NSG122 & NSG124 Milestone Exam #1 2026 | Herzing University | Latest Update |
Most Tested Questions & Verified Answers | Graded A+
1. Eye Drop Admin - Teach - NSG122 - 07.03.03
• Check medications 2x before entering patient’s room (1st when retrieving it and 2nd when
preparing it)
• Always implement the 6 rights of medication administration (right patient, medication, route,
dose, time, & documentation)
• Use hand hygiene upon entering patient’s room
• Introduce self and explain procedure to patient
• Verify patient with 2 identifiers
• Confirm allergies against patient records
• 3rd medication check in the patient’s room against the MAR before administration
• Scan barcode on medication
• Bring bed down to a comfortable working position
• Don clean gloves
• Clean patient’s eyes (inner to outer canthus)
• Have patient tilt head back (unless it’s contraindicated in their chart)
• Remove cap of eye drops & never touch the inside of the cap bc you can contaminate the entire
bottle
• Have patient look up at the ceiling
• Move lower eyelid down and place a drop into the lower conjunctival sac
• Make sure not to touch the cornea with the eye drops
• Also do not let the bottle touch the patient’s eyes, eyelids, or eyelashes
• Once designated amount of drops are instilled, close the eye & apply gentle pressure to the
lacrimal duct to prevent the medication from falling into the tear ducts (also minimizes any
systemic effects of the medication)
• Advise patient not to rub their eyes
• Document medication administration into MAR
• Use hand hygiene when leaving patient room
2. ***Pressure Ulcer - Assessment - pre-test item not graded***
4 stages:
• Stage 1 Pressure Injuries are localized areas of erythema that the skin remain intact.
• Stage 2 Pressure Injuries includes a partial-thickness loss of skin with exposed dermis. The
wound bed is viable, pink or red, moist, and may also present as an intact or ruptured serum-
filled blister. Adipose tissue is not visible and deeper tissues are not visible. Granulation tissue,
slough, and eschar are not present.
• Stage 3 Pressure Injuries have full-thickness loss of skin. In a stage 3 pressure injury, adipose
and granulation tissue are often visible.
• Stage 4 Pressure Injuries (unstageable) are also full thickness skin loss with exposed fascia,
muscle, tendon, ligament, or bone.
,3. ***Shearing Force - pre-test item not graded***
Shear - results when one layer of tissue slides over another layer. Shear separates the skin from
underlying tissues. The small blood vessels and capillaries in the area are stretched and possibly
tear, resulting in decreased circulation to the tissue cells under the skin. Patients who are pulled,
rather than lifted, when being moved up in bed or from bed to chair or stretcher are at risk for injury
from shearing forces. A patient who is partially sitting up in bed is susceptible to shearing force
when the skin sticks to the sheet and underlying tissues move downward with the body toward the
foot of the bed. This may also occur in a patient who sits in a chair but slides down.
4. Allergic Reaction - NSG124 - 01.02.04
Allergic Reaction - an immune response. For an allergic reaction to occur, there must be prior
sensitization of the immune system.
Once the immune system has been sensitized to a drug, re-exposure to that drug can trigger an
allergic response. The intensity of allergic reactions can range from mild itching to severe rash to
anaphylaxis. Anaphylaxis is a life-threatening response characterized by bronchospasm, laryngeal
edema, and a precipitous drop in blood pressure. Estimates suggest that less than 10% of ADRs are
of the allergic type.
The intensity of an allergic reaction is determined primarily by the degree of sensitization of the
immune system, not by drug dosage. Put another way, the intensity of allergic reactions is largely
independent of dosage. As a result, a dose that elicits a very strong reaction in one allergic patient
may elicit a very mild reaction in another. Furthermore, because a patient's sensitivity to a drug can
change over time, a dose that elicits a mild reaction early in treatment may produce an intense
reaction later on. Very few medications cause severe allergic reactions. In fact, most serious
reactions are caused by just one drug family—the penicillins. Other drugs noted for causing allergic
reactions include the nonsteroidal anti-inflammatory drugs (e.g., aspirin) and the sulfonamide group
of compounds, which includes certain diuretics, antibiotics, and oral hypoglycemic agents.
