vaginal bleeding
Acute DVT
253
Q

minipills

A

progestin only
Less effective
Change the cervical secretion/mucus
Recommended for new moms because they do not go into breastmilk

254
Q

when can oxytocin be used

A

can only be used if cervix is ripe and fetal lungs are mature
IV infusion only

255
Q

4 drugs for postpartum hemorrhage

A

Oxytocin (pitocin)
Misoprostol (PG) (cytotec)
Carboprost tromethamine (PG) (hemabate)
ergot alkaloids (Methylergonovine) (Methergine)

256
Q

how is testosterone prepared

A

PO (both are 17 alpha = hepatotoxic)
Transdermal - can be transferred w/ skin to skin contact! - more consistent level
Nasal gel
Implantable pellets - 3-6 months
Buccal tablets
IM (T cypionate and T enanthate) - long acting - more consistent level

257
Q

MOA of tamulosin

A

alpha 1 antagonist

  • relaxes smooth muscle in bladder neck and prostate capsule to decrease dynamic obstruction
  • does not decrease PSA
258
Q

which drugs target mechanical obstruction of BPH

A

5 alpha reductase inhibitors

  • finteraride
  • dutasteride (longer ½ life)

decreases serum PSA

259
Q

can insulin be given PO or IM?

A

no

260
Q

which 2 diabetes drugs cause weight gain and hypoglycemia

A

Sulfonylureas (3Gs!)

  • glimepiride
  • glipizide
  • glyburide

Meglitinides (Glinides)

  • nateglinide (shorter acting)
  • repaglinide

both need a working pancreas to release insulin!!

261
Q

what drugs work best for lowering LDL?

A

first, Monoclonal antibody PCSK9 inhibitors

second, HMG COA inhibitors (statins)

262
Q

AEs of statins

A
  • myopathies (aches, tenderness, weakness) → can lead to CK + K+ increase which can lead to renal injury
  • should measure CK at start
  • rhabdo = skeletal muscle breakdown
  • hepatotoxicity
263
Q

fibric acid derivatives: MOA

A

Inhibit hepatic extraction of free fatty acids so the liver cannot synthesize as many TGs
lowervs VLDL by 40-55%

264
Q

heparin MOA

A
  • suppress thrombin and factor Xa
  • hepatic metabolism/renal excretion
  • cannot cross the placenta
  • ½ life =1.5 hours
  • large and polar
265
Q

AEs of heparin

A

hemorrhage

  • spinal/epidural hematoma with LP/epidural anesthesia
  • HIT → drop in platelets will be the sign
  • hypersensitivity reactions
266
Q

heparin antidote

A

protamine sulfate

267
Q

what factors does warfarin impact

A

decreases production of factors II, VII, IX, X to decrease fibrin production
*doesn’t impact existing factors

268
Q

does warfarin cross the placenta and breastmilk

A

yes - CI in pregnancy

269
Q

Direct Xa Inhibitor

A

Rivaroxaban

270
Q

rivaroxaban MOA

A
  • selective binding and inhibition of factor Xa → decreased production of thrombin → inhibition of fibrin mesh
  • rapid onset
  • PO
  • CYP450
271
Q

HIT

A

potentially fatal immune mediated disorder characterized by reduced platelet counts and paradoxical increase in thrombotic events
Development of antibodies against heparin platelet protein complexes
Antibodies activate platelets and damage endothelium → promote thrombosis and loss of circulating platelets
Can lead to DVT, PE, MI

272
Q

abciximab

A

GP IIb/IIIa Receptor antagonist –> block IIb/IIIa receptors on platelets → inhibit the final step in platelet aggregation from all factors

273
Q

MOA of alteplase

A

binds with plasminogen to form an active complex → catalyzes the conversion of other plasminogen molecules into plasmin = enzyme that digests the fibrin network of clots + degrades fibrinogen and other clotting factors
1/2 life = 5 minutes

