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Np4-Tos 250930 012320

The document is a comprehensive reviewer for the Philippine Nurses Licensure Examination, focusing on Nursing Practice 4 topics such as Nutrition, Gastrointestinal Disturbances, Metabolism, Endocrine, and various disorders affecting perception and coordination. It includes detailed sections on malnutrition, oral and esophageal disorders, and their nursing interventions, emphasizing assessment, management, and prevention strategies. Key clinical manifestations, risk factors, and nursing diagnoses are also outlined to aid in exam preparation.

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Donna Mabalot
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0% found this document useful (0 votes)
1K views28 pages

Np4-Tos 250930 012320

The document is a comprehensive reviewer for the Philippine Nurses Licensure Examination, focusing on Nursing Practice 4 topics such as Nutrition, Gastrointestinal Disturbances, Metabolism, Endocrine, and various disorders affecting perception and coordination. It includes detailed sections on malnutrition, oral and esophageal disorders, and their nursing interventions, emphasizing assessment, management, and prevention strategies. Key clinical manifestations, risk factors, and nursing diagnoses are also outlined to aid in exam preparation.

Uploaded by

Donna Mabalot
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd

PHILIPPINE NURSES LICENSURE EXAMINATION

Nursing Practice 4 Reviewer


According to the Newly TOS
MHEL, RN’25, MD’31

Topic Outline:

A. Nutrition and Gastrointestinal Disturbances


1.​ Malnutrition
2.​ Oral and Esophageal Disorder
3.​ Absorption and Elimination
3.1. Intestinal Mobility
3.2. Malabsorption Syndrome
3.3. Structural and Obstructive Bowel Disorders

B. Metabolism and Endocrine


1.​ Metabolic Disorders affecting the:
1.1. Liver
1.2. Biliary Tract
1.3. Pancreas (DM)
2.​ Endocrine Disorders
2.1. Hypofunction (thyroid gland, parathyroid,
adrenal glands, pituitary glands)
2.2. Hyperfunction (thyroid glands, parathyroids,
adrenal glands, pituitary glands)

C. Perception and Coordination Disturbances


1.​ Neurologic
1.1. Degenerative
a.​ Multiple Sclerosis
b.​ Parkinson’s Disease
c.​ Myasthenia Gravis
1.2. Cerebrovascular Accidents
1.3. Alzheimer disease and Dementia
1.4. Traumatic Lesions
1.5. Neuropathies
1.6. Peripheral Nerve and Spinal Cord Diseases

2.​ Musculoskeletal Dysfunction


2.1. Musculoskeletal Trauma
2.2. Metabolic Bone Disorders
2.3. Musculoskeletal Infections
2.4. Occupation-Related Muscular Disorders
2.5. Musculoskeletal Modalities
a.​ Cast
b.​ Splints
c.​ Braces

3.​ Vision Disorders


3.1. Impaired Vision
a.​ Cataract
b.​ Glaucoma
c.​ Retinal Detachment
3.2. Ocular and Orbital Trauma
3.3. Infections and Inflammatory Conditions
3.4. Consequences of Systemic Diseases

4.​ Hearing and Balance Disorders


4.1. Conditions of External Ear, Middle Ear, and
Inner Ear

1
PHILIPPINE NURSES LICENSURE EXAMINATION
Nursing Practice 4 Reviewer
According to the Newly TOS
MHEL, RN’25, MD’31

A. Nutrition and Gastrointestinal Disturbances Nursing Interventions


1. General goals
a.​ Prevent complications (infection, refeeding
Malnutrition
syndrome).
b.​ Restore nutritional status safely.
It is an imbalance between nutrient/energy intake and the c.​ Promote growth/weight gain and functional recovery.
body’s needs. It includes undernutrition (wasting, stunting, d.​ Educate family on feeding and follow-up.
underweight, micronutrient deficiencies) and overnutrition
(overweight/obesity). 2. Priorities & safety
a.​ Stabilize life-threatening problems (shock, severe
dehydration, hypoglycemia, hypothermia).
Classification of Malnutrition b.​ Treat infections.
c.​ Start therapeutic feeding per severity
Undernutrition
3. Management of Severe Acute Malnutrition (SAM) for
1. Acute Recent; low weight for height; severe children (WHO steps)
Malnutrition or acute malnutrition (SAM) is a.​ Emergency treatment: Treat hypoglycemia,
Wasting life-threatening. hypothermia, dehydration, electrolyte imbalance, and
infection. (Use special low-sodium ReSoMal for
2. Chronic low height-for-age, long-term deprivation rehydration in malnourished children; avoid rapid IV
Malnutrition or (mostly in children). rehydration except in shock).
Stunting b.​ Nutritional rehabilitation:
-​ Stabilization phase: F-75 therapeutic milk
3. Underweight low weight-for-age (combination of acute (low-protein, low-energy formula) to stabilize
+ chronic). metabolic status (WHO protocol).
-​ Rehabilitation phase: F-100 or
4. Protein 3 Types: ready-to-use therapeutic foods (RUTF) for
Energy 1. Marasmus - severe energy deficiency, catch-up growth.
Malnutrition muscle wasting, minimal edema. c.​ Micronutrient supplementation (vitamin A, zinc in
(PEM) 2. Kwashiorkor - protein deficiency with diarrhea, folic acid/iron when no infection risk per
edema, fatty liver, hypoalbuminemia. local protocol).
3. Marasmic-kwashiorkor - mix, very d.​ Follow-up & community care.
poor prognosis.
4. Route of feeding
5. 1. Vitamin A - can cause vision a.​ Oral: preferred if safe. Fortify diet (energy-dense
Micronutrient problems foods), oral nutritional supplements.
deficiencies 2. Iron - can lead to anemia, fatigue, and b.​ Enteral feeding (tube): when oral intake is insufficient
impaired brain function but GI tract functional (start early within 24–48 hrs if
3. Iodine - can cause goiters and critically ill if indicated).
intellectual disabilities c.​ Total Parenteral nutrition (TPN): when GI tract not
usable or insufficient enteral route; strict aseptic
Overnutrition technique; monitor for line infections, hyperglycemia,
(Excessive consumption of calories and unhealthy diet. This liver dysfunction.
can lead to diseases such as diabetes, heart disease and
some cancers) 5. Monitor for refeeding syndrome
a.​ Check/replace phosphate, K, Mg before and during
Overweight BMI is 25 to 29.9 feeding for high-risk patients; start low-calorie feeding
and progress slowly; monitor vital signs, fluid balance,
Overweight Class 1 - BMI of 30 - 34.9 daily weights, electrolytes.
Class 2 - 35 - 39.9
Class 3 - BMI of 40 or greater 6. Wound care & infection control:
a.​ Optimize protein intake for wound healing; treat
infections aggressively.
Etiology and Risk Factors:
1. Inadequate dietary intake (quantity/quality), disease/infection Nursing diagnosis:
(diarrhea, HIV/TB), malabsorption. 1. Imbalanced nutrition: less than body requirements related to
2. Food insecurity, poverty, poor feeding practices, maternal inadequate intake and malabsorption as evidenced by weight
malnutrition, inadequate healthcare, poor sanitation. loss, BMI <18.5, muscle wasting, low serum albumin.
3. Political or economic systems, inadequate a.​ Goals: Gain weight, improved muscle mass, normal
education/household resources. lab trends.
4. Infants <2 years, children under 5, pregnant/lactating b.​ Interventions: Dietitian referral, high-calorie
women, the elderly, chronically ill (cancer, HIV), post-op high-protein meals, oral supplements, monitor
patients. intake/output and weights, teaching. Evaluate weight
changes.
Assessment
1. History 2. Risk for infection related to impaired immune function from
a.​ Diet history (24-hr recall, food frequency), weight loss malnutrition.
timeline, GI symptoms (diarrhea, vomiting), appetite a.​ Interventions: Strict infection control, monitor temps,
changes, chronic illness, social history (food access, early antibiotics for suspected infection, nutritional
caregiver skills). support to improve immunity.

2. Physical exam 3. Risk for electrolyte imbalance related to refeeding.


a.​ General: cachexia (biglaang pagpayat), muscle a.​ Interventions: Baseline and daily electrolyte
wasting, low subcutaneous fat, edema (pitting in monitoring, slow feeding, prophylactic thiamine,
kwashiorkor), altered mental status, hypotension, electrolyte replacement.
brady/tachy, hypothermia.
b.​ Skin/hair: thin, brittle hair; hyperpigmentation Complications to remember (exam favorites)
/dermatosis (kwashiorkor). a.​ Infection, hypothermia, hypoglycemia, dehydration,
c.​ Oral cavity: glossitis, cheilosis (vitamin deficiencies). electrolyte disturbances, refeeding syndrome,
d.​ Abdomen: hepatomegaly (fatty liver in kwashiorkor). cardiac/respiratory failure, poor wound healing,
e.​ Growth charts for children: BMI and MUAC cognitive and developmental delays in children.
(mid-upper arm circumference).
2
PHILIPPINE NURSES LICENSURE EXAMINATION
Nursing Practice 4 Reviewer
According to the Newly TOS
MHEL, RN’25, MD’31

Oral and Esophageal Disorder Candidiasis (Oral Thrush)

Anatomy and Physiology Pathophysiology:


1. Mouth (oral or buccal cavity) Opportunistic fungal infection caused by Candida albicans;
a.​ Digestion starts from the mouth Normally present in the oral cavity, overgrows when host
b.​ Mechanical digestion occurs through mastication immunity is decreased or normal flora is disrupted.
(chewing)
c.​ Chemical digestion occurs through the mechanism of Common in infants, immunocompromised (HIV, cancer, TB),
salivary amylase (enzyme na nasa laway), we also diabetics, and those on prolonged antibiotics or corticosteroids.
call it ptyalin which breaks down starches to maltose.
d.​ Deglutition (swallowing) occurs once the food is Clinical Manifestations
broken down into small pieces and well mixed with Earliest or Pathognomonic sign: milky white or white, curd-like
saliva (food bolus) plaques on tongue, buccal mucosa, palate, or oropharynx.

2. Esophagus Easily scraped off, leaving a red/bleeding base; Burning


a.​ Serve as a passage for food bolus from mouth to sensation, sore throat, dysphagia; Angular cheilitis (cracks at
stomach by peristalsis. mouth corners).
b.​ The distal end of the esophagus is guarded by lower
esophageal sphincter (LES). It is also known as Infants: feeding difficulty, irritability.
cardiac sphincter wherein it prevents gastric reflux.
Prevention
1. Practice good oral hygiene.
Oral Cancer
2. Rinse mouth after inhaled corticosteroids.
3. Avoid unnecessary/prolonged antibiotics.
Pathophysiology: 4. Control blood sugar (diabetics).
Malignant tumor in the oral cavity (lips, tongue, floor of mouth, 5. Sterilize feeding bottles, pacifiers.
buccal mucosa, pharynx). 6. For HIV/AIDS: regular antifungal prophylaxis if recurrent.

Most common type: Squamous Cell Carcinoma (SCC) (arises Nursing Interventions
from epithelial lining). 1. Maintain oral hygiene:
2. Use soft toothbrush or gauze.
Major risk factors: 3. Avoid alcohol-based mouthwashes.
1. Tobacco (cigarette, cigar, chewing) – #1 4. Diet: Encourage soft, bland, non-irritating foods.
2. Alcohol (synergistic with smoking) 5. For infants: Sterilize nipples/pacifiers; apply antifungal
3. HPV infection (especially oropharyngeal cancers) suspension with cotton swab.
4. Chronic irritation (ill-fitting dentures, poor oral hygiene) 6. Pain relief: Topical anesthetic rinses (if ordered).
5. Prolonged sun exposure (lip cancer). 7. Finish antifungal treatment even if lesions resolve.

Clinical Manifestations Medical Management


Earliest sign (PNLE favorite!): Painless, non-healing ulcer or 1. First-line (topical):
lesion. a.​ Nystatin oral suspension – swish and swallow.
Other findings: Lump, thickening, or white/red patches b.​ Clotrimazole troches (lozenges).
(leukoplakia or erythroplakia), Soreness, difficulty 2. Systemic (for severe/recurrent cases):
chewing/swallowing, Voice changes, foul breath, ear pain, a.​ Fluconazole (Diflucan) oral/IV.
Dysphagia, bleeding, weight loss, loose teeth, palpable b.​ Ketoconazole, itraconazole alternatives.
cervical nodes. 3. Infants: Nystatin suspension applied with dropper/cotton
applicator.
Prevention
1. Stop smoking and alcohol (most effective).
Stomatitis
2. Regular oral examination (for high-risk clients).
3. Good oral hygiene; treat dental problems early.
4. Use lip sunscreen for chronic sun exposure. Pathophysiology:
5. HPV vaccination (for oropharyngeal protection). Inflammation of the oral mucosa; it can affect lips, cheeks,
gums, tongue, palate and throat.
Nursing Interventions
1. Airway first! Monitor for obstruction (tongue/floor of mouth Risk factors (HSV or Candida infection, chemotherapy,
tumors). mechanical irritation, nutritional deficiency, and systemic illness
2. Nutritional support: like immunosuppression) > mucosal cell injury (hindi na
a.​ High-protein, high-calorie diet (wound healing) maayos na nagreregenerate ang cell) > inflammatory response
b.​ Soft or liquid diet pre-op/post-op. (redness, pain, or swelling) > epithelial breakdown (ulcer or
c.​ Tube feeding if severe dysphagia. sore formation) > secondary infection > systemic impact.
3. Maintain airway patency (priority!).
4. Assess for bleeding and edema.
5. Support communication (pen, whiteboard). Types of Stomatitis
6. Encourage expression of feelings (body image).
7. Pain management (analgesics, oral rinses). Primary It’s an independent condition
8. Mouth care: non-irritating rinses, avoid alcohol-based
mouthwash. 3 Types:
1. Aphthous (canker sores) - benign, small,
Medical Management shallow with erythematous halo; often stress
1. First-line / Definitive treatment: related.
a.​ Surgery = gold standard wide excision, glossectomy, 2. Herpetic sores - caused by HSV; may recur
mandibulectomy). (cold sores or fever blisters)
2. Radiation therapy – for small tumors or adjunct. 3. Traumatic or Denture - mechanical,
3. Chemotherapy – for advanced/metastatic cases, combined chemical or thermal irritation; poorly fitting
with radiation. dentures
4. Reconstructive surgery – restores function/appearance
post-resection. Secondar Occurs as symptoms or complications of
y another condition; can be due to infection,
chemotherapy, radiation or systemic diseases.

