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Clinical Med (Year 2) > Pharm (Exam 3) > Flashcards

Pharm (Exam 3) Flashcards

1
Q

What are the geriatric issues with drug use?

A
  • Increased drug use
  • Altered response to drug
  • Adverse drug reaction
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2
Q

What is the concept of “appropriate” drug use in the elderly?

A
  • Elderly patients take more drugs because they suffer more illnesses
  • Consequently they also suffer more adverse drug reactions
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3
Q

What is polypharmacy defined as?

A
  • over 5 meds
  • Better definition is use of any inappropriate/ unnecessary meds
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4
Q

What is an indicator of polypharmacy?

A

Patient’s drug regimen includes one or more unnecessary medications

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5
Q

What are the features of polypharmacy?

A
  • No apparent reason for drug
  • Duplicate drugs
  • Contraindicated drugs
  • Interacting drugs
  • Inappropriate dose
  • Use of drugs to treat adverse drug reactions (ADRs)
  • Improvement when drugs discontinued
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6
Q

What are the consequence of polypharmacy?

A
  • More adverse drug reactions
  • More drug interactions
  • Financial, adherence issues
  • Creates vicious cycle
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7
Q

Describe the cycle of polypharmacy starting at elderly take more drugs

A

Elderly take more drugs –> increase risk of side effects –> increase symptoms –> more drugs prescribed –> Elderly take more drugs

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8
Q

When the elderly take drugs there is an altered response, what are the pharmacokinetic and pharmacodynamic changes?

A
  • Pharmacokinetic: Elderly handle drugs differently
  • Pharmacodynamic: Drugs affect elderly differently
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9
Q

Where does drug metabolism occur and what are the changes of this site in the elderly?

A

Liver
- Decreased mass
- Decreased blood flow
- Decreased enzyme activity

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10
Q

Where does drug excretion occur and what are the changes of this site in the elderly?

A

Kidney
- Decreased mass
- Decreased blood flow, GFR
- Decreased tubular function

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11
Q

Why is drug elimination often decreased or delayed in older adults?

A

Decline in liver and kidney function

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12
Q

Pharmacodynamic changes in the geriatric population can occur at what two levels?

A
  • Cellular level
  • Systemic level
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13
Q

How do pharmacodynamic changes occur at the cellular level in the geriatric population?

A
  • Receptor binds
  • Transmembrane signaling
  • Intracellular response
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14
Q

What pharmacodynamic changes can occur at the systemic level in the geriatric population?

A

Decline in homeostatic mechanisms
- Orthostatic circulatory response
- Posture/balance
- cognitive function
- muscle strength/endurance
- others

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15
Q

Name some additional factors that can affect the elderly drug profile

A
  • Disease, comorbidity
  • Nutrition, general health
  • Inadequate drug testing
  • Patient education, adherence
  • Hoarding & sharing
  • other chemicals
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16
Q

What are some examples of societal drugs?

A
  • Alcohol
  • nicotine
  • caffeine
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17
Q

What are some examples of over the counter drugs?

A
  • Laxatives
  • analgesics
  • vitamins
  • many others
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18
Q

What is an adverse drug reaction?

A

any unwanted, potentially harmful effect

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19
Q

What dose can adverse drug reactions occur at in the elderly? What are they often misinterpreted as?

A
  • Occurs at recommended dosage
  • Misinterpreted as symptoms
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20
Q

T/F: The elderly are 2-3 times more likely to experience adverse drug reactions

A

True

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21
Q

T/F: Even though elderly experience adverse drug reactions more often the reactions are not any more severe than in other age groups

A

False- More severe

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22
Q

What are some risk factor for adverse drug reactions?

A
  • > 75 year old
  • small stature
  • multiple drugs
  • high risk drugs
  • organ dysfunction
  • previous adverse drug reactions
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23
Q

What are some ways to prevent adverse drug reactions and inappropriate drug use in older adults?

A
  • Adequate evaluation
  • “Low & slow” prescribing
  • Periodic re-eval of long term meds
  • early recognition of ADRs
  • education/communication
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24
Q

Where did marijuana (MJ) come from?

A
  • Cultivated 12,000 yrs ago in west/central Asia
  • Used for medicinal purposes > 4000 yrs
  • Spread throughout Asia/Europe
  • Brought to Western world in 1500-1600’s
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25
Q

Marijuana was used extensively through Europe in 1800’s and well into 20th century in US for medical use because physicians documented benefits in treating what?

