MANILA TYTANA COLLEGES

Manila Doctors College of Nursing

Pres. Diosdado Macapagal Blvd., Metropolitan Park Pasay City

DRUG ANALYSIS

Name :_Rosete, Christine Marie M.__ Year & section:_3 -

A________________
Course:__BS Nursing_____________ Date of submission:__09/ 14/
2020___

DRUG NAME MECHANISM OF ACTION MAJOR ADVERSE NURSING IMPLICATIONS

EFFECTS

- Nitroglycerin - The patient’s blood pressure is 158/96 mm Hg, This drug ● Headache ● Periodically monitor BP and
(Anti-anginals) will inhibit the movement of calcium ions across the ● Dizziness cardiac rhythm because
- 3 tablets membrane of myocardial and arterial muscle cells, altering ● Orthostatic there is an increased risk of
-Sublingual the action potential and blocking muscle cell contraction. hypotension hypotensive episodes
This effect depresses myocardial contractility, slows ● Tachycardia ● Provide comfort measures to
Page 853 pdf cardiac impulse formation in the conductive tissues, and ● Flushing help the patient tolerate drug
relaxes and dilates arteries, causing a fall in blood ● Palpitations effects
pressure and a decrease in venous return. ○ Small frequent meals
- These effects decrease the workload of the heart and ○ Access to bathroom
myocardial oxygen consumption. facilities
-May interact with nitrate receptors in vascular smooth- ○ Remove clutters in the
muscle cell membranes. This interaction reduces environment
nitroglycerin to nitric oxide, which activates the enzyme ● Monitor blood pressure
guanylate cyclase, increasing intracellular formation of closely because of the
cGMP. Increased cGMP level may relax vascular smooth increased risk of hypotension
muscle by forcing calcium out of muscle cells, causing and falls especially in elderly
vasodilation. Venous dilation decreases venous return to patients who are taking
the heart, reducing left ventricular end-diastolic pressure several medications.
and pulmonary artery wedge pressure. Arterial dilation ● Assist or suggest patient to
decreases systemic vascular resistance, systolic arterial rise slowly to minimize
pressure, and mean arterial pressure. Thus, nitroglycerin dizziness when standing up
reduces preload and afterload, decreasing myocardial because of the increased risk
workload and oxygen demand. It also dilates coronary of orthostatic hypotension.
arteries, increasing blood flow to ischemic myocardial Advise to lie down at the first
tissue. sign of dizziness.
● For sublingual use, teach the
-2005, A nitrate that reduces cardiac oxygen demand by patient how to give the
decreasing left ventricular end- diastolic pressure prescribed form of
(preload) and, to a lesser extent, systemic vascular nitroglycerin. Advise and
resistance (afterload). Also increases blood flow through instruct patient to place tablet
the collateral coronary vessels. under his tongue. Instruct
him not to swallow or chew
the drug but let it dissolve
and explain that moisture in
his mouth helps drug
absorption; or have the
patient to take the drug with
a glass of water.
● Drug may cause headaches,
 especially at the beginning of
therapy. Advise patient to
notify prescriber immediately
about severe headache.