3
PHILIPPINE NURSES LICENSURE EXAMINATION
Nursing Practice 4 Reviewer
According to the Newly TOS
MHEL, RN’25, MD’31

d.​ Post procedure (WOF bleeding and perforation)


Clinical Manifestations 2. Barium Swallow (Using a barium sulfate and then xray)
Earliest sign: Painful, erythematous oral mucosa. a.​ Evaluates anatomical abnormalities
b.​ Preprocedure: assess for allergies and kidney
Other: Small, round or oval ulcers with red halo (aphthous); function (BUN and creatinine; NPO dapat
Burning sensation, difficulty eating/swallowing; Swelling, c.​ Post procedure: Increase the oral fluid intake
bleeding, halitosis. (2000-3000 ml)
d.​ Normal/Expected: white stool (24-72 hrs after
Severe cases: multiple ulcers, risk of secondary infection, procedure); white substance is the barium sulfate
nutritional compromise.
3. Esophageal pH monitoring
Prevention a.​ Measure amount and frequency of acid reflux probe in
1. Maintain good oral hygiene. esophagus
2. Avoid irritants (spicy foods, tobacco, alcohol). b.​ Normal ph in this area is more than 4 which is slightly
3. Use well-fitted dentures. acidic
4. Adequate nutrition (vitamins, minerals).
5. Rinse mouth after corticosteroid inhalers or chemotherapy. Nursing Interventions: (Food should go down)
1. Diet
Nursing Interventions a.​ Fluids in between meals (decreases abdominal
1. Oral care: Soft-bristled brush or sponge swabs. distention)
2. Avoid alcohol-based mouthwashes. b.​ Fiber should be high (delays gastric emptying >
3. Encourage bland, soft, non-irritating diet. increases satiety > prevents overeating)
4. Pain relief: topical anesthetic gels/rinses (lidocaine). c.​ SFF (6-10 meals a day)
5. Monitor hydration and nutrition (offer high-calorie, 2. Position
high-protein shakes). a.​ HOB 30-45 degrees or side lying position (left) as
6. Educate about avoiding triggers (citrus, spicy, salty foods). alternative
3. Medications
Medical Management a.​ Antacids - neutralizes the pH; “carbonates or
1. Topical treatments: hydroxide” (Ex. Aluminum Hydroxide)
a.​ Benzocaine, lidocaine rinses for pain. b.​ Histamine 2 Receptor Blockers - decreases HCL
b.​ Antifungals (nystatin suspension) if Candida. production; ends with “tidine” (Ex. Ranitidine)
c.​ Antivirals (acyclovir) if herpetic stomatitis. c.​ Proton Pump Inhibitors - decreases HCL
2. Systemic therapy: production; ends with “prazole” (Ex. Omeprazole)
a.​ Analgesics for severe pain. d.​ Prokinetics - increases motility (Ex. Metoclopramide)
b.​ Multivitamins/iron supplements if deficient. 4. AVOID 5CsAFPS
3. Chemotherapy or radiation-induced stomatitis: Magic a.​ Coffee, Citrus Fruits, Cigarette (Nicotine increases
mouthwash (mixture of lidocaine, diphenhydramine, antacids). HCL; therefore decreasing saliva production),
Carbonated Drinks (can cause abdominal distention),
and Chocolates.
Gastroesophageal Reflux Disease
b.​ Alcohol
c.​ Fatty Foods (slowest food to digest that leads to
Backflow of HCL and gastric contents from stomach to abdominal distention)
esophagus. d.​ Peppermint (muscle relaxant)
e.​ Spicy Foods (worsens the sign and symptoms of
Causes GERD)
1. Weak LES (Low Esophageal Sphincter) or Cardia (should be 5. AVOID
close after eating to prevent backflow). a.​ Increases intraabdominal pressure such as straining,
2. Slow motility (Mabagal ang paggalaw ng pagkain sa heavy lifting, tight clothes and bending below the
stomach, hindi makababa sa small intestine that will result to waist.
abdominal distention > Increased Intraabdominal Pressure > 6. AVOID drugs that increases HCL and decreases motility
will open the LES (ANAC)
3. Pyloric Stenosis (narrowed, hindi na makababa ang food) a.​ Aspirin - increases HCL production
b.​ NSAIDs - inhibits prostaglandin synthesis
Normally, this should be the action of these 2 sphincter c.​ Anticholinergics or antispasmodics
d.​ Calcium Channel Blocker - smooth muscle relaxant
Lower Esophageal Pyloric Sphincter
Sphincter
Hiatal Hernia
Relaxes (open) during food Relaxes (open) during
intake gastric emptying (2-5 hours We also called it diaphragmatic hernia; abnormal protrusion of
after meal) the stomach to the hiatus (opening of diaphragm).
Contracts (closes) during
gastric emptying (2-5 hours Contracts (closes) upon food Factors
after meal) intake 1. Increase intraabdominal pressure
a.​ Pregnancy
Clinical Manifestations: b.​ Ascites
1. Indigestion burns your throat, larynx, and esophagus. c.​ Tumor
2. Dyspepsia d.​ Obesity
3. Heartburn or pyrosis (most common reported complaint after
meals or at the evening) Confirmatory - EGD
4. Globus (feeling of fullness) Two Types of Hernia
5. Laryngitis (Hoarseness of voice) or dry cough
6. Odynophagia (Painful swallowing) Sliding Hernia Paraesophageal or Rolling
7. Dysphagia (Dumudulas pataas ang (Ang gastroesophageal
tiyan at opening ng junction ay nanatili sa
Diagnostic Tests esophagus) normal na pwesto pero may
1. Endoscopy part ng tiyan na gumugulong
a.​ Visualize the esophageal lining pataas sa tabi ng
b.​ Can also take biopsies (WOF most fatal esophagus)
complications: Barret’s esophagus, has risk for
esophageal cancer)
c.​ Pre-procedure is NPO
4
PHILIPPINE NURSES LICENSURE EXAMINATION
Nursing Practice 4 Reviewer
According to the Newly TOS
MHEL, RN’25, MD’31

b.​ Often combined with fundoplication to prevent GERD.


Most common; Rare; asymptomatic; GERD
asymptomatic; GERD like like negative symptoms;
symptoms. Feeling of fullness
Complications: Strangulation > Decrease BP > Necrosis Esophageal Varices
Surgery (for GERD and Hiatal Hernia)
1. Fundoplication - reinforces LES (strengthen and tighten) Dilated, tortuous veins in the lower esophagus; Caused by
portal hypertension (most often from liver cirrhosis).
3 Types Increase Portal venous pressure > blood diverted to fragile
collateral veins in the esophagus > risk of rupture and massive
Nissen Wrap fully around esophagus (360 degrees); upper GI bleeding (life-threatening).
strong reinforcement; best control of reflux
Clinical Manifestations
Risk: may cause dysphagia and gas bloat 1. Often asymptomatic until rupture.
syndrome 2. Earliest sign of rupture: Hematemesis (vomiting blood).
3. Other bleeding signs:
Toupet Wrap around back (posterior) side of esophagus a.​ Melena (black tarry stool)
(270 degrees); control reflux and less dysphagia b.​ Hematochezia (rare, if massive)
risk than Nissen. c.​ Hypovolemic shock: tachycardia, hypotension, cold
clammy skin
Dor Fundus is wrapped in front of the esophagus; 4. Signs of portal hypertension: ascites, splenomegaly, caput
often used when doing procedures for achalasia medusae
or when myotomy is performed 5. Signs of cirrhosis: jaundice, palmar erythema, spider
angiomas

Achalasia Prevention
1. Prevent rupture:
a.​ Avoid straining, heavy lifting, coughing, vomiting
Failure to relax; Rare esophageal motility disorder due to loss (increases intra-abdominal pressure).
of ganglion cells in the myenteric plexus that results to 2. Avoid alcohol (common precipitant in cirrhosis).
impaired peristalsis + failure of the Lower Esophageal 3. Adhere to beta-blocker therapy (propranolol, nadolol) to
Sphincter (LES) to relax. lower portal pressure.
4. Regular endoscopy for high-risk patients.
Results in:
1. Food stuck in esophagus Nursing Interventions
2. Esophageal dilation (proximal to LES) 1. Priority: Airway, breathing, circulation (ABC).
3. Functional obstruction at gastroesophageal junction 2. During active bleeding:
a.​ Maintain airway (risk of aspiration from massive
Clinical Manifestations hematemesis).
1. Earliest sign: Progressive dysphagia (initially solids, then b.​ Establish large-bore IV access for fluids & blood
liquids). transfusion.
2. Pathognomonic sign: Bird’s beak appearance on barium c.​ Monitor VS, CVP, urine output, detect shock early.
swallow (narrowed LES with dilated esophagus). d.​ Prepare for endoscopic intervention (band
3. Other symptoms: ligation/sclerotherapy).
a.​ Regurgitation of undigested food (at night, it increases 3. If balloon tamponade (Sengstaken-Blakemore tube):
aspiration risk) a.​ Monitor airway (risk of aspiration, tube displacement).
b.​ Substernal chest pain or pressure after eating b.​ Keep scissors at bedside (in case tube slips and
c.​ Weight loss and nutritional deficiencies obstructs airway).
d.​ Heartburn-like sensation (but due to stasis, not acid) 4. Long-term:
a.​ Teach patients to avoid alcohol, irritants.
Prevention b.​ Stress low-salt diet if ascites present.
(Since cause is idiopathic/degenerative, prevention is focused
on complications) Medical Management
1. Eat slowly, chew food thoroughly 1. Emergency (acute bleed):
2. Drink water with meals a.​ Endoscopic variceal ligation (banding) = first line
3. Avoid eating before bedtime to reduce regurgitation risk b.​ Endoscopic sclerotherapy (alternative if ligation
4. Elevate head of bed to prevent nocturnal aspiration unavailable).
2. Vasoactive drugs:
Nursing Interventions a.​ Octreotide (first choice, less side effects)
1. Monitor for aspiration (priority: airway). b.​ Vasopressin (potent but increases cardiac risk, often
2. Encourage small, frequent meals with fluids. combined with nitroglycerin).
3. Position: High-Fowler’s during meals, semi-Fowler’s after c.​ Balloon tamponade (Sengstaken-Blakemore tube) for
meals. temporary measure only
4. Provide soft or liquid diet to reduce dysphagia risk. 3. Definitive management (portal decompression):
5. Educate on meal timing: avoid lying down immediately after a.​ TIPS (Transjugular Intrahepatic Portosystemic Shunt)
eating. = gold standard for refractory bleeding.
6. Pre-op & post-op care if surgical (Heller myotomy or
pneumatic dilation).
7. Monitor for nutritional status and weight loss. Absorption and Elimination
Stomach
Medical Management It is located at LUQ of the abdomen. It has an approximate
1. First-line (non-surgical): capacity of 1,500 mls.
a.​ Pneumatic balloon dilation (endoscopic), it stretches
LES. Functions of Stomach:
2. Pharmacologic (less effective): 1. Storage, mixing, and liquefaction of bolus of food into a
a.​ Calcium channel blockers (nifedipine) semisolid mixture called chyme.
b.​ Nitrates (isosorbide dinitrate), relax LES. 2. 1,500 - 3,000 ml of gastric juice is secreted by the glands in
3. Definitive treatment / Gold standard: the gastric mucosa. The gastric juice is composed of mucus,
a.​ Heller Myotomy (surgical division of LES muscle HCl, pepsinogen, and water. Gastrin (a hormone) is secreted
fibers). directly into the bloodstream.
5
PHILIPPINE NURSES LICENSURE EXAMINATION
Nursing Practice 4 Reviewer
According to the Newly TOS
MHEL, RN’25, MD’31

3. Digestion of protein starts in the stomach through the action 6. If prolonged, can lead to dehydration & electrolyte imbalance
of pepsin, which converts protein into polypeptides.
a.​ Pepsinogen (inactivated enzyme) is converted into Prevention
pepsin (activated form) in the presence of HCl. 1. Early ambulation post-surgery
b.​ Digestion of emulsified fats also starts in the stomach 2. Chewing gum post-op (stimulates bowel motility)
due to the presence of small amounts of gastric 3. Use non-opioid pain control when possible.
lipase. 4. Correct electrolyte imbalances promptly (especially
4. The acid in the stomach is also responsible for the reduced potassium)
activity of harmful bacteria that may have been taken in with
food. It also provides a favorable medium for the absorption of Nursing Intervention
calcium and other minerals. 1. Priority: Assess bowel sounds and abdominal girth regularly.
5. Through peristalsis, carbohydrates are emptied within 1-2 2. NPO (nothing by mouth) until peristalsis returns.
hours; proteins within 3-4 hours; fats within 4-6 hours. Once 3. Insert nasogastric tube for decompression if severe
acidic chyme is formed, slow peristalsis waves travel from the vomiting/distention.
fundus to the pylorus. Pressure builds up and pyloric sphincter 4. Maintain IV fluids and electrolytes (especially potassium).
opens. 5. Encourage early ambulation and repositioning.
6. Administer prescribed prokinetic agents (e.g.,
metoclopramide).
Small Intestines 7. Provide comfort measures (frequent mouth care for NPO
(6 meters long or 20-22 feet) patients).
Main function: Digestion and absorption of nutrients
Medical Management
1. Duodenum (first 25 cm) - receives chyme from stomach; 1. Conservative first-line:
mixes with bile (fat digestion) and pancreatic enzymes a.​ Bowel rest (NPO) + NG decompression + IV fluids.
(protein, carbs, and fat digestion); begins chemical 2. Correct underlying cause:
digestion. a.​ Stop opioids / offending drug
b.​ Replace electrolytes
2. Jejunum (middle 2.5 m) - main site for absorption of c.​ Treat peritonitis or sepsis if present
carbohydrates, proteins, vitamins, minerals, and water 3. Surgical intervention: Only if bowel obstruction is suspected
soluble nutrients; rich in villi and microvilli (increases the and does not resolve.
absorptive surface area)
Remember: MONITOR POTASSIUM (Hypokalemia can further
3. Ileum (last 3.5 m) - absorbs vitamin b12 and bile salts; worsen paralytic ileus)
complete nutrient absorption before contents pass to large a.​ Potassium is essential for smooth muscle contraction
intestine. b.​ Low potassium > weak peristalsis > lalo pang titigil
ang bowel motility
Large Intestine
(1.5 meters or 5-6 feet)
Main function: water and electrolyte absorption and stool Irritable Bowel Syndrome
formation
Functional disorder of intestinal motility regulation (it can be too
1. Cecum - pouch like structure where ileum joins; receives fast (diarrhea) or too slow (constipation) or alternating.
chyme through ileocecal valve; appendix is attached here
(role in immunity) Cause is idiopathic or unknown.

2. Colon (ascending, transverse, descending sigmoid) - Factor


absorbs water, sodium, chloride, potassium; houses Stress > visceral hypersensitivity > increase pain even in
intestinal flora (bacteria that synthesize vitamin k and b normal GIT activity such as peristalsis, pressure, or stretching.
complex; compact chyme into semi-solid stool.
Types
3. Rectum - stores feces until defecation; stretch receptors 1. IBS-C - Constipation
triggering urge to defecate. 2. IBS-D - Diarrhea
3. IBS-M - Mixed (alternating)
4. Anal Canal - final passage for stool elimination; 4. IBS-U - Unidentified
controlled by internal (involuntary) and external (voluntary)
sphincters. Clinical Manifestations
1. Abdominal pain related to or associated with:
a.​ Change in frequency and appearance or bristol stool
Intestinal Mobility chart
b.​ Defecation (before and during), it is GI activity that will
cause pain
Paralytic Ileus 2. Common complaint:
a.​ Abdominal pain triggered by food intake and relieved
by defecation
Functional intestinal obstruction due to absence of intestinal b.​ Abdominal distention
peristalsis (paggalaw ng intestine para itulak ang pagkain at
dumi) (no mechanical blockage); Caused by neurogenic or Managements
muscular impairment of GI motility. 1. Avoid stress
2. Diet
Common after: a.​ Fiber (if IBS-C = high fiber dahil constipation) (If
1. Abdominal surgery (most common) IBS-D = low fiber dahil diarrhea)
2. Peritonitis b.​ Use food diary to avoid triggers
3. Electrolyte imbalance (low potassium) c.​ Fluids in between meals
4. Drugs (opioids, anticholinergics) 3. LOW FODMaP - can cause bloating or further diarrhea; it
5. Spinal cord injury will ferment in the colon that will cause gas, pain, and
discomfort.
Clinical Manifestations a.​ low Fermentable Oligosaccharides - gas forming
1. Earliest sign: Absent bowel sounds (listen ≥5 minutes). b.​ low Disaccharides - lactulose or milk (meron silang
2. Abdominal distention, bloating osmotic laxative effect that pulls water into the colon
3. Nausea and vomiting (may be bilious or feculent) na pwedeng magworsen ng bloating, cramping, and
4. Constipation / no passage of stool or flatus diarrhea)
5. Abdominal discomfort or pain (dull, diffuse) c.​ Monosaccharide (high fructose) - apple, pears, or
6
PHILIPPINE NURSES LICENSURE EXAMINATION
Nursing Practice 4 Reviewer
According to the Newly TOS
MHEL, RN’25, MD’31

watermelon (it will trigger IBS because it will be poorly Lactase enzyme tablets before dairy intake can help.
absorbed.
d.​ Polyols - stone fruit - sugar alcohol (peaches, plum, or Nursing Interventions
cherries) 1. Assess diet history (timing of symptoms after dairy).
2. Educate on hidden sources of lactose (processed foods,
and medications with lactose fillers).
Medications 3. Encourage calcium and vitamin D supplementation (since
1. Antispasmodics - decrease motility milk is avoided).
2. Alosetron - for IBS-D 4. Teach alternatives: yogurt (lower lactose), fortified non-dairy
3. Lubiprostrone - for IBS-C milk.
4. Probiotics - decreases gas
Medical Management
1. No cure. Just symptoms control
Malabsorption Syndrome

Short Bowel Syndrome


Celiac Disease
Malabsorption disorder caused by surgical removal or
congenital loss of a large portion of the small intestine.
It is a gluten-sensitive enteropathy.
Small intestine is the major site of nutrient absorption kapag
Autoimmune reaction > ingestion of gluten (protein in wheat, nacut or missing, the body cannot absorb enough:
rye, barley, oats) damages the villi of the small intestine > 1. Fluids
Results in malabsorption of nutrients (fat, carbs, protein, 2. Macronutrients (carbs, protein, fat)
vitamins, minerals). 3. Micronutrients (vitamins & minerals)
4. Severity depends on length and location of resection:
Clinical Manifestations a.​ Loss of ileum could lead to worst malabsorption (esp.
1. Earliest / common signs: bile salts, B12).
a.​ Chronic diarrhea (steatorrhea = fatty, foul-smelling b.​ Loss of jejunum could lead to partial adaptation
stool) possible by ileum.
2. Abdominal bloating, cramping and flatulence
3. Malnutrition signs: Clinical Manifestations
a.​ Weight loss 1. Chronic diarrhea (main symptom)
b.​ Anemia (iron, folate, B12 deficiency) 2. Steatorrhea (fatty, foul-smelling stool)
c.​ Vitamin D & calcium deficiency > bone pain, 3. Malnutrition, weight loss
osteopenia 4. Dehydration, electrolyte imbalance
4. Children: Growth retardation, irritability, delayed puberty 5. Vitamin deficiencies:
a.​ B12 deficiency > megaloblastic anemia (if ileum
Prevention removed)
1. Only prevention (lifelong strict gluten-free diet). b.​ Fat-soluble vitamins (A, D, E, K) > bone disease and
2. Avoid BROW foods: Barley, Rye, Oats, Wheat. bleeding problems
3. Encourage gluten-free substitutes: rice, corn, potato, soy, 6. Failure to thrive in children
quinoa.
Prevention
Nursing Interventions 1. Prevent further bowel damage:
1. Priority: Maintain strict gluten-free diet. a.​ Careful surgical decision-making (avoid unnecessary
2. Monitor for malnutrition & anemia. resections).
3. Teach patient & family to read labels for hidden gluten. 2. Early aggressive nutritional support post-surgery.
4. Provide supplementation (iron, folate, calcium, Vit. D, B12). 3. Patient teaching: strict diet modification + adherence to
5. Encourage small, frequent, nutrient-dense meals. nutritional supplements.
6. AVOID BROW
a.​ Barley, Rye, Oats and Wheat Nursing Interventions
1. Priority: Monitor for fluid & electrolyte imbalance.
Medical Management 2. Maintain accurate I&O; monitor weight daily.
1. No cure > only management is lifelong gluten-free diet. 3. Provide a high-calorie, high-protein diet in small frequent
meals.
Complications if untreated: Malnutrition, anemia, 4. Recommend complex carbs; restrict simple sugars.
osteoporosis, high risk for intestinal lymphoma. 5. Supplement with:
a.​ Vitamin B12 (if ileum resected)
b.​ Fat-soluble vitamins (A, D, E, K)
Lactose Intolerance
c.​ Calcium, magnesium, iron
Lactase deficiency (enzyme in small intestine brush border). 6. Administer antidiarrheal medications as ordered.

