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General OTOHNS > Biomedical principles and wound healing, common medication basics > Flashcards

Biomedical principles and wound healing, common medication basics Flashcards

1
Q

What are the 7 CanMEDS roles?

A
  1. Communicator - therapeutic relationship, relevant history, listen effectively, discuss appropriate information
  2. Collaborator - Consult effectively, MDT
  3. Professional - Integrity, honesty, and compassion, interpersonal behaviours, practice medicine ethically consistent with obligations
  4. Scholar - CME, facilitate learning, critically appraise the literature, contribute to new knowledge
  5. Health Advocate - Identify determinants of health, for patients and community, recognize and respond
  6. Leader (formerly Manager) - Utilize and allocate resources, health care organization, use information technology
  7. Medical Expert - diagnostic and therapeutic skills, effective patient care, access and apply information, consultation
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2
Q

What are 5 grounds for discharge patients from your practice?

A
  1. Changing scope of practice
  2. Patient poses a safety risk to office staff
  3. Patient is abusive
  4. Patient fails to respect professional boundaries
  5. Physician leaving medical practice
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3
Q

What are the 3 important aspects to informed consent as per the Royal College?

A
  1. Disclosure: Information about the risks and benefits of the proposed test or treatment as well as any alternatives, presented in language that the patient can understand
  2. Capacity: The ability to understand and appreciate the consequences of a particular decision or lack of decision. If in doubt, consultation from a psychiatrist, hospital attorney, or ethicist may be helpful. The ultimate judge of a patient’s capacity is court. If patient is incapable, seek consent from the appropriate subsitute decision maker
  3. Voluntary: The ability to make treatment choices without undue external coercion
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4
Q

What are 4 standards for how a patient decision should be made, in decreasing order of priority?

A
  1. Wishes: Prior expressions by the patient, while competent, that seem to apply to the actual decision that needs to be made
  2. Values & beliefs
  3. Best interests: This is more important for children, where the decision maker is usually the parent. Decisions should be respected unless they would cause direct and serious harm to the child.
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5
Q

Define competence

A

Possession of the required knowledge, skill, and experience to perform a particular task reliably and produce an appropriate outcome.

Categorical variable. One is competent, or not, to provide a particular service or perform a particular operation

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6
Q

Discuss the FDA Drug Risk Classification System

A

Category A: Controlled studies in humans show no risk to the fetus

Category B: No human studies, but safe in animal studies

Category C: No human studies, but adverse effects seen in animal studies

Category D: Evidence of human risk to fetus, but benefits may outweigh risks in certain situations

Category X: Controlled studies in animals or humans demonstrate fetal abnormalities. Risks clearly outweigh benefits.

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7
Q

Describe 3 features unique to laser light

A

3 C’s

  1. MonoCHROMATIC (= single wavelength)
  2. Collimated (= unidirectional, no divergence)
  3. Coherent (= in phase)
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8
Q

What does LASER stand for?

A

Light Amplification by Stimulated Emission of Radiation

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9
Q

Describe the physics of laser light emission

A
  • Electrons orbit around a nucleus at a stable energy level
  • Photon bumps electron to higher energy level, putting it in excited/unstable state
  • If struck by 2nd photon, unstable electron emits 2 identifical photons (= STIMULATED EMISSION). These photons are identical wavelength, direction & phase (laser light characteristics)
  • Each emitted photon stimualtes emission of further identical photons in cascading effect
  • HIGH REFLECTANCE MIRROR perpetuates cascade by directing photons back through laser medium
  • PARTIALLY TRANSMISSIVE MIRROR allows transmission of small amount of coherent photons (“laser beam”)
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10
Q

Discuss the mechanism of action and reversal agents of the following antiplatelets/anticoagulants:
1. Warfarin
2. ASA
3. Plavix (Clopidogrel)
4. Rivaroxaban (Xarelto), Apixaban (Eliquis)
5. Dabigatran/Argatroban
6. Unfractionated heparin
7. LMWH

A

Warfarn:
- Inhibits Vitamin K dependent clotting Factors
- 1972 C+S: Factors 10, 9, 7, 2, C, S
- Reversal: Vitamin K (or Octaplex, which contains Vitamin K factors)

ASA:
- Blocks COX-1, which normally inhibits platelet generation of thromboxane A2, which stimulates platement aggregation
- Result = decreases platelet aggregation
- Reversal: DDAVP, Tranexamic acid, platelet transfusion

Plavix = Clopidogrel
- Irreversibly inhibits the ADP receptor (which is normally important for platelet activation)
- Result = Decreases platelet activation
- Reversal: DDAVP, Tranexamic acid, platelet transfusion

Rivaroxaban (Xarelto), Apixaban (Eliquis)
- Selective factor Xa inhibitor (“Xa-ban”)
- Reversal: None

Dabigatran/Argatroban
- Direct thrombin inhibitor - IIa - (anti-thrombin - “at” in name)
- Reversal: None

Unfractionated Heparin:
- Intrinsic pathway (XII, XI, IX) and common pathway (X, II)
- Reversal: Protamine

LMWH:
- Common pathway (X, II)
- Reversal: None

Coagulation pathway notes

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11
Q

Patient that presents with recurrent post-op bleeding, history of easy bruising, and blood in urine. What is the suggested work-up?

A
  1. Medication review
  2. Liver/renal function
  3. CBC + smear
  4. PTT, INR
  5. Fibrinogen
  6. vWF antigen (quantity study) + activity (quality study)
  7. Special blood tests (cnosult hematology)
    - Specific factors
    - Platelet function tests
    - 50:50 mix (pt blood: normal blood) to determine factor insufficiency (PT/PTT values correct) vs. presence of inhibitor (PT/PTT values don’t correct)
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12
Q

What is the most common causes of blood dyscrasias?

