Final Flashcards
1
Q
How many mg/mL is 2% lidocaine
A
20mg/mL
2
Q
How is remifentanil metabolized
A
By esterases
3
Q
Cytochrome p450 enzymes metabolize what
A
Lidocaine and midazolam
4
Q
Proton pump inhibitors end in -_
A
-prazole
5
Q
Serotonin 5-HT3 inhibitors (antiemetic properties) end in -_
A
-estrone
6
Q
Propofol is metabolized where
A
The liver
7
Q
Atenolol is metabolized where
A
The kidney
8
Q
-olol
A
Beta blocker
9
Q
-sartan
A
Angiotensin II Receptor Blocker (lowers BP by relaxing blood vessels)
10
Q
-inol
A
Xanthine oxidase inhibitors like allopurinol, prevent gout
11
Q
-pril
A
Angiotensin converting enzymes like lisinopril treat hypertension and heart failure
12
Q
Metformin
A
Diabetes
13
Q
Glargine
A
Insulin
14
Q
Humulin
A
Insulin
15
Q
Hemostasis tripod, mechanism
A
Primary hemostasis (platelets) Coagulation (chemical) Vasoconstriction (mechanical)
16
Q
Hemostasis tripod is balanced by _ activity
A
Anticoagulant
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
18
Q
Platelets adhere to one another via _ and _
A
Surface receptor glycoprotein IIb/IIIa
And
Fibrinogen
2b/3a and Fib.
19
Q
Two arachidonic acid vasoconstrictors
A
Thromboxane A2
Prostaglandins
20
Q
Platelet surface provides site for what two things
A
Generation of thrombin
Subsequent fibrin formation
21
Q
Tissue Factor - Factor VII pathway or extrinsic system steps
A
- TF exposed to blood
- Complex forms b/t TF and FVII
- FVII is activated to FVIIa
- TF/FVIIa complex binds and activates FX
- FX converts prothrombin (FII) to thrombin (FIIa) which requires FV as cofactor
7-10 PT to T
22
Q
Coagulation alternate/secondary pathway
A
- TF/FVIIa complex activates FIX
- FIXa and CFVIII activate FX
- PT to T
8,9,10 T
23
Q
Coagulation 3rd pathway
A
- Thrombin activates FXI
- FXIa activates FIX
- More thrombin
T -> 9 -> 10 -> T
24
Q
Thrombin mediates _
A
Fibrinogen cleavage
25
What is the ultimate step in the coagulation cascade
Cross-linking of fibrin by thrombin activated factor XIII
26
3 natural anticoagulation mechanisms, where they work
Tissue factor pathway inhibitor (TFPI) - duh
Protein C - degrades CF V and VIII
Antithrombin III - inactivates T and FXa
27
Heparin strongly enhances _
Antithrombin III
28
_ degrades fibrin
Plasmin
29
How is plasmin formed
t-PA and u-PA activate plasminogen to plasmin
30
Most common coagulation disease
vW disease
31
3 types of vWDisease
1. Reduced conc. (10-45%)
2. dysfunctional vWF
3. Absent vWF (homozygous for gene defect)
32
Treatment of vWD
Type I and IIa treated with _
Severe forms
Desmopressin (DDAVP)
| Transfused factors
33
How long after surgery do you have to keep up vWD treatment
4-7 days
34
Hemophilia A is a disorder of what
FVIII
35
Treatment of hemophilia A
desmopressin (mild to moderate)
| Factor 8 transfusion (severe)
36
Hemophilia B affects what
IX
37
2 hypercoagulable coagulation Diseases
Protein C/S deficiency
| Factor V Leiden (factor V resists inactivation)
38
_ is the source of coagulation factors
Liver
39
Where are Protein C,S and fibrinogen made
Liver
40
What is MELD
Model for end stage liver disease score. Predicts 3 month mortality
41
T/F patients with renal failure often present with coagulation abnormalities and are at risk for enhanced bleeding
True
42
How to treat prolonged bleeding time in patients with renal disease
desmopressin
43
How does aspirin work
Inhibits platelet membrane associated cyclooxygenase
44
How long does aspirin effect last and why
Lasts until new, unaffected platelets can be made. Around 10 days
45
Discontinue aspirin for dental procedures?
NO
46
What is clopidogrel and what does it do
Oral anti-platelet prodrug metabolized by liver. Binds irreversibly to P2Y12ADP receptor on platelet surface.
47
What is Dipyramidole
Antiplatelet by inhibition of phosphodiesterase
48
The most potent inhibitors of platelet aggregation are _
Glycoprotein receptor IIb/IIIa inhibitors
49
How does Coumadin work
It’s an oral vitamin K antagonist
50
What does vitamin K do in the coagulation pathway?