A
  • Anxiety
  • Sleep disorders
  • Headache/migranes
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26
Q

Marijuana was used extensively through Europe in 1800’s and well into 20th century in US for medical use… what happened?

A
  • 1937: US government placed extreme legal & financial restrictions on medical use
  • Made it difficult or impossible to prescribe or recommend MJ for therapeutic reasons
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27
Q

T/F: Restrictions of marijuana occurred against the advice of AMA

A

True

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28
Q

In 1970, MJ was classified as Schedule I controlled substance and reconfirmed in July 2016 what is a Schedule I substance?

A
  • High abuse potential
  • no current accepted medical use
  • Lacks adequate safety
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29
Q

What is the current status of MJ use as of November 2021?

A
  • Some form of medical MJ is available in 36 states & Washington DC
  • Recreational MJ currently approved in 18 states
  • MJ use decriminalized in most other states
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30
Q

What is MJ?

A
  • Species of Cannabis plant (3 primary species C. sativa, C. indica, C. ruderalis)
  • Typically refers to C. sativa (contains high levels of psychoactive substance called cannabinoids)
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31
Q

Species of Cannabis that are low in psychoactive substances are classified as what?

A

Hemp (C. ruderalis)

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32
Q

What is the active ingredient in MJ?

A

Cannabinoids

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33
Q

There are 2 important cannaboids (THC & CBD) which one produces most of psychoactive effects and high association with MJ?

A

THC

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34
Q

T/F: CBD is not as psychoactive as THC but may provide certain medicinal effects

A

True

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35
Q

How do cannabinoids affect humans?

A

Through Endogenous cannabinoid system

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36
Q

What are the 3 primary components of endogenous cannabinoid system?

A
  • Cannabinoid receptors
  • Substance produced within the body (endocannabinoids)
  • Enzymes that synthesize and degrade endocannabinoids
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37
Q

There are two primary subtypes of Cannabinoid receptor (CB1 & CB2). Where are CB1 receptors found?

A
  • Found throughout nervous system
  • Especially prevalent in pain pathways
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38
Q

There are two primary subtypes of Cannabinoid receptor (CB1 & CB2). Where are CB2 receptors found and what is the function?

A
  • Found on immune & hematopoietic tissues
  • Generally modulate immune responses and inflammation
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39
Q

CB1 may help modulate pain but it also produces most of what effects?

A

psychotropic effects (cannabinoid high)

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40
Q

Which cannabinoid receptor may provide immunosuppression and anti inflammation without psychotropic effects?

A

CB2

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41
Q

A specific drug or exogenous cannabinoid that affects only CB2 may produce beneficial effects without what side effect?

A

Psychotropic effects

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42
Q

What are the 2 primary substances of endocannabinoids?

A
  • Anandamide
  • 2 arachidonylglycerol (2-AG)
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43
Q

What are endocannabinoids produced by?

A

By CNS & peripheral tissues when tissues are injured or disturbed

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44
Q

What are some physiological processes that endocannabinoids can play a role in regulating?

A
  • Appetite
  • Digestion
  • Metabolism
  • Thermoregulation
  • Reproduction
  • Cardiovascular response
  • Fluid/ electrolyte balance
  • immune responses
  • learning
  • memory
  • stress responses
  • pain perception
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45
Q

Both Anandamide and 2-AG are degraded by what?

A

Fatty acid amide hydrolase (FAAH)

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46
Q

What are the implications of Anandamide and 2-AG?

A

Drugs that enhance synthesis or inhibit breakdown may be beneficial

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47
Q

What are the enzymes Anandamide and 2- AG synthesized from?

A

Anandamide: NAPE-PLD enzyme
2- AG: DAGL

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48
Q

What are the sources of cannabinoid?

A
  • Marijuana plant
  • Edible products
  • Synthetic THC and/or CBD
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49
Q

What are administration methods of cannabinoid?

A
  • Inhaled (smoking, vaporization)
  • Oral (tablets, mucosal sprays, edible products)
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50
Q

What are some pros to smoking administration route of cannabinoids?

A
  • Provide rapid onset & effects
  • Easy to adjust dose
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51
Q

What are some cons to smoking administration route of cannabinoids?

A
  • May damage respiratory tissues
  • May contain toxins in plant vaporization
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52
Q

In regards to oral administration of cannabinoids, what is the pro and cons of edibles?

