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Pharmacology 2 > Test 2 Study Guide > Flashcards

Test 2 Study Guide Flashcards

1
Q

What is the half life of Factor II

A

65 hours

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2
Q

What is the half life of Factor VII

A

5 hours

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3
Q

What is the half life of Factor IX

A

25 hours

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4
Q

What is the half life of Factor X

A

40 hours

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5
Q

Which factors are not manufactured by the liver?

A

III - Thromboplastin (vascular walls)

IV - Calcium (diet)

VIII:vWF vonWilibran Factor (vascular endothetlial)

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6
Q

Aprotinin MOA

A

Aprotinin - Antifibrinolytic Agents
Inhibits plasmin, therefore fibrin breakdown is slowed.
Used during cardiac surgery to decrease intraoperative blood loss
I. Aprotinin MOA (PG 449 4th ed)
a. a naturally occurring serine protease inhibitor hat decreases activation of plasminogen and the activity of plasmin
b. Classified as an anti-fibrinolytic, anticoagulant, platelet protective, and anti-inflammatory drug.
c. Possible anaphylactic and analphylactoid reactions
i. Derived from bovine lungs
ii. Rate of occurrence is 2.8%

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7
Q

Protamine MOA

A

Protamine used for reversing anticoagulation
Protamine found in salmon sperm
How: + charged alkaline protamine combines with the - charged acid heparin to form a stable complex that is devoid of anticoagulant activity
Dose of protamine required to antagonize heparin is typically 1mg for every 100units of circulating heparin activity

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8
Q

Side effects of Protamine?

A

Side effects

Hypotension
Rapid IV injection of protamine may be associated with histamine release, causing facial flushing, tachycardia, and hypotension.

Pulmonary hypertension
In rare cases, protamine neutralization of heparin can result in secretion of thromboxane and 5-hydroxy tryptamine (serotonin) manifesting as pulmonary vasoconstriction, Pulmonary hypertension, and bronchoconstriction

Allergic reactions
Pretreatment with histamine-receptor antagonists followed by a slow trial of protamine infusion

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9
Q

MOA for Aspirin?

A

Blocks production of thromboxane A2
Since platelets do not synthesize new proteins, the action of ASA on platelet cyclooxygenase is permanent lasting the life of the platelet (7-10 days)
Complete inactivation is achieved with 160 mg/day

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10
Q

MOA of Dipridamole?

A

Cilostazol and several of its metabolites are cyclic AMP (cAMP) phosphodiesterase III inhibitors (PDE III inhibitors), inhibiting phosphodiesterase activity and suppressing cAMP degradation with a resultant increase in cAMP in platelets and blood vessels, leading to inhibition of platelet aggregation and vasodilation.

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11
Q

MOA of Dextran

A

Dextran - In preclinical studies, the mechanism of action is thought to be related to the blockage of the uptake of tissue plasminogen activator by mannose-binding receptors. This process has a direct effect by enhancing endogenous fibrinolysis.

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12
Q

MOA of thienopyridines

A

Thienopyridines: Clopidogril, Prasugrel and Ticagrelor
Ticlid (Ticlopidine)
Plavix (Clopidogrel)
Work at the G protein receptors
Inhibits adenylyl cyclase which results in lower levels of cyclic AMP and thereby less platelet activation

Dose
Ticlid loading 500 mg followed by 250 mg/day
Plavix loading 300 mg followed by 75 mg/day
Inhibition of platelets persists for 3-4 days after D/C

Adverse effects
Nausea, vomiting and diarrhea
Neutropenia

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13
Q

MOA of Glycoprotein IIb/IIIa Inhibitors

A

Glycoprotein IIb/IIIa Inhibitors

Platelet surface integrin
Glycoprotein is a receptor for fibrinogen and von Willebrand factor which anchor platelets to foreign surfaces and to each other, thereby mediating aggregation

The receptor is activated by platelet agonists
Thrombin, collagen, or thromboxane A2
Inhibition of the glycoprotein binding blocks platelet aggregation induced by any of the agonist

Examples Reopro (abciximab), Integrilin (Eptifibatide)

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14
Q

OTC supplements that can cause enzyme induction

A

St. John’s Wort
Used as an antidepressant and anxiolytic.
extract inhibits reuptake of serotonin, norepinephrine, dopamine, and MAO; acts as a tricyclic.
Increased cytochrome P450 activity
May interfere with digoxin pharmacokinetics
avoid MAOIs, SSRIs, and ephedrine
St John’s: happy pill via NT reuptake inhibition. Can decrease dig, induces CP450.