How does this relate to Coumadin
Carboxylates FII, VII, IX, and X
Coumadin blocks this carboxylation
51
Coumadin has a _ dose-effect relationship
Variable
52
New oral anticoagulants affect what
Inhibit factor Xa
53
T/F you may want to discontinue new oral anticoagulants before oral surgery
True
54
Heparin is what, how does it work
IV or subcut. Anticoagulant
| Binds to antithrombin III
55
How to monitor effects of heparin
PTT or
| Whole blood activated clotting time
56
What are low molecular weight heparins, why use?
More favorable antithrombic effect and less bleeding complications
57
Pentasaccharides work where
| Treat what
Xa
| Treat DVT and PE
58
What is heparin induced thrombocytopenia
Immune response to heparin characterized by thrombocytopenia and thromboembolism
59
3 signs that might point to a defect in the coagulation system
Abnormal bruising
Petechiae
Splenomegaly
60
Which screens do you need if someone shows signs of a bleeding tendency
Platelet count
PTT
PT/INR
61
The PT value reflects coagulation of the _ coagulation pathway
TF-VIIa
62
aPTT
What does it measure
Common use
Activated partial thromboplastin time
Measures slower “intrinsic” pathway. Requires all clotting factors except VII.
Commonly used to monitor anticoagulation with heparin
63
Gold standard for platelet function analysis
Platelet aggregometry (PAA)
64
Why can we use empiric therapy for odontogenic infections?
The bacteria in odontogenic infections are fairly predictable and there is often not enough time for cultures to grow
65
Pros and cons of bactericidal drugs
Pros:
Rely less on immune system
Quicker
Maintain effect longer
Con:
Post antibiotic effects
66
Example of an organism with high PAE
| What is PAE
Azithromycin
| Post antibiotic effect - persistent suppression of bacterial growth after brief exposure to antibiotic
67
When to stop taking antibiotics
When sure patient is on their way to recovering based on clinical eval
68
3 adverse effects of antibiotics
Toxicity
Allergy
Superinfection
69
Antifungals are toxic to what
Liver
70
Penicillin and aminoglycosides can be toxic to what
Kidneys
71
C diff overgrowth aka
Pseudomembranous colitis
72
Which type of AB has the widest spectrum
Beta-lactate
73
Why is penicillin V good for oral microbes
It is narrow spectrum to oral microbes
74
When are β lactamase resistant penicillins indicated
For proven staph infections only
75
When to use amoxicillin
Ear infection
UTI
SBE prophylaxis
If culture indicates
76
T/F extended spectrum penicillins are indicated for head and neck infections
FALSE
77
What is augmentin
When to use?
Amoxicillin and clavulonic acid
Rapid growing oral infection, or oral microbes in a distant site (bite wound)
78
Unasyn: what and when to use and why
Ampicillin + sulbactam
Similar spectrum to augmentin, used for serious infections in hospital due to increasing resistance to PCN G
79
most frequent DOC for odontogenic infection
PCN V
80
When to use metronidazole
Significant anaerobic component
81
When to use first gen ceph
Community staph
Surgical wound prophy
Odontogenic infection in patient with mild penicillin allergy
SBE and TJR prophy
82
How do macrolides work
Bind 50s ribosomal unit, inhibiting RNA dependent protein synth
83
Macrolides end in -
Mycin
84
Clarithromycin is good for killing _
H. influenza
85
When to use clarithromycin
Sinus infection
Mild to moderate odontogenic infection in PCN allergic patient
Pneumonia
86
Azithromycin is good at killing
Strep and g- anaerobes
87
Clindamycin kills what 4 things
Strep
Staph
Actinomycetes
Anaerobes
88
Risk of clindamycin
Wide spectrum, can cause pseudomembranous colitis
89
Metronidazole kills what
Anaerobes
90
Tetracycline uses
Resistant hospital acquired infections
H pyloris
Topical
Dry socket
91
4 things that make pain worse
Anxiety
Increased symp output
Poor rest
Inadequate oral intake
92
3 orders or neurons
1 periphery to spine
2 spine to thalamus
3 thalamus to sensory cortex
93
Both opioids and non-opioids act where
Centrally and peripherally to interrupt ascending nociceptive impulses
94
How do NSAIDs work
Inhibit cyclooxygenase
95
Cox 1 is responsible for what
Gastric mucosal barrier
Renal function
Platelet aggregation
Vasoconstriction
96
Cox2 is responsible for what
Pain, inflammation, fever
Renal function
Platelet inhibition
Vasodilation
97
Why are NSAIDs bad for asthma patients
Blocking cox1 can result in overproduction of leukotrienes that can make asthma worse
98
3 absolute contraindications for NSAIDs
Allergy
Pregnancy
Erosive or ulcerative GI conditions
99
Why not use cox-2 inhibitors exclusively?
