N271 Test 3

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Last updated 7:32 AM on 4/22/26
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140 Terms

1
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Practice Question: What should the nurse check before administering verapamil (a calcium channel blocker)?

Heart rate and blood pressure.

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Practice Question: What is the therapeutic effect of digoxin?

Digoxin increases cardiac contractility (positive inotropic effect).

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Practice Question: Which patient is the highest priority: a patient with unstable angina or a patient with a myocardial infarction who has a headache?

The patient with unstable angina is the highest priority.

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Practice Question: What is barrel chest?

Barrel chest is an increased anterior-posterior diameter of the chest caused by air trapping, commonly seen in COPD.

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Practice Question: What is the most accurate way to measure oxygenation status in patients with COPD?

Arterial blood gases (ABGs) are the most accurate measurement of oxygenation.

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Practice Question: What do these values indicate

pH 7.52, PaCO₂ 30 , PaO₂ 70 , HCO₃ 26 .

uncompensated respiratory alkalosis

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Practice Question: What type of medication is cromolyn sodium?

Cromolyn sodium is a mast cell stabilizer.

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Practice Question: What drug classes do the following medications belong to: albuterol, montelukast, and salmeterol?

Albuterol is a SABA,

montelukast is a leukotriene

salmeterol is a LABA.

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Practice Question: What is the first-line treatment for a patient with tachypnea and low SpO₂?

Albuterol nebulizer treatment.

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Practice Question: What is a common drug suffix for angiotensin II receptor blockers (ARBs)?

ARBs end in "-sartan".

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Practice Question: When should propranolol be held?

Propranolol should be held if the patient's heart rate is low (bradycardia).

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Practice Question: What is a common side effect of ACE inhibitors?

A persistent dry cough is a common side effect of ACE inhibitors (-pril).

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Practice Question: Which medication is a leukotriene receptor blocker?

Montelukast (Singulair) is a leukotriene receptor blocker.

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Practice Question: What is an important consideration when diabetic patients take beta blockers?

Beta blockers (-olol) can mask symptoms of hypoglycemia.

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Practice Question: Which beta blocker is commonly considered appropriate for a patient with diabetes?

Atenolol

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Practice Question: When does a patient require further teaching about blood pressure medications?

If the patient believes they can stop taking medication once their blood pressure becomes normal.

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Practice Question: What should the nurse do if a patient recovering from a myocardial infarction develops chest pain during ambulation?

Stop the ambulation to prevent further cardiac stress.

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Practice Question: Why should nonselective beta blockers be used cautiously in patients with respiratory conditions?

They can cause bronchoconstriction by blocking beta-2 receptors.

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Practice Question: What complication can occur if a patient does not rinse their mouth after using an inhaled corticosteroid?

White patches in the mouth (oral candidiasis or thrush).

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Practice Question: When should a patient take nitroglycerin?

Nitroglycerin should be taken at the onset of chest pain.

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Asthma Def

A chronic inflammatory airway disease with reversible bronchoconstriction.

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Asthma Clinical Manifestations

Wheezing

Chest tightness

Cough (often at night)

Dyspnea

Prolonged expiration

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Status asthmaticus indicates?

life-threatening emergency

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Asthma Diagnostics

Spirometry: ↓ FEV1 (improves with bronchodilator)

Peak flow monitoring

ABGs:

Early: respiratory alkalosis

Late: respiratory acidosis (bad sign)

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Asthma Medications

Rescue (Quick Relief)

Short-acting beta-2 agonists (SABA)

Albuterol

Control (Long-Term)

Inhaled corticosteroids (first-line)

LABAs (with steroids only)

Leukotriene modifiers (montelukast)

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Asthma Nursing Interventions

High Fowler's

Stay with patient during attack

Administer bronchodilator FIRST

Oxygen as needed

Monitor peak flow

Teach inhaler technique

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COPD (Chronic Obstructive Pulmonary Disease) def and 2 types

A progressive, irreversible lung disease causing airflow limitation.

Includes

Chronic bronchitis

Emphysema

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COPD Pathophysiology

Chronic inflammation

Increased mucus production

Loss of lung elasticity

Air trapping → hyperinflation

Destruction of alveoli (especially in emphysema)

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COPD Risk Factors

Smoking (most common)

Long-term pollutant exposure

Alpha-1 antitrypsin deficiency

Age > 40

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COPD S/S

Chronic cough

Thick sputum

Dyspnea on exertion → at rest

Barrel chest (From increased trapped air causing increased diameter of chest)

Prolonged expiration

Use of accessory muscles

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COPD Late Signs

Cyanosis

Clubbing

Polycythemia

Cor pulmonale (right-sided heart failure)

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COPD Diagnostics

Spirometry: ↓ FEV1/FVC ratio (<70%)

ABGs:

Early: respiratory alkalosis

Late: respiratory acidosis

Chest x-ray: hyperinflation, flattened diaphragm

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COPD Medications

Bronchodilators (albuterol, ipratropium)

Long-acting beta agonists (LABAs)

Inhaled corticosteroids

Systemic steroids for exacerbations

Oxygen therapy (LOW flow 1-2 L NC)

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COPD NI

COPD patients are often CO₂ retainers — avoid high oxygen flow rates.