DRUG NAME MECHANISM OF ACTION MAJOR ADVERSE NURSING IMPLICATIONS

EFFECTS

- Morphine - Binds with and activates opioid receptors (mainly mu  Euphoria ● Before giving morphine,
sulfate receptors) in brain and spinal cord to produce analgesia ● Seizures make sure opioid antagonist
(Opioid and euphoria. ● Dizziness are available
Analgesic) -(2005) Unknown; binds with opiate receptors in the CNS, ● Bradycardia ● Monitor respiratory and
- 5 mg altering both perception of and emotional response to ● Shock circulatory status carefully
- IV push pain. ● Cardiac arrest and frequently because
● Nausea respiratory depression and
- The analgesic of choice for acute MI is morphine sulfate ● Vomiting severe hypotension can
(Duramorph, Astramorph) administered in intravenous ● Constipation develop. Life-threatening
boluses. Morphine reduces pain and anxiety. It reduces ● Thrombocytopenia depression can occur even
preload, which decreases the workload of the heart. ● Respiratory when morphine is taken as
Morphine also relaxes bronchioles to enhance depression prescribed and is not
oxygenation. The cardiovascular response to morphine is ● Apnea misused or abused.
monitored carefully, particularly the blood pressure, which ● Respiratory arrest ● Slowly inject the drug directly
can be lowered, and the respiratory rate, which can be into tubing of free-flowing I.V.
depressed. Because morphine decreases sensation of solution over 4 to 5 minutes
pain, ST-segment monitoring may be a better indicator of because rapid I.V injection
subsequent ischemia than assessment of pain. may increase adverse
reactions.
 -The patient is experiencing chest pain that radiates to the ● Expect morphine to cause
left shoulder and left jaw. Pain begins at the nociceptors in physical and psychological
the peripheral nervous system which sends signals to the dependence. Provide patient
brain and spinal cord if “possible threat” stimuli are safety by putting the side
perceived. Nociceptors transmit painful stimulus to the rails up and assisting the
spinal cord. The signal is then carried through patient.
spinothalamic tract to the thalamus, then to the
somatosensory cortex where pain is perceived. The brain
produces endogenous opioids which binds to opioid
receptors, which are abundantly present in the central and
peripheral nervous system. This drug binds with opioid
receptors (specifically mu receptor) for activation. If mu
receptor is activated, it will produce analgesia that will then
result to relief of pain.

DRUG NAME MECHANISM OF ACTION MAJOR ADVERSE NURSING IMPLICATIONS

EFFECTS

- Tissue - Binds to fibrin in a thrombus and converts trapped ● Cerebral hemorrhage ● Closely monitor patient for
Plasminogen plasminogen to plasmin. Plasmin breaks down fibrin, ● Arrhythmias signs of bleeding, especially
Activator fibrinogen, and other clotting factors, which dissolves the ● GI bleeding (cathflo at arterial puncture sites.
(Thrombolytic thrombus. activase) Bleeding is the most
enzyme) - (2005) Binds to fibrin in a thrombus and locally converts ● Spontaneous common adverse effect and
- 5 mg/day plasminogen to plasmin, which starts local fibrinolysis bleeding may occur internally and at
- PO ● Cholesterol external puncture sites.
-The patient is experiencing chest pain. Chest pain or embolization ● Advise patient to limit
angina happens due to plaque that blocks of coronary ● Anaphylaxis physical activity during
artery causing inadequate amount of blood going to the ● Venous thrombosis alteplase administration to
heart. Once the plaque rupture, platelets in the blood will ● Sepsis (cathflo reduce risk of injury and
result to blood clots that will completely occlude the artery, activase) bleeding.
resulting to myocardial infarction thereby increasing ● Minimize bleeding by
respiratory rate. avoiding compressible
-This drug act on existing clot causing it to dissolve by puncture sites.
directly or indirectly activating circulating protein called ● Monitor blood pressure and
plasminogen which then converts into plasmin. The heart rate and rhythm
plasminogen is converted into plasmin by activating tissue frequently during and after
plasminogen activator found in the endothelial cells. therapy.
Plasmin breaks down fibrin, fibrinogen, and other clotting ● Monitor continous ECG for
factors, through fibrinolysis which dissolves the thrombus. arrythmias during drug
This effect allows the blood in the artery to facilitate therapy. Coronary
increased blood flow going to the heart as the clot is thrombolysis is linked with
dissolved, reducing chest pain. arrythmias caused by
repurfusion of ischemic
myocardium.
● Monitor vital signs and
neurologic status carefully.
Keep the patient strict on bed
rest.
● Treat minor bleeding by
applying direct pressure if
accessible and appropriate;
continue to monitor.
● Tranexamic acid stops
fibrinolysis by inhibiting
binding of plasminogen to
firbin as well as conversion of
 plasminogen to plasmin

