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Pharm II > Final > Flashcards

Final Flashcards

1
Q

How many mg/mL is 2% lidocaine

A

20mg/mL

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2
Q

How is remifentanil metabolized

A

By esterases

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3
Q

Cytochrome p450 enzymes metabolize what

A

Lidocaine and midazolam

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4
Q

Proton pump inhibitors end in -_

A

-prazole

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5
Q

Serotonin 5-HT3 inhibitors (antiemetic properties) end in -_

A

-estrone

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6
Q

Propofol is metabolized where

A

The liver

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7
Q

Atenolol is metabolized where

A

The kidney

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8
Q

-olol

A

Beta blocker

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9
Q

-sartan

A

Angiotensin II Receptor Blocker (lowers BP by relaxing blood vessels)

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10
Q

-inol

A

Xanthine oxidase inhibitors like allopurinol, prevent gout

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11
Q

-pril

A

Angiotensin converting enzymes like lisinopril treat hypertension and heart failure

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12
Q

Metformin

A

Diabetes

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13
Q

Glargine

A

Insulin

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14
Q

Humulin

A

Insulin

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15
Q

Hemostasis tripod, mechanism

A 
Primary hemostasis (platelets)
Coagulation (chemical)
Vasoconstriction (mechanical)
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16
Q

Hemostasis tripod is balanced by _ activity

A

Anticoagulant

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17
Q

In primary hemostasis, platelets adhere to disrupted VESSEL WALL via _ and _

A

Platelet surface membrane glycoprotein receptor Ib
And
von Willebrand factor

1b and vWF

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18
Q

Platelets adhere to one another via _ and _

A

Surface receptor glycoprotein IIb/IIIa
And
Fibrinogen

2b/3a and Fib.

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19
Q

Two arachidonic acid vasoconstrictors

A

Thromboxane A2

Prostaglandins

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20
Q

Platelet surface provides site for what two things

A

Generation of thrombin

Subsequent fibrin formation

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21
Q

Tissue Factor - Factor VII pathway or extrinsic system steps

A
  1. TF exposed to blood
  2. Complex forms b/t TF and FVII
  3. FVII is activated to FVIIa
  4. TF/FVIIa complex binds and activates FX
  5. FX converts prothrombin (FII) to thrombin (FIIa) which requires FV as cofactor

7-10 PT to T

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22
Q

Coagulation alternate/secondary pathway

A
  1. TF/FVIIa complex activates FIX
  2. FIXa and CFVIII activate FX
  3. PT to T

8,9,10 T

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23
Q

Coagulation 3rd pathway

A
  1. Thrombin activates FXI
  2. FXIa activates FIX
  3. More thrombin

T -> 9 -> 10 -> T

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24
Q

Thrombin mediates _

A

Fibrinogen cleavage

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25
Q

What is the ultimate step in the coagulation cascade

A

Cross-linking of fibrin by thrombin activated factor XIII

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26
Q

3 natural anticoagulation mechanisms, where they work

A

Tissue factor pathway inhibitor (TFPI) - duh
Protein C - degrades CF V and VIII
Antithrombin III - inactivates T and FXa

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27
Q

Heparin strongly enhances _

A

Antithrombin III

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28
Q

_ degrades fibrin

A

Plasmin

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29
Q

How is plasmin formed

A

t-PA and u-PA activate plasminogen to plasmin

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30
Q

Most common coagulation disease

A

vW disease

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31
Q

3 types of vWDisease

A
  1. Reduced conc. (10-45%)
  2. dysfunctional vWF
  3. Absent vWF (homozygous for gene defect)
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32
Q

Treatment of vWD
Type I and IIa treated with _
Severe forms

A

Desmopressin (DDAVP)

Transfused factors

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33
Q

How long after surgery do you have to keep up vWD treatment

A

4-7 days

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34
Q

Hemophilia A is a disorder of what

A

FVIII

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35
Q

Treatment of hemophilia A

A

desmopressin (mild to moderate)

Factor 8 transfusion (severe)

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36
Q

Hemophilia B affects what

A

IX

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37
Q

2 hypercoagulable coagulation Diseases

A

Protein C/S deficiency

Factor V Leiden (factor V resists inactivation)

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38
Q

_ is the source of coagulation factors

A

Liver

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39
Q

Where are Protein C,S and fibrinogen made

A

Liver

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40
Q

What is MELD

A

Model for end stage liver disease score. Predicts 3 month mortality

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41
Q

T/F patients with renal failure often present with coagulation abnormalities and are at risk for enhanced bleeding

A

True

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42
Q

How to treat prolonged bleeding time in patients with renal disease

A

desmopressin

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43
Q

How does aspirin work

A

Inhibits platelet membrane associated cyclooxygenase

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44
Q

How long does aspirin effect last and why

A

Lasts until new, unaffected platelets can be made. Around 10 days

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45
Q

Discontinue aspirin for dental procedures?