Without lactase > lactose (milk sugar) is not digested > Medical Management
instead, fermented by colonic bacteria> leads to gas, bloating, 1. Nutritional support:
diarrhea, abdominal pain. a.​ TPN (Total Parenteral Nutrition) if initial & severe
cases.
NOT autoimmune, NOT structural, purely enzyme deficiency. b.​ Gradual introduction of enteral feeding to promote
intestinal adaptation.
Clinical Manifestations 2. Medications:
1. Earliest/common signs after dairy intake: a.​ Antidiarrheals (loperamide)
a.​ Abdominal bloating, cramping b.​ Proton pump inhibitors (decreases gastric acid >
2. Flatulence decreases diarrhea)
3. Watery diarrhea (osmotic) c.​ Teduglutide (enhances intestinal absorption, if
4. Hearing Borborygmi (rumbling sounds) available).
5. No blood or mucus in stool (unlike IBD). 3. Definitive treatment: Small bowel transplant (last resort).

Prevention
1. Avoid or limit lactose-containing foods (milk, soft cheese, ice
cream).
2. Use lactose-free or plant-based substitutes (soy milk,
almond milk, lactose-free dairy).
3. Gradually reintroduce small amounts to assess tolerance.
7
PHILIPPINE NURSES LICENSURE EXAMINATION
Nursing Practice 4 Reviewer
According to the Newly TOS
MHEL, RN’25, MD’31

Surgery
Pancreatic Insufficiency VS Bile Salt Deficiency
1. Appendectomy - laparoscopic or laparotomy
a.​ If there’s an abscess > delay the surgery (drain the
abscess first) use penrose drain and continue the
Pancreatic Insufficiency Bile Salt Deficiency surgery
2. Post-op management
Lack of enzymes (lipase, Lack of bile salts a.​ High fowlers position
protease, amylase); (emulsification of fat will fail) b.​ Use morphine as medication
c.​ IV fluids during first 24 hours
Caused by chronic Caused by liver disease, bile d.​ Allow food kapag returned gag reflex and peristalsis
pancreatitis or pancreatic duct obstruction, ileal e.​ Ambulation during first day
cancer disease or resection
Stool is Steatorrhea (greasy Stool is steatorrhea as well Diverticulosis VS Diverticulitis
and bulky)
Could lead to deficiency of
Could result in deficiency of Vitamin A,D,E,K as well Diverticulosis Diverticulitis
Vitamin A,D,E,K + protein
wasting. Signs: Bleeding tendency Outpouching of intestinal Chronic constipation and
due to vitamin K loss, mucosa (paglabas ng lining episodes of diarrhea (active
Signs: severe weight and pruritus and jaundice ng bituka sa mga part ng phase)
muscle loss intestinal wall)
Definitive treatment is to Inflammation of 1 or more
Definitive treatment is correct the underlying cause Common site is sigmoid diverticula; accumulation of
pancreatic enzymes such stone removal, (LUQ); low fiber that leads to bacteria is cause; diagnosed
replacement manage liver disease constipation; diagnoses by abdominal CT scan
through colonoscopy (using dye)

Structural and Obstructive Bowel Disorders Management: Management:


1. High fiber and fluid intake 1. High fiber if constipated,
2. Laxative or lactulose but during active phase
Appendicitis (diarrhea) is low fiber dapat.
2. High fluid intake
3. Monitor for peritonitis
May obstruction sa appendix lumen usually cause fecalith (rigid or board like abdomen)
(hard stool stone) or swollen lymph tissue after infection >
mucus and bacteria will build up inside this blocked appendix
Manifestations:
(so since blocked, ‘yung mga content inside appendix is hindi
1. Cramping abdominal pain in LLQ
maka-escape > increasing pressure inside appendix > traps
2. Infection - fever and increase WBC
bacteria them multiply > infection starts > pressure also blocks
3. Injury - rupture or perforate (hematochezia or fresh blood
blood flow > ischemia > ischemia + infection is inflammation
in stool)
where appendix becomes swollen, red, and painful.
4. Obstruction - increase gas that could lead to bloating or
flatulence
Possible complications if untreated
1. Perforation > peritonitis (infections spread to peritoneum)
2. Abscess formation (localized pus collection)
3. Sepsis (life threatening) Peritonitis

Causes of Ruptured Appendicitis Inflammation of the peritoneum, the thin membrane lining the
1. Increase peristalsis abdominal cavity; Usually caused by infection (bacterial,
2. Increase IAP fungal) or chemical irritation (gastric acid, bile, pancreatic
3. Vasodilation > increase blood flow > swelling or edema enzymes, foreign bodies).

Diagnostics: Pathophysiology
1. CT scan 1. Infection enters peritoneal cavity triggers inflammatory
2. Ultrasound response
2. Increased capillary permeability that leaks fluid into
Clinical Manifestations peritoneal cavity (ascites, third-spacing)
1. McBurney’s - pain ⅓ from the iliac region 3. Bacterial proliferation > systemic response > septic shock if
2. Rovsing’s - palpation in LLQ will cause pain in the RLQ untreated
3. Durphy’s - pain triggered by coughing
4. Blumberg - rebound tenderness Clinical Manifestations
5. Psoas - pain on passive extension of the right thigh 1. Earliest sign: Abdominal pain (usually diffuse, aggravated by
6. Obturators - eliciting pain on passive internal rotation of the movement)
hip with knee flexed 2. Other common signs:
7. High WBC due to infection a.​ Abdominal rigidity or “board-like” abdomen (pathog)
8. Bowel sound is late b.​ Rebound tenderness (Blumberg sign)
a.​ If decrease or absent + no pain, could mean rupture c.​ Fever, tachycardia, hypotension
9. (+) fever d.​ Nausea, vomiting, anorexia
e.​ Absent bowel sounds > paralytic ileus
Management f.​ Guarding > voluntary or involuntary
1. Suspected Appendicitis - do not give analgesic because it
will mask the pain or rupture Diagnostic Tests
a.​ Give analgesic once confirmed or diagnosed 1. Elevated WBC count (leukocytosis)
2. GI activity decreased - NPO or bedrest 2. Abdominal X-ray: free air under diaphragm if perforation
3. Avoid the causes of rupture such as increase peristalsis and 3. Peritoneal fluid analysis: cloudy, purulent, bacteria positive
intraabdominal pressure.
4. Compress Nursing Interventions
a.​ Cold is RECOMMENDED to decrease pain 1. Assess abdominal pain, distension, rigidity, bowel sounds,
b.​ NEVER use hot compress because it will promote vitals (watch for shock)
vasodilation 2. Monitor I&O, electrolytes, CBC, signs of sepsis
5. Position - low or semi-fowlers and minimized movement or 3. Positioning: Semi-Fowler’s to reduce abdominal pressure &
peristalsis ease breathing

8
PHILIPPINE NURSES LICENSURE EXAMINATION
Nursing Practice 4 Reviewer
According to the Newly TOS
MHEL, RN’25, MD’31

4. NPO - to prevent further peritoneal irritation; NG tube if


Gastric Ulcer VS Duodenal Ulcer
vomiting/distension
5. IV fluids to restore third-space fluid loss (isotonic
crystalloids)
6. AVOID any pain killers to prevent the mask of pain Gastric Ulcer Duodenal Ulcer
7. Antibiotic administration as prescribed, broad-spectrum
initially Pain triggered by food intake Pain triggered by gastric
(gnawing pain, hunger like emptying (burning pain)
Medical Management pain and persistent)
1. First-line Pain relieved by food intake
a.​ IV broad-spectrum antibiotics (ceftriaxone + Pain relieved by vomiting
metronidazole) With melena (old and dark
2. Definitive treatment / Gold standard With hematemesis > vomitus stool)
a.​ Surgery (laparotomy / laparoscopy) to repair cause + blood
(perforation, appendectomy)
3. Post-op care: continue antibiotics, monitor for complications
(abscess, sepsis) Hemorrhoids

Peptic Ulcer Disease Increased pressure in rectal veins > veins swell and dilate >
Increased pressure are caused by:
Ito ay open sore or ulcer sa lining ng stomach or duodenum 1. Straining
dahil sa mataas na HCl production at mababang mucus 2. Pregnancy
production for protection 3. Prolonged sitting
4. Portal hypertension
Factors 5. Increase intraabdominal pressure
1. Stress (chronic) - will trigger the parietal cells,
enterochromaffin and G cells to increase the acid secretion These causes result to increased anorectal area pressure >
2. Drinks such as caffeinated or decaffeinated (coffee beans) weakening of supporting tissues around the anal canal
3. Smoking and drinking alcohol
4. Drugs such as aspirin and NSAIDs shall be avoided Two Types
5. Infection due to H. Pylori from raw meets 1. Internal - above anal sphincter; painless unless it prolapse
2. External - below anal sphincter; thrombosis > congestion of
Diagnostic Tests: blood > stasis of blood
1. Upper endoscopy - direct visualization of GIT
2. Serum test - detects antibodies to H. Pylori Clinical Manifestations
3. FOBT - detects duodenal ulcer and hidden blood in stool 1. Pain
4. Urea breath test - patient will ingest urea + specialized 2. Itching > swelling of blood vessels > irritation of nerve
carbon isotope > H. Pylori will breakdown endings > trigger itchy sensation
a.​ If H. Pylori is present, detect labeled CO2 3. Bleeding upon defecation > strain > dilated blood vessels >
rupture or tear
Nursing Interventions (stomach distention is directly
proportional to HCl production)
1. SFF (6-10 meals a day) Degree of Prolapse
2. Diet as tolerated
a.​ Active phase - if painful, should be bland diet to First Don’t prolapse
decrease HCl production
b.​ Chew slowly and thoroughly Secon Prolapse due to defecation
c.​ Milk is limited for about 200-400 ml a day d
3. Avoid factors
Third Prolapse in anal area through manual reduction
Medications
1. Antacids - best time is 1-2 hours after meals Fourth Prolapse fully in anal area; need surgery
a.​ Sodium Bicarbonate - metabolic acidosis
b.​ Calcium Carbonate - hypercalcemia and constipation
c.​ Aluminum Hydroxide - constipation Interventions
d.​ Magnesium Hydroxide - diarrhea 1. Good personal hygiene
2. Gastric Protectants or Cytoprotective 2. Avoid straining (the internal type could prolapse)
a.​ Sucralfate - forms barrier or coating (best time is 3. Regular bowel movement - increase fiber and OFI, do
before meals) ambulation and exercise
b.​ Misoprostol - prostaglandin analog (increases mucus 4. Comfort/Reduced engorgement
production, with meals, contraindicated with pregnant) a.​ Cold compress - vasoconstriction (external)
3. H2 receptor antagonist or blocker - decreases HCl b.​ Sitz Bath (warm, shallow bath that soaks only the
production before meals dapat, onset is 90 minutes hips, buttocks and perineal area)
4. Proton Pump Inhibitors - decreases HCl production (30
minutes before meals) Medical Management
5. Antibiotics - combined with PPI + bismuth subsalicylate. Ex: 1. Hydrophilic Bulk Forming Agents - stool softener (psyllium
a.​ Tetracycline + Metronidazole husk)
b.​ Amoxicillin + Clarithromycin 2. Analgesic ointments - topical like lidocaine
3. Suppositories - prevent straining
Surgery 4. Astringents - dehydrates hemorrhoids (witch hazel), it
1. Vagotomy - cut the branches of vagus nerve located in decreases the size.
stomach to decrease the HCl production
2. Gastrectomy Surgery
a.​ Total - from esophagus to small intestine 1. Sclerotherapy - shrink and hardening (prevent prolapse)
b.​ Subtotal Antrectomy - removal of the lower portion of 2. Rubber Band Ligation - decrease blood flow > necrosis > fall
stomach (fundus + body to small intestine) off
3. Anastomosis - reconnecting or reattaching 3. Stapled hemorrhoidopexy - surgical staples > prolapsed
a.​ Billroth I - gastroduodenostomy hemorrhoids
b.​ Billroth II - gastrojejunostomy 4. Hemorrhoidectomy - not immediate, if only conservative
treatments are not working.

Post-op Interventions
9
PHILIPPINE NURSES LICENSURE EXAMINATION
Nursing Practice 4 Reviewer
According to the Newly TOS
MHEL, RN’25, MD’31

1. Prone or side lying position to decrease anal pressure


2. Ice pack during first 24 hours to promote vasoconstriction, to
decrease bleeding
3. Sitz Bath - temp is 31-41 degrees, 3-4 x a day for 20 mins.
4. Diet - Increase OFI and fiber
5. AVOID prolonged sitting to decrease anal pressure
6. Use stool softener like psyllium husk or decosate sodium.

Gastritis
Inflammation of gastric lining or mucosa

Causes: highly seasoned food, smoking, alcohol drinking,


gastric ulcer, radiation and chemotherapy, H. Pylori, highly
acidic substance, highly alkaline substance, aspirin and
NSAIDs.

Acute Chronic
(Sudden inflammation) (Repeated inflammation or
scars or fibrosis)
Mnemonics: HEAD

Hiccups, Epigastric Pain, Halitosis, Reflux, Sour Taste,


Anorexia, and Dyspepsia. Early Satiety, Anorexia,
Epigastric Pain
WOF: Bleeding
WOF: Pernicious anemia
due to Vitamin B12
deficiency

Interventions
1. Acute bleeding - rest the GI (NPO to promote healing then
pwede na mag ice chips, liquid, then solid)
2. Bland diet to decrease the HCl production
3. Medications are antacids, gastric protectants, H2 Blockers,
PPI, and antibiotic
4. Supplement for chronic such as Vitamin B12
5. AVOID causes
Dumping Syndrome

Rapid gastric emptying; Once bumaba ang food sa small


intestine, tumataas ang concentration. Since walang ability
ang small intestine to absorb high concentration, blood vessels
will compensate through vasodilation. Water from blood
vessels will shift to small intestines. Now, the blood vessels
has low volume, showing shock-like symptoms.

It will also manifest postprandial hypoglycemia (since mabilis


ang absorption or gastric emptying, pancreas will be triggered
and release high insulin, therefore, glucose will be transport
inside the cell.

Interventions: (Food should stay)


1. Diet
a.​ High protein (absorb for 3-4 hours)
b.​ High fiber - delays gastric emptying
c.​ Carbohydrate low - mabilis matunaw for about 1-2
hours especially the sweet or simple carbs for about
30 mins to 1 hour.
d.​ SFF meals, taken in between meal (decrease
abdominal distention)
e.​ AVOID concentrated foods
2. Position - lie down after meals 20-30 minutes
3. Medications are anticholinergic or antispasmodics
4. Vitamin B12 should be given due to loss of intrinsic factor
(given monthly via IM)

10
PHILIPPINE NURSES LICENSURE EXAMINATION
Nursing Practice 4 Reviewer
According to the Newly TOS
MHEL, RN’25, MD’31

B. Metabolism and Endocrine


Cardiac Associated with severe right sided
Cirrhosis congestive heart failure and results in
Liver enlarged, edematous and congested
liver. The liver becomes anoxic, resulting
Anatomy of the Liver in liver cell necrosis and fibrosis.