High Fowler's position

Pursed-lip breathing

Tripod positioning

Encourage small frequent meals

Energy conservation

Smoking cessation education

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Quick-Relief (Rescue) Medication and Use for Respiratory

Short-Acting Beta₂ Agonists (SABA)

Albuterol (Proventil)

First-line for acute asthma attack

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Short-Acting Beta₂ Agonists (SABA) Mechanism

Stimulates beta₂ receptors → bronchodilation (relaxes airway muscles)

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Short-Acting Beta₂ Agonists (SABA) Side Effects

Tachycardia

Tremors

Nervousness

Palpitations

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Short-Acting Beta₂ Agonists (SABA) Important Considerations

Always carry rescue inhaler

Use before exercise for exercise-induced asthma

If using >2 days/week → asthma not controlled

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Long-Term Control (Maintenance) Medications for Respiratory

Used daily to prevent inflammation and attacks

Types

1. Inhaled Corticosteroids (ICS) - FIRST-LINE MAINTENANCE

2. Long-Acting Beta₂ Agonists (LABA)

3. Leukotriene Receptor Antagonists

4. Anticholinergics

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Inhaled Corticosteroids (ICS) Mechanism

↓ Airway inflammation

↓ Mucus production

↓ Airway hyperresponsiveness

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Inhaled Corticosteroids (ICS) Side Effects

Oral candidiasis (thrush)

Hoarseness

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Inhaled Corticosteroids (ICS) NI

Rinse mouth after use

Use spacer

Not for acute attacks

Most important drug class for long-term asthma control

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Long-Acting Beta₂ Agonists (LABA) Examples

Salmeterol

Formoterol

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Long-Acting Beta₂ Agonists (LABA) Important Considerations and Combination with other meds

IMPORTANT

Do not use alone in asthma

Must be combined with corticosteroid

Often combined as:

Advair

Symbicort

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Leukotriene Receptor Antagonists Example

Montelukast (Singulair)

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Leukotriene Receptor Antagonists Mechanism

Blocks leukotrienes → ↓ inflammation & bronchoconstriction

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Leukotriene Receptor Antagonists Uses

Mild persistent asthma

Exercise-induced asthma

Allergic rhinitis

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Leukotriene Receptor Antagonists Side Effects

Neuropsychiatric effects (black box warning)

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Anticholinergics Example and uses

Example: Ipratropium

Used more commonly in COPD, but may be added in acute asthma exacerbation.

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Mast Cell stabilizers Examples and Uses

Cromolyn/Intal/Nasalcrom

Inhaled anti-inflammatory used to prevent asthma symptoms and bronchospasm, not to treat asthma attacks.

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Pneumonia Patho

Bacteria (commonly Streptococcus pneumoniae) enter the lower airway, triggering an inflammatory response. This leads to alveolar edema and exudate formation, which impairs gas exchange.

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Pneumonia Risk Factors

Advanced age (>65) or very young (children/babies)

Immunocompromised status (HIV, Chemo)

Immobility (post-op, stroke)

Chronic diseases (COPD, Asthma, Heart Failure)

Aspiration risk (dysphagia, altered LOC)

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Pneumonia S/S

Productive Cough: Often "rust-colored" or purulent sputum

Fever & Chills: Usually high grade in bacterial cases

Pleuritic Chest Pain: Sharp pain on inspiration

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Pneumonia NI

Nursing care revolves around the "ABCs" and clearing that airway.

Acute Phase

Oxygen Administration: Maintain O2 > 92% (or per HCP orders).

Different oxygen delivery device depending on severity of hypoxia

Positioning: High-Fowler's (90 degrees) to maximize lung expansion.

Fluids: Increase intake to 2-3L/day to thin out thick secretions (unless contraindicated by HF).

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Pneumonia Tx

Antibiotics: Broad-spectrum first, then narrow-spectrum after culture results.

Antipyretics: Acetaminophen for fever/pain.

Bronchodilators: To open airways if wheezing is present.

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Pneumonia Patient Education

Finish the Course: Stress the importance of completing all antibiotics to prevent resistance.

Vaccination: Encourage the Pneumococcal vaccine and annual Flu shot.

Oral Care: Especially important for ventilated or immobile patients to prevent VAP (Ventilator-Associated Pneumonia).

Smoking Cessation: Vital for long-term lung health.

