Brainscape's Knowledge GenomeTM

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


See full index

Pharm Drugs > Antibiotics, antifungal, antivirals, and cancer > Flashcards

Antibiotics, antifungal, antivirals, and cancer Flashcards

1
Q

Ibuprofen

A

NSAID
CV risk
Nephrotoxicity
Safest for GI risk

Advil
Motrin

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

naproxen (Aleve)

A

NSAID

Safest for CV risk

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

indomethacin

A

NSAIDs oral

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

Aspirin Ind,MOA,AE

A

Indications: analgesia, antipyretic, anti-inflammatory, antithrombotic
MOA: irreversibly inhibits cox 1 and cox2 enzymes and forms prostaglandin derivative
decreases formation of prost. precursors
thromboxane= dec. platelet aggregation
Route:PO and rectal
AE: GI, bleeding/bruising, rash, photosensitivity, bronchospasm
*Avoid if Hx of GI bleed or under 12 or recent flu (reyes syndrome)
*low dose is selective for cox1- cardioprotection
*need increased doses for analgesia and inflammatory

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

celecoxib (Celebrex)

A

NSAID, COX-2 selective, use if GI risk but no CV risk

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

meloxicam (mobic)

A

NSAIDs oral

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

diclofenac (Voltaren gel, Flector patch)

A

Topical NSAID
Solution (Pennsaid)
Gel (voltaren)
Patch (Flector)

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

trolamine salicylate (aspercreme)

A

Topical NSAID

Aspercreme

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

codeine

A

Opioid

*Antitussive

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

hydrocodone

A

opioids

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

hydrocodone with acetaminophen ()

A

Opioid

*Vicodin

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

morphine ()

A

Opioid
*MS Cotin
Can accumulate after extended dosing

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

oxycodone ()

A

Opioid

  • Oxycotin
  • negligible levels of metabolites (OK for liver)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

oxycodone with acetaminophen ()

A

Opioid

*Percocet

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

fentanyl ()

A

Opioid
*Duragesic
Dont apply heat to patch

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

hydromorphone ()

A

Opioid

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

meperidine ()

A

opioid

  • Demerol
  • neurotoxic metabolite esp with decrease liver function
  • anxiety and seizures
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

tramadol

A

opioid

Risk of Sezure

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

methadone

A

Opioid

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

cortisone

A

corticosteroids

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

prednisone

A

Corticosteroids
Synthetic version of corticosteroids to treat RA (and other diseases)
MOA: decreases inflammation and supresses immune system

Route: PO, IV, Intraarticular, Topical

Short term AE: inc blood glucose, mood changed, fluid retention

Long term AE: osteoporosis, inc fracture risk, thin skin, muscle wasting, poor wound healing, adrenal supression, cushing disease, inc infection risk

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

methylprednisolone

A

corticosteroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

prednisolone

A

corticosteroids

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

triamcinolone

A

corticosteroids

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

betamethasone

A

corticosteroids

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

methotrexate

A

Non Biological
Gold Standard for RA
Also treats SLE

MOA: unknown in RA
Route: PO x1 week

Give with folic acid to reduce GI, hepatic, and hematological toxicity
Common AE: N/V/D, alopecia, malaise

Less Common: hepatoxicity, nephrotoxicity, thrombocytopenia, bone marrow suppression

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

hydrochloroquine

A

Non-biologic DMARD
anti-malarial

MOA: impacts mediator of inflammatory response

AE: GI, renal toxicity

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

adalimumab (Humira)

A

Biologic TNF inhibitors
DMARDs

MOA: bind to TNF alfa

AE: headache, infection

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

etanercept (Enbrel)

A

Biologic TNF inhibitors
DMARDs

MOA: bind to TNF alfa

AE: headache, infection

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

rituximab (Rituxan)

A

Biologic Non-TNF DMARDs

MOA: impacts inflammation

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

lidocaine

A

anesthetics

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

adalimumab (Humira)

A

TNF inhibitor

DMARD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

etanercept (Enbrel)

