Drugs Flashcards

1
Q

What is the anticipated bacteria for skin and reconstructive surgery?

A

Staphylococcus spp.

Commonly associated with surgical site infections in skin and reconstructive procedures.

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2
Q

Which antimicrobial is recommended for skin and reconstructive surgery?

A

Cefazolin

A first-line antibiotic for preventing infections.

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3
Q

What bacteria are anticipated in head and neck surgery?

A

Staphylococcus spp., Streptococcus spp., anaerobes

These bacteria can contribute to surgical site infections in this area.

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4
Q

What are the recommended antimicrobials for head and neck surgery?

A

Clindamycin or cefazolin

Effective options for managing potential infections.

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5
Q

What is the anticipated bacteria for elective orthopedic procedures?

A

Staphylococcus spp.

Key bacteria involved in infections from elective orthopedic surgeries.

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6
Q

What antimicrobial is recommended for elective orthopedic procedures?

A

Cefazolin

Used to prevent infections in elective orthopedic surgeries.

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7
Q

What are the anticipated bacteria for open fractures in orthopedic surgery?

A

Staphylococcus spp., Streptococcus spp., anaerobes

These bacteria increase the risk of infections in open fractures.

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8
Q

What antimicrobials are recommended for open fractures?

A

Cefazolin or clindamycin, ± aminoglycoside or fluoroquinolone

Enrofloxacin should be avoided with known or potential Streptococcus canis infections.

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9
Q

What is the anticipated bacteria for thoracic surgery?

A

Staphylococcus spp.

Associated with surgical site infections in thoracic procedures.

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10
Q

What antimicrobial is recommended for thoracic surgery?

A

Cefazolin

A common choice to prevent infections in thoracic surgeries.

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11
Q

What is the anticipated bacteria for abdominal surgery (nongastrointestinal)?

A

Staphylococcus spp.

Key bacteria that can lead to infections in non-gastrointestinal abdominal surgeries.

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12
Q

What antimicrobial is recommended for abdominal surgery (nongastrointestinal)?

A

Cefazolin

Used to prevent infections during these procedures.

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13
Q

What bacteria are anticipated in upper gastrointestinal surgery?

A

Gram-positive cocci, enteric Gram-negative bacilli

Important bacteria to consider for upper GI surgical infections.

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14
Q

What antimicrobial is recommended for upper gastrointestinal surgery?

A

Cefazolin

Effective in preventing infections during upper GI surgeries.

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15
Q

What bacteria are anticipated in hepatobiliary surgery?

A

Clostridium spp., Gram-negative bacilli, anaerobes

These bacteria can cause infections in hepatobiliary surgical procedures.

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16
Q

What antimicrobial is recommended for hepatobiliary surgery?

A

Cefoxitin

Chosen for its effectiveness against the anticipated bacteria.

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17
Q

What bacteria are anticipated in lower gastrointestinal surgery?

A

Enterococci, Gram-negative bacilli, anaerobes

Key bacteria that may lead to infections in lower GI surgeries.

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18
Q

What antimicrobial is recommended for lower gastrointestinal surgery?

A

Cefoxitin

Recommended to prevent infections in lower GI procedures.

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19
Q

What bacteria are anticipated in urogenital surgery?

A

Streptococcus spp., Staphylococcus spp., Escherichia coli, anaerobes

Important to consider for potential infections in urogenital surgeries.

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20
Q

What antimicrobials are recommended for urogenital surgery?

A

Cefazolin or ampicillin

Effective in preventing infections during urogenital procedures.

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21
Q

Which antibiotics inhibits cell wall synthesis?

A
  • β-lactams
  • glycopeptides (vancomycin),
  • bacitracin

This category is crucial for disrupting bacterial cell wall integrity.

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22
Q

Which antibiotics impair cell membrane function?

A

Polymyxin B, colistin

These antibiotics target the bacterial cell membrane, leading to cell death.

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23
Q

Which antibiotics inhibit protein synthesis?

A

Through binding either to a single (tetracyclines, chloramphenicol, macrolides, lincosamides) or both (aminoglycosides) ribosomal subunits

This interference prevents bacteria from producing essential proteins.

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24
Q

Which antibiotics inhibit DNA synthesis and replication?

A
  • Novobiocin
  • quinolones
  • metronidazole

These antibiotics disrupt the processes necessary for bacterial DNA replication.

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25
Q

Which antibiotic class inhibits DNA-dependent RNA polymerase?