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15
Q

Drugs that block factor II and X

A

Heparin
Heparin is a negatively charged Mucopolysacharide
Unfractionated heparin (UFH) is an extract of porcine intestines or bovine lung
Heparin is stored in the mast cells
Does not cross the placenta
Thrombin (IIa) and factor Xa are inhibited

LMWH
Derived from standard grad UFH by chemical to yield a molecular weight of 4,000 to 5,000 daltons
LMWH mainly removed by non-saturable renal excretion
Effect prolonged with renal failure
Protamine does not neutralize LMWH

Fondaparinux
Synthetic anticoagulant
Inhibits factor Xa but no direct activity against thrombin
Administer SQ
Elimination half-life 15 hours
Eliminated by kidneys-use with caution in renal failure
Clinical Use: DVT, PE, Alternative pt. with HIT

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16
Q

Heparin and its LMW derivatives, MOA

A

Heparin - Heparin acts as an anticoagulant by binding to ATIII enhancing the rate of thrombin AT III complex formation by 1,000 to 10,000 times. Thrombin (IIa) and factor Xa are inhibited

Heparin MOA
Has an anti-activated factor X to anti-activated factor II activity of about 1:1

LMWH MOA
Enoxaparin has a corresponding ratio that varies between 4:1 and 2:l
Care should be taken to delay surgery for 12 hours after the last dose

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17
Q

aPTT

A

Activated partial thromboplastin time (aPTT)
Intrinsic pathway
Heparin tx is usually monitored to maintain the ratio of the aPTT within a defined rage of approximately 1.5 to 2.5 times normal value*
Typically 30 -35 seconds
Heparin prolongs aPTT
*** easily corrected by omitting a dose due to brief half-life (23 min to 2.48 hr)
NEW some hospitals have changed to anti Xa assay instead of aPTT monitoring because of the variability with low dose regimens

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18
Q

ACT

A

Activated Clotting Time
At high heparin concentration the ACT is used to monitor anticoagulation
Performed by mixing whole blood with and activating substance that has a large surface area such a celite
Influenced by:
Hypothermia
Thrombocytopenia
Presence of aprotinin
Preexisting coagulation deficiencies (fibrinogen, factor XII and factor VII)

ACT

  • ACT may be influenced by hypothermia, thrombocytopenia, presence of contact activation inhibitors (aprotinin), and preexisting coagulation deficiencies (fibrinogen, factor XII, factor VII)
  • The control ACT is usually 90 to 120 seconds
  • Asequate if the ACT is >300 seconds, questionable with ACT between 180 and 300 seconds, and inadequate at < 180 seconds
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19
Q

PT INR

A

Prothrombin Time/ International Normalized Ratio
Extrinsic pathway
Treatment with oral anticoagulants is best guided by Prothrombin time (PT)
INR addresses the problem of variability
INR is the ratio of a patients prothrombin time to a normal control
Most indication a moderate anticoagulant effect with a target INR
2.0 to 3.0 is appropriate*
Unexpected fluctuations in the dose respond to warfarin may reflect change in died

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20
Q

Proteins C and S what happens when they are low

A

Protein C
When activated by thrombin, degrades cofactors Va and VIIIa
Greatly diminishes activation of prothrombin and factor X

Protein S
Cofactor for activated Protein C

Low Protein C and S will result in a hypercoagulability state via future activation of prothrombin and factor X

Protein C is a natural anticoagulant

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21
Q

PONV risk factors and what PONV is associated with

A

Patient
Female, Non-smoker, Hx of motion sickness, Previous Hx PONV, Obesity, Young, Anxiety, Full Stomach, DM, Pain, Movement, Hypovolemia

Surgical
Duration, Prolonged exposure to lipophilic drugs, Laparotomy/ Laparoscopic, GYN, Procedures, ENT, Breast, Plastic, Orthopedic, Highest risk male genitalia

Anesthetic
Inhalational agents, N2O, Neostigmine, Opioids, Barbiturates, Ketamine, Etomidate

Factors, Surgery-related (Children)
Adenotonsillectomy, Orchiopexy, Middle ear surgery, Otoplasty, Strabismus repair, Anxiety

22
Q

PONV has been associated with:

A

PONV has been associated with:
Morbidity including dehydration, Electrolyte abnormalities, Wound dehiscence, Bleeding, Esophageal rupture (Boerhaave’s syndrome), Airway compromise
BE AWARE AND PROPHYLACTICALLY TREAT PONV!!!