Location Clinical Manifestations


1. Right upper quadrant (RUQ) of the abdomen, beneath the 1. Anorexia (initial manifestation), weakness, and weight loss.
diaphragm These s/sx are due to inability of the liver to metabolize
2. Partially under the rib cage (protective) nutrients and store fat-soluble vitamins (ADEK)
2. Fever - normal physiologic response if you have liver tissue
Size & Weight damage.
1. 1.2–1.5 kg in adults 3. Jaundice, pruritus, and tea colored urine - due to increased
2. Largest internal organ serum bilirubin levels.
4. Bleeding - due to decreased vitamin K absorption that
Blood Supply (dual) results in reduced synthesis of clotting factors.
1. Hepatic artery - delivers oxygen-rich blood from aorta 5. Risk to develop infection
2. Portal vein - delivers nutrient-rich blood from GI tract
Remember: Portal hypertension leads to hepatosplenomegaly,
Venous Drainage: caput medusae (dilated vein in abdomen), spider angioma,
1. Hepatic veins - going to inferior vena cava palmar erythema, ascites, esophageal varices, internal
hemorrhoids, leg varicosities, dependent edema, and small,
Hexagonal structure nodular liver.
1. Central vein + surrounding hepatocytes
2. Portal triad at corners: hepatic artery + portal vein + bile duct 6. Liver cirrhosis can also lead to asterixis (liver flap) - coarse
tremor characterized by rapid nonrhythmic extension and
Physiology of the Liver flexion of the wrist and fingers.
7. Hepatic encephalopathy - end stage hepatic failure and
Metabolic Functions cirrhosis caused by elevated serum ammonia. It is
1. Carbohydrate metabolism characterized by the following manifestations
a.​ Glycogenesis: glucose to glycogen a.​ Confusion or disorientation
b.​ Glycogenolysis: glycogen to glucose b.​ Delirium or hallucination
c.​ Gluconeogenesis: amino acids or lactate to glucose c.​ Fetor hepaticus or the fruity, musty breath odor of
2. Protein metabolism chronic liver disease.
a.​ Synthesizes albumin & clotting factors (II, VII, IX, X) d.​ Hepatic coma - irreversible
b.​ Converts ammonia into urea (detoxification) 8. Hepatorenal syndrome - progressive renal failure
3. Lipid metabolism associated with hepatic failure. Characterized by sudden
a.​ Synthesizes cholesterol, triglycerides, phospholipids decrease in urinary output, elevated BUN and creatinine,
b.​ Produces bile for fat digestion decreased urine sodium and secretion, and increased urine
4. Vitamin & Mineral Storage osmolarity.
a.​ Vitamins: A, D, E, K, B1
b.​ Minerals: iron, copper Interventions
1. Promote rest
Detoxification & Excretion 2. Diet
1. Metabolizes drugs, alcohol, and toxins a.​ High calorie (2,000 to 3,000 a day)
2. Excretes bilirubin (from RBC breakdown) into bile b.​ High carbohydrates to maintain weight
c.​ Low protein
Bile Production d.​ Fat restriction
1. 600–1000 mL/day e.​ Provide vitamin supplements ADEKB and C.
2. Bile emulsifies fats > aids digestion & absorption in small 3. Skin care to relieve pruritus
intestine a.​ Wash the skin with warm water and mild soap
b.​ Change position at regular intervals
Immunologic Function c.​ Change linens and gowns as needed
1. Kupffer cells > phagocytosis of bacteria, old RBCs, and d.​ Keep cool environment
debris e.​ Apply lotion as prescribed like calamine lotion
4. Prevent trauma or injury to prevent bleeding
Liver Cirrhosis a.​ AVOID or minimize parenteral injection, use small
gauge needle
b.​ Apply pressure at injection for about 5 minutes
Chronic progressive disease characterized by diffuse damage c.​ AVOID vigorous nose blowing.
to the cells with fibrosis and nodular regeneration. Repeated 5. Protect from infection
causes of hepatic cells cause the form of a scar in liver tissue; 6. Elevate the HOB to minimize SOB.
It is a persistent increase in pressure within the portal vein that 7. Relieve ascites
develops as a result of obstruction to blood flow. a.​ Monitor daily weights, abnormal girth, and intake and
output every shift.
b.​ Restrict sodium and fluid intake
Types of Liver Cirrhosis
c.​ Administer diuretics as prescribed. DOC is
spironolactone.
Alcoholic or Alcohol induced; cellular necrosis causes
d.​ LeVeen peritoneo or venous shunt - used for clients
Laennec’s widespread scar tissue, with fibrotic
with chronic ascites.
Cirrhosis infiltration of the liver
8. Prevent rupture of esophageal varices
a.​ Advise the client to avoid screaming, shouting, or
Postnecrotic Occurs after massive liver necrosis. It yelling.
Cirrhosis occurs as a complication of acute viral b.​ Administer Inderal (Propranolol) to reduce portal
hepatitis or exposure to hepatotoxins. hypertension.
9. Reduce ammonia formation.
Biliary Develops from chronic biliary obstruction, a.​ DOC: lactulose
Cirrhosis bile stasis, and inflammation resulting in 10. AVOID medications such as narcotics, sedatives,
severe obstructive jaundice. barbiturates, and acetaminophen.
11. AVOID ASA to prevent bleeding
12. AVOID alcohol.
11
PHILIPPINE NURSES LICENSURE EXAMINATION
Nursing Practice 4 Reviewer
According to the Newly TOS
MHEL, RN’25, MD’31

Clinical Manifestations
Biliary Tract
1. Earliest sign: intermittent right upper quadrant (RUQ) pain /
biliary colic
Gallbladder 2. Other signs
1. Concentrates the bile produced by the liver a.​ Jaundice (yellowing of skin & sclera)
2. The gallbladder stores 50-70 ml of concentrated bile. b.​ Dark urine, clay-colored stools (obstructive pattern)
3. Bile is composed of water, cholesterol, bile salts, c.​ Fever & chills - may indicate ascending cholangitis
electrolytes, and phospholipids. 90-95% of this volume is (Charcot’s triad)
water. d.​ Nausea, vomiting
4. Bile is important in fat emulsification and intestinal e.​ Pruritus due to bile salt accumulation
absorption of fatty acids, cholesterol, and other lipids.
5. Bile also aids in excretion of conjugated bilirubin from the Diagnostic Tests
liver and prevents jaundice. 1. Elevated bilirubin (direct)
2. Elevated alkaline phosphatase (ALP) & GGT
3. Ultrasound / MRCP → shows stones in CBD
Cholecystitis VS Cholelithiasis
4. ERCP → diagnostic and therapeutic

Cholecystitis Cholelithiasis Prevention


1. Maintain healthy weight & diet to prevent gallstone formation
Inflammation of the Presence of the gallstones (low fat, high fiber)
gallbladder in the gallbladder 2. Early management of gallstones to prevent migration into
CBD
Causes: Cause: 3. Avoid prolonged fasting or rapid weight loss > increases risk
1. Calculous - obstruction by Imbalance in bile of gallstones
gallstone components that result to
2. Acalculous - trauma, cholesterol, bilirubin, and Nursing Interventions
sepsis, or prolonged fasting calcium salts crystallize > 1. Assess RUQ pain, jaundice, vitals, stool/urine changes
stone form 2. Monitor: liver function tests, bilirubin, signs of infection
It’s obstructing the cystic (fever, chills)
duct or common bile duct, Stones can obstruct duct 3. Pain management opioids as prescribed
therefore bile is being causing pain or cholecystitis 4. NPO or low-fat diet until obstruction resolved
trapped 5. Prepare for procedures ERCP, cholecystectomy
Symptoms: 6. IV fluids: maintain hydration if vomiting occurs
Symptoms: 1. May be asymptomatic
1. RUQ pain may radiate to 2. Sudden RUQ pain after Medical Management
right shoulder or scapula fatty meal (colicky pain) 1. First-line:
2. Nausea, vomiting and 3. May progress to a.​ Endoscopic Retrograde Cholangiopancreatography) >
fever cholecystitis if obstruction stone removal & stent if needed
3. Jaundice, clay colored persist 2. Broad-spectrum antibiotics if cholangitis present
stool or dark urine 3. Definitive / Gold Standard:
Diagnostics: a.​ Surgical removal (cholecystectomy) if gallbladder
Diagnostics: 1. Ultrasound - stone visible stones present
1. Ultrasound - thickened 2. ERCP for ductal stones
gallbladder wall
2. Murphy's sign (+) - sharp Management: Pancreas (DM)
pain in RUQ during 1. May not need treatment if
inspiration asymptomatic Pancreas perform both exocrine and endocrine functions. Its
2. If symptomatic - address it exocrine function is to secrete pancreatic amylase, lipase, and
Management: by giving analgesics or trypsin.
1. NPO comfort measure
2. IV Fluids 3. If not resolved, proceed 1. Amylase - completes digestion of carbohydrates
3. Analgesics or antibiotics with cholecystectomy 2. Lipase - complete digestion of fats
4. NG tube if vomiting 3. Trypsin - complete digestion of proteins
5. Definitive is
cholecystectomy The endocrine function of pancreas involves the Islets of
Langerhans. It has two cell types such as beta and alpha cells.
Post-cholecystectomy Beta cells secretes insulin to transport glucose inside the cell.
1. Encourage deep breathing and coughing exercise to Alpha cells secretes glucagon which stimulates glycogenolysis
avoid atelectasis or pneumonia in the liver.
2. Semi fowler’s position
3. Diet: clear liquids > soft diet > low fat diet
4. Encourage early ambulation Diabetes Mellitus Type 1
5. If T-tube or drain is present, REPORT sudden increase
and output foul odor Absolute insulin deficiency due to the autoimmune destruction
6. SFF, avoid fatty greasy, and spicy foods of beta cells (in CBC, you will see a (+) islet cell antibodies).
7. Light ambulation soon after surgery; AVOID heavy lifting
for 4-6 weeks. Classic manifestation: 3P’s + 1
1. Polydipsia
2. Polyphagia
Choledocholithiasis 3. Polyuria - due to osmotic diuresis, may diuretic effect ang
glucose, since maraming glucose sa blood vessels, hihilahin
Presence of gallstones in the common bile duct (CBD). niya ang tubig na nasa loob ng cell.
4. Hyperglycemia - since walang insulin, walang magtransport
Often arises from gallstones formed in the gallbladder that ng glucose inside cell. Therefore, dadami ang glucose sa blood
migrate into the CBD. vessels.

Stone obstructs bile flow > bile stasis > Leads to biliary colic, Renal glucose threshold - 180 mg/dl
cholangitis, or pancreatitis if the pancreatic duct is involved > 1. Once our body reaches beyond the threshold, it will start
Obstruction > jaundice due to bilirubin accumulation excreting glucose in urine = glycosuria.

12
PHILIPPINE NURSES LICENSURE EXAMINATION
Nursing Practice 4 Reviewer
According to the Newly TOS
MHEL, RN’25, MD’31

Management
1. Insulin - primary treatment kase nga absolute ang deficiency Long Acting 6-8 hours 12-16 hours 20-30 hours
2. Diet (Ultralente)
3. Exercise
Glargine 1 hour no peak 24 hours
Acute Complication
Diabetic Ketoacidosis - since walang glucose ang Remember: Give snacks during peak. Snack should be simple
nakakapasok sa loob ng cell, it will result to cell hunger that will carbohydrates (ex. fruit juice).
trigger the brain to look for an alternative source of food. The
fats and protein will be broken down as an alternative. Once fat AVOID exercise during peak action. Possibly that is also the
is broken down, may byproduct siya na ketones and this is peak of lowest blood sugar levels.
acidic in nature. So accumulation of ketones will result to
acetone breath during the kussmaul’s breathing.
Oral Hypoglycemic Agent

Diabetes Mellitus Type 2


OHA Mechanism of Action
DM 2 has 2 types. Let’s compare it.
Sulfonylureas Stimulate beta cells to
First gen: Tolazamide or release more insulin
Relative Insulin Deficiency Insulin Resistance Tolbutamide
Second gen: Glibenclamide
Beta cells not producing Common factor is obesity. or Glimepiride
enough insulin.
Technically, diba kapag Biguanides (metformin) Increased sensitivity to
Same symptoms like Type 1 obese ang tao, marami insulin (addressing insulin
the 3P’s and Hyperglycemia. siyang fats? Ang lipids from resistance)
this fat is uunahan ang
insulin na magbind sa insulin Thiazolidinediones Increased sensitivity to
receptor. Therefore, walang (rosiglitazone and insulin (addressing insulin
glucose ang makakapasok pioglitazone) resistance)
sa loob ng cell.
Alpha Glucosidase Inhibits the breakdown of
Management Inhibitors starches and some form of
1. Oral hypoglycemic agents - ordered when blood sugar level (Acarbose or Miglitol) sugar in the intestines
is unregulated or uncontrolled.
2. Diet
3. Exercise - primary treatment, it improves the insulin Pancreatitis
sensitivity.
Inflammation of the pancreas due to autodigestion by
Insulin Administration pancreatic enzymes (esp. trypsin).

Causes
4 R’s of Insulin
1. Gallstones (most common) > obstruct CBD > reflux of
1. Roll - do not shake the insulin vial (it will cause bubbles >
bile/enzymes
insufficient amount). Roll it gently.
2. Alcohol use (second most common) > toxic to pancreatic
2. Rotate - rotate injection site at least 1 inch apart to prevent
cells
lipodystrophy (pagkapal or pagnipis ng subcutaneous tissue).
3. Refrigerate - place as much as possible to the farthest area
Process
na hindi sa coolest area. For example, sa compartment lang ng
1. Obstruction or injury > premature activation of enzymes
ref.
inside pancreas
4. Room temperature - inject or administer at room temp
2. Enzymes digest pancreatic tissue > inflammation, edema,
level. Opened vial of insulin may be stored at the room temp
necrosis
within 1 month only.
3. May lead to systemic complications (ARDS, shock, DIC).
Mixing of NPH and Regular Insulin
Types
1. Inject air sa NPH or cloudy first
1. Acute pancreatitis - sudden, reversible if treated; can be
2. After ng cloudy, sa clear or regular ka naman mag inject ng
mild or severe
air.
2. Chronic pancreatitis - progressive, irreversible damage,
3. Draw insulin sa regular or clear first.
leads to diabetes, steatorrhea
4. Lastly, draw insulin sa NPH or cloudy.
Clinical Manifestations
Remember: when injecting air to cloudy insulin, make sure
1. Earliest sign - severe epigastric pain radiating to the back,
that syringe doesn’t touch the insulin.
worse after meals or alcohol
2. Other common signs:
Type of Insulin a.​ Nausea, vomiting
b.​ Abdominal distension, tenderness
Type Onset Peak Duration c.​ Absent bowel sounds (ileus)
d.​ Low-grade fever, tachycardia, hypotension (shock
Rapid Acting 10-15 mins 30 mins 1 hour risk)
(Humalog) 3. Pathognomonic signs:
a.​ Grey Turner’s sign - bluish flank discoloration
Short Acting 30 mins - 2-4 hours 4-6 hours (retroperitoneal bleed)
(Regular or 1 hour b.​ Cullen’s sign - bluish periumbilical discoloration
Humulin R) (intra-abdominal bleed)

Intermediate 2-4 hours 6-12 hours 16-20 hours Diagnostics


(Humulin N or 1. Increase Serum amylase and lipase (lipase more specific)
NPH) 2. Increase Blood glucose (insulin)
3. Increase WBC, hypocalcemia (tetany risk)
4. CT scan > best imaging to assess severity
13
PHILIPPINE NURSES LICENSURE EXAMINATION
Nursing Practice 4 Reviewer
According to the Newly TOS
MHEL, RN’25, MD’31

Nursing Interventions the frequent swallowing as well.


1. NPO - absolute rest of pancreas 2. Laryngeal nerve damage - assess for persistent hoarseness
2. NG tube suction - to relieve nausea/vomiting & reduce (NORMAL ang hoarseness within 24 hours)
stimulation 3. Hypocalcemia - early manifestation is paresthesia; late sign
3. Position - Semi-Fowler’s or side-lying with knees flexed > is trousseous sign, chovstek’s sign, and tetany.
decreases pain 4. Hypocalcemia may cause Laryngospasm - prepare calcium
4. Monitor vitals, fluid & electrolytes (esp. calcium), urine gluconate at bed side, tracheostomy set, suction machine and
output oxygen.
5. Pain management
a.​ IV opioids (morphine/hydromorphone)
Parathyroid Gland
6. IV fluids - aggressive hydration (prevent shock)
7. Monitor for complications: hypocalcemia
(Chvostek/Trousseau signs), ARDS, and sepsis Location
8. AVOID alcohol, low-fat diet, report recurrence 1. Small, oval endocrine glands located on the posterior
surface of the thyroid gland.
2. Usually four (2 superior + 2 inferior), but number can vary
Endocrine Disorders
(some people have 2–6).

