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Med 412 > Week 32 Asthma > Flashcards

Week 32 Asthma Flashcards

1
Q

Pharmacogenetics

A

Study of how single gene variation may impact on the variability of an individuals response to medication.

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2
Q

Pharmacogenomics

A

Field of research that studies how the genome can influence response to medication.

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3
Q

Describe how genetic differences contribute to inter-individual variability in drug response

A

Various SNPs alter pharmacodynamics and pharmacokinetics which further affect:
Drug metabolism - affects drug levels
Forensics
Drug choice in ancestry groups
Links with monogenic disorders - don’t need to know about the condition - but causes a serious condition d/t metabolism pathway

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4
Q

How are safe drug use prinicples employed considering genetic differences and inter-individual variability in drug response?

A

Drugs have more than one stage of metabolism with multiple receptors/enzymes. Therefore any genetic variations can impact pharmacokinetics.
Need to know/check for ancestry interactions/personal interactions.

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5
Q

Outline indications for genomic testing and referral to genetic specialists

A

Testing:
Precision medicine and targeted treatment.
Disease surveillance.
Anticipatory guidance.
Familial implications.
Ending diagnostic odyssey

Referral:
Identify hereditary disease.
Identify multisystem disease.
Education of developmental differences.
Prenatal diagnosis.

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6
Q

Discuss the WHO ladder of pain tx

A
  1. Non-opiate: NSAIDS, acetimenophen
  2. Weak opiates
  3. Strong opiates
  4. Regional anesthesia
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7
Q

Which is the best NSAID for disrupting platelet activity?

A

Aspirin

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8
Q

What are the most important side effects of NSAIDS

A

Gi ulcers
Increase risk of MI
Increase risk of kidney dysfunction

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9
Q

Method of action of opiates

A

Inhibit voltage gated Ca influx to presynaptic terminal - blocks neurotransmitter release.
Opens K channels - hyperpolarizes neurons and inhibits action potential.

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10
Q

Common opiates

A

Morphine
Hydromorphone (Dilaudid)
Oxycodone (Oxycontin)
Percocet (Acetaminophen + Oxycodone)
Codein - some gets converted to morphine.
Meperidine (Demerol)
Fentanyl

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11
Q

Effects of opiates

A

Analgesia
Euphoria/dysphoria/hallucination
Respiratory depression
Decrease GI motility
Miosis
Sedation
Physical dependence

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12
Q

Mechanism of cannabinoids for pain control

A

Inhibit voltage gated Ca influx to presynaptic terminal - blocks neurotransmitter release.
Opens K channels - hyperpolarizes neurons and inhibits action potential.

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13
Q

Common cannabinoids used for pain control

A

Cesamet (nabilone) - THC
Sativex (nabiximol) - THC/CBD

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14
Q

Side effects of cannabinoids

A

Drowsiness/sedation
Dizziness
Psych disturbances
Euphoria
Acute psychosis/dissociation
1st episode psychosis
Unmask schizophrenia
Speech disorder/ataxia
Impaired memory
Irritibility/agitation
Appetite changes
GI issues

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15
Q

What is the most common side effect of cannabinoids

A

Sedation

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16
Q

Method of action of ketamine

A

Inhibits post synaptic ligand gated Ca channel - decreases glutamate release.
Activation of NMDA receptor leads to hyperalgesia and allodynia.

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17
Q

How does NMDA antagonism lead to anesthesia?

A

Blocks glutamate binding.
Inhibit ligand gated Ca influx.
Suppresses thalamocortical signalling - cuts it off completely.
Inhibits central sensitization in the spinal cord by increasing glutamate release.

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18
Q

How are ketamine’s effects on glutamate paradoxical

A

Inhibits and enhances glutamate transmission depending on:
Dosage
Brain region
Timing
Cell type
100mg high dose - loss of consciousness.
10mg low dose - preferentially blocks NMDA receptors on inhibitory interneurons -> excitation.

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19
Q

Method of action of A2 agonists

A

Activation of A2 receptors ->
Inhibits cAMP ->
less Ca entry ->
less glutamate release.

