NURSING CARE OF CLIENTS WITH DIGESTIVE PROBLEMS

GASTROINTESTINAL TRACT
MOUTH
o Ingestion and mastication
PHARYNX
o Passageway for air, food, fluids
EPIGLOTTIS
o Flap the open and closes to prevent food or fluids enter the trachea
ESOPHAGUS
o Secretes mucus, passageway and facilitates movement of food
STOMACH
o Temporary storage
o Break down food by churning & churning to turn it into CHYME consistency (heavy
cream)
● Parts:
○ Lower Esophageal or Cardioesophageal sphincter
○ Fundus
○ Body
○ Pylorus
○ Pyloric Sphincter
○ On the gastric lining:
- Gastric Pits
- Gastric Glands
- Intestinal Cells
- Parietal cells - produces and secretes gastric juice HCL acid (pH1) and Intrinsic
Factors (Vit. B12 binding protein)
- Mucous Neck Cells - production of sticky mucus and clings to mucosa as
protection from HCL and digestive enzymes.
- Chief cells - production of protein-digesting enzymes (Pepsin)

SMALL INTESTINE
●Chemical digestion
● Absorption of nutrients, vitamins, electrolytes
● Parts:
○ Duodenum
○ Pancreatic Duct
■ Pancreas - secretes pancreatic enzymes
■ Trypsin - breakdown protein
■ Amylase - starch
■ Lipase - fats
 ■ Alkaline in pH because of high concentration of bicarbonate, alkaline pH help
neutralize acid
○ Ampulla of Vater
○ Common Bile Duct
■ Gallbladder - stores and secretes bile
● Emulsify fats
● Absorbs fats and fat soluble Vits (ADEK)
■ Liver - Produces Bile
● Yellow to green fluid containing bile salts, bile pigments (Bilirubin),
cholesterol
○ Jejunum
○ Ileum
■ Ileocecal valve

2 TYPES OF CONTRACTIONS
1. Peristalsis
- propels contents toward the colon
2. Segmentation
- produces mixing waves that move contents back and forth in churning motion

LARGE INTESTINE
● Water and Na Ion absorption temporary storage of fecal matter; Elimination.
● Parts:
○ Ileocecal Valve
○ Cecum
○ Appendix
○ Colon
- Ascending
- Transverse
- Descending
○ Sigmoid
○ Rectum
○ Anal canal, internal and external sphincter

Components Of Large Intestine:

● Bacteria, assist in completing the breakdown of the waste materials (undigested / unabsorbed
proteins and bile salts)
● 2 types of colonic secretions:
1. Bicarbonate solution – to neutralize.
2. Mucus – protects the colonic mucosa.
Peristalsis:
● Slow and weak – move the colonic components.
● Intermittent and strong propel contents for considerable distance.
WASTE PRODUCT OF DIGESTION
● FECES consist of:
o Undigested food
o Inorganic materials
o Water
o Bacteria
● Brown color – results from the breakdown of bile by the intestinal bacteria.
● Fecal odor is chemically formed by the intestinal bacteria.

ACCESSORY DIGESTIVE ORGANS

Teeth
Salivary glands
● Secretes 1.5L of saliva a day to lubricate and facilitate swallowing.
● Contains mucus, water, enzyme, ptyalin or salivary amylase to break down starches.
- Parotid
- Submandibular
- Sublingual
Pancreas
Liver / Gallbladder
● Metabolism of CHON, CHO, and FATS
● Secretes bile
● Detoxifies various substances (drug and hormones)
● Vitamin metabolism – stores vit. A, B, K, and B12

HEALTH HISTORY
● Collection of subjective data
● Nursing health history
1. Present health concern
2. Past health history
3. Family history
4. Lifestyle and health pattern
PRESENT HEALTH HISTORY
➔ To help elicit information about the current symptoms: Use COLDSPA mnemonic as your
guide.
● CHARACTER – Describe the sign or symptom
e.g. - Abdominal pain
- Dyspnea
- Intestinal gas
❖ BELCHING – expulsion of gas from stomach to mouth.
❖ FLATULENCE – expulsion of gas from the rectum.
- Nausea & Vomiting
- Change in bowel habits and stool characteristics.
● ONSET – when it is started?
● LOCATION – Where? Radiating?
● DURATION – How long it last? Recurring?
● SEVERITY – mild, mod, severe? Pain scale.

TYPES OF ABDOMINAL PAIN

1. Visceral Pain
● Caused by distension hollow organs or stretching of solid organs
● Description: Crampy, Achy, Dull, Burning, Colicky, Poorly Localized.
● Onset: Gradual
2. Parietal Pain
● Caused by inflammation or irritation of parietal peritoneum e.g. appendicitis, peritonitis
● Description: Sharp, stabbing pain, Steady and severe, Tenderness, Guarding, Rigidity,
Rebound, Well Localized.
● Onset: Sudden

REFERRED ABDOMINAL PAIN:

- Pain occurs, travels or refers from the primary site
and becomes highly localized at DISTANT SITES

PAST HEALTH HISTORY

● Any gastrointestinal disorder or conditions in the past?
● Had any infections?
● Had any abdominal surgery or trauma?
● Taking any prescribed or OTC medications?
FAMILY HISTORY
● Any history of GIT diseases or disorders in the family?
LIFESTYLE AND HEALTH PRACTICES
● Alcohol consumption and cigarette smoking
● Coffee and food preferences and consumption
● Activities, exercises, stress level
Key Points For Assessment:
● Explain each aspect of the examination to ease anxiety level and obtain cooperation.
● Provide privacy.
● Position on supine with knee flexed
● Sequence of the abdominal assessment; not to alter
● Patterns of bowel sounds.
- Inspection
- Auscultation
 - Percussion (use diaphragm of the stethoscope)
- Palpation
● Void first (distended bladder interfere accurate examination)
● Observe verbal and non – verbal cues.

INSPECTION
OBSERVE COLORATION OF SKIN
● Redness, Pale, Yellowish, Bruises, Hematoma
- Inspect for stretch marks/scars (ask the source of scar, measure the length, document the
location and appearance of scar)
● Nonhealing, redness, inflamed, keloids
- Assess for lesions and rashes
● Changes in mole size, color, border symmetry, wounds
- Inspect the umbilicus
● Purple or bluish discoloration around umbilicus (Cullen’s Signs)
- Indicate intra-abdominal bleeding, deviated, everted
INSPECT ABDOMINAL CONTOUR
● Distended or generalized protuberant from obesity, air or fluid accumulation, scaphoid
(sunken) seen with severe weight loss
- Assess abdominal symmetry
● from organ enlargement, large masses, bulging of abdominal wall from hernia, bowel
obstruction
- Inspect abdominal movement when breathing
● Diminished abdominal respiration
- Observe aortic pulsation
● Exaggerated pulsation with abdominal aortic aneurysm
- Observe for peristaltic wave
REGIONS AND QUADRANTS OF ABDOMEN
 ORGANS PER QUADRANT CONDITIONS PER REGION

NATURE OF VOMITUS

DIARRHEA
Causes:
● Infectious agents (Escherichia coli, Salmonella, Shigella,Campylobacter, Glardia, Amoeba,
Clostridium difficile, Cyclospora, Cryptosporidium, Rotavirus)
● Food poisoning
● Drugs (antibiotics, magnesium)
● Fecal impaction
● Bowel disease (irritable bowel syndrome, ulcerative colitis)
● Malabsorption syndromes (lactose Intolerance, Celiac sprue, fat malabsorption)
● Short bowel syndrome
Characteristics Of Stool:
1. Appearance
● Tarry black (melena) - Upper GI bleed
● Bright red blood - Lower GI bleed
● Blood streaking on surface of stool or on toilet paper - Lower rectal or anal bleeding
2. Other characteristics with specific problem
● Bulky, greasy, foamy, foul smelling, gray with silvery sheen-steatorrhea (fatty stool)
● Light gray "clay colored" (due to absence of bile pigment, acholic)-biliary obstruction
● Mucus or pus visible-chronic ulcerative colitis
● Small, dry, rocky-hard masses-constipation obstruction
● Marble-sized stool/ pellets-spastic colon syndrome

DYSPHAGIA (DIFFICULTY IN SWALLOWING)

➔ onset (acute or gradual), intermittent, continuous

CONSTIPATION
➔ frequency, consistency, color, blood/mucus, size. Change in bowel habits, diet.
➔ CAUSES:
● Inadequate fluid intake psychological factors
● Electrolyte imbalances
● Hormonal abnormalities
● Mechanical bowel obstruction, ileus
● Drugs (laxative abuse, anticholinergic agents, opiates)
● Loss of innervation (Hirschsprung's disease)
● Neuromuscular (paralysis, spinal cord injury or sacral lesion, multiple sclerosis)
● Anorectal disorders (hemorrhoids, fecal impaction, cancer, abscess, fissures)

DISORDER OF THE MOUTH

STOMATITIS
➔ Inflammation of the oral cavity
➔ Types:
1. Primary
- APHTHOUS STOMATITIS or canker sores
- Most common type
- Benign and non-contagious
2. Secondary
- Candidiasis or oral thrush
- May be due to overgrowth of normal flora
Etiology:
● Infection e.g. herpes zoster or cytomegalovirus,
syphilis etc.
● Allergy to coffee, potatoes, cheese, nuts, citrus fruits
● Vitamin deficiency eg. Vitamin B folate, zinc and iron
● Systemic disease e g. HIV chronic renal failure,
inflammatory bowel disease
● Irritants eg. tobacco and alcohol
● Chemotherapy and Radiation
● Trauma
● CANKER SORES- whitish gray center and erythematous ring
● Whitish plaque-like lesion, appears red and sore when wipe away - COMMON IF WITH
CANDIDIASIS
● Dysphagia
● Dry or hot sensation on area of lesions
● Elevation of temperature - RARE
● Pain
Laboratory Assessment
● COMPLETE BLOOD COUNT- may reveal INFECTION.
● CYTOLOGIC CULTURE and GRAM STAIN TESTING - to identify the CAUSATIVE
MICROORGANISM
Nursing Care:
● Provide ORAL CARE EVERY 2 HOURS and twice at night
● Use SOFT-BRISTLED TOOTHBRUSH OR FOAM SWABS to stimulate gums and
clean the oral cavity
● Use SODIUM BICARBONATE solution (baking soda), WARM SALINE or
Chlorhexidine 2% aqueous mouth wash in rinsing the mouth Avoid
COMMERCIAL MOUTHWASHES
● Provide SOFT, BLAND and NON ACIDIC foods
● Apply TOPICAL ANALGESICS or ANESTHETICS as prescribed
● Administer prescribed medication

DRUG THERAPY
TYPES OF STOMATITIS DRUG CONSIDERATIONS
General Tetracycline Syrup USUAL DOSE –
2500mg/10ml for 10 days
INSTRUCTION: rinse for 2
mins then swallow
Herpes Simplex Acyclovir (Zovirax) USUAL DOSE – 5mg/kg for
1 hour IV q 8hr
INSTRUCTION: make sure
client has no renal problem
Fungal Nystatin (Mycostatin) USUAL DOSE – 600,000
units QID oral suspension
Anti-Inflammatory Agents and Immune Modulators
● Triamcinolone in Benzocaine
● Dexamethasone
● Amlexanox
●Amlexanox
●Thalidomide
Symptomatic Topical Agents For Pain
● Benzocaine
● Camphor phenol
● 15 ml 2 % viscous Lidocaine gargle of mouthwash every 3 hours ( maximum of 8 doses per
day)

DISORDER OF THE GASTROINTESTINAL SYSTEM (DISORDERS OF THE

ESOPHAGUS)

GASTROESOPHAGEAL REFLUX DISEASE (GERD)

● BACKWARD FLOW (reflux) of gastrointestinal contents into the esophagus
● MOST COMMON upper GI disorder
● common in PEOPLE OVER AGE 45
● Considered a disease process when acid is excessive and causes undesirable symptoms such as
pain and respiratory distress

Cause:
● INAPPROPRIATE RELAXATION of lower esophageal sphincter or inability of the
LES to close fully
Predisposing Factors:
● Ingestion of LARGE INTESTINE
● Condition associated with DECREASED GASTRIC EMPTYING
● Recumbent or SUPINE positioning after eating.
● Insertion of nasogastric tube (NGT)
● INCREASED INTRAABDOMINAL and INTRAGASTRIC PRESSURE e.g.
pregnancy, wearing of tight belts, obesity, bending over, ascites
Factors That Relax Lower Esophageal Sphincter
● Fatty foods, Chocolates
● Caffeinated beverages
● Citrus fruits, tomatoes and tomato products
● Alcohol
● Nicotine in cigarette smoke
● High levels of estrogen and progesterone
 ● Medication e.g calcium channel blockers (calcibloc,anticholinergic drugs ( AS04)

Subjective Data:
● HEARTBURN - suggest reflux.
● DYSPHAGIA - suggest narrowing of lumen.
Objective Data:
● Dyspepsia - MOST COMMON SYMPTOM; occurs 30-60 minutes after meals and
with reclining position.
● Regurgitation- with sour or bitter taste
● Hypersalivation
● Dysphagia
● Odynophagia- sharp substernal pain on swallowing
● Eructation (belching)
● Pyrosis- burning sensation in the esophagus.
● Chronic cough
● Aspiration pneumonia
● Respiratory Distress
Diagnostic Tests
● 24-hour ambulatory esophageal pH monitoring-most accurate method allows for
observation of the frequency of reflux episodes and their associated symptoms
● Upper endoscopy
● Esophageal manometry (measures the rhythmic muscle contractions
● (peristalsis) that occur in esophagus when swallowing)
Diet Therapy
● Avoid CAFFEINATED AND CARBONATED foods.
● Avoid SPICY and ACIDIC FOODS
● SMALL FREQUENT FEEDINGS (4-6 small meals)
● Avoid food 3 hours before going to bed.
● Standing, Sitting or High Fowler’s position after eating
Lifestyle Changes
● ELEVATED HEAD OF THE BED 6-8 inches for sleep
● DO NOT LIE DOWN 3-4 hours after eating.
 ● Avoid NICOTINE and ALCOHOL
● LOSE WEIGHT- if the patient is obese.
● Avoid CONSTRICTIVE CLOTHING, STRAINING or BENDING OVER.

