NR 508 Week 3 TD and Quiz
PART 1:
Elliot is a 74 year-old male who presents to your clinic with complaints of frequent
nosebleeds (4 in the past week) and several severe bruises scattered variously
throughout his anatomy (increased INR). The patient is also complaining of a
runny nose, cough, and head/chest congestion. He has a history of chronic atrial
fibrillation and is currently prescribed and taking warfarin. Approximately 3 weeks
previously, he started taking over-the-counter cimetidine (Tagamet, H2
antagonist) for heartburn he was experiencing. Below is a list of the patient’s
medications, his physical examination, and his laboratory findings:
Medications
Digoxin 0.25 mg QD Cimetidine OTC BID
Pseudoephedrine SR 120 BID Warfarin 7 mg QD
Allergies: NKDA
Physical Examination
VS: BP: 180/95, HR 75, irregularly HEENT: WNL
irregular, RR 17
Weight: 95 kg (209 lbs)
ABD: + Bowel Sounds EXT: Bruising on arms and legs
NEURO: Alert & Oriented x 3 GEN: Well developed, well-nourished
male
ECG: atrial fibrillation
Laboratory
Na 143 mEq/L N K 4.5 mEq/L N
Cl 99 mmol/L (95-105) N CO2 25 mEq/L (23-29) N
BUN 18 mg/dL (8-21) N SCr 0.9 mg/dL (0.8-1.3) N
INR 4.8 (2-3) H Hct 42% (40-52% m) N
Hbg 15 mg/dL (13-17 m) N Digoxin 3.8 ng/ml (0.5-2) H
What problems should be identified in this patient? HTN possibly r/t
Pseudoephedrine intake and/or afib, chronic Afib, high INR reason for
bruising, digoxin overdose, possible Viral URI d/c pseudoepi and start
on zyrtec OTC and Tylenol prn , GERD, drug-drug interaction
between cimetidine and warfarin , flu swab to r/o flu, check for H.
Pylori, make sure pt’s diet hasn’t changed.
What are the precise mechanisms of action of each drug?
What do you think is contributing to the patient’s
hypertension? Pseudoephedrine intake, however we must consider he
could have HTN unrelated to this med as well so follow up in one week.
, Are there any drug interactions that you can identify as associated with
this current drug regimen, and if so how, mechanistically, are they
occurring? drug-drug interaction between cimetidine and warfarin
What is the clinical significance of these interactions? Cimetidine
increases anticoagulation effect of vitamin K antagonists ie warfarin
Please try to remember to include the physiology behind how a drug
works on the body (more than just a sentence or two). Specifically, we
want to look at how a drug works on the body, and what the body does
to the drug. This often includes examining pharmacodynamics as well
as pharmacokinetic properties that play a role in drug interactions.
Elliot presents to the office today with complaints of frequent epistaxis,
bruising, GERD, and symptoms of a viral upper respiratory infection (URI).
He has a history of atrial fibrillation (afib) and is taking warfarin for
anticoagulation and digoxin for contractility. After assessing the patient and
examining the results of his lab work, additional problems were identified,
which include hypertension (HTN) most likely related to the
pseudoephedrine, an increased INR level which is likely the cause of his
epistaxis and bruising, and an increased Digoxin level, also referred to as
digoxin overdose or toxicity.
The precise mechanisms of action of each drug are as follows:
Pseudoephedrine SR 120 BID. Pseudoephedrine directly effects alpha- and
beta-adrenergic receptors as well as indirectly causes the release of
norepinephrine (PDR, 2017). Pseudoephedrine acts directly on alpha
receptors in the mucosa of the respiratory tract causing vasoconstriction and
subsequent reduction of nasal congestion, hyperemia, edema, and an
increase in sinus drainage and nasal airway patency (PDR, 2017).
Pseudoephedrine also stimulates beta2 – adrenergic receptors that have the
potential to relax bronchial smooth muscle, although bronchodilation is
uncommon (PDR, 2017). Pseudoephedrine can increase the irritability of the
myocardium, which can effect ventricular conduction, especially in patients
with as underlying cardiac issue (PDR, 2017). Adverse cardiovascular
reactions include hypertension, arrhythmias, chest tightness, palpitations,
and tachycardia (Lexicomp, 2017).
Cimetidine OTC BID. Cimetidine impedes effects of histamine at the H2-
receptor, known as the basolateral membrane of the parietal cell, resulting in
, gastric acidity and gastric acid volume reduction (PDR, 2017). Cimetidine
does not decrease acid-output as well as proton-pump inhibitors; it also does
not seem to alter gastric motility, esophageal pressure, gastric emptying, or
secretion rates of the pancreas and gallbladder (PDR, 2017). It does weakly
exhibit anti-androgenic effects (PDR, 2017).