5. Tylenol (Acetaminophen) - Lab Check - NSG124 - 03.03.03
Mechanism of Action:
Differences between the effects of acetaminophen and aspirin are thought to result from selective
inhibition of cyclooxygenase, the enzyme needed to make prostaglandins and related compounds.
Whereas aspirin can inhibit cyclooxygenase in both the CNS and the periphery, inhibition by
acetaminophen is limited to the CNS; acetaminophen has only minimal effects on cyclooxygenase at
peripheral sites. By decreasing prostaglandin synthesis in the CNS, acetaminophen is able to reduce
fever and pain. The inability to inhibit prostaglandin synthesis outside the CNS may explain the
absence of anti-inflammatory effects, gastric ulceration, and adverse effects on the kidneys and
platelets.
Pharmacokinetics:
,Acetaminophen is readily absorbed following oral dosing and undergoes wide distribution. Most of
each dose is metabolized by the liver, and the metabolites are excreted in the urine. The plasma
half-life is approximately 2 hours.
Acetaminophen can be metabolized by two pathways: (major and minor)
Major Pathway - acetaminophen undergoes conjugation with glucuronic acid and other compounds
to form nontoxic metabolites.
Minor Pathway - acetaminophen is oxidized by a cytochrome P450–containing enzyme into a highly
reactive toxic metabolite: N-acetyl-p-benzoquinoneimine.
Adverse Effects:
Adverse effects are extremely rare at therapeutic doses. Acetaminophen does not cause gastric
ulceration or renal impairment and does not inhibit platelet aggregation. In addition, there is no
evidence linking acetaminophen with Reye's syndrome.
Acetaminophen use has also been associated with Stevens-Johnson syndrome (SJS), acute
generalized exanthematous pustulosis (AGEP), and toxic epidermal necrolysis (TEN). SJS and TEN
are characterized by painful rash, blistering of the skin and mucous membranes, and detachment of
the epidermis. These are considered medical emergencies, as they can result in death. Recovery
can take weeks to months. AGEP is characterized by pustular lesions that predominantly affect the
upper trunk and body folds. AGEP usually resolves within 2 weeks of onset. These reactions can
occur at any time, even if the patient has taken acetaminophen previously. If a rash appears while
taking acetaminophen, the drug should be stopped, and the patient should seek medical attention.
Alcohol:
Regular alcohol consumption increases the risk of liver injury from acetaminophen—but only if
acetaminophen dosage is excessive. Three mechanisms are involved. First, alcohol induces
synthesis of the P450-containing enzyme in the minor metabolic pathway, thereby increasing
production of acetaminophen's toxic metabolite. Second, stores of glutathione are depleted in
chronic alcoholics. As a result, the liver is unable to convert the toxic metabolite to a nontoxic form.
Third, chronic alcohol abusers often have pre-existing liver damage, which renders them less able to
tolerate injury from acetaminophen.
Some authorities recommend that if a person drinks alcohol on a regular basis, they should
consume no more than 2000 mg of acetaminophen a day (one-half the normal maximum).
Although therapeutic doses of acetaminophen may be safe for alcohol drinkers, high doses certainly
are not. Accordingly, to alert the public to the potential risk of combining alcohol with
acetaminophen, the FDA requires that acetaminophen labels bear the following statement: Alcohol
Warning: If one consumes three or more alcoholic drinks every day, ask a doctor whether
acetaminophen or other pain relievers/fever reducers should be taken.
Warfarin:
, There is evidence that acetaminophen may increase the risk of bleeding in patients taking warfarin
(an oral anticoagulant). The best guess is that acetaminophen may inhibit warfarin metabolism,
which would cause warfarin levels to rise. Although this interaction has not been proved, caution is
advised. Accordingly, for patients taking more than 1 gm of acetaminophen daily for several days,
responses to warfarin should be monitored closely. Occasional use of acetaminophen is not a
concern.