A

Rifamycins

This class is important for blocking RNA synthesis in bacteria.

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26
Q

Which antibiotics inhibit folic acid and consequently DNA synthesis.

A
  • Sulfonamides
  • trimethoprim

These antibiotics interfere with the metabolic pathway required for DNA synthesis.

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27
Q

Name Bactericidal Antiobitics

A

BANG Q RIP
- Beta-lactams (penicillins, cephalosporins, carbapenems): Amoxicillin, cefazolin, meropenem
- Aminoglycosides: Tobramycin, gentamicin, amikacin
- Nitroimidazoles: Metronidazole
- Glycopeptides: Vancomycin
- FluoroQuinolones: Ciprofloxacin, levofloxacin, moxifloxacin
- Rifampicin
- Polymyxins

  • Cyclic Lipopeptides: Daptomycin
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28
Q

Name Bacteriostatic Antiobitics

A

MS. COLT

  • Macrolides: Azithromycin, clarithromycin, erythromycin
  • Sulfonamides: Sulfamethoxazole
  • Chloramphenicol
  • Oxazolidinones: Linezolid
  • Lincosamides: Clindamycin
  • Tetracyclines: Doxycycline, minocycline
  • Glycylcyclines: Tigecycline
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29
Q

Antiobiotics that Penetration the Blood-Brain Barrier:
Good Penetration

A
  • Third-generation cephalosporins
  • Fluoroquinolones
  • Metronidazole
  • Sulfonamides
  • Chloramphenicol
  • Trimethoprim
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30
Q

Antiobiotics that Penetration the Blood-Brain Barrier:
Moderate Penetration (with meningitis)

A
  • Tetracyclines: especially doxycycline and minocycline
  • Erythromycin
  • Penicillins
  • Rifampin
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31
Q

Antiobiotics that Penetration the Blood-Brain Barrier:
Poor Penetration

A
  • First- and second-generation
  • Cephalosporins
  • Aminoglycosides
  • Clindamycin
  • Vancomycin
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32
Q

The most important mechanism of bacterial resistance to β-lactam antibiotics is

A

enzymatic inactivation by β-lactamases by cleavage of the 4-member β-lactam ring

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33
Q

β-Lactams impair the development of bacterial cell walls by interfering with \_\_\_\_\_\_\_ enzymes responsible for the formation of the cross-links between peptidoglycan strands. These enzymes are associated with a group of proteins in both gram-positive and gram-negative bacteria called the \_\_\_\_\_\_\_ \_\_\_\_\_\_\_ which comprise the cell wall. B-lactam drugs mimic PBP substrate and thus inhibit \_\_\_\_\_\_ \_\_\_\_\_\_\_ \_\_\_\_\_\_.

A
  • transpeptidase
  • penicillin-binding proteins (PBPs)
  • cell wall synthesis
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34
Q

Beta lactams are excreted

A

Renally

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35
Q

Aminoglycosides need only a short contact with bacteria to kill them and, as such, are \_\_\_\_\_\_\_\_ \_\_\_\_\_\_\_\_ in their actions. Their main site of action is the \_\_\_\_\_\_ \_\_\_\_\_\_ \_\_\_\_\_\_ through which they interfere with protein synthesis. To reach the ribosome, they must first cross the lipopolysaccharide (LPS) covering (gram-negative organisms), the bacterial cell wall, and finally the cell membrane.

A
  • concentration dependent
  • membrane-associated bacterial ribosome
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36
Q

Features of aminoglycosides:
- The antibacterial activity of the aminoglycosides depends on an effective concentration of antibiotic outside the cell.
- Anaerobic bacteria and induced mutants are generally resistant, because they lack appropriate transport systems.
- With low oxygen tension, as in hypoxic tissues, transfer into bacteria is diminished.
- Divalent cations (eg, calcium and magnesium) located in the LPS, cell wall, or membrane can interfere with transport into bacteria because they can combine with the specific anionic sites and exclude the cationic aminoglycosides.
- Passive movement of aminoglycosides across bacterial cell membranes is facilitated by an alkaline pH; a low pH may increase membrane resistance more than 100-fold.
- Changes in osmolality also can alter the uptake of aminoglycosides.
- Some aminoglycosides are transported more efficiently than others and thus tend to have greater antibacterial activity. - Synergism is common when aminoglycosides and β-lactam antibiotics (penicillins and cephalosporins) are used in combination.

A
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37
Q

What does the antibacterial activity of aminoglycosides depend on?