A

NO

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46
Q

What is clopidogrel and what does it do

A

Oral anti-platelet prodrug metabolized by liver. Binds irreversibly to P2Y12ADP receptor on platelet surface.

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47
Q

What is Dipyramidole

A

Antiplatelet by inhibition of phosphodiesterase

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48
Q

The most potent inhibitors of platelet aggregation are _

A

Glycoprotein receptor IIb/IIIa inhibitors

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49
Q

How does Coumadin work

A

It’s an oral vitamin K antagonist

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50
Q

What does vitamin K do in the coagulation pathway?

How does this relate to Coumadin

A

Carboxylates FII, VII, IX, and X

Coumadin blocks this carboxylation

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51
Q

Coumadin has a _ dose-effect relationship

A

Variable

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52
Q

New oral anticoagulants affect what

A

Inhibit factor Xa

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53
Q

T/F you may want to discontinue new oral anticoagulants before oral surgery

A

True

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54
Q

Heparin is what, how does it work

A

IV or subcut. Anticoagulant

Binds to antithrombin III

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55
Q

How to monitor effects of heparin

A

PTT or

Whole blood activated clotting time

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56
Q

What are low molecular weight heparins, why use?

A

More favorable antithrombic effect and less bleeding complications

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57
Q

Pentasaccharides work where

Treat what

A

Xa

Treat DVT and PE

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58
Q

What is heparin induced thrombocytopenia

A

Immune response to heparin characterized by thrombocytopenia and thromboembolism

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59
Q

3 signs that might point to a defect in the coagulation system

A

Abnormal bruising
Petechiae
Splenomegaly

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60
Q

Which screens do you need if someone shows signs of a bleeding tendency

A

Platelet count
PTT
PT/INR

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61
Q

The PT value reflects coagulation of the _ coagulation pathway

A

TF-VIIa

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62
Q

aPTT
What does it measure
Common use

A

Activated partial thromboplastin time

Measures slower “intrinsic” pathway. Requires all clotting factors except VII.

Commonly used to monitor anticoagulation with heparin

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63
Q

Gold standard for platelet function analysis

A

Platelet aggregometry (PAA)

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64
Q

Why can we use empiric therapy for odontogenic infections?

A

The bacteria in odontogenic infections are fairly predictable and there is often not enough time for cultures to grow

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65
Q

Pros and cons of bactericidal drugs

A

Pros:
Rely less on immune system
Quicker
Maintain effect longer

Con:
Post antibiotic effects

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66
Q

Example of an organism with high PAE

What is PAE

A

Azithromycin

Post antibiotic effect - persistent suppression of bacterial growth after brief exposure to antibiotic

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67
Q

When to stop taking antibiotics

A

When sure patient is on their way to recovering based on clinical eval

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68
Q

3 adverse effects of antibiotics

A

Toxicity
Allergy
Superinfection

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69
Q

Antifungals are toxic to what

A

Liver

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70
Q

Penicillin and aminoglycosides can be toxic to what

A

Kidneys

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71
Q

C diff overgrowth aka

A

Pseudomembranous colitis

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72
Q

Which type of AB has the widest spectrum

A

Beta-lactate

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73
Q

Why is penicillin V good for oral microbes

A

It is narrow spectrum to oral microbes

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74
Q

When are β lactamase resistant penicillins indicated

A

For proven staph infections only

75
Q

When to use amoxicillin

A

Ear infection
UTI
SBE prophylaxis
If culture indicates

76
Q

T/F extended spectrum penicillins are indicated for head and neck infections

A

FALSE

77
Q

What is augmentin

When to use?