A

CONGENITAL:
1. Von Willebrand disease (most common)
2. Hemophilia A (VIII)
3. Hemophilic B (IX)
4. Specific factor deficiency
5. Platelet dysfunction
6. Fibrinogen dysfunction/insufficiency

ACQUIRED: Medical conditions
1. Liver disease
2. Renal disease
3. ITP
4. Bone marrow pathology

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13
Q

Regarding Hemophilia A, discuss:
1. What is the genetics and inheritance?
2. What is it?
3. Symptoms?
4. Treatment?

A

GENETICS:
- X-linked recessive

HEMOPHILIA A:
- Factor VIII (8) deficiency

SYMPTOMS:
1. Easy bleeding
2. Hemarthrosis
3. GI
4. Brain bleeds

TREATMENT:
1. Mild: Desmopressin DDAVP (Releases more VIII from vessel walls)
2. Severe: Plasma exchange or give IV factor VIII

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14
Q

Regarding Hemophilic B, discuss:
1. What is it?
2. Genetics?
3. Clinical presentation
4. Treatment

A

HEMOPHILIA B:
- Factor IX (9) deficiency

GENETICS:
- X-linked recessive

CLINICAL PRESENTATION:
- Similar to Hemophilia A, but IX has a longer half life and therefore symptoms are less severe

TREATMENT:
- IV Factor IX infusions

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15
Q

Regarding von Willebrand’s disease, discuss:
1. What is it?
2. Pathophysiology?
3. What are the different types?
4. How is it typically treated?

A

VON WILLEBRAND’S DISEASE (vWD):
- Von Willebrand factor transports factor VIII, which helps stabilizes platelet adhesion and aggreggation

FOUR TYPES:
1. Type 1 = Autosomal dominant (80%)
- Insufficient quantity of vWF
- Asymptomatic, nosebleeds
- Tx: Desmopressin (increases factor VIII and von Willebrand factor and also improves platelet function)

  1. Type 2 = Autosomal dominant
    - Defective qualiity of vWF
    - Moderately symptomatic
    - Tx: Desmopressin
  2. Type 3 = Autosomal recessive (rare)
    - Absence of vWF completely
    - Life-threatening internal hemorrhage
  3. Acquired
    - vWF antibody that clears vWF; OR
    - vWF molecules are sheered/destroyed by intracardiac devices
    - Associations: Hypothyroidism, AV stenosis, Left ventricular assistance device (LVAD)
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16
Q

What is the active ingredient in each of the following:
1. Gelfoam
2. Surgicel
3. Tisseel
4. Floseal

A

Gelfoam = Purified porcine skin gelatin
Surgicel = Oxidized cellulose (plant derirved), is also bactericidal
Tisseel = Human thrombin + human fibrinogen + Ca2+ chloride, and bovine aportinin (inhibitor of proteases like plasmin)
Floseal = Human thrombin + bovine gelatin granules
Avitene = Microfibrillar collagen (bovine into microcrystals), induces intrinsic pathway

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17
Q

Distinguish “Euthaniasia and assisted suicide” from “decisions to forego treatment”

A

Euthanasia and assisted suicide: injection of a lethal substance or the provision of a lethal overdose

Decisions to forego treatment involve the non-initiation or discontinuation of a life-sustaining treatment such as CPR, ventilator, tube feeding, etc. The law permits discontinuation, even though it leads to death, under defined conditions.

Think: They were going to die anyways, and you are not saving them. Which does not mean you are killing them.

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18
Q

Define clinical equipoise

A

Exists when the experts of the medical community is unable to achieve consensus on the preferred treatment.

Assumption that there is not one ‘better’ intervention present (for either the control or experimental group) during the design of a randomized controlled trial (RCT).

A true state of equipoise exists when one has no good basis for a choice between two or more care options.

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19
Q

What are 5 conditions that must be met for ethical research

A
  1. The existence of clinical equipoise (Sound foundation of previous work must give good reason to believe that the proposed question is debatable)
  2. Good design
  3. Research interventions are not likely to cause serious harm to research subjects
  4. Approval by a Research Ethics Board (IRB)
  5. Interventions will acheive the intended result
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20
Q

Describe the 4 phases of clinical trials

A
  1. Phase I: DOSE
    - Tolerance and Pharmacologic properties
    - Determine spectrum of toxicity
    - End point is the maximally tolerated DOSE
    - Healthy patients only
  2. Phase II: RESPONSE RATE (per dose)
    - Efficacy of a drug in a specific disease and stage at a defined dose
    - Define activity within tolerable levels of toxicity
    - Endpoint is Response Rate
    - All patients
  3. Phase III: RESPONSE RATE & DURATION, DFS & OS
    - Comparison of 2 therapies in a randomized manner
    - Endpoints are response rate, response duration, disease free survival, overall survival
    - All patients
  4. Phase IV: POST RELEASE
    - Post release to assess long term complications

Note:
- Phase I done in healthy subjective
- Phase 2 and 3 done in all patients

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21
Q

What are the Oxford levels of evidence?