A

An effective concentration of antibiotic outside the cell

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38
Q

Which types of bacteria are generally resistant to aminoglycosides?

A

Anaerobic bacteria and induced mutants

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39
Q

Why are anaerobic bacteria resistant to aminoglycosides?

A

They lack appropriate transport systems

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40
Q

How does low oxygen tension (hypoxic tissues) affect aminoglycoside transport into bacteria?

A

Diminishes transfer into bacteria

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41
Q

What role do divalent cations (eg, Ca & Mg) located in the LPS, cell wall or memmbrane play in aminoglycoside transport?

A

They can interfere with transport by combining with anionic sites

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42
Q

What effect does alkaline pH have on aminoglycoside movement across bacterial membranes?

A

Facilitates passive movement

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43
Q

By how much can a low pH increase membrane resistance to aminoglycosides?

A

More than 100-fold

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44
Q

What can alter the uptake of aminoglycosides?

A

Changes in osmolality

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45
Q

Why do some aminoglycosides have greater antibacterial activity than others?

A

They are transported more efficiently

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46
Q

What is a common interaction when aminoglycosides are used in combination with β-lactam antibiotics?

A

Synergism

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47
Q

Fill in the blank: The transport of aminoglycosides is diminished in _______ tissues.

A

Hypoxic

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48
Q

Fill in the blank: Lidocaine, bupivacaine, ropivacaine, levobupivacaine, and mepivacaine were reported to have dose- and time-dependent deleterious effects on chondrocytes that appeared to be made worse by the coadministration of corticosteroids. _______ at concentrations of 0.5% or less was found to be the least chondrotoxic anesthetic.

A

Ropivacaine

49
Q

What are the hypotensive effects observed after IV administration of opioids?

A

Minimal hypotensive effects are observed after IV administration

This suggests that while opioids can affect blood pressure, the impact is generally not significant.

50
Q

What cardiac effects may occur after rapid IV administration of opioids?

A

Bradycardia and/or tachycardia with hypotension

This can be due to histamine release, especially with Meperidine and occasionally with Morphine.

51
Q

How do opioids affect respiratory rate and tidal volume?

A

Minimally affected

This indicates that opioids do not significantly impair respiratory function in terms of rate and volume.

52
Q

What type of antiarrhythmic effects do opioids produce?

A

Some antiarrhythmic effects due to decreases in sympathetic nervous system activity

53
Q

What is the effect of low dose dopamine (0.5-2 mcg/kg/min)?

A

Vasodilation through activation of dopaminergic receptor

Low dose dopamine primarily affects dopaminergic receptors, leading to vasodilation.

54
Q

What receptors are preferentially stimulated at intermediate dose dopamine (5-10 mcg/kg/min)?

A

Beta receptors

Intermediate dose dopamine enhances cardiac contractility through stimulation of beta receptors.

55
Q

What is the effect of intermediate dose dopamine (5-10 mcg/kg/min) on cardiac contractility?

A

Increased cardiac contractility

This dose primarily acts on beta receptors, enhancing the heart’s ability to contract.

56
Q

What receptors are primarily stimulated at high dose dopamine (10-20 mcg/kg/min)?

A

Alpha receptors

High dose dopamine leads to significant alpha receptor stimulation, impacting vascular tone.

57
Q

What is the effect of high dose dopamine (10-20 mcg/kg/min)?

A

Vasoconstriction

The stimulation of alpha receptors at high doses results in vasoconstriction.

58
Q

What type of adrenergic activity does Dobutamine exhibit?

A

a+, B1+++, B2+++

Dobutamine primarily stimulates alpha and beta adrenergic receptors, with a strong emphasis on beta-1 and beta-2 receptors.

59
Q

What is the effect of Dobutamine on cardiac contractility?

A

strong increase

Dobutamine is known for its potent positive inotropic effects, leading to enhanced cardiac contractility.

60
Q

What is the effect of Dobutamine on systemic vascular resistance?

A

reduced

Unlike other inotropic agents, Dobutamine has a minimal effect on systemic vascular resistance, which can be beneficial in certain clinical scenarios.

61
Q

What is Misoprostol?

A

Synthetic analogue of prostaglandin E1 (PGE1)

Misoprostol is used in various medical applications, including gastrointestinal protection.

62
Q

What are the two main functions of Misoprostol?

A
  • Acid-INHIBITORY
  • Mucosal-PROTECTIVE properties

These functions help protect the stomach lining and reduce acid secretion.