A

Amoxicillin and clavulonic acid

Rapid growing oral infection, or oral microbes in a distant site (bite wound)

78
Q

Unasyn: what and when to use and why

A

Ampicillin + sulbactam

Similar spectrum to augmentin, used for serious infections in hospital due to increasing resistance to PCN G

79
Q

most frequent DOC for odontogenic infection

A

PCN V

80
Q

When to use metronidazole

A

Significant anaerobic component

81
Q

When to use first gen ceph

A

Community staph
Surgical wound prophy
Odontogenic infection in patient with mild penicillin allergy
SBE and TJR prophy

82
Q

How do macrolides work

A

Bind 50s ribosomal unit, inhibiting RNA dependent protein synth

83
Q

Macrolides end in -

A

Mycin

84
Q

Clarithromycin is good for killing _

A

H. influenza

85
Q

When to use clarithromycin

A

Sinus infection
Mild to moderate odontogenic infection in PCN allergic patient
Pneumonia

86
Q

Azithromycin is good at killing

A

Strep and g- anaerobes

87
Q

Clindamycin kills what 4 things

A

Strep
Staph
Actinomycetes
Anaerobes

88
Q

Risk of clindamycin

A

Wide spectrum, can cause pseudomembranous colitis

89
Q

Metronidazole kills what

A

Anaerobes

90
Q

Tetracycline uses

A

Resistant hospital acquired infections
H pyloris
Topical
Dry socket

91
Q

4 things that make pain worse

A

Anxiety
Increased symp output
Poor rest
Inadequate oral intake

92
Q

3 orders or neurons

A

1 periphery to spine
2 spine to thalamus
3 thalamus to sensory cortex

93
Q

Both opioids and non-opioids act where

A

Centrally and peripherally to interrupt ascending nociceptive impulses

94
Q

How do NSAIDs work

A

Inhibit cyclooxygenase

95
Q

Cox 1 is responsible for what

A

Gastric mucosal barrier
Renal function
Platelet aggregation
Vasoconstriction

96
Q

Cox2 is responsible for what

A

Pain, inflammation, fever
Renal function
Platelet inhibition
Vasodilation

97
Q

Why are NSAIDs bad for asthma patients

A

Blocking cox1 can result in overproduction of leukotrienes that can make asthma worse

98
Q

3 absolute contraindications for NSAIDs

A

Allergy
Pregnancy
Erosive or ulcerative GI conditions

99
Q

Why not use cox-2 inhibitors exclusively?

A

Poor efficacy in 3rd molar model
Expensive
Increased emboli
Contraindicated in sulfa allergy

100
Q

How does Acetaminophen work

A

Prostaglandin synthesis inhibition in the CNS

101
Q

Daily maximum of acetaminophen

A

3,000 mg/day

2,000 if liver disease

102
Q

Mu vs kappa side effects

A

μ - dependence, constipation

κ - dysphoria, psychomimetic

103
Q

Strength of the code opioids

A

Oxy>hydro>codeine

104
Q

Why do we use the code opioids with acetaminophen

A

Synergistic with acetaminophen

105
Q

T/F it is the acetaminophen, not the opioid that dictates the dose/frequency when combined

A

True

106
Q

How much of the effect of the code opioids is from being converted vs the parent drug

A

Codeine = entirely from conversion to morphine

Hydrocodone = 1/2 effect from parent, 1/2 from conversion

Oxycodone = almost entirely from parent drug

107
Q

When to use tramadol

A

Chronic pain

108
Q

How does pre-emotive analgesia work

A

It inhibits prostaglandin synthesis

109
Q

Why are non-opioids first line for dental pain

A

Most has inflammatory component

110
Q

T/F there is evidence that ibuprofen is safer and more effective than other

A

FALSE

111
Q

How is NSAID dose chosen

A

According to contribution of inflammation to the pain experienced

112
Q

Non-narcotic scheduled dosing

A

Ibuprofen 600 mg Q6h

Acetaminophen 650 mg Q6h

113
Q

What is used for breakthrough pain

A

Tylenol + codeine (Tylenol 2,3,4)
Tylenol + hydrocodone (Norco)
Tylenol + oxycodone (percocet)

114
Q

Of drug OD deaths, opioids were what %

A

66%

115
Q

Opioid prescribing rules:
Days for adults/minors
Dosing average limit

A

7 days adults, 5 days minors

Can’t average >30 MED over the period

116
Q

Optimum pain management

A

Pre-emptive analgesics
Long acting LA
Step 1 plan for routine non-opioids
Step 2 plan for prn opioids