Poor efficacy in 3rd molar model
Expensive
Increased emboli
Contraindicated in sulfa allergy
100
How does Acetaminophen work
Prostaglandin synthesis inhibition in the CNS
101
Daily maximum of acetaminophen
3,000 mg/day
| 2,000 if liver disease
102
Mu vs kappa side effects
μ - dependence, constipation
κ - dysphoria, psychomimetic
103
Strength of the code opioids
Oxy>hydro>codeine
104
Why do we use the code opioids with acetaminophen
Synergistic with acetaminophen
105
T/F it is the acetaminophen, not the opioid that dictates the dose/frequency when combined
True
106
How much of the effect of the code opioids is from being converted vs the parent drug
Codeine = entirely from conversion to morphine
Hydrocodone = 1/2 effect from parent, 1/2 from conversion
Oxycodone = almost entirely from parent drug
107
When to use tramadol
Chronic pain
108
How does pre-emotive analgesia work
It inhibits prostaglandin synthesis
109
Why are non-opioids first line for dental pain
Most has inflammatory component
110
T/F there is evidence that ibuprofen is safer and more effective than other
FALSE
111
How is NSAID dose chosen
According to contribution of inflammation to the pain experienced
112
Non-narcotic scheduled dosing
Ibuprofen 600 mg Q6h
| Acetaminophen 650 mg Q6h
113
What is used for breakthrough pain
Tylenol + codeine (Tylenol 2,3,4)
Tylenol + hydrocodone (Norco)
Tylenol + oxycodone (percocet)
114
Of drug OD deaths, opioids were what %
66%
115
Opioid prescribing rules:
Days for adults/minors
Dosing average limit
7 days adults, 5 days minors
| Can’t average >30 MED over the period
116
Optimum pain management
Pre-emptive analgesics
Long acting LA
Step 1 plan for routine non-opioids
Step 2 plan for prn opioids
117
T/F nausea is an allergic reaction
False
118
S&S of allergic rxn
Skin rash/hives
Wheezing
Swelling
Anaphylaxis
119
2 main uses for corticosteroids in dentistry
Trismus and edema
120
Contraindications to corticosteroids
```
Chronic infection
Peptic ulcer
Diabetes
Poor wound healing
Caution with NSAID use
```
121
When to consider stress dose of steroid?
20 mg prednisone per day for
2+ weeks
In the past 2 months
122
P wave represents
Atrial depolarization
123
QRS complex represents what
Ventricular depolarization and implies contraction
124
T wave
Repolarization of ventricles
125
```
Volume-pressure diagram
X
Y
Flow direction
Stroke volume
```
X is Lventricular volume
Y is L intraventricular pressure
Flow is counter clockwise
Stroke volume is x direction b/t two volume lines
126
Aortic valve opens at what pressure
80 mm Hg
127
Nodal cells vs muscle cell potential
Nodal is more curved
| Myocyte looks like cursive r
128
```
Cardiac muscle action potential
Phase 0:
Cardiac cell _
Membrane becomes more _
_ open
_ enters
Membrane potential reaches _
```
```
Depolarizes
Positive
Fast Na channels open
Na enters
Membrane potential reaches +20
```
129
```
Cardiac muscle action potential
Phase 1:
_ close
Cell begins to _
_ open
_ exit
```
Fast Na channels close
Cell begins to repolarize
K channels open
K ions exit
130
```
Cardiac muscle action potential
Phase 2:
_ open
Membrane charge _
Repolarization is delayed
```
Slow Ca channels open
| membrane charge is balanced
131
```
Cardiac muscle action potential
Phase 3:
_ close
_ stay open
_ rushes out
Cell _
```
Slow Ca channels close
K channels stay open
K rushes out
Cell depolarizers
132
Cardiac muscle action potential
Phase 4:
Cell membrane averages _
-90 mV
133
Ohm’s law
Voltage = current x resistance
134
Hemodynamics law relating to ohms law
MAP =
Pressure = flow x resistance
MAP = CO x SVR
135
CO =
HR x SV
136
Alpha 1 receptors are located in _
Vasculature
137
Alpha 2 receptors are located _
In brain, nerves
138
Beta 1 receptors are located _
Heart
139
Beta 2 receptors are located
Lungs, Vasculature
140
Inotropy vs chronograph
Ino - how hard
| Chrono - how fast
141
Symp nerve layout
Short pregang -> ACh -> long post gang -> NE -> end organ
142
On catacholamines:
Hydroxyl substitutions affects what:
Amine substitutions affects what:
Side chain distance affects what:
OH subs: increase β and α activity
Amine subs: larger increases β activity
Side chain length increases symp activity, substitution increases duration
143
Dopamine is made where
Kidney
144
Dopamine function at low, moderate, and high levels
Low: binds D1, increased renal flow