A

TNF inhibitor

DMARD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

rituximab (Rituxan)

A

Non TNF inhibitor

DMARD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

piperacillin/tazobactam (Zosyn)

A

antibiotic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

azathromycin

A

macrolides

CYP450 inhibitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

lidocaine

A

Regional anesthetics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

vancomycin

A

antibiotic

glycopeptide

hypotension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

amoxicillin

A

penicillin antibiotic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

amoxicillin/clavulanate (Augmentin)

A

penicillin antibiotic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

piperacillin/tazobactam (Zosyn)

A

penicillin antibiotic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

cephalexin (Keflex)

A

Cephalosporins Antibiotic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

ceftriaxone (Rocephin)

A

cephalosporin antibiotic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

cephalexin

A

Cephalosporins

Keflex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

gentamicin

A

Aminoglycosides antibiotic
ototoxicity
Nephrotoxicity

Usage p. aeeruginosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

azithromycin (Z-pack)

A

macrolide antibiotic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

doxycycline

A

tetracycline antibiotic

Photosensitivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

clindamycin

A

lincosamide antibiotic that can cause cdiff

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

ciprofloxacin

A

Fluoroquinolone Antibiotic

tendon rupture
phototoxicity
hypoglycemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

levofloxacin (Levaquin)

A

Fluoroquinolone Antibiotic

tendon rupture
phototoxicity
hypoglycemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Treatment for pain cancer

A

Mild: NSAIDS, Acetaminophen, short acting opioid

Moderate: short acting opioid

Severe: strong opioid or long acting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

cancer concerns

A 
Increased fall risk
fatigue
pain
emotional distress
Chemo induced peripheral neuropathy
decrease cognition
decreased muscle strength (sarcopenia)
cardiac and pulmonary damage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

nystatin

A

antifungal
Treats FI
Route: PO, Topical
AE: PO- N/V/D, cramps, topical-rash, urticaria (hives/itching)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Pharmacotherapy: Immunotherapy

A

hormones and drugs that use the immune system to treat cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Pharmacotherapy: Targeted therapy

A

DAmage cancer cells by blocking specific genes or proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Pharmacotherapy: chemotherapy

A

Drugs that inhibit growth and replication of cancer cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Radiation Considerations

A

FATIGUE!!!

Radiation fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Chemotherapy effects

A 
myelosuppression
NVD
stomatitis
reproductive dysfunction
hair loss

**try Nadir after chemotherapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Neoadjuvant therapy

A

treatment used before primary treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Adjuvant therapy

A

used after primary treatment in conjunction with other therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Cancer treatment goals

A

Cure, control, or palliation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

cancer cure

A

chemotherapy, biotherapy, radiation, and/or surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Cell life cycle and cancer

A

G0: rest stage- cells considered resistant to exposure from many chemotherapeutic agents

G1: pre DNA: protein synthesis

G2: premitosis: all cellular and structural compnents needed..checkpoint for cell sructures

M: mitosis- cell division PMAT= 2 daughter cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What is cancer?

A

uncontrolled cell growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Types of vaccines

A

Inactivated (killed pathogen)

Subunit or conjugated (piece of pathogen)

Live attenuated (weakened pathogen)- avoid if immunocompromised

Toxoid (pathogen toxin)

**AE: injection site reaction, fever, headaches

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Primary concern with antifungals

A

damage to liver and kidneys (fluid retention)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Fluconazole and Ketoconazole

A

Azoles that treat FI

AE: N/V, photophobia, cardiac arrhythmia, menstrual irregularities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Azoles

A

Broad Spectrum

PO: fluconazole and ketoconazole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Polyenes

A

Nystatin and Amphotericin B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Types of drugs for Fungal Infections

A

Polyenes and Azoles

Common CYP interactions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Drug target for fungal infections

A

Cell membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Types of fungal infections (2)

A

Superficial (ring worm or vaginal yeast infection) and systemic (meningitis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Fungal Infections

A

aka mycoses

Risk for FI increased after antibacterial use, immunisuppression, pregnancy, diabetes, elderly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Rehab concerns: Antiviral