117
Q

T/F nausea is an allergic reaction

A

False

118
Q

S&S of allergic rxn

A

Skin rash/hives
Wheezing
Swelling
Anaphylaxis

119
Q

2 main uses for corticosteroids in dentistry

A

Trismus and edema

120
Q

Contraindications to corticosteroids

A 
Chronic infection
Peptic ulcer
Diabetes
Poor wound healing
Caution with NSAID use
121
Q

When to consider stress dose of steroid?

A

20 mg prednisone per day for
2+ weeks
In the past 2 months

122
Q

P wave represents

A

Atrial depolarization

123
Q

QRS complex represents what

A

Ventricular depolarization and implies contraction

124
Q

T wave

A

Repolarization of ventricles

125
Q 
Volume-pressure diagram
X
Y
Flow direction
Stroke volume
A

X is Lventricular volume
Y is L intraventricular pressure
Flow is counter clockwise
Stroke volume is x direction b/t two volume lines

126
Q

Aortic valve opens at what pressure

A

80 mm Hg

127
Q

Nodal cells vs muscle cell potential

A

Nodal is more curved

Myocyte looks like cursive r

128
Q 
Cardiac muscle action potential
Phase 0:
Cardiac cell _
Membrane becomes more _
_ open
_ enters
Membrane potential reaches _
A 
Depolarizes
Positive
Fast Na channels open
Na enters
Membrane potential reaches +20
129
Q 
Cardiac muscle action potential
Phase 1:
_ close
Cell begins to _
_ open
_ exit
A

Fast Na channels close
Cell begins to repolarize
K channels open
K ions exit

130
Q 
Cardiac muscle action potential
Phase 2:
_ open
Membrane charge _
Repolarization is delayed
A

Slow Ca channels open

membrane charge is balanced

131
Q 
Cardiac muscle action potential
Phase 3:
_ close
_ stay open
_ rushes out
Cell _
A

Slow Ca channels close
K channels stay open
K rushes out
Cell depolarizers

132
Q

Cardiac muscle action potential
Phase 4:
Cell membrane averages _

A

-90 mV

133
Q

Ohm’s law

A

Voltage = current x resistance

134
Q

Hemodynamics law relating to ohms law

MAP =

A

Pressure = flow x resistance

MAP = CO x SVR

135
Q

CO =

A

HR x SV

136
Q

Alpha 1 receptors are located in _

A

Vasculature

137
Q

Alpha 2 receptors are located _

A

In brain, nerves

138
Q

Beta 1 receptors are located _

A

Heart

139
Q

Beta 2 receptors are located

A

Lungs, Vasculature

140
Q

Inotropy vs chronograph

A

Ino - how hard

Chrono - how fast

141
Q

Symp nerve layout

A

Short pregang -> ACh -> long post gang -> NE -> end organ

142
Q

On catacholamines:
Hydroxyl substitutions affects what:
Amine substitutions affects what:
Side chain distance affects what:

A

OH subs: increase β and α activity
Amine subs: larger increases β activity
Side chain length increases symp activity, substitution increases duration

143
Q

Dopamine is made where

A

Kidney

144
Q

Dopamine function at low, moderate, and high levels

A

Low: binds D1, increased renal flow
Med: binds β1 and increases BP, HR
High: binds α1 and causes vasoconstriction

145
Q

Effect of epinephrine that makes it useful in emergency (epi pen) situations

A

Mast cell stabilization

146
Q

How much epi do you give kids/adults in anaphylaxis

A

150 mcg kids

300 mcg adults

147
Q

What does phenylephrine do, where does it bind

A

α1 causes intense vasoconstriction

148
Q

Digoxin is a _

It causes _

A

Cardiac glycoside

Longer and harder contractions

149
Q

3 main mechanisms of action of antihypertensive agents

A
  1. Effect on autonomic nervous system
  2. Inhibition of the renin-angiotensin-aldosterone system
  3. Peripheral vasodilation
150
Q