A
  • Pro: Easy convenient, no respiratory issues
  • Con: long delay before onset/peak effects; difficult to adjust dose
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53
Q

In regards to oral administration of cannabinoids what is the best method for regulating dose but what is a con to this method?

A
  • Tablets/capsules
  • Con: long delay before onset/peak
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54
Q

In regards to oral administration of cannabinoids what is the positives of using oromucosal sprays?

A
  • Rapid onset
  • Fairly easy to adjust dose
  • Avoids 1st pass effect
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55
Q

Plant based (marijuana):
- Route?
- Onset?
- Peak?
- Duration?

A
  • Route: Inhaled by smoking or vaporization
  • Onset: Within minutes
  • Peak: 15-30 min
  • Duration: 2-3 hours
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56
Q

Edible products
- Route?
- Onset?
- Peak?
- Duration?

A
  • Route: Oral
  • Onset: 30-90 min
  • Peak: 2-3 hours
  • Duration: 4-12 hours
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57
Q

Synthetic THC
- Route?
- Onset?
- Peak?
- Duration?

A
  • Route: oral (tablets)
  • Onset: 30-60 min
  • Peak: 1-4 hours
  • Duration: 4-12 hours
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58
Q

Plant extracts
- Route?
- Onset?
- Peak?
- Duration?

A
  • Route: oral mucosal sprays
  • Onset: 10-15 min
  • Peak: 2-4 hours
  • Duration: Unknown
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59
Q

Topical administration of products containing CBD have become popular what are some of these products?

A
  • Cream
  • Lotion
  • Salve
  • Can penetrate through skin to treat subcutaneous structures
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60
Q

T/F: Topical & Transdermal Administration products often contain other ingredients and the amount and frequency of use varies depend on each product

A

True

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61
Q

What are some prescription products of cannabinoids?

A
  • Plant based (marijuana)
  • Synthetic THC (tablets)
  • Synthetic THC & CBD (in equal amounts)
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62
Q

Prescription cannabinoids: Dronabinol (tablet)
- Trade name?
- Cannabinoid?
- Approved indications?
- Current status?

A
  • Trade name: Marinol
  • Cannabinoid: THC
  • Approved indications: Anti- emetic for CINV, Appetite stimulant for HIV/AIDs
  • Current status: Received FDA approval in 1985, currently available in US as schedule III controlled substance
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63
Q

Prescription cannabinoids:
Nabilone (tablet)
- Trade name?
- Cannabinoid?
- Approved indications?
- Current status?

A
  • Trade name: Cesamet
  • Cannabinoid: THC
  • Approved indications: Anti-emetic for CINV
  • Current status: Received FDA approval in 1985, currently available in US as a schedule II controlled substance
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64
Q

Prescription cannabinoids:
Nabiximols
- Trade name?
- Cannabinoid?
- Approved indications?
- Current status?

A
  • Trade name: Sativex
  • Cannabinoid: THC & CBD
  • Approved indications: Spasticity in MS pain in advanced cancers
  • Current status: Approved for use in UK, Canada, other countries; Phase 3 clinical trials in US
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65
Q

Prescription cannabinoids:
Cannabidiol
- Trade name?
- Cannabinoid?
- Approved indications?
- Current status?

A
  • Trade name: Epidiolex
  • Cannabinoid: CBD
  • Approved indications: Drug resistant epilepsy in children
  • Current status: Approved by FDA in June, 2018 to treat seizures in Lennox-Gastaut and Dravet syndrome
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66
Q

What are some neuromusculoskeletal indications for cannabinoids?

A
  • Pain (cancer, neuropathic pain, fibromyalgia, arthritis, chronic back/neck pain, others)
  • Spasticity (esp MS)
  • Seizures (esp resistant seizure in children)
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67
Q

What are some other clinical applications of cannabinoids?

A
  • Nausea, vomiting, appetite stimulant
  • Glaucoma
  • Anxiety, Psychosis (maybe)
68
Q

Why are there contradictory results of the clinical effects of cannabinoids?

A
  • Different products/sources
  • Types of cannabinoids (THC, CBS, others)
  • Administration routes
  • Doses
  • Past experience with MJ
69
Q

What is the difference between inhalation and oral route of cannabinoids?