A

Exercise tolerance may be affected (malaise, fatigue, INFs may cause flu like symptoms, anemia)

Track vital signs and Rate of PE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Rehab concerns: HIV

A

Opportunistic infections: look out for long term antibiotics and wash hands

Neuromuscular: pain, dysfunction, myopathy, peripheral neuropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Biktarvy

A

Antiretroviral agents in combo

Treatment for naive patients

bictegravir/emtricitabine/tenofovir alafenamide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Triumeg

A

dolutegravir/abacavir/lamivudine

Antiretroviral agents in combo

Treatment for naive patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Types of Antiretroviral agents

A 
NRTI
NNRTI
Protease Inhibitor
Entry Inhibitors
Integrase inhibitor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

HAART

A

treatment for HIV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

HIV treatment

A

HAART= highly active antiretroviral treatment

Synergistic drug-drug interation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Direct-Acting Antivirals (DAAs)

A

AE: fatigue, weakness, and headache

Also when combined with amiodarone will see bradycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Chronic Hepatitis C

A

In the past treatments hardly tolerated, now there are 11 DAA products to cure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Hepatitis B Treatment

A

Interferon- (injection) but causes flu like symptoms

Nucleoside/nucleotide analogs- (PO) better tolerated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Hepatitis A

A

Pre and post exposure prophylaxis

Vaccine, immune globulin, rest and hydration, antiemetics (nausea), antipyretics (fever)

2-6 months of recovery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Hepatitis

A

inflammation of the liver caused by a virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Treatments for the flu

A

Oseltamavir (Tamiflu)

Baloxavir (Xofluza)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Antiviral endings

A
  • ovir
  • ivir
  • alfa
  • ine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Life cycle of a virus

A 
Attachment to host cell
Entry
Replication
Assembly
Release (budding or host cell lysis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

What is a virus

A

A very small invader that can only replicate in a host cell and enters the body via skin, mucous membranes, GI or respiratory tract.

3 components: envelope, capsid, nucleic acid core

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Macrolide

A

antibiotic that fights Atypical pathogens causing pneumonia- this is a CYP450 inhibitor (look out for DDIs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Fluroquinolone

A

Used to treat community acquired pneumonia- look out for tendon rupture

92
Q

Pneumonia

A

Leading cause of death
Causes: bacteria, virus, or mycoplasmas

Inflammation affecting parenchyma of the lungs

Transmission: airborne pathogens, circulation, sinus or contiguous infection, aspiration

May be nosocomial (hospital acquired) which is more deadly

93
Q

MRSA (Methicillin resistant Staphylococcus aureus)

A

On skin
Spread via contact
Treatments: linezoid and quinupristin/dalfopristin

94
Q

Clostridium Difficile (Cdiff)

A

Gram +
Transmission: contact or fecal to oral
Symptoms: diarrhea, cramping, fever
Occurs when normal GI flora interrupted

**can survive up to 5 months

DOC:
metronidazole (IV)
vancomycin

95
Q

TB therapeutic concerns

A

Liver and kidney issues
visual disturbances
CN VIII damage
neurological symptoms

Beware of resistance due to resistant strain of TB infection or noncompliance with medications

96
Q

Two Main Treatment Goals: TB

A

Contain and cure infection

This process can last months to a year

97
Q

Latent vs. Active TB

A

Latent TB: carries bacteria without symptoms

Active: individuals are infectious and can spread disease

98
Q

TB symptoms

A

fever, night sweats, malaise, weight loss

99
Q

How does tuberculosis take effect?

A

Myobacterium tuberculosis is inhaled into lungs, aveoli and surrounded by macrophages to set off an immune response

100
Q

How is TB transmitted?

A

airborne particles

101
Q

What contributes to drug resistance?