Drug Therapy
ANTACIDS
● GENERIC NAME: Aluminum or Magnesium Hydroxide
● BRAND NAMES: Maalox, Mylanta
● INDICATION: management of heartburn
● ACTION: elevates gastric pH and deactivates pepsin
● SIDE EFFECTS: constipation and diarrhea
● CLIENT INSTRUCTIONS: take the antacid 1 hour before and 2-3 hours after meals.

HISTAMINE RECEPTOR ANTAGONISTS

Drug Names:
● famotidine (Pepcid)
● ranitidine (Zantac)
● cimetidine (Tagamet)
● nizatidine (Axid)
INDICATION: management of heartburn
ACTION: suppresses secretion of gastric acid by blocking the histamine receptor sites
DRUG INTERACTION: CIMETIDINE may have significant interactions with WARFARIN,
THEOPHYLLINE, PHENYTOIN, NIFEDIPINE and PROPRANOLOL

PROTON PUMP INHIBITORS

Drug Names:
● omeprazole (Priolosec)
● lansoprazole (Prevacid)
● rabeprazole (Aciphex)
● pantoprazole (Protonix)
● esomeprazole (Nexium)
INDICATION: management of heartburn
ACTION: inhibits gastric acid secretion by blocking enzymes associated with the 30-60 minutes
before meals final stage of acid production
CLIENT INSTRUCTIONS: should be taken 30-60 minutes before meals
Other Drugs:
METOCLOPRAMIDE (Plasil) (GI stimulant) antiemetic
● ACTION- increase rate of gastric emptying and relaxation of the pyloric sphincter
● ADVERSE EFFECTS- fatigue, anxiety, ataxia and hallucinations
SURGICAL MANAGEMENT
LAPAROSCOPIC NISSEN
FUNDOPLICATION (LNF)
● WRAPPING AND ANCHORING
fundus around the lower esophageal sphincter

Nursing Care After Surgery:

● Elevate the head of the bed at least 30 degrees to lower the diaphragm and facilitate lung
expansion.
● Facilitate insertion of NGT to prevent excessive tightening of the fundoplication.
● Monitor drainage of NGT (should be normal yellowish green within the first 8 hours after
surgery)
● Check placement every 4-8 hours Avoid alcohol, caffeinated and carbonated foods.
● Monitor for dysphagia (sign that fundoplication is too tight).
● Monitor for gas bloat syndrome.
● Administer simethicone 80 mg QID for excessive gas as per doctor’s order.

ENDOSCOPIC THERAPIES
STRETTA PROCEDURE
● PURPOSE- to inhibit the activity of the vagus nerve.
● use of radiofrequency energy through needles to induce THERMAL BURN in the
gastroesophageal junction; tiny lesions occur initially and as it heals, it tightens the tissues and
increase muscle mass at the LES
● Lasts 45 minutes; recovery time is 1-2 days.
Procedure:
- Outpatient endoscopic procedure
- 45 minutes, conscious sedation
- Delivery of temperature-controlled
radiofrequency energy
- Significant reduction in GERD
symptoms
- Significant reduction in esophageal acid
exposure
- Low incidence of side-effects as compared to anti-reflux surgery
● Note: Based upon peer-reviewed literature evaluating each procedure separately (not compared
prospectively)
ENTERYX PROCEDURE
● PURPOSE: to tighten the lower esophageal sphincter
● INJECTION OF SOFT, SPONGY PERMANENT IMPLANT made of liquid polymeric
material into the LES muscle
Patient Care After Endoscopic Therapies
● Maintain on CLEAR LIQUIDS for 24 hours
● After the DAY 1-shift to SOFT DIET such as custard, pureed vegetables, mashed potatoes
● Avoid NSAIDs and ASPIRIN for 10 days Give LIQUID MEDICATIONS as much as possible
● Avoid NGT INSERTION for at least 1 month.
● Watch out for CHEST or ABDOMINAL PAIN, BLEEDING, DYSPHAGIA, SHORTNESS
OF BREATH, NAUSEA of VOMITING.

HIATAL HERNIA
➔ opening in the diaphragm through which the esophagus passess becomes enlarged and part of
the upper stomach moves up into the lower portion of the thorax
➔ Occurs more often in women than in men
2 TYPES OF HIATAL HERNIAS
● TYPE 1 - Sliding occurs when the upper stomach and the gastroesophageal junction are
displaced upward and slide in and out of the thorax
● Para esophageal occurs when all of the part of the stomach pushes through the diaphragm
beside the esophagus
Clinical Manifestations
● Pyrosis
● Regurgitation
● Dysphagia
● Intermittent epigastric pain
● Fullness after eating
● Large hiatal hernia Intolerance to food, nausea and vomiting
● X ray
● Barium enema
● Esophagogastroduodenoscopy
● Esophageal manometry
● Chest CT scan
Management
● Frequent small frequent feeding
● Not to recline 1 hr. after eating Elevate head of the bed 4-8 inches.
● Surgical Hernia repair for patient with gastric outlet obstruction or suspected strangulation:
Post operative report immediately belching, vomiting, gagging, abdominal distention and
epigastric chest pain.

DISORDER OF THE STOMACH AND SMALL INTESTINE (DISTURBANCES IN

DIGESTION)
GASTRITIS
➔ inflammation of the stomach mucosa
Classification:
● Acute - includes erosive gastritis and stress ulcers
● Chronic - includes non- erosive gastritis.
Types Of Chronic Gastritis
● TYPE A - inflammation of the glands in the fundus
and body
● TYPE B - inflammation of the glands from fundus
to antrum
● Atrophic – diffuse inflammation and destruction of
deeply located glands.

ETIOLOGY
ACUTE GASTRITIS
 local irritants (drug, alcohol,
corrosive substances)
 bacterial invasions by
salmonella, E. Coli and H. pylo
CHRONIC GASTRITIS
 may occur due to bile acid
reflux (complication of gastrojejunal
surgery or peptic ulcer disease)
 chronic use of irritants

PATHOPHYSIOLOGY

ILLUSTRATION OF MALDIGESTION CHRONIC GASTRITIS

ACUTE GASTRITIS CHRONIC GASTRITIS

 Rapid onset of epigastric pain  Vague epigastric pain
 Pain not relieved by food  Pain relieved by food
 Anorexia  Anorexia
 Nausea and vomiting  Nausea and vomiting
 Dyspepsia  Intolerance of fatty or spicy
 Gastric hemorrhage food
 Hematemesis  Pernicious anemia
Diagnostic Test
➔ Esophagogastroduodenoscopy with biopsy
Drug Therapy
● H2 Receptor Antagonists
● Antacids
● Proton Pump Inhibitors
● Vitamin B12 (if there is pernicious anemia)
● Triple therapy (if there us H. Pylori in bipsy)
○ 1 Bismuth subsalicylates or proton pump inhibitor (omeprazole)
○ 1 Antibiotic (metranidazole)
○ 1 Antibiotic (tetracycline, clarithromycin, amoxicillin)
● DRUGS TO AVOID- aspirin, ibuprofen.
● Instruct client to limit intake of goods and spices that cause distress e.g. tea, cola, chocolate,
mustard, pepper, and hot spices.
● Instruct client to avoid alcohol and tobacco.
● Give soft, bland diet and smaller, more frequent meals.
Stress Reduction
● Progressive muscle relaxation
● Cutaneous stimulation
● Guided imagery
● Distraction
Surgical Management
● partial / total gastrectomy
● Pyloroplasty- surgery to widen the
opening in the lower part of the
stomach (pylorus) so that the stomach
contents can empty into the small
intestine.
● Vagotomy- surgical procedure that
involves resection of the vagus nerve to reduce acidity of the stomach.

PEPTIC ULCER DISEASE

● Ulceration of the gastric mucosa, duodenum and rarely the lower esophagus and jejunum
● Types
○ Gastric ulcer
○ Duodenal ulcers
○ Stress ulcers (Curling’s Ulcer or Cushing's Ulcer)- result of critical illness and severe
physical or emotional stress
❖ Curling’s Ulcer- due to hypovolemic shock
❖ Major surgery- sepsis, severe burns, and hypoxia
❖ Cushing's Ulcer- aftermath of cerebral trauma which cause stimulation of vagus and increase
Hcl production
PATHOPHYSIOLOGY

PARAMETER GASTRIC ULCER DUODENAL ULCER

Age Usually 50 years or older
Gender Male/female ration 1:1
Blood Group No differentiation
General Nourishment May be malnourished
Stomach acid production Normal secretion or
hyposecretion
Clinical course Healing and recurrence
Pain Occurs 30-60 minutes after
meal; at night rarely
PARAMETER GASTRIC ULCER
Pain Accentuated by ingestion of
food
Response to Treatment Healing with the appropriate
therapy
Hemorrhage Hematemesis more common
than melena
Malignant change Perhaps in less than 10%
Recurrence Tends to heal and recurs often
in the same location
Usually 50 years or older
Male/female ration 1:1
Most often type O
Usually well nourished
Hypersecretion
Healing and recurrence
Occurs 1.5-3hours after a
meal; at night 1-2 am
DUODENAL ULCER
Relieved by ingestion of food
Healing and appropriate
therapy
Melena more common than
hematemesis
Rare
60% recurrence in the same
year

Predisposing Factors
● Stress
● Irregular hurried meals
● Smoking and alcoholism
● caffeinated , fatty, spicy, acidic foods
● Ulcerogenic medications- Aspirin, NSAIDs, Steroids
● GI disorders- Gastritis, Zollinger- Ellison Syndrome
● Type A personality
● Type O blood
Complications
● Hemorrhage
● Perforation
● Pyloric obstruction
● Intractable Disease

ASSESSMENT:
History
● Alcohol and tobacco use
● Use of corticosteroids, aspirin, and NSAIDs
Clinical Manifestation
● Epigastric tenderness
● Rigid, board like abdomen with rebound tenderness
● Diminishing hyperactive bowel sounds
● Dyspepsia
● Vomiting
Diagnostic Tests
● Low hemoglobin and hematocrit
● Positive occult blood test
● Barium examination
● Esophagogastroduodenoscopy (most accurate)
● Elevated immunoglobulin G antibodies (suggest H.Pylori Infection)
● Fecalysis
DRUG THERAPY
Triple Therapy (most successful region)
● Bismuth compound or proton-pump inhibitor (omeprazole)
● Metronidazole
● Tetracycline or clarithromycin and amoxicillin
Hyposecretory Drugs
● Histamine Receptor Antagonists
● Proton Pump Inhibitors
● Prostaglandin Analogues
○ Misoprostol (cytotec)
○ Lower gastric secretion and higher resistance of mucosa to injury
○ CONTRAINDICATION: pregnancy
Mucosal Barrier Fortifiers
● SUCRALFATE (CARAFATE)
● Action: forms a seal over the ulcer, protecting if from irritation
● Instruction: take 1 hour before meals and at bedtime
● Side effect: constipation
Diet Therapy
● Bland diet
● Small frequent feedings (6 small meals/day)
● Avoid caffeine-containing foods (coffee, tea, or cola)
● Avoid tobacco and alcohol
Management For Hypervolemia
● Monitor vital signs intake and output
● Monitor serum electrolytes to determine need for replacement.
● Administer isotonic solutions (NSS or lactated Ringer’s).
● Perform blood transfusion as prescribed to expand blood volume.
● If there is active bleeding, administer Fresh Frozen Plasma.
● Monitor the following:
○ Signs of SHOCK (hypotension, chills, palpitations, diaphoresis, weak thready pulse)
○ Occult blood
○ Hematocrit, hemoglobin and coagulation studies
● Perform GASTRIC DECOMPRESSION OR LAVAGE.
● AVOID NSAIDs to minimize GI bleeding.
● Vasopressin (Pitressin) a vasoconstricting drug.

ENDOSCOPIC THERAPY
● Goal: Promote blood clot formation
● Methods of Endoscopic Therapy
○ Thermal Contact- heater probe or multi electrocoagulation
○ Inject bleeding site with diluted epinephrine
○ Laser therapy
○ Mechanical clip
Client Preparation
● Administer SEDATIVES e.g. midazolam and meperidine.
● Place on NPO 6 hours prior to the procedure.
Care After Procedure
● Resume diet once gag reflex is present
Management For Perforation
● Replace lost fluids, blood, and electrolytes
● Administer antibiotics
● Place on NPO
● Gastric lavage or decompression
● Monitor for signs of septic shock (fever, pain, tachycardia, lethargy, or anxiety)
Surgical Management For Obstruction
● Gastroduodenostomy (Billroth I)
● Gastrojejunostomy (Billroth II)
● Partial Gastrectomy
● Pyloroplasty enlargement of the pyloric sphincter
Client Preparation
● Insert NGT connected to suction to remove secretions and empty the stomach.
Post- Operative Care
● Monitor placement, patency, and drainage of NGT
● Monitor for Dumping Syndrome

EARLY SIGNS (WITHIN 30 MINUTES LATE SIGNS (90 MINUTES-3 HOURS

AFTER FEEDING) AFTER FEEDING)
 Vertigo  Dizziness
 Tachycardia  Light-headedness
 Syncope  Palpitations
 Pallor  Diaphoresis
 Desire to lie down  Confusion
Management For Dumping Syndrome
● Small frequent feeding.
● Do not take fluids with meals.
● Advise a high- protein, high- fat, low to moderate carbohydrate diet.
● Administer pectin to prevent syndrome.