Also hyperpolarizes postsynaptic membrane -> less transmission of nociceptive pain.

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20
Q

Method of action of gapapentinoid

A

Inhibit voltage gated Ca channels
Inhibits serotonin receptors

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21
Q

Examples of gabapentinoids

A

Gabapentin (neurotonin)
Mirogabalin (Tarlige)
Phenibut (Anvifen, Fenibut, Noofen)
Pregabalin (lyrica)

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22
Q

What drugs produce analgesia through suppression of voltage gated Ca channels?

A

Nabilone
Gabapentin
Fentanyl
Clonidine

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23
Q

Which drug produces analgesia through suppression of ligand gated Ca channels?

A

Ketamine

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24
Q

2 main techniques of regional anesthesia

A

Epidural
Spinal (below L1/2 - lasts 4 hours)

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25
Benefits of epidural
Pain control Less general anesthesia Infusion/patient controlled Less systemic opiates = less side effects
26
Method of action of general anethesia
Increases inhibitory neurotransmitters (GABA, glycine) Decreases excitatory neurotransmitters (Glutamate, Ach, 5-HT, NMDA)
27
What drug is best for predictable and fast offset pharmacokinetic?
Propofol
28
What is the major factor for deposition of gases in the various components of the airway?
Solubility. More soluble - further into the lungs.
29
What is the major factor for deposition of particles in the various components of the airway?
Size. PM.25 - gets into the lungs. PM0.1- gets deep into the lungs (deisel exhaust and cig smoke)
30
Phases of particle deposition
Impaction, >5, nasopharynx: get trapped in mucous Sedimentation, 1-5, small airways: get trapped and moved by cilia Diffusion, <0.1, alveoli: get into blood stream
31
Factors determining lung response
Deposition Clearance/detoxification Biologic activity of substance.
32
Ventilation
RRXVt
33
Modifiable factors for that influence toxicity of pollutants
Activity (how/when) - VENTILATION is key in acute context. Location (inside/outside/work/home) Reduction of CV risks Use of air cleaners Use of masks Use of antioxidants and medications
34
Factors that affect clearance
Site of deposition Health of lung defences; nasal filtering (mouth breather?) Cough/sneeze reflex Alveolar macrophages Bactericidal enzymes/antibodies Lymphatic system.
35
What is the strongest predictor of the likelihood and type of effect of a pollutant?
Dose of exposure.
36
Asthma definition
Heterogenous disease, usually characterized by chronic airway inflammation. it is defined by the history of respiratory symtpoms such as wheeze, shortness of breath, chest tightness and cough that vary over time and in intensity, together with variable expiratory airflos limitation.
37
Characteristics of asthma
Airway inflammation Bronchial hyper-responsiveness Variable degree of airflow obstruction
38
S&S of asthma
Wheezing Shortness of breath Chest tightness Cough
39
Asthma tiggers
Exercise Allergen Irritants Viral infection
40
Main defining factor for asthma symptoms vs, for example, COPD
Variable in time!
41
Asthma phenotypes
Allergic Non-allergic Adult-onset Asthma with persistent airflow limitation Asthma with obesity
42
Two core mechanisms in the pathophysiology of asthma
Airway inflammation Airway remodelling
43
Allergic inflammation pathway
Allergen presented to dendritic cell. Dendritic cell processes antigen and presents to T helper. T helper becomes Th2 and releases IL4, IL5, IL13. Cytokines cause B cell to produce IgE. IgE and cytokines further stimulate eosinophils, mast cells, basophils. Granulocytes produce more cytokines, leukotrines, histamine, and toxic granule products that cause airway smooth mm constriction, airway hyperresponsiveness, and eventual remodelling.
44
Epithelial damage pathway