A

overuse/misuse
international OTC antibiotics
Antibiotics in livestock

102
Q

Types of Resistance

A

Innate: organism isnt susceptible

Acquired: Inactivated drug, modify drug target, export drug from bacteria, or bypass antibiotic inhibition

103
Q

Antimicrobial resistance

A

when bacteria or other microbes become resistant to the effects of a drug after being exposed to it

104
Q

Sulfamethoxazole/trimethoprim (Bactrim)

A

Sulfonamides

Steven-Johnsons syndrome

105
Q

Sulfonamides

A

Sulfamethoxazole/trimethoprim (Bactrim, SMX/TMP)

Broad coverage of Gram - and +

AE: can cause allergy or steven johnson syndrome

106
Q

Metronidazole (Flagyl)

A

Nitroimidazole antibiotic

Metallic taste
neuropathy

107
Q

Nitroimidazole

A

Metronidazole (Flagyl)

Use: Anaerobes

AE: GI, metallic taste,
Uncommon: peripheral neuropathy

108
Q

Fluroquinolones

A

Ciprofloxacin
Levofloxacin (levaquin)

Gram -
AE: GI, Photosensitivity
Rare: tendon rupture, significant hypoglycemia

109
Q

Lincosamides

A

Clindamycin

Gram +

GI and can Cause cdiff

110
Q

Tetracyclines

A

Doxycycline

Broad coverage gram + and - and atypicals

AE: GI or photosensitivity

111
Q

Macrolides

A

Azithromycin (Z-pak)

Some gram + and -

AE: GI issues, QT prolongation, CYP450 inhibitor (DDI)

112
Q

Aminoglycosides

A

Gentamicin

Usage: Gram +, P. aeruginosa

AE: ototoxicity and nephrotoxicity

113
Q

Glycopeptides

A

Vancomycin

MRSA, Cdiff
Increasing resistance (VRE)

AE: Hypotension

114
Q

Cephalosporins

A

Cephalexin (Keflex), ceftriaxone (Rocephin)

Nosocomial infections, surgical prophylaxis

GI and Hypersensitivity

115
Q

Penicillins

A

Amoxicillin, Amoxicillin/clavulanate (Augmentin) and Piperacillin/tazobactam(Zosyn)

Broad coverage of Gram+ and Gram-

AE: GI and hypersensitivity

116
Q

MOA for antibacterials

A 
Cell wall
cell membrane
protein synth
dna synth
dna strand
117
Q

Broad vs Narrow

A

effective against many or few types of infection

118
Q

3 considerations for selecting treatment

A 
Bacterial factors (identify and susceptibility)
Host specific factors (allergies, renal function, ect)
Drug specific factors (DDI, route, ect)
119
Q

Bactericidal

A

kill bacteria

120
Q

Bacteriostatic

A

inhibit bacterial growth, requires an immune host

121
Q

Gram negative

A

Positively charged but favors negatively charged compounds

Thinner cell wall (5-7 strands)

122
Q

Gram Positive

A

Is negatively charges but favors positvely charged compounds

Thick cell wall (20-30 strands)

123
Q

Antibiotic

A

Drug that is only actively against bacteria

124
Q

Antimicrobial

A

Drug that is active against bacteria, virus, fungi, or parasite

125
Q

Propofol

A

general anesthetic

causes loss of consciousness

126
Q

General Anesthesia rehab concerns

A

Neuromuscular Weakness

Impaired airway clearance

Immune function suppressed

In older adults pulmonary complications or reduced cough reflex

127
Q

Local Anesthetics (AE and duration)

A

AE: rare but possible: CNS stimulation progressing to depression, CV issues, respiratory depression

Duration: 20 min up to 6 hours

128
Q

Local Anesthetics (MOA, Advantages, diadvantages)

A

MOA: reversibly bind a receptor site within the pore of the Na+ channels in nerves ->block ion movement through the pore ->blocks action potential for nerve conduction, especially at small myelinated axons that carry nociceptive input

Advantages: quick recovery, low systemic toxicity, confined to nerve tissue

Disadvantages: incomplete analgesia, longer time to anesthesia

129
Q

Regional Anesthetics (route and categories)

A

Route: topical, infiltration anesthesia, peripheral nerve block, IV regional block, epidural or spinal administration

Categories:
central neuraxial block: epidural or intrathecal space
peripheral nerve block: near a nerve or the plexus innervating the are undergoing surgery
field block: adjoining tissues so the drug will diffuse to the surgical area for minor hand or foot procedures

Can be used in combo w/ decrease general anesthesia dose

130
Q

Where does inhaled general anesthetics create a hang over effect?