GASTROENTERITIS
● Inflammation of the mucous membranes of the stomach and the intestinal tract.
● CLASSIC MANIFESTATION- increase in the frequency and water content of the stools or
vomiting.
Types
● VIRAL- caused by Norwalk virus or rotavirus.
● BACTERIAL- caused by E. coli, campylobacter enteritis or shigellosis.
PATHOPHYSIOLOGY

Assessment
● Nausea and vomiting (first 2 days of illness)
● Diarrhea
● Myalgia
● Headache
● Malaise
● Abdominal tenderness
Signs of Dehydration
● Poor skin turgor
● Dry mucous membranes
● Hypotension
● Oliguria

Management
● FLUID REPLACEMENT
○ Monitor vital signs, I and O and weight (1kg weight loss is equivalent to 1L loss).
○ Administer HYPOTONIC IV FLUIDS
○ (0.45% NaCI)
○ Oral Rehydration Salts (Oresol)
○ If with HYPOKALEMIA- incorporate potassium supplements
○ Observe standards precautions
● DIET THERAPY
○ IF NOT ACTIVELY VOMITING- clear liquids with electrolytes.
○ IF VOMITING- NO
○ IF TREATED- crackers, toast, and jelly.
○ IF IMPROVING- bland diet.
○ AVOID caffeine.
● DRUG THERAPY
○ Racecadotril (Hidrasec) and LOPERAMIDE (IMODIUM)- to inhibit peristalsis.
○ BISMUTH SUBSALICYLATES (PEPTO-BISMUL)- to reduce watery volume of stool
(suppresses H. Pylori and assist in healing of mucosal lesions).
○ ANTIBIOTICS
➢ NORFLOXACIN OR CIPROFLOXACIN
➢ If caused by bacteria
➢ TRIMETHOPRIM- SULFAMETHOXAZOLE (BACTRIM)
DISORDER OF THE LOWER GI TRACT (DISORDERS
OF THE GASTROINTESTINAL SYSTEM

INFLAMMATORY BOWEL DISEASES

ULCERATIVE COLITIS
● Chronic inflammatory process affecting the mucosa and submucosa of the SIGMOID COLON
and RECTUM.
CROHN’S DISEASE (REGIONAL ENTERITIS)
● Subacute or chronic inflammatory bowel disease affecting segmental areas along the ENTIRE
WALL OF THE GI TRACT; most commonly noted within the TERMINAL ILEUM.

PATHOPHYSIOLOGY

CLINICAL
MANIFESTATIONS

DRUG THERAPY
● Salicylate Compounds
○ Drug name- Sulfasalazine (Azulfidine).
○ Indication- Management of ulcerative colitis.
○ Action- inhibits prostaglandin synthesis to reduce inflammation.
○ Adverse effects- leukopenia and anemia.
○ Client Instruction
 ➢ Take the drug with a full glass of water
➢ Take the drug after meals to prevent GI discomfort.
● Oral or Intravenous Corticosteroids
○ Drug name- Prednisone
○ Indication- to reduce inflammation
○ Adverse Effects- hyperglycemia, osteoporosis, peptic ulcer disease, increased risk for
infection
● Immunosuppressive Drugs
○ Should be given in combination with steroids to be effective.
○ Drug name- cyclosporine, mercaptopurine.
○ Indication- to reduce inflammation.
○ Adverse Effects- thrombocytopenia, leukopenia, anemia, renal failure, infection, headache,
stomatitis, hepatotoxicity.
● Anti- Diarrheal Drugs
○ Diphenoxylate HCI and loperamide (imodium)
● Infliximab (Remicade)
○ Given for refractory disease or for toxic megacolon an immunoglobulin G that neutralizes
activity of tumor necrosis factor.
Diet Therapy
● If the client has severe symptoms:
○ NPO
○ Total Parenteral Nutrition (TPN)
● Avoid:
○ Whole- wheat grains
○ Nuts
○ Fresh fruit and vegetables lactose containing foods caffeinated beverages
○ Pepper
○ Alcohol smoking
Surgical Management
● Indications for Surgery
○ Bowel perforation
○ Toxic megacolon
○ Hemorrhage
○ Colon cancer
○ Failure of conventional treatment

TOTAL PROCTOCOLECTOMY WITH

PERMANENT ILEOSTOMY
➔ Terminal ileum is pulled through the
abdominal wall and forms a stoma or ostomy.

Pre-operative Care
● Administer oral or parenteral antibiotics such as neomycin sulfate (Mycifradin) as bowel
antiseptic.
● Administer laxative or edema.
Post-operative Care
● Monitor color, odor, consistency of ileostomy output (effluent).
● Instruct client to report any foul or unpleasant odor (it may indicate intestinal blockage or
infection).
● Instruct the client to wear a pouch system at all times.
● Apply a skin barrier to prevent irritation and injury to the skin.

TOTAL PROCTOCOLECTOMY WITH CONTINENT ILEOSTOMY

● Alternative to traditional ileostomy with external pouch.
● Creation of an internal reservoir called a Kock’s ileostomy or ileal reservoir to be drained
periodically.
Post-operative Care
● Monitor character and quality of effluent.
● Teach the client to drain stoma when sensation of fullness is felt.
● Apply a small dressing to keep stoma moist.

TOTAL COLECTOMY WITH ILEOANAL ANASTOMOSIS

● Removal of the colon and rectum with anastomosis of the ileum and the anal canal.

DISCHARGE INSTRUCTION FOR CLIENTS WITH ILEOSTOMY

Skin Care
● Use pectin- based skin barrier to protect skin from irritation.
● Use skin sealants and ostomy skin creams.
● Monitor skin for irritation.
Pouch Care
● Empty pouch when it is 1⁄3 full
● Change pouch at intervals such as before meals, before bedtime, before walking in the
morning, 2-4 hours after meals.
Diet
● Chew food thoroughly
● Be cautious in taking high-fiber and high-cellulose foods such as popcorn, peanuts, coconut,
string beans, shrimp and lobster, rice, skinned vegetables (tomatoes, corn and peas)
Medications
● Avoid taking enteric- coated and capsule medications
● Do not take laxative or enema.
● Contact physician of no stool ‘has passed in 6-12 hours.
DANGER SIGNS!
● Drastic increase or decrease in effluent.
● Stomal swelling, abdominal cramping, distention, and absence of drainage.
Interventions for Danger Signs
● Remove pouch.
● Lie down and assume knee-chest position.
● Begin abdominal massage.
● Apply moist towels to the abdomen.
● Drink hot tea.
● Contact the health care provider.

IRRITABLE BOWEL SYNDROME

● Also known as SPASTIC BOWEL OR MUCUS COLITIS
● Different from ulcerative colitis because there is no inflammation or ulceration present.
Risk Factors
● Emotional stress or anxiety, depression
● Diverticulitis
● Intolerance to gastric stimulants such as caffeine or
spicy foods or lactose
● Diet high in fats
● Smoking and alcohol
● CAUSE: UNKNOWN
● INCIDENCE: Common among women, Caucasians and Jewish population.
Pathophysiology and Clinical Manifestations

Diagnostic Test
● Contrast studies
● Barium enema
● Colonoscopy
● Manometry and electromyography- to study intraluminal pressure changes that generated
spasticity.
Nursing Interventions
● Administer anti-diarrheals antispasmodics, bulk-forming laxatives as ordered.
● Encourage high-fiber diet and avoid fatty and gas forming foods (carbonated beverages,
cauliflower or beans).
● Instruct client to avoid and tobacco.
● Encourage to increase oral fluids intake but should not be taken with meals because it can
result to distention.
● Instruct with meals because it can result to distention.
● Instruct on lifestyle changes (regular exercise, adequate rest periods, stress management).
● Anticholinergics and Ca channel blocker.
DIVERTICULOSIS AND DIVERTICULITIS TWO FORMS OF DIVERTICULAR
DISEASE
1. DIVERTICULOSIS
● asymptomatic multiple out-pouching of the intestinal mucos.
2.) WITHOUT INFLAMMATION DIVERTICULITIS
● Symptomatic multiple out-pouching of the intestinal mucosa WITH INFLAMMATION;
causes retention of hardened stool: 20% of patients with diverticulosis results to diverticulitis.
Incidence
● More common in older adults
● More prevalent in men
Predisposing Factors
● Diet low in fiber
● Diet high in refined carbohydrates
Complications
● Bowel perforation and peritonitis
● Bowel obstruction
● Hemorrhage
● Shock
Pathophysiology

Assessment:
● Acute onset of crampy abdominal pain in the left lower quadrant
● Abdominal distention
● Low-grade fever
● Chronic constipation with intervals of diarrhea
● Occult bleeding
● Nausea and vomiting
Diagnostic Test:
● Barium enema and colonoscopy (contraindicated if there is diverticulitis due to the danger of
perforation)
● Complete blood count - increase ESR and WBC
● Urinalysis
● CT Scan - procedure of choice & can reveal abscess.
Nursing Interventions:
● Instruct client to eat high fiber foods
● Encourage to increase fluids.
● Administer bulk laxatives and anticholinergics as prescribed.
● Encourage client to lose weight and avoid activities that increase intra-abdominal pressure
such as straining at stool (Valsalva maneuver), vomiting, lifting, bending, lifting or
● tight clothing.
Surgical Management
● Colon resection with temporary colostomy

APPENDICITIS
● Inflammation of the vermiform appendix
● More common in males 10-30 years of age
Etiology
● Obstruction by fecal impaction, kinking of the appendix,
● parasites or infections.
● Low fiber diet
● High intake of refined carbohydrates
Pathophysiology

Assessment:
● Acute abdominal pain at RLQ or
● McBurney's point (halfway between the umbilicus and the anterior iliac crest)
● Anorexia, nausea and vomiting
● Rigid and guarded abdomen
● Blumberg sign (rebound tenderness)
● Rovsign sign upon palpation LLQ pain in the RLQ increases.
● Fever (temperature of 38-38.5 °C)
● Psoas or Copes psoas or Obraztsova’s
● Sign (lateral position with right hip flexion)
● Decreased or absent bowel sound
Diagnostic Test
● WBC Count
- Leukocytosis: WBC above 10,000/mm3
- Perforation: suggested if WBC is above
● 20.000/mm3
● Increase neutrophils.
● Ultrasound may reveal enlarged appendix by at least 6mm.
● Pregnancy Test for female to rule out ectopic pregnancy.
● Urinalysis to rule out UTI or renal calculi.
● CT Scan
- Ordered if symptoms are recurrent or prolonged
- May reveal presence of fecalith
● Neuro-Spec imaging uses a technetium labeled anti-CD 15 monoclonal antibody that
selectively binds to neutrophils at the at injection site.
● Uses gamma camera.
● Diagnosis within 1 hour.
Management
● Maintain patient on NO for possible admission.
● Administer IV fluids as prescribed to prevent fluids and electrolytes imbalance.
● Maintain patient in semi-Fowler's position to prevent
● upward spread of infection.
● DO NOT GIVE LAXATIVE NOR
● ENEMA to prevent perforation of the appendix.
● DO NOT APPLY LOCAL HEAT to prevent inflammation
● and perforation.
● Instead apply COLD compress
Surgical Management
LAPAROSCOPY
● A small incision in the umbilicus is made and a small endoscope is used to visualize the
appendix.
● If diagnosis is not definitive.
LAPAROTOMY
● An open approach in which large abdominal incision is made.
APPENDECTOMY
● Removal of the inflamed appendix
● Guided with laparoscopy.
● Done with spinal anesthesia.
Nursing Care for Appendectomy
● Maintain client flat on bed for 6-8 hours.
● Monitor for return of sensation in the lower extremities.
● Maintain on NPO until peristalsis returns.
● Instruct client to ambulate after 24 hours. Tell the client that he can resume normal activities
within 2-4 weeks.

PERITONITIS
● Inflammation of the peritoneum, the serous membrane lining the abdominal cavity and
covering the viscera.
2 Types of Peritonitis
1. PRIMARY
- acute bacterial infection resulting from contamination of the peritoneum through the
vascular system.
- May occur from tuberculosis, cirrhosis, and ascites.
2. SECONDARY
- Bacterial invasion resulting from acute bacterial abdominal disorder.
- May occur from gangrenous bowel, visceral perforation, bile leakage, blunt or penetrating.
Trauma (gunshot wound).
Pathophysiology

Clinical Manifestation
● RIGID, BOARDLIKE ABDOMEN (CLASSIC SIGN)
● Abdominal pain diffuse and becomes localized near the site of inflammation.
● Distended abdomen'
● Nausea, anorexia, and vomiting
● Diminishing bowel sounds
● Inability to pass flatus or feces.
● Rebound tenderness in the abdomen.
● High fever
● Dehydration
● Oliguria
● Hiccup’s
Diagnostic Assessment
● ELEVATED WBC: 20,000/MM?
● Hgb and Hct may be low.
● Altered levels of K+, Na +. CI -
● Abdominal x-ray may show free air and fluid in the peritoneum.
● CT Scan or ultrasound - changes in abdominal organs
● Peritoneal Lavage may reveal the following:
- WBC: 500/ml
- RBC: 50,000/ml
● Gram stain: (+ bacteria
- Culture reveals: E. coli, klebsiella, proteus, pseudomonas. If untreated can result to septic
shock and death
Management
● Administration of the following as prescribed.
 - IV fluids to replace lost fluids (isotonic)
- Broad spectrum antibiotics
- Oxygen if there is dyspnea due to ascites
● Analgesics (meperidine or morphine)
- Antiemetics (metoclopramide)
● Monitor daily weight, intake and output to monitor fluid status.
● Side lying with knees flexed to lessen pain.
● NGT insertion to decompress the stomach and intestine.
● Maintain client on NPO.
Surgical Management
● Abdominal surgery guided by exploratory laparotomy.
● Appendectomy if there is appendicitis.
● Colon resection with or without colostomy if there is bowel perforation.
Nursing Care After Surgery
● Maintain patient in SEMI-FOWLER'S POSITION to promote drainage of peritoneal contents
and allow adequate lung expansion.
● Perform PERITONEAL IRRIGATION as prescribed
● Check for presence of abdominal distention or pain (suggestive of irrigate retention)
● Assess incision, dressing and drains.
● Instruct client to AVOID LIFTING for at least 6 weeks.
Complications
● Sepsis- major cause of death
● Wound evisceration and dehiscence.

HEMORRHOIDS
● Dilated and painful veins in the rectum, anal canal, inside or outside the anal sphincter.
Classifications
● Internal- hemorrhoids ABOVE the anal sphincter.
● External- hemorrhoids BELOW the anal sphincter.