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Hypertension

Essential/primary vs secondary hypertension

Hypertensive crisis is BP over 180/120. Emergency, treat with anti-hypertensives

Causes of hypertension:

Adrenergic nervous system

Baroreceptors

RAAS

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Beta blockers end in? Examples

(-alol)

Non-selective: blocks beta 1&2 (propranolol, carvelilol, sotalol, labetolol)

Selective: blocks just beta 1 (atenolol, bisoprolol, metoprolol, esmolol)

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Beta blockers Mechanisms

Decrease HR and BP and myocardial oxygen demand

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Beta blockers Uses

HTN, MI, HF

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Beta blockers Important Considerations

Check HR and BP before giving. Hold for HR under 60 or SBP under 90-100mmHg

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Non-selective vs selective beta blockers contraindications

Avoid non-selective in COPD/emphysema/asthma as they can cause bronchoconstriction/bronchospasm

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Who should beta blockers not be given to and why?

Caution in diabetes as they can mask tachycardia which can be a symptom of hypoglycemia

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Beta Blocker Side Effects

bradycardia, hypotension, depression, erectile dysfunction, fatigue

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Calcium channel blockers end in? Examples

(-pines)

amlodipine, felodipine, nicardipine, nisoldipine

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Calcium channel blockers Mechanism

Decrease HR, contractility, vasodilators

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Calcium channel blockers Uses

Used in HTN, angina, dysrhythmias

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Calcium channel blockers Side Effects

bradycardia, hypotension, constipation

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Calcium channel blockers What to monitor for?

(BP, HR), LFTs (Liver Function), ECG

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ACE inhibitors end in? Examples

(-prils)

Ex Captopril, Benazepril, lisinopril, enalapril

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ACE inhibitors Side effects

dry cough, hyperkalemia, angioedema (life threatening)

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Anti-hypertensives: Angiotensin II Receptor Blockers (ARB) end in?

(-sartans)

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What are ARB's similar to and extra uses?

Similar to ACE inhibitors but can be used if they cause cough or angioedema

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Chest pain Types

Stable- chest pain with activity that stops with rest

Unstable- chest pain at rest or chest pain not relieved by rest. No troponin elevation. Treatment similar to MI.

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Nitroglycerin Mechanism

Vasodilator- decreases preload, decreased myocardial oxygen demand

Improves blood flow to the heart and relieves angina

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Nitroglycerin Use

angina

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Nitroglycerin Contradindications

Check BP before giving, hold if SBP under 90-100 mmHg

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Nitroglycerin Side Effects

headache, hypotension, dizziness, flushing

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Nitroglycerin Routes and Indications

SL (acute chest pain),

Transdermal patch (prevention),

IV (emergency).

Not swallowed

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Nitroglycerin Patient Education

Sit before taking in case of dizziness due to drop in BP

If prescribed for angina, take three doses, 5 min apart, if no relief, call emergency services (ie 911). Persistent pain can indicate MI.

Headache is expected side effect

Do not take with erectile dysfunction medication as the combination can cause a dangerous drop in BP.

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Myocardial infarction

Complete blockage of coronary artery leading to lack of oxygen to heart muscle and cell death

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Myocardial infarction Lab Indications

Elevated troponin can indicate damage to myocardium.

Checked at baseline and every few hours to see if it rises or falls.

If it rises and stays high, evidence of MI

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MONA Acronym use

emergency treatment for chest pain

Morphine- pain relief

Oxygen for O2 under 90%

Nitroglycerin- vasodilator

Aspirin- antiplatelet to decrease further clotting at site of vessel blockage

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Heart failure

inability of heart to pump effectively to oxygenate body

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Digoxin Mechanism

Increases contractility of heart muscle (positive inotrope)

Decreases heart rate

Improves cardiac output in heart failure and controls rate in A fib

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Before giving digoxin what should be noted

Check apical pulse for one minutes (Hold if under 60 BPM)

Monitor potassium- if low, greater chance of digoxin toxicity (dig competes with K at the cellular level)

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Digoxin toxicity symptoms

N/V

Decreased appetite

Fatigue

Bradycardia

Vision changes (yellow/green halos)

Dysrhythmias- can be fatal

Loop diuretics like Lasix can increase risk of toxicity

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Digoxin Antidote

digoxin immune Fab (Digibind)

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Digoxin Patient Education

take pulse before taking dig, do not double dose, report N/V or vision changes, irregular pulse. Maintain consistent potassium intake.

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Pain Pathway

Transduction

Nociceptors (nerve endings found in skin, muscle, connective tissue, circulatory system, abdominal/pelvic/thoracic viscera) are stimulated

Nerve action potentials progress through spinal cord and then to brain

Trasnmission

Specialized sensory fibers transmit impulses to CNS from nociceptors

Large mylenated fibers (A-delta) transmit impulses quickly (sharp, stinging, localized pain)

Unmylenated fibers (C fibers) transmit impulses that are poorly localized and evoke emotional responses like displeasure and anxiety. Excessive stimulation of C fibers can result in chronic pain conditions.