A

Adipose tissue

131
Q

General anesthetics- Intravenous types

A 
Barbiturates (thiopental)
Dissociative (ketamine)
Misc (etomidate, propofol)
Opioids (fentanyl)
Benzodiazepines (midazolam)

Quick onset and quick recovery

May be used with inhaled too

132
Q

General Anesthetics- types of inhaled

A 
Gas (nitrous oxide)
Volatile Liquids (halothane)
133
Q

How are general anesthesia goals achieved?

A

Balanced anesthesia: combo of IV and inhaled anesthetics, analgesics and neuromuscular blocking agents

134
Q

Goal of general anesthesia

A

loss of consciousness, analgesia, amnesia, skeletal muscle relaxation, inhibition of sensory and autonomic reflexes

135
Q

General Anesthesia- Medullary Paralysis

A

Can have respiratory or cardiovascular collapse

136
Q

General Anesthesia- Surgical Anesthesia

A

Completely unconscious and respiration is more regular

137
Q

General Anesthesia- Delirium/Disinhibition

A

Will lose consciousness and respirations may change

138
Q

General Anesthesia- Analgesia/Induction

A

May or may not remember but generally still conscious

139
Q

Anesthesia (3 categories)

A

General: Iv and inhaled
Regional: Intrathecal and epidural
Local: Injection and topical

140
Q

Anesthesia (3 categories)

A

General: Iv and inhaled
Regional: Intrathecal and epidural
Local: Injection and topical

141
Q

Patient-controlled analgesia (PCA) side effects

A

Pharmacological side effects (AE to meds)

Problems with delivery

142
Q

PCA- types of anesthetics

A

Opioids (Morphine, fetanyl, hydromorphine)

Local anesthetics (epidural)

143
Q

Patient Controlled Anaglesia (PCA) dosing strategies

A

Load Dosing, Demand Dosing, Lockout interbal, 1 and 4 hour limits, background infusion rate

Measures successful vs. total demand

144
Q

What does PCA do?

A

Enables continuous pain control and lowers incidence side effects

145
Q

What is patient-controlled analgesia (PCA)?

A

Patient self administers analgesic via small pumps worn, implanted devices, or pumps on a pole

Route: Catheters, IV, Intrathecal, epidural space

146
Q

Other rehab concerns with SLE drugs

A

Viral infections
Fungal infections
Photosensitivity

147
Q

Rehab Concerns w/ SLE drugs (Bacterial Infections)

A

80 % of infections

soft tissue infection can lead to sepsis

148
Q

Rehab concerns w/ SLE drugs (immunosupression)

A

Pts w/ SLE already risk for infection

Increased risk with DMARDS and steroids

149
Q

Immunosuppressants for SLE

A

Methotrexate and azathioprine are most common

MOA: Decrease the immune response so body does not attack itself

AE: N/V

Boxed warning: serious infection, secondary malignancy

150
Q

SLE treatment (severe)

A

High Dose steroids

Immunosuppressants

151
Q

SLE treatment (mild/moderate)

A

NSAIDS
Steroids
Antimalarials
Immunosupressants

152
Q

systemic lupus erythematosus (SLE)

A

chronic inflammatory autoimmune disease affecting variety of organs

Direct infiltration of immune complexes into organs and joints -> destruction of tissue -> clinical symptoms

153
Q

Corticosteroids

A

Short term RA treatment

NSAIDS can help
Opioids for pain

154
Q

Janus Kinase Inhibitors

A 
Biological DMARD
RA
Route:PO
Common AE: infection, nasopharyngitis
Boxed warning: infections
Tofacitinib (Xeljanz)
Baricitinib (Olumiant)
155
Q