Risk Factors
● Familial tendency
● Straining at stool
● Prolonged sitting or standing
● Pregnancy, prolonged labor
● Obesity
● Portal hypertension
● Anal intercourse
● Colon malignancy
Pathophysiology

Assessment
● Bleeding with defecation of hard stool and pain – due to stretching and irritation of mucosa.
● External hemorrhoids- extreme pain due to thrombosis and edema; appear reddish blue lump.
● Internal hemorrhoids- not usually painful, until it bleeds & prolapse when enlarged; some
protrude during defecation and retracts after defecation.
Diagnostic Test
● Digital rectal examination
● Sigmoidoscopy
● Colonoscopy rules out colorectal CA
Nursing Interventions
● Instruct client on the importance of HIGH-FIBER DIET and INCREASED FLUID INTAKE.
● Instruct client to take STOOL SOFTENERS and use ointments such as dibucaine, anti-
inflammatory, or astringents medication that causes contraction or constriction of tissues).
● Apply ICE PACKS for several hours followed by warm packs.

Surgical Management
● HEMORRHOIDECTOMY- removal of hemorrhoid- Internal and external packing secured
by a T-binder.
● Cryosurgery - application of extreme low temperature to destroy or remove diseased tissue
(prolonged wound healing)
● Rubber band ligation- internal hemorrhoids (anoscope & small rubber band).
Pre-operative Care
● Advise low residue diet.
● Administer stool softeners.
Nursing Care After Hemorrhoidectomy
● Watch out for bleeding.
● Place the client in PRONE OR SIDE-LYING POSITION
● Administer analgesics as prescribed.
● Administer stool softeners.
● Offer warm Sitz baths 3-4 times a day.

DISORDER INVOLVING THE ACCESSORY ORGANS DISORDERS OF THE

GASTROINTESTINALSYSTEM

CHOLELITHIASIS AND
CHOLECYSTITIS
● CHOLELITHIASIS- STONE FORMATION in the gallbladder and accessory ducts.
● CHOLEDOCHOLITHIASIS- stone formed at the Common Bile Duct.
● CHOLECYSTITIS- INFLAMMATION of the gallbladder.
Risk Factor:
● Female gender
● Fat (Obesity)
● Fair (Caucasian)
● Forty (age)
● Fertile (multigravida; use of contraceptive pills)

Pathophysiology

S/sx:
Diagnostic Test
ULTRASONOGRAPHY
● Dx.procedure of choice. Accurate, can be used even if pt liver dysfunction and jaundice. 95%
stone detection
ENDOSCOPIC RETROGRADE CHOLANGIOPANCREATOGRAPHY (ERCP)
● Visualization of gallbladder, cystic duct, common hepatic duct, and common bile duct.
IV CHOLANGIOGRAM
● Radiographic image of the bile ducts that is obtained by cholangiography.
● Prolonged Prothrombin time
● CBC – leukocyte

CHOLECYSTOGRAPHY
● (gall bladder imaging)
Types Of Cholecystography:
1. ORAL - done 10 HOURS after administration of contrast medium
2. INTRAVENOUS - done 10 MINUTES after administration of contrast medium.

ORAL CHOLECYSTOGRAPHY
➔ radiographic examination of the gallbladder.
Purposes Of Oral Cholecystography
1. To defect gallstones
2. Assess the ability of the gallbladder to fill, concentrate and store a dye like, iodine - based
radiopaque contrast medium.
Nursing Interventions
● Administer MEPERIDINE HCL (drug of choice) as prescribed for pain relief.
● AVOID ADMINISTERING MORPHINE!!!
- it may cause spasm of the sphincter of Oddi
● Use BAKING SODA or CALAMINE-CONTAINING LOTIONS for pruritus.
● Encourage LOW-FAT DIET
● Administer BILE SALTS such as Chenodeoxycholic acid (chenodiol)or Ursodioxycholic acid
(UDCA) ursodiol.
 - Used to dissolve gallstones.
Surgical Management:
➔ Cholecystectomy
Preoperative Nursing Care:
● Administer IV fluids to replace electrolytes.
● Administer vitamin K injection, especially if prothrombin time is prolonged as per doctor's
order.
Postoperative Nursing Care:
● Place patient in SEMI-FOWLER'S POSITION to promote lung expansion
● NGT DECOMPRESSION to prevent gastric distention.
● LOW-FAT DIET for 2-3 months
● Encourage ambulation after 24 hours.
● Encourage to resume normal activities within 2-3 days.
● Monitor T-Tube if common bile duct exploration was done.

T - TUBE INSERTION
Purpose:
➔ to DRAIN BILE
Drainage Characteristics:
● It should be BROWNISH RED for the first 24 hours.
● It should be 300-500 ML for the first 24 hours.
Nursing Responsibilities:
● Place drainage bottle or Jackson Pratt AT THE LEVEL OF THE INCISION.

PANCREAS
● Large, elongated accessory organ of digestion.
● secretes bicarbonate and pancreatic enzymes aiding in the process of digestion (exocrine
function-amylase
lipase, trypsin)
● contains the islets of Langerhans composed of beta cells secreting insulin and alpha cells
secreting glucagon.

PANCREATITIS
➔ Inflammation of the pancreas
➔ CAUSE is unknown; linked with autodigestion.
Types Of Pancreatitis:
1. Acute - vary from mild, self-limiting disorder to severe, fatal and does not respond to any
treatment.
- edema and inflammation confined to the pancreas
2. Chronic -continuous and prolong with fibrosis
Risk Factor:
● Alcohol abuse
● MEDICATIONS
● Antihypertensives, diuretics, antimicrobials.
● immunosuppressives, oral contraceptives
● GI DISORDERS: Biliary obstruction and intestinal diseases
Pathophysiology

Other Manifestation
● Grey Turner's Spot or sign Bluish flank discoloration
● Cullen sign
● Bluish periumbilical discoloration.
Diagnostic Test
● Elevated serum and urinary amylase, serum lipase, serum bilirubin, alkaline phosphatase, and
sedimentation rate
● White blood cell count
● Fecal fat determinations
● Blood and urine glucose
Nursing Interventions
● Administer MEPERIDINE HCL (DEMEROL) as ordered
● AVOID MORPHINE SULFATE!!!
● Place client on NPO DURING ACUTE PHASE
● bland, LOW-FAT DIET, LOW CHON, HIGH CHO; avoid alcohol.
● NGT DECOMPRESSION insertion to remove gastrin and prevent further stimulation of the
pancreas.
● Administer CALCIUM SUPPLEMENTS (WITH
● VITAMIN D) if there is hypocalcemia.
● Administer INSULIN as ordered if there is hyperglycemia.
Surgical Management
➔ Pancreatectomy
● surgical removal of part or all of the part of pancreas.

LIVER CIRRHOSIS
● Irreversible chronic inflammatory disease characterized by massive degeneration and
destruction of hepatocytes resulting in a disorganized lobular pattern of regeneration.
Types/Causes:
1) LAENNEC'S- caused by ALCOHOLISM or hepatotoxic drugs.
2) POST-NECROTIC- caused by viral HEPATITIS or industrial hepatotoxins.
3) BILIARY - caused by BILIARY PROBLEMS
4) CARDIAC - caused by CONGESTIVE HEART FAILURE (CHF)

HEPATITIS
Types:
● Hepatitis A (HAV): Infectious H.
● Hepatitis B (HBV): Serum H.
● Hepatitis C (HCV): non-A, non-B / Post-transfusion H.
● Hepatitis D 9HDV): Delta H.
Pathophysiology:

PORTAL HYPERTENSION
● Normal portal vein pressures range from 5-10 mm Hg.
● Refers to elevated pressures in the portal venous system.
● Venous pressure more than 5 mm Hg greater than the inferior vena cava pressure is defined as
portal hypertension.
PATHOGENESIS OF EDEMA IN LIVER CIRRHOSIS

Assessment:

Diagnostic Test
● LIVER BIOPSY (definitive test)
● Abdominal x-ray
● Ct scan
● Endoscopy
● Elevated Aspartate Aminotransferase (AST)SGOT) 4.8-19U/L, Alanine
● Aminotransferase (ALT)(SGT) 2.4-17 U/L, bilirubin TB0-0.9mg/dL
● Prolonged prothrombin time (PT) (N) 11-16 seconds.
● Decreased serum albumin.
● CBC reveals anemia.
● Serum ammonia = Normal: 150-250mg/dL, 10-80 ug/dl.
Preparing A Patient For Ultrasound Of The Liver
● Place patient on NPO 8-12 hours
● before the procedure
● Administer laxative a night before the test.
● Maintain adequate hydration.
Preparing A Patient For Liver Biopsy
● Place patient on NPO 2-4 hours before the test
● ADMINISTER VITAMIN K
● Monitor prothrombin time.
● Position patient in LEFT LATERAL POSITION with pillow under right shoulder.
● Instruct to HOLD BREATH 5-10 seconds during needle insertion.
Nursing Care After Liver Biopsy
● Turn the patient to sides q4 hours.
● Place on bed rest for 24 hours
● Monitor for signs of bleeding.
Nursing Interventions
● Place client on BED REST with bathroom privileges
● Offer LOW-PROTEIN, HIGH
● CARBOHYDRATES and vitamins (ADEK, B-complex)
● RESTRICT AMOUNT OF ORAL FLUIDS and eliminate alcohol intake
● Provide meticulous skin care.
● Monitor weight, intake and output and ABDOMINAL GIRTH
● Assist in paracentesis if necessary.
● Monitor for bleeding of esophageal varices.
● Perform tap water or NSS enema as per doctor's order.
● Avoid giving aspirin (causes bleeding) and sedatives (hepatotoxic).
Medication For Patient With Cirrhosis
1) ANTACID - to prevent GI bleeding.
2) SPIRONOLACTONE - (Potassium-sparing diuretic) - diuretic of choice to manage ascites;
does not cause hypokalemia.
3) FUROSEMIDE - diuretic given if a patient has hyperkalemia after prolonged use of
spironolactone.
4) VITAMIN K - prevents bleeding tendencies.
5) INTRAVENOUS ALBUMIN - to manage ascites and edema.
6) DUPHALAC (Lactulose) reduces levels of ammonia.
7) NEOMYCIN SULFATE - reduce colonic bacteria responsible for ammonia formation.
Prevention Of Bleeding Of Esophageal Varices
● Avoid Valsalva maneuver.
● Avoid bending or stooping.
● Avoid hot spicy foods.
● Avoid lifting heavy objects.
Interventions For Bleeding Of Esophageal Varices
● Place patient in SEMI-FOWLER'S
● POSITION to prevent aspiration.
● Suction the mouth.
● Perform gastric lavage with tap water.
● Insert SENGSTAKEN-BLAKEMORE TUBE
● Administer: IV fluids, blood transfusion as ordered
● Administer VASOPRESSIN to constrict splanchnic arteries.
Preparing A Patient For Paracentesis
● Ask to empty the bladder to prevent puncture.
● Check serum protein studies.
● Place patient in sitting or upright position
Nursing Care After Paracentesis
● Check urine output.
● Watch out for board-like abdomen (sign of PERITONITIS)
● Monitor for signs of hypovolemic shock.

THE ENDOCRINE SYSTEM

ANTERIOR PITUITARY GLAND DYSFUNCTION

POSTERIOR PITUITARY GLAND DYSFUNCTION
(ANTERIOR) HYPERPITUITARISM (+BASOPHILIC OR EOSINOPHILIC TUMOR)
 POSTERIOR PITUITARY GLAND

(ANTERIOR) HYPOPITUITARISM (+CHROMOPHOBIC TUMOR)

 POSTERIOR PITUITARY GLAND (HYPOPITUITARISM)

OTHER ORGANS/GLANDS INVOLVED IN ENDOCRINE SYSTEM

REVIEW OF NORMAL STRUCTURES AND FUNCTIONS

ENDOCRINE SYSTEM
➔ is made of hormones secreting glands that helps maintain and regulate vital functions such as:
● Response to stress and injury
● Growth and development
● Reproduction
● Ionic homeostasis
● Energy metabolism
Major Organs
● Pituitary
● Thyroid and Parathyroid in the neck
● Adrenals
● Pancreas
● Ovaries or Teste

THE PITUITARY GLAND

➔ The Pituitary Gland, also known as the hypophysis, and master gland
Two Parts
1. Anterior Pituitary (Adenohypophysis)
2. Posterior Pituitary (Neurohypophysis)
Anterior Pituitary (Adenohypophysis) secretes:
● Growth Hormones (GH) or Somatotropin
● Prolactin (Mammotropic, Lactotropic, Luteotrophic)
● Gonadotropic Hormones (LH and FSH)
● Thyrotropic Hormones (TSH)
● Adrenocorticotropic Hormone (ACTH)
● Melanocyte-Stimulating Hormone (MSH)
Posterior Pituitary (Neurohypophysis) secretes:
● Antidiuretic Hormone (ADH)
● Oxytocin

THE THYROID AND PARATHYROID

➔ Thyroid gland is located in the neck in close approximation to the first part of the trachea. In
humans, the thyroid gland has a “butterfly” shape
➔ Close examination of a thyroid gland will reveal one or more small, light-colored nodules on
or protruding from its surface - these are parathyroid glands (meaning “beside the thyroid”)
The Thyroid secretes:
● Thyroxine (T4)
● Triiodothyronine (T3)
● Thyrocalcitonin
The Parathyroid secretes:
● Parathormone (PTH)

THE ADRENAL GLANDS

➔ The two adrenal glands are located immediately anterior to the kidneys
Two Regions Ovaries
● Adrenal Medulla (inner) - which is a source of the catecholamines epinephrine and
norepinephrine
● Adrenal Cortex (outer) - which secretes several classes of steroid hormones, glucocorticoids
and mineralocorticoids
The Adrenal Cortex
● Glucocorticoids
● Mineralocorticoids
● Androgens
The Adrenal Medulla
● Epinephrine (adrenaline)
● Norepinephrine (noradrenaline)

THE PANCREAS
➔ An elongated organ nestled next to the first part of the small intestine. The endocrine
pancreas refers to those cells within the pancreas that synthesize and secrete hormones
➔ The endocrine portion of the pancreas take the form of many small cluster of cells called
Islets of Langerhans
Pancreatic Secretions
● Endocrine - insulin and glucagon - secreted to blood
● Exocrine - digestive enzymes (acinar cells), aqueous NaHCO3 solution (duct cells) - secreted
to the duodenum collectively as pancreatic juice
Three major cell types:
● Alpha Cells (A Cells) - secrete the hormone glucagon
● Beta Cells (B Cells) - produce insulin and cells
● Delta Cells (D Cells) - secretes the hormone somatostatin, which is also produced by a
number of other endocrine cells in the body.