274
Q

indications for alteplase

A

Remove thrombi that ALREADY exist

Acute MI
Acute ischemic stroke
Acute massive PE
Not for hemorrhagic stroke

275
Q

how to decrease risk of acute bleeding episodes

A

Minimizing physical manipulation of patient
Avoid SQ or IM injections
Minimize invasive procedures
Minimized concurrent use of anticoags
Minimize concurrent use of antiplatelet drugs
Fall risk
Can’t give after epidural → risk for spinal cord hemorrhage

276
Q

which diuretic causes the most diuresis

A

loop diuretics (ex: furosemide)

277
Q

AE of loop diuretics

A

Hyponatremia, Hypochloremia
Dehydration
Hypokalemia
ototoxicity

278
Q

where do thiazide diuretics act

A

Blocks NaCl & K+ reabsorption in early DCT so blocks water absorption

279
Q

AE of thiazide diuretics

A

-Hyponatremia, Hypochloremia
Dehydration
-Hypokalemia
-increase in uric acid levels

280
Q

where do potassium sparing diuretics work

A

Act on late DCT and collecting ducts

*least amount of diuresis

281
Q

MOA for spironolactone

A

Blocks aldosterone which stops production of Na+/K+ exchange protein
K+ retention, Na+/H2O excretion

282
Q

MOA for non aldosterone antagonists

A

Directly inhibits Na+/K+ exchange in DCT

Leads to K+ retention, Na+/H2O excretion

283
Q

when are osmotic diuretics used

A

Only used in certain situations like severely increased ICP or Intraocular pressure

284
Q

AEs/cautions of mannitol (osmotic diuretic)

A

Edema since it can exist capillary beds (not BBB)

Caution with HF and pulmonary edema risk

285
Q

how should IV potassium be given

A

diluted and infused slowly (10 mEq/hour)

286
Q

which drugs prevent CV remodeling the best

A

ACE inhibitors

first line of defense = the strongest

287
Q

AEs of the ACE inhibitors

A 
First dose hypotension
Dry Cough
Hyper K+ b/c aldosterone is inhibited 
Toxic to fetus
Renal failure

Rare:Angioedema, Neutropenia

288
Q

MOA of ARBs

A

block effects of ang II at receptor

289
Q

why do ACE inhibitors cause coughing?

A

ACE is also called Kinase II in some cells → by blocking Kinase II → build up of bradykinin → vasodilation, cough, angioedema (side effects)

290
Q

MOA of aliskiren

A

inhibit release of renin → block entire RAAS

291
Q

where do dihydropyridines (nifedipine) act?

A

on vascular smooth muscle leading to
arteriole vasodilation → decreases afterload, lowers arterial pressure

-reflex tachycardia/contractility increase

292
Q

where do nondihyrdopyridines act and what is the effect

A

vascular smooth muscle and heart leading to:

  • arteriole vasodilation
  • ↓ HR, ↓ AV node conductivity, ↓ contractility
  • decrease afterload, increase coronary perfusion
293
Q

2 nondihyrdopyridines

A
  • verapamil

- diltiazem

294
Q

which vasodilator acts on the arterioles

A

hydralazine

will lead to reflex tachy and contractility

295
Q

venous dilator

A

nitroglycerin

296
Q

if you have active chest pain…

A
  • take sublingual tab asap
  • if there is no relief after 5 mins → call 911
  • 3 doses in 15 minutes
  • don’t chew or swallow
297
Q

what is contraindicated with nitroglycerin

A

PDE5 (ED drug) inhibit cGMP breakdown - also results in vascular smooth muscle relaxation → orthostatic hypotension, major vasodilation

298
Q

nitroglycerin patient instructions

A
  • use lowest effective dose because tolerance can develop rapidly
  • at least 8 drug free hours a day - at night
  • avoid abrupt withdrawl to avoid coronary vasospasm
299
Q

MOA of digoxin

A
  • selectively inhibits Na+/K+/ATPase pump
  • Build up Ca++ intracellularly (increased actin/myosin interactions) → increases contractility (inotropy) → increased workload
300
Q

class I antiarrhythmic drugs

A

Na+ channel blockers

301
Q

class II Antiarrhythmic drugs

A

Beta blockers

302
Q

class III Antiarrhythmic drugs

A

K+ channel blockers

303
Q

class IV Antiarrhythmic drugs

A

Ca++ channel blockers

304
Q

how do beta blockers affect the heart

A

Block binding of epi and norepi in nodal and non nodal tissue
Decrease SA node automaticity
Inhibit AV response by prolonging refractory period and slowing conduction
decreased myocardial contractility