A
  1. LEVEL 1
    - 1a: SR and/or meta-analysis of RCTs
    - 1b: Individual (well conducted) RCTs
  2. Level 2
    - 2a: SR of cohort studies
    - 2b: Individual cohort study or low-quality RCTs
  3. Level 3
    - 3a: SR of case-control studies
    - 3b: Individual case-control study or phase II interventional (uncontrolled) study
  4. Level 4
    - Case series, low quality case-control study, or cohort studies
  5. Level 5
    - Expert opinion
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22
Q

What are the AAP Grade of Evidence?

A
  1. Grade A (Oxford 1): Systematic review of multiple RCTs
  2. Grade B (Oxford 2-3): Randomized trials or observations studies with dramatic effects or highly consistent evidence
  3. Grade C (Oxford 4): Non-randomized, or historically controlled studies, including case-control and observational studies
  4. Grade D (Oxford 5): Case reports, mechanism-based reasoning, or reasoning from first principles
  5. Grade X: Exceptional situations where validating studies cannot be performed and there is a clear preponderance of benefit over harm
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23
Q

What are the AAO Grades of Recommendation?

A

AAP Grade A:
- Data shows preponderance of benefit over harm (or vice versa for negative recommendations) = Strong recommendation
- Data shows balance of benefit and harm = Option

AAP Grade B:
- Data shows preponderance of benefit over harm (or vice versa for negative recommendations) = Strong recommendation or recommendation
- Data shows balance of benefit and harm = Option

AAP Grade C:
- Data shows preponderance of benefit over harm (or vice versa for negative recommendations) = Recommendation
- Data shows balance of benefit and harm = Option

AAP Grade D:
- Data shows preponderance of benefit over harm (or vice versa for negative recommendations) = Option
- Data shows balance of benefit and harm = No recommendation

AAP GRADE X:
- Data shows preponderance of benefit over harm (or vice versa for negative recommendations) = Strong recommendation or recommendation

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24
Q

Describe the pregnancy risk categories and give an example drug for each

A
  1. A = Safe in human trials (e.g. synthroid, folate)
  2. B = Safe in animal trials, no human evidence (e.g. metformin)
  3. C = Risk not ruled out (e.g. prednisone)
  4. D = Adverse events in humans, but benefit may outweigh risk (e.g. benzos, anti-epileptics)
  5. X = Adverse events in humans (e.g. warfarin, thalidomide, retinoids)
  6. N = Not classified (e.g. acetaminophen)
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25
Q

What are the 4 tenets of biomedical ethics?

A
  1. Autonomy
  2. Beneficence
  3. Non-maleficence
  4. Justice
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26
Q

How do you disclose medical errors (according to CMPA guide)

A
  1. Avoid speculation
  2. Comment only on own involvement
  3. Document the harm and the disclosure
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27
Q

Define Genotype vs. Phenotype

A

Genotype: The genetic constitution of a locus (position on a specific gene)

Phenotype: The observable characteristics of an organism controlled by a specific genetic locus

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28
Q

Define Endotype

A

Pathobiological form of a disease (e.g. Type II CRS)

An endotype is a subtype of a health condition, which is defined by a distinct functional or pathobiological mechanism. Different than phenotype which is just characteristics

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29
Q

Define Allele

A

A particular form of a gene on each chromosome

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30
Q

Define Homozygosity vs. Heterozygosity

A

Homozygosity: Two identical alleles at an autosomal gene locus (e.g. PP dominant, aa recessive)

Heterozygosity: Two different alleles at an autosomal gene locus (e.g. Bb)

See Image Vancouver notes Page 3

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31
Q

Describe the 3 common forms of Mendelian inheritance

A
  1. Autosomal dominant inheritance (75% expression)
  2. Autosomal recessive inheritance (25% expression)
  3. Sex-linked inheritance (males)
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32
Q

Describe 5 non-Mendelian inheritance patterns

A
  1. Mitochondrial inheritance: Maternal mitochondria inherited from ovum (all offspring affected)
  2. Mosaicism: presence of both normal and abnormal cells within the same organism, can be somatic or germline
  3. Genetic imprinting (“silenced”): expression depends on parent of origin (e.g. if allele inherited from the father is imprinted and thereby silenced, only the allele from the mother is expressed)
  4. Uniparental disomy: Offspring inherits both copies of a chromosome pair/allele from a single parent
  5. Dynamic/spontaneous mutation (trinucleotide repeats)

MM-GUD

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33
Q

How do you identify the pattern of inheritance based on pedigrees:
1. Autosomal dominant
2. Autosomal recessive
3. X-linked dominant
4. X-linked recessive

A

AUTOSOMAL DOMINANT
- Every generation

AUTOSOMAL RECESSIVE
- Skips generations

X-LINKED DOMINANT:
- All daughters of a male who has the trait will also have the trait
- Sons may have the trait if their mother has the trait
- Sons can not inherit this from their mothers

X-LINKED RECESSIVE:
- Only males will have the trait, skips generations

Kevan Gen #136

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34
Q

What are the equivalent doses of opioids using 1mg of Dilaudid, for:
1. Dilaudid
2. Oxycodone
3. Morphine
4. Codeine

A

= Hydromorphine 1mg PO
= Oxycodone 2.5mg PO (no IV form)
= Morphine 5mg PO
= Codeine 30mg PO

IV/SQ doses usually half, except Hydromorphone is usually 5x more potent when given parentally

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35
Q

What is the conversion of morphine to fentanyl patch?

A

Total daily dose of morphine PO (mg) divided by 2 = Fentanyl patch dose (mcg/h)

Morphine 50mg PO = Fentanyl 25mcg/h

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36
Q

How do you calculate the breakthrough dosage for opioids?