THE OVARIES AND TESTES

➔ The gonads, the primary reproductive organs, are the testes in the male and the ovaries in the
female. These organs are responsible for producing the sperm and ova, but they also secrete
hormones and are considered to be endocrine glands.
Testes
➔ Males sex hormones, as a group are called androgens
➔ The principal androgen is testosterone, which is secreted by the testes.
This steroid hormone is responsible for:
● The growth and development of the male reproductive structures
● Increased skeletal and muscular growth
● Enlargement of the larynx accompanied by voice changes
● Growth and distribution of body hair
● Increased male sexual drive
Ovaries
➔ Two groups of female sex hormones are produced in the ovaries, the estrogens and
progesterone
➔ These steroid hormones contribute to the development and function of the female
reproductive organs and sex characteristics
At the onset of puberty, estrogens promotes:
● The development of the breast
● Distribution of fat evidenced in the hips, legs, and breast
● Maturation of reproductive organs such as the uterus and vagina
● Repair endometrium after menstruation
Progesterone causes:
● The uterine lining thickens in preparation for pregnancy.
Regulation of Hormones
➔ The secretion of many hormones is initiated by a negative-feedback system

NURSING CARE OF PATIENTS

WITH DISTURBANCES IN ENDOCRINE FUNCTIONS

DISORDERS OF THE PITUITARY GLAND

HYPERPITUITARISM
➔ oversecretion of one or more of the hormones secreted by the pituitary gland caused by a
secreting pituitary tumor, typically a benign adenoma.
Three Major Types of Pituitary Tumors
A. Eosinophilic Tumor
● Enlargement involves all tissues and organs (gigantism)
● Many of these patient suffer from headaches and visual disturbances because the tumors exert
pressure on the optic nerves
B. Basophilic Tumor
● Give rise to Cushing’s Syndrome with features largely attributable to hyperadrenalism,
including masculinization and amenorrhea in females, truncal obesity, hypertension, osteoporosis
and polycythemia
C. Chromophobic Tumor
● Represent 90% of pituitary tumors
● Produce no hormones but destroy the pituitary gland causing hypopituitarism
● Patient with this disease are often obese and somnolent and exhibit fine, scanty hair, dry, soft
skin, a pasty complexion and small bo0nes
● They also experience headache, loss of libido and visual defects progressing to blindness
● Other signs and symptoms include polyuria, polyphagia, lowering of the basal metabolic rate
and a subnormal body temperature.
Signs and Symptoms of Hyperpituitarism
Systemic
● Excessive or abnormal growth patterns
● Abnormal milk secretion (galactorrhea)
● Overstimulation of one or more of the target glands resulting in the release of excessive
thyroid, sex, or Adrenocortical hormones
Local
● Blindness due to pressure in the optic nerve
● Headaches
● Somnolence (state of being drowsy)
Diagnostic Evaluation
1. Radiologic
2. Laboratory testing
● A sensitive and specific immunologic staining method that helps determine the nature
of the hormones synthesized and secreted by pituitary tumors.
● Plasma levels of GH, LTH, FSH, and LSH
3. Metrizamide - accentuated CT scan

GIGANTISM
➔ which is an overgrowth of the long bones, develops in children before the age at which the
epiphyses of the bones close. Individuals suffering from gigantism may grow as tall as 8 or 9
feet.

ACROMEGALY
➔ is an adult disease that develops following closure of the epiphyses of the long bones.
➔ Marks by both increases in bone thickness and hypertrophy of the soft tissues.
Intervention
Drug:
● Bromocriptine (Parlodel) lower GH level and prolactin level
● Octreotide and Lanreotide (Somatostatin Analog) used preoperatively to improve patient
condition and shrink the tumor
● Hypophysectomy treatment of choice

Hypophysectomy
● Partial or complete removal of pituitary gland
● Indications:
○ Pituitary tumors
○ Diabetic retinopathy
○ Metastatic cancer of breast or prostate
● Surgical approaches:
○ Craniotomy - transfrontal
○ Transsphenoidal - incision via inner aspect of upper lip and gingiva
Nursing Interventions after Transsphenoidal Hypophysectomy:
● Keep head elevated to promote venous drainage for 2 weeks
● Maintain nasal pack as per doctor’s order
● Provide good oral care
● Avoid blowing of nose and other activities that increase ICP
● Report output greater than 900 ml / 2hrs

CUSHING’S DISEASE
➔ Oversecretion of ACTH by a basophilic tumor, which in turn results in oversecretion of
adrenocortical hormones

SEXUAL DISTURBANCE
➔ Excess secretion of gonadotropic hormones from pituitary tumors produces sexual precocity
in children
➔ Excess Prolactin secretion causes amenorrhea or galactorrhea (excessive flow of milk) in
women.
Nursing Interventions
● Help the client accept the altered body image that is irreversible
● Assist family to understand what the client is experiencing
● Help the client recognize that medical supervision will be required for life
● Help the client understand the basis for the change in sexual functioning
● Assist the client in expressing feelings
● Care for the client following a hypophysectomy:
○ Protect from stress situations
○ Protect from infection
○ Follow and maintain an established schedule for hormone replacement
● Follow a nursing care for the client undergoing intracranial surgery:
 ○ Perform neurologic assessments
○ Measure specific gravity of urine, and check daily weight to identify complication of
DI
○ Check nasal drainage for glucose to determine presence of CSF
○ Encourage deep breathing but not coughing
○ Institute measures to prevent constipation

HYPOPITUITARISM
➔ Deficiency of one or more of the hormones produced by the anterior lobe of the pituitary
➔ When both the anterior and posterior lobes fail to secrete hormones, the condition is called
PANHYPOPITUITARISM
Causes:
● Hypophysectomy
● Non-secreting pituitary tumors
● Pituitary dwarfism
● Postpartum pituitary necrosis
● Functional disorders
Specific Disorders resulting to Hypopituitarism
● Dwarfism
● Secondary Adrenocortical insufficiency
● Myxedema (severe hypothyroidism)
● Sexual and reproductive disorders
Intervention
● Removal
● Permanent replacement of the hormones secreted by the target organ
● Medication
○ Corticosteroids for correction of secondary Adrenocortical insufficiency
○ Thyroid hormone for treatment of Myxedema
○ Sex hormone to correct hypogonadism

DWARFISM
Nursing Intervention:
● Monitor effects of hormone replacement
● Discuss the importance of adhering medical regimen on a long term basis
● Allow client ample time to verbalize feelings regarding the long term nature of the disease and
impact on daily life
● Provide adequate rest periods
Types Of Dwarfism
● Disproportionate Dwarfism - some average size parts of the body and some shorter than
normal parts of the body
● Proportionate Dwarfism - the individual is smaller than the average all over
DIABETES INSIPIDUS (ADH DEFICIENCY)
➔ Disorder of the posterior lobe of the pituitary gland characterized by a deficiency of ADH
(vasopressin).
Causes of ADH insufficiency
1. Vasopressin deficiency (ADH deficiency) due to
● Abnormalities in the hypothalamus and primary gland from familial or idiopathic causes
primarily diabetes Insipidus
● Destruction of the gland by tumors in the hypothalamo pituitary region, trauma, infectious
process, vascular accidents or metastatic tumors from breast or lung (secondary diabetes
Insipidus).
● Medications such as phenytoin (Dilantin), alcohol, and lithium carbonate
2. Nephrogenic" diabetes Insipidus
● Owing to an inherited defect, the kidney tubules cannot reabsorb water.
● This condition also may develop secondary to potassium depletion or pyelonephritis.
Assessment
Major Manifestations
● Polyuria –urine output greater than 250 ml per hour
● Polydipsia- drinks 2L-20L of fluid daily and craves for cold water
● Urine specific gravity of 1.001 to 1.005
Diagnostic Exams
1. Water deprivation test - is carried out by withholding fluids for 8-12 hours or until 3%-5% of
the body weight is lost
● the patient is weighed frequently during the test
● plasma and osmolality studies are performed at the beginning and end of the test
● the inability to increase the specific gravity and osmolality of the urine is characteristic of
diabetes insipidus
2. Does not respond to ADH injection (only for Nephrogenic D. I.)
3. Plasma level of ADH
Intervention
1. Desmopressin (DDAVP) is a synthetic vasopressin given intranasally, insufflated through the
nose. Largely replaced vasopressin for long term treatment of persons with severe D. I.
2. Surgical resection of tumor
3. Vasopressin injection (aqueous Pitressin) or vasopressin tannate (Pitressin Tannate).
● Pitressin typically alleviates polyuria, and usually polydipsia for 24 - 72 hours.
4. Chlorpropamide (diabinese) and thiazide are used in mild forms
Nursing Management
● Physical assessment and continue monitoring of F and E imbalance status: I and O, daily
weight, skin turgor, electrolyte levels
● Replace fluid by mouth or parenterally
● Monitor response to ADH replacement
● Teach clients on long term vasopressin therapy the need for daily weight records, recognition
of polyuria.
● Advised wearing of medical identification bracelet
SIADH (SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE)
➔ Excessive ADH secretion from the pituitary gland
➔ Opposite of diabetes Insipidus.
➔ Patient cannot excrete a dilute urine
➔ Retain fluids
➔ Develop sodium deficiency
Cause: trauma, stroke, malignancies of lungs, medications, stress
Clinical Manifestations
● Headache
● nausea / vomiting
● muscle cramps
● restlessness
● lethargy
● confusion
● decreased reflexes
● seizure
● coma
● Death
Medical Management
● Eliminating underlying cause
● Establish Airway
● Restricting fluid intake as per doctor’s order
● Mannitol (hypertonic solution)
● Lasix / Bumex (loop diuretic)
● Corticosteroids
● Positioning
Nursing Management
● Close monitoring of fluid and intake, daily weight, urine and blood chemistries and neurologic
status.
● Monitoring and regulating IVF accurately
● Administer medications as per doctor’s order. Assessment of patients for side effects of
treatment of SIADH
● Assess for pain, anxiety, and depression; and provide interventions to improve pain
management and coping ability.
● Monitor signs and symptoms of complications

DISORDERS OF THE THYROID GLAND

➔ Thyroid Enlargement (Simple Goiter, Non-toxic Goiter, Nodular Goiter)
➔ The thyroid gland needs iodine in order to synthesize and secrete its hormones.

GOITER
Types of Goiter
1. Endemic (iodine Deficient ) Goiter
● is principally caused by nutritional iodine deficiency.
● It is twice as prevalent in women as in men.
● Commonly developed in adolescents, pregnant women and nursing mothers residing
in iodine deficient regions.
2. Sporadic Goiter
● is not restricted to any geographic area.
Causes:
● Genetic defects resulting in faulty iodine metabolism
● Ingestion of large amounts of nutritional goitrogens (e.g. cabbage, soybeans, peanuts, peaches,
peas, strawberries, spinach, and radishes)
● Ingestion of medicinal goitrogens, e.g. thiouracil (propylthiouracil), thiocarbamides
(aminothiazole, tolbutamide) and iodine in large doses.
Diagnosis and Assessment
● the goiter grows large enough to distort the appearance of the neck
● they may also experience respiratory distress and difficulty swallowing if the goiter is very
large.
Medical Management
Pharmaceutical Management
● strong iodine solution (Lugol’s solution) or saturated solution of potassium iodine (SSKI
drops).
● Thyroid hormone replacement with sodium levothyroxine (Synthroid), Desiccated thyroid
(thyroid USP) and sodium liothyronine (Cytomel),
● When administering thyroid preparations, assess the individual carefully for symptoms of
thyrotoxicosis, (tachycardia, increased appetite, diarrhea, sweating, agitation, tremors,
palpitation)
Surgical Management
● Subtotal thyroidectomy

HYPERTHYROIDISM (THYROTOXICOSIS; OVERACTIVE THYROID)