Non TNF inhibitors

A 
Biological DMARD
RA
Route: IV or subcut
Common AE: injection reactions, increased LFTs, antibody devlopment
Boxed Warning: serious infections
Rituximab (Rituxan)
Abatacept (Orencia)
Tocilizumab (Actemra)
Sarilumab (Kevzara)
Anakinra (Kineret)
156
Q

TNF inhibitors

A

Biological DMARD
RA

Route: IV or subcut
Common AE: headache, infection, antibody development, infusion reactions

Boxed warnings: serious infections
◦Adalimumab (Humira)
◦Golimumab (Simponi)
◦Infliximab (Remicaide)
◦Certolizumab pegol (Cimzia)
◦Etanercept (Enbrel)
157
Q

Hydroxychloroquine

A

Non-biologic DMARD
RA
Treats Lupus too (reduces disease progression and prolongs survival)

◦MOA: impacts mediators of inflammatory response
◦Route: PO
◦Common AE: GI and skin reactions
◦Rare AE: retinal toxicity (regular ophthalmologic exams)
◦Addresses symptoms but not progression
◦Used for other disease states too (lupus, malaria, etc)

158
Q

RA Treatment

A

Nonbiological DMARD
Biological DMARD (TNF inhibitors, NonTNF inhibitors and Janus Kinase inhibitors)
MOA: inflammation usually

159
Q

rheumatoid arthritis (RA)

A

A chronic, progressive, systemic, inflammatory autoimmune disease

Often swollen and inflamed

160
Q

Glucosamine- Chondroitin

A

Not recommended
But possibly help with OA
Antithrombotic effect

161
Q

Intraarticular Steroids

A

OA treatment
Injections
Trimacincolone (Kenalog)
Methylprednisolone (Depo-Medrol)

162
Q

Intraarticular hyaluronate

A

For hip or knee OA
MOA: visoelastic solution to provide joint lubrication
AE: injection site pain, swelling, rash

163
Q

Treatment for OA

A

Tylenol, if not topical NSAID, corticosteroids, tramadol, or oral NSAID

Second line: opioids, surgery, intraarticular hyaluronate

If over 75 Topical NSAID or Capsaicin or tramadol (avoid oral NSAIDs)

164
Q

Osteoarthritis (OA)

A

Slow, progressive degeneration of joint surfaces (cartilage all the way to bone)

Inc thickness of subchondral bone reduces ability to absorb energy= more strain on articular cartilage-> cartilage erodes and bones directly contact each other

165
Q

Capsaicin cream

A

Neuropathic Treatment

AE: burning sensation and erythema

166
Q

Gabapentin (Neurontin)

A

Neuropathic
GABA analog and anticonvulsant
AE: dizziness and drowsiness
INEXPENSIVE

167
Q

Stimulus Independent- paroxysms

A

shooting or shock like

168
Q

Stimulus Independent- paresthesia

A

numbness or tingling

169
Q

Stimulus Independent- mechanical allodynia

A

normal stimulus that shouldnt cause pain but does

170
Q

Stimulus Independent- Hyperalgesia

A

experiencing more pain than we would expect

171
Q

Stimulus Independent

A

results from mechanical, thermal, or chemical stimuli

172
Q

Stimulus Dependent

A

Shooting, shock-like, aching, crushing, burning

173
Q

Neuropathic Pain

A

associated with disease or injury to PNS or CNS
Causes: Diabetes, immune deficiencies, shingles, trauma, MS, ischemic issues, cancer, drugs, ect.
Due to damage nocioreceptors are highly sensitive to stimuli or produce pain signals w/o a stimulus

174
Q

Diclofenac (Voltaren)

A

NSAID (topical)

175
Q

NSAIDs

A

Indications: analgesia, antipyretic, anti-inflammatory
MOA: reversibly inhibits COX1 and 2 (decrease prostiglandins precursors)
AE: GI, inc BP, nephrotoxicity, CV risk (variable)
Look out for GI Bleed, elderly, and renal issues
May impact muscle repair