2 types of Ca channel blockers

A

Dihydropuridines

Non-dihydropuridines

151
Q

Dihydropuridines end in _ and act on the _

A

Dipine

Act on peripheral vasculature

152
Q

2 non-dihydropuridines

Work on _

A

Verapamil and diltiazem

Work mainly on heart

153
Q

Beta blockers end in _ or _

A

-olol or -alol

154
Q

2 types of beta blockers

A

Selective and non-selective

155
Q

How to remember selective vs. non selective beta blockers

A

Non selective are > m (except labetelol)

Or selectives are Mae
Non selectives are stpl

156
Q

What antihypertensive agent should not be used in obstructive lung disease

A

Non-selective beta blocker

157
Q

β1 blockers work where

β2 blockers work where

A

Heart

Lungs

158
Q

ACE inhibitors end in _

A

-pril (lisinopril)

159
Q

What do ACE inhibitors do

A

Prevent angiotensin I from being converted to angiotensin II

160
Q

ARBs end in _ and do what

What does ARB stand for

A

-sartan
Prevent angiotensin II from binding

gerARB butler this is SARTAN

Angiotensin receptor blocker

161
Q

Primary vs secondary diuretics

A

1˚ decrease intravascular volume

2˚ direct arterial vasodilation

162
Q

3 classes of diuretics and endings of each

A 
Thiazides, end in -thiazide except -thalidone
Loop diuretics
-semide
K sparing
-one
163
Q

Alpha 2 agonists do what

End in _

A

Prevent the release of NE from post ganglionic nerve fibers by negative feedback

-idine

164
Q

Two types of alpha 1 antagonists, endings

What do they do

A

Selective -zosin
Non-selective -amine

Cause vasodilation, used in oraverse to cause faster lido metabolism

165
Q

Nitrites vs nitrates

A

Nitrites can cause cyanide poisoning

Nitroglycerine is a nitrate which causes coronary dilation

166
Q

Hydralazine does what

A

K into vascular cells, vasodilation

167
Q

Class I and III antiarrythmics do what, 2 examples

A

Rhythm control
Procainamide
Amiodarone

168
Q

Class II and IV antiarrythmics do what, 2 examples

A

Rate control
Metoprolol
Diltiazem

169
Q

Pharmacokinetic vs pharmacodynamic drugs

A

Kinetic - kick drugs butt, what the body does to drugs

Dynamic- what drugs do to you to make you die

170
Q

4 pharmacokinetic changes

A

Altered rates of absorption
Altered protein binding
Altered metabolism rate
Altered excretion rate

171
Q

2 possible outcomes with altered rates of absorption

A

Drug increases absorption of another

Drug decreases absorption of another

172
Q

If a drug is more highly bound by proteins in the plasma, it’s effect is _

A

Lower. Unbound drug has its therapeutic effect

173
Q

Potentiation reaction:

A

Creation of toxic effect from one drug (not toxic) due to the presence of another drug. The second drug is not affected

174
Q

What happens if you take Zantac and halcyon together

A

Zantac increases absorption of triazolam and patient may become over sedated or stop breathing

175
Q

Diabetic Americans
How many don’t know theyre diabetic
How many are prediabetic
How many prediabetics don’t know

A

1/10
1/4
1/3
9/10

176
Q

Impaired fasting plasma glucose level

Impaired oral glucose tolerance

A

100-125

140-199 (2 hours)

177
Q 
HbA1c:
Normal
Prediabetic
Diabetes
Controlled diabetes
A

4.0-5.6
5.7-6.4
>6.5
<7.0

178
Q

Diabetes assumptions:
_ patients may display baseline dysglycemia

_ may be induced by surgical stress

A

> 30%

Hyperglycemia

179
Q

3 things diabetics can’t properly metabolize

A

Carbs
Proteins
Lipids

180
Q

4 Causes of diabetes

A
  1. Type 1: complete lack of insulin production
  2. Inadequate insulin production
  3. Tissue insensitivity to insulin (obesity)
  4. Ineffective or destroyed insulin
181
Q

Only _% of type 2 diabetics have no comorbid conditions

A

14%

182
Q

Most common cause of death in diabetics

A

Cardiovascular disease

183
Q

3-4-5 rule

A

1 g of ingested glucose will raise blood sugar 3,4, or 5 mg/dL depending on weight

184
Q

If patient doesn’t take insulin, assume insulin requirement of _

A

60 units

Pharm II (2 decks)

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