➔ Excessive synthesis and secretion of endogenous or exogenous thyroid hormones by the
thyroid
Causes, Incidence, and Risk Factors
● Graves disease
● Toxic multinodular goiter
● Toxic adenoma
● Thyroiditis
● Tumors of the testes or ovaries
● Inflammation (irritation and swelling) of the thyroid due to viral infections or other causes
● Ingestion of excessive amounts of thyroid hormone
● Ingestion of excessive iodine
Symptoms
● Weight loss
● Polyphagia
● Diaphoresis
● Nervousness
● Restlessness
● Heat intolerance
● Increased sweating
● Fatigue
● Insomnia
● Frequent bowel movements
● Menstrual irregularities in women
Assessment
● increased heart rate
● Systolic blood pressure may be elevated
● thyroid enlargement or goiter.
Laboratory Exams
● Serum TSH is usually decreased
● T3 and free T4 are usually elevated
● Triglycerides
● T3RU
● Radioactive iodine uptake
● Glucose test
● Cholesterol test
● Antithyroglobulin antibody
Thyroid Scan
● Measures the affinity of the thyroid gland for radioactive iodine( Normal 15-40%)
● Preparation
● No diagnostic test with contrast medium for the past 3 mos.
● No foods or drugs with iodine for 2weeks prior to test
● Discontinue contraceptive pills
● NPO6-8hrs if 131 is used
● IV No fasting
Treatment
● Antithyroid medications (Thyroid Inhibitors)
● Examples: Iodine (Lugol’s Solution), Methimazole (Tapazole), PTU (Propylthiouracil)
● Major S/E:
○ Agranulocytosis (decreased WBC)
○ Skin disturbances (hypersensitivity)
○ N/V (irritation of gastric mucosa)
○ Decreased metabolism
○ Iodine: bitter taste; stains teeth (local oral effect on B teeth and mucosa
Nursing Interventions
● Report the occurrence of any S/E to the physician , especially sore throat and fever.
● Avoid crowded places and potentially infectious situations
● Administer liquid iodine prep dilute in beverage of choice through a straw
● Assess client for signs of hypothyroidism
● Radioactive iodine Therapy
● Thyroidectomy (If the thyroid must be removed with radiation or surgery, replacement thyroid
hormones must be taken for the rest of the person's life)
● Beta-blockers (propranolol and atenolol)
Complications of Thyroidectomy
● rapid heart rate, congestive heart failure, and atrial fibrillation.
● thyroid crisis or "storm"
● Fever
● decreased mental alertness
● abdominal pain may occur
● increases the risk for osteoporosis
Nursing Interventions
● Monitor V/S, I&O
● Provide cool, quiet environment
● Provide adequate rest; promote normal thought processes (minimize sleep disruption); use
safety measures to reduce risk of trauma or fall
● Provide high caloric, protein, CHO, vitamin diet without stimulants, extra fluids; restrict
stimulants (tea, coffee, alcohol)
● IVF therapy as prescribed
● Weigh client daily
● Provide eye protection: ophthalmic medicine
● Provide emotional support
● Be alert for complications: corneal abrasion, heart disease, thyroid storm
● Maintain skin integrity
● Explain procedures to client and encourage verbalization of feelings
● Thyroidectomy: Preoperative care
● administer prescribed antithyroid drugs to achieve euthyroid state
● teach coughing, DBE, and use of hands to support neck and to avoid strain on suture lines
Pre-Operative
● Achieve euthyroid state by Lugol’s Administration and any antithyroid drug as per doctor’s
order
● Takes 2-3 weeks to decrease the vascularity of the thyroid and prevent postoperative
hemorrhage
Postoperative care
● semi-fowler’s position without pillows
● Limit head movement
● Avoid tension on suture line
● check dressing esp. back of neck
● observe for respiratory distress caused by tracheal edema
● be alert for signs of hemorrhage
● instruct patient: talking limited, note any hoarseness – may indicate injury in laryngeal nerve
● observe for signs of tetany: Chvostek’s sign, Trousseau’s sign
● calcium gluconate IV at bedside
● Have tracheostomy set and suction machine ready at bedside
● observe for signs of thyroid storm (high fever, tachycardia, irritability, delirium, coma)
● gradual increase ROM of neck

GRAVE’S DISEASE (TOXIC DIFFUSE GOITER, EXOPHTHALMIC GOITER)

➔ It is predominantly a disorder of females.
➔ It affects women four times as often as it does men, especially young women between the
ages of 20 and 40.
Causes
● Over functioning of the entire gland
● Single or multiple functioning adenomas of thyroid cancer
● Over treatment of myxedema with thyroid hormone
Hallmarks of Graves' disease
● Hyperthyroidism
● Thyroid gland enlargement
● Exophthalmos (abnormal protrusion of the eyes).
● Dermopathy) skin lesions
Etiology
● Graves' disease is an autoimmune disorder.
● have circulating autoantibodies that react against thyroglobulin.
● thyroid-stimulating immunoglobulins (TSI) are present in the serum of 80 to 90 percent of
hyperthyroid individuals.
● Assessment and Diagnosis
● extremely agitated and irritable, with a hand tremor at rest.
● Weight loss occurs owing to the quickened metabolism.
● the person's bodily processes literally "speed up”
Signs & Symptoms
● loose bowel movements
● heat intolerance
● profuse diaphoresis
● Tachycardia
● Tremors
● skin become warm and smooth
● hair appears thin and soft.
● emotions are adversely may be cyclic, ranging from mild euphoria to extreme fatigue and
depression, again followed by episodes of over activity
Assessment
● Graves' disease is diagnosed on the basis of
○ the person's often striking physical appearance (enlarged neck, protruding eyes, agitated
expression)
○ the symptoms of agitation, restlessness, and weight loss; and
○ The serum thyroid hormone levels, 24 hour radio-iodine uptake, and T3 resin uptake are
usually all elevated
The three major forms of therapy
1. Antithyroid medication e.g, Propylthiouracil and Methimazole
2. Radioiodine e.g. 131 Iodine (1311) therapy
3. Surgery
Nursing Intervention
● Provide an environment that is restful both mentally and physically.
● Explain to significant others that any bizarre, difficult behavior is likely to be temporary and
should steadily improve with intervention.
● Maintain a quiet, understanding manner when caring.
● Accept their irritation and emotional outburst as normal expressions of the disease.
● Incorporate occupational therapy into care planning
● Provide a well-balanced diet
● Provide cool environment
Thyroid Storm
● Uncontrolled and potentially life-threatening hyperthyroidism due to sudden and excessive
release of thyroid hormone into the bloodstream
Precipitating factors
● Stress
● Infection
● Unprepared thyroid surgery
Clinical manifestations
● hyperpyrexia, diarrhea, dehydration, extreme tachycardia, arrhythmias, extreme irritation,
delirium, coma, shock and death if not adequately treated
Management
● Drug therapy: antithyroid drugs Propylthoiuracil(PTU), Hydrocortisone, sedatives, cardiac
drugs, oxygen administration, Iodine to lower output of T4
● Immediate management of hyperthermia, tachycardia and prevention of vascular collapse
Nursing intervention
● Administer IV therapy as ordered

HYPOTHYROIDISM
➔ The thyroid gland fails to produce enough thyroid hormones.
● Myxedema - Adult hypothyroidism
● Cretinism – Hypothyroidism in infants and children
Causes:
● Hashimoto's thyroiditis (the most common, an autoimmune disease) - Chronic progressive
disease of thyroid gland caused by infiltration of lymphocytes
● progressive destruction of the parenchyma and hypothyroidism if untreated
● Medications: lithium, iodine compounds, antithyroid medications
● Radiation to the neck and head
● congenital defects
● surgical removal of the thyroid gland
● inflammatory conditions.
Risk factors
● age over 50 years
● female gender
● Obesity
● thyroid surgery
● exposure of the neck to X-ray or radiation treatments
Symptoms
Early Symptoms Late Symptoms
 weakness  slow speech
 fatigue  dry flaky
 cold skin
intolerance  thickening of
 constipation the skin
 weight gain  puffy face,
(unintentional) hands and feet
 depression  decreased
 joint or taste and smell
muscle pain  thinning of
 thin, brittle eyebrows
fingernails  hoarseness
 thin and  abnormal Note: Patient with
brittle hair menstrual periods Hypothyroidism are
 paleness Hypersensitive to
narcotics and barbiturates
Laboratory Examinations:
● T4 test (low)
● serum TSH (high in primary hypothyroidism, low or low-normal in secondary
hypothyroidism)
● increased cholesterol levels
● increased liver enzymes
● increased serum prolactin
● low serum sodium
● complete blood count (CBC) that shows anemia
Treatment
● Replace the deficient thyroid hormone (Synthetic levothyroxine)
○ Examples: Levothyroxine sodium (Synthroid), Liothyronine sodium (Cytomel),
Liothrix (Euthroid, Thyrolar)
● Administration of high dose glucocorticoids every 8 to 12 hrs for 24 hrs. followed by low dose
therapy as per doctor’s advised.
Major S/E:
● Increased metabolism
● Hyperactivity
● Cardiac stimulation
Nursing Care:
● Take the medication as scheduled at the same each day
● Take radial pulse; notify physician if greater than 100 beats/min
● Monitor V/S to detect changes in CV status and ability to respond to stress
● Monitor ECG tracings to detect arrhythmias
● Provide warm environment and prevent chilling
● Administer fluids and all prescribed drugs with caution
● WOF and teach patients signs of complications
A. Angina pectoris
B. Cardiac failure: dyspnea, palpitations
C. Myxedema coma: weakness, syncope, slow pulse rate, subnormal temperature, slow
respirations, lethargy
● Adequate hydration and roughage in diet (high fiber)
● Control of dietary intake to limit calories and reduce weight
● Low calorie,high protein, increase fiber and fluids
● Patient teaching on continued HRT through life; regular medical check-up; energy
conservation techniques and the need to increase activity gradually; how and when to take
medications
Complications:
● Myxedema coma, the most severe form of hypothyroidism
● Symptoms and signs of myxedema coma include:
- unresponsiveness
- decreased breathing
- Low blood pressure
- low blood sugar
- below normal temperature.
Other complications:
● heart disease
● increased risk of infection
● Infertility
● miscarriage.

HYPERPARATHYROIDISM
➔ is excessive production of parathyroid hormone by the parathyroid glands
Types of Hyperparathyroidism
1. Primary hyperparathyroidism
● Parathyroid hormone is produced without regard to the calcium levels.
● It is caused by enlargement of one or more of the parathyroid glands.
2. Secondary hyperparathyroidism
● when the body produces extra parathyroid hormone because the calcium levels are too low.
3. Tertiary hyperparathyroidism
● If the parathyroid glands continue to produce too much parathyroid hormone even though the
calcium level is back to normal
Symptoms:
● Fatigue
● Back pain
● Joint pain
● Fractures of long bones
● Decreased height
● Increased urine output
● Increased thirst
● Upper abdominal pain
● Loss of appetite
● Nausea
● Muscular weakness
● Muscle pain
● Depression
● Personality changes
● Stupor and possibly coma
● Itching of the skin
● Blurred vision (because of cataracts)
● Bone pain or tenderness
Laboratory Examination:
● Serum calcium is increased.
● Serum phosphorus is decreased.
● Serum alkaline phosphatase may be increased.
● Intact parathyroid hormone (PTH) in the blood is increased.
● Bone X-ray shows bone reabsorption or fractures.
● Imaging of the kidneys or ureters may show calcification or obstruction.
● Reduced bone mineral density on bone densitometry (DEXA)
● Urinary calcium may be increased.
Treatment:
Treatment depends upon the severity and cause of the condition.
● In primary hyperparathyroidism, if the calcium level is very high or symptoms are present,
surgery may be necessary to take out the gland that is overproducing the hormone.
● Secondary hyperparathyroidism is treated by restoring the calcium back into the normal range,
usually by giving calcium and vitamin D alone or in combination, depending on the underlying
disorder.
Nursing Interventions:
● Strain the urine, observing for stones
● Encourage fluid intake, especially fluids such as cranberry juice to acidify the urine
● Assist the client in ambulating to help prevent demineralization
● I/O monitoring
● Combat constipation
● Limit intake of foods high in calcium especially milk / dairy products
Complications:
Complications that result from excess calcium deposits within the body
● Skeletal damage
● Urinary tract infection due to kidney stones and obstruction
● Peptic ulcer disease
● pancreatitis
● Pseudogout

HYPOPARATHYROIDISM
➔ is having insufficient parathyroid hormone, which causes abnormal low blood levels of
calcium and phosphorus.
Causes:
● Lack of PTH.
● Blood calcium levels fall, and phosphorus levels rise.
● Injury to the parathyroid glands during head and neck surgery.
● Side effect of radioactive iodine treatment for hyperthyroidism
● PTH secretion also may be impaired when blood levels of magnesium are low
● When blood pH is too high, a condition called metabolic alkalosis.
Symptoms:
● Tingling lips, hands, and feet
● Muscle cramps
● Pain in the face, legs, and feet
● Abdominal pain
● Dry hair
● Brittle nails
● Dry, scaly skin
● Cataracts
● Weakened tooth enamel in children
● Muscle spasms called tetany (can lead to spasms of the larynx, causing breathing difficulties)
● Convulsions (seizures)
Laboratory Examinations:
● Low serum calcium level
● High serum phosphorus level
● Low serum parathyroid hormone level
● Low serum magnesium level (possible)
● Abnormal heart rhythms on ECG
● Urine calcium
Treatment:
● Goal to increase serum Ca level to 9 to 10 mg/dl and eliminate the symptoms
● Ca Chloride or Ca gluconate given IV for emergency treatment
- Calciferol (vit D) to help raise serum calcium levels
- Parathormone injections
- High calcium diet
- Aluminum hydroxide to decrease absorption of phosphorus from the GI tract
Nursing Interventions:
● Observe for respiratory distress and have emergency equipment available to perform a
tracheostomy
● Maintain seizure precautions
● Monitor serum Ca and phosphate levels
● Check V/S frequently
● Provide a calm environment free of harsh stimuli
● Provide a drug and dietary instruction including elimination of milk, cheese and egg yolks
because of high phosphorus content

ADDISON'S DISEASE
➔ adrenal hormone deficiency caused by damage to the outer layer of the adrenal gland (adrenal
cortex).
Alternative Names:
● Adrenocortical hypofunction
● Chronic adrenocortical insufficiency
● Adrenal insufficiency
Causes:
Damage to the adrenal cortex caused by the following:
● autoimmune disease
● infections such as tuberculosis, HIV, or fungal infections Hemorrhage, blood loss
● Tumors
● Use of blood-thinning drugs (anticoagulants) , anticonvulsants and rifampicin
Risk factors:
● Type I diabetes
● Hypoparathyroidism
● Hypopituitarism
● Pernicious anemia
● Testicular dysfunction
● Graves' disease
● Chronic thyroiditis
● Candidiasis
● Dermatitis herpetiformis – eruption of itching papules, vesicles and lesions resembling hives
typically in clusters
● Vitiligo – skin disorder manifested by smooth white spots to various parts of the body
● Myasthenia gravis – progressive weakness of voluntary muscles
Symptoms:
● Extreme weakness
● Fatigue
● emaciation
● Nausea and vomiting
● Chronic diarrhea
● Loss of appetite
● Darkening of the skin - patchy skin color
- Unnaturally dark color in some
locations
- Paleness may also occur
● Mouth lesions on the inside of a cheek
● Slow, sluggish, lethargic movement
● Changes in the blood pressure or heart rate
Assessment and Laboratory Examinations:
● Blood pressure is low.
● Cortisol level is low.
● Serum sodium is low.
● increased potassium.
● An abdominal x-ray may show adrenal calcification.
● An abdominal CT scan may show adrenal calcification, enlargement or atrophy.
Medical Management:
● Immediate treatment for combating circulatory shock
● Restoring blood circulation
● Administering fluids and corticosteroids
● Monitoring V/S
● Placing pt in a recumbent position with legs elevated
● Hydrocortisone (Solu-Cortef) via IV D5NSS
● Vasopressor amines maybe required if hypotension persist
Nursing Interventions:
● Monitor V/S, be alert for elevation of temperature (infxn, DHN), alterations in PR and rhythm
and alterations in BP
● Observe for signs of Na and K imbalance
● MIO and weigh daily
● Administer steroids as ordered
● Administer steroids with antacid to limit ulcerogenic factor of the drug
● Put the client in a private room to prevent contact with clients having infectious diseases
● Limit the number of visitors