Med: binds β1 and increases BP, HR
High: binds α1 and causes vasoconstriction
145
Effect of epinephrine that makes it useful in emergency (epi pen) situations
Mast cell stabilization
146
How much epi do you give kids/adults in anaphylaxis
150 mcg kids
| 300 mcg adults
147
What does phenylephrine do, where does it bind
α1 causes intense vasoconstriction
148
Digoxin is a _
| It causes _
Cardiac glycoside
| Longer and harder contractions
149
3 main mechanisms of action of antihypertensive agents
1. Effect on autonomic nervous system
2. Inhibition of the renin-angiotensin-aldosterone system
3. Peripheral vasodilation
150
2 types of Ca channel blockers
Dihydropuridines
| Non-dihydropuridines
151
Dihydropuridines end in _ and act on the _
Dipine
| Act on peripheral vasculature
152
2 non-dihydropuridines
| Work on _
Verapamil and diltiazem
| Work mainly on heart
153
Beta blockers end in _ or _
-olol or -alol
154
2 types of beta blockers
Selective and non-selective
155
How to remember selective vs. non selective beta blockers
Non selective are > m (except labetelol)
Or selectives are Mae
Non selectives are stpl
156
What antihypertensive agent should not be used in obstructive lung disease
Non-selective beta blocker
157
β1 blockers work where
| β2 blockers work where
Heart
| Lungs
158
ACE inhibitors end in _
-pril (lisinopril)
159
What do ACE inhibitors do
Prevent angiotensin I from being converted to angiotensin II
160
ARBs end in _ and do what
| What does ARB stand for
-sartan
Prevent angiotensin II from binding
gerARB butler this is SARTAN
Angiotensin receptor blocker
161
Primary vs secondary diuretics
1˚ decrease intravascular volume
| 2˚ direct arterial vasodilation
162
3 classes of diuretics and endings of each
```
Thiazides, end in -thiazide except -thalidone
Loop diuretics
-semide
K sparing
-one
```
163
Alpha 2 agonists do what
| End in _
Prevent the release of NE from post ganglionic nerve fibers by negative feedback
-idine
164
Two types of alpha 1 antagonists, endings
What do they do
Selective -zosin
Non-selective -amine
Cause vasodilation, used in oraverse to cause faster lido metabolism
165
Nitrites vs nitrates
Nitrites can cause cyanide poisoning
| Nitroglycerine is a nitrate which causes coronary dilation
166
Hydralazine does what
K into vascular cells, vasodilation
167
Class I and III antiarrythmics do what, 2 examples
Rhythm control
Procainamide
Amiodarone
168
Class II and IV antiarrythmics do what, 2 examples
Rate control
Metoprolol
Diltiazem
169
Pharmacokinetic vs pharmacodynamic drugs
Kinetic - kick drugs butt, what the body does to drugs
Dynamic- what drugs do to you to make you die
170
4 pharmacokinetic changes
Altered rates of absorption
Altered protein binding
Altered metabolism rate
Altered excretion rate
171
2 possible outcomes with altered rates of absorption
Drug increases absorption of another
| Drug decreases absorption of another
172
If a drug is more highly bound by proteins in the plasma, it’s effect is _
Lower. Unbound drug has its therapeutic effect
173
Potentiation reaction:
Creation of toxic effect from one drug (not toxic) due to the presence of another drug. The second drug is not affected
174
What happens if you take Zantac and halcyon together
Zantac increases absorption of triazolam and patient may become over sedated or stop breathing
175
Diabetic Americans
How many don’t know theyre diabetic
How many are prediabetic
How many prediabetics don’t know
1/10
1/4
1/3
9/10
176
Impaired fasting plasma glucose level
| Impaired oral glucose tolerance
100-125
140-199 (2 hours)
177
```
HbA1c:
Normal
Prediabetic
Diabetes
Controlled diabetes
```
4.0-5.6
5.7-6.4
>6.5
<7.0
178
Diabetes assumptions:
_ patients may display baseline dysglycemia
_ may be induced by surgical stress
>30%
| Hyperglycemia
179
3 things diabetics can’t properly metabolize
Carbs
Proteins
Lipids
180
4 Causes of diabetes
1. Type 1: complete lack of insulin production
2. Inadequate insulin production
3. Tissue insensitivity to insulin (obesity)
4. Ineffective or destroyed insulin
181
Only _% of type 2 diabetics have no comorbid conditions
14%
182
Most common cause of death in diabetics
Cardiovascular disease
183
3-4-5 rule
1 g of ingested glucose will raise blood sugar 3,4, or 5 mg/dL depending on weight
184
If patient doesn’t take insulin, assume insulin requirement of _
60 units