23
Q

Modifiable risk factors

for PONV

A 
Modifiable risk factors
•Use of volatile anesthetics
•Intraoperative use of opioids
•Surgical/anesthetic time
•Smoking (tobacco use decreases PONV risk)
24
Q

Non-modifiable risk factors for PONV

A 
Non-modifiable risk factors
•Female sex
•Young age (<50)
•History of PONV
•Surgical location (abdominal/pelvic, ENT, breast)
•Surgical technique (laparoscopic)
25
Q

Cranial nerves associated with vomiting center

A

Activation of the vomiting center sends signals via (cranial nerves V, VII, IX, X, and XII)*** through vagal parasympathetic fibers and the sympathetic chain to the skeletal muscle through alpha motor neurons

Trigeminal = V
Facial = VII
Glossopharyngeal = IX
Vagus = X
Hypoglossal = XII
26
Q

Location of the vomiting center

A
  • Emesis controlled by vomiting center which lies in the (medulla oblongata)*** which consists of the nucleus of the tractus solitarius and parts of the reticular formation.
  • Cephalad to vomiting center is the CRTZ (Chemoreceptor trigger zone)*** which detects noxious chemicals in blood stream
  • Site in which many antiemetics prevent or treat PONV
  • At the base of Fourth ventricle in area of Postrema*****
  • Rich with receptors for serotonin, dopamine, histamine, ACh, Substance P
  • Very vascular and lacks blood brain barrier.*****
  • Because its location and exposure it can be directly stimulated by toxins, metabolites, and drugs that circulate in the blood and cerebrospinal fluid.***
27
Q

Anticholinergics Drugs that cross BBB

A

Anticholinergics

Atropine & Scopolamine- CROSSES THE BLOOD BRAIN BARRIER

28
Q

Benzamine Drugs that cross BBB

A

Benzamine

Metoclopramide (reglan) - Crosses the BBB

29
Q

5-HT3 Receptor Antagonists

Drugs that cross BBB

A

5-HT3 Receptor Antagonists - Cross BBB

Aprepitant - Crosses the BBB

30
Q

H1 Receptor Antagonists - First-generation drugs Drugs that cross BBB

A

GI Motility
H1 Receptor Antagonists - First-generation drugs - tend to produce sedation, (crosses BBB)
Diphenhydramine

31
Q

H2 Receptor Antagonists Drugs that cross BBB

A

H2 Receptor Antagonists

Cimetidine (Tagamet) - Cross the BBB

32
Q

PPI Drugs that cross BBB

A

PPI

Omeprazole - Crosses BBB

33
Q

Droperidol (Inapsine)

A

Droperidol (Inapsine)
Dose 0.625-1.25 mg (adults)

Dose 50-75 mcg/kg (peds)

34
Q

Dexamethasone (Decadron)

A

Dexamethasone (Decadron) - Dose 4-10 mg for adults. Minimum 5 mg effective prophylactic dose needed

35
Q

Odansetron (Zofran)

A

Odansetron (Zofran)
Dose 4-8 mg IV over 2-5 min

Peds >2 yrs: 0.05-0.15 mg/kg (max 4 mg)

36
Q

Dolasetron (Anzemet)

A

Dolasetron (Anzemet)
Dose 12.5 mg IV 15 min before end of anesthesia

Peds: 0.35mg/kg IV

37
Q

Aprepitant (Emend)

A

Aprepitant (Emend) - Dose 40 mg PO 3 hr before induction

38
Q

Ephedrine

A

Ephedrine - 5-10 mg IV q 5-10 min; q 3-4 hr max 150 mg in 24hr

Peds: 3mg/kg over 24 hr

39
Q

Cannabinoids

A

Cannabinoids - Dose 2.5 mg BID

40
Q

Cimetidine (Tagamet)