Size & Shape


Thyroid Gland
1. About 3–5 mm in diameter (size of a grain of rice).
2. Flat, oval, yellowish-brown.
Butterfly shaped gland located at the base of the neck, below
the adams apple. Structure
1. Each gland is surrounded by a thin fibrous capsule.
3 Hormones Composed of:
1. T3 (Triiodothyronine) - for metabolism a.​ Chief cells - secrete parathyroid hormone (PTH)
2. T4 (Thyroxine) - for heat production b.​ Oxyphil cells - function not well understood, may
3. Thyrocalcitonin - for calcium regulation increase with age

Thyrocalcitonin - pinapasok ang calcium sa blood to bones Physiologic Function (PNLE High-Yield)
(calcium deposition) 1. Main hormone: Parathyroid Hormone (PTH)
Parathormone (PTH) - release by parathyroid gland; 2. Function: Regulates calcium and phosphorus balance
activation of osteoclast; bony matrix is crashed > calcium is a.​ Increase blood calcium (by stimulating bone
released to blood (Bone resorption) resorption, increasing GI absorption via vitamin D
activation, and increasing renal calcium reabsorption)
b.​ Decrease blood phosphate (increases renal
Hypothyroidism VS Hyperthyroidism
excretion)

Remember na laging opposite ang calcium at phosphate.


Hypothyroidism Hyperthyroidism
(Remember DRY and (Remember WET and
SLOW) FAST) Hypoparathyroidism VS Hyperparathyroidism

Hyposecretion of thyroid Hypersecretion of thyroid


hormones hormones Hypoparathyroidism Hyperparathyroidism

Manifestations: Manifestations: Hypocalcemia and Hypercalcemia and


1. Decreased T3 (decreased 1. Increased T3 (increased Hyperphosphathemia Hypophosphatemia
metabolism) - weight gain, metabolism) - weight loss,
constipation, bradycardia, diarrhea, tachycardia, Management: Management:
hypotension, slowed hypertension 1. Dietary calcium, calcium 1. To correct hypercalcemia,
physical and mental 2. Increased T4 (Increased supplementation (calcium we are using NSS, loop
reactions thermoregulation) - heat gluconate, oral calcium), diuretics, calcitonin,
2. Decreased T4 (decreased intolerance, diaphoresis vitamin D, and mithracin and increasing oral
thermoregulation) - dry skin, 3. Increased Thyrocalcitonin parathormone supplement, fluid intake.
cold intolerance - fine tremors 2. Amphogel (Aluminum 2. To correct low phosphate,
3. Decreased thyrocalcitonin 4. Others - exophthalmos hydroxide) we are giving dietary
- fatigue, brittle nails, (protrusion of eyeball) and phosphate and phosphate
lethargy dalrymple’s sign. preparation as prescribed.
4. Others - enlarged tongue
and increased sensitivity to Management:
narcotics and sedatives 1. Provide cool and and non Adrenal Glands
stimulating environment
Management: 2. Provide high calorie and
1. Provide warm low fiber diet It is also called the suprarenal gland.
environment 3. Protects eye, instill
2. Low calorie, cholesterol, artificial tears 1. Adrenal Cortex - producing GMA (CAS)
and high fiber diet 4. Fluid and electrolyte a.​ Glucocorticoid - Cortisol (Increases blood glucose,
3. Weight reduction replenishment immunosuppressant or stress hormone).
4. Pharmacotherapy 5. Pharmacotherapy - beta b.​ Mineralocorticoid - Aldosterone (sodium and water
(Levothyroxine sodium, blockers or calcium channel reabsorption; sodium retention and potassium
thyrolar, thycar, and cytomel) a. Anti-thyroid meds - can be excretion)
a solution or tablet, but u c.​ Androgen - Sex Hormone (secondary sex
need to WOF its adverse characteristics; will make you appear as man or
effect which is woman during puberty)
agranulocytosis or
neutropenia 2. Adrenal Medulla (Chromaffin Cells)
6. Surgery a.​ Adrenaline/Epinephrine
b.​ Noradrenaline/Norepinephrine
c.​ These 2 hormones are producing catecholamines
Post Thyroidectomy which activates fight and flight response or SNS,
1. WOF bleeding - assess the dressing in front and back and means isipin mo kapag na-activate to is hinahabol ka

14
PHILIPPINE NURSES LICENSURE EXAMINATION
Nursing Practice 4 Reviewer
According to the Newly TOS
MHEL, RN’25, MD’31

ng maraming aso (mataas HR, RR, BP, and etc.) many other endocrine glands.

Two Major Lobes


Adrenal Cortex Disorders
1. Anterior Pituitary (Adenohypophysis)
a.​ 75% of the gland
b.​ Derived from oral ectoderm (Rathke’s pouch)
Cushing Syndrome Addison’s Disease c.​ Controlled by hypothalamic releasing/inhibiting
(Increased GMA-CAS) (Decreased GMA-CAS) hormones via hypophyseal portal system
d.​ Hormones:
Hyperglycemia, Hypoglycemia, -​ GH (Growth Hormone) for growth,
Hypernatremia, Hyponatremia, metabolism
Hypokalemia Hyperkalemia -​ TSH (Thyroid-Stimulating Hormone) for
thyroid gland
Clinical Manifestations: Clinical Manifestations: -​ ACTH (Adrenocorticotropic Hormone) for
1. Gynecomastia (male); 1. Dehydration - could lead adrenal cortex
Hirsutism (female) to hypovolemic shock -​ FSH & LH for gonads (spermatogenesis,
2. Edema, moon face, 2. Weight loss ovulation, estrogen/testosterone)
buffalo hump 3. Bronze pigmentation of -​ PRL (Prolactin) for lactation
3. Truncal obesity (adipose skin (pathognomonic sign)
tissue accumulation) weight 2. Posterior Pituitary (Neurohypophysis)
gain Management: a.​ 25% of the gland
4. Increase susceptibility to 1. Diet is increase b.​ Extension of the hypothalamus (nerve tissue)
infection carbohydrate and sodium; c.​ Hormones are made in the hypothalamus (supraoptic
decrease potassium & paraventricular nuclei) but stored & released here
Management: d.​ Hormones:
1. Decrease carbohydrates 2. Increase fluid -​ ADH (Antidiuretic Hormone / Vasopressin)
and sodium; increase for water reabsorption in kidneys
potassium -​ Oxytocin for uterine contraction, milk
2. Decrease fluid intake let-down reflex
3. Surgery - unilateral or
bilateral adrenalectomy Clinical PNLE Notes
(complication is addisonian 1. Hypersecretion:
crisis > management is a.​ Increased GH will lead to Acromegaly (adults),
hormonal replacement Gigantism (children)
therapy) b.​ Increased Prolactin will lead to Galactorrhea, infertility
4. There will be an 2. Hyposecretion:
insensible fluid loss = not a.​ Panhypopituitarism will lead to dwarfism, amenorrhea,
measurable or observe hypothyroidism, adrenal insufficiency
water loss, that’s why hindi 3. Posterior disorders:
fully restricted ang fluid (add a.​ Decreased ADH will lead to Diabetes Insipidus
500 cc in 24 hour collection) b.​ Increased ADH will lead to SIADH (Syndrome of
5. Prevent infection Inappropriate ADH Secretion)

Adrenal Medulla Diseases Diabetes Insipidus

Remember “DI”
Pheochromocytoma 1. DIcreased ADH
Tumor in chromaffin cells of the adrenal medulla; usually 2. Dami Ihi; Dalas Ihi;
benign. 3. DIlute urine; DIcreased urine specific gravity (Normal is
1.010-1.030)
It results to increase production of cathecolamines > Increase 4. DIhydration (Hypernatremia)
HR and BP
Management
Clinical Manifestations 1. Fluid administration
1. Hypertension (they may be unresponsive to antihypertensive 2. Administer desmopressin as ordered (it’s a synthetic
drugs which is considered as hypertensive crisis) vasopressin)
2. Headache a.​ The assessment parameter if we need to administer
3. Heavy sweating is the urine specific gravity
4. Tachycardia
5. Tremors Diagnostic Test
1. Water deprivation test - if madami pa rin ang ihi at clear kahit
Diagnostic Test hindi pinainom = (+) fluid deprive test.
1. Vanillylmandelic Acid Test (VMA test) - metabolite of
catecholamine production Syndrome of Inappropriate ADH secretion (SIADH)

Management Increase ang ADH, so excessive ang water retention.


1. Surgery (Adrenalectomy)
2. AVOID food high in tyramine > cheese, chocolate, beer and Clinical Manifestations
processed meat. 1. Decreased fluid excretion
3. AVOID stimulants 2. Concentrated urine
4. AVOID stress and activities that worsen condition 3. Hypervolemia - good indicator is neck vein distention or
5. Promote rest blood vessel distention
4. Dilutional Hyponatremia - bumababa amg concentration ng
sodium sa blood kase marami ang water.
Pituitary Gland
REMEMBER: Hindi common ang EDEMA sa SIADH.
Small, pea-shaped endocrine gland (0.5–1 gram); Located at
the base of the brain, in the sella turcica of the sphenoid bone; Management
Connected to the hypothalamus by the pituitary stalk 1. Fluid restriction
(infundibulum); Called the “master gland” because it regulates 2. Diuretics - loop and vasopressin receptor antagonist
3. Demeclocycline - diuresis (it’s an antibiotic actually that
15
PHILIPPINE NURSES LICENSURE EXAMINATION
Nursing Practice 4 Reviewer
According to the Newly TOS
MHEL, RN’25, MD’31

promotes water diuresis)


4. Surgery - removal of tumor kase possible na kaya
dumadami ang secretion ng ADH is because of tumor pero
benign.

16
PHILIPPINE NURSES LICENSURE EXAMINATION
Nursing Practice 4 Reviewer
According to the Newly TOS
MHEL, RN’25, MD’31

C. Perception and Coordination Disturbances


Clinical Manifestations
1. Pathognomonic sign - CHARCOT’S TRIAD
Neurological Nursing
a.​ Scanning speech - syllabication of words
b.​ Intention Tremors
Degenerative means progressive, irreversible deterioration of c.​ Nystagmus - dancing eyes
neurons or nervous system structures. Usually chronic,
worsening overtime and no complete cure. Nursing Interventions
1. Promote ambulation - walking!
2. Minimize spasticity - use warm compress
Cranial Nerves 3. Minimize effect of immobility
a.​ Pressure ulcer - turn every 2 hours and use padding
I. Olfactory Sensory Smell over bony prominence
b.​ Pneumonia - turning; increase OFI; cough exercise
II. Optic Sensory Vision c.​ Venous stasis - elevate legs and use compression
stockings
III. Oculomotor Motor Eye Movement; UPward 4. Prevent injury - walk with feet apart!
Pupil constriction
Parkinson’s Disease
IV. Trochlear Motor Eye Movement:
DOWNward
Chronic, progressive neurodegenerative disorder of the basal
V. Trigeminal Both Facial sensation and ganglia; Caused by decreased dopamine (from degeneration
mastication of substantia nigra cells).

VI. Abducens Motor Eye movement: Destruction of Substantia Nigra > Dopamine deficiency >
LATERAL imbalance between dopamine & acetylcholine > impaired
movement, posture, coordination.
VII. Facial Both Facial expression and
taste Clinical Manifestations
4 Cardinal Signs
VIII. Sensory Hearing 1. Resting tremor > “pill-rolling tremor” (earliest, common sign)
Vestibulocochlear 2. Rigidity > stiffness, “cogwheel rigidity”
3. Bradykinesia > slowness of movement (pathognomonic
IX. Both Swallowing and taste hallmark)
Glossopharyngeal 4. Postural instability (stooped posture, shuffling gait)

Postural Changes
X. Vagus Both Muscle movement
a.​ Propulsive Gait - head and neck bent forward
through pharynx or
b.​ Shuffling Gait - short sliding steps
larynx; sensation in ear
c.​ Festinating Gait - faster (doesn’t stop unless meets an
obstruction
XI. Accessory Motor Sternocleidomastoid &
Trapezius muscle
5. Other Manifestations
a.​ Micrographia - small handwriting
XII. Hypoglossal Motor Tongue Movement b.​ Mask like facies - expression less

Neurologic Assessment Nursing Interventions


Level of Consciousness - most sensitive indicator of 1. Safety first - fall precautions, assistive devices
neurologic function 2. Promote mobility - ROM exercises, encourage ambulation
with wide-based gait
a.​ Practice walking in marching music (sensory,
Glasgow Coma Scale reinforcement)
b.​ Finger exercises such as buttoning shirt, crochet and
Eye Movement 4 - spontaneously etc.
(4) 3 - eye open in response to speech 3. Nutrition - soft diet, small frequent meals, high-fiber & fluids
2 - pain stimuli (finger pressure and (prevent constipation), upright while eating
supraorbital pressure) 4. Swallowing - position upright, suction PRN, thickened liquids
1 - no response 5. Communication - allow time to speak, use short sentences

Verbal Response 5 - oriented to time, person, and place Medical Management


(5) 4 - confused 1. First-line drug:
3 - inappropriate words a.​ Levodopa + Carbidopa (Sinemet) > gold standard for
2 - incomprehensible sounds symptom control
1 - no response 2. Other drugs
a.​ Dopamine agonists (bromocriptine, pramipexole)
Motor Movement 6 - obeys command b.​ Anticholinergics (benztropine) > reduce
(6) 5 - moves to localized pain tremors/rigidity
4 - flexed to withdraw from pain c.​ MAO-B inhibitors (selegiline) > slow dopamine
3 - abnormal flexion or decorticate breakdown
2 - abnormal extension or decerebrate 3. Surgical: Deep brain stimulation (for advanced cases)
1 - no response
Myasthenia Gravis
(Remember: Mind to Ground)
Multiple Sclerosis

Autoimmune disorder affecting the myoneural junction; Caused


Irreversible demyelinating disease of the CNS; Sensitized T by thymic hyperplasia or tumor; Result to weakness of
cells attack myelin sheath and oligodendoglial cells (cells that voluntary muscles
produced myelin in the CNS); The result will show impaired
transmission of the nerve impulses. Clinical Manifestations (Descending Paralysis)
1. Ptosis
17
PHILIPPINE NURSES LICENSURE EXAMINATION
Nursing Practice 4 Reviewer
According to the Newly TOS
MHEL, RN’25, MD’31

2. Diplopia
3. Blank facial expression Diagnostic Test
4. Dysphonia - voice impairment 1. CT Scan - initial diagnostic test for stroke
5. Difficulty in chewing and swallowing 2. MRI
a.​ Priority is AIRWAY; risk for aspiration before 3. 12 lead ECG - used for atrial fibrillation (strongly support
breathing problem ischemic stroke)
6. Respiratory failure Medical Management of Ischemic Stroke:
7. Weakness of extremities 1. Thrombolytic therapy (main treatment) - TSA or Tissue
Plasminogen Activator; Best is Alteplase
Diagnostic Test Consideration: stroke must be ischemic; age must be 18 years
1. Tensilon test or Acetylcholinesterase Inhibitor Test old or older; onset is 3 hours or less dapat mabigay na (Wala
a.​ Uses edrophonium chloride (tensilon) via IV ng magagawa if beyond 3 hours)
b.​ 30 seconds after injection facial muscle weakness
including ptosis, if it resolve for 5 mins (it confirms 2. Anticoagulant - warfarin (coumadin)
diagnosis) If contraindicated - aspirin is best option (can be given together
c.​ Atropine (anticholinergic) - antidote or cholinergic with clopidrogel)
crisis
2. MRI - enlarged thymus gland Medical Management of Hemorrhagic Stroke:
1. Antihypertensive - control BP
Nursing Interventions 2. Fresh Frozen Plasma and Vitamin K - increase clotting
1. Teaching focuses on strategies to conserve energy factor from liver; plasma contains all clotting factors
2. Minimize risk of aspiration 3. Anticonvulsant - phenytoin (dilantin) (Advise proper oral
a.​ Rest before meal to conserve energy care, can cause gingival hyperplasia).
b.​ Sit upright neck flexed while swallowing
3. Eye problem - eye dryness
a.​ Use artificial tears Clinical Management
b.​ Tape the eyes Manifestation