CUSHING'S SYNDROME EXCESSIVE CORTICOSTEROID

➔ Additional symptoms that may be associated with this disease
● weight gain (unintentional)
● Buffalo hump
● skin spots, red
● skin blushing/flushing
● muscle atrophy or thin extremities
● fatigue
● bone pain or tenderness
● high blood pressure
Assessment and Laboratory Examination:
● Serum cortisol, urinary cortisol and low dose dexamethasone suppression test
● cranial MRI or cranial CT scan may show pituitary tumor
● abdominal CT may show adrenal mass
● glucose test is elevated
● potassium test may be low
● Increase serum Na
● white blood cell count may be elevated
Treatment:
● Cushing's syndrome caused by drug therapy with corticosteroids, the drug must be slowly
decreased under medical supervision.
● Cushing's disease is caused by a tumor, surgery to remove the tumor is recommended.
(HYPOPHYSECTOMY)
● Radiation is needed as well.
● Hydrocortisone (cortisol) replacement therapy is needed after surgery, and sometimes forever.
Nursing Interventions:
● Monitor vital signs, MIO, daily weight, blood glucose and electrolytes
● Protect the client from exposure to infections
● Minimize stress in the environment by limiting visitors and explaining procedures carefully
● Instruct client regarding diet and supplementation; encourage diet rich in nutrient dense foods
such as fruits and vegetables, whole grains and legumes to improve and maintain nutritional
status and prevent any possible drug-induced nutrient deficiencies
Other management:
● Increased protein and potassium but decrease calories and sodium
● Medication:
● Aminoglutethimide (Cytadren)
● Mitotane (Lysodren)
● Ketoconazole (Nizoral)
●Trilostane (Modastane)
● Surgery: adrenalectomy

DIABETES MELLITUS
➔ A group of metabolic diseases characterized by increased levels of glucose in the blood
resulting from defects in insulin secretion, insulin action or both (American Diabetes Association
2016).
Major Types:
1. INSULIN-DEPENDENT DIABETES - formerly called juvenile type; has rapid onset and
requires insulin administration
2. NON-INSULIN DEPENDENT DIABETES – formerly called adult onset type, often can be
controlled with diet
3. GESTATIONAL DIABETES - occurs during pregnancy usually during 2nd and 3rd
Trimester
Assessment:
● Polyphagia
● Polydipsia
● Polyuria
● Hyperglycemia
● Weight Loss
● Blurred Vision
● Slow Wound Healing
● Vaginal Infections
● Weakness & Paresthesias
● Signs Of Inadequate Feet Circulation
APPROACH TO DIABETES MELLITUS:
● nutritional therapy
● low glycemic index
● exercise
● oral hypoglycemic agents/insulin
● education`
● Monitoring
EXERCISE GUIDE DIABETIC FITNESS:
● Frequency - 3x a week
● Intensity - 60-80% of Maximal Heart Rate
● Time - AEROBIC ACTIVITY 20-30mins. With 5-10mins. WARM-UP
Oral Hypoglycemic Agents:
● Sulfonylureas
- Chlorpropamide (Diabinase)
- Tolbutamide (Orinase)
- Glimepinide (Solosa)
- Acetohexamide (Dymelor)
● Prandial Glucose Regulator
- Repaglinide (Novonorm)
- Rosiglitazone (Avandia)
● Non-sulfonylureas
- Metformin (Glucophage)
- Precose (Acarbose)
- Rosiglitazone (Avandia)
Major S/E of Antidiabetics
● Irritability
● Confusion
● Tachycardia
● Tremor
● Moist skin
● Headache
● Hunger
● Oral hypoglycemics
○ Skin rash
○ Jaundice
○ Pruritus
○ Allergic reactions
Nursing care for patients taking antidiabetics
● Assess clients for signs of hypoglycemia
● Instruct client to use proper medication procedure
● Comply with dietary program
● avoid alcohol
● Be prepared for hypoglycemic incidents (rapid acting glucose solution, hard candy, orange
juice)
Insulin Administration
● Administer all form of insulin subcutaneously
● Use only regular insulin for IV administration
● When mixing insulin, draw regular insulin into the syringe first
● Rotate sites of administration
Major Complications of Diabetes Mellitus
● HYPOGLYCEMIA
● DIABETIC KETOACIDOSIS (DKA)
● HYPERGLYCEMIC HYPEROSMOLAR NONKETOTIC SYNDROME (HHNS)
Causes of Hypoglycemia
● Too much insulin
● Excessive intake of antidiabetic agents
● Unusually high levels of exercise
● Insulin potentiating drugs
Signs of Hypoglycemia
● Sweating
● Tremor
● Tachycardia
● Palpitations
● Nervousness
● Hunger
Simple Carbohydrate to Treat Hypoglycemia
● 3 or 4 commercially prepared glucose tablets- CHILD: 2-3 GLUCOSE TABS
● 4-6 ounces of fruit juice or regular soda- CHILD: 1⁄2 CUP OR 120 ML OF ORANGE JUICE
OR SUGAR-SWEETENED JUICE
● 6-10 Life Savers or hard candy- CHILD: 3-4 HARD CANDIES OR 1 CANDY BAR
● 2-3 teaspoons of sugar or honey- CHILD: 1 SMALL BOX OF RAISINS
● 10-15 g of simple carbohydrate

DIABETIC KETOACIDOSIS
Assessment
● 3 main clinical features:
○ Hyperglycemia
○ DHN and electrolytes loss
○ Acidosis
● 3 Ps
● Blurred Vision
● Marked fatigue
● Headache
● Hypotension
● Weak, rapid pulse
● Anorexia, nausea, vomiting & abdominal pain
● Acetone breath (fruity odor)
● Kussmaul respirations
● Mental status changes
Management for DKA
● Treating hyperglycemia
● Correcting dehydration thru rehydration, electrolytes loss and acidosis

HYPERGLYCEMIC HYPEROSMOLAR NONKETOTIC COMA

● A metabolic disorder of type 2 resulting from a relative deficiency initiated by an illness that
raises the demand for insulin.
● Management same with DKA
● Kussmaul respirations- Deep, rapid respiration characteristic of diabetic acidosis or other
conditions causing acidosis.

Chronic Complications of
 ● Peripheral Neuropathies- Result from thickening of vessel walls that supply peripheral
nerves causing alteration in sensory perception.
● Retinopathy- Microangiopathy of the retina leading to retinal microvascular occlusion,
eventually leading to blindness.
● Nephropathy- Thickening of glomerular basement membrane resulting in hardening and
thickening of the glomeruli.
● Macrovascular disease- Atherosclerosis

The GIT System: Anatomy and Physiology

 The GIT is composed of two general parts

 The main GIT starts from the mouth → Esophagus→ Stomach→ SI→ LI
 The accessory organs are the
o Salivary glands
o Liver
o Gallbladder
o Pancreas

The GIT ANATOMY

The Mouth (oral or buccal cavity)

 Contains the lips, cheeks, palate, tongue, teeth, salivary glands, masticatory/facial muscles and
bones
 Anteriorly bounded by the lips
 Posteriorly bounded by the oropharynx
 Digestion starts from the mouth
 Mechanical digestion occurs through mastication (chewing)
 Chemical digestion occurs through the action of salivary amylase (ptyalin), which breaks down
starches to maltose
 Deglutition (swallowing occurs, once the food is broken down into small pieces and well mixed
with saliva (food bolus)
 The food is broken down by the teeth and mixed with saliva.
 Saliva is excreted by three pairs of glands:
- The parotid gland (below the ear)
- The submandibular (under the tongue)
- The sublingual (under the tongue)
 Saliva contains water, mucus and the enzyme salivary amylase.

Functions of Saliva

 It lubricates food with mucus, making it easier to swallow.

 It contains the enzyme salivary amylase, which acts on cooked starch turning some of it into
maltose.
 It keeps the mouth and teeth clean.
 The ball of food that leaves the mouth is known as a bolus.

Functions of the Tongue

 Taste: it is covered with thousands of taste buds. These are sensitive to salt, sweet, sour and
bitter chemicals in food and drink.
 They help us enjoy food and drink and warn us when food, drink are off or inedible.
 Chewing: the tongue aids chewing by moving the food around the mouth, pushing it between the
teeth and covering it with saliva, which contains enzymes that start the digestive process.
 The food is turned into a partially digested mass known as a bolus.
 Swallowing: when the food is ready to travel to the stomach, the tongue pushes it to the back of
the mouth.

Our 3 types of teeth:

1. Incisors - front teeth

2. Canines - pointy teeth
3. Molars - back teeth
*They are all shaped differently to help us eat and digest food

So how many teeth do humans have?

We have 2 sets
- 20 baby teeth
- 32 adult teeth

Why do they fall out?

 Just like some animals, we are born with two sets of teeth
 The baby teeth fall out so the adult teeth can grow in

The Mouth

 Important for the mechanical digestion of food

 The saliva contains SALIVARY AMYLASE or PTYALIN that starts the INITIAL digestion of
carbohydrates
 The Esophagus

 A hollow collapsible tube

 Serves as passage for food bolus from mouth to stomach by peristalsis
 Measures 10 inches in length
 Made up of stratified squamous epithelium
 The distal end of the esophagus is guarded by lower esophageal sphincter (LES) otherwise
known as the cardiac sphincter that prevents gastric reflux
 The food passes into the pharynx (a muscular tube behind the mouth) and down the oesophagus.
 The epiglottis a small flap of cartilage blocks the entrance to the larynx, this stops the food going
down the wrong way and prevents choking.
 The upper third contains skeletal muscles
 The middle third contains mixed skeletal and smooth muscles
 The lower third contains smooth muscles and the esophago-gastric/ cardiac sphincter is found
here
 Functions to carry or propel foods from the oropharynx to the stomach
 Phases in swallowing:
o Phase 1 - Voluntary stage of swallowing
 Bolus - voluntarily squeezed or rolled posteriorly against the palate
 Swallowing cannot be stopped
o Phase 2 - Pharyngeal stage of swallowing
 Bolus reaches posterior mouth & pharynx stimulates receptors initiate
series of automatic pharyngeal muscle contraction
o Phase 3 - Esophageal stage of swallowing
 Conducts food rapidly to the stomach

Two types of peristaltic movements:

1° peristalsis:

- continuation of a peristaltic wave

- begins in pharynx & spreads into esophagus
- passes in 8-10 sec

2° peristaltic waves:

- results from the distention of esophagus

- begins if the 1° wave failed to push the food down

 It is a J-shaped, elastic organ.

 Food enters it from the oesophagus through the cardiac sphincter.
 The cardiac sphincter, is a valve that stops back flow of the stomach`s contents.
 Food leaves the stomach through the pyloric sphincter into the duodenum (first part of the
small intestine).
 it is located in the LUQ of the abdomen that has a capacity of 1,500 ml.
  The functions of the stomach are generally to digest the food (proteins) and to propel the
digested materials into the SI for final digestion
 The stomach has the following regions: cardiac region, fundus, body and antrum or pyloric
region
 It has greater and lesser curvature
 Considered as the most dilatable organ
 The Glands and cells in the stomach secrete digestive enzymes:

The GIT PHYSIOLOGY

Stomach:

1. Parietal cells- HCl acid and Intrinsic factor

2. Chief cells- pepsin digestion of PROTEINS!
3. Antral G-cells- gastrin
4. Argentaffin cells- serotonin
5. Mucus neck cells- mucus

Mechanical digestion – storage, mixing and liquefaction of bolus of food into a semisolid
mixture called chyme. The rugaue liquefy solid food particles through grinding motion

Secretion – 1,500 to 3,000 mls. Of gastric joice is secreted by the glands inhe gastric mucosa.
The gastric juice is composed of mucus, HCL, pepsinogen and water. Gastrin (a hormone) is
secreted into the bloodstream

Chemical digestion – digestion of protein starts in the stomach through the action of pepsin
which converts proteins into polypeptides

 Amylase from the salivary glands is inactivated by the acidity in the stomach so CHO digestion
stops
 Pepsinogen (inactive enzyme) is converted into pepsin (active form) in the presence of HCL
 Milk is curdled and casein is free, through the action of renin. Digestion of emulsified fats also
starts in the stomach due to the presence of small amounts off gastric lipase

Protection : the acid medium is responsible for the reduced activity of harmful bacteria that may
have been taken in with food. It also provides a favorable medium for the absorption of calcium
and other minerals
Absorption: Minimal water, alcohol, glucose, and some drugs are absorbed through the gastric
mucosa
Controls passage of chyme into duodenum through peristaltic waves, CHO are emptied within 1
to 2 hours, protein 3 to 4 hours. Once acidic chyme is formed, slow peristaltic waves travel from
the fundus to the pylorus thus there will be pressure build up and trigger the pyloric sphincter to
open
 SMALL INTESTINE

The Small intestine

 6 meter long ( 20 to 22 feet) that extends from the pyloric sphincter to the ileocecal valve
 divided into 3 parts: the Duodenum, Jejunum and Ileum
 The duodenum contains the two openings for the bile and pancreatic ducts
 The ileum is the longest part (about 12 feet)
 Majority of the digestive process is completed in the duodenum
 Complete digestion of foods set in

1. Mucus secretion goblet cells and duodenal (Brunner’s glands) secretes mucus to protect the
mucosa
2. Secretion of enzymes
 Brush border cells secretes sucrase, maltase and enterokinase which acts on
disaccharides (CHO).
 Peptidase acts on polypeptides (CHON)
 Enterokinase activates trypsinogen from the pancreas
4. Secretion of hormones
 Endocrine cells sceretes cholecystokinin, secretin, and enterogastrone that regulate
the secretion of bile, pancreatic juice and gastric juice

The GIT Physiology

SYMPATHETIC

 Generally INHIBITORY!
 Decreased gastric secretions
 Decreased GIT motility
 But: Increased sphincteric tone and constriction of blood vessels

PARASYMPATHETIC

 Generally EXCITATORY!
 Increased gastric secretions
 Increased gastric motility
 But: Decreased sphincteric tone and dilation of blood vessels

LARGE INTESTINE

 It deals with waste.