Digoxin 0.25 mg QD. Na-K-ATPase controls intracellular potassium and
sodium (PDR, 2017). Digoxin prevents the action of the Na-K-ATPase
membrane pump (PDR, 2017). The restriction causes an increase in
intracellular sodium, which stimulates an increase in intracellular calcium
concentrations (PDR, 2017). The thought is that the increased calcium
concentrations facilitate the activation of proteins responsible for
contraction, such as actin and myosin (PDR, 2017). Basically, digoxin
increases the velocity and force of myocardial contraction but it also takes
specific action on electrical activity within the myocardium (PDR, 2017). In
afib, it will decrease the amount of times atrial depolarization reaches the
ventricle, which will slow the ventricle rate (PDR, 2017).
Warfarin 7 mg QD. Warfarin restricts the synthesis of vitamin k-dependent
anticoagulation proteins C and S and coagulation factors of II, VII, IX, and
X. Precisely, warfarin restricts the C1 subunit of the vitamin K epoxide
reductase (VKORC1) enzyme that decreases regeneration of vitamin K
epoxide (PDR, 2017). Vitamin K is a cofactor for the carboxylation of
glutamate residues to gamma-carboxylation on the N-terminal areas of the
vitamin k-dependent proteins (PDR, 2017). Carboxylation permits
coagulation proteins encounter the conformational change that is required in
order to activate them (PDR, 2017). Warfarin produces its anticoagulation
effects by preventing vitamin K epoxide reductase and potentially vitamin K
reductase, which leads the vitamin K depletion and confines the gamma-
carboxylation of vitamin K-dependent coagulant proteins (PDR, 2017). The
amount of effect on vitamin K-dependent proteins depends on the dose and
possibly the patient’s VKORC1 genotype. Warfarin lengthens prothrombin
time (PT), which responds to 3 out of 4 vitamin K-dependent coagulations
factors, those being II, VII, and X (PDR, 2017). Each of the factors are
different in regards to their degradation half life; factor II’s half life is 60
hours, factor VII is 4 to 6 hours, factor IX is 24 hours, and factor X is 48-72
hours (PDR, 2017). Proteins C and S have specific half lives as well, protein
C is approximately 8 hours while protein S has approximately 30 hours
(PDR, 2017).
PART 1:
Elliot is a 74 year-old male who presents to your clinic with complaints of frequent
nosebleeds (4 in the past week) and several severe bruises scattered variously
throughout his anatomy (increased INR). The patient is also complaining of a
runny nose, cough, and head/chest congestion. He has a history of chronic atrial
fibrillation and is currently prescribed and taking warfarin. Approximately 3 weeks
previously, he started taking over-the-counter cimetidine (Tagamet, H2
antagonist) for heartburn he was experiencing. Below is a list of the patient’s
medications, his physical examination, and his laboratory findings:
Medications
Digoxin 0.25 mg QD Cimetidine OTC BID
Pseudoephedrine SR 120 BID Warfarin 7 mg QD
Allergies: NKDA
Physical Examination
VS: BP: 180/95, HR 75, irregularly HEENT: WNL
irregular, RR 17
Weight: 95 kg (209 lbs)
ABD: + Bowel Sounds EXT: Bruising on arms and legs
NEURO: Alert & Oriented x 3 GEN: Well developed, well-nourished
male
ECG: atrial fibrillation
Laboratory
Na 143 mEq/L N K 4.5 mEq/L N
Cl 99 mmol/L (95-105) N CO2 25 mEq/L (23-29) N
BUN 18 mg/dL (8-21) N SCr 0.9 mg/dL (0.8-1.3) N
INR 4.8 (2-3) H Hct 42% (40-52% m) N
Hbg 15 mg/dL (13-17 m) N Digoxin 3.8 ng/ml (0.5-2) H
What problems should be identified in this patient? HTN possibly r/t
Pseudoephedrine intake and/or afib, chronic Afib, high INR reason for
bruising, digoxin overdose, possible Viral URI d/c pseudoepi and start
on zyrtec OTC and Tylenol prn , GERD, drug-drug interaction
between cimetidine and warfarin , flu swab to r/o flu, check for H.
Pylori, make sure pt’s diet hasn’t changed.
What are the precise mechanisms of action of each drug?
What do you think is contributing to the patient’s
hypertension? Pseudoephedrine intake, however we must consider he
could have HTN unrelated to this med as well so follow up in one week.