305
Q

AEs of beta blockers

A

bradycardia, hypotension, fatigue

306
Q

how to CCBs affect the heart

A

Decrease APs generate by SA node and can block AV nod, decrease HR, and block calcium entry into myocardial cells to decrease contractility

act mainly on AV node

307
Q

AEs of CCBs

A

bradycardia

decreased contractility

308
Q

amiodarone

A

K+ channel blocker

used emergently for someone in v tach

309
Q

amiodarone AE

A

Torsades

Long term use: need to look out for:
Liver toxicity
Pulmonary toxicity
Thyroid toxicity

310
Q

do CCBs and beta blockers have the same effect on the heart?

A

yes

311
Q

MOA of adenosine

A

Binds to A1 receptors → activates opening of K+ channels → hyperpolarization, inhibition of pacemaker cells

half life = 10 seconds

312
Q

What drug class is indomethacin and what is it used for?

A

COX inhibitor, tocolytic

313
Q

What are the two classes of calcium channel blockers?

A

Nondihydropyridines (verapamil and diltiazem)

Dihydropyridines (nifedipine)

314
Q

What drug class does nifedipine fall under?

A

Dihydropyridines (calcium channel blocker)

315
Q

What are the classes of RAAS drugs?

A

ACEs (prils)
ARBs (sartans)
Direct Renin Inhibitors (DRIs; aliskiren)
Aldosterone antagonists (spironolactone, eplerenone)

316
Q

What are the effects of dihydropyridines?

A
  • Decreased afterload
  • Decreased coronary artery vasoconstriction
  • Reflex tachycardia & increased contractility
317
Q

What are the effects of nondihydropyridines?

A
  • Decreased afterload & increased coronary perfusion
  • Decreased HR (SA node) decreased nodal conduction (AV node)
  • Decreased myocardial contractility
318
Q

What is the main AEs of concern with vasodilation of venous vessels?

A

orthostatic hypotension

319
Q

What is the main AEs of concern with vasodilation of arterial vessels?

A

Reflex tachycardia

320
Q

Does hydralazine vasodilate arteries or veins?

A

Direct arteriole vasodilation, causes reflex tachycardia and contractility

321
Q

What is the drug of choice for HTN emergencies?

A

Sodium nitroprusside (venous and arteriolar vasodilator)

322
Q

Does nitroglycerine vasodilate venous or arteriole vessels?

A

Venous vasodilation

323
Q

What is the indication for nitroglycerin?

A

Angina (active chest pain):

  • Administer sublingual asap
  • No relief after 5mins: call 911
  • Take up to 3 doses Q5mins
324
Q

What is the MOA of digoxin?

A

Mechanism: selectively inhibits Na+/K+/ATPase pump

  • Build up of Ca++ intracellularly (increased actin/myosin interactions)
  • Increased contractility
325
Q

What is digoxin’s electrical effects on the heart?

A
  • Decreased SA node automaticity
  • Decreased AV node conduction velocity & increased refractory period
  • Increased automaticity in Purkinje Fibers (can lead to ectopic foci –> ventricular dysrhythmias)
326
Q

What are the classes of antidysrhythmics?

A

Class I: Na+ channel blockers (Phenytoin, lidocaine)
Class II: beta blockers (propanolol, esmolol)
Class III: K+ channel blockers (amiodarone)
Class IV: Ca+ channel blockers (verapamil, diltiazem)

327
Q

What are AEs of beta blockers as antiarrhythmic drugs?

A

bradycardia, hypotension, fatigue

328
Q

Which antiarrhythmic drug has “torsades” as an AE?

A

Class III: K+ channel blocker (amiodarone)

329
Q

What should be monitored when giving Class III channel blockers?