Medical Management Motor Loss


1. Anticholinesterase medication
a.​ Pyridostigmine (mestinon) and neostigmine - first line Hemiplegia Passive ROM
therapy, it inhibits breakdown of acetylcholine
2. Corticosteroid - suppress immune response Hemiparesis Active ROM
3. Thymectomy - surgical removal of thymus gland
Ataxia Support on initial ambulation; provide
supportive device like cane
Myasthenic Cholinergic
Dysphagia Aspiration Precaution:
Underdosage Overdosage 1. Test pharyngeal or gag reflex using
tongue depressor
If use tensilon test, it will If use tensilon test, it will 2. Started on thick liquid; upright position
relieve worsen and tuck the chin toward the chest; place
food on unaffected side of mouth; allow
Use antidote which is ample time to eat
atropine
Verbal Deficits
Cerebrovascular Accidents or Stroke
Expressive ”Write” as alternative method of
Functional abnormality of the CNS from disruption of blood Aphasia communication
supply to part of the brain. (Broca’s Area) Ex. Magic slate; If you cannot write, use
picture boards.
2 Major Categories
1. Ischemic Receptive ”Read” as alternative method
2. Hemorrhage Aphasia Si nurse ang magsusulat
(Wernicke’s
Ischemic Hemorrhagic
area)
Decrease perfusion to brain Bleeding into the brain
Global Aphasia Use gestures, actions, or pictures
tissue tissue, ventricles, and
(Both) (Allow sufficient time to respond)
subarachnoid space.
Causes:
Visual Fields
Atherosclerosis, thrombus, 2 Types:
embolism, DM, HPN, atrial 1. Primary - from rupture of
fibrillation (quivering or small blood vessels caused Homonymous Loss of half of the visual field
nanginginig) by uncontrolled HPN. Hemianopsia Remember: Kung nasaan ang affected
2. Secondary - associated side of vision, ayon dun ang paralyzed
Pathophysiology: with AVMS (congenital, side of the body
Disruption of blood flow > tangled arteries and veins),
ischemia (prolong lack of cerebral aneurysm, Management:
O2) > tissue necrosis > neoplasm or medication 1. Objects should be in unaffected; also
infarction (basta hindi uncontrolled approached in unaffected.
HPN) 2. Instruct patient to scan affected side
by head turning

Assessment of Stroke Sensory Loss


1. Balance - sudden loss of balance or coordination
2. Eyes - double vision or unable to see at one eye Agnosia Unable to recognize objects through
3. Face - facial drooping (ask patient to smile) sensory system
4. Arm - does one arm drift downward? Does a person raise
both arms in the air? Management: assisting patient in self
5. Speech - slurring speech (ask to repeat words) care but ensuring to promote
6. Time - call 911

18
PHILIPPINE NURSES LICENSURE EXAMINATION
Nursing Practice 4 Reviewer
According to the Newly TOS
MHEL, RN’25, MD’31

eat/swallowing issues).
independence 7. Support family coping & caregiver burden.
Joint Deformities and Contractures
Traumatic Lesions
1. When bed rest - put pillow in axillary; apply splint at night
on affected extremity; reposition every two hours; ROM Traumatic lesions simply means an injury to body tissue
exercises caused by external physical force; Examples are skull fracture
and brain injury.

Alzheimer Disease and Dementia Lesions - any abnormal change or damage to tissue
Traumatic - caused by trauma.
Dementia (General Term)
A broad syndrome characterized by progressive decline in Skull Fracture
cognitive function (memory, judgment, language, reasoning)
severe enough to interfere with daily life.
Break in the continuity of the skull from forceful trauma; Brain
Causes: injury may or may not be present.
1. Alzheimer’s Disease (most common)
2. Vascular dementia (after multiple strokes) Types of Skull Fracture
3. Lewy Body dementia
4. Frontotemporal dementia Simple Linear Break in the continuity of the bone
Alzheimer’s Disease (Specific type of Dementia) Comminuted Splintered fracture line or nadurog
A progressive, irreversible neurodegenerative disease that is
the most common cause of dementia.
Depressed Skull displaced downward or
lumubog
Pathophysiology
1. Amyloid plaques and neurofibrillary tangles form in the brain.
2. Loss of acetylcholine (ACh) > impaired memory & learning. Basilar Skull Fracture Fracture of the base of the skull
3. Neuronal death & brain atrophy > cognitive & functional
decline. Signs:
1. Raccoons eye - pre-orbital
Clinical Manifestations edema
Dementia (general) 2. Rhinorrhea - CSF in nose
1. Memory loss (especially short-term) 3. Otorrhea - CSF in ear
2. Impaired judgment & abstract thinking 4. Battle sign - bruising mastoid
3. Personality & behavior changes bone
4. Loss of ability to perform ADLs
5. Progressive disorientation (time, place, person) Test Fluid for Glucose
Use 4x4 gauze pad and collect the fluid leaking. Yellowish or
Alzheimer’s Disease (more specific progression) halo ring sign indicates CSF leakage (produced by glucose)
1. Early stage:
a.​ Forgetfulness, difficulty finding words Diagnostic Tests
b.​ Disorientation in familiar places 1. CT scan - to diagnose skull fracture
c.​ Mood/behavior changes 2. MRI - to diagnose brain injury
2. Middle stage:
a.​ Increased confusion, wandering, agitation
b.​ Difficulty with ADLs Brain Injury
c.​ Personality changes, hallucinations/delusions
3. Late stage:
a.​ Severe memory loss, inability to recognize family Types of Brain Injury
b.​ Loss of verbal communication
c.​ Incontinence, immobility Concussion Jarring of the brain (naalog)
d.​ Total dependence
Contusion Brain is bruised or damaged (nauntog)
Management
No cure > goal is to slow progression & support patients/family. Diffuse Axonal Widespread axonal shearing (naputol)
1. Medications Damage Poor prognosis
a.​ Cholinesterase inhibitors like Donepezil,
Rivastigmine, Galantamine - increases ACh levels. Intracranial Bleeding inside cranium
b.​ NMDA receptor antagonist: Memantine > protects Hemorrhage
brain cells. a. Epidural Hematoma
c.​ Antipsychotics or antidepressants (for behavior & b. Subdural Hematoma
mood).
2. Supportive care
a.​ Maintain routine & structured environment (to Meninges - protective layer of brain and spinal cord; It has 3
decrease confusion). layers:
b.​ Safety precautions (wandering, falls, choking) 1. Dura mater
c.​ Provide cues (clocks, calendars, labels). 2. Arachnoid mater
d.​ Promote independence as long as possible. 3. Pia mater
e.​ Support caregivers (respite care, education).
Epidural Hematoma Subdural Hematoma
Nursing Care (PNLE favorites)
1. Provide a calm environment to decrease agitation. Outer bleeding (outside Below the dura bleeding
2. Use simple, clear instructions. dura)
3. Encourage frequent orientation (introduce self, use Between dura and
clocks/calendars). Between skull and dura arachnoid;
4. Maintain safety (lock hazardous items, fall precautions). (meninges); Source of bleeding is
5. Avoid restraining unless necessary ( if increased agitation). Source of bleeding is venous;
6. Provide nutritional support (risk of forgetting to

19
PHILIPPINE NURSES LICENSURE EXAMINATION
Nursing Practice 4 Reviewer
According to the Newly TOS
MHEL, RN’25, MD’31

arteries and rapid hematoma Slow hematoma Diagnostic Test


development development 1. Xray
2. CT Scan
3. MRI
Neuropathies or Peripheral Nerves Management
1. Prevent further injury
Disorder or damage of the peripheral nerves (nerves outside 2. Assess - ask if can move hands and feet
the brain and spinal cord) a.​ Any vehicle accident, assume that it is SCI unless
stated and tested
Neuro - nerves 3. Immobilize in flat, firm surface (spine board) and head and
Pathy - disease or disorder neck in neutral position (jaw thrust)
4. Maintain in extended position - AVOID sitting
Symptoms depend on which nerves are affected: 5. Transport the patient as unit
1. Sensory nerves - numbness, tingling, burning or pain 6. DO NOT align the body parts
2. Motor nerves - muscle weakness or paralysis
3. Autonomic nerves - abnormal sweating, GI problem, or BP Musculoskeletal Dysfunction or Orthopedics Nursing
instability

The total bones that we have is 206, it becomes fewer as we


Trigeminal Neuralgia (Tic Doulourex) age. Newborn bones: 270 (they have 4 coccyx that fuses as
they age.
Condition of CNS (Trigeminal); abnormally firing of electrical
impulse; cause is unknown and irreversible. Sequence of the spinal cord (CTLSC)
1. Cervical
Manifestation 2. Thoracic
1. Primary symptoms; pain is innervated by 3 branches 3. Lumbar
a.​ Characteristics are abrupt, unilateral, shooting, 4. Sacral
stabbing, and burning pain. 5. Coccyx
2. Involuntary contraction of facial muscles - painful twitching
Common Bones:
Management 1. Sternum - also known as breast plate
1. DOC: Carbamazepine (Anticonvulsant) a.​ Xiphoid process
2. Pain occurs within any stimulation of the branches; so dapat -​ Cartilage under sternum
less stimulated -​ Used as landmark to measure the length of
a.​ Washing of face - water, room temp, use cotton pads GIT (Nose > ear lobes > xiphoid process or
b.​ Eating and drinking - food and drinks should be room vice versa)
temp; sa unaffected side dapat ang pagchew. 2. Clavicle - also known as the collarbone, shoulder girdle
c.​ Brushing of teeth is avoided, use mouthwash instead. 3. Scapula - also known as shoulder blades; located at the
d.​ Less shaving of facial hair back of clavicle
e.​ AVOID direct pressure to face
Fracture
Bell’s Palsy Defined as a break in bone continuity due to trauma,
pathologic disease (osteoporosis, cancer), or stress.
Facial paralysis; unilateral inflammation of CN 7 (facial nerve);
cause is unknown and this is reversible; complete recovery Classified as
1. Closed (simple): skin intact
Manifestations 2. Open (compound): skin broken > increase infection risk
1. Distorted face, excessive lacrimation, and drooling 3. Complete vs. incomplete (greenstick, common in kids)
2. Pain sa face, eyes, and behind ear. 4. Comminuted: bone splinters into many fragments
5. Impacted: ends are driven into each other
Management (general concept is to facial exercise) 6. Pathologic: secondary to bone disease
1. DOC: Prednisone (corticosteroid)
2. Massage face in a gentle upward motion Clinical Manifestations
3. Facial exercise 1. Earliest sign: Pain at the site
a.​ Wrinkle forehead 2. Pathognomonic: Bone deformity/abnormal angulation
b.​ Blowout cheeks 3. Other signs:
c.​ Whistle a.​ Swelling, tenderness
4. AVOID exposure to cold drafts b.​ Loss of function
c.​ Crepitus (grating sound/feeling)
d.​ Shortening of limb (esp. hip fracture)
Spinal Cord Diseases e.​ Bruising/hematoma

There is a loss of transmission of impulses; injury in the spinal Prevention


cord, vertebral column, or intervertebral disc. 1. Adequate calcium & vitamin D intake
2. Weight-bearing exercise to strengthen bones
3. Fall prevention: assistive devices, remove home hazards
Location of Injuries (elderly)
4. Protective gear during sports, helmets, seatbelts
Cervical SCI Innervates diaphragm and arms; respiratory
paralysis, quadriplegia, tetraplegia, which Nursing Interventions
are life threatening 1. Immobilize immediately (splints, sling, traction)
2. Neurovascular assessment = 5 P’s:
Thoracic Innervates abdominal muscle and bowel a.​ Pain (earliest)
SCI movement; cannot cough (management is b.​ Pallor
pneumonia precaution) and possible c.​ Pulselessness
paralytic ileus. d.​ Paresthesia
e.​ Paralysis
Lumbar SCI Innervates bladder and legs (bladder 3. Elevate affected limb (reduce swelling)
paralysis; paraplegia) 4. Apply ice in first 24–48 hrs
5. Cover open fractures with sterile dressing > prevent infection
20
PHILIPPINE NURSES LICENSURE EXAMINATION
Nursing Practice 4 Reviewer
According to the Newly TOS
MHEL, RN’25, MD’31

6. Do not attempt to realign bone in the ward inflammation


7. Monitor for compartment syndrome: pain unrelieved by 5. Elevate - prevent edema by promoting venous return and
analgesics = EMERGENCY prevent internal bleeding
8. Encourage isometric exercises to prevent muscle atrophy if 6. Splint - for immobilization
immobilized
Medical Management
1. First-line: Immobilization (splints, casts, traction) Other Management:
2. Definitive treatment: 1. Sling - protect upper extremities
a.​ Closed reduction + cast/splint (non-surgical 2. Crutches - protect lower extremities
realignment) 3. Relative test - rest the affected extremities only for faster
b.​ Open Reduction with Internal Fixation (ORIF): healing and recovery due to faster circulation and perfusion on
surgical, plates/screws/rods the affected side.
c.​ External fixation: pins outside skin, used for severe 4. PROMOTE gradual ambulation unless may surgery. (If may
open fractures surgery, advise bed rest).
3. Gold standard for open fracture: surgical debridement + IV
antibiotics
Sprain vs Strain
4. Pain control: NSAIDs, opioids
5. Tetanus prophylaxis for open wounds Lateral curvature of the spine; asymmetrical shoulder and
pelvis (hindi pantay); sternum moves with the spine as the ribs
are attached to it; we have letter S and C curvature.
Dislocation and Sublaxation
Common to female teenagers.
Dislocation - complete displacement of a bone from its joint
capsule. Physical Examination
Subluxation - partial/incomplete dislocation of the joint. 1. Adams Forward Bend Test - bend and look both sides of
scapula > prominence of scapula = possible scoliosis
Usually caused by trauma, sports injuries, or falls. May 2. Xray - confirmatory diagnostic test
damage surrounding ligaments, blood vessels, and nerves >
medical emergency. Complication
1. Pulmonary Impingement - due to asymmetry of spine; some
Clinical Manifestations parts of the lungs are compressed and unable to fully utilize >
1. Pain (sudden, severe at the joint) reduce vital capacity > reduce oxygen.
2. Obvious deformity of the joint
3. Loss of function or immobility Management
4. Shortened or malaligned limb (if hip/shoulder) 1. Milwaukee Brace
5. Swelling and bruising a.​ Reduce curvature; used for 3 years with gradual
6. Tenderness on palpation adjustment; worn for 23 hours a day (1 hour removed
for hygiene or swimming)
Nursing Interventions b.​ Best exercise for spine abnormality is swimming
1. Immobilize joints immediately in the position found (do not c.​ Use at the top of cotton shirt
attempt to reduce in the ward). d.​ Harness/Traction ot braces concern is to prevent skin
2. Apply cold packs/ice first 24 hrs → reduce swelling. breakdown
3. Neurovascular assessment (5 P’s) e.​ DO NOT apply anything on the skin unless
4. Elevate extremity to minimize edema. prescribed.
5. Provide analgesics and muscle relaxants as ordered 2. Harrington Red Insertion - also known as spinal fusion;
Medical Management slight spine curvature can undergo surgery.
1. First-line - Closed reduction (manual realignment by MD,
often under sedation).
Metabolic Bone Disorders
2. Definitive treatment:
a.​ Closed reduction + immobilization (cast, splint, sling).
b.​ Open reduction (surgery) if closed reduction fails or if
Osteoporosis
fracture complicates.
c.​ Rehabilitation/physical therapy to restore mobility “Silent thief of bones”; Imbalance between bone resorption
(osteoclast activity increase) and bone formation (osteoblast
activity decrease)
Sprain vs Strain
Leads to low bone mass, fragile bones, increases fracture risk;
They are both damage to connective tissues which connects Common in postmenopausal women (estrogen deficiency =
the structures of the body. accelerated bone loss) and elderly.