A
  • Inhalation: Offers faster onset of effects but potential harm to lungs
  • Oral: Delayed effects and less predictable
70
Q

What are some adverse systemic effects of MJ on CV, Pulmonary & GI?
- Note effects are seen primarily in heavy/habitual MJ users

A
  • CV: Increase HR, BP, myocardial O2 demand, increased risk ischemic stroke
  • Pulmonary: airway inflammation, airflow obstruction, wheezing, cough, increase sputum
  • GI: Increased nausea/vomiting (hyperemesis syndrome)
71
Q

What are some acute CNS effects of MJ?
- Note type and severity depend on THC content, prior MJ use, use with other drugs

A
  • MJ high (giddiness, increased perception, euphoria, mellowing out
  • Some users: Confusion, hallucinations, panic run, paranoia
  • Decreased cognition, alertness, rxn time
  • Decreased balance, coordination
72
Q

What are some chronic CNS effects of MJ?

A
  • Long term adverse effects are not well understood
  • Info obtained from heavy/habitual recreational users may not apply to Medical MJ
  • Major concern often summarized as “Cannabis Use Disorder”
73
Q

What is Cannabis use disorder?

A
  • Taken in larger amounts, over a longer period than intended
  • Persistent desire, unsuccessful efforts to cut down or control use
  • Great deal of time is spent in activities necessary to obtain, use or recover from its effects
  • Craving or a strong desire or urge to use cannabis
  • Failure to fulfill obligations at work, school, home
  • Persistent or recurrent social or interpersonal problem
  • Important social, occupational, or recreational actives are given up or reduced
  • Cannabis use is continued despite knowledge of having a persistent/recurrent physical or psychological problem
74
Q

Tolerance of cannabinoids is defined as by as?

A

Either of the following
- A need for markedly increased amounts of cannabis to achieve intoxication or desired effect
- Markedly diminished effects with continued use of the same amount of cannabis

75
Q

A patient is considered to be going through withdrawal from canabis when either?

A
  • Characteristic withdrawal syndrome for cannabis
  • Cannabis (or a closely related substance) is taken to relieve or avoid withdrawal symptoms
76
Q

T/F: Compulsive drug seeking/obsession has not been documented in individuals using cannabis

A

False- There has been documentation
Tolerance and withdraw can occur but intensity not on scale of opioids

77
Q

Is MJ a gateway drug?

A
  • Most MJ users do not progress to harder drugs
  • Early MJ use is associated with use of other drugs (including alcohol, nicotine)
78
Q

MJ should be avoided if there is a history of what?

A
  • Addiction
  • Mental health issues (depression, psychosis)
  • Developing CNS
79
Q

What are the potential positive effects on rehab with the use of canabis?

A
  • Decrease pain, spasticity, seizures
  • Decrease disability, increase HRQoL
80
Q

What are some possible adverse effects on rehabilitation with the use of cannabis?

A
  • Decrease balance, coordination, rxn time
  • Adverse CV, respiratory effects
  • Excessive, inappropriate use or concomitant use with other drugs
81
Q

What is some information we can tell our patients about cannabis use?

A
  • Smoking is not the only administration method
  • Oral/edible forms are available but have certain drawback (delay before effects)
  • MJ is composed of many compounds (cannabinoids)
  • Certain cannabinoids (THC, CBD) have been isolated, can be given as pills/tablets
  • At present, several rx products containing THC, CBD or bothdrugs are available in US and others may be approved soon
82
Q

T/F: PT can advise or recommend use of cannabis when it is legal

A

False - DO NOT they must consult their physician

83
Q

What is some advice to give patients using cannabis?

A
  • Advice about slower rxn time, decreased attention
  • Inform about interaction with other drugs
84
Q

What are the classic symptoms of Parkinson disease?

A
  • Rigidity
  • Resting tremor
  • Bradykinesia
  • Postural instability
85
Q

What is the primary cause of Parkinsonism?

A
  • Degeneration of dopaminergic neurons in substantia nigra
  • Normally there is balance between dopamine (DA) & Ach in basal ganglia
    PD: Decreased DA results in increased Ach
86
Q

What is the rationale for levodopa therapy?

A
  • Attempt to increase dopamine content in basal ganglia
  • Direct administration of dopamine ineffective because of blood brain barrier
  • Must provide precursors to dopamine (levodopa - L- DOPA)
87
Q

What is Carbidopa and when is it used?

A
  • Carbidopa: Inhibits dopa decarboxylase, prevents premature conversion
  • Used with L-dopa because L-dopa will be converted to dopamine before reaching the brain
88
Q

Oral administration of dopamine is not an effective treatment of Parkinson disease because?