Vaccines:
Acetaminophen and other analgesic-antipyretics can blunt the immune response to childhood
vaccines. Accordingly, routine use of these drugs to prevent vaccination-associated pain and/or
fever should be discouraged.
Therapeutic Uses:
Acetaminophen is indicated for relief of pain and fever. Because acetaminophen is not associated
with Reye's syndrome, the drug is preferred to NSAIDs for use by children suspected of having
chickenpox or influenza. Because it does not cause GI injury, acetaminophen is preferred to NSAIDs
for patients with peptic ulcer disease. In addition, acetaminophen may be a safe alternative to aspirin
for patients who have experienced aspirin hypersensitivity reactions. Because of its weak anti-
inflammatory actions, acetaminophen is not useful for treating arthritis or rheumatic fever.
Acute Toxicity - Liver Damage:
Overdose with acetaminophen can cause severe liver injury and death. The cause is the
accumulation of the toxic metabolite (discussed earlier). In the United States, acetaminophen
overdose—intentional or unintentional—is the leading cause of acute liver failure, accounting for
about 50% of all cases. Risk of liver injury is increased by fasting, chronic alcohol use, and by taking
more than 4000 mg of acetaminophen a day.
Signs and Symptoms:
The principal feature of acetaminophen overdose is hepatic necrosis. Severe poisoning can
progress to hepatic failure, coma, and death. Early symptoms of poisoning (nausea, vomiting,
diarrhea, sweating, abdominal discomfort) belie the severity of intoxication. It is not until 48 to 72
hours after drug ingestion that overt indications of hepatic injury appear.
Treatment:
Liver damage can be minimized by giving acetylcysteine [Mucomyst , Acetadote], a specific
antidote to acetaminophen. Acetylcysteine reduces injury by substituting for depleted glutathione in
the reaction that converts the toxic metabolite of acetaminophen to its nontoxic form. When given
within 8 to 10 hours of acetaminophen overdose, acetylcysteine is 100% effective at preventing
severe liver injury. Even when administered as much as 24 hours after poisoning, it can still provide
significant protection. Acetylcysteine may be administered PO or IV.
Most Tested Questions & Verified Answers | Graded A+
1. Eye Drop Admin - Teach - NSG122 - 07.03.03
• Check medications 2x before entering patient’s room (1st when retrieving it and 2nd when
preparing it)
• Always implement the 6 rights of medication administration (right patient, medication, route,
dose, time, & documentation)
• Use hand hygiene upon entering patient’s room
• Introduce self and explain procedure to patient
• Verify patient with 2 identifiers
• Confirm allergies against patient records
• 3rd medication check in the patient’s room against the MAR before administration
• Scan barcode on medication
• Bring bed down to a comfortable working position
• Don clean gloves
• Clean patient’s eyes (inner to outer canthus)
• Have patient tilt head back (unless it’s contraindicated in their chart)
• Remove cap of eye drops & never touch the inside of the cap bc you can contaminate the entire
bottle
• Have patient look up at the ceiling
• Move lower eyelid down and place a drop into the lower conjunctival sac
• Make sure not to touch the cornea with the eye drops
• Also do not let the bottle touch the patient’s eyes, eyelids, or eyelashes
• Once designated amount of drops are instilled, close the eye & apply gentle pressure to the
lacrimal duct to prevent the medication from falling into the tear ducts (also minimizes any
systemic effects of the medication)
• Advise patient not to rub their eyes
• Document medication administration into MAR
• Use hand hygiene when leaving patient room
2. ***Pressure Ulcer - Assessment - pre-test item not graded***
4 stages:
• Stage 1 Pressure Injuries are localized areas of erythema that the skin remain intact.
• Stage 2 Pressure Injuries includes a partial-thickness loss of skin with exposed dermis. The
wound bed is viable, pink or red, moist, and may also present as an intact or ruptured serum-
filled blister. Adipose tissue is not visible and deeper tissues are not visible. Granulation tissue,
slough, and eschar are not present.
• Stage 3 Pressure Injuries have full-thickness loss of skin. In a stage 3 pressure injury, adipose
and granulation tissue are often visible.