Clinical Manifestations
sTrain Sprain 1. Earliest sign is back pain (due to microfractures in
(Tendon) (Ligaments) vertebrae)
2. Most common sites of fracture are vertebrae, hip (femoral
Tendons connect bones to Ligaments connects bone to neck), wrist (Colles’ fracture)
muscles like quadriceps, bone like carpals in hand or 3. Loss of height, stooped posture, kyphosis (“dowager’s
hamstring, calf, biceps, and metatarsals in feet hump”)
triceps.
Cause: twisting injury or Nursing Interventions
Cause: Overuse, sudden stretch 1. Priority - prevent falls & fractures
overstretching, or improper a.​ Encourage safe mobility (assistive devices, non-slip
lifting Manifestation: joint footwear, proper lighting at home)
instability and inability to 2. Educate on diet rich in calcium & Vit D
Manifestation: muscle bear weights 3. Promote weight-bearing activities within tolerance
spasm and weakness 4. Pain management (heat, NSAIDs as ordered)
5. Encourage compliance with osteoporosis meds
Management (PRICES)
1. Protect Medical Management
2. Rest 1. First-line / Gold Standard diagnostic test: Dual-energy X-ray
3. Ice - prevent bleeding, pain, and inflammation Absorptiometry (DEXA scan)
4. Compress - used of elastic bandages, prevent swell or a.​ First-line drug: Bisphosphonates (Alendronate or
Fosamax) – inhibit bone resorption
21
PHILIPPINE NURSES LICENSURE EXAMINATION
Nursing Practice 4 Reviewer
According to the Newly TOS
MHEL, RN’25, MD’31

2. Other meds
Rheumatoid Arthritis VS Osteoarthritis
a.​ Calcitonin (decrease bone resorption)
b.​ SERMs (Raloxifene) – mimic estrogen on bones
c.​ Teriparatide (PTH analog, increase bone formation)
for severe cases RA OA
d.​ Calcium + Vit D supplementation
Autoimmune (immune Degenerative “wear and
system attacks synovial tear” of cartilage.
Osteomalacia membrane)
Usually starts at 50 years
Metabolic bone disease in adults caused by defective Usually starts at 30 years old; Asymmetrical (localized
mineralization of bone > soft, weak bones. old; Symmetrical both sides. weight bearing joints)

Cause: Improves with activity or Worsens with activity;


1. Vitamin D deficiency > low calcium & phosphate absorption movement; worse after rest Relived by rest
> impaired bone hardening.
2. Childhood version = Rickets. It has systemic symptoms No systematic symptoms,
3. Often confused with Osteoporosis but: such as fatigue, fever, just localized only.
a.​ Osteoporosis = low bone density weight loss, anemia and
b.​ Osteomalacia = defective mineralization (bone is soft, nodules No systemic deformities, just
not brittle). bony enlargements
Swan neck deformity and
Clinical Manifestations ulnar deviation Heberden’s nodes and
1. Earliest sign: Bone pain and tenderness (spine, pelvis, legs). Bouchard's nodes
2. Muscle weakness (everytime walking, climbing stairs). Soft tender rheumatoid
3. Waddling gait (due to weak muscles & soft bones). nodules Mild or no inflammation, joint
4. Easy fatigue. may feel hard
5. Classic triad: “Bone pain + muscle weakness + vitamin D Marked inflammation
deficiency = Osteomalacia.” X-ray is the confirmatory
Diagnostics will show diagnostic; will show joint
Prevention increase ESR and CRP space narrowing
1. Adequate sunlight exposure (15–30 mins/day).
2. Diet rich in vitamin D & calcium (milk, fish, eggs, fortified Medications are Medications are the same
food). methotrexate, NSAIDs or with RA
3. Vitamin D supplementation in at-risk groups (elderly, corticosteroids
pregnant, malabsorption, chronic renal disease). Priority nursing care are pain
4. Avoid excessive phosphate-binding antacids (decreases Priority nursing care are joint relief, weight reduction,
absorption of vit D). protection, energy exercise that is low impact
conservation, ROM during and joint support.
Nursing Interventions remission
1. Encourage safe sun exposure.
2. Prevent falls & fractures (use assistive devices, safety
measures at home). Musculoskeletal Infections
3. Monitor for signs of hypocalcemia (tetany, muscle spasms).
4. Provide pain relief and assist with mobility. Musculoskeletal infections are bacterial, fungal, or viral
infections that affect the bones, joints, muscles, or surrounding
Medical Management soft tissues.
1. First-line: Vitamin D supplementation (Calciferol,
Ergocalciferol). They usually occur after trauma, surgery, open fractures, or
2. If renal disease: Active form of vitamin D (Calcitriol). spread from nearby skin infections
3. Calcium & phosphate supplements as needed.

Osteomyelitis
Rickets

Severe infection of bone and bone marrow, usually caused by


Metabolic bone disorder in children due to Vitamin D deficiency bacteria (Staphylococcus aureus, most common).
that will lead to defective bone mineralization.
Infection > inflammation > edema > vascular congestion >
Leads to soft, weak, deformed bones (failure of growing bone decreased blood flow > bone necrosis (sequestrum) > chronic
to calcify); Childhood counterpart of Osteomalacia (adult form). infection.
Clinical Manifestations Types
1. Earliest sign: Delayed growth & bone pain. 1. Acute Osteomyelitis > recent onset (days–weeks).
2. Skeletal deformities: 2. Chronic Osteomyelitis > persistent/recurrent infection with
a.​ Bowed legs (genu varum) dead bone (sequestrum).
b.​ Knock knees (genu valgum)
c.​ Enlarged wrists & ankles Clinical Manifestations
3. “Rachitic rosary” (beading of ribs at costochondral junction) 1. Earliest sign: Localized bone pain (constant, throbbing).
4. Delayed closure of fontanels, delayed tooth eruption. 2. Swelling, redness, warmth over site.
5. Weakness, irritability, easy fatigue. 3. Fever, chills, malaise (systemic signs).
4. Limited movement of affected limb.
Nursing Interventions 5. Chronic cases: Sinus tract drainage, non-healing ulcer,
1. Promote a diet high in vitamin D and calcium. necrotic bone.
2. Encourage safe sun exposure for children.
3. Monitor growth and development milestones. Nursing Interventions
4. Provide orthopedic support for deformities (braces if 1. Strict aseptic wound care.
prescribed). 2. Immobilize affected limbs to decrease pain and prevent
5. Fall prevention > soft bones = high fracture risk. spread.
3. Elevate extremity to reduce swelling.
4. Provide pain management (analgesics, comfort measures).
5. Encourage high-protein, vitamin C diet > wound healing.

22
PHILIPPINE NURSES LICENSURE EXAMINATION
Nursing Practice 4 Reviewer
According to the Newly TOS
MHEL, RN’25, MD’31

6. Monitor for signs of sepsis (tachycardia, hypotension, fever). a.​ Tinel’s sign: tapping median nerve at wrist > tingling
b.​ Phalen’s test: flexing wrist for 60 sec >
Medical Management tingling/numbness
1. First-line - IV broad-spectrum antibiotics > tailored after
culture results (usually 4–6 weeks). Prevention
2. Debridement of necrotic bone (sequestrectomy). 1. Avoid repetitive wrist strain (ergonomic tools, frequent
3. Chronic cases: May require bone graft or amputation. breaks).
4. Pain control with NSAIDs or opioids. 2. Use wrist supports or splints for high-risk jobs.
3. Early treatment of wrist inflammation (arthritis, injury).

Nursing Interventions
Cellulitis
1. Splint wrist in neutral position (esp. at night).
2. Encourage ROM exercises for fingers/wrist.
Acute bacterial infection of the skin and subcutaneous tissue 3. Teach ergonomic practices (computer/typing positions).
(not localized, unlike abscess) 4. Pain management: cold packs, NSAIDs as ordered.
5. Monitor for sensory/motor loss > may indicate worsening
Commonly caused by: compression.
1. GABHS 6. Prepare for surgery if conservative measures fail.
2. Staphylococcus aureus
Musculoskeletal Modalities
Pathophysiology
Break in skin (wound, scratch, insect bite, ulcer, surgical
incision) > bacteria enter dermis > infection spreads rapidly
Traction
through connective tissue & lymphatic channels >
inflammation, edema, erythema.
Reduce muscle spasm before surgery; pulling force;
Risk Factors immobilize; and prevent fracture.
1. Diabetes mellitus (poor wound healing).
2. Immunocompromised clients. Component of Traction
3. Poor hygiene. 1. Splint - immobilize the traction
4. Chronic venous insufficiency / lymphedema. 2. Rope - maintains the tension
5. Skin trauma (cuts, insect bites, surgery). 3. Pulley - responsible for the direction of pull
4. Sandbag - contains weight
Clinical Manifestations
1. Red, warm, swollen, tender skin (classic sign).
2. Rapidly spreading erythema with poorly defined borders. Types of Traction
3. Pain and tenderness on palpation.
4. Fever, chills, malaise (systemic signs). Skin Traction
5. Lymphadenopathy in affected area. Uses light materials such as bandage, straps, and
6. In severe cases, blisters, abscess, necrosis. adhesives; prevent skin breakdown because skin is intact in
this type of traction ; 5-7 lbs sandbag weight
Complications DO NOT apply anything on skin
1. Sepsis.
2. Necrotizing fasciitis. Russells Tibia and fibula fracture
3. Chronic edema/lymphangitis.
4. Gangrene (if untreated). Bucks Fracture is in femur

Nursing Interventions Bryant’s Buttocks slightly elevated off the bed and
1. Elevate affected extremity > reduces edema. knee slightly flexed (usually for kids;
2. Apply warm, moist compress > promotes circulation & congenital hip dysplasia)
healing.
3. Strict aseptic wound care. Halter Strap that is placed in the chin, usually
4. Administer antibiotics (usually IV for severe cases). used for cervical fractures
Medical Management
1. First-line antibiotics: Skeletal Traction
a.​ Mild cases > oral (cephalexin, dicloxacillin, Uses screw, rods, and pins; drilled on the outer layer of
clindamycin). bone called periosteum; prevent infection through pin care;
b.​ Severe cases > IV (cefazolin, ceftriaxone, vancomycin 15-40 lbs sandbag weight
if MRSA suspected).
2. Analgesics for pain. Balance Also called as Thomas Splint with Pearson
3. Treat underlying causes (wounds, ulcers, diabetes). Suspension Attachment; sandbag is usually 40 lbs due
Traction to this heavy weight, another traction is
Occupational-Related Muscular Disorders applied called pearson
attachment;usually accompanied by
trapeze to change position; reduce pulling
Carpal Tunnel Syndrome force and reduce muscle spasm.

Halovest Drill at periosteum of skull; prevent


Compression of the median nerve as it passes through the movement of neck and spinal cord
carpal tunnel (wrist); Caused by repetitive hand/wrist motion,
inflammation, or swelling; Results in pain, numbness, and An important tool is a wrench to loosen or
tingling in the thumb, index, middle, and radial half of the ring remove bolts when a patient is having
finger. DOB.
Clinical Manifestations
1. Earliest sign: Numbness/tingling in thumb and first 3 fingers Cast
(esp. at night).
2. Other common signs:
a.​ Hand pain radiating to forearm It’s a rigid external immobilizing device encasing an extremity
b.​ Weak grip, clumsiness, dropping objects or body part; maintains bone alignment, supports healing, and
c.​ Thenar muscle atrophy in advanced cases prevents deformity.
3. Special tests (pathognomonic):
23
PHILIPPINE NURSES LICENSURE EXAMINATION
Nursing Practice 4 Reviewer
According to the Newly TOS
MHEL, RN’25, MD’31

eye.
Plaster Synthetic Remember: Light is one of the requisites of vision; main
refracting surface of the eyes.
Sinemento; white or grayish Fiberglass (hindi mabilis
color; conventional; dries mabasag); dries within Refractory ability - eyes ability to bend light so that it focuses
within 24-72 hours; heavy; 20-30 minutes; light weight; properly on the retina.
use damp cloth to clean wash with water
Pupil - space that dilates and constricts in response to light
Cast Care a.​ Normal shape is round
1. Direct air current b.​ Protective mechanism - too bright; constricts or miosis
2. Handle the cast while it’s wet using palms, DO NOT use any c.​ Adaptive mechanism - too dark; dilate or mydriasis
other objects Iris - color portion of the eye; give pigments; regulate the size
3. Elevate it with pillow to promote venous return of the pupil.
4. Hotspot may indicate infection - REFER!
5. If itchiness occur, use BLOWER at cool setting Lens - colorless, biconcave structure; responsible for
a.​ If not relieved, refer for prescription of antihistamine accommodation (ability to focus for near vision; ability to
6. Petal the cast - hibla ng cast can cause skin irritation, cut it refocus for distant vision)
using scissor. DO NOT PILE. If it’s just small, place adhesive
tape inside and out. Conjunctiva - membrane that cushions the eye; covers the
sclera and inside of eyelids; lubricates the eye.

Splints Ciliary body - adjusting the shape of lens for focusing;


produces aqueous humor (fluids that nourishes the eye; jeep
Non-circumferential device that immobilizes an injured part; cornea healthy; maintain normal IOP of 10-21.
Allows for swelling, unlike casts.
Note: Elevated IOP is normal in the morning.
Indications
1. Initial management of fractures before definitive cast Vitreous Chamber - area between lens and retina that
2. Sprains, tendon injuries, post-op support contains vitreous humor; gel like structure that occupies ⅔ of
3. When swelling is expected (to prevent compartment the eyes volume; maintain the normal shape of the eyes.
syndrome)
Cataract
Nursing Interventions
1. Check circulation and skin integrity under splint
2. Avoid wrinkles > may cause pressure sores Painless, clouding or opacity of the lens (impaired vision)
3. Educate patient on loosening Velcro straps if too tight
4. Elevate extremity to reduce swelling Causes
1. Senile (pagtanda)
Remember: Splints are preferred in acute swelling phase of 2. Congenital (inborn)
fractures 3. Trauma (injury)

Manifestations
Brace 1. Blurred vision > decreasing visual acuity (disturbed sensory
perception, risk for injury, self care deficit)
External support device that stabilizes, aligns, or corrects 2. White, milky, grayish pupil
deformities; Used long-term (chronic conditions). 3. Gradual and painless loss of vision

Types/Uses Diagnostics
1. Knee brace – ligament/tendon injuries 1. Snellen chart - measure decline in visual acuity
2. Ankle-foot orthosis (AFO) – foot drop, neuromuscular 2. Slit lamp examination - visual opacity of lens
disorders 3. Indirect ophthalmoscopy - rule out retinal disease
3. Spinal brace – scoliosis, post-op spine surgery
4. Wrist brace – carpal tunnel Management:
1. Priority is safety
Nursing Interventions a.​ Use eyeglasses or contact lenses
1. Monitor for skin breakdown (inspect bony prominences b.​ Lensectomy (last resort)
daily) 2. Pre-op - use mydriatics ointment (para mag dilate ang pupil)
2. Apply over clean cotton clothing to protect skin a.​ Given every 10 minutes for 4 doses
3. Encourage ROM exercises for unaffected joints 3. Artificial lens implant (Intraocular lens)
4. Ensure correct fitting and adjustment (too tight = impaired
circulation) Glaucoma

Remember: Braces are for long-term support, not immediate Increased IOP > optic nerve damage (nacocompress ang
fracture management nerve due to pressure) > loss of vision (irreversible)

Cause: inability of the aqueous humor to drain from the eyes.


Vision Disorders Risk factor: age and genetics
The eye is a sphere in shape. It has 3 layers:
Anterior chamber: space between cornea and iris
1. Sclera - outermost fibrous layer; white Posterior chamber: space between lens and iris
2. Choroid - middle vascular layer; brown
3. Retina - innermost layer; neural tissue; extension of the (These 2 chambers are filled with aqueous humor)
optic nerve; it is also a visual receptive layer; composed of 10
microscopic layers. Open Angle Glaucoma
a.​ Macula - central vision (macular degeneration > loss
of central vision) Painless; partial blockage of the trabecular meshwork,
b.​ Rods - night vision therefore it gradually increases the resistance; usually bilateral.
c.​ Cons - bright vision (too much light can cause
blindness) Manifestations:
1. Asymptomatic in early stage
Cornea - transparent structure that attracts light to enter the 2. Tunnel vision
3. Blurring of vision
24
PHILIPPINE NURSES LICENSURE EXAMINATION
Nursing Practice 4 Reviewer
According to the Newly TOS
MHEL, RN’25, MD’31