63
Q

What are the three functions that Misoprostol increases?

A
  • Bicarbonate secretion
  • Mucus production
  • Mucosal blood flow

These functions contribute to its protective effects on the gastrointestinal tract.

64
Q

How does Misoprostol affect gastric acid secretion?

A

Decreases intracellular cAMP -> decreased H+/K+-ATPase pump activity -> decreased gastric acid secretion

This mechanism helps in reducing acidity in the stomach.

65
Q

What is the half-life of Misoprostol?

A

Short half-life of 30 minutes

Due to its short half-life, Misoprostol is often administered multiple times a day.

66
Q

How often should Misoprostol be administered due to its half-life?

A

3 to 4 times a day

Frequent dosing is necessary to maintain its therapeutic effects.

67
Q

What type of hepatic injury is associated with NSAID hepatotoxicity?

A

Intrinsic hepatic injury

This injury is predictable and dose-related due to high exposure during metabolism.

68
Q

Which NSAIDs are specifically mentioned as causing intrinsic hepatic injury?

A

Aspirin, acetaminophen

These drugs are known for their potential hepatotoxic effects.

69
Q

What is the timing of idiosyncratic injury associated with Rimadyl?

Idiosyncratic - an abnormal physical reaction by an individual to a food or drug

A

Approximately 19 days after starting

This injury is not dose-related and is considered rare.

70
Q

True or False: Injury from Rimadyl is dose-related.

A

False

It is rare and unpredictable with vague clinical signs.

71
Q

What are some clinical signs of injury from NSAIDs?

A

Vague clinical signs such as vomiting and anorexia

These signs can be nonspecific and may not directly indicate liver injury.

72
Q

Which dog breed is particularly noted for susceptibility to NSAID hepatotoxicity?

A

Labradors

This breed shows a notable predisposition to idiosyncratic injury from certain NSAIDs.

73
Q

What is the mechanism by which acidic NSAIDs cause gastrointestinal injury?

A

Acidic NSAID -> lipophilic -> diffuses into gastric mucosa

This direct effect leads to injury in the gastric or intestinal lining.

74
Q

What is the indirect effect of NSAIDs on the gastrointestinal tract?

A

PG inhibition

Prostaglandins (PG) have a cytoprotective effect on the GI mucosa.

75
Q

What are the 4 functions of endogenous PGE2 play in the gastrointestinal tract?

A
  1. Maintains gastric mucosal layer
  2. Quality of gastric mucus
  3. Mucosal blood flow
  4. Production of gastric acid

These are four essential functions of PGE2 in the GI system.

76
Q

Where are Mucous neck cells located?

A

Body, antrum

Mucous neck cells secrete mucus.

77
Q

What do Chief cells produce?

A

Pepsinogen

Pepsinogen is activated to pepsin in the acidic environment of the stomach.

78
Q

What is secreted by the Surface epithelium?

A

Mucus, bicarbonate

These substances help protect the stomach lining from gastric acid.

79
Q

Which hormones are produced by Endocrine cells?

A

Gastrin, Histamine, Serotonin

These hormones regulate gastric functions.

80
Q

Fill in the blank: Parietal cells are located in the _______.

81
Q

Fill in the blank: Chief cells are primarily found in the _______.

82
Q

True or False: Mucous neck cells are responsible for producing pepsinogen.

A

False

Pepsinogen is produced by Chief cells, not Mucous neck cells.

83
Q

What percentage of body weight does water constitute in adult animals with appropriate BCS?

A

Approximately 60%

84
Q

What fraction of total body water does the intracellular compartment account for?

A

2/3 of total body water

85
Q

What percentage of body weight is represented by the intracellular compartment?

A

40% of body weight

86
Q

What fraction of total body water does the extracellular compartment account for?

A

1/3 of total body water

87
Q

What percentage of body weight is represented by the extracellular compartment?

A

20% of body weight

88
Q

What are the two divisions of the extracellular compartment and their respective percentages?

A
  • 25% plasma (AKA intravascular)
  • 75% interstitial
89
Q

Where does the movement of fluid from intravascular to extravascular occur?

A

At the capillary

90
Q

Which COX enzyme’s inhibition leads to ulceration in the duodenum?

A

COX-2

Inhibition of COX-2 is specifically linked to duodenal ulceration.

91
Q

What is produced by Parietal cells?

A

Acids and intrinsic factor

Intrinsic factor is essential for vitamin B12 absorption.