• Stage 4 Pressure Injuries (unstageable) are also full thickness skin loss with exposed fascia,
muscle, tendon, ligament, or bone.
,3. ***Shearing Force - pre-test item not graded***
Shear - results when one layer of tissue slides over another layer. Shear separates the skin from
underlying tissues. The small blood vessels and capillaries in the area are stretched and possibly
tear, resulting in decreased circulation to the tissue cells under the skin. Patients who are pulled,
rather than lifted, when being moved up in bed or from bed to chair or stretcher are at risk for injury
from shearing forces. A patient who is partially sitting up in bed is susceptible to shearing force
when the skin sticks to the sheet and underlying tissues move downward with the body toward the
foot of the bed. This may also occur in a patient who sits in a chair but slides down.
4. Allergic Reaction - NSG124 - 01.02.04
Allergic Reaction - an immune response. For an allergic reaction to occur, there must be prior
sensitization of the immune system.
Once the immune system has been sensitized to a drug, re-exposure to that drug can trigger an
allergic response. The intensity of allergic reactions can range from mild itching to severe rash to
anaphylaxis. Anaphylaxis is a life-threatening response characterized by bronchospasm, laryngeal
edema, and a precipitous drop in blood pressure. Estimates suggest that less than 10% of ADRs are
of the allergic type.
The intensity of an allergic reaction is determined primarily by the degree of sensitization of the
immune system, not by drug dosage. Put another way, the intensity of allergic reactions is largely
independent of dosage. As a result, a dose that elicits a very strong reaction in one allergic patient
may elicit a very mild reaction in another. Furthermore, because a patient's sensitivity to a drug can
change over time, a dose that elicits a mild reaction early in treatment may produce an intense
reaction later on. Very few medications cause severe allergic reactions. In fact, most serious
reactions are caused by just one drug family—the penicillins. Other drugs noted for causing allergic
reactions include the nonsteroidal anti-inflammatory drugs (e.g., aspirin) and the sulfonamide group
of compounds, which includes certain diuretics, antibiotics, and oral hypoglycemic agents.
5. Tylenol (Acetaminophen) - Lab Check - NSG124 - 03.03.03
Mechanism of Action:
Differences between the effects of acetaminophen and aspirin are thought to result from selective
inhibition of cyclooxygenase, the enzyme needed to make prostaglandins and related compounds.
Whereas aspirin can inhibit cyclooxygenase in both the CNS and the periphery, inhibition by
acetaminophen is limited to the CNS; acetaminophen has only minimal effects on cyclooxygenase at
peripheral sites. By decreasing prostaglandin synthesis in the CNS, acetaminophen is able to reduce
fever and pain. The inability to inhibit prostaglandin synthesis outside the CNS may explain the
absence of anti-inflammatory effects, gastric ulceration, and adverse effects on the kidneys and
platelets.
Pharmacokinetics:
,Acetaminophen is readily absorbed following oral dosing and undergoes wide distribution. Most of
each dose is metabolized by the liver, and the metabolites are excreted in the urine. The plasma
half-life is approximately 2 hours.
Acetaminophen can be metabolized by two pathways: (major and minor)
Major Pathway - acetaminophen undergoes conjugation with glucuronic acid and other compounds
to form nontoxic metabolites.
Minor Pathway - acetaminophen is oxidized by a cytochrome P450–containing enzyme into a highly
reactive toxic metabolite: N-acetyl-p-benzoquinoneimine.
Adverse Effects:
Adverse effects are extremely rare at therapeutic doses. Acetaminophen does not cause gastric
ulceration or renal impairment and does not inhibit platelet aggregation. In addition, there is no
evidence linking acetaminophen with Reye's syndrome.