A

Blocking K+ channels, can lead to prolonged QT interval.

AE: torsades

330
Q

What are AEs of class IV antiarrhythmics?

A

bradycardia, decreased contractility

331
Q

What are CIs of class IV antiarrhythmics?

A

high grade heart blocks, heart failure

332
Q

What is the route of administration and half life of adenosine?

A

IV, 10 seconds

333
Q

What are the CIs of adenosine?

A

high-grade heart blocks

334
Q

What are the AEs of digoxin?

A

AEs: arrhythmias, AV block, toxicity (Digibind)

335
Q

Between esters and amides, which has higher allergic reaction rates?

A

esters

336
Q

How are esters and amides metabolized?

A

Esters are metabolized by plasma esterases.

Amides are metabolized by hepatic enzymes.

337
Q

What is Methemoglobinemia?

A

AE from topical benzocaine.

  • Converts Hgb –> metHgb (form that cannot release O2 to tissues).
  • Most common in <2yrs (contraindicated)
338
Q

What are drug examples of esters?

A

Cocaine
Chloroprocaine
Benzocaine

339
Q

What class of drug is lidocaine?

A

Amide

340
Q

Is there cross sensitivity between esters and amides? What does this mean?

A

No, there is no cross sensitivity. If you’re allergic to esters, you can give amides instead.

341
Q

What is a rare but fatal reaction of inhaled anesthetics?

A

Malignant hyperthermia

342
Q

What is the MOA of most IV anesthetics?

A

+GABA transmission

Barbiturates, benzodiazepines, propofol, etomidate

343
Q

What are the CNS effects of local anesthetics?

A

CNS excitation (seizures) –> CNS depression (coma, sedation, death)

344
Q

What are the CV effects of local anesthetics?

A

Na+ block = decreased myocardial excitability

  • bradycardia, heart block, decreased contractility, cardiac arrest
  • vasodilation
345
Q

What are the AEs of propofol?

A

Hypotension, bradycardia, respiratory depression, no muscle paralysis, CNS depression

346
Q

What are s/s of propofol infusion syndrome?

A
  • Metabolic acidosis
  • Cardiac failure
  • Renal failure
  • Rhabdomyolysis
  • Can be fatal
347
Q

What should be monitored during propofol infusion syndrome?

A

CPK (marker of muscle injury)

348
Q

Opioid tolerance develops to all effects except which ones?

A

Constipation and miosis

349
Q

What drug is used to reverse the effects of opioids?

A

Naloxone (Narcan)

***reversal of opioid OD

350
Q

What is the purpose of Naltrexone?

A

Block euphoric effects of opioids

351
Q

What should be monitored when giving methadone?

A

AE: prolongation of QTc –> torsades

- EKG prior to administration

352
Q

Which strong opioid creates a toxic metabolite with metabolism?

A

Meperidine

353
Q

Because meperidine creates a toxic metabolite when metabolized, what is the standard practice when prescribing this drug?

A

Keep use <48 hours

Keep dose < 600mg/24hrs

354
Q

In the liver, what is codeine converted to?

A

10% of dose is converted to morphine in liver

355
Q

What is unique about codeine?

A

10% of dose is converted to morphine in liver

  • Some people lack gene = cannot gain analgesic effects
  • Some people are “ultrarapid metabolizers”
356
Q

What is an AE of Buprenorphine?

A

Block kappa, partially agonize mu

AE: Prolongs QTc

357
Q

Which neurotransmitters are modulated in drugs for Parkinson’s/AD/MS?

A

Dopamine and ACh

358
Q

When administering Levadopa, what concurrent medication should you avoid?

A

MAO inhibitor (risk for severe HTN)

359
Q

What is a key AE of Levodopa?

A

Dyskinesias

360
Q

Which vaccines are live?

A

MMR, varicella, rotavirus, poliovirus (if oral)

361
Q

Between benzodiazepines and barbiturates, which one has a ceiling effect on GABA?

A

Benzodiazepines only potentiate GABA.

Barbiturates agonize GABA receptor directly, no ceiling effect to sedation/respiration depression.