A

Dopamine is unable to pass from blood stream into the brain

89
Q

What are the side effects of L-dopa therapy?

A
  • GI irritation
  • Hypotension
  • Psychotropic, behavioral effects
  • Dyskinesias
  • Freezing of gait
  • others
90
Q

There is fluctuation in response to L-dopa. What is the end-of-dose akinesia?

A
  • Also called “wearing off” or “fading effect”
  • Decreased response toward end of dose cycle
91
Q

Response fluctuations within dose cycles of L-dopa is known as what?

A

On-off phenomenon

92
Q

An inhaled form of L-Dopa is available (Inbrija) what is it used to treat?

A

“Off” episodes if already treated with levodopa/carbidopa

93
Q

What can begin to occur after 4-5 years of L-dopa therapy?

A

Benefits may be lost or dyskinesias become intolerable

94
Q

What is the mechanism of dopamine agonist used for treating Parkinson? When can they be used?

A
  • Mechanism: Cross blood brain barrier and directly stimulate dopamine receptors
  • Used as initial treatment in early PD
95
Q

What are some problems of dopamine agonists?

A
  • Nausea/vomiting
  • Confusion, hallucinations
  • Postural hypotension
  • Increased dyskinesia
96
Q

What is COMT enzyme?

A
  • COMT (Catechol-O-methyltransferase)
  • Enzyme that breaks down L-dopa in peripheral tissues
97
Q

What does COMT inhibitors do?

A
  • Allow more L-dopa to reach the brain
  • May decrease fluctuations, increase on time
98
Q

What are the problem with COMT inhibitors?

A
  • GI distress (esp diarrhea)
  • Orthostatic hypotension
  • Increased dyskinesia
99
Q

What do anticholinergic agents do?

A
  • Decrease acetylcholine influence
  • May help decrease rigidity & tremor
100
Q

What does MAO-B inhibitors do?

A
  • Inhibit monoamine oxidase type B (MAO- B)
  • Prolong dopamine effects in brain
101
Q

What are the problems with MAO-B inhibitors?

A

No major concerns

102
Q

What does Amantadine do?

A
  • Blocks NMDA receptor in brain
  • Decreases influence of excitatory amino acids (glutamate)
  • Decrease chance of dyskinesias
103
Q

What are the problems with Amantadine? (antiparkinson med)

A
  • Orthostatic hypotension
  • Psychotropic effects
  • Skin discoloration
104
Q

What are the antiparkinson drugs impact on rehabilitation?

A
  • Coordinate rehab sessions with drug therapy
  • Optimal treatment time (30-60 min after meds)
  • Recognize synergistic effects of physical rehab & drug therapy
105
Q

What are some examples of anti-infectious agents?

A
  • Antibacterials
  • Antivirals
  • Antifungals
106
Q

What is the common goal of anti-infectious agents?

A

Selective toxicity

107
Q

What is bacteria? And how is it different from a human cell?

A
  • Single cell microorganisms
  • Different from human cells in structure/function (rigid cell membrane, different ribosomes, different nucleic acid metabolism)
108
Q

What are the 3 general categories of antibacterial drugs?

A
  1. Inhibit cell wall synthesis & function
  2. Inhibit protein synthesis
  3. Inhibit DNA/RNA synthesis & function
109
Q

How does inhibition of cell wall synthesis & function occur?

A
  • Bacterial membrane more rigid than human.. contain peptidoglycan
  • Certain agents inhibit wall synthesis or create hole in lipid bilayer
110
Q

How does inhibition of protein synthesis occur?

A
  • Bacterial ribosomes (50S) slightly different from human
  • Certain agents bind to bacterial ribosome… inhibit protein synthesis
111
Q

How does inhibition of DNA/RNA function occur?

A
  • Nucleic acid metabolism different in bacteria versus human
  • Certain drug decrease DNA synthesis by inhibiting folic acid production
  • Other directly inhibit bacterial DNA/RNA synthesis function
112
Q

Overall antibacterial drugs can be selectively toxic because bacteria?

A
  • Have more rigid membrane
  • Have different ribosomes
  • Have different DNA/RNA synthesis & function
113
Q

Antibacterial drugs: additional features
- Effects?
- Spectrum?
- Resistance?

A
  • Effects: bactericidal vs bacteriostatic
  • Spectrum: Broad vs narrow spectrum
  • Resistance: Strains develop natural defense against drugs
114
Q

What are some common resistant strains to antibacterial drugs?