4. Headache
Types and Causes
Diagnostic Tests:
1. Visual field testing Rhegmatogenous Tear in the surface of retina > fluids
2. Perimetry - determine the extent of visual field from vitreous humor space is going to
3. Non-contact tonometry - puff of air is introduced to cornea subretinal space; due to trauma
and resistance is noted.
4. Goldmann Applanation Tonometry - a machine is used to Traction Retinal Fibrovascular tissues of the eyes pull
press cornea Detachment the retina away from its surface; due
5. Fundoscopy - assess condition of optic disc and note the to tumor growth
cupping.
Management: Exudative Retinal Injury eye trauma is the cause;
The goal is to decrease the IOP. Detachment It has inflammatory process or
1. Increase the uveoscleral outflow (eyedrop is the 1st line infection
intervention)
a.​ Prostaglandin Analogs - Latanoprost (side effect is Manifestations:
significant grown of eyelashes and iris discoloration) 1. Veil like or curtain like vision
b.​ Miotics - constrict the pupil 2. (+) sensation of particles floating across visual field when
2. Reduce production of aqueous humor looking at light background (SIGN OF BLEEDING)
a.​ Carbonic anhydrase inhibitors like Dorzalamide 3. Defects in visual field; areas of vision may be blank.
b.​ Topical beta blockers which is timolol
3. Health teaching for proper use of eyedrops Diagnostics
a.​ Sit upright and tilt your head back and put the 1. Color fundus photography - detects presence of retinal
eyedrop container close but do not touch the eyes. lesions
a.​ Before the procedure, pupil should be fully dilated
Surgical Management b.​ Use mydriatic eyedrop
1. Trabeculectomy - creation of new channel around 2. Indirect Ophthalmoscopy - noninvasive, utilizes hand-held
conjunctiva to facilitate drainage of aqueous humor. lens and light source to examine interior part of the eyes
3. Slit lamp examination
Closure Angle Glaucoma 4. Optical Coherence Tomography and ultrasound - method of
choice for complete retinal assessment
Acute, painful, and more dangerous. Management (Prevent further retinal detachment)
1. Maintain bed rest and application of patches
Causes: 2. AVOID eye stress, avoid jerky and sudden movement
1. Obstruction of the passage of the aqueous humor to a.​ Move gradually
trabecular meshwork and canal of schlemm > blockage of
aqueous humor Surgical Management
2. Pupillary block 1. Scleral Buckling - compression to indent the scleral wall and
attach 2 retinal layers together
Manifestations 2. Pneumatic Retinopexy - a gas bubble will be injected into
1. Rapid increase of IOP > headache, nausea, and vomiting the vitreous cavity to push the detached retina to the surface.
2. Conjunctival hyperemia 3. Cryosurgery or Retinal Cryopexy - freezing probe is applied
3. Corneal edema > hazy cornea on the surface of the sclera to cause a minimal damage >
4. Oval shaped pupil, dilated, unreactive to light and scarring that will facilitate retinal surface to reattach the
accommodation detached retina.
5. Decreased visual acuity
6. Halos around lights Post-Op Interventions
1. PREVENT increased IOP
Diagnostics: 2. WOF signs of bleeding (severe eye pain and presence of
1. Tonometry floaters)
2. Perimetry a.​ If positive report immediately to MD
3. Ophthalmoscopy - visual internal structure of eye 3. Proper positioning
4. Gonioscopy - examine anterior chamber of the eye; it a.​ AVOID coughing, sneezing, and valsalva maneuver
differentiate the open and close glaucoma. (high fiber diet)
b.​ AVOID bending head below the waist and vigorous
Management activities within 3 weeks
1. AVOID anticholinergic drugs - pupil dilation 4. Advised to take prescribed medications
2. Hyperosmotic agents (acetazolamide or diamox) 5. Follow up check ups
a.​ Decreases IOP by reducing fluid formation
b.​ Increases osmotic gradient
3. Topical ocular hypotensive agents Ocular and Orbital Trauma
a.​ Pilocarpine - cholinergic agonist (mitotic - eye drops)
b.​ Betaxolol or timolol - beta blockers
4. Analgesics Penetrating Eye Injury
5. Antiemetics
A full-thickness wound of the eyeball caused by a sharp object
Surgery
or high-velocity projectile.
1. Laser iridotomy - laser incision in the iris to release blocked
aqueous humor.
Examples: knife, glass, metal fragment, wood splinter,
explosion debris.
Retinal Detachment
Unlike blunt trauma, this actually pierces the cornea or sclera
that can cause permanent blindness
Pulls retinal cells away from the layer of blood vessels that
supply O2 and nourishment; Total loss of vision if left Manifestations
untreated; painless and ocular emergency! 1. Conjunctival laceration > severe pain
2. Hemorrhage > blood shot eye; Hyperemia
3. Marked loss of vision

25
PHILIPPINE NURSES LICENSURE EXAMINATION
Nursing Practice 4 Reviewer
According to the Newly TOS
MHEL, RN’25, MD’31

Management 3. Teach proper instillation of eye drops/ointments:


1. Never remove the penetrated foreign object a.​ DO NOT touch the dropper to eye.
2. Stabilize the object b.​ Pull down lower eyelid > instill medication.
a.​ Do not put on pressure patch on the affected eye c.​ Emphasize hand hygiene before & after touching
b.​ Avoid excessive eye movement (keep IOP [intraocular eyes.
pressure] decrease) d.​ Instruct patient not to rub eyes (prevents worsening &
3. Prevent excessive bleeding spread).
4. Topical corticosteroid (prednisone) > antiinflammatory
5. Antifibrinolytic: aminocaproic acid > stops bleeding Medical Management
6. Enucleation = complete removal of the eyeball (if needed 1. Bacterial - Topical broad-spectrum antibiotics (erythromycin
a.​ Criteria for Enucleation: ointment, ciprofloxacin drops).
-​ Extensive, irreparable damage 2. Viral - Symptomatic (cold compress, artificial tears);
-​ Light perception absent self-limiting (1–2 weeks).
3. Allergic - Antihistamine or mast-cell stabilizer eye drops
Note: Enucleation is done 2 weeks after injury to prevent (olopatadine).
sympathetic ophthalmia. 4. Severe cases - Corticosteroid drops (ONLY if prescribed by
ophthalmologist).
Splash Injury Corneal Ulcer

An ocular emergency where chemicals or foreign liquids (alkali, Open sore or lesion of the cornea > INFECTION; It cannot
acid, detergents, or other irritants) splash into the eye. easily fight off infection (it is avascular, so walang blood flow)

Considered a chemical burn of the eye; Alkali burns (ammonia, Causes:


lye, lime) are more dangerous than acids because they 1. Trauma
penetrate deeper. 2. Prolonged misuse of contact lens

Management: Manifestations
1. Immediate, continuous irrigation is needed 1. Pain
2. Redness
What can be used? 3. Foreign body sensation
1. Tap water at home 4. Increased lacrimation
2. Normal saline (0.9% NaCl, PNSS) - hospital setting 5. Increased sensitivity to light or photophobia

Other Care: Diagnostics:


1. Analgesics 1. Eye examination (Right eye, Left eye, them both eyes)
2. Tetanus antitoxin 2. Slit Lamp - specialized microscope that provides detailed
3. Antibiotics assessment of the eye structure
3. Fluorescein staining - uses contrast agent (dye) to visualize
Note: Immediate referral is necessary. blood vessels of the eye.
a.​ Advise the patient na normal lang ang golden skin
and deep yellow discoloration of urine
Infections and Inflammatory Conditions
Management
1. Urgent treatment is needed
Conjunctivitis
2. Eye patch - rest the eyes
a.​ Abrasion is starting healing within 24-48 hours
Inflammation of the conjunctiva (thin transparent membrane 3. Antibiotic eyedrop as per MD
lining eyelid & sclera); Often called “pink eye.” 4. Use protective eye shields.

Types:
Consequences of Systemic Diseases
1. Bacterial – Staphylococcus aureus, Streptococcus
pneumoniae, H. influenzae.
2. Viral – usually Adenovirus (common, highly contagious). 1. Diabetes Mellitus
3. Allergic – immune reaction to pollen, dust, etc. a.​ Disorder - diabetic retinopathy
4. Transmission: direct contact (hands, towels, eye secretions) b.​ Pathophysiology - chronic hyperglycemia >
microvascular damage in retina > capillary leakage,
Clinical Manifestations neovascularization
1. Earliest sign > Redness of the sclera (hyperemia). c.​ Visual Consequences - blurred vision, floaters (due to
2. Other signs & symptoms: vitreous hemorrhage), vision loss or blindness if
a.​ Itching (allergic type) untreated
b.​ Purulent discharge with eyelid crusting (bacterial)
c.​ Watery discharge (viral) 2. Hypertension
d.​ Gritty/foreign body sensation a.​ Disorder - hypertensive retinopathy
e.​ Mild photophobia b.​ Pathophysiology - chronic high BP > arteriosclerosis
f.​ Tearing (epiphora) of retinal vessels > retinal ischemia, hemorrhage
3. Usually no severe pain or vision loss (differentiates from c.​ Visual Consequences - narrowed arterioles (“copper
keratitis/uveitis). wiring”), retinal hemorrhages, exudates, papilledema,
blurred vision
Prevention
1. Frequent handwashing (most effective). 3. Hyperthyroidism / Graves’ Disease
2. Avoid sharing towels, pillowcases, cosmetics. a.​ Disorder - thyroid eye disease (exophthalmopathy)
3. Proper contact lens hygiene (no overnight use, use sterile b.​ Pathophysiology - autoimmune inflammation of orbital
solutions). tissues
4. Isolation from school/work until 24 hrs after starting c.​ Visual Consequences - proptosis (bulging eyes),
antibiotics (bacterial). diplopia (double vision), corneal exposure
(ulceration) and possible optic neuropathy (vision
Nursing Interventions loss)
1. Apply warm compresses for bacterial conjunctivitis >
loosens crusts. 4. Autoimmune Diseases (SLE, RA)
2. Apply cool compresses for allergic conjunctivitis → relieves a.​ Disorder - retinal vasculitis, uveitis
itching. b.​ Pathophysiology - immune-mediated inflammation of
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PHILIPPINE NURSES LICENSURE EXAMINATION
Nursing Practice 4 Reviewer
According to the Newly TOS
MHEL, RN’25, MD’31

ocular vessels Problems occur if:


c.​ Visual Consequences - blurred vision, photophobia, 1. Overproduction of cerumen
redness, and risk of permanent vision loss if untreated 2. Narrow or tortuous ear canal
3. Improper cleaning (cotton buds push wax deeper) leads to
5. Chronic Kidney Disease conductive hearing loss.
a.​ Disorder - uremic retinopathy
b.​ Pathophysiology - toxin accumulation > vascular Clinical Manifestations
damage > retinal edema and hemorrhage 1. Hearing loss (conductive, gradual)
c.​ Visual Consequences - blurred vision and visual field 2. Ear fullness or pressure
defects 3. Itching of ear canal
4. Tinnitus (ringing in the ear)
6. Infectious Diseases (e.g., HIV/AIDS, Syphilis) 5. Dizziness/vertigo (sometimes)
a.​ Disorder - opportunistic ocular infections 6. Pain (if secondary infection present
b.​ Examples: CMV retinitis > floaters, blind spots, vision
loss or Ocular syphilis > uveitis, retinal lesions Nursing Interventions
1. Assess degree of hearing loss, otoscopic exam (if trained).
2. Educate about proper ear hygiene, avoid self-trauma.
7. Nutritional Deficiencies 3. Prepare patient for cerumen removal:
a.​ Disorder - Vitamin A deficiency a.​ Cerumenolytics before irrigation (to soften wax).
b.​ Pathophysiology - impaired photoreceptor function b.​ Irrigation with warm saline (unless perforated
c.​ Visual Consequences - night blindness (nyctalopia), tympanic membrane suspected).
xerophthalmia > corneal ulceration and blindness c.​ Manual removal by physician (curette, suction).
4. Monitor for pain, vertigo, bleeding, or signs of otitis externa
after removal.
Hearing and Balance
5. Provide reassurance: hearing usually returns after wax
removal.
Anatomy of the Ear
The ear is divided into three main parts: external, middle, and Medical Management
inner ear. Each has structures and functions essential for 1. First-line:
hearing and balance. a.​ Cerumenolytics (carbamide peroxide, hydrogen
peroxide, mineral oil, glycerin) > softens wax.
1. External Ear b.​ Definitive treatment (Gold standard) - Irrigation with
Components: warm saline (if tympanic membrane is intact).
a.​ Auricle (pinna) - collects sound waves, directs them 2. Alternative: Manual removal (curette, suction, forceps) by
to ear canal ENT.
b.​ External auditory canal - 2.5–3 cm; channels sound
to tympanic membrane; contains ceruminous glands
Otitis Externa
(earwax)
(Outer Ear)
c.​ Tympanic membrane (eardrum) - thin, semi
transparent membrane; vibrates in response to sound
waves Infection of outer ear or inflammation of external auditory canal

Function: Sound collection & initial transmission Common causes:


1. Bacteria - pseudomonas; staphylococcus aureus
2. Middle Ear (Tympanic cavity) 2. Trauma to ear canal - when cleaning the ear
Components: 3. Stagnant water in the ear canal (swimmer’s ear)
a.​ Ossicles (smallest bones in body):
-​ Malleus – attached to tympanic membrane
Acute Otitis Media
-​ Incus – connects malleus to stapes
(Middle Ear)
-​ Stapes – connects to oval window of inner
ear
b.​ Eustachian tube - connects middle ear to Middle ear infection
nasopharynx; equalizes pressure
c.​ Oval window & round window - transmit vibrations to Common causes:
inner ear 1. Bacteria - Staphylococcus aureus, streptococcus
pneumoniae and haemophilus influenzae
Function: Amplifies sound waves; protects inner ear via
pressure equalization Complications:
1. Mastoiditis - difficult to treat; red, dull, and thick tympanic
3. Inner Ear membrane
Components: Note: Antibiotics cannot penetrate the bony structure of the
a.​ Cochlea - spiral-shaped; contains organ of Corti → mastoid; therefore, the treatment is mastoidectomy or
converts sound vibrations into nerve impulses tympanoplasty
(hearing) Manifestations of Otitis Externa and Media:
b.​ Vestibule - central part; detects linear acceleration 1. Ear pain or otalgia
(balance) 2. Foul smelling ear discharge
c.​ Semicircular canal - detect rotational movement 3. Muffled hearing > decrease hearing acuity
(balance) 4. Temporary hearing loss
d.​ Vestibulocochlear nerve (CN VIII) - transmit hearing & 5. Hyperthermia
balance info to brain
REMEMBER: Lie on the affected ear (promote drainage or
Function: Hearing & equilibrium secretions)

Nursing Interventions for EARDROPS


Cerumen Impaction
1. Clean the outer and remove any debris that may cause
(Outer Ear)
obstruction
2. Put the patient in unaffected ear
Accumulation of earwax (cerumen) that blocks the external 3. Hold the bottle for 1-2 minutes before instilling eardrops to
auditory canal; Normally, cerumen protects/lubricates the ear provide warm
canal & traps debris. 4. Gently pull the outer ear
5. Drop medication in ear canal
6. Press tragus in pumping motion
27
PHILIPPINE NURSES LICENSURE EXAMINATION
Nursing Practice 4 Reviewer
According to the Newly TOS
MHEL, RN’25, MD’31

7. Let the patient be still in 5 minutes of the patient first before talking; DO NOT shout and
exaggerate the movement of lips when talking.
REMEMBER: If the patient is 3 years old or below, pull the
pinna down and backward; if above 3 years old, pull the pinna
up and backward. Conductive Sensorineural

Air conduction from middle Sound waves in both air and


Otosclerosis and inner ear is impaired bone is impaired
(Middle Ear)
Sounds on the affected ear Sounds reaching affected
Abnormal growth of bone tissue near the middle ear appears louder ear will be perceived to be
(progressive hearing loss that may lead to deafness); usually lesser than unaffected ear
affected are young adults male Causes:
1. Diseases in the middle Causes:
Cause: ear such as otosclerosis and 1. Inner ear disease
1. Development of bone tissue near the stape (it vibrate to otitis media 2. Damaged cochlear nerve
transmit sounds to inner ear) > immobile stape > stiffening and 2. Outer ear obstruction
fixation (Cerumen Impaction)
Risk Factors:
1. Family history
2. Temporal bone fracture (abnormal bone remodelling) Weber Test Rinne Test

Manifestations: Uses bone conduction to Air conduction is greater


1. Decrease hearing acuity test lateralization of sounds than bone conduction
2. Conductive hearing loss
A vibrating tuning fork is 2 position of tuning fork
Surgical Management placed on the patient’s head (shifting):
1. Stapedectomy - surgical removal of stapes; with or forehead. 1. 2 inches from the opening
Fenestration - implanting titanium prosthesis of ear canal (AC)
Normal: sounds should be 2. Against the mastoid bone
Complication is facial nerve damage heard equally on both ears (BC)
Sensorineural hearing
Post operative management loss - kapag mas malakas Normal: dapat mas malakas
1. Avoid getting the wound wet sa unaffected side sa AC kaysa sa BC
2. Avoid anything that increases the pressure such as blowing Conductive hearing loss - Conductive hearing loss -
of nose, coughing, bending the hips, and valsalva maneuver. kapag mas malakas ang mas malakas ang BC sa AC
sound sa affected side
Meniere’s Disease
(Inner Ear)
Also called Endolymphatic Hydrops; (+) recurrent attacks

Labyrinth - balance system connected to cochlea with 3


semicirculars canal filled with fluid which is endolymph
responsible for sending head directions.

Endolymph - specialized fluid around the inner ear that fills


membranes of labyrinth; it detects sound and maintains
balance.

Causes of meniere’s disease:


1. Excessive endolymph in the labyrinth > increasing pressure
> disruption of sensory signals > damaged
vestibulococchlear nerve

Manifestations:
1. Feeling of fullness around the ear
2. Imbalance - priority is safety
3. Meniere’s triad
a.​ Vertigo
b.​ Tinnitus
c.​ Sensorineural hearing loss
Medical Management:
1. Diuretic
2. Antiemetics (promethazine)
3. Vestibular suppressants (meclizine, diphenhydramine, and
diazepam)

Interventions (Health Education)


1. Non-stimulating environment
2. Limit sodium intake
3. Limit fluid intake
4. AVOID
a.​ Rapid head movement
b.​ Ambulation
c.​ Flickering lights
d.​ Driving
e.​ Anything that increases ICP

Hearing Disorder
Talk to the patient in front and at normal pace; Get the attention
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