A

Prescribe 10% of the Total daily dose (regular and PRNs), q1h

Example:
- When using fentanyl, calculate 10% of the breakthrough dose for morphine SQ q1h, or multiply by 2 for morphine PO q1h
- Fentanyl 25mcg/h = 50mg PO morphine total daily dose = morphine 5mg PO q1h breakthrough; or morphine 2.5mg SQ q1h

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37
Q

How do you calculate the dosage for long-acting opioids?

A

Add up the total daily opioid dose, including regular and breakthrough; then divide by 2

Prescribe long acting form q12h

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38
Q

What are the equivalent doses for Steroids, using 5mg prednisone; for:

  1. Dexamethasone
  2. Triamcinolone (Kenalog)
  3. Methylpred/Solumedrol
  4. Prednisone/Prednisolone
  5. Hydrocortisone
  6. Cortisone
A

Dex = 0.75 mg
Triamcinolone = 4mg
Methylprednisolone = 4mg
Prednisone = 5mg
Hydrocortisone = 20mg
Cortisone = 25mg

39
Q

List all the different types of side effects of steroids/oral prednisone

A
  • a. Metabolic – Hyperlipidemia, Hypertension, edema
  • b. Endocrine – Adrenal suppression, Hyperglycemia
  • c. Ocular – Cataracts, steroid-induced glaucoma
  • d. Gastrointestinal – Weight gain, increased appetite
  • e. Musculoskeletal – Osteoporosis, increased fracture risk, AVN of the hip
  • f. Dermatologic – Delayed wound healing, skin fragility
  • g. Other: Insomnia, increased infectious risk
40
Q

Discuss the mechanism of action, coverage, and examples of the following antibiotics:
1. Penicillins
2. Cephalosporins
3. Vancomycin
4. Macrolides
5. Clindamycin
6. Aminoglycoside
7. TMP/SMX
8. Quinolones
9. Metronidazole
10. Carbapenems

A
  1. Penicillins
    - Coverage: Staph/Strep
    - Beta lactams
    - Inhibits penicillin binding protein and prevents cross linking of peptidoglycans strands of cell wall - inhibits cell wall formation
    - Bactericidal
    - 20% resistance (due to heavy use)
  2. Cephalosporins
    - Beta lactams
    - Same MOA as penicillin
    - 15% cross reactivity to penicillin
  3. Vancomycin
    - Glycopeptide
    - Same MOA as penicillin
    - Blocks peptidoglycan polymerization
  4. Macrolides
    - Coverage: Strep, Pertussis, H. flu
    - Binds 50S subunit and prevents translocation / protein synthesis
    - Bacteriostatic, 20-40% resistance
    - Erythromycin, Clarithromycin, Azithromycin
  5. Lincomycin antibiotics (e.g. Clindamycin)
    - Coverage: Staph, Strep, anaerobes
    - Binds 50S ribosomal subunit and prevents translocation / protein synthesis
    - Bacteriostatic, 30% resistance
  6. Aminoglycoside
    - Coverage: anaerobic gram-negative bacilli
    - MOA: Binds 30S ribosomal subunit and prevents protein synthesis
    - Bacteriostatic
    - Gentmicin, Tobramycin, Streptomycin, Amikacin, Neomycin
  7. TMP/SMX
    - TMP inhibits DHFR (Dihydrofolate reductase) - catalyzes the reduction of dihydrofolate to tetrahydrofolate (THF). THF is needed for the action of folate-dependent enzymes and is thus essential for DNA synthesis and methylation.
    - SMX competes with PABA (Para-aminobenzoic acid) for incorporation into folic acid
  8. Quinolones
    - Coverage: Pseudomonas, broad spectrum gram positive and negative
    - MOA: Inhibits DNA gyrase and topoisomerase to prevent DNA synthesis
    - Bacteriocidal, 1% resistance
    - e.g. Ciprofloxacin (excellent pseudomonas and general gram +, no strep coverage); Other quinolones have better broad spectrum gram + coverage
  9. Metronidazole
    - Coverage: obligate anaerobes
    - MOA: Enters intracellular then activation leads to release of metabolites (free radicals) that damage DNA
    - Bacteriocidal
  10. Carbapenems
    - Beta lactam, similar MOA to penicillins
    - Imipenem, Meropenem
41
Q

What are the contraindications to systemic Ciprofloxacin and why?
When is systemic Cipro indicated in kids?

A

CONTRAINDICATIONS:
1. Allergy and hypersensitivity
2. History of tendon rupture associated with quinolone antibiotic
3. Children under 18 years old (theoretical incidence of tendinitis, tendon rupture, arthropathy)
4. Pregnancy (Class C)
5. Long QT
6. May exacerbate Myasthenia gravis and Eaton-Lambert

SPECIAL INDICATIONS IN CHILDREN:
1. Anthrax
2. Plague
3. Uncomplicated UTI (not first line)
4. Relative infections with pseudomonas

42
Q

What are 4 antibiotics that cross the blood-brain barrier?

A
  1. Flagyl
  2. Ceftriaxone
  3. Ampicillin
  4. Chloramphenicol
43
Q

Describe the mechanism of action of the following antifungal medications:
1. Nystatin
2. Fluconazole
3. Amphotericin B

A

NYSTATIN:
- Binds to ergosterol found in fungal cell membranes
- Causes formation of pores in the membrane
- Leads to leakage of intracellular contents –> cell death

FLUCONAZOLE:
- Inhibits ergosterol synthesis causing cell membrane breakdown, leakage of intracellular contents and cell death

AMPHOTERICIN B:
- Similar to nystatin

44
Q

What are 4 causes of antimicrobial resistance?