A

Cimetidine (Tagamet) - 300 mg IV Q 6hr

41
Q

Famotidine (Pepcid)

A

Famotidine (Pepcid) - Dose 20-40 mg

42
Q

Metoclopramide

A

Metoclopramide - 10 to 20 mg IV

43
Q

Drugs with dopaminergic effects

A

Benzamine
Metoclopramide (reglan)
Has antidopaminergic effect (don’t give w/ parkinsons, dementia, or alztimers)
Not to be used with Parkinson’s restless leg syndrome, or pts with movement disorders related to dopamine

Benzodiazepines
Midazolam - May decrease synthesis and release of dopamine within the CRTZ*

Butyrophenones
Droperidol - black box warning prolonged QT syndrome
Haloperidol - EPS may occur due to dopamine blockade
Butyrophenones should not be used with Parkinson’s, Restless leg syndrome or other diseases with dopamine blockage

44
Q

Drug considerations with eye surgery

A

Dramamine:
Treats PONV and Motion sickness
Inhibition of the integrative functioning of the vestibular nuclei by decreasing vestibular and visual input
Manipulation of the ocularcardiac reflex with strabismus surgery
Dramamine blocks the ocularcardiac reflex

45
Q

Drug considerations with ear surgery

A

Scopolamine MOA- blocks transmission to the medulla due to overstimulation of vestibular apparatus of the inner ear

46
Q

Drug considerations with Parkinson’s patients

A

Ondansetron (zofran) - Does not alter dopamine, histamine, adrenergic or cholinergic receptor (can use with Parkinson )

47
Q

Antacids

A

Antacids are drugs that neutralize (remove hydrogen ions) from gastric contents or decrease the secretion of hydrogen chloride into the stomach.

Oral antacids have been used for centuries. In current practice, the oral antacids used most often are salts of aluminum, calcium, and magnesium; the hydrogen ions in stomach acid react with the base, forming a stable compound.

As hydrogen ions are consumed, the pH of the stomach contents increases. The best known example would be sodium bicarbonate, NaHCO3, which in the stomach would combine with HCl to produce NaCl, H2O, and CO2.
NaHCO3 + HCL → NaCl + H20 + Co2

48
Q

Citric acid & Sodium citrate (Bicitra)

A

Citric acid & Sodium citrate (Bicitra)
•Mixes with gastric fluid
•Rapidly buffers gastric fluid
•Raises gastric pH
•Passes through the stomach into small intestine to be absorbed into bloodstream
•Metabolized to sodium bicarb which raises gastric pH
•Sodium bicarb eliminated in urine

49
Q

Calcium carbonate

A

Calcium carbonate
• Can produce metabolic alkalosis with chronic therapy. The plasma concentration of calcium is increased transiently. Symptomatic hypercalcemia may occur in patients with renal disease.
•The administration of calcium carbonate–containing antacids may result in hypophosphatemia. Even small amounts of calcium carbonate–containing antacids evoke hypersecretion of hydrogen ions (acid rebound).6
•The release of CO2 in the stomach may cause eructation and flatulence. Constipation is minimized by including magnesium oxide with calcium carbonate. Acute appendicitis has been reported due to impacted calcium carbonate fecaliths.

50
Q

Complications Antacid

A

Complications Antacid

  • Increase urine and gastric volume pH causes the following
  • Bacterial overgrowth in the duodenum and small intestine

Milk alkali syndrome :
Increase Ca, BUN, Creatinine, systemic alkalosis due to large amounts of Ca carbonate and >1L of milk per day

Phosphorus Depletion
Due to ingestion large amounts of aluminum salts due to binding of phosphate ions in GI tract and preventing absorption
Beneficial in ESRD due to decrease plasma phosphate risk of toxicity
Anorexia, skeletal muscle weakness, malaise.
Osteomalacia, Osteporosis may occur. Phosphate supplements may be needed

51
Q

NK1 inhibitor drugs crosses the BBB

A

Aprepitant - Crosses the BBB

Pharmacology 2 (11 decks)

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