176
Q

NSAID mechanism of action

A

Stimulus signals arachidonic acid
Which inc. inflammation, cytokines, and activates COX1 and COX2
COX2 does vasodilation, vascular perm, cytokine release, leukocyte migration, and pain
COX1 does fever and neurotransmission- always present
When NSAID blocks these enzymes anti-inflammatory, analgesia and antipyretic happen

177
Q

Acetaminophen

A

not an NSAID
Tylenol
Indications: analgesia and antipyretic
MOA: inhibits prostaglandin synthesis in CNS
Route: PO,IV, Rectal
AE: Hepatoxicity
*SIP enzymes break it into metabolites that are toxic to the liver

178
Q

Opioids

A

Codeine, Hydrocodone, Vicodin, Morphine, Oxycodone, Percocet, Fetanyl, Hydromorphone, Meperdine

  • Binds to receptors in CNS to inhibit asc pain pathway
  • Dont develop tolerance to constipation and miosos
  • anaglesia, antitissive
  • PO, rectal, IM, IV, topical, subcut, epidural, intrathecal, transmucosal
179
Q

Opioid Antagonists

A

naltrexone (vivitrol)- PO- 4 maintenance of abstinence- not acute overdose
naloxone (evizio/narcan)- IV,IM,Subcut, Intranasal- acute overdose or respiratory depression

*reverses respiratory depression and euphoria

180
Q

Strong vs mild mu agonist

A

Strong: all but codeine and tramadol

181
Q

Substantia Gelatinosa

A

gate keeper

rich in opioid receptors

182
Q

Categories of Pain

A

Nocioceptive: injury, stabbing, aching
Neuropathic: burining, tingling sensation
Psychogenic: origin to psych

183
Q

Pain Pathway

A

Pain signal to brain via ascending pathway to brain stem to spinal cord
Injury: produce cytokines which release prostaglandins
Sensory nerve fibers (afferent) respond to prostaglandins (1st order)
2nd order goes up spinothalamic tract to brain to thalmus
3rd order relays yo somatosensory cortec on opposite sides of the brain
Dorsal horn of SC- substance P activates next cell, so no sub P= inhibit

184
Q

A fibers

A

myelinated and are localized pain

185
Q

C fibers

A

unmyelinated and diffuse pain

186
Q

Mechanism of pain

A

Descending Pathway: Neurons in gray matter signals to silence 2nd order and travels down dorsal horn to inhibit
Substantia gelatinosa: gate keeper 2 regulate transmission of nocioceptive fibers
This blocks release of substance p and inhibits pain

187
Q

Opiod mechanism of action

A

Drug passes BBB
Lipid soluble passes quicker
Opioids bind to opioid receptors (G-coupled)
Cause presynaptic and postsynaptic inhibition
Blocks pain by stopping desc and thus stopping the pain loop with ascending pathway

188
Q

DDI-Antagonistic

A

Effect

189
Q

DDI- Synergistic

A

Response> sum of response to both

positive: HIV cocktail viral load suppression
negative: CNS depression with opioid and benzo

190
Q

Drug-Drug Interactions (DDI) definition

A

The effect will be altered or modified when more than one drug is given because one drug changes another drug’s action.

191
Q

Statins

A

Lower blood cholesterol
Block HMG-CoA to prevent liver from making chol
Can be used for leukemia, dementia, lung cancer, OP
Can induce myopathy (muscular weakness)

192
Q

Receptor Change antagonism

A

Desensitization due to long term exposure to agonist

193
Q

Pharmacokinetic antagonism

A

One drug induces or inhibits the metabolism of another

194
Q

Physiologic antagonism

A

2 drugs with opposite effects

195
Q

Chemical antagonism

A

2 substances that diminish the effect

196
Q

Response and Drug Dose Graph

A

Smallest curve is most potent
Shortest curve is also probably the partial agonist b/c there was not a high response
Most effective curve is the quickest one to reach 100 percent response