A
  1. Inactivation of drug (e.g. by beta lactamases)
  2. Alteration of target site
  3. Alteration of metabolic pathway
  4. Reduced drug accumulation (permeability into tissues)
45
Q

Name 4 augmented penicillins

A
  1. Amoxicillin- Clavulanate
  2. Ticarcillin-Clavulanate
  3. Ampicillin-Sulbactam
  4. Piperacillin-Tazobactam
46
Q

Name 4 antibiotics which can cross the blood-brain barrier

A
  1. Ampicillin
  2. Ceftriaxone
  3. Ceftazidime
  4. Flagyl
  5. Chloramphenicol
  6. Fluoroquinolones
  7. Septra
47
Q

What is the difference between ester and amide anesthetics?

A
  • Amides are biotransformed in the liver
  • Esters are hydrolyzed in the bloodstream by plasma esterases (or can be in liver as well)
48
Q

What are ester anesthetics? List 4 examples

A
  • Metabolized by plasma and liver cholinesterase
  • Higher pKa (acid dissociation) compared to amides, therefore low local uptake
  • No uncommon to be allergic to these compounds

EXAMPLES:
1. Cocaine
2. Procaine
3. Tetracaine
4. Benzocaine

One “i” in the name

49
Q

What are amide anesthetics? List 6 examples

A
  • Metabolized by liver dealkylation
  • Rare allergies to these drugs
  1. Lidocaine (Xylocaine)
  2. Bupivacaine
  3. Mepivacaine
  4. Prilocaine
  5. Ropivacaine

Two “i” in the name; Amide has more “i” than ester”

50
Q

What is the mechanism of action of lidocaine?

A
  • Inhibits sodium influx through voltage-gated Na channels in the neuronal cell membrane, preventing formation of an action potential
51
Q

What is the mechanism of action of cocaine?

A
  • Vasoconstriction effect: Through inhibition of norepinephrine, dobutamine, and serotonin reuptake; which causes catecholamine side effects
  • Local anesthetic effect: Through blockage of sodium channels
52
Q

What is the side effect of Prilocaine?

A
  • Methemoglobinemia with doses > 500- 600mg (condition in which there is low amount of hemoglobin available for oxygen transport; conversion of some or all of the four iron species from the reduced ferrous (Fe2+) state to the oxidized ferric (Fe3+) state)
53
Q

What is the ingredient in hurricaine spray?

A
  • 20% Benzocaine in polyethylene glycol base
  • Can cause methemoglobinemia (Fe2+ to Fe3+) at doses > 500mg
54
Q

What is the pharmacologic action of mucolytics (N-acetylcysteine)

A
  • Depolymerizes mucopolysaccharides, making them more soluble
55
Q

What is the pharmacologic action of antihistamines?

A
  • Reversible inhibition of histamine receptors
  • H1-receptor blockers
56
Q

What are the contents of EMLA? What does it stand for?

A

EMLA = Eutectic mixture of local anesthetic

Emulsified 2.5% prilocaine and 2.5% lidocaine

Reliability increases effect if applied for > 1 hour

57
Q

What is Ametop?

A

4% Tetrocaine gel

Best if applied for > 30-45 minutes

58
Q

What are the maximum doses, onset, and duration of action of various local anesthetics?

A

4% Cocaine:
- Max dose: 1mg/kg

0.5% Bupivacaine:
- Max dose: 2mg/kg
- Onset: 5-10 minutes
- Duration 3-8 hours

0.5% Bupivacaine + Epi:
- Max dose: 3mg/kg
- Onset 5-10 min
- Duration: 3-8 hours

1% Lidocaine:
- Max dose: 4-5mg/kg
- Onset: 1-5min
- Duration: 30-90 min

1% Lidocaine + Epi:
- Max dose: 6-7mg/kg
- Onset: 1-5min
- Duration: 60-180min

1-2-3-4-5-6-7 Max doses

59
Q

What does % of anesthetic solution mean?

A

1% = 1g / 100mL = 10mg/mL

0.5% = 5mg/mL
1% = 10mg/mL
2% = 20mg/mL

60
Q

How many mg/mL in various epinephrine concentrations?

A

1:1000 (1g/1000mL) = 1mg/mL
1:10000 (1g/10000mL) = 1mg/10mL = 0.1mg/mL
1:100000 (1g/100000mL) = 1mg/100mL = 0.01mg/mL
1:200000 (1g/200000mL) = 1mg/200mL) = 0.01mg/2mL = 0.005mg/mL

61
Q

Pediatric dosing of local anesthesia for lidocaine

A

1.8cc of 2% lidocaine per 20lbs

4mg/kg maximum

62
Q

What are the signs of lidocaine toxicity?

A
  1. CNS stimulation (3mcg/cc)
    - Light-headedness
    - Tinnitus
    - Circumoral numbness
    - Metallic taste
    - Double vision
    - Slurred Speech
    - Anxiety
    - Tremors
  2. CNS depression (5mcg/cc)
    - Seizures
    - Respiratory depression/arrest
    - Coma
  3. Cardiovascular excitation, then depression (8mcg/cc)
    - Palpitations, tachycardia
    - Bradycardia, ventricular fibrillation, hypotension, asystole

2nd number is rate of absorption?

63
Q

What are the signs and symptoms of lidocaine toxicity?

A
  1. Circumoral numbness
  2. Facial tingling
  3. Restlessness
  4. Vertigo
  5. Tinnitus
  6. Slurred speech
  7. Tonic-clonic seizures
64
Q

Describe the management of Lidocaine Toxicity

A
  1. Stop procedure
  2. ABCs
  3. Place IVs + O2
  4. Fluids/vasopressors as needed
  5. Benzos (prevent seizures), Succinylcholine for seizures
  6. Lipid emulsion therapy (intralipid)
  7. Management of cardiac arrhythmias - initiate ACLS protocol as indicated
65
Q

Why does local infection decrease efficacy of local anesthetics?

A
  • Drug must be non-ionized to diffuse through lipid cell membranes
  • Infected tissues are more acidic (lower pH) –> increase ionization of drug –> reduces local drug diffusibility and concentration
66
Q

What are the side effects of corticosteroids?

A

“A Fucking CCUSSHINGOID Eh?”

A: Acne
F: Fluid imbalance
C: Cushinoid habitus/central obesity
C: Cataracts
U: Ulcers (Peptic Ulcer disease)
S: Skin - striae, tinning, bruising
S: Sleep and behaviour/mood disturbances
H: Hirsutism
I: Immunosuppression/infections
N: Necrosis (Avascular necrosis of the hip)
G: Glucosuria
O: Osteoporosis
I: Increased BP (hypertension)
D: Diabetes control issues (Hyperglycemia)
E: Electrolyte disturbances

67
Q

List the contraindications to corticosteroid treatment

A

The BAD Guy dOPPPes

T: TB (known latent TB)
B: Brittle diabetic
A: Allergy to corticosteroid (rare but reported, due to a component in the formulation)
D: Diverticulitis
G: Glaucoma
O: Osteoporosis
P: Poorly controlled hypertension
P: Peptic ulcer disease
P: Psychosis

68
Q

List 6 types of topical decongestants

A
  1. Ephedrine
  2. Epinephrine
  3. Phenylephrine
  4. Oxymetazoline
  5. Xylometazoline
  6. Cocaine
69
Q

List 2 types of systemic decongestants

A
  1. Phenylephrine
  2. Pseudoephedrine
70
Q

What receptors do the following decongestants target?

  1. Epinephrine
  2. Phenylephrine
  3. Oxymetazoline
  4. Ephedrine
A
  • Alpha: Vasoconstriction, decreased smooth muscle activity
  • Beta: Cardiac effects
  1. Epinephrine
    - Alpha 1, 2
    - Beta 1, 2, 3
  2. Phenylephrine
    - Alpha 1-adrenergic receptor agonist
  3. Oxymetazoline
    - Alpha 1
    - Partial alpha 2
  4. Ephedrine
    - Alpha and beta receptors
71
Q

Where are the emetic centres of the brain and what receptors are present in those locations?

List 5 classes of antiemetics and some examples

A

Emetic Centres:
1. Medulla (reticular formation) - ACh and Histamine receptors present
2. Chemoreceptor trigger (CRT) zone in 4th ventricle - Dopamine receptors present

Classes of Antiemetics:
1. Antidopaminergic: Metoclopramide, phenothiazines (chlorpromazine)
2. Anticholinergic: Scopolamine
3. 5HT3 receptor antagonist (found on Vagus in CRT zone): Ondansetron
4. Steroids: Dexamethasone
5. Antihistamines (H1): Diphenhydramine (Benadryl), Dimenhydrinate (Gravol)

72
Q

What are expectorants? Provide some examples

A

Expectorants:
1. Thins/dries secretions
2. Increase transport

Examples:
1. Antimuscarinics: Scopolamine, Glycopyrrolate, Atropine
- Scopolamine and Glyco are potent antisialagogues, stimulates secretions in respiratory tract
- Atropine mostly vagolytic (increases sympathetics), produces greatest increase in HR

  1. Iodide salts
  2. Ammonium salts
  3. Guaifenesin (helps eliminate sputum from respiratory tract)
73
Q

Describe the mechanism of action of botulinum toxin (Botox).
How long until the onset of paralysis from injection time, and length of overall effect?
What is the toxic dose?

A

MOA:
- Binds to receptors and is internalized at the pre-synaptic terminal
- Causes irreversible blockage of neuromuscular junction by cleaving SNARE proteins (SNAP-25) responsible for acetylcholine containing vesicle release in the presynaptic neuron
- Leads to flaccid paralysis
- Wears off through regeneration of fresh synaptic terminals

1 unit = Lethal dose in 50% of mice

  • Effect in 48-72 hours (Presynaptic vessels depleted)
  • 90 days for affect to wear off (although new axons begin sprouting at 28 days)
  • Toxic dose = 2700-3000 units
74
Q

How many botox exotoxins are there? Which ones are the most clinically useful?

A

7 (A to G) exotoxins
A is the longest lasting

Active form has a heavy chain for binding, and a light chain for intracellular toxicity

75
Q

List 9 differential functions for botox in the head and neck
`

A
  1. Facial dystonias (e.g. blepharospasm, torticollis)
  2. Laryngeal/pharyngeal disorders
  3. Forehead rhytids
  4. Ptyalism (drooling)/sialorrhea
  5. Frey’s syndrome
  6. Migraines
  7. Palatal myoclonus
  8. Facial palsy - weakn the normal side for symmetry
  9. Post laryngectomy / radiotherapy speech disorders
76
Q

What are 6 contraindications to botox?

A
  1. Prior allergic reaction
  2. Pregnancy (category C) or breastfeeding
  3. Injection into areas of infection or inflammation
  4. Myasthenia Gravis, Eaton Lambert syndrome, motor neuron disease
  5. Medications that decreased NM transmission (can have botulism like effects at high doses) - Aminoglycoside, Penicillamine, Quinine, Calcium channel blockers
  6. Jehovah’s witness - albumin in solution

A PIMP:
Allergy
Pregnancy
Infection
Myasthetia gravis
Penicillin

77
Q

What are common medications used in Rhinology?

A
  1. Phenylephrine - alpha adrenergic agonist
    - Contraindicated in HTN, CAD, Glaucoma
  2. Xylometazoline/Oxymetazoline - direct alpha adrenergic
  3. Topical Epinephrine - intraoperatively for vasoconstriction
  4. Ipratropium - anticholinergic - used in vasomotor rhinitis
    - Contraindicated in narrow angle glaucoma
78
Q

Describe the nomenclature of various monoclonal antibodies

A

For each drug name ending in X is derived from:

  1. -omab = mouse
  2. -ximab = chimeric (multiple genotypes)
  3. -xumab = humanized
  4. -umab = human
79
Q

Regarding malignant hyperthermia, discuss:
1. Epidemiology
2. Inheritance
3. Pathophysiology
4. Etiology
5. Presentation
6. Investigations
7. Treatment
8. Complications

A

EPIDEMIOLOGY:
1. 1 in 15000 children (more common in children)
2. 1 in 50-100000 adults

INHERITANCE:
- Autosomal dominant
- Reduced penetrance
- Variable expressivity
- 30+ mutations

ETIOLOGY:
- Abnormal RYANODINE RECEPTOR causes buildup of Calcium in skeletal muscle sarcoplasmic reticulum; then a trigger causes sudden massive Ca release and hypermetabolic state
- Associated with halogenated inhalational anesthetics (iso/des/sevoflurane)
- Depolarizing muscle relaxants (Succinylcholine)

PATHOPHYSIOLOGY:
1. Buildup of calcium in skeletal muscle SR
2. Trigger causes sudden release of calcium and increase in calcium in muscle sarcoplasm
3. Further exacerbated by decreased reuptake of calcium from sarcoplasmic reticulum
4. Causes increase in muscle contraction/spasm and breakdown

PRESENTATION:
1. Fever
2. SNS activation: Tachycardia, Tachypnea
3. Cyanosis
4. Rapid O2 consumption
5. Hypercarbia (rise in EtCO2 is first sign you will see on monitor)
6. Rhabdomyolysis
7. Metabolic (lactic) and respiratory (CO2) acidosis
8. Hyperkalemia (secondary to acidosis)
9. DIC
10. Multiorgan failure (secondary to myoglobulinemia, metabolic exhaustion)

INVESTIGATIONS:
1. Immediate labs: Urine myoglobin, LDH, CK/CPK (Creatinine Phosphokinase), ALP
2. Muscle biopsy
3. CHCT (Caffeine Halothane Contracture Test) - using muscle biopsy & in vitro MH challenge - only offered at 5 hospitals in north america
4. Genetic testing

TREATMENT:
1. ABCs
2. Discontinuation of precipitating agent
3. Dantrolene 1mg/kg slow IV push up to 10mg/kg (stabilizes and reverses Calcium release)
4. Cooling
5. 100% oxygen
6. Cardiovascular support

COMPLICATIONS:
1. Brain damage.
2. Cardiac arrest.
3. Death.
4. Heart failure.
5. Internal bleeding.
6. Kidney failure.
7. Pulmonary edema.
8. Skeletal muscle degeneration (like rhabdo)

80
Q

Briefly describe the plain radiographic views of the head

A
  1. Lateral
  2. Towne’s = looking down, 30% from central ray, AP film (good for skull, petrous apex, mastoid, foramen magnum)
  3. Caldwell = looking down, 25-30 degrees (skull) from central ray, 15 degrees (sinuses) from the central ray, PA film (good for frontal sinus)
  4. Waters = Head tipped back, 45 degrees from central ray, PA film (Good for maxillary sinus)
  5. Submentovertex (basal or bucket handle view) = Maximal extension, AP film, good for skull base, sphenoid, and zygoma
81
Q

What are two absolute contraindications to IV iodinated contrast for CT?

A
  1. Previous adverse reaction
  2. Severe renal insufficiency (especially in multiple myeloma, DM, nephrotoxic meds)

Iodide absorbs x-rays which results in less x-rays on the sensor –> appears brighter
- 2-3x increase the risk of thyroid dysfunction
- Iatrogenic hypothyroid - wolf chaikoff effect (reduction in thyroid hormone levels caused by ingestion of a large amount of iodine)

82
Q

What are 8 relative contraindications to IV iodinated contrast for CT?

A
  1. Advanced age
  2. Asthma
  3. Atopy
  4. Beta-blockers
  5. Cardiac disease
  6. Dehydration
  7. Expected thyroid radio-ablation (within 6 weeks)
  8. Renal failure

ABCDEF

83
Q

What are precautions for patients on metformin receiving IV contrast?

A
  1. Causes AKI with lactic acidosis
  2. Stop metformin for 48 hours post-CT
  3. Check renal funtion prior to resumption
84
Q

List 5 general advantages of MRI

List 6 general disadvantages of MRI

A

ADVANTAGES:
1. Better soft tissue definition than CT
2. Multiplanar capability
3. Clear delineation of arteries, veins, major cranial nerves
4. Absence of ionizing radiation
5. Absence of beam-hardening artifacts from dental implants

DISADVANTAGES:
1. Prolonged data collection times
2. Higher sensitivity to patient motion
3. Contraindications: pacemakers, certain implants, metallic foreign bodies
4. Inferior bony detail
5. Claustrophobia may prohibit examination
6. Higher equipment cost and exam cost

85
Q

List 5 absolute and 4 relative contraindications to MRI

A

ABSOLUTE:
1. Pacermakers (most common) and pacer-wires
2. Swan-Gantz catheter
3. Cochlear or brainstem implants (older models not compatible with MRI)
4. Ocular (do x-ray) or metallic foreign bodies
5. Certain aneurysm clips

RELATIVE:
1. Cardiac valve (relative, usually safe)
2. Vascular clips (relative, usually safe)
3. Orthopedic prosthesis (relative, usually safe)
4. Claustrophobia (relative, premedicate)

86
Q

List 7 types of absorbable sutures, their strength duration, and absorption duration

A
  1. Catgut: Strength 4-10 days, Absorption 10 days
  2. Chromic catgut: Strength 10-14 days, absorption 20 days
  3. Dex/Polyglycolic: Strength 14-21 days, absorption 60-90 days
  4. Vicryl/POlyglactic: Strength 20-30 days, absorption 60-90 days
  5. PDS/Polydiaxone: Strength 40-60 days, absorption 180 days
  6. Maxon/polyglyconate: Strength 40-60 days; absorption 180-210 days
  7. Monocryl/polyglecaprone
87
Q

List 5 types of non-absorbable sutures and some of their features

A
  1. Silk - braided, high tissue reactivity
  2. Polyester (Dacron, ethibond) - braided (mersilene) but usually coated
  3. Nylon - braided or monofilament, will degrade in about 2 years
  4. Polypropylene (prolene, surgilene) - monofilament, does not lose tensile strength
  5. Steel
88
Q

Describe the 4 phases of wound healing

A

A. COAGULATION
- Hemorrhage with exposure of platelets
- Formation of platelet plug and degranulation
- Release of mediators that cause initial vasoconstriction (TXA2), vasodilation (5-HT, Histamine), epithelial proliferation (EGF, TGF) and chemotaxis (PDGF)

B. INFLAMMATION
- Infiltration of leukocytes which scavenge cellular debris, foreign bodies, and other by-products
- PMNs in first 48 hours
- Transition to monocyte/macrophages predominance by days 3-4

C. PROLIFERATION/FIBROPLASIA
- Fibroblasts attracted to wound as of day 2 (max at day 15)
- Start extensive collagen III synthesis
- Reepithelialization by basal cells at 15µm/h (EGF)
- New capillary growth into matrix via angiogenesis (VEGF)

D. REMODELLING
- Inflammation subsides, angiogenesis decreases, fibroplasia slows
- Type III collagen synthesized early in the repair process –> replaced by Type I collagen in this phase until the normal skin ratio of 4:1 (Type I to III collagen) is realized
- By 3 months scar achieves 80% of original strength - never reaches 100%

89
Q

What are the effects of radiation on tissue healing? List the acute, intermediate, and late effects.

A

ACUTE:
- Severity related to the radiation fraction
- Reduction in proliferation of fibroblasts, myofibroblasts, endothelial cells

INTERMEDIATE:
- 3-6 months after radiation
- Diminished endothelial & connective tissue proliferation

LATE:
- Related to total radiation dosage, hyalinization of collagen, rupture of elastic fibrils, fibrinous exudate deposition, induction of atypical fibroblasts, hyalinization & sclerosis of blood vessels (obliterative endarteritis)
- Narrowed vessel lumen = decreased O2 delivery to tissues

90
Q

What are 4 effects of steroids on wound healing?

A
  1. Decreased leukocyte and monocyte migration and phagocytosis
  2. Inhibition of keratinocyte & fibroblast mitosis (slows reepithelialization)
  3. Vasoconstriction, results in decreased oxygen and nutrient delivery
  4. Decreased collagen formation
91
Q

What are the factors in nutrition that most influence wound healing?

A
  1. Vitamin A deficiency - impaired collagen synthesis and epithelialization
  2. Vitamin C deficiency - prevents hydroxylation of proline & lysine for production of collagen
  3. Zinc deficiency slows wound healing by preventing cell proliferation
  4. Magnesium
  5. Arginine

CAZAM

92
Q

Discuss keloid and hypertrophic scarring

A
  • Most common in dark skinned individuals
  • Overgrowth of dense fibrous scar
  • Hypertrophy = within the border of original skin injury, generally < 4mm above the skin
  • Keloid = raised >4mm above skin and grow beyond the original incision
  • Increased collagen, decreased fibroblasts
  • Grow over time, most common places - earlobes, shoulder, cheeks, and chest
  • Never completely disappear to leave skin with normal texture
  • 1/3 of cases flatten and soften
  • Can develop anywhere on the body (appears histologically the same as normal scar tissue; major decrease in size in 10 years)
93
Q

What are six treatment options for keloids?

A

SCLERI

S: Silicone gel sheeting/pressure
C: Cryotherapy
L: Laser therapy
E: Elastic compression
R: Radiotherapy
I: Intralesional steroids

94
Q

Your post-op patient in PACU is having an MI.
What is your first move?
When is the most common time for peri-operative MI?
What are the risk factors for post-op MI?

A

Most common time = POD3

Suspected MI - first move = Give 100% O2 (most common cause of peri-op MI is hypoxia)

RISK FACTORS:
1. CHF (S3)
2. MI in last 6 months
3. >5 PVCs / min
4. Abnormal ECG rhythm or PACs
5. Age > 70 years old
6. Emergency OR

General OTOHNS (9 decks)

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