Acetaminophen use has also been associated with Stevens-Johnson syndrome (SJS), acute
generalized exanthematous pustulosis (AGEP), and toxic epidermal necrolysis (TEN). SJS and TEN
are characterized by painful rash, blistering of the skin and mucous membranes, and detachment of
the epidermis. These are considered medical emergencies, as they can result in death. Recovery
can take weeks to months. AGEP is characterized by pustular lesions that predominantly affect the
upper trunk and body folds. AGEP usually resolves within 2 weeks of onset. These reactions can
occur at any time, even if the patient has taken acetaminophen previously. If a rash appears while
taking acetaminophen, the drug should be stopped, and the patient should seek medical attention.
Alcohol:
Regular alcohol consumption increases the risk of liver injury from acetaminophen—but only if
acetaminophen dosage is excessive. Three mechanisms are involved. First, alcohol induces
synthesis of the P450-containing enzyme in the minor metabolic pathway, thereby increasing
production of acetaminophen's toxic metabolite. Second, stores of glutathione are depleted in
chronic alcoholics. As a result, the liver is unable to convert the toxic metabolite to a nontoxic form.
Third, chronic alcohol abusers often have pre-existing liver damage, which renders them less able to
tolerate injury from acetaminophen.
Some authorities recommend that if a person drinks alcohol on a regular basis, they should
consume no more than 2000 mg of acetaminophen a day (one-half the normal maximum).
Although therapeutic doses of acetaminophen may be safe for alcohol drinkers, high doses certainly
are not. Accordingly, to alert the public to the potential risk of combining alcohol with
acetaminophen, the FDA requires that acetaminophen labels bear the following statement: Alcohol
Warning: If one consumes three or more alcoholic drinks every day, ask a doctor whether
acetaminophen or other pain relievers/fever reducers should be taken.
Warfarin:
, There is evidence that acetaminophen may increase the risk of bleeding in patients taking warfarin
(an oral anticoagulant). The best guess is that acetaminophen may inhibit warfarin metabolism,
which would cause warfarin levels to rise. Although this interaction has not been proved, caution is
advised. Accordingly, for patients taking more than 1 gm of acetaminophen daily for several days,
responses to warfarin should be monitored closely. Occasional use of acetaminophen is not a
concern.
Vaccines:
Acetaminophen and other analgesic-antipyretics can blunt the immune response to childhood
vaccines. Accordingly, routine use of these drugs to prevent vaccination-associated pain and/or
fever should be discouraged.
Therapeutic Uses:
Acetaminophen is indicated for relief of pain and fever. Because acetaminophen is not associated
with Reye's syndrome, the drug is preferred to NSAIDs for use by children suspected of having
chickenpox or influenza. Because it does not cause GI injury, acetaminophen is preferred to NSAIDs
for patients with peptic ulcer disease. In addition, acetaminophen may be a safe alternative to aspirin
for patients who have experienced aspirin hypersensitivity reactions. Because of its weak anti-
inflammatory actions, acetaminophen is not useful for treating arthritis or rheumatic fever.
Acute Toxicity - Liver Damage:
Overdose with acetaminophen can cause severe liver injury and death. The cause is the
accumulation of the toxic metabolite (discussed earlier). In the United States, acetaminophen
overdose—intentional or unintentional—is the leading cause of acute liver failure, accounting for
about 50% of all cases. Risk of liver injury is increased by fasting, chronic alcohol use, and by taking
more than 4000 mg of acetaminophen a day.
Signs and Symptoms:
The principal feature of acetaminophen overdose is hepatic necrosis. Severe poisoning can
progress to hepatic failure, coma, and death. Early symptoms of poisoning (nausea, vomiting,
diarrhea, sweating, abdominal discomfort) belie the severity of intoxication. It is not until 48 to 72
hours after drug ingestion that overt indications of hepatic injury appear.
Treatment:
Liver damage can be minimized by giving acetylcysteine [Mucomyst , Acetadote], a specific
antidote to acetaminophen. Acetylcysteine reduces injury by substituting for depleted glutathione in
the reaction that converts the toxic metabolite of acetaminophen to its nontoxic form. When given
within 8 to 10 hours of acetaminophen overdose, acetylcysteine is 100% effective at preventing
severe liver injury. Even when administered as much as 24 hours after poisoning, it can still provide
significant protection. Acetylcysteine may be administered PO or IV.