362
Q

What are differences between 1st and 2nd generation anti-psychotics?

A

1st gen: extrapyramidal symptoms, cheaper, more drug interaction d/t CYP450 metabolism

2nd gen: metabolic effects (weight gain, DM, dyslipidemia), risk for CV events, more expensive

363
Q

What are the s/s of neuroleptic malignant syndrome?

A

rigidity, decrease bowel activity, normal pupils, gradual onset

364
Q

What are the s/s of serotonin syndrome?

A

tremor, hyperreflexia, dilated pupils, hyperactive bowel activity, rapid onset

365
Q

What class of drug does Chlorpromazaine belong to?

A

Conventional antipsychotics

Prolongs QT interval
AE = sedation, orthostatic hypotension, anticholinergic side effects

366
Q

What class of drug does Haloperidol belong to?

A

Conventional antipsychotics

Prolongs QT interval, cheaper, EPS symptoms early

367
Q

What is the SSRI prototype?

A

Fluoxetine

368
Q

Between FGAs and SGAs, which is safer in pregnancy?

A

SGAs

369
Q

What is the antidote for Tylenol?

A

acetylcysteine

370
Q

What is the antidote for opioid reversal?

A

Naloxone (Narcan)

371
Q

What class of drug does bupropion fall under?

A

Atypical antidepressant.

372
Q

What are the uses of lithium?

A

Antiepileptic, bipolar disorder/mood stabilizer

373
Q

What are other uses for valproate and carbamazepine, other than epilepsy?

A

Mood stabilizers, bipolar disorder

374
Q

What are the classes of drugs used for depression?

A 
SSRIs (Fluoxetine)
SNRIs (Venlafaxine)
TCAs (amitriptyline)
MAOIs (Nonselective, MAO-B selective)
Atypical antidepressants (Bupropion)
375
Q

What depression drug classes should you avoid tyramine-rich foods?

A

MAOs and TCAs

376
Q

How does tyramine and MAOIs lead to excessive NE?

A

MAO-A –> decreased NE breakdown
High concentration of NE in nerve terminals
Tyramine stimulates NE release
Excessive NE occurs

s/s = severe HA, tachycardia, HTN, N/V

377
Q

What are effects of lithium toxicity?

A

Tremor, vision changes, agitation, slurred speech, thirst, polyuria (bc block of ADH), renal toxicity (monitor BUN/Cr)

378
Q

How does hypernatremia affect lithium administration?

A

Decreases lithium in the body, causing subtherapeutic effects

379
Q

Which vaccines are given PO?

A

Poliovirus (if given live, attenuated)

Rotovirus

380
Q

What two drugs augment levodopa

A

Carbidopa (decarboyxlase inhibitors)

Entacopone (COMT inhibitor)

381
Q

What are the AEs of Phenytoin?

A
  • CNS = sedation, nystagmus, ataxia, diplopia
  • Gingival hyperplasia = swelling, tenderness, bleeding
  • Dermatologic effects = measles-like rash or worse (SJS, TEN)
  • Teratogenic
  • CV = dysrhythmias & hypotension w/ IV injection –> DILUTE, INFUSE SLOWLY
  • Necrosis w/ IV extravasation
382
Q

What schedule is ketamine

A

III

383
Q

Benzo antidote

A

Flumazenil

384
Q

What schedule is most benzodiazepines?

A

IV

385
Q

What is the main difference between 1st and 2nd generation anti-psychotics?

A

1st: extrapyrimidal symptoms
2nd:

386
Q

What is notable about varenicline?

A

Most effective for secession of nicotine.

387
Q

Which anti-depressant class have cardiotoxicity as an AE?

A

TCAs

388
Q

What drug classes should you avoid with MAOs?

A

TCAs, Levodopa

389
Q

What drug do you use for anxiety?

A

Buspirone

390
Q

What are the three classes of bronchodilators?

A

beta2 agonists, methylxanthines, anticholinergics

391
Q

What is notable about inhaled bronchodilators?

A

Local, no systemic effects (Quantrenarymonium)

392
Q

What drug is most effective for acute bronchospasms?