, Are there any drug interactions that you can identify as associated with
this current drug regimen, and if so how, mechanistically, are they
occurring? drug-drug interaction between cimetidine and warfarin
What is the clinical significance of these interactions? Cimetidine
increases anticoagulation effect of vitamin K antagonists ie warfarin
Please try to remember to include the physiology behind how a drug
works on the body (more than just a sentence or two). Specifically, we
want to look at how a drug works on the body, and what the body does
to the drug. This often includes examining pharmacodynamics as well
as pharmacokinetic properties that play a role in drug interactions.
Elliot presents to the office today with complaints of frequent epistaxis,
bruising, GERD, and symptoms of a viral upper respiratory infection (URI).
He has a history of atrial fibrillation (afib) and is taking warfarin for
anticoagulation and digoxin for contractility. After assessing the patient and
examining the results of his lab work, additional problems were identified,
which include hypertension (HTN) most likely related to the
pseudoephedrine, an increased INR level which is likely the cause of his
epistaxis and bruising, and an increased Digoxin level, also referred to as
digoxin overdose or toxicity.
The precise mechanisms of action of each drug are as follows:
Pseudoephedrine SR 120 BID. Pseudoephedrine directly effects alpha- and
beta-adrenergic receptors as well as indirectly causes the release of
norepinephrine (PDR, 2017). Pseudoephedrine acts directly on alpha
receptors in the mucosa of the respiratory tract causing vasoconstriction and
subsequent reduction of nasal congestion, hyperemia, edema, and an
increase in sinus drainage and nasal airway patency (PDR, 2017).
Pseudoephedrine also stimulates beta2 – adrenergic receptors that have the
potential to relax bronchial smooth muscle, although bronchodilation is
uncommon (PDR, 2017). Pseudoephedrine can increase the irritability of the
myocardium, which can effect ventricular conduction, especially in patients
with as underlying cardiac issue (PDR, 2017). Adverse cardiovascular
reactions include hypertension, arrhythmias, chest tightness, palpitations,
and tachycardia (Lexicomp, 2017).
Cimetidine OTC BID. Cimetidine impedes effects of histamine at the H2-
receptor, known as the basolateral membrane of the parietal cell, resulting in
, gastric acidity and gastric acid volume reduction (PDR, 2017). Cimetidine
does not decrease acid-output as well as proton-pump inhibitors; it also does
not seem to alter gastric motility, esophageal pressure, gastric emptying, or
secretion rates of the pancreas and gallbladder (PDR, 2017). It does weakly
exhibit anti-androgenic effects (PDR, 2017).
Digoxin 0.25 mg QD. Na-K-ATPase controls intracellular potassium and
sodium (PDR, 2017). Digoxin prevents the action of the Na-K-ATPase
membrane pump (PDR, 2017). The restriction causes an increase in
intracellular sodium, which stimulates an increase in intracellular calcium
concentrations (PDR, 2017). The thought is that the increased calcium
concentrations facilitate the activation of proteins responsible for
contraction, such as actin and myosin (PDR, 2017). Basically, digoxin
increases the velocity and force of myocardial contraction but it also takes
specific action on electrical activity within the myocardium (PDR, 2017). In
afib, it will decrease the amount of times atrial depolarization reaches the
ventricle, which will slow the ventricle rate (PDR, 2017).
Warfarin 7 mg QD. Warfarin restricts the synthesis of vitamin k-dependent
anticoagulation proteins C and S and coagulation factors of II, VII, IX, and
X. Precisely, warfarin restricts the C1 subunit of the vitamin K epoxide
reductase (VKORC1) enzyme that decreases regeneration of vitamin K
epoxide (PDR, 2017). Vitamin K is a cofactor for the carboxylation of
glutamate residues to gamma-carboxylation on the N-terminal areas of the
vitamin k-dependent proteins (PDR, 2017). Carboxylation permits
coagulation proteins encounter the conformational change that is required in
order to activate them (PDR, 2017). Warfarin produces its anticoagulation
effects by preventing vitamin K epoxide reductase and potentially vitamin K
reductase, which leads the vitamin K depletion and confines the gamma-
carboxylation of vitamin K-dependent coagulant proteins (PDR, 2017). The
amount of effect on vitamin K-dependent proteins depends on the dose and
possibly the patient’s VKORC1 genotype. Warfarin lengthens prothrombin
time (PT), which responds to 3 out of 4 vitamin K-dependent coagulations
factors, those being II, VII, and X (PDR, 2017). Each of the factors are
different in regards to their degradation half life; factor II’s half life is 60
hours, factor VII is 4 to 6 hours, factor IX is 24 hours, and factor X is 48-72
hours (PDR, 2017). Proteins C and S have specific half lives as well, protein
C is approximately 8 hours while protein S has approximately 30 hours
(PDR, 2017).