Irritants cause epithelial damage, which then causes epithelium to release inflammatory mediators. Damage causes direct release of alarmins (IL25, IL33, TSLP). Alarmins then: 1. Stimulate natural T2 helper cells which further stimulates T2 cytokine release. 2. Stimulate T2 helper cells leading to release of IL4, IL5, IL13. Cytokines cause B cell to produce IgE. IgE and cytokines further stimulate eosinophils, mast cells, basophils. Granulocytes produce more cytokines, leukotrines, histamine, and toxic granule products that cause airway smooth mm constriction, airway hyperresponsiveness, and eventual remodelling.
45
What is the main T helper cell involved in asthma and what Cytokines does it release?
Th2: IL4 - IgE production, eosinophil recruitment IL5 - Eosinophilic inflammation IL9 - Mast cell release, IgE production, Mucus hypersecretion IL13 - IgE production, Eosinophil recruitment, Goblet cell metaplasia, Bronchial hyperreactivity
46
What WBC is predominant in asthma and what are its effects?
Eosinophil: Epithelial damage, Bronchoconstriction, Mucous hypersecretion
47
What supports growth of smooth muscle in asthmatics
Mast cells.
48
Major pathologic changes in airway remodeling
Proliferation and hyperplasia of goblet cells and submucosal glands. Increased deposition of subepithelial collagen. Airway smooth muscle hyperplasia. Microvascular changes.
49
What factors contribute to viable airway obstruction in asthma? Which one is not reversible?
Contraction of smooth muscle: inflammation/bronchoconstriction Thickening of the airway: remodelling/edema Mucus plugging. Remodelling is not reversible.
50
Risk factors for mortality d/t asthma
History of poorly controlled asthma. Prior hx of near fatal asthma.
51
Consider asthma if a patient presents with any of
Frequent episode of breathlessness. Chest tightness. Wheezing. Cough.
52
Aggravating factors associated with asthma dx
Viral resp. tract infections. Exercise. Exposure to aeroallergens/irritants.
53
Relieving factors associated with asthma dx.
Bronchodilators. Anti-inflammatory therapy.
54
Signs of severe airflow obstruction
Wheezing Tachypnea Decreased breath sounds Accessory mm use Indrawing
55
Pre/post bronchodilator spirometry for asthma dx.
Need less than lower limit of normal FEV1/FVC. FEV1/FVC improved by >=12% AND 200ml after bronchodilator.
56
Peak expiratory flow variability
Peak expiratory flow increases by >=20% after bronchodilator or over time with treatment. Or varies over 8% in a day. Useful for asthma at workplace vs not working.
57
Positive challenge test
Methacholine challenge: Methacholine causes bronchoconstriction. Low dose given, increasing until reaction occurs. Reaction within certain dose range = (+) Look for decrease FEV1 by >20% w/<4mg/ml. Exercise challenge: Breathing test pre and post exercise. If FEV1 drops >10-15% = (+)
58
What is needed for accurate dx of asthma?
Proper history for suspicion of asthma. Spirometry test. Confirm with methacholine challenge test.
59
Goals of asthma management
Achieve good symptom control Minimize future risk of exacerbation Minimize future risk of fixed airflow limitation. Minimize side effects from treatment.
60
Steps of asthma management
Assess Adjust Review Confirm diagnosis. Environmental control, education, written action plan. Meds.
61
Step wise rx for asthma control
SABA +ICS (LTRA 2nd line) +LABA **always needs to be used with ICS b/c LABA d/n treat inflammation(adults), Increase ICS (kiddos) +LTRA
62
Comorbidities that can worsen asthma
chronic rhinosinusitis GERD OSA obesity aspergillus allergy vocal chord dysfunction
63
Risk factors for exacerbation
Hx of previous severe exacerbation. Poorly-controlled asthma as per guidelines. More than 2 SABA per year. Current smoker.
64
When to consider adding controller therapy (ICS)
When reliever is used >2x/week during the day. When reliever is used >1/week during the night.
65
Pharm therapy for not well-controlled asthma
ICS + SABA
66
Pharm therapy for well-controlled asthma
Assess for risk of exacerbation. Higher risk: ICS + SABA Lower risk: SABA or consider ICS + SABA
67
Triple therapies
ICS LABA Anticholinergics
68
Expiratory wheeze indicates the obstruction is where?
Intra-thoracic.
69
Inspiratory stridor indicates the obstruction is where?
Extra-thoracic.
70
Bronchiectasis
dilation of the airways
71
Thumb sign indicates
Thickened epiglottis
72

Med 412 (17 decks)

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