A

Short acting beta agonist (albuterol)

393
Q

What are the names of the long acting beta2 agonists?

A
  • Salmeterol

- Formoterol

394
Q

What class of drug is theophylline?

A

Methylxanthines, used for bronchodilation and ADHD

Low TI, variable metabolism

395
Q

What are drug examples of short and long acting anticholinergic drugs?

A

Short acting: ipratropium

Long acting: tiotropium

396
Q

What are three ways glucocorticoids suppress inflammation?

A

Decrease inflammatory mediators, decrease edema of airway mucosa, decrease infiltration of inflammatory cell

397
Q

What drug is used for allergic rhinitis?

A

Intranasal phenylephrine (Decrease nasal congestion via nasal vasoconstriction)

398
Q

Which anti-inflammatory drug is safest?

A

Cromolyn, has rare AEs

MOA: stabilizes membrane of mass cells to decrease histamine release

399
Q

What is the MOA of glaucoma drugs?

A
  • Alpha2 agonists: decrease aqueous humor
  • Beta blockers: decrease aqueous humor
  • Carbonic anhydrase inhibitors: decrease aqueous humor
  • Prostaglandin analogues: increases outflow of aqueous humor
400
Q

What are the four classes of glaucoma drugs?

A
  • Beta blockers: timolol
  • Prostaglandin analogues: latanoprost
  • Alpha2 agonists: brimonidine
  • Carbonic anhydrase inhibitors: dorzolamide
401
Q

What are the AEs of glucocorticoids when used topically?

A

AE: local reactions, thinning of skin with long -term use (increased with higher potency, dressing, large area)

402
Q

What are the AEs of keratolytics when used topically?

A

i.e. salicylic acid

AE: rarely, toxicity with long -term, high-dose use

403
Q

What are the AEs of Azelaic acid?

A

itching, burning, pigment reduction

404
Q

What are the AEs of topical antibiotics?

A

i.e. benzoyl peroxide

AE: peeling, drying

405
Q

For ezcema, what are the first and second line treatments?

A

First line: Moisturizers, Topical glucocorticoids​

Second line: Topical immunosuppressants: tacrolimus (AE: erythema, pruritis)

406
Q

What are the defensive factors against peptic ulcer disease?

A

Mucous, bicarbonate, prostaglandins, blood flow

407
Q

What drugs decrease the aggressive factors of peptic ulcer disease?

A

PPIs, H2RAs, antacids, antibiotics

408
Q

What drugs increase the defensive factors of peptic ulcer disease?

A

Misoprostol, Suprolafate

409
Q

What are the concerns with decreasing aggressive factors?

A

Increase gastric pH causing bacterial growth, absorption affected, delayed gastric emptying time

410
Q

What is notable about famotidine?

A

Large volume of distribution, can cross BBB

411
Q

What are the two classes of antisecretory agents?

A

Histamine 2 receptor blockers, proton pump inhibitors

412
Q

What population do you not use misoprostol in?

A

Pregnant

413
Q

What are the 5 classes of laxatives?

A

Bulk forming laxatives, surfactant laxatives, stimulant laxatives, osmotic laxatives, selective mu antagonist

414
Q

What class of drug has the fastest effect on constipation?

A

Stimulant laxatives (castor oil)

415
Q

What is a risk with all laxatives?

A

Dehydration

416
Q

What class of drug does docusate fall under?

A

Surfactant laxatives

417
Q

What class of drug does Senna fall under?

A

Stimulant laxatives

418
Q

Which pathway does ondansetron affect?

A

CTZ pathway

419
Q

What neurotransmitter does Haloperidol antagonize?

A

Dopamine —> CTZ pathway

420
Q

Which antiemetics affect the CTZ pathway?

A

Serotonin antagonists
Substance P/neurokinin 1 antagonists
Dopamine antagonists

421
Q

How is amphotericin B given

A

IV only

422
Q

what kind of drug is allopurinol

A

xanthine oxidase inhibitor

423
Q

what drug is used for hyperparathyroidism

A

Cinacalcet

Pharmacology (6 decks)

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