DRUG NAME MECHANISM OF ACTION MAJOR ADVERSE NURSING IMPLICATIONS

EFFECTS

- Heparin - Binds with antithrombin III, enhancing antithrombin III’s ● Hemorrhage ● Give heparin only in IV route
(Anticoagulant) inactivation of the coagulation enzymes thrombin (factor ● Overly prolonged or subcutaneous because
- bolus of 8000 U IIa) and factors Xa and XIa. At low doses, heparin inhibits clotting time I.M. use causes risk for
factor Xa and prevents conversion of prothrombin to ● Thrombocytopenia bleeding, hematoma,
thrombin. Thrombin is needed for conversion of fibrinogen ● White clot syndrome irritation, and pain. Explain
to fibrin; without fibrin, clots can’t form. At high doses, (WHAT IS THIS) also that heparin can’t be
heparin inactivates thrombin, preventing fibrin formation ● Anaphylactoid taken orally
and existing clot extension. reactions ● Inform patient about
- (2005) Accelerates formation of antithrombin III- thrombin increased risk of bleeding.
complex and deactivates thrombin, preventing conversion Take safety precautions to
of fibrinogen to fibrin. prevent bleeding, such as
having patient to use a soft-
-stimulates the anti thrombin III and then the antithrombin bristled toothbrush because
3 will inactivate (inhibit) factors (2,7) 9,10,11,12.= leads to bleeding is a major adverse
inhibition of secondary hemostasis. Heparin is fast acting effect of heparin therapy.
and sa blood ang site of action. Inhibition of 2ndary Bleeding may occur at any
hemostasis= inhibition of the coagulation casket= site.
inihibition of the formation of vibrant fibers= ● Keep protamine sulfate on
hand to use as an antidote
(unfractionated heparin inhibits factors 9, 10, 11, 12 and for heparin toxicity. Be aware
factor 2(thormbin; low molecular weight heparin stimulates that each milligram of
antithrombin 3 to inhibit only factor 10a protamine sulfate neutralizes
-heparin affects intrinsic pathway of coagulation when 100 unites of heparin.
there is internal trauma to the vascular system ● Watch closely if patient is
How? Heprin will bind in the natural occuring substance in receiving heparin therapy
the body and enchances the activity os this sustance and nitroglycerin I.V.
(antithrombin 3). Antithomrnin 3 inhibits the enzyme that because PTT may decrease
will play a role in the clotting process (specifically prevents and then rebound after
the acitvation of thrombin) =alter clotting bec we are nitroglycerin is discontinued.
gonna prevent the conversion of fibrinogen to fibrin= Monitor PTT closely, and be
slower clotting time and prevent clots and if may existing prepared to adjust heparin
clot, it will prevent the clot to getting bigger and potentially dose, as prescribed.
breaking off and going into circulation ● READ pg 901 for more
HEPARIN DOES NOT BREAK AN EXISTING CLOT (2005)

Factor 10 a converts prothormbin to thrombin

Thrombin converts fibrinogen to fibrin= lead to formation of
fibrin clot.Firbin forms a fibrous mesh that impedes the
flow of blood. Fibrin is broken down by plasmin (which is
converted from plasminogen)

-The patient is experiencing chest pain with a respiratory

rate of 30 breaths per minute due to the blockage in the
coronary artery, thus increase in oxygen demand. This
drug will bind and enhance the activity of antithrombin III.
Antithrombin III inhibits coagulation enzyme thrombin and
coagulation factor Xa and XIa. Factor Xa converts
prothrombin to thrombin and then thrombin converts
fibrinogen to fibrin which leads to formation of fibrin clot,
 impeding the flow of blood. But because of this drug,
formation of clots will be prevented, and the clotting time
will be slowed down. This effect will prevent clots from
impeding the flow of the blood allowing more blood to pass
by the artery and more oxygen thereby reducing chest
pain and respiratory rate.