A
  • VRSA
  • MRSA
  • VRE
  • PRSP
115
Q

What are some common mechanisms that cause antibacterial drug resistance?

A
  • Develop drug-destroying enzymes
  • Alter or mask drug binding site
  • Change enzyme targeted by drugs
  • Decrease drug penetration
  • Develop drug efflux pumps
116
Q

In prevention of bacterial resistance how is antibacterial stewardship achieved?

A
  • Avoid overuse (esp broad spectrum)
  • Use narrow spectrum whenever possible
117
Q

What is the treatment of bacterial resistance?

A

Provide second drug to overcome resistance

118
Q

To prevent the development of drug resistant bacteria practitioners should do what?

A
  • Antibacterial resistance can be reduced by using narrow spectrum drugs
  • Obtaining culture/sensitivity test to help select best drug
  • Not using antibacterial drugs to treat viruses & other pathogens
119
Q

How can a PT help reduce or prevent the spread of resistant strains?

A
  • Handwashing
  • Sterilize equipment
  • Patient & family education (avoid exposure to contagious people, take anti bacterials as directed, discard old/expired anti-infectious drugs)
120
Q

What are the adverse effects of antibacterial drugs?

A
  • Minor problems
  • Hypersensitivity, allergic reactions
  • UV sensitivity
  • Ototoxicity
121
Q

What are some rehab concerns when a patient is taking antibacterial drugs?

A

Be alert for tendon pain & possible tendinopathy

122
Q

What is the adverse effects of fluoroquinolone? (a common example of inhibition of DNA/RNA)

A
  • May increase risk of tendon damage, possible rupture
  • Often large, wt bearing tendons (can be others)
123
Q

There is an increased risk of Fluorquinolone tendon damage in?
(a common example of inhibition of DNA/RNA)

A
  • Older patients
  • Renal failure
  • Taking glucocorticoids
124
Q

When can tendon damage from Fluoroquinolone occur and how is it treated?
(a common example of inhibition of DNA/RNA)

A
  • Occur: Onset can be rapid
  • Tx: Stop drug, protect tendon
125
Q

How does viral replication occur?

A
  • Virus absorbs onto host cell
  • Virus penetrates into host cell, releases genetic material
  • Viral DNA or RNA takes over host cell, uses cell to make new viruses
  • Symptoms related to loss of host cell function, other direct viral effects
126
Q

T/F: Antiviral drugs are not specific

A

False
- Fairly specific often act on only one type of virus
- Typically inhibit viral enzymes

127
Q

Why are viral infections more difficult to treat than other types of infections?

A
  • Viruses penetrate into human cells & cannot be killed easily without harming the human cells
  • Viruses use a host cell to reproduce and replicate more viruses
  • Most antiviral drugs cannot kill the virus after it has moved into the host cell without also killing the host cell
128
Q

What are interferons and what are the important functions?

A
  • Small proteins, produced endogenously
  • Functions: Control cell division/differentiation & Control immune responses
129
Q

What are some specific interferons and what can they be used for?

A
  • Interferon alfa n-3: condylomata
  • Interferon alfacon-1: hepatitis C
  • Interferon alfa 2b: Condylomata, hep B & C, certain cancers
130
Q

What are antiviral vaccines typically made from and when are they administered?

A
  • Typically made from modified virus
  • Administered prior to exposure to virus
131
Q

What do antiviral vaccines do?

A

Stimulate immune system to produce virus - specific cellular and antibody responses

132
Q

What are the 3 primary types of antiviral vaccines?

A
  1. Live attenuated vaccine
  2. Inactivated vaccine
  3. Subunit vaccine
133
Q

What is live attenuated vaccine?

A
  • Pathogen (usually virus) has been weakened, often by repeated cell cultures
  • Mimics actual infection but causes very mild symptoms
134
Q

Live attenuated vaccine typically produce a good immune response but is contraindicated in?

A
  • Immunocompromised patient
  • Pregnant women
135
Q

What is non-live vaccines?

A
  • Pathogen inactive by heat, radiation or chemicals
  • Does not replicate in body
136
Q

T/F: Non-live vaccines are not contraindicated in Immunocompromised patients

A

True
- Does not replicate in body

137
Q

Since the immune response is not as strong in non-live vaccine what might individuals need?

A

Primary and booster doses for long-term response

138
Q

What is subunit vaccines?