92
Q

What is the effect of COX-1 inhibition on the gastrointestinal tract?

A

Decreased mucus production

This reduction can lead to increased susceptibility to gastric injury.

93
Q

Which COX enzyme’s inhibition leads to ulceration in the duodenum?

A

COX-2

Inhibition of COX-2 is specifically linked to duodenal ulceration.

94
Q

What is the potency of Methadone compared to morphine?

A

2x

Methadone is twice as potent as morphine.

95
Q

Does Methadone cause histamine release?

A

Does NOT

Methadone does not trigger histamine release.

96
Q

What is the duration of action for Methadone?

A

3-4 hours

Methadone has a duration of action ranging from 3 to 4 hours.

97
Q

Methadone acts as an antagonist for which receptor?

A

N-methyl-D-aspartate (NMDA)

This antagonism may lead to fewer excitatory responses in certain animals, such as cats.

98
Q

What is the risk associated with systemic use of aminoglycosides?

A

Ototoxicity

99
Q

Does topical administration of aminoglycosides in the middle ear result in ototoxic considerations?

100
Q

What type of administration of aminoglycosides does NOT result in ototoxic considerations in the vestibular apparatus?

A

Topical administration in the middle ear

101
Q

True or False: Topical aminoglycosides are ototoxic when applied to the middle ear.

102
Q

What type of anesthetic is Ketamine?

A

Dissociative anesthetic

Acts via antagonism of N-methyl-D-aspartate receptors.

Dissociative anesthetics are a class of drugs that produce a state of altered consciousness characterized by:
- Dissociation: Separation of perception from cognition, leading to a feeling of detachment from the body and environment.
- Analgesia: Pain relief.
- Sedation: Drowsiness and loss of consciousness.

103
Q

What effects does Ketamine have on muscle and reflexes?

A

Muscle rigidity and retention of laryngeal reflexes due to dissociative state

104
Q

What effect does Ketamine have on salivation in dogs and cats?

A

Increases salivation

Notable in both dogs and cats

105
Q

What type of effect does Ketamine have on the sympathetic nervous system?

A

Mild sympathomimetic effect

Leads to an increase in myocardial work

106
Q

What happens to cardiac output in cases of depleted sympathetic reserves when using Ketamine?

A

Decrease in cardiac output

Example condition: septic shock

107
Q

What effect does Ketamine have on intracranial and intraocular pressures?

A

Increases intracranial and intraocular pressures

108
Q

How is Ketamine metabolized and what is the caution regarding its elimination?

A

Metabolized to norketamine; renal elimination

Caution with decreased renal function

109
Q

What percentage of the administered dose of Ketamine is excreted unchanged in urine in cats?

A

Approximately 50%

110
Q

What is the duration of action for Ketamine?

A

15-20 minutes

111
Q

What is Clopidogrel?

A
  • A thienopyridine medication that undergoes hepatic metabolism to acquire antiplatelet activity
  • Thienopyridine, a class of antiplatelet drugs that inhibit platelet aggregation by blocking the ADP receptor on platelets, used to prevent stroke and other serious vascular events

Clopidogrel is commonly used to prevent blood clots in various cardiovascular conditions.
AKA Plavix

112
Q

What is the mechanism of action (MOA) of Clopidogrel?

A

Irreversible blocks ADP (adenosine diphosphate), binds P2Y12-ADP on platelets, preventing activation of integrin IIb/IIa

This action inhibits fibrinogen binding and platelet aggregation.

113
Q

How long does it take for Clopidogrel to onset its effects?

A

About 2 days

It reaches steady state in approximately 5-7 days.

114
Q

What additional effect does Clopidogrel have besides antiplatelet activity?

A

Inhibits serotonin, leading to vasomodulatory effects

This helps mitigate the ischemic impact of venous thromboembolism (VTE).

115
Q

Fill in the blank: Clopidogrel is a _______ that requires hepatic metabolism to acquire antiplatelet activity.

A

thienopyridine

Thienopyridine, a class of antiplatelet drugs that inhibit platelet aggregation by blocking the ADP receptor on platelets, used to prevent stroke and other serious vascular events

116
Q

True or False: Clopidogrel prevents platelet activation by binding to P2Y12-ADP on PLT.

117
Q

What is ADP’s role in clotting

A

ADP (adenosine-5-diphosphate) is a nucleotide released by platelets that plays a crucial role in activating platelets and initiating the formation of blood clots

118
Q

Diltiazem drug class

A

A Ca+ channel blocker