DRUG NAME MECHANISM OF ACTION MAJOR ADVERSE NURSING IMPLICATIONS

EFFECTS

- Aspirin - Blocks the activity of cyclooxygenase, the enzyme ● Tinnitus ● Instruct patient to take aspirin
(Antiplatelet) needed for prostaglandin synthesis. Prostaglandins, ● Hearing loss with food or after meals
important mediators in the inflammatory response, cause ● Nausea because it may cause GI
local vasodilation with swelling and pain. With blocking of ● GI bleeding upset if taken on an empty
cyclooxygenase and inhibition of prostaglandins, ● Leukopenia stomach
inflammatory symptoms subside. Pain is also relieved ● Thrombocytopenia ● Instruct patient to stop taking
because prostaglandins play a role in pain transmission ● Prolonged bleeding aspirin and notify prescriber if
from the periphery to the spinal cord. Aspirin inhibits time any symptoms of stomach or
platelet aggregation by interfering with production of ● Hepatitis intestinal bleeding occur
thromboxane A2, a substance that stimulates platelet ● Rash such as passage of black,
aggregation. Aspirin acts on the heat-regulating center in ● Angioedema bloody, or tarry stools or if
the hypothalamus and causes peripheral vasodilation, ● Reye’s syndrome patient is coughing up blood
diaphoresis, and heat loss or vomit that looks like coffee
(2005) In low doses, aspirin also appears to impede grounds
clotting by blocking formation of the platelet-aggregating ● Monitor elderly patients
substance, thromboxane A2. closely because they may be
 more susceptible to aspirin’s
-When platelet becomes activated, arachidonic acid is toxic effects.
released form phospolipid membrane then convert to ● Ask about tinnitus. This
prosta H2 by cyclooxygenase-1 enzym (cox1), finally reaction usually occurs when
prosta h2 is futher metabolized to thromoxane A2 which is blood aspirin level reaches or
released form the platelet to stimulate activation of new exceeds maximum for
platelets as well as promote their aggregation (platelet therapeutic effect
agreggation= clot?), WHAT ASPirIn DoeS is it irreversaby ● (2005) Monitor patient for
inactivate cox 1 = dirsupting clot formation hypersensitivity reactions
such as anaphylaxis or
-The patient’s blood pressure is 154/96mmHG and is asthma
experiencing chest pain and was diagnosed to have
myocardial infarction due to the blockage in the coronary
artery caused by a subsequent thrombus formation as the
plaque ruptures in the artery. The artery has endothelial
cells. The endothelial cells that make up the inner surface
of the blood vessels release chemical mediators: nitric
oxide and prostacyclin. Nitric oxide dilates the artery while
prostacyclin binds to receptors located on platelets. This
binding prevents platelet activation and aggregation. If
there is damaged in the artery, there will be inadequate
nitric oxide and prostacyclin which will result to
vasoconstriction and platelet aggregate. Platelets adhere
to exposed collagen which causes platelets to change
shape and release granules containing chemical
mediators such as ADP, thrombin, thromboxane a2,
serotonin and platelet-activating factor which attracts and
activate more platelets that come to the site of injury in the
 artery. Thromboxane activates the glycoprotein 2b/3a
receptors which binds circulating fibrinogen that initiates
platelets to form aggregates. When platelet becomes
activated, phospholipid membrane in the cells release
arachidonic acid. Arachidonic acid is released if there is
tissue injury. The arachidonic acid will then be converted
to prostaglandin by cyclooxygenase-1 enzyme (COX-1).
Prostaglandin is further metabolized to thromboxane A2
which is released form the platelets to stimulate activation
of new platelets as well as promote platelet aggregation.
-This drug inactivates and inhibits the production of
thromboxane A2 which will then result to disrupting
platelet aggregation in the artery and then disrupts clot
formation. When the thrombus caused by platelet
aggregation is disrupted, blood flow in the artery will not
be impeded and the workload of the heart will be
decreased thereby reducing blood pressure and reducing
chest pain.

DRUG NAME MECHANISM OF ACTION MAJOR ADVERSE NURSING IMPLICATIONS

EFFECTS

- Metoprolol - Inhibits stimulation of beta1-receptor sites, located ● Fatigue ● Monitor patient’s heart rate.
tartate mainly in the heart, resulting in decreased cardiac ● Dizziness •Advise patient to notify
(Antihypertensive excitability, cardiac output, and myocardial oxygen ● Hypotension prescriber if pulse rate falls
) demand. These effects help relieve angina. Metoprolol ● Heart failure below 60 beats/minute or is
- 5 mg/ 5 minutes also helps reduce blood pressure by decreasing renal ● AV block (WHAT IS significantly lower than usual.
(total of 15 mg); release of renin THIS?) ● Monitor blood pressure
TID; -(2005)Unknown. A selective beta blocker that selectively frequently. metoprolol masks
- IV push blocks beta1- adrenergic receptors; decreases cardiac common signs and
output, peripheral resistance, and cardiac oxygen symptoms of shock
consumption; and depresses renin secretion. ● Store drug at room
temperature and protect from
-The patient is having a blood pressure of light. Discard solution if it’s
154/96mmHg.This drug selectively inhibits beta 1 discolored or contains
receptors which are pressure sensitive neuron which particles
regulates blood pressure. Once the beta receptor is ● Check page 766 of MSN
inhibited, it will not stimulate the adrenal medulla to book
release catecholamines resulting to decrease in heart rate
and stroke volume as well as cardiac output and
myocardial oxygen demand which will result in decreased
blood pressure.