A
  • Fragment of pathogen are used as antigens to stimulate immune response
  • Not infectious, but often less effective or might need periodic boosters
139
Q

What type of vaccines are COVID-19 vaccines?

A

mRNA vaccines

140
Q

How do mRNA vaccines work?

A
  • mRNA synthesized in lab, injected to instruct human cells to manufacture harmless proteins related to COVID
  • Immune cells (T,B lymphocytes) recognize “viral” proteins as invaders and synthesize virus - specific antibodies
  • Viral antibodies attach to virus, prevent insertion into healthy human cells
141
Q

What is AIDS associated with?

A

Human immunodeficiency virus (HIV)

142
Q

What is HIV?

A

Retrovirus that attacks T4 lymphocytes

143
Q

What does loss of lymphocytes have an impact on?

A
  • Impaired immune function
  • Opportunistic infections
  • Certain cancers
144
Q

What are some anti-HIV drugs?

A
  • Reverse transcriptase inhibitors (RTIs)
  • Protease inhibitors
  • HIV entry inhibitors
  • Integrase inhibitors
145
Q

What is the action of reverse transcriptase inhibitors?

A

Prevent conversion of viral RNA to viral DNA (reverse transcription)

146
Q

What are the agents of reverse transcriptase inhibitors and what is their function?

A
  • Nucleoside RTI: act as false substrate
  • Non Nucleoside RTIs: Block active site on reverse transcriptase
147
Q

What is HIV protease?

A

Key enzyme in final steps of HIV synthesis

148
Q

What is the mechanism of protease inhibitors?

A

Mimic viral components… block protease function

149
Q

What is the suffix of several protease inhibitors agents?

A

-avir

150
Q

What is the mechanism of HIV entry inhibitors?

A

Impair ability of HIV to fuse with & enter host (CD4) lymphocytes

151
Q

What is the mechanism of integrase inhibitors?

A

Inhibit HIV integrase … enzyme that splices viral DNA into host cell DNA

152
Q

What are the adverse effects of anti-HIV drugs?

A
  • Myopathy, neuropathy (RTI, integrase inhibitors)
  • Lipodystrophy syndrome (protease inhibitors, integrase inhibitors)
  • Blood dyscrasias, GI distress, immune reactions (all groups)
153
Q

What is the current combination strategy of anti-HIV drugs?

A
  • Highly active antiretroviral therapy (HAART)
  • Usually 2 nucleoside RTIs, plus a non-nucleoside RT, integrase inhibitor or a protease inhibitor
  • Other drugs added or substituted to maintain antiviral effects and avoid developing resistance
154
Q

What is the newer strategy of long acting injections of anti- HIV drugs?

A
  • IM injection of Cabenuva
  • 600 mg IM (initial) followed by 400 mg IM a month
155
Q

What are some other common medications in AIDS used to treat opportunistic infections?

A
  • Antibacterials
  • Antivirals
  • Other antimicrobials
156
Q

What are some other common medications in AIDS used to treat cancers?

A
  • Interferons
  • Others
157
Q

What are some current/future strategies against AIDS?

A
  • Modify, optimize HAART strategies
  • On-going drug development
  • Prevention
158
Q

Fungal infections are from? And where are they often found?

A
  • Fungal infections: mycosis
  • Infections often superficial or local
159
Q

T/F: Other mycoses are systemic and serious in immunocompromised host

A

True

160
Q

What is the suffix of common antifungal drugs ?

A
  • Imidazoles
  • “-azole”
161
Q

What is the mechanism of Imidazoles? (Common antifungal drug)

A

Inhibit enzymes that synthesize membrane components

162
Q

There are several other chemical classifications of anitfungals. what do these drugs usually do?

A

Generally impair membrane integrity or biochemistry of fungal cells

163
Q

What are the adverse effects of topical-local antifungals?

A
  • Few serious side effects
  • Excessive use may cause resistance
164
Q

What are some adverse effects of systemic use antifungals?

A
  • Headache, Gi problems common
  • Other serious side effects can occur
165
Q

Antifungal drugs are relatively safe when administered (topically or orally), but the risk of liver toxicity and other serious side effects increases substantially when these drugs are given (topically or orally)

A
  • Topically
  • Orally
166
Q

What are the characteristics of a virus?

A
  • Viral DNA or RNA core
  • Surrounded by protein shell (capsule)

Clinical Med (Year 2) (17 decks)

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