Perception

Perception is the result of neural processing of pain sensation in the brain

Includes awareness and interpretation of meaning of sensation

Perception influenced by attention, distraction, anxiety, fear, fatigue, previous experience

Modulation

Neurons from nociceptors, somatosensory receptors and descending neurons meet at spinal cord and interact

Person experiencing pain may shake or press painful area spontaneously to reduce pain

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Acute pain

Acute pain results from tissue injury and resolves when the injury heals, usually in less than 3 months

Can be accompanied by signs/symptoms of pain from stimulation of sympathetic nervous system

Symptoms: elevated HR, RR, BP

Adequate management of pain during acute phase (with opioid or non-opioid medications) may prevent future chronic pain

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Chronic pain

Pain is considered chronic when it lasts more than several months beyond the expected healing time (usually more than 6 months)

Cause can be difficult to ascertain

Peripheral sensitization- reduction in threshold and increase in responsiveness of nociceptors.  Occurs when the peripheral terminals of the primary sensory neurons are exposed to inflammatory mediators and damaged tissue

Central sensitization- changes in the properties of neurons in the CNS.  Abnormal state of responsiveness or increased gain of the nociceptive inputs.  Reduced threshold for activation by peripheral stimuli

Pain can be present with no change in vital signs

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Somatic Pain

Superficial (skin, mucus membranes) and Deep (muscles, bones, joints, tendons).

Common Causes: Lacerations, burns, fractures, sprains, arthritis, muscle cramps, and tumor-related tissue damage

Symptoms: Specific, localized pain that is sharp (superficial) or dull/aching (deep), tender to touch, and may limit movement.

Treatment Options: Common treatments include OTC medications (NSAIDs, acetaminophen), muscle relaxants, physical therapy, heat/cold packs, and in some cases, opioids. 

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Visceral Pain

Felt in internal organs such as the heart, lungs, gastrointestinal tract, or pelvic organs (uterus, bladder).

Causes: Common causes include chronic inflammation (e.g., irritable bowel syndrome), obstruction (e.g., kidney stones), infection, reduced blood flow (ischemia), and tumor growth.

Symptoms: Often described as a deep, aching, dull, or colicky pain, accompanied by autonomic reflexes like nausea, vomiting, sweating, and feelings of intense anxiety.

Referred Pain: Visceral pain can be "referred" to different locations on the skin, such as cardiac pain felt in the arm or jaw, or gallstone pain felt in the back, or pelvic pain felt in the shoulder.

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Neuropathic Pain

Complex and sometimes disabling chronic pain caused by lesions or disease of the somatosensory nervous system.

Results from actual damage to the nerves as opposed to pain signals being sent through nerves

Damage can be caused from surgery, tumor growth, viral infection, trauma, etc

Can be constant ache with intermittent bursts of pain

Can happen long after an injury

Ex postherpetic neuralgia, diabetic neuropathy, trigeminal neuralgia, spinal cord compression

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Localized pain

Pain at a specific site of injury (ex cut to hand)

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Radiating pain

Pain that is perceived to extend or spread out from one area of the body to another.

Ex Burners and stingers are injuries that occur when nerves in the neck and shoulder are stretched or compressed (squeezed together) after an impact.

Common in contact or collision sports

Injuries are named for the stinging or burning pain that spreads from the shoulder to the hand.

A burner or stinger can feel like an electric shock or lightning bolt down the arm.

In most cases, burners and stingers are temporary, and symptoms quickly go away

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Referred pain

When there is pain perception at a location other than the site of the painful stimulus, it is known as referred pain (ex. pain brought down the neck, shoulders, and back following a myocardial infarction or shoulder pain after a pelvic procedure)

Referred pain may be visceral (pain from an organ) or somatic (pain from deep tissues such as muscles or joints)

Can be felt some distance from site of injury

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Pain: Aspirin

Anti-inflammatory agents - antipyretic and analgesic

Blocks prostaglandins

Used to prevent clotting in suspected MI

Risks of GI upset, bleeding

Signs of toxicity: tinnitus, dizziness, headache, hyperventilation

Risk of Reye syndrome in young people with viral illness

Typically presents in children as vomiting and confusion with rapid progression to coma and death. Begins in the days following recovery from a viral illness during which aspirin was administered.

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Pain: Tylenol

Antipyretic (Acts directly on the thermoregularoty cells in the hypothalamus to cause sweating and vasodilation, causing release of heat and lowering of fever.)

Analgesic (mechanism not known)

DO NOT EXCEED 1 GM/6 HRS DUE TO RISK OF LIVER TOXICITY

Adverse effects: rash, chest pain, liver toxicity