197
Q

Selectivity

A

Only bind to Beta 1 or Beta 2

198
Q

Specificity

A

only bind to alpha or beta

199
Q

Antagonist

A

Occupy receptors but do not activate

200
Q

Agonist

A

Drugs occupy receptors= activate

201
Q

Partial Agonist

A

Does not fit receptor exactly
Lower dose= agonist effect
Higher does= less response b/c it blocks receptors where agonists would usually bind

202
Q

Non-competitive antagonist

A

Greatly diminishes effect, increasing agonist will not overcome antagonist

203
Q

Competitive Antagonist

A

Antagonist and agonist compete for receptor, higher concentration wins

204
Q

ED50

A

Effective dose to get 50 % of expected response

Lower ED50= more potent drug b/c less drug is needed for greater effect

205
Q

Emax

A

maximal response, receptors filled

206
Q

Other drug targets

A

Enzymes and Non-human cells (penicillin-bacteria cell wall and oseltamauir-infected cells)

207
Q

Boxed Warning

A

Calls attention to serious risks associated with medicine

208
Q

Receptor Types (Name and describe all 4)

A

Ligand- quick, ligand binds, voltage gated channels open to transmembrane protein to allow ion flow
G- Protein- quick- transmembrane receptors cross 7 times- intracellular effects
Kinase- hours- ligand binds and makes receptors pair up (ex:insulin, GLU4, uptake glucose)
DNA- hours- intracellular with lipophilic ligand, receptor binds ligand and DNA to activate or depress gene expression (ex levothyroxine)

209
Q

Therapeutic Index

A

Ratio of TD50 to ED50

Lower the TI= more likely AE/toxicity

210
Q

Lipid soluble meds…

A

Cross BBB quicker

211
Q

Elimination/Excretion

A
  • removal of a drug from the body
  • Kidneys and liver
  • First order (most common- proportional to concentration- 1/2 life) and second order (not proportional to conc- steady downward slope)
  • 1/2 life= how long it takes to eliminate half the drug
  • A drug is cleared after 5 (1/2) lives
212
Q

Metabolism

A

CYP enzymes: break down molecule into active or inactive products
**Some drugs inhibit CYP which inc. drug concentration and may inc. likelihood of AE

213
Q

Distribution Vd?

A

Vd=total conc of drug in body/plasma
higher Vd= more drug in tissue
highly protein bound= less active drug in tissue

214
Q

Absorption (Entheral, Parentheral, Diffusion-3, Bioavailability, First Pass)

A

Enteral (GI) vs. Parentheral (not GI)
Passive Diffusion via lipid memebrane or aqueous channel or carrier mediated
Bio-availability: % of drug in systemic circulation (varies with pH, gut motility, and food)
First Pass: In liver, liver takes out most of the drug (PO)

215
Q

Pharmacokinetics

A

What the body does to the drug (ADME)

216
Q

Pharmacodynamics

A

How the drug affects the body (MOA, Potency, Efficacy)

217
Q

FDA Clinical Trails 1-4

A

One: small, healthy, for safety
Two: Small, diseased, for efficacy
Three: Large, long, and randomized
Four: After approval and post marketing

218
Q

Schedule V

A

Medical use and little to no abuse (ex: antidiarrheal, antitussive, analgesia)

219
Q

Schedule IV

A

Medical use and low abuse (ex: tramadol, xanax, ambien)

220
Q

Schedule III

A

Medical use and mid abuse (ex:codeine & anabolic steroids)

221
Q

Schedule II

A

Medical Use and High abuse (ex: cocaine, meth, fetanyl, addy, oxy, hydros)

222
Q

Schedule I

A

No medical use and high abuse ex:heroin, LSD, MaryJ

223
Q

Brand

A

owned by manufacturer & uppercase

224
Q

Generic

A

official name & lowercase

225
Q

off-label

A

Using drugs for something not approved by the FDA (ex:different ages, diseases, or doses)

226
Q

Off Patent

A

~20 years later other companies can make the drug without permission from the original manufacturers

Pharm Drugs (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions