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A1 > A3 - Pharm/Med > Flashcards

A3 - Pharm/Med Flashcards

1
Q

If calling EMT, need to consider who they are

A

EMT-P
Paramedics - 3 year training, fully prepared to do life support.

Others are EMT-B, EMT-I, EMT-A (basic, to advance, top is paramedic).

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2
Q

If pt complains of severe SOB and chest pain, immediately

A

engage nasal canula with 02, flow rate 1-5. Know med hx. Know the contents of your rescue drugs, know how to use them. Own the liability.

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3
Q

95% Sp02, after a few minutes, you bump to

A

99%.

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4
Q

—- for MI

A

aspirin

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5
Q

Contraindications for aspirin for MI:

A

Hx of peptic ulcers, allergy (only true contraindication)

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6
Q

Viagra

A

No nitro - do not assume women don’t take this - they can take it for pulmonary HTN

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7
Q

Contraindication for nitroglycerin

A

If BP plumets from starting point (hypotension), vasodilators (phosphodiesterase-5 inhibitors).

Know that <90SBP is not a good standard - BP is relative to starting BP.

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8
Q

Contraindication for nitroglycerin

A

If BP plumets from starting point (hypotension), vasodilators (phosphodiesterase-5 inhibitors).

Know that <90SBP is not a good standard - BP is relative to starting BP.

Significant bradycardia (under 50), tachycardia over 100,
right ventricular MI, severe aortic stenosis.
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9
Q

Only drug that improves survivability of MI

A

Aspirin - NOT nitro - exception is vasospastic angina, which is incredibly rare.

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10
Q

With MI, oxygen really helps if

A

hypoxic

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11
Q

With MI, oxygen really helps if

A

hypoxic

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12
Q

Drop in BP from baseline to contraindicate Nitro

A

over 25%

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13
Q

If bradycardia (HR under 50) or if tachycardia (HR over 100) do not administer

A

nitro

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14
Q

If you give nitro, you need to have —– in order to maintain pressure if needed.

A

IV bore access

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15
Q

Right ventricular MI - why no nitro?

A

This MI is highly dependent on venous pressure to maintain flow. If you vasodilate, you can push the patient over and kill them.

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16
Q

How to tell if Right Ventricular MI

A

Either clinical signs (don’t know this) or RV infarction

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17
Q

Generally, never reduce SBP below —— for non HTN pts

A

110 mmHg

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18
Q

About – mm for cemented, — mm for screw retained

A

8, 5

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19
Q

Always ask about

A

headaches

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20
Q

— mm from IAN/mental foramen

A

2

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21
Q

Literature states that you need—- mm of facial bone - lingual needs — mm

A

2, 1

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22
Q

Thngs you need in emergency kits

A 
 Pt Assessment Equipment  CPR Equipment
 Epi
 Ntg
O2
 Albuterol
ASA
 Oral Glucose
 Benadryl
 Lorazepam (Ativan) (this is less necessary and is only OK if you are comfortable with using it)
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23
Q

If you have benzos in your emergency kit, you need to be able to

A

ventilate (they can lose airway). Know the risks and own it for each item.

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24
Q

Use for epi in emergency kits

A

anaphylaxis

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25
Q

Use fro Ntg in emergency kits

A

Iatrogenic HTN crisis

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26
Q

Use for O2 in emergency kits

A

hypoxia

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27
Q

Use for albuterol in emergency kits

A

reactive airway

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28
Q

Use for ASA (aspirin) in emergency kits

A

acute MI

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29
Q

Use for Oral Glucose in emergency kits

A

hypoglycemia (conscious)

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30
Q

Use for benadryl in emergency kits

A

Allergic Rx (oral or IV/IM)

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31
Q

Use for lorazepam/ativan in emergency kits

A

seizure

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32
Q

Blood flow to heart during

A

diastole - otherwise pressure is too high.

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33
Q

Inotropy

A

 Strength of contraction

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34
Q

 Chronotropy

A

 Rate of contraction (Heart Rate)

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35
Q

Dromotropy

A

 Electrical impulse conduction speed

 (magnitude of delay in the AV Node)

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36
Q

Bathmotropy

A

 Sensitivity to being depolarized (threshold of excitation)

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37
Q

 Lusitropy

A

 Rate of myocardial relaxation

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38
Q

 SV is affected by

A

Preload, Contractility, & Afterload

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39
Q

 CO =

A

HR x (Preload, Contractility, Afterload)

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40
Q

 Stroke volume of the heart —- as the volume of blood in the ventricles (before contraction) increases.

A

increases

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41
Q

Ejection fraction

A

% of blood ejected from a contraction

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42
Q

4-6 implants on maxilla - (6 for brachiocephalic pts)

A

in 7, 10, 13, 4 positions

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43
Q

MAP =

A

CO*SVR (Cardiac output * systemic vascular resistance

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44
Q

Systemic Vascular Resistance

A

Afterload

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45
Q

MAP =

A

1/3Sys + 2/3Dias

Dia+ 1/3 PP (pulse pressure) - PP = Sys-Dia

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46
Q

General hypotension management

A

MAP>65

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47
Q

Under cardiogenic shock, you can tolerate MAP —

A

60

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48
Q

Central venous presure

A

IVC and SVC pressure in thoracic cavity - effectively preload. About 5mmHg

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49
Q

CPP

A

Cerebral perfusion pressure

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50
Q

CPP =

A

MAP – ICP (Intracranial Pressure)

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51
Q

 CBF =

A

Cerebral blood flow

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52
Q

CBF =

A

CPP/CVR (cerebral vascular resistance)

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53
Q

 CVR has an —- range

A

autoregulatory

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54
Q

CO2 is a cerebral —— (via pH)

A

vasodilator

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55
Q

Coronary Perfusion Pressure

A

The other CPP

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56
Q

Left ventricular coronary perfusion is intermittent and only occurs during —–

A

diastole

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57
Q

 In contrast, right ventricular blood flow occurs during

A

both systole and diastole

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58
Q

Coronary perfusion pressure CPP =

A

DAP – EDRAP
 (DAP) Diastolic Aortic Pressure
 (EDRAP) End Diastolic Right Atrial Pressure

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59
Q

 Left V entricular CPP 

A

CPP = DAP – EDLVP

 (EDLVP) End Diastolic Left Ventricular Pressure

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60
Q

HTN crisis symptoms

A 
 Headache w/  Confusion
 Anxious/agitated  Nausea/V omiting
 Tinnitus
 Blurred vision
 Seizure
 CP, SOB, ACS symptoms  CV A symptoms
 Renal Failure
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61
Q

MAP – tells you how the

A

body & brain are being perfused  This should be your initial & primary focus

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62
Q

 Diastolic Pressure – tells you

A

how the heart is being perfused  Low diastolic pressures should be concerning

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63
Q

Systolic Pressure –

A

Easiest to obtain and interpret, but least relevant  High systolic spikes can be a risk for hemorrhagic & vasospastic vascular
injuries

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64
Q

 Extreme Hypertension without symptoms is

A

not a medical emergency. But it can become one.

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65
Q

FiO2 -

A

fraction of inspiratory oxygen.

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66
Q

PEEP:

A

What you breath against when you exhale.

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67
Q

Atelectasis:

A

airway collapses.

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68
Q

Alveolar recruitment =

A

recovering from atelectasis (airway collapse.

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69
Q

A-a gradiant -

A

partial pressure of o2 in alveolar sac vs arterial blood. Takeaway, if pulse ox is different from oxygen applied. This could be a massive amount of causes.

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70
Q

Lung compliance -

A

how well they can open up vs how stiff their alveolar sacs are.

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71
Q

Cold finger - can skew

A

pulse ox.

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72
Q

 Infinitely ↑ V/Q =

A

dead space. Infinitely ↓ V/Q = shunting

V/Q = ventilation/perfusion ratio

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73
Q

Diabetic ketoacidosis:

A

Hyperventilating to blow off as much CO2 as possible to remove protons. If you ventilate a patient, you want to go to a targeted end tidal CO2.

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74
Q

Respiratory Acidosis:

A

Drop in pH, rise in pCO2, rise in HCO3 (but mostly normal).

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75
Q

Respiratory Acidosis: causes

A

Respiratory depression (due to drugs, CVA, seizure, etc), COPD, asthma

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76
Q

Respiratory Alkalosis:

A

Increase in pH, decrease in pCO2, decrease in HCO3 (mostly normal)

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77
Q

Respiratory Alkalosis: causes

A

hyperventilation (panic, pain)

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78
Q

Metabolic acidosis:

A

Decrease pH, normal decrease in pCo2, decrease in HCO3

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79
Q

Metabolic acidosis: causes

A

Diabetic ketoacidosis, shock, kidney failure

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80
Q

Metabolic alkalosis

A

increase in pH, normal increase in pCO2, increase in pHCO3

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81
Q

Metabolic alkalosis causes

A

bicarbonate overdose, prolonged vomiting.

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82
Q

Adrenergic

A

 Activated by Catecholamines  Epinephrine
 Norepinephrine  Dopamine
 Levonordefrin
 Postsynaptic Junction (Sympathetic)

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83
Q

Cholinergic

A

 Activated by Acetylcholine (ACh)  2 main types
 Nicotinic (binds Nicotine)  Presynaptic Junction
(Sympathetic & Parasympathetic)  Brain
 Skeletal muscle (Somatic)
 M uscarinic (binds M uscarine)
 Postsynaptic Junction (Parasympathetic)
 Brain

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84
Q

alpha 1 main function

A

Vasoconstriction in the skin, GI, Kidneys

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85
Q

Activating alpha 1 results in

A

↑ SVR

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86
Q

Alpha 1 agonist

A

Decongestants (Phenylephrine) Levonordefrin (including epi, norepi, dopa)

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87
Q

Alpha 1 antagonists

A

Labetalol Carvedilol Phentolamine

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88
Q

alpha 2 main function

A

Inhibits the release of norepinephrine (mild negative feedback of 1) Mildsedation

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89
Q

Alpha 2 activation results in

A

↓ SVR

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90
Q

Alpha 2 agonist

A

Clonidine

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91
Q

Alpha 2 antagonist

A

Phentolamine

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92
Q

Beta 1 main function

A

↑ HR, ↑ SV, (↑ all 5 properties of the heart) ↑ Renin secretion

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93
Q

Beta 1 activation results in

A

↑ CO ↑ BP

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94
Q

Beta 1 agonist

A

Isoproterenol Dobutamine

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95
Q

Beta 1 antagonists

A

Selective & Non-selective Beta Blockers

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96
Q

Beta 2 main function

A

Bronchodilation

Vasodilation in Skeletal Muscles & Cor Art

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97
Q

Beta 2 activation results in

A

↑ Airway ↓ BP

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98
Q

Beta 2 agonist

A

Albuterol Terbutaline

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99
Q

Beta 2 antagonist

A

Non-Selective Beta Blockers

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100
Q

β3 main function

A

Lipolysis Relax Bladder

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101
Q

The Main Cardiovascular & Pulmonary effects are mediate by the —-

 Excitation (— Vagal tone)
 Inhibition (— Vagal tone)

A

Vagus Nerve, CN X

↑

↓

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102
Q

Muscarinic cholinergic receptors

A

parasymp

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103
Q

Muscarinic cholinergic receptors

Agonist (Cholinergic)

A

 Pilocarpine
 Indirect (Cholinesterase Inhibitors)
 *stigmines (ex. Neostigmine)

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104
Q

Muscarinic cholinergic receptors

Antagonists (Anticholinergic)

A

 Atropine

 Ipratropium Bromide  Diphenhydramine

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105
Q

Vagal tone is — tone. Know that it is a balance between —-. If you bring one up, it drops the other.

A

parasympathetic

symp and parasymp

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106
Q

Antagonists matter: The listed drugs combat against

A

parasymp drugs (decrease vagal tone, increase symp tone). You see the exact opposite with epi, airway drops.

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107
Q

Shock is defined as a state of

A

cellular and tissue hypoxia due to reduced oxygen delivery and/or increased oxygen consumption or inadequate oxygen utilization. This most commonly occurs when there is circulatory failure manifested as hypotension (ie, reduced tissue perfusion). Shock is initially reversible, but must be recognized and treated immediately to prevent progression to irreversible organ dysfunction. “Undifferentiated shock” refers to the situation where shock is recognized but the cause is unclear.

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108
Q

Spinal shock is different -

A

red warm, hypoperfusing.

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109
Q

Distributive shock

A

 Septic, Neurogenic, Anaphylaxis, Drug/Toxin, Endocrine

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110
Q

 Cardiogenic shock

A

 Cardiomyopathic, Arrythmic, Mechanical (valvular disfunction)

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111
Q

 Hypovolemic shock

A

 Hemorrhagic, Non-hemorrhagic (dehydration)

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112
Q

 Obstructive shock

A

 Pulmonary Vascular (PE, PH), Mechanical (Pericarditis, Tension Pneumo)

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113
Q

 Combined shock

A

 many patients with circulatory failure have a combination of more than one form of shock (multifactorial shock)

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114
Q

Steps of shock

When shock first occurs, body compensates by (step 1)

A

increased minute ventilation
increased CO
vasoconstriction

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115
Q

Steps of Shock

When compensatory mechs don’t work, (Step 2)

A

adrenal response
pituitary response
renin-angiotensin system activation

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116
Q

Compensated shock

A

Vasoconstriction maintains organ blood supply, perfusion decreases, skin becomes clammy. Vitals are stable.

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117
Q

Decompensated shock

A

BP decreasing. vascular tone decreases, organ dysfunction imminent.

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118
Q

Irreversible shock

A

profound hypotension

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119
Q

Tuberculin syringe

A

1cc

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120
Q

Diphenhydramine (benadryl) instructions

A

Dilute & give slow (< 25 mg/min)

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121
Q

Promethazine (phenergan) instructions

A

Dilute & give slow

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122
Q

D50 instructions

A

Large IV only, Never kids, NO INFILTRATION

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123
Q

D50 - 50% —- in water. Only approved for —- (subclavian, femoral). Acceptable in a peripheral line in an emergency. Extremely —-. If you inject into a small vein, it won’t cause problems. If you inject into a large vein, and you blow it, you get necrosis. Make sure that you have a patent IV, do a saline flush.

A

dextrose

central line

hypertonic

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124
Q

 D25 (Dextrose 25%) instructions

A

No infiltration

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125
Q

Ephedrine instructions

A

Dilute & give slow

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126
Q

Phenylephrine instructions

A

Dilute & give slow

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127
Q

Dopamine instructions

A

see manufacturer

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128
Q

Labetolol instructions

A

give slowly

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129
Q

Epi 1:1000 instructions

A

NEVER IV (IM, SC only) IM best

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130
Q

Labetalol for —-

A

htn crisis.

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131
Q

ACLS - epi for cardiac arrest is —– When anaphylaxis is in consideration, —— NEVER give this IV, always IM.

A

1: 10,000 1mg epi IV.
1: 1,000.

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132
Q

For adult, 0.3mg epi for anaphylactic (for 1:100,000 give 0.3 ml). Given IV, it caused a —- cardiac event.

A

vasospastic

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133
Q

Pediatric dose for epi is —-mg/kg.

A

0.01

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134
Q

O2 & N2O tanks should get a —- test and —- inspection every 5 years.

A

hydro

visual

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135
Q

 Only use designated

A

“O2 safe” washers & O-rings

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136
Q

 The 3 most common oxygen delivery systems “IF” a Pt is breathing adequately on their own

A

 NC (Nasal Cannula)
 Simple Mask
 Non-Rebreather Mask (w/ & s/) Reservoir Bag

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137
Q

Oxygen:  SpO2 —-is the target

A

94% - 99%

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138
Q

Nasal canula can give up to

A

6L/min

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139
Q

Mask can give up to

A

10L/min

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140
Q

Non rebreather mask can give up to

A

15 L/min

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141
Q

Hypoxic drive fear:

A

Don’t put oxygen on people with bad COPD because of this. These patients are no longer regulated by CO2 levels. your main drive to breath is CO2 and pH. COPD patients live at high CO2 levels, and the control centers in the brain stop paying attention to it. Only thing driving ventilation is hypoxic drive (partial pressure of oxygen). Low partial pressure of oxygen = desire to breath. If they are UNCONSCIOUS (conscious can breath on their own), and their O2 sat is 90% and you bump them to 100%, they will stop breathing. However, this is taking a truth the wrong way. You never withold O2 from hypoxic person. Instead, you need to be prepared to ventilate the patient (control their breathing for them w/positive pressure ventilation).

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142
Q

Self-inflating Bag Valve Mask BVM

A

Positive pressure breathing - if they aren’t breathing on their own.

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143
Q

 Positive End Expiratory Pressure

A

 Maintains alveolar recruitment
 Auto PEEP ~ 3-4 cm H2O  Natural level of PEEP
 Useful range 5-20 cm H2

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144
Q

Problem with NRM @1-2Lpm -

A

not enough flow, you won’t get enough air. These patients will become hypercapnic (retain CO2). At this phase, you will not be washing out CO2. Nonrebreather masks need to have high flow to compensate.

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145
Q

Bronchospasm

 Can be caused by

A

 Asthma
 COPD
 Allergic Reaction (Anaphylaxis)
 Side effect of Decongestants & Non-Selective Beta Blockers

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146
Q

Nebulizer meds - Be weary of —- in response to administering these drugs. If they have an HR of —-, albuterol will cause that to spike.

A

tachycardia

135

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147
Q

Nebulizer will work at — per minute. This will administer Beta2 agonists much more efficiently.

A

8l

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148
Q

Some patients are allergic to albuterol. Then you use ——– (hits —– nervous system and turns it off. Doesn’t directly stimulate, instead downgrades —- stimulus. You can combine them, but albuterol can be constantly given over multiple doses).

A

hypertropium bromide

parasymp

vagal

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149
Q

Critical Vitals (for medical emergencies)

A

 HR, BP, RR, SpO2, LOC (AVPU)
 prn Vitals
 Blood Glucose, Temp, ETCO2, ECG

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150
Q

Heart Rate(HR)

A

 Methods of obtaining  ECG (heart monitor)
 Pulse Ox
 Automatic BP monitors
 Palpation (Redneck ECG)
 RRR
 Location
 Radial (>70 mm Hg)  Femoral (>50 mm Hg)  Carotid (>40 mm Hg)

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151
Q

 Radial (>— mm Hg)  Femoral (>—- mm Hg)  Carotid (>——- mm Hg)

A

70, 50, 40

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152
Q

Cuff too small = — reading, and vice versa.

A

high

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153
Q

 Tachypnea
 Rapid breathing > —
 Bradypnea
 Slow breathing < —

A

20

12

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154
Q 
SpO2 (Saturation of peripheral Oxygen)  Usually adequate if ≥ ---%
 There must be a ---- to work 
 False negative:
------
 False positive
-------
A

94

detectable pulse

 Hypoperfusion, vasoconstriction, obstruction (fingernail polish), callouses, dislodgement

 CO, methemoglobinemia, anemia,

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155
Q

AVPU

A

 Alert
 V erbal – respond to verbal stimuli
 Physical – respond to physical stimuli
 Unresponsive – noogies and titty twisters are ineffective

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156
Q

 Levels of awareness

 CAO x4

A

(Conscious Alert & Oriented) Who

Where When Why

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157
Q

Typically in a stroke MCA - you usually run into —- weakness. Normally for MCA in lower face. Above the eyebrows has bilateral innervation, below has contralateral innervation.

A

contralaterral

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158
Q

 3 general types of syncope

A 
 Cardiac &amp; blood vessel related  Arrythmias, embolism, etc.
 Reflex
 V asovagal
 Prolonged standing, Emotional stress, Pain
 Situational
 Straining, Coughing, Swallowing
 Carotid Sinus
 Orthostatic (postural hypotension)
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159
Q

Syncope management

A

 Assist Pt to supine position  NO Trendelenburg
 Clear airways  Support ABCs
 Suction and roll over to lateral recumbent if needed.  Consider ammonia inhalant
 Vitals, q5 min.
 If Pt does not respond to Tx, 911

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160
Q

General Shock Management

A

 Lay patient supine, protect & maintain a patent airway  Not Trendelenburg
 Lateral recumbent prn (e.g. passive regurgitation)
 Whichever side is most convenient & best access to airway  Pregnant – left (keep fetus off of IVC)
 Keep Pt warm  Support ABCs  Vitals
 Large bore IV
 Crystalloid fluid bolus if not contraindicated
 100 – 500 cc depending on the situation  Reassess
 May need to repeat fluid bolus

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161
Q

Adult

 Mild allergix rxn:

A

 Benadryl (Diphenhydramine)  25-50 mg PO

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162
Q

Adult moderate allergic rxn:

A 
 Moderate
 Benadryl (Diphenhydramine)
 25-50 mg Deep IM
 Some places recommend 100 mg
 25-50 mg IV
 diluted slow push (< 25 mg/min)
 H2 Antagonist  Steroid
 Bronchodilator  Fluid bolus
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163
Q

 Anaphylactic Shock is the

A

rapid onset of a serious allergic reaction that can cause death. Involving 2 or more body systems.

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164
Q

 Any one of these three criteria will diagnose anaphylaxis

A

 1) Acute onset of skin or mucosal reaction, PLUS:  Either Respiratory or Hypotension signs/symptoms
 2) If an exposure to a likely allergen has occurred, PLUS 2 or more of:  Skin, Resp, BP, or GI symptoms
 3) Reduced BP (30% drop) after a known allergen exposure

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165
Q

Adult anaphylaxis tx

A

 0.3 – 0.5 mg (300 - 500 mcg) Epinephrine 1:1,000 given IM in the middle half of the anterolateral thigh area

 0.3 – 0.5 mL of 1:1,000 epi
 It’s nice, but not mandatory to inject in a clean manner
 If using a TB syringe, you get to opportunity to aspirate and reduce the risks of an intravascular injection
 Can be given SQ but IM is better

 Call 911
 Repeat epi q5-15 minutes prn  Stabilize ABC
 High-flow O2
 Low threshold for intubation

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166
Q

Adult anaphylaxis if coughing or wheezing:

A

 Observe for Pt’s response to Tx
 Take vitals signs
 Put Pt on a heart monitor, pulse ox, & NiBP (q5 min)
 Look for Anaphylaxis signs/symptoms improvement Lookforcardiacresponsetotheepi. Especiallylifethreatingcardiacevents.
 Albuterol Neb prn (if cough, wheezing)
 Start 2 large bore IVs
 Give H1 & H2 antagonist IV
 Give Steroid (IV or IM, depending on drug)
 May need large volumes of crystalloids (IV fluids like NS & LR)
 If hypotension persists, prepare epi drip (1:10,000) at 0.1-1 mcg/kg/min

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167
Q

Pediatric Anaphylaxis

A

 Same as adult but doses are weight dependent  Epi Pen uses 0.15 mg (150 mcg) of Epi 1:1000
 Proper dose is 0.01 mg/kg (max 0.3 mg)
 IV fluids are 20 mL/kg

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168
Q

Bronchospasm

A

 Can be caused by  Asthma
 COPD
 Allergic Reaction (Anaphylaxis)
 Side effect of Decongestants & Non-Selective Beta Blockers
 Frontline treatment is to administer a bronchodilator into the lungs

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169
Q

Nebulizer:

Albuterol

A

 (2.5 mg/3 mL) – q5 min prn (up to 4 doses)

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170
Q

Nebulizer

Albuterol + Ipratropium Bromide (DuoNeb)

A

 (3 mg* + 0.5 mg) - once

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171
Q

Nebulizer

Ipratropium Bromide (Atrovent)

A

 (0.5 mg/2.5 mL) - once

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172
Q

Contraindications & precautions to Albuterol & Ipratropium

A

 Rare allergy to preservatives in Albuterol  Use Ipratropium Bromide only
 Tachycardia & HTN
 Weigh risks vs benefits of Tx
 May cause arrythmias  Manage prn

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173
Q

Heart attack can either be

A

STEMI or NONSTEMI

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174
Q

Impossible to distinguish between

A

NOn-STEMI or unstable angina

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175
Q

Contraindications to Ntg

A

 Phosphodiesterase-5 Inhibitors in the last 48 hours
 Allergy to Ntg
 Significant drop in systolic BP from baseline (≥ 25%)
 Avoid dropping SBP below 110 if previously normotensive  Significant bradycardia (<50)
 Tachycardia (>100)
 Right ventricular MI
 Severe aortic stenosis
 (?) Do you have large bore IV access?

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176
Q

Chest pain aspirin dose

A

 ASA 325 mg chewable PO

 Only contraindication is if known anaphylactic allergy to ASA

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177
Q

If chest pain and hypoxic,

A

 O2 if hypoxic

 Keep SpO2 between 94%-99%

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178
Q

OK to give nitro if:

A

 Consider SL Ntg 0.4 mg IF:
 No Phosphodiesterase-5 Inhibitors in the last 48 hours (are they pitching a tent?)  No allergy to Ntg
 No significant bradycardia (<50)
 No tachycardia (>100)
 No significant drop in systolic BP from baseline (≥ 30 mm Hg)
 No severe aortic stenosis
 Avoid dropping SBP below 110 if previously normotensive
 If a large bore IV is established & a right ventricular MI has been ruled out
 Then consider Ntg if systolic BP will not be dropped below 110 mm Hg  If no, then only consider if Pt is hypertensive

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179
Q

HTN Crisis tx options in dental office

A 
 Tx Options in the dental office
 Anxiolysis
 Calm atmosphere
 N2O
 Sedation (IV , PO)
 Analgesia
 Get Pt out of pain...safely
 Clonidine 0.1 mg (alpha 2 agonist)  Prophylactic for problem Pts
 Ntg (0.4 mg SL)
 Labetalol
 Blocks alpha &amp; beta
 5-20 mg slow IV push (over 2 min) q10 min  Watch for bradycardia
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180
Q

If pt is taking non-selective beta blocker, what can happen with epi

A

iatrogenic HTN Crisis - You will effectively get unopposed alpha 1 stimulation

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181
Q

Non-selective beta blocker with epi - HTN Crisis tx

A

 Tx w/ Ntg 0.4 mg SL assuming no contraindications are present.

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182
Q

Complications with treating HTN Especially with Labetalol & Clonidine

A

 Reflex tachycardia (Bradycardia for Labetalol)  Hypotension
 Especially after the patient leave your office
 Too rapid of a reduction in BP can precipitate a stroke (Cerebral Blood Flow Curve)
 Rebound Hypertension
 May occur up to 4-8 hours later
 Often patients get observed in a hospital setting  Can precipitate a stroke
 Reducing CPP during an ischemic stroke  ↑ MAP is a protective reflex during a stroke
 Thought to maintain perfusion to the penumbra

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183
Q

 TIA – Transient Ischemic Attack

A

 a brief episode of neurological dysfunction with a vascular cause, with clinical symptoms typically lasting less than one hour, and without evidence of infarction on imaging.

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184
Q 
CVA (Cerebrovascular accident)
Core Infarction  ----
CVA
    Penumbra
------
A

Irreversible

 Tissue we’re trying to save  Time = brain cells

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185
Q

Middle cerebral artery syndrome most common ischemic stroke

A

 Hemiparesis or hemiplegia of the lower half of the contralateral face
 Hemiparesis or hemiplegia of the contralateral upper and lower extremities
 Sensory loss of the contralateral face, arm and leg
 Ataxia of contralateral extremities
 Speech impairments/aphasia: Broca’s area, Wernicke’s or Global aphasia as a result of a dominant hemisphere lesion (usually the left brain)
 Perceptual deficits: hemispatial neglect, anosognosia, apraxia, and spatial disorganization as a result of a non-dominant hemisphere lesion (usually the right brain)
 Visual disorders: déviation conjuguée, a gaze preference towards the side of the lesion; contralateral homonymous hemianopsia
 Note: faciobrachial deficits greater than that of the lower limb

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186
Q

If stroke is suspect, engage Cinci Prehospital Stroke Scale

A

Ask pt to smile
Have them slowly extend both arms out for 10 seconds - look for irregular movement or arm drifting down
Ask them to say something

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187
Q

Stroke pt: Contraindication to fibrinolytic therapy:

A 
intracranial hemmorhage visible on CT
Hx of the above
Systolic BP over 180, Diastolic BP over 110
Serious head trauma in last 3 months
Thrombocytopenia and coagulopathy
Blood glucose over 400mg/dl or under 50
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188
Q

If you suspect a stroke:

A 
Get glucose reading
Admin O2 to keep SpO2 over 94%
Perform Cinic prehospital stroke scale
If positive, record time of onset
Get phone of family/contact
Maintain body temp
Obtain 12 lead EKG during transport
Protect extremities
Early notification of ED is critical
Consider paramedic intercept, air if needed

If severe or delayed response, give long bore IV access with 0.9% normal saline 100ml per hour- avoid dextrose in absence of hypoglycemia

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189
Q

Prehospital Stroke Management Summary

A

 911
 Support ABC’s  Position Pt
 Supine for ischemic stroke (~85%)
 30 ̊ degree head elev ation for hemorrhagic stroke (~15%)  Anticipate&TolerateHTN(permissivehypertension)
 Systolic commonly 180 – 220
 Treat if > 220/120
 Document time of onset
 “Last known well time”
 3 hour window for fibrinolytic drugs (tPA)
 can be extended to 4.5 hours for some
 EndovascularMechanicalThrombectomycanbeextendedmuchlonger
 Monitor & document vitals
 Check blood sugar (Avoid hyper & hypoglycemia)  Hypoglycemia can mimic CVA
 Have Pt’s HHx & med list ready for EMS
 Including what you administered to the Pt

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190
Q

If hypoglycemic:
 Oral Glucose (any kind) ONLY IF the patient can obey commands, take
the glucose and eat it safely on their own. If not…

A

 D10 give IV slowly infuse until >80 mg/dL
 D50 – Give IV. Very Hypertonic, caustic if extravasation. Avoid tissue infiltration. Give very slowly. Be careful not to cause a blood glucose spike.
D25–pediatric. SameprotocolasD50  Glucagon 1 mg IM

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191
Q

DKA

A

 DiabeticKetoacidosis  Typically w/ type I DM  Onsetwithinhours
 MOA
 ↓Insulin + ↑Glucagon → ↑Glucose  → Osmotic Diuresis → Dehydration  ↓Insulin → ↑Fatty Acids
 → Ketone Bodies → ↓pH
 Metabolic Acidosis, fruity breath
 Compensatoryhyperventilation  Kussmaul Respirations

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192
Q

HHS

A

 HyperosmolarHyperglycemicState  Typically w/ type II DM
 Onsetwithindays
 Relativeinsulindeficiency
 Noketosisdueto“some”insulin  VERYhyperglycemic
 NormalornearnormalpH

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193
Q

 If first seizure, atypical for Pt, hypoxic, or >5 min (Status Epilepticus), then 911 & Tx

A

 Lorazepam (Ativan)

 0.1 mg/kg (max 4 mg) @ rate < 2mg/min. q5-10 minutes.  Preferred IV . Can be given IM.

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194
Q

Adrenal crisis symptoms

A

Pallor, dizziness, headache, weakness/lethargy, ab pain, etc. etc.

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195
Q

Tx for adrenal crisis

A

20mL/kg bolus of normal saline, repeat up to 60 ml/kg

Hydrocortisone 100mg iM/IV/IO

Glucose 25 gm of D50 for adults, kids over 12 2.5ml/kg D10, kids under 12 1ml/kg 25% Dextrose

Vasopressors can be used for shock refractory to going to full 60 ml/kg bolus.

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196
Q

The pathophysiology for the development of MRONJ induced by bisphosphonates or
monoclonal antibodies is not fully elucidated, however it is well accepted as being multifactorial
and includes the following:

A 
Inhibition of osteoclast induced bone resorption
 Inhibition of bone remodeling cycles
 Systemic or local inflammation
 Localized infection
 Inhibition of angiogenesis
 Localized soft tissue toxicity
 Localized trauma such as a tooth extraction, and
Immune dysfunction.i
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197
Q

For patients who have taken an oral BP for less than 4 years and have concurrently taken —–, the physician should be asked to consider discontinuation of the oral BP or monoclonal antibody for at least 2 – 3 months (drug-holiday) prior to the intended oral surgery.

A

glucocorticosteroids or other antiangiogenic medications

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198
Q

Lab test for bisphosphonate pts:

A
  1. serum-NTX (s-NTX)

2. serum-BSAP (Bone Specific Alkaline Phosphatase)

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199
Q

Test result range for bisphosphonate pts

A

s-NTX 7.5 – 16.5 nmolBCE/L

s-BSAP: 7.9-29.0 U/L

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200
Q

Non-Specific Beta Blockers

Treatment,

A

Angina, Dysrhythmia, Tremors, Glaucoma, Hypertension, Migraine, M.I., Pheochromocytoma

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201
Q

Non-Specific Beta Blockers action

A

Competitively block stimulation of beta receptors by Epi and Norepi

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202
Q

Non-selective beta blockers (common used drugs)

A

Propranolol - Rx Inderal Nadolol - Rx Corgard

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203
Q

Selective beta blockers (commonly used drugs)

Selective Selective B-1

A

Atenolol - Rx Tenormin Metoprolol - Rx Lopressor

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204
Q

Non-Selective Beta Blockers with Epi

A

Massive unopposed alpha vasoconstriction Hypertensive crisis

Significance rating 1

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205
Q

Tricyclic Antidepressants tx

A

Tx: depression, anxiety, neuropathic

pain, nocturnal enuresis

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206
Q

TCA drug examples

A

Imipramine - Rx Tofranil Amitriptyline - Rx Elavil

Doxepin - Rx Sinequan

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207
Q

TCA with Epi

A

Block active reuptake of amine neurotransmitters Get potentiation of affected neurotransmitter
Epi subject to same affects

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208
Q

COMT Inhibitors A New Drug Interaction?
COMT Inhibitors
Tx
Drug examples

A

Parkinson’s Disease – Tolcapone (Rx Tasmar) – Entacapone (Comtan)

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209
Q

Catechol-O-Methyl-Transferase

A

Enzyme responsible for inactivating catechols – levodopa
– vasoconstrictors
• epinephrine • levonordefrin

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210
Q

COMT Inhibitors with Epi

400 mg of Entacapone + Epinephrine ›——–

A

Tachycardia

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211
Q

COMT Inhibitors with Epi Reasonable Precaution

One carpule of 1:100,000 epinephrine and monitor patient’s —— for 5 minutes

A

B.P. and pulse

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212
Q

COMT Inhibitors with Epi Patients at Risk

A

Low COMT activity Selegiline - Rx Eldepryl
specific (MAO)-B inhibitor
high doses block (MAO)-A also
both pathways for epinephrine metabolism are blocked

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213
Q

COMT Inhibitors with Epi

A

Significance rating 1

Also unique to Tolcapone is acute liver failure - watch Tylenol

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214
Q

Monoamine Oxidase Inhibitors

A

Antidepressants Antimicrobial
Marplan and Parnate -Furazolidone - Rx Furoxone Antiparkinson
– Selegiline - Rx Eldepryl

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215
Q

MAO Inhibitors

A

Prevent metabolism of drugs metabolized by MAO
Block intraneuronal breakdown of norepi - increases the pool of neurotransmitter capable of being released by amphetamine, pseudoephedrine
and tyramine

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216
Q

MAO Inhibitors with Epi

A

No evidence of problem with epi or levonordefrin - reason COMT
Bureaucracy?

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217
Q

MAO Inhibitors

A

Remember Sudafed and MAO – sinus elevations Remember MAOI’s and Meperidine -Rx Demerol
– Muscle rigidity, stupor, agitation, increased temperature, hallucinations, death (?) Talwin, Nubain

218
Q

TCA with Epi Boakes Found

A

Increase in systolic B.P. & Dysrhythmia

Tofranil potentiates epi 3 X and Potentiates Levonordefrin 6-8 X

219
Q

TCA with Epi
Persson and Siwers 1975
2 1/2 Carpules of Lido 2% with Epi 1:100,000
– causes —– – increased systolic pressure —–
Hgover baseline
Brown and Lewis in 3-0 1988 Prolonged use of TCA’s
– desensitization to —–
– decrease chance of —–

A

headache

45 mm

adrenergic vasoconstrictors

interaction significance

220
Q

TCA with Epi Treatment Plan

A
  • No levonordefrin
  • no epi cord
  • no greater 1:100,000 epi
  • 1/3 maximum dose
  • wait 30 minutes before re-injecting
221
Q

Thyroid Hormones and Vasocontrictors

A
  • Thyroxine - Rx Synthroid

* May cause dysrhythmias, ⇑ cardiac output, ischemia • Significance rating 4

222
Q

Cocaine

A
  • Has L.A. action

* Blocks the re-uptake of norepi and dopamine • Enhances adrenergic neurotransmitter release

223
Q

Efficacy of Articaine: A New Amide Local Anesthetic

A
  • Articaine 4% with Epi 1:100,000 vs. Xylo 2% with Epi 1:100,000 • 882 received Articaine
  • 443 received Xylocaine
  • No difference between two groups
224
Q

Articaine vs. Citanest Forte

A

• Articaine 4% with Epi 1:200,000 found to be no different than Citanest Forte (Epi 1:200,000

225
Q

Articaine

A
  • Same recommended maximum dose as Xylocaine 7 mg per Kg.
  • Formulation is twice as strong - WHY?
  • Has epi 1:100,000 - ? Mandibular blocks
  • Prilocaine (Citanest Epi 1:200,000)
  • lower recommended dose - WHY?
226
Q

COX-1 constitutively express

A

Good things – Prostaglandins that aid in kidney perfusion, anti-coagulation, vasodilation, GI protection

227
Q

COX-2 induced by:

A

Cytokines, Growth factors, Endotoxin; Leads to inflammation cascade

228
Q

NSAID actions:

A

ANALGESIC, ANTI-INFLAMMATORY, ANTIPYRETIC, INHIBIT:
Ccloyxygenases, Prostaglandins, and Thromboxanes
NSAIDs Lack unwanted side effects of the opioids and on the CNS: Respiratory ↓ & physical dependence. Do not change the perception of sensory modalities other than pain. Chronic post-op pain is often from inflammation and is well controlled by NSAIDs
• Hypersensitivity reactions:
• Cross hypersensitivity - Usually not IgE mechanism
• Shunting towards leukotriene synthesis can lead to Bronchospasm & anaphylaxis
• Do not use another NSAID; Use acetaminophen

229
Q

PRE-EMPTIVE ANALGESIA

A

• INHIBITS THE “FORMATION” OF PROSTAGLANDINS; HAVE ON BOARD BEFORE START
DIONNE J. CLIN. PHARMACOL. 1983; JACKSON, MOORE, JADA 1989

230
Q

NSAID Contraindications:

A

• CURRENT HX: NEPHROPATHY, EROSIVE ULCERATION OF GI, ANTICOAGULANT TX, HEMORRHAGIC DISORDER, PRIOR HX OF NSAID/ASA ALLERGY OR INTOLERANCE, CONCURRENT ANTIHYPERTENSIVE THERAPY (RELATIVE)

231
Q

NSAID • Short term use:

A

LITTLE EFFECT ON RENAL FUNCTION IN NORMAL PATIENT

232
Q

NSAID • Side effects:

A

⇑ BP (FLUID RETENTION), DIZZINESS, RASH, GI IRRITATION
(ULCER), RENAL PAPILLARY NECROSIS + OTHER RENAL MEDULLARY
CHANGES, LICHEN PLANUS

233
Q

NSAID • Half-Life:

A

T1/2β 2 HR.; 400 mg. PEAK PLASMA LEVEL 29 ug/ml IN 90 MIN.;

3ug/ml IN 8 HR.; NON DETECTED IN 12 HR.

234
Q

o SpinalFusion/NSAIDS

A

In a retrospective study of 83 patients undergoing spinal fusion, those patients who postoperatively used NSAIDs for longer than 3 months showed only 37% fusion rate compared to a 93% fusion rate in patients not taking NSAIDs. Deguchi M, Rapoff AJ, Zdeblick TA. Posterolateral fusion for isthmic spondylolisthesis in adults: analysis of fusion rate andclinical results. J Spinal Disord 1998;11M459–64.

235
Q

COX-2EffectsonFractureHealing

A

The healing of stabilized tibia fractures was delayed in COX-2 knockouts compared to wild-type animals and to COX-1 knockouts. In radiographic analysis at 21 days post-fracture normal healing found in 8 out of 10 wild-type mice five out of six COX- 1 knockouts three out of eight COX-2 knockouts
Zhang X, Schwarz EM, Young DA, Puzas JE, Rosier RN,OʼKeefe RJ. Cyclooxygenase-2 regulates mesenchymal cell differentiation into the osteoblast lineage and is critically involved in bone repair. J Clin Invest 2002;109M1405–15.

236
Q

o Indomethacinvs.Coxibs on fracture healing

A 
Celecoxib or Rofecoxib evaluated in femur fracture in rats All three drugs inhibited fracture healing
8 week results healed:
Control 7/7
Indomethacin 6/8
Celecoxib 0/6
Rofecoxib 0/5
Acetaminophen vs. Celecoxib
237
Q

o Femur fracture repair in rats
Acetaminophen - —
Celecoxib - ——-
Bergenstock M, et al. A comparison between the effects of acetaminophen and celecoxib on bone fracture healing in rats. J Orthop Trauma 2005;19M717-23

A

no delayed healing

impaired healing when observed at 8 weeks

238
Q

o Boneformationprocess

A

Ostoclasts➙resorption➙free up BMPs BMPs➙osteoblasts➙bone formation
Prostaglandins & bone forma Ostoclasts➙resorption➙free up BMPs

239
Q

Prostaglandins &BMP; bone formation

A

PGs ↑ # and activity of osteoclasts = bone resorption
PGs ↑ replication and differentiation of osteoblasts = bone formation
PGs ↑ blood supply through vasodilation & ↑ angiogen

240
Q

COX-1:

A

expressed in normal bone and at bone fracture sites

241
Q

COX-2:

A

up-regulated during initial stages of bone repair

242
Q

Osteoclasts and osteoblasts produce —-

A

PGs (PGE2)

243
Q

Selective COX-2 inhibitors reduce risk of

A

GI adverse events

244
Q

Excessive PGE2 formation can result in —-
Controlling PGE2 formation may be good
However, PGE2 in the right concentration promotes —–
What should we do?
Conclusion: This study provides preliminary data that suggest that systemic administration of —- may reduce bone loss around dental implants in the first year of service

A

bone loss

bone formation

flurbiprofen

245
Q

• ACETAMINOPHEN:

A

• PROSTAGLANDIN PATHWAYS IN CNS - COX-3 INHIBITOR
• LITTLE Peripheral INFLUENCE; LITTLE ANTI-INFLAMMATORY
• NONE OF NSAID PERIPHERAL SIDE EFFECTS
• ONLY INHIBITS CYLCOOXYGENASE IN AREAS OF LOW PEROXIDE
FORMATION i.e. HYPOTHALAMUS
• SITES OF INFLAMMATION USUALLY HAVE HIGH PEROXIDES
GENERATED BY LEUKOCYTES - REF. MARSHALL 1987
• EQUAL IN POTENCY AND EFFICACY TO ASPIRIN ∴ INFERIOR TO
IBUPROFEN AND OTHER NSAIDs
• HEPATOTOXICITY: TOXIC DOSE 10-15 Grams; LOWER TOXICITY IF:
DEPLETED GLYCOGEN; CHRONIC ALCOHOLISM MAX. DAILY DOSE IS 2 Grams VS NORMAL 4 Grams; Normal maximum daily dose is 4 grams per 24 hours – no liver failure,
alcoholism, or age is less than 65
• If a patient consumes alcohol routinely, and you prescribe acetaminophen, then the patient must continue to drink the alcohol

246
Q

• When pain is expected give pre-operative doses of NSAIDs (cox-1 & 2 inhibitors) optimize this NSAID dosage
• Keep a steady-state blood level of NSAID (not prn)
• Prevent pain and inflammation vs trying to beat it later
• Add acetaminophen (cox-3 inhibitor) if ——
• If NSAID-acetaminophen (inhibiting Cox 1,2,3) combination is ineffective
then add a —–

A

the NSAID does not control pain

narcotic for “break through” pain

247
Q

Analgesic algorithm:

A

Step 1: start with ibuprofen 600mg. or flurbiprofen 100mg one hour pre-
op
Step 2: continue ibuprofen 600mg. q 6 hrs for 3-5 days or flurbiprofen 100mg bid for 3 to 5 days
Step 3: if ibuprofen is not controlling pain then add acetaminophen 500- 1000mg q 6 hrs.
Step 4 add a narcotic + acetaminophen combination drug (i.e. Lortab 10/325) one or two tablets q 4 to 6 hrs as needed.
Discontinue the previously prescribed individual acetaminophen
No opioids if patient has taken MAO inhibitors in previous 14 days

248
Q

• Tramadol (UltramTM) has both an

A

opioid and antidepressant

• component

249
Q
  • Tramadol parent drug is like a —–

* Tramadol metabolite –m1- weak agonist on —–

A

tri-cyclic antidepressant

mu receptors good
for chronic pain

250
Q

n Caffeine increases —- of aspirin & Tylenol, but not the —–

A

potency

efficacy

251
Q

n Sedative/anxiolytics: —- to analgesic efficacy

A

No benefit

252
Q

Antiemetic

• Use to TX —-

A

n & v of opioids; cannot prevent n & v of opioids

253
Q

Steroid - ANTI-INFLAMMATORY ACTION

Supraphysiological doses mech. of action: decrease in

A

inflammatory mediators; synthesize an enzyme that degrades bradykinin

254
Q

Steroid
IMMUNOSUPPRESSANT EFFECTS
Antibody production ↓ by —- steroid dose, not —- dose
Will retard —– activity
Steroids ↑ migration of —— to sites of infection – Very important!

A

large

moderate

lymphocyte

anti-inflammatory monocytes

255
Q

STEROIDS- THE BAD SIDE

Chronic steroid therapy leads to

A

suppression of HPA axis, compromised immune status osteoporosis and increased blood sugar levels

256
Q

ADDITIONAL STEROIDS

If patient takes daily steroids:

A

double, triple, 4x, 5x (procedure dependent) their normal daily steroid dose for the day of surgery, then taper off over the next 5 to 7 days to normal dose or give IV short acting steroids and longer acting IM suspension steroids

257
Q

“A single dose of glucocorticoid, even a large one, is virtually

A

without harmful effects, and ad
short course of therapy (up to 1 week), in the absence of specific contraindications, is unlikely to be harmful” Goodman & Gillmans – 10th edition

258
Q

STEROIDS

All steroids are equipotent;

A

they do vary in: potency, half-life, mineralcorticoid activity, and salt retention – fluid retention

259
Q

STEROID REGIMEN

A

Oral – use the dose packs available (i.e. medrol dose pak)
Pt. takes all of the first row in the AM prior to surgery (or splits dose – 1/2 in am and 1⁄2 in early afternoon then follow directions for following days

260
Q

STEROID REGIMENS
IV OR IM
use —– (solution – clear)
give —– prior to surgery, this will last 24 - 48 hrs.
Give IM for longer duration: —–
This will last 5 to 7 days. NOTE never give suspensions IV

A

dexamethasone sodium phosphate 4mg/ml

4 – 8 mg IV or IM

Depo-medrol 40 mg/ml suspension (white suspension) give 1 –2 ml

261
Q

Steroids

CONTRAINDICATIONS

A

(even short term use)
Uncontrolled diabetes, Immunocompromised, Active peptic ulcers, Osteoporosis
Active herpetic or fungal infections, Avoid high dose in pts. with psychoses

262
Q

Dexamethasone Rx:

Single Implant, Small Flap

A

0.75mg - 5432110 regimen

263
Q

Dexamethasone Rx:

Single implant, mid flap

A

0.75mg - 6543211 regimen

264
Q

Dexamethasone Rx:

Multiple implants, large lafp

A

0.75mg 6543211 regimen

265
Q

Dexamethasone Rx:

Full arch, large flap

A

0.75mg - 7654321

266
Q

Dexamethasone Rx:

RCT

A

21000000

267
Q

Dexamethasone Rx:

Crown and Bridge (if even needed*)

A

2100000

268
Q

Dexamethasone Rx:

3rd molar complete bony impaction x 4

A

6543211

269
Q

Dexamethasone Rx:

3rds max only x 2

A

5432110

270
Q

Dexamethasone Rx:

3rds mand only

A

6543211

271
Q

Dexamethasone Rx:

Single tooth ext.

A

5432110

272
Q

Dexamethasone Rx:

Older, medically compromised, or petite pt: modify dose

A

1/4 to 1/2 above doses.

273
Q

Dexamethasone Rx:

Diabetic - well controlled

A

None at all if not well controlled

1/4 dose above.

274
Q

Dexamethasone Rx:

Cardiovascular compromised

A

1/4 to 1/2 above dose or none at all.

275
Q

Dexamethasone Rx: Equivalent rules and usage to

A

Prednisone 5mg

276
Q

Beta-lactams - Penicillin only indicated for

A

minor infections – this includes dental abscesses

277
Q

Ampicillin Greater activity against

A

gram (-) because it penetrates the gram (-)

cell membrane

278
Q

Beta lactam Downside: Beta-lactamases inactivate

A

+ Multiple resistant bacterial strains

279
Q

Cephalasporins -

A

Broader spectrum than (3-lactams; More stable to (3-lactamases; 1st generation (cephalexin): gram (+) activity and anaerobes sensitive; Later generations (Cefaclor, Cefotaximer, Cefepine): improved gram(-) activity. Less expensive than Augmentin®; Less bacterial resistance. Most effective treatment for sinusitis Cellulitis + other soft tissue infections

280
Q

Tetracyclines -

A

Broad spectrum; Bacteriostatic for many gram (+) and (-) aerobes and anaerobes Bound to developing teeth and bones. Inhibits bone growth; Used to treat Helicobacter pylori (HP) in combination with other meds HP. Exists in maxillary sinus of pts with gastric HP infections.
Problem: opportunistic candida infections; sun sensitivity

281
Q

Doxycycline (Vibramycin)

A

Dose: 100 mg 1 or 2 a day for 14 days; Contraindications: Food Pregnancy - Category D Adverse events: GI Drug interactions: anti- epileptics

282
Q

Macrolides -

A 
Erythromycin Gram (+) and Gram (-) activity Low doses bacteriostatic High doses bactericidal. Suitable alternative for penicillin allergic pt. Drug interactions (inhibits P450 enzymes in liver); Increases serum concentrations Theophylline, warfarin,
cyclosporine, methylprednisolone, digoxin; Decreases activity Plavix
283
Q

Azithromycin:

A

Less activity against staphylococci and streptococci; Greater activity against HP
Penetrates tissues better (exceeding serum concentration by 10 – 100 fold).
Slowly released from tissues with a tissue half-life of 2 to 4 days and an elimination half-life of 3 days. FDA warning Heart Risks March 2013: May cause prolong cardiac repolarization and QT interval. High risk patients: history of existing QT-interval prolongation torsade de pointes, Congential long QT syndrome, uncompensated heart failure, hypokalemia, hypomagnesemia or significant bradycardia
Clindamycin- Activity against streptococci staphylococci, pneumococci
Enterococci and gram(-) aerobes resistant (does not penetrate gram(-) outer membrane) (Clostridium difficile is resistant) Well absorbed orally – food does not reduce absorption significantly

284
Q

Fluoroquinolones -

A 
Excellent Gram (-) aerobes and little gram(+) activity
Newer agents more gram (+) activity Well absorbed. Wide volume of distribution Since most dental infections have high concentrations of anaerobes – and most fluoroquinolones demonstrate no activity against anaerobes – rarely a good choice for dental infections
285
Q

Metronidazole -

A

Great anaerobic activity Well absorbed widely distributed. Anaerobic bacteria reduce the nitro group to give the antimicrobial activity. Do not consume alcohol
– re.disulfiram-like reaction Potentiates warfarin anticoagulants

286
Q

Therapeutic regimen -antibiotics

A

Step 1. Penicillin-like antibiotic meets criteria for activity against anaerobic gram (-)
and aerobic gram (+) bacteria. Amoxicillin logical 1st choice, with exception of anaerobes possessing beta-lactamase activity (–) then consider Augmentin® - BUT very expensive, so cephalexin (demonstrates greater stability than penicillins and less expensive than Augmentin®
Step 2. If the beta-lactam antibiotic (cephalexin) fails to bring resolution after 48 to 72 hours, then consider improving anaerobe coverag
James L. Rutkowski DMD, PhD 14
a. Add metronidazole 500 mg initially followed by 250 mg every 8 hours for 7 to 10 days. (Keep patient on the beta lactam antibiotic) OR b. Change to clindamycin 300 mg 1st time then 150 mg q 6 h (discontinue beta- lactam)

287
Q

Antibiotics + oral contraceptives -

A

rifampin (TB) only confirmed; anecdotal reports;
Oral contraceptive failure 0.5 - 1.0 % (teens 8%); enterohepatic recycling studies do not substantiate the possible drug interaction

288
Q

Sugical prophylaxis:

A

adequate serum within 2 hrs. of incision; serum level should not be continued for more than 24 hrs. prolonged prophylaxis results in growth of resistant organisms) 1 or 2 additional doses; oral amoxicillin, cephalexin, penicillin VK, clindamycin,
Intravenous cefazolin

289
Q

Medical prophylaxis -

A

Compromised immune function; poorly controlled insulin dependent Diabetes, renal failure with dialysis evidence of significant malnutrition or alcoholism; symptomatic HIV; immunosuppressant drugs; radiation of head or neck Inflammatory arthropathies including rheumatoid arthritis and systemic
lupus erythematosus;
First 2 yrs. following joint placement previous prosthetic joint infections (?)

290
Q

INHIBITORS OF CLOTTING FACTOR SYNTHESIS

A

Warfarin (Coumadin®)
Rivaroxaban (Xarelto®)
Apixaban (Eliquis®)

291
Q

INHIBITORS OF THROMBIN ®

A

Heparin, Lepirudin (Refludant )

Dabigatran Etexilate Mesylate (Pradaxa®)

292
Q

PREVENTION OF PLATELET AGGREGATION

A

Ticlopidine (Ticlid®) Clopidogrel (Plavix®) Tirofiban (Aggrastat®) Eptifibatide (Integrilin®) Prasugrel (Effient®) Ticagrelo (Brilinta®)
ASA (acetylsalicylic acid - aspirin)

293
Q

HEPARIN

A

POTENTIATES THE ANTICOAGULANT ACTIVITY OF ENDOGENOUS ANTITHROMBIN III; EFFECT IN 24 HRS.

294
Q

WARFARIN (COUMADIN)

A

ACTS IN LIVER BY INHIBITING REDUCTION OF VIT. K TO A FORM NEEDED FOR SYNTHESIS OF FACTORS VII, IX, X, AND PROTHROMBIN

295
Q

Coumadin peak effect takes

A

TAKES 3 – 4 DAYS

296
Q

Coumadin antidote

A

ANTIDOTE – VIT. K; REQUIRES 12 –24 HRS.

MAY REQUIRE TRANSFUSION

MONITOR WITH INR (INTERNATIONAL NORMALIZED RATIO) STANDARDIZES THE VARIOUS LABORATORIES THROMBOPLASTINS (human or rabbit)

297
Q

Dabigatran (Pradaxa®) Boehringer Ingelheim

A

• For prevention of stroke and systemic embolism (blood clots) in patients with atrial fibrillation
• Specific direct thrombin inhibitor
• First replacement for warfarin (Coumadin®) since Coumadin was approved in 1954
• Rapid onset of action (peak plasma level within 0.5 to 4 hours)
• 1/2 life
o Healthy patient: 12 - 14 hours
o Elderlypatient:14-17hours
o Severe renal dysfunction: up to 27 hours
• Wide therapeutic margin

298
Q

Dabagatran

A

Few drug interactions, No significant food interactions
Acts by inhibiting thrombin, an enzyme in the blood that is involved in blood clotting
Thrombin (serine protease) enables the conversion of fibrinogen to fibrin during the coagulation cascade, its
prevention prevents the development of a thrombus.
Recommended dose is a 150 mg orally once or twice daily
Warfarin therapy requires patients to undergo periodic monitoring with blood tests, INR monitoring not necessary for dabigatran.
Measurement of Effect
At therapeutic doses prolongs the activated partial thromboplastin time (aPTT)
Oral dose of 150 mg twice daily, the median peak aPTT is approximately twice that of control values
James L. Rutkowski DMD, PhD 17
Twelve hours after the last dose, the median aPTT is 1.5x control More accurate thrombin clotting time (TT) and ecarin clotting time (ECT)
INR test is relatively insensitive to the activity of dabigatran and may not be elevated in patients on dabigatran.
Absorption and Metabolism
Minor bleeding event, delay the next dose - consult physician Ref. Costantinids et al. BMC Oral Health (2016) 16\5; Managing patients taking novel oral anticoagulants (NOAs) in dentistry: a discussion paper
on clinical implications Not metabolized by CYP enzymes
After oral administration, dabigatran etexilate is converted to dabigatran through esterase-catalyzed hydrolysis of
the molecule in plasma
Dabigatran is not a substrate, nor inhibitor, nor inducer of CYP 450 Enzymes

299
Q

Dabigatran and Risk of Bleeding

A

? risk of bleeding and can cause significant, and sometimes fatal, bleeding
Drugs that can increase the risk of bleeding include antiplatelet agents and chronic use of NSAIDs
RE-LY trial, life-threatening bleeding occurred at an annualized rate of 1.5% for Pradaxa 150 mg and 1.8% for warfarin.
Discontinuing Pradaxa for surgery places the patient at an? risk of stroke
If anticoagulation must be temporarily discontinued for any reason, therapy should be restarted as soon as
possible.
Dental patients who may have a high risk of bleeding if taking Pradaxa include those over 75 years of age, or are taking
aspirin, or long term NSAIDs, or clopidogrel (Plavix®) or prasugrel (Effient®). RE-LY study Connolly SJ, Ezekowitz MD, Yusuf S, et al, “Dabigatran Versus Warfarin in Patients With Atrial Fibrillation,”
N Engl J Med, 2009, 361(12):1139-51.

300
Q

Dabagatran life threatening bleed

A

Administration of prothrombin complex concentrates
Administration of idarucizumab: Rx - Praxind - (monoclonal antibody)
Rapidly (within minutes) reverses bleeding effects of dabigatran
Discontinuing for elective surgery places patients at an increased risk of stroke and if discontinued restart as soon as
possible
Wynn, TL. New antiplatelet and anticoagulant drugs. Gen Dent. 2012;608-11
Risk of post-op bleeding is similar to those patients who take warfarin with an INR of 2 to 3

Connolly et al. Re-LY steering committee and investigators. Dabigatran versus warfarin in patients with atrial fibrillation

301
Q

Dabagatran life threatening bleed

A

Administration of prothrombin complex concentrates
Administration of idarucizumab: Rx - Praxind - (monoclonal antibody) Rapidly (within minutes) reverses bleeding effects of dabagatran
Discontinuing for elective surgery places patients at an increased risk of stroke and if discontinued restart as soon as
possible

302
Q

Dabigatran dental treatment

A

For aggressive oral surgical procedures - get consult on discontinuation of drug. TT or aPTT performed 6 to 12 hours prior to surgery
Restart dabigatran once a stable clot has formed (24 - 48 hours) following surgery

303
Q

Rivaroxaban (Xarelto)

A

Mechanism: Factor Xa inhibitor
In coagulation cascade factor X → Xa (produces fibrin)
Prophylaxis of deep vein thrombosis (DVT), which may lead to pulmonary embolism (PE) in pts undergoing knee or hip
replacement surgery
10 mg once daily
5 -6% pts have “a bleeding event” Measurement of Effect
Prolongs prothrombin time (PT) and activated partial thromboplastin time (aPTT) Predictive treatment values not established
No data on INR use
Hip replacement - 35 days Knee replacement - 12 days
Rapid onset (peak plasma level 2.5 - 4 hours) 1/2 life 5.7 to 9.2 hours
patients >75 yo = 12 to 13 hours

304
Q

Rivaroxaban (Xarelto) Dental considerations

A

↑ bleeding occurs with 10mg/day Consult (? for simple surgery)
No reports of interactions with amoxicill, cephalexin, cefazolin, ampicillin, & clindamycin
No interruption for simple surgery
Complex oral surgery or patients at increased risk for bleeding (especially severe renal impairment) discontinue 24
hours in advance Get consult
Restart within 24 to 48 hours Analgesia use acetaminophen

305
Q

Rivaroxaban (Xarelto®) Drug interactions

A

Inhibitors of CYP3A4: Ketocanazole (antifungal), Clarithromycin (Biaxin®), Erythromycin
NSAIDS
Opioids

306
Q

Apixaban (Eliquis)

A

Direct anti-coagulant
Rapid onset -bioavailability 60% Peak plasma level 1-3 hours
1/2 life 12 hours
No Reversal agent
If post-op bleeding - delay subsequent dose Do not stop for oral surgery - be reasonable

307
Q

ANTIPLATELET DRUG

DIPYRIDAMOLE (PERSANTINE)

A

PREVENTS PLATELET ADHESION TO ENDOTHELIAL SURFACES MIXED WITH ASA
ENHANCES ANTITHROMBOTIC ON ARTIFICIAL SURFACES VALVULAR & CARDIAC PROSTHESES
DIALATES CORONARY ARTERIES

308
Q

PLAVIX® - CLOPIDOGREL

A

BLOCKS THE ADP RECEPTOR WHICH PREVENTS THE BINDING OF FIBRINOGEN TO THAT SITE DOES NOT ALTER THE RECEPTOR
REDUCES # OF FUNCTIONAL ADP RECEPTORSMONITOR WITH
PLATELET AGGREGATION
INITIAL 2 TO 4 WEEKS MAY CAUSE THROMBOCYTOPENIA – CHECK
PLATELETS RARELY NECESSARY TO D/C
SURGERY IF MULTIPLE SITES OR EXTENSIVE ? – get consultation DISCONTINUE
7 DAYS PRIOR TO PROCEDURE (RARELY NECESSARY!)

309
Q

Prasugrel (EffientTM)

A

Antiplatelet agent and aggregation inhibitor
For ♦ thrombotic cardiovascular events (stent thrombosis
Pro-drug
Irreversibly blocks P2Y12 component of adenosine diphosphate (ADP) receptors on platelets for their lifespan
James L. Rutkowski DMD, PhD 21
Normal platelet activity does not return (new platelets in 5 to 9 days after D/C Loading dose 60 mg followed by maintenance dose of 10 mg daily. Should take with ASA 75 to 325 mg daily
Genetic variants in liver metabolizing enzymes do not affect efficacy Undergoes rapid intestinal and serum metabolism via esterase-mediated hydrolysis to a thiolactone (inactive metabolite), which is then converted, via CYP3A4 & CYP2B6 enzyme oxidation, to the active metabolite designated as R-138727.

310
Q

Ticagrelor (Brilinta)

A

Reduce rate of thrombotic cardiovascular events in pts with acute coronary syndrome (ACS): unstable angina, non-ST
elevation MI, ST elevation MI More effective than clopridogrel Drug interactions
Inhibitors of CYP3A4:Ketocanazole , Itaconazole , Voriconazole , Clarithromycin (Biaxin®), Erythromycin, NSAIDs
Mechanism of action: An active, reversible platelet inhibitor
CYP3A4 converts ticagrelor to another active reversible platelet inhibitor - which is the
major active metabolite
Act at the ADP-receptor
Loading dose 180 mg then 90 mg BID
Give with loading dose ASA 325 mg then 75 - 100 mg. Daily
ASA doses above 100 mg/day reduce effectiveness of ticagrelor and should be avoided
Dental considerations
Do NOT D/C without consultation
Expect bleeding and echymosis
Patients often have SOB
No coagulation parameters suggested
Ways to stop bleeding: Pressure, Surgicel, Avitene, Laser, Bovie (cautery), Electosurge (cautery), Bovine thrombin, Hemostyat, Injecting local anesthesia with epinephrine, Ice Packs, Burnish bone, Ligate vessel

311
Q

Infection and Wound Healing

A

Difficulty managing infections: Hyperglycemia reduces phagocytic activity of
granulocytes facilitates growth of microorganisms
Oral Complications of Diabetes
Uncontrolled diabetes mellitus: Xerostomia, infection, poor healing; 1 risk and
severity of periodontal disease
Burning mouth syndrome; Oral fungal infections (Candida,
mucomycosis)

312
Q

Insulin dependent Diabetic s u r g e r y requirements

A

Review HbA1C (ideal <7 mg%)
Stable patient , knowledgeable patient, not extensive procedure & within your comfort
level – ? need for consult
If not stable, poor knowledge base for patient, extensive procedure – consult

313
Q

• EMDOGAIN® FORMULATION

A

• Treatment of Periodontal Defects
Purified acidic extract of developing embryonal enamel derived from
six month-old
piglets. Purpose is to act as a tissue-healing modulator that would mimic
the events
that occur during root development and to help stimulate periodontal
regeneration

314
Q

Emdogain

• Mechanism of Action)

A

EMD adsorbs both to hydroxyapatite and collagen
binds to denuded dental rootEMD forms insoluble spherical complexes
Detectable amounts remain at the treated site on the root surface for up to 2 wks
Gestrelius et al., 1997
This appears to be a sufficient period of time to permit recolonization by periodontal ligament cells or undifferentiated
cells
Also contains TGF-β1

315
Q

Bisphosphonate: Mechanism of Action

A

Nitrogen containing BPs are incorporated into the osteoclasts
Inhibits farnesyl diphosphate synthase (enzyme involved in cholesterol synthesis) that Leads to ↓ geranylgeranyl diphosphate. This is the
protein that is involved in attachment of other proteins and molecules to the cell membr ane

316
Q

Sx sponge -

A

Use these in the back of the throat to act as a throat screen. This is a bit more sturdy than gauze, and they can be autoclaved. Even place during times when you can’t do rubber dam isolation due to anatomy.

317
Q

Epinephrine: know:

A

Alpha 1 (small blood vessels, causes vasoconstriction)

318
Q

1:100,000 epi in 1 carp is 0.—–, or ——– in a carp.

A

0.018mg, or 18 micrograms

319
Q

Systolic BP goes up—— on average with each carpule on older patients, it has less of an effect on BP in healthier younger patients. 18 micrograms isn’t much, but it does change things.

A

5-10 mmHg

320
Q

With high bp, check —–, and consider looking into sedation.

A

headache, vision, general health - verify that it is anxiety

321
Q

Beta 1: makes heart beat —–. —– takes epi from IA artery, to heart. *Adds methyl group to epi to where it no longer can fit on to beta 1 receptor, effectively deactivates it. If pt is having an excessive beta 1 response, ——, calm things down, and it should drop eventually.

A

faster and stronger

COMT

versed, nitrous

322
Q

Once heart rate rises too much, you can have —–, which can lead to arrythmia and MI. You have to consider that over time, you have more and more necrotic heart tissue. Pulse is important for this exact reason.

A

necrotic areas refract the nervous response

323
Q

Beta 2 are also activated by epi - in large blood vessels, bronchioles, causes dilation. There are also alpha 1 receptors on large vessels, but they are far outnumbered, so the beta 2 response is the predominant effect. You lower diastolic BP —– with every carpule of anesthetic w/epi.

A

5-10 mmHg

324
Q

Legitimate I+D,

A

do I+D and Rx for antibiotics. Never take out the tooth with this procedure.

325
Q

MIC-90

A

SErum concentration of antibiotic needed to inhibit 90% of species.

326
Q

Can only kill —% of bacteria at any given time, due to mechanism of action of antibiotics. — are always dormant. With amox TID, you never get to stable blood levels for long periods of time. MIC-90 - after 2 days dose, you are less than a tenth of a percent of bacteria remaining.

A

90, 10%

327
Q

Clavulonic acid -

A

preferred substrate to help the amoxicillin in augmentin get through.

328
Q

Pen allergy: Most allergic manifestations are

A

maculopapular or urticarial skin reactions.

329
Q

Cross allergies exist between cephalosporin and beta lactams. If the patient has multiple, send to allergist, try to figure out which one was mild diarrhea (maybe helped with probiotic). If ever uncertain, give

A

low dose, have albuterol inhaler ready, have them sit in office for a few hours. Or give steroid, then have them take the antibiotic, as the steroid will blunt the allergic rxn.

330
Q

Cephalosporins
• •
Most effective treatment for

A

sinusitis Cellulitis + other soft tissue infections

331
Q

Cephalosporins
• •
Most effective treatment for

A

sinusitis Cellulitis + other soft tissue infections

332
Q

Tetracyclines: •

Used to treat

A 
Helicobacter pylori (HP) in combination with other meds
•

HP exists in maxillary sinus of pts. with gastric HP infection

333
Q

Tetracycline inhibits

A

Inhibits bone growth

334
Q

Tetracycline other oddities

A

Opportunistic Candida infections Sun Sensitivity

335
Q

Doxycycline: •

A 
Contraindications
Food
• •
•
Pregnancy - Category D 
Adverse events: GI
Drug interactions: anti-epileptics
336
Q

Macrolides decrease activity of

A

plavix (P450 inhibition in liver)

337
Q

Azithromycin - why is this macrolide attractive?

A

It doesn’t inhibit P450.

338
Q

Problem with azithromycin:

A

May cause prolonged cardiac repolarization and QT interval

High risk patients: history of existing QT-interval prolongation torsade de pointes, congential long QT syndrome, uncompensated heart failure, hypokalemia, hypomagnesemia or significant bradycardia

339
Q

Fluoroquinolones:

A

Don’t really kill anaerobes, completely useless for dental infections. Can cause damage to tendons**

340
Q

Not a bacteria in the oral cavity can survive a beta lactam and metronidazole. The problem is that you can’t have —-

A

booze.

341
Q 
Metronidazole
• • • •
• • •
Great --- activity
Well absorbed
Widely distributed
---- bacteria reduce the nitro group to give the antimicrobial activity
May give a ---- taste
Do not consume alcohol – re. ---- reaction 
Potentiates (improves) -----
A

anaerobic

Anaerobic

metallic

disulfiram-like

warfarin anticoagulants

342
Q

Step 1 for antibiotic regimen:

A

amox, or cephalexin depending on how anaerobic.

343
Q

Cephalexin Rx:

A

Cephalexin 1000mg initially, followed by 500mg q6h for 7-10 days.

344
Q

Step 2 for antibiotic regimen

A

A. Add metronidazole 500 mg initially followed by 250 mg every 8 hours for 14 days.
OR
B. D/C cephalexin and begin clindamycin 300 mg initially follow by 150 mg every 6 hours for 7 to 10 day.

345
Q

Acute infection arising in under 2 days:

A

Pen VK 1000 mg initially, then 500 mg q 6 h or
Amoxicillin 1000 mg initially, then 500 mg q 8 h or
Cephalexin 1000 mg initially, then 500 mg q 6 h (all of the above for 7 to 10 days or longer)

If Penicillin allergy: Clindamycin 300 mg initially, then 150 mg q 6 h or Cephalexin (for 7 to 10 days)or Azithromycin (5 days)

346
Q

Chronic infection over 2 days

A

Think Anaerobes: Add Metronidazole 500 mg 1
time then 250 q 8 hr for 14 days
or

Clindamycin 300 mg initially, then 150 mg q
6 h for 7 to 10 days

347
Q

General rule for antibiotics -step 1

A

Pencillin 500-1000 mg QID Cephalexin 500-1000 mg QID Erythromycin 250-500 mg QID Amoxicillin 500-1000 mg TID For 2-3 days
If better continue If not better, then:

348
Q

General rule for antibiotics step 2

A 
•
500 mg stat then 250 mg TID
Add Metronidazole
•
With to Clindamycin
•
150-300 mg QID
•
If not successful then:
•
Culture &amp; sensitivity
•
•
Always consider incise &amp; drain and moist heat
349
Q

It is this doctor’s opinion that every sx patient should have

A

antibiotic prophylaxis. Consider chlorhexidine rinse to lower bacteria in the mouth.

350
Q

Surgical Prophylaxis
•Use —– regimen
•Plus 1 or 2 additional doses (for lengthy surgeries)
• Oral amoxicillin, penicillin VK, cephalexin, clindamycin
• IV Cefazolin, then oral cehalexin

A

bacterial endocarditis prophylaxis

351
Q

Note with renal failure, need to coordinate with nephrologist to have antibiotics taken after —.

A

dialysis

352
Q

When to prophylax electively with antibiotics:

A 
Compromised immune function
Poorly controlled insulin dependent diabetic patient (may continue antibiotic for 7 to 10 days)
Renal failure with dialysis (may continue antibiotic for 7 to 10 days)
Evidence of significant malnutrition or alcoholism (may continue antibiotic for 7 to 10 days)
Symptomatic HIV (may continue antibiotic for 7 to 10 days)
Immunosuppressant drugs

Inflammatory arthropathies, including rheumatoid arthritis and systemic lupus erythematosus
•First 2 years following joint replacement (?)
•Previous prosthetic joint infections

353
Q

Joint replacement: if it heals properly, in —– it is encapsulated by fibrous tissue and is avascular and cannot be infected. You need CT to determine full osseointegration, and you need to be pain free. When in doubt, just consult with the surgeon.

A

6 weeks

354
Q

How long should surgical prophylaxis be administered for

A

B. Beginning within 2 hours prior of the surgical procedure and discontinued so the blood antibiotic blood level is not detected within 24 hours following placement of the final suture

355
Q

Avoid metronidazole with — patients

A

lithium

356
Q

No booze for 3 days after —- tx

A

metronidazole

357
Q

Erythromycin, Clarithromycin or Metronidazole with Oral Anticoagulants
l
Can get marked increase in —-

A

Warfarin levels

358
Q

Glucocorticosteroids - help with pain management tremendously over long periods of time.

Step 1: if the patient is OK with it, give a —- injection to keep the pt numb for that time. Worst post-op pain is within ——. Always give a post-op call the evening of the procedure. Have desk staff call the morning after the procedure to check for pain, and check for numbness, let them know if they have pain and swelling, go on.

A

marcaine

3-6 hours, and marcaine helps

359
Q

Recommendation, vast majority of sx patients get 1 antibiotic dose 1-2 hours preoperatively. It will take 24-48 hours post-operatively to develop infection, so if the patient develops pain or swelling, get a call. NSAID given IV (ketoralac), or you can do IM but it is painful. If tylenol/ibuprofen regiment doesn’t work, alltram 50mg-100mg every 12hr can work.

A

Vast majority of pts given glucocorticosteroids that can last 3-7 days. Often, opioids can cause problems with function during medication. Only thing oral opioids are truly good at is preventing cough and diarrhea. If taking opioids, day 6, 7, will start dependence.

360
Q

7 days or less, steroids are great. Often, —- can start if you have too high of a dose. Consider 1 short acting, 1 long acting in each arm.

A

anxiety

361
Q

Everytime you cut a cell membrane, — will rush out. Phospholipase A2 act on these ——, which organizes them into —–. This is then acted on my lipooxygenase, COX-1 and COX-2. Steroids block ——, and you block formation of a lot of arachidonic acid. Then COX-1 does good things, COX-2 causes inflammation and thus pain. Lipooxygenase however makes slow reacting substances of anaphylaxis - leukotrienes. These can cause asthma attacks, feeling of slowness and motion issues.

A

phospholipids

arachidonic acid

phospholipase A2

362
Q

COX-1 acts on —- that makes good things happen. —– formation, helps protect stomach lining. Creates prostacyclin PGI-2. Helps with perfussion of blood through kidneys, which also helps with blood pressure. Dilates small blood vessels preventing blood clot formation. Also puts out low levels of PGE2, which repairs microfractures in the bone.

A

arachidonic acid

Prostaglandin

363
Q

Now that said, Ibuprofen blocks off —– to some degree. Only use NSAIDS for —-, 6-10 days at the absolute most, because we cannot hamper —-

A

COX-1

3-5 days

COX-1.

364
Q

COX-2: cause pain, redness, swelling, everything bad comes from COX-2. That said, you need this, because when you do a bone injury, COX-2 puts out significantly more —- than COX-1 to repair and induce bone formation. This principle is also why COX-2 selective inhibitors are not a great idea, because you have significantly less —- and thus you interfere with new bone formation.

A

PGE-2

PGE-2

365
Q

Analgesics: Ibuprofen 200-400 mg is an analgesic dose to get rid of pain. To get rid of inflammation you need —–.** 800mg every 8 hours has no noticeable effect on GI upset compared to 600mg every 6 hours for 2-3 days. After that, transition to 600 mg every 6 hours. If you go every 8 hours, the last few hours will be without analgesia.

A

2400 mg in 24 hours

366
Q

If you give someone an aspirin tablet and have an asthmatic attack with it, you probably can’t give them

A

any other NSAID. They have a ton of cross-class hypersensitivity.

367
Q

If you take a COX-1, COX-2 inhibitor for prolonged periods of time, you create a ton of —-, and are prone to rashes. If you block both COX-1 and COX-2 for too long, you have a —— problem, whereas —— can be taken long-term. THIS WILL BE ON THE EXAM

A

leukotrienes, leukotriene

COX-2 blockers

368
Q

If NSAID intolerance, use

A

acetaminophen

369
Q

If they only have —-, get a med consult for NSAIDs.

A

1 kidney

370
Q

Stomach ulcers?

A

no NSAIDS. If it was 5 years ago, again get a med consult, consider lower dose.

371
Q

If mild allergy after prolonged NSAID use, and it has been —–s, use.

A

6 week

372
Q

Concurrent antihypertensive therapy - all pts taking antihypertensives tend to have —-. COX-2 selective are better at this. If someone is taking antihypertensives, you need to know their baseline BP, give 600mg Ibuprofen every 6 hours for a week, check BP day 1, day 3, day 5, 7, 10. This will 100% be on the exam. Pt on antihypertensives can take NSAIDS for 3-5 days, have them check their BP at above day, or bring them into the office to check.

A

renal problems

373
Q

Increase BP due to perfussion in kidneys. Usually NSAIDS raise diastolic BP by —–.

A

10mmHg

374
Q

If pt presents with —-, check their NSAID consumption.

A

lichen planus

375
Q

PGs ↑ # and activity of osteoclasts, replication and differentiation of osteoblasts, angiogenesis and vasodilation= —–

A

bone resorption

376
Q

COX-1: expressed in normal bone and at bone fracture sites
COX-2: up-regulated during —–
Osteoclasts and osteoblasts produce — (PGE2)

A

initial stages of bone repair

PGs

377
Q

Glucocorticosteroids Long-term chronic use—– expession and therefore PG production

A

↓ COX-2 - result is bone loss

378
Q

Glucocorticosteroids Long-term chronic use—– expession and therefore PG production

A

↓ COX-2 - result is bone loss

379
Q

Celebrex - someone takes it all the time, stop it —– If someone is self-medicating with ibuprofen, stop —— and you can’t use this as the analgesia post-op. Tylenol and steroids can help.

A

2weeks before, 2 weeks after.

2 weeks before, 2 weeks after,

380
Q

Flurbiprofen is just ibuprofen with —- - it is ——. Low dose is a minor improvement of bone, 100mg flurbiprofen helped bone formation and maintenance tremendously. 30 days ———–r - if they need it give 100mg flurbiprofen twice a day.

A

fluoride

bone sparing

2 weeks before, 2 weeks afte

381
Q

The problem is that flurbiprofen has a lot of —- associated problems with 30+ days of use. Do not volunteer this, only when a patient is extremely weary of going without NSAID for those 2 weeks pre-op. 30 days is an extremely firm number.

A

GI

382
Q

NSAID: Clinical recommendations:
Limit routine NSAID use —– thereafter PRN and/or switch to Acetaminophen with/without narcotic
•
Use a non-specific COX inhibitor

A

to 5 days

383
Q

If chronic NSAID use: use

A

Use Flurbiprofen 50 – 100 mg twice a day
Monitor patients blood pressure
Take drug free holidays.

384
Q

ASA Dose for MI/Stroke prevention:

81 MG. INHIBITS

A

THROMBOXANES, BUT NOT PROSTACYCLIN (PGI2)

SO PREVENTS CLOTTING AND STILL ALLOWS VASODILATION AND PREVENTION OF PLATELET CLUMPING

385
Q

ASA dose during MI;

325 MG. PREVENTS CLOTTING BY

A

THROMBOXANES
• BUT THERE IS MUCH MORE TBX2 DUE TO RELEASE FROM MONCYTES AND
EOSINOPHILS

386
Q

Acetaminophen: Only Inhibits Cylcooxygenase In Areas Of Low —–

A

Peroxide Formation (wounds never have this)

387
Q

Acetaminophen: Much more narrow window of toxicity than ibuprofen. If you take 2 tylenol every 2 hours, you would have hepatotoxicity and be in liver failure. You have lower toxicity if you have depleted —-

A

glycogen (everyone over 65, or anyone who has more than 3 alcoholic beverages daily).

388
Q

Levonordefrin = what is in carbocaine. It is an analog of —– - has little or no —-. As a result, you don’t have vasodilation. Often, carbocaine with this drug has more levonordefrin to meet the parameters that epinephrine. It is 1/5th as strong, but they give 5x as much of it. At least with epi, and you spike systolic BP, you bring diastolic BP down with beta 2 activity. With levonordefrin, you raise systolic bp and maintain diastolic bp. This is the worst drug to use in the cardiac unstable pt.

A

epinephrine

beta 2

389
Q

With selective beta blockers, you won’t have ==== rising, as beta 1 is only blocked. Vasoconstriction will be balanced with vasodilation in large vessels.

A

heart rate

390
Q

Non-selective beta blockers

A

Propranolol - Rx Inderal

Nadolol - Rx Corgard

391
Q

With non-selective blockers, you have non-combated —-.

A

vasoconstriction

392
Q

When dealing with hypertensive crisis or bradycardia: —– is the reason for the bradycardia, (BP = CO*Rate). —- is released when htn crisis occurs, and your HR plummets. You must deal with BP first and foremost. Nobody dies from bradycardia in the dental office. Atropine = anticholinergic, halts bradycardia.

A

hypertension

Acetylcholine

393
Q

Seizure to blood vessel rupture due to —- = subarachnoid hemherage. In this situation, nitroglycerin pill under the tongue would have stopped the problem.

A

high BP

394
Q

Nitrous is a —–.

A

vasodilator

395
Q

Do not be afraid of administering nitro - unless they came in —- (systolic less than 90), 1 tablet will not do just about much of anything. If you have someone with a headache or indigestion, just consider administering.

A

hypotensive

396
Q

You can readminister nitro every—– minutes, but never below 90 systolic bp. Once the patient is unconscious or has slurred speech (once they’ve had a stroke at the exact moment), do not give nitro. The reason for this is that they need a higher BP to keep the brain perfusing.

A

3-5

397
Q

Question: What side effect would you expect if epinephrine is administered to a patient taking Inderal 40 mg daily?

A

Htn crisis

398
Q

TCAs
Within 2 weeks, —% of the postsynaptic receptors will get internalized, then you don’t have as many receptors. You then still feel good due to receptor saturation, not receptor activation.

Drug interaction between epi and TCAs whenever dosage changes upwards or whenever TCAs are prescribed - within 2 weeks (due to 50% of receptors going away by this 2 weeks time).

A

50

399
Q

TCA with Epi
Block active reuptake of —– Get potentiation of affected neurotransmitter
Epi subject to same affects

A

amine neurotransmitters

400
Q

COMT Inhibitors with Epi

A

tachycardia can results

401
Q

COMT Inhibitors with Epi

A

tachycardia can results

402
Q

Secondary way for epi metabolism - MAO monoamineoxidase. The issue is that this doesn’t work as fast. If you have a pt with a —-, they won’t metabolize it as quickly. So, you must use less epinephrine.

A

COMT inhibitor

403
Q

Eldepryl is a MAO inhibitor - this is when someone’s health has progressed further for parkinson’s, etc. If they are only taking MAO inhibitor but not COMT, you can

A

still use epi just less. If both, you cannot use epinephrine.

404
Q

Biggest drug combo to be worried about with epi?

A

B. COMT (Comtan, Tasmar) inhibitor with a high dose MAO-B inhibitor (Eldepryl)

405
Q

Hold your —- meds for after the dental appointment.

A

thyroid

406
Q

Thyroid hormone and vasoconstrictors

A

• May cause dysrhythmias, ⇑ cardiac output, ischemia

407
Q

—- after endo, you will not have sensitivity issues.

A

2mg dextramethosone

408
Q

Never give steroid for more than – days. In medicine, they do and they have to contend with all of the problems. —- therapy is ideal.

A

7

2-4 day

409
Q

If you give a diabetic pt a steroid, let them know that their glucose levels will —-. Short term —— (>250mg/dl) is not a big deal, but over a long term it is tremendously damaging.

A

rise

ketoacidosis

410
Q

Steroids also potentiate catecholamines, so it —- htn.

A

boosts

411
Q

Chronic steroid use gives the opposite response - —–. Vs giving it one time when you mix it in with graft material. If you take 10mg prednisone for more than 2 weeks, you see the beginning of bone loss.

A

osteoporosis

412
Q

Always use low or moderate doses (high dose for ——).

A

dysthesia/parasthesia

413
Q

With steroids, That said, no matter the dose, —- activity will drop. —— have a lifespan of 7 days. Most have a lifespan of 3-4 weeks. Every day you make —-, and the problems arise when you are taking the steroid long enough to have each daily batch affected so that all you have are affected ——.

A

lymphocyte

Lymphocytes (go to T and B cells)

lymphocytes

lymphocytes

414
Q

No steroid in the presence of

A

noticeable infection, even though the doses will not cause problems.

415
Q

Never stop steroid dose

A

abruptly - always taper.

416
Q

If patient takes daily steroids:

A

Double, triple, or even greater, their daily dose
•
of the steroid on the day of surgery
Taper the dose off over the next several days
•
to the their traditional dose
Or give IV short acting steroids and longer
•
acting IM suspension steroids

417
Q

Steroid Relative Contraindications


A 
Peptic ulcer
Diabetes mellitus • Hypertension
Pregnancy
• •
Osteoporosis
 •
• Psychosis
  •
• •
Epilepsy Renal failure
418
Q

Problem with pre-op steroids:

A

strong inducer of the same enzyme that metabolizes benzos, so you just made your job a lot tougher.

419
Q

Steroids at time of nerve injury limit

A

inflammation (inflammation is the cause of the nerve damage).

420
Q

If a1c is 7 or less, give—- of steroid dose for diabetics. It won’t be the same effect, but it’ll help. Greater than —–, your call (I personally wouldn’t). High BP, even when controlled with meds, give —% of dose of steroid.

A

25-30%

7.5, never give a steroid. 7-7.5

30-50

421
Q

This is “OR” never use dexamethasone and prednisone —–.

A

simultaneously

422
Q

• These medicaYons dosage needs to be increased if give dexamethasone

A

AnYanxiety and anYpsychoYc drugs AnYhypertensives
Hypoglycemics
sympathomimeYcs

423
Q

Definitive contraindications for steroid use

A 
Diabetes
Pregnancy
Immuno-compromised
Active peptic ulcer
Osteoporosis
Active herpetic or fungal infections
Avoid high doses in patients with psychoses
424
Q

Definitive contraindications for steroid use

A 
Diabetes
Pregnancy
Immuno-compromised
Active peptic ulcer
Osteoporosis
Active herpetic or fungal infections
Avoid high doses in patients with psychoses
425
Q

Zoran (Ondansetron) -

A

4mg and 8 mg
•
Selective 5-HT3 (serotonin) receptor antagonist
Used to treat N&V caused by surgery or medications
•
used to treat cancer (chemotherapy or radiation)
Do Not administer if the patient is taking
•
apomorphine
• •
Do not adminiister if the patient has PKU Erythromycin drug interaction

426
Q

Note: not every NSAID is created equal - ——- will not have as much of an effect on risk of post-op bleeding.

A

celebrex or COX-2 selective

427
Q

If excess bleeding, keep pt in office for —-, keep track of them for 24 hours.

A

5 hours

428
Q

If someone is on coumadin and you give a Rx, go on lexicomp to be sure tha the antibiotic won’t

A

potentiate coumadin. Antibitoics longer than 3-4 days will likely increase INR.

429
Q

When in doubt, a consult over —is not a terrible idea, especially if you have someone claiming little to no medication.

A

75

430
Q

With eliquis, If excess bleeding, hold for

A

1 day, if still going, hold for 2 days and inform physician.

431
Q

Aspirin - Never stop, never go less than —-, just have them ramp it down. If they go off aspirin, they can have hypercoagulopathy.

A

325 or 81

432
Q

Plavix

A

No lab tests monitor it, no antidotes. Never stop it. The first 2 weeks they can have thrombocytopenia purpura (decreased platelets), and usually this follows stent placement. Do not do sx on these pts.

433
Q

Above —, don’t worry. Under —, don’t do sx, give sugar. Use their glucometer for consistency if possible.

No regular —- the day of the procedure, get them eating ASAP.

A

140

100

insulin

434
Q

If diabetes pt takes medicine orally, be sure that they eat a ——– breakfast

A

high protein

435
Q

•Epinephrine causes increased — and increased

A

gluconeogenisis

glycolysis (∴ ↑ blood glucose)

436
Q

•Glucocorticosteroids increased

A

gluconeogenisis (∴ ↑ blood gluscose)

437
Q

EPINEPHRINE WITH INDERAL OR CORGARD (or high dose selective β-1
bockers)

A

CAN LEAD TO A BAD DAY – HYPERTENSIVE CRISIS

438
Q

ACETAMINOPHEN IN THE ALCOHOLIC

A

– KEEP HIM DRINKING, THIS ISN’T THE TIME TO QUIT!

439
Q

ACETAMINOPHEN IN THE ALCOHOLIC

A

– KEEP HIM DRINKING, THIS ISN’T THE TIME TO QUIT!

440
Q

ACETAMINOPHEN IN THE ALCOHOLIC

A

– KEEP HIM DRINKING, THIS ISN’T THE TIME TO QUIT!

441
Q

Idea is that activated bound platelets dump —– If the receptors for said factors are present, any given growth factor will start causing changes. Concentration of the platelets is purely dependent on the homeostasis of the body. The idea is to concentrate these platelets 7x, so that we can have the optimal dose of healing for bone. Note: this technique will cause scarring.

A

growth factors.

442
Q

Buffy coat PRP is ——. This will reach out 8 nanometers to physically coax stem cells in. The effect is felt up to —-. It is also —-, meaning that the stem cells will be induced.

A

chemotactic - it will call in stem cells to help improve healing with demineralized bone grafts

1.5cm away

mitogenic

443
Q

PRF: no concrete evidence to that it is —-. Ultimately, buffy coat PRP is the ideal.

A

chemotactic

444
Q

So why bother with both PRF and PRP? PRP lasts — days, and after—-days, PRP and PRF are a wash. 7 days +, PRF is releasing more growth factors, and can continue doing so for 30 days.

A

10-12

5-7

445
Q

PRP Always grab — top first, turn over — times to mix —– thoroughly to prevent clotting. Red top is last to prevent it from clotting.

A

yellow

12

sodium citrate

446
Q

Optimal speed for WBC: —- RPM for 10-12 minutes. Tape will create optimal dose for growth factors. 4.5% weight volume is the sweet spot that this marker creates.

A

3100

447
Q

If the PPP is —–, the pt had a high-fat meal within the last 24 hours. Recommend that they get their cholesterol checked.

A

cloudy

448
Q

Blood supply to bone graft in first 72 hours is practically nil. If you take —-, you more or less bypass this.

A

PRP with WBCs

449
Q

Pure PRP does not have

A

WBCs, is not as favorable.

450
Q

PRP does not work without a

A

carrier (collagen or bone grafting material).

451
Q

To have true chemotaxis, you need to have

A

WBCs.

452
Q 
PRPTechniques
•
blood collected with anticoagulant
immediately processed by centrifugation
platelet concentration completed within one hour separates blood into 3 layers
• • •
Common points
A

Platelet-Poor Plasma (PPP) Platelet-Rich Plasma (PRP) Red Blood Cells (RBCs)

453
Q

Choukroun’s PRF (Platelet-Rich Fibrin)
•
•
•

A

whole blood collected without anticoagulant and immediately centrifuged
natural process occurs for the easy collection of a leukocyte- and platelet-rich bring (L-PRF) clot
no anticoagulant, thrombin, or calcium chloride

454
Q

PRP, PRF: dont use —- to prepare

A

bovine thrombin - anaphylaxis

455
Q

BC-PRP mainly beneficial if used with

A

demin bone

456
Q

BC-PRP mainly beneficial if used with

A

demin bone

457
Q

Venipuncture: •—– are the crucial structures to avoid
–found deep to the Basilic Vein in the medial aspect of the arm –DO NOT probe or explore this DEEP in this area with the
needle
–If patient experiences a shooting pain down to the fingers or up to the shoulder, terminate the procedure immediately

A

Median nerve and Brachial artery

458
Q

Venipuncture: •Uncontrolled hematoma –Can lead to ——

A

compression nerve injury

459
Q

• Surfaces contaminated with blood must be cleansed with

A

– Sodium hypochlorite

460
Q

• Hemolyzed: — • Lipemic: —– • Icteris: —-

A

red

cloudy

yellow (juandice)

461
Q

Which blood test is critically affected by hemolyzed specimen

A

Potassium

462
Q

Specimens are rejected by the laboratory for all of the following reasons: (Must Know)

A
  • Clots in a lavender stopped tube (contains EDTA) • Collec;on in the wrong tube
  • Incompletely filled light blue stopper tubes
463
Q

Quality Issue: Hemolysis

A

Causes and PrevenGon Rupturing of RBCs
Due to poor “sGck” CollecGng from hematoma
Residual alcohol Improper mixing

464
Q

SERUM =

A

Liquid por;on of blood obtained when specimen is allowed to clot

465
Q

PLASMA =

A

Liquid por;on of blood obtained when blood is collected

with an an;coagulant

466
Q

Liquid Por;on of Blood Collec;on Tube Aier Centrifuging
(Must Know)
• Non-an;coagulated tube—–
• Heparinized (Green top) or —– tube (Yellow top) - —-

A

(Red top) - Serum

Tri-sodium citrate

Plasma

467
Q

An;-coagulated, un-centrifuged blood specimen
(Must Know)
• Referred to as —-

A

Whole Blood

468
Q

An;-coagulated, un-centrifuged blood specimen
(Must Know)
• Referred to as —-

A

Whole Blood

469
Q

Transferring blood from a syringe to an evacuated tube:

Must Know

A

Use a blood transfer device Needle-less transfer of blood

Prevents transfer injuries Maintains integrity of blood Sterile

470
Q

Yellow anti-coagulated ACD Tube

• • • • •

A

ACD = Acid, Citrate, Dextrose Prevents cloeng by binding calcium Dextrose preserves the red cells Mix 12 Gmes (gently inversion) Provides PRP

471
Q

Failure to gently and immediately mix an an;-coagulated specimen may result in: (Must Know)

A

• Clot Forma;on

472
Q 
Plain Red Clot Tube
Red Top
  • Contains NO anGcoagulant
• Contains ---- as a clot acGvator
• Mix 5 times
• Blood clots in about 30 minutes
• Provides PRF membrane
A

silica

473
Q

Which tube will be rejected by lab if not completely full

A

Light blue

474
Q

Tube with EDTA (purple) cannot be used for

A

Determining a calcium level

475
Q

Tubes with Separa;on Gels

Must Know

A

*• Gold hemogard closure tubes
• Light green herogard closure tubes
• red with gray marked rubber stopper tubes

*red stoppers do not contain separation gel

476
Q

Blood collec;on Order

A 
(Must Know)
1. Yellow
2. Light Blue 3. Red
4. Lavender
Acronym: YLRL (yellow light, red light)
477
Q

Must Do Items

Must Know

A
  • Correct pa;ent iden;fica;on • Assure quality of specimen

* Correct ;ming of collec;on

478
Q

The Most important step in the venipuncture procedure is: (Must Know)

A

• Iden;fying the Pa;ent

479
Q

The minimum required number of pa;ent iden;fiers required by the joint commission is:
(Must Know)

A

2

480
Q

To avoid test interference the maximum ;me a tourniquet can remain on the pa;ent’s arm is:

A

1 min

481
Q

Areas that should not be used for blood collec;on are: (Must Know)

A
  • From a hematoma

* An arm with a running IV • An arm with a fistula

482
Q

The needle is inserted into the vein:

Must Know

A

• Bevel up at a 15 - 30 degree angle

483
Q

Bracing the hand holding the needle assembly against the pa;ent’s arm accomplishes what:
(Must Know)

A

• Prevents excess needle movement

484
Q

A hematoma may be caused by:

Must Know

A
  • Removing the tourniquet AFTER removing the needle
  • Bandaging the pa;ent’s arm immediately aier needle removal (not confirming clot forma;on)
  • Having the pa;ent bend the elbow and apply pressure
485
Q

Prior to bandaging the puncture site, the phlebotomist should: (Must Know)

A
  • Examine the site for bleeding

* Apply pressure for at least 5 minutes

486
Q

What should the phlebotomist do once the last required tube is filled: (Must Know)

A

• Filled tube is removed from the vacutainer holder

487
Q

Pushing the evacuated tube through the stopper tube puncturing needle before entering the vein will result in: (Must Know)

A

• Failure to obtain the specimen

– Reason: the vacuum is no longer available for pulling the blood into the vacutainer tube

488
Q

Upon comple;on of the blood collec;on, the holder is: (Must Know)

A

• Discarded with needle a\ached

489
Q

Remember to include —– when labeling vials of blood

A

Patient Name, date, time

490
Q

When blood is not obtained when the needle is inserted into the vein, the phlebotomist may try: (Must Know)

A
  • Gently advancing the needle
  • Gently pulling the needle back
  • Inser;ng a new tube into the holder
491
Q

When blood collected in a syringe must be placed in vacutainer tube the phlebotomist should:
(Must Know)

A
  • The needle safety device is ac;vated
  • The needle is discarded
  • A blood transfer device is a\ached to the syringe
492
Q

When an vacutainer tube is pushed onto the needle, and blood begins to flow into the tube, but then stops. This can be caused by:
(Must Know)

A

• Collapsing of the vein
• The bevel of the needle is res;ng on the vein
wall
• The vein is occluded (valve is present)

493
Q

Lymphedema-

A

swelling caused by lymph accumula;on in the ;ssues causing increased suscep;bility for infec;ons
Do NOT collect blood from same side as mastectomy
•
MASTECTOMY
Use other arm or if double mastectomy, use hand or
•
perform capillary s;ck

494
Q

The first thing a phlebotomist should do when a pa;ent develops syncope is: (Must Know)

A

• Remove the tourniquet and needle

495
Q

Older pa;ents are more prone to hematoma forma;on because: (Must Know)

A

• The veins of geriatric pa;ents have decreased elas;city

496
Q

For children, use veins in —— . Other sites include the —–.

A

antecubital fossa

medial wrist or dorsal side of the hand

497
Q

When performing venipuncture on a pediatric pa;ent, the phlebotomist may require:
(Must Know)

A

• A pediatric requisi;on • Small vacutainer tubes

498
Q

Use the Platelet-Poor- Plasma (PPP)

A

Place gauze soaked with PPP over the incision
•
areas to promote coagulation

499
Q

Osteoclasts actively controlled by

A

PTH

500
Q

Periosteium composition

A

• Periosteum: 2 layers of special connective tissue • *toughouterlayerofdensecollagen
*inner cambium layer in direct contact with bone, containing functional osteoblasts

501
Q

• Periosteum’s osteoblasts have great —– potential, so it has to be positioned carefully after surgery to nurture the graft and underlying bone. A major source of blood supply to graft.

A

osteogenic

502
Q

General rule of thumb with BMPs:

A

keep it at the site of use - use the sponge!

503
Q

General rule of thumb with BMPs:

A

keep it at the site of use - use the sponge!

504
Q

Purpose of emdogain

A

serve as chemical mimic to hertzwig root sheath to hopefully induce attachment and cementoblast differentiation

505
Q

Emdogain results

A

It works, but rarely true perio attachment, and we don’t fully know what is going on yet.

506
Q

Emdogain results

A

It works, but rarely true perio attachment, and we don’t fully know what is going on yet.

507
Q

—- is the key bone forming hormone. As we age, you lose this —– (men lose it later in life, as it is converted from —–).

A

Estrogen

testosterone

508
Q

Cortical bone is where you go for —-. Calcium is extremely important in your practice ultimately. Your patient needs enough calcium intake and vitamin D (absorbs calcium) to form/remodel bone. Recommendation: if you have a case that has failures, or if you have an extremely large case, get a —– reading if all else is normal.

A

BMPs

vitamin D

509
Q

For postmenopausal pts, use —– calcium, vitamin D, vitamin K (Keeps calcium in bone) combo. You cannot have a patient on —- take this.

A

ossteok

coumadin

510
Q

Lack of estrogen also leads to decreased —- - bone becomes brittle. Bisphosphonate pts also experience —– issues and remodeling issues (over 2.5-3 years, because the bone is dead).

A

collagen

511
Q

Demineralized freeze dried bone: took bone from donor, treat it with acid, and in doing so, you wash away all of the mineral component or a portion of it, and you free up BMPs that are captured in mineral matrix, and now these are available to stimulate any stem cells in situ. Every bone graft that you do, particularly in an older male/female needs to have a component of demin bone because of this.

A

Problem with this bone, it is 3-7% mineralized, and as such it doesn’t look like much on an x-ray. So, you can’t use 100% of this bone with sinus lifts. Thus, some add mineralized bone, which absorbs slower and is radiopaque.

512
Q

Osteoblasts: Located in two areas:

A

in periosteum and endosteum lining vascular canals in bone

513
Q

Osteoclasts dissolve bone, releasing

A

BMPs • BMPaffectsundifferentiatedmesenchymalstemcells, turning them into osteoblasts, and thus stimulating new bone production.

514
Q

Thus, if you really need to put a membrane, make sure it is right where your incision line is, unless you scored your flap (in which case the periosteum is destroyed, and you should only place a membrane where you scored the flap). Recommend laying flap, sling suture, emdogain on adjacent teeth.

A

Periosteum’s osteoblasts have great osteogenic potential, so it has to be positioned carefully after surgery to nurture the graft and underlying bone. A major source of blood supply to graft.

515
Q

• Phase I Woven bone

A
  • Develops quickly but does not last long

* Disorganized but highly mineralized

516
Q

• Composite bone:

A

transition between phase I and II

• Mixture of the two types of bone

517
Q

• Phase II Lamellar bone

A

• Replaces woven bone slowly
• Extremely strong, well organized protein
and mineral structure

518
Q
  • Osteoblastsandstemcellsingraftsurvive

* Osteocytes die —–

A

3-5days

immediately

519
Q

• Plateletsingraftdegranulatewithinhoursandrelease —-

A

PDGFs

520
Q

Because of O2 gradient and PDGFs, capillary buds

from recipient site appear by—–

A

day 3, and form a complete network by day 14

521
Q

By day 10, osteoid minerals are beginning to form from —- of graft, —- in graft, and circulating —- that are attracted to the wound (osteoinduction

A

endosteal osteoblasts

stem cells

stem cells

522
Q

By 3-4 weeks, osteoid production is consolidating graft by building on graft’s fibrin network——-

A

(osteoconduction)

This is Phase I Regeneration which forms woven bone

523
Q

• Osteoinduction=

A

stimulatingosteogenesis even in areas where bone is not normally found

524
Q

More BMPs in —- - so you want to use a mix of demin —– bone (you want variable chunk sizes - 150-500microns of this - different sizes leaves gaps for vascular ingrowth) and mineralized —– bone (250-750 micron).

A

cortical

cortical

cancellous

525
Q

Demin will resorp over—–, mineralized will resorb over —– weeks. Both are resorbing at around the same time. Typically you can go into grafts at 12 weeks if you use PRP.

A

8-12 weeks

10-16

526
Q

The larger the particles, the —–

Porosity (100 -500 um), the more scaffolding it provides the —–

A

longer it takes to resorb

quicker it resorbs

527
Q

Biooss or salvinoss (dr rut uses this at —-% ratio of every graft).

A

20

Dr. recommends with 20% xenograft to wait 16-20 weeks to place/re-enter (with PRP).

528
Q

• Smallerparticles

A
  • Resorbfaster
  • Lessfibrous encapsulation
  • Moreboneingrowth
  • Fasterboneingrowth
  • Provides a large surface area around which more bone may form
529
Q

• Largerparticles

A
  • Resorbsslower

* Morestructuralintegrity

530
Q

Minimum pore size of —- necessary for bone to grow into the material

A

100 μm

531
Q

Recommends 70/30

A

min demin

532
Q

When in doubt, extend flap —- to have greater closure capabilities. Consider putting PRF, dermal matrix over titanium mesh if they have a really thin biotype, as they may not be able to handle thermal changes. If alloderm is exposed, you have a problem, but if you have PRF you have a better chance of keeping that mesh in there for longer.

A

distally

533
Q

When doing onlay grafts, nothing in the mouth for —weeks, essix after that time. Not recommended to do a flipper for these cases.

A

3

534
Q

Doc does not recommend block grafts, as his concern is that they never truly osseointegrate. With particulates, putty, tenting screws, you can get a preferred outcome. If you do a block graft, you decorticate both bone and block. Blocks worked fine until the patient went —–. Once they lost the estrogen, they tended to have implant failure. Hypothesis is that it was never truly live bone. Osteotomies in these bones also didn’t tend to bleed. Allosulpt is mentioned a few times - what is it?

A

post-menopausal

535
Q

Best mix for grafting: mix of 7030 min to demin bone, 20% xeno, membrane. Up to 3mm of opening, —-. 3-5mm, PRF is fine, tissue will move over —- a day, within 2 weeks it will be closed. Greater than —-, you need to consider doing something to help closure. Put PRF down first, then put ——

A

PRF or collagen is fine

0.5mm

5 mm

PTFE membrane stippled side up (nonexpanding).

536
Q

Recommendation: chlorhexidine can interfere with —-, which is essential for soft tissue healing. That said, if it is infected (localized), chlorhexidine is great.

A

fibroblast formation

537
Q

Oracell (ADM)

A

• Subepithelial connective tissue grafting – Flap
– Tunnelling
• Thickening of thin biotypes
• Collagen barrier applications
• DO NOT leave exposed
• Predictable if covered with preferably native soft tissue
• If any is exposed - cover with a perio pack

538
Q

Socket grafting grade 1

A

Particulate bone, collagen

539
Q

Socket grafting grade 2

A

particulate bone with membrane to retain material, putty

540
Q

Socket grafting grade 3

A

allosculpt, tenting screws, membranes or barriers

541
Q

Autogenous bone is great for grafting adjacent to ——-

A

exposed implant threads

542
Q

Dr. Rut bone graft mix:

A

7030 min, demin cortical allograft.

A1 (5 decks)

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