 It extends from the ileocecal valve to the anus and measures approximately 1.5m long. (5 to 6
feet long)
 It consists of the following:
o The caecum: a small pouch; the ileum empties its contents into the caecum
through the ileo-caecal valve.
o The colon: ascending, transverse, descending colon.
o The appendix: narrow tube attached to the caecum.
o The final segments of the large intestine are the rectum and he anus

The GIT ANATOMY

The Large intestine

 Approximately 5 feet long, with parts:

1. The cecum- widest diameter, prone to rupture
2. The appendix
3. The ascending colon
4. The transverse colon
5. The descending colon
6. The sigmoid- most mobile, prone to twisting
7. The rectum

1. Motor activities: haustral churning and peristalsis

2. Secretion: the mucus protects the mucosa from injury, binds fecal particles into a formed mass,
lubricates and allows passage of fecal residue and counteracts the effects of acid-forming
bacteria
3. Absorption of water, sodium and chloride – approximately 800 to 1,00 mls. Of water is
absorbed in the large intestine
4. Vitamin synthesis – colonic bacterial flora synthesize vitamin K, thiamine, riboflavin, vitamin
B12, folic acid, biotin and nicotinic acid
5. Formation of feces – fecal material is ¾ water and ¼ solid material
6. Defecation – the act of expelling feces from the body

4 MAJOR FUNCTION GIT/DIGESTIVE SYSTEM

1. Motility
2. Secretion
3. Digestion
4. Absorption

ASSESSMENT OF CLIENTS WITH GASTROINTESTINAL DISORDER

The GIT Physiology: LIVER

 Functions to store excess glucose, fats and amino acids

 Also stores the fat soluble vitamins- A, D and the water soluble- Vitamin B12
 Produces the BILE for normal fat digestion
 The Von Kupffer cells remove bacteria in the portal blood
 Detoxifies ammonia into urea

The GIT anatomy

The gallbladder

 Located below the liver

 The cystic duct joins the hepatic duct to become the bile duct
 The common bile duct joins the pancreatic duct in the sphincter of Oddi in the first part of the
duodenum

The GIT Physiology

 Stores and concentrates bile

 Contracts during the digestion of fats to deliver the bile
 Cholecystokinin is released by the duodenal cells, causing the contraction of the gallbladder and
relaxation of the sphincter of Oddi

The pancreas

 A retroperitoneal gland
 Functions as an endocrine and exocrine gland
 The pancreatic duct (major) joins the common bile duct in the sphincter of Oddi

The GIT Physiology

 The exocrine function of the pancreas is the secretion of digestive enzymes for carbohydrates,
fats and proteins
 Pancreatic amylase carbohydrates
 Pancreatic lipase (steapsin) fats
 Trypsin, Chymotrypsin and Peptidases proteins
 Bicarbonate to neutralize the acidic chyme. Stimulated by SECRETIN!

Gastrointestinal Assessment
Laboratory Procedures
COMMON LABORATORY PROCEDURES

FECALYSIS

 Examination of stool consistency, color and the presence of occult blood.

 Special tests for fat, nitrogen, parasites, ova, pathogens and others

FECALYSIS: Occult Blood Testing

 Instruct the patient to adhere to a 3-day meatless diet

 No intake of NSAIDS, aspirin and anti-coagulant
 Screening test for colonic cancer

Upper GIT study: barium swallow

 Examines the upper GI tract

 Barium sulfate is usually used as contrast

Upper GIT study: barium swallow

 Pre-test: NPO post-midnight

 Post-test: Laxative is ordered, increase pt fluid intake, instruct that stools will turn white, monitor
for obstruction

Lower GIT study: barium enema

 Examines the lower GI tract
 Pre-test: Clear liquid diet and laxatives, NPO post-midnight, cleansing enema prior to the test

Lower GIT study: barium enema

 Post-test: Laxative is ordered, increase patient fluid intake, instruct that stools will turn
white, monitor for obstruction

Gastric analysis

 Aspiration of gastric juice to measure pH, appearance, volume and contents

 Pre-test: NPO 8 hours, avoidance of stimulants, drugs and smoking
 Post-test: resume normal activities

EGD (esophagogastroduodenoscopy)

 Visualization of the upper GIT by endoscope

 Pre-test: ensure consent, NPO 8 hours, pre-medications like atropine and anxiolytics
 Intra-test: position : LEFT lateral to facilitate salivary drainage and easy access
 Post-test: NPO until gag reflex returns, place patient in SIMS position until he awakens, monitor
for complications, saline gargles for mild oral discomfort

Lower GI- scopy

 Use of endoscope to visualize the anus, rectum, sigmoid and colon

 Pre-test: consent, NPO 8 hours, cleansing enema until return is clear
 Intra-test: position is LEFT lateral, right leg is bent and placed anteriorly
 Post-test: bed rest, monitor for complications like bleeding and perforation

Cholecystography

 Examination of the gallbladder to detect stones, its ability to concentrate, store and release the
bile
 Pre-test: ensure consent, ask allergies to iodine, seafood and dyes; contrast medium is
administered the night prior, NPO after contrast administration
 Post-test: Advise that dysuria is common as the dye is excreted in the urine, resume normal
activities

Paracentesis

 Removal of peritoneal fluid for analysis

 Pre-test: ensure consent, instruct to VOID and empty bladder, measure abdominal girth
 Intra-test: Upright on the edge of the bed, back supported and feet resting on a foot stool

Liver biopsy
 Pretest
 Consent
 NPO
 Check for the bleeding parameters
 Intratest
o Position: Semi fowler’s LEFT lateral to expose right side of abdomen
 Post-test: position on RIGHT lateral with pillow underneath, monitor VS and complications like
bleeding, perforation. Instruct to avoid lifting objects for 1 week

The NURSING PROCESS in GIT Disorders

Assessment

 Health history Nursing History

 PE
 Laboratory procedures

The ABDOMINAL examination

The sequence to follow is:

 Inspection
 Auscultation
 Percussion

Physiologic responses to GIT dysfunction

1. Halitosis
• commonly known as bad breath, is a condition characterized by an unpleasant odor
emanating from the mouth
. • It can be caused by various factors, including:
1. Poor Oral Hygiene: Inadequate brushing, flossing, and tongue cleaning can lead to
the accumulation of food particles and bacteria in the mouth, resulting in bad breath.
2. Food and Drink: Certain foods and beverages, such as onions, garlic, coffee, and
alcohol, can cause temporary bad breath due to their strong odors.
3. Tobacco Use: Smoking and other forms of tobacco consumption can contribute to
halitosis by leaving a foul-smelling residue in the mouth and lungs.
4. Dry Mouth: Saliva helps cleanse the mouth and neutralize acids produced by bacteria.
A lack of saliva, often caused by dehydration, medication side effects, or certain medical
conditions, can lead to bad breath.
5. Dental Issues: Gum disease, tooth decay, oral infections, and poorly fitting dental
appliances (such as dentures) can harbor bacteria and produce malodor.
6. Medical Conditions: Halitosis can sometimes be a symptom of underlying health
problems, including respiratory infections, sinusitis, digestive disorders, diabetes, liver or
kidney disease, and some cancers.

To address halitosis, individuals can take the following steps:

1. Maintain good oral hygiene by brushing your teeth twice a day, flossing daily,
and cleaning the tongue with a tongue scraper or toothbrush.
2. Stay hydrated by drinking plenty of water throughout the day to stimulate
saliva production. 3. Avoid tobacco use and limit consumption of odorous foods
and beverages.
4. Visit a dentist regularly for professional cleanings and to address any dental
issues.
5. If halitosis persists despite oral hygiene efforts, consult a healthcare
professional to rule out any underlying medical conditions that may be
contributing to the problem.
2. Dysphagia
• Dysphagia is a medical condition characterized by difficulty swallowing. It can
occur at different stages of the swallowing process: oral (mouth), pharyngeal
(throat), or esophageal (esophagus). Dysphagia can result from various underlying
causes, including:
• Neurological Disorders: Conditions such as stroke, Parkinson's disease,
multiple sclerosis, and ALS (amyotrophic lateral sclerosis) can affect the
nerves and muscles involved in swallowing, leading to dysphagia. •
Structural Abnormalities: Structural issues in the mouth, throat, or
esophagus, such as tumors, strictures, or narrowing of the esophagus, can
impede the normal swallowing process.
• Muscle Weakness or Dysfunction: Weakness or dysfunction of the
muscles involved in swallowing, which can be caused by conditions like
muscular dystrophy or myasthenia gravis, may result in dysphagia.
• Gastroesophageal Reflux Disease (GERD): Chronic acid reflux can
cause irritation and inflammation of the esophagus, leading to swallowing
difficulties.
 • Aging: Normal aging can lead to changes in the muscles and tissues
involved in swallowing, increasing the risk of dysphagia in older adults.
• Traumatic Injuries: Injuries to the head, neck, or chest, such as those
resulting from accidents or surgery, may cause damage to the structures
involved in swallowing.
• Symptoms of dysphagia can vary depending on the underlying cause but may include:
1. Difficulty initiating swallowing
2. Feeling of food sticking in the throat or chest
3. Choking or coughing while eating or drinking
4. Regurgitation of food or liquids
5. Pain or discomfort during swallowing
6. Unintentional weight loss or malnutrition due to difficulty eating
• Treatment for dysphagia depends on the underlying cause and severity of symptoms. It
may include:
✓ Dietary modifications, such as soft or pureed foods or thickened liquids, to make
swallowing easier
✓ Swallowing therapy with a speech-language pathologist to improve swallowing
function and coordination
✓ Medications to treat underlying conditions like GERD or neurological disorders
✓ Surgical interventions to address structural abnormalities or remove obstructions
✓ Use of feeding tubes for individuals who are unable to swallow safely or adequately
✓ If you or someone you know is experiencing difficulty swallowing, it's essential to
seek evaluation and treatment from a healthcare professional, such as a speech-language
pathologist, gastroenterologist, or otolaryngologist (ENT specialist)

3. Odynophagia
• A medical term used to describe pain or discomfort experienced while swallowing.
Unlike dysphagia, which refers to difficulty swallowing, odynophagia specifically
focuses on the sensation of pain associated with swallowing.
• Causes by various factors, including:
1. Infections: Conditions such as pharyngitis (inflammation of the throat), tonsillitis
(inflammation of the tonsils), or esophagitis (inflammation of the esophagus) caused by
bacterial, viral, or fungal infections can lead to pain during swallowing.
2. Trauma: Injuries to the mouth, throat, or esophagus due to trauma or surgery can
cause pain and discomfort during swallowing.
3. Gastroesophageal Reflux Disease (GERD): Chronic acid reflux can lead to irritation
and inflammation of the esophagus, resulting in odynophagia.
4. Esophageal Disorders: Conditions such as esophageal ulcers, strictures (narrowing of
the esophagus), or motility disorders can cause pain during swallowing.
5. Tumors or Growths: Benign or malignant growths in the mouth, throat, or esophagus
can obstruct the passage of food and cause pain with swallowing.
 6. Medications: Certain medications, particularly those that can irritate the lining of the
esophagus, may cause odynophagia as a side effect.
7. Radiation Therapy: Radiation treatment for head and neck cancers can lead to
inflammation and damage to the tissues of the mouth, throat, and esophagus, resulting in
pain while swallowing.
• Symptoms of odynophagia may include:
1. Sharp or stabbing pain in the throat or chest while swallowing
2. Pain that worsens with swallowing solid foods, liquids, or both
3. Discomfort or burning sensation in the throat or chest 4. Difficulty eating or drinking
due to the pain associated with swallowing
• Treatment for odynophagia depends on the underlying cause and may include:

✓ Medications to treat infections, reduce inflammation, or manage acid reflux

✓ Dietary modifications, such as consuming soft or liquid foods to minimize irritation
✓ Pain management strategies, including over-the-counter pain relievers or prescription
medications
✓ Lifestyle modifications, such as avoiding spicy or acidic foods, quitting smoking, or
elevating the head while sleeping to reduce acid reflux
✓ Surgical interventions or other procedures to address structural abnormalities or
remove obstructions causing pain with swallowing.

4. Pyrosis
• another term for heartburn, a common symptom characterized by a burning sensation in the
chest or throat. It occurs when stomach acid flows back up into the esophagus, causing irritation
and inflammation of the esophageal lining.
• Pyrosis typically occurs after eating or when lying down, and it can be exacerbated by certain
foods, beverages, or lifestyle factors.
• Causes
1. Gastroesophageal Reflux Disease (GERD): Chronic acid reflux, where stomach acid
frequently flows back into the esophagus, is a common cause of pyrosis. GERD can result from a
weakened lower esophageal sphincter (the valve that prevents stomach acid from flowing back
up) or other factors contributing to increased stomach acid production.
2. Hiatal Hernia: A hiatal hernia occurs when part of the stomach protrudes into the chest
through the diaphragm. This can weaken the lower esophageal sphincter, allowing acid to reflux
into the esophagus and causing pyrosis.
3. Dietary Factors: Certain foods and beverages, such as spicy or acidic foods, citrus fruits,
tomatoes, chocolate, caffeine, alcohol, and fatty or fried foods, can trigger pyrosis in susceptible
individuals.
4. Overeating: Consuming large meals or lying down shortly after eating can increase the
likelihood of experiencing pyrosis by putting pressure on the stomach and promoting acid reflux.
5. Obesity: Excess body weight can contribute to pyrosis by putting pressure on the abdomen
and increasing the risk of acid reflux.
6. Smoking: Smoking can weaken the lower esophageal sphincter and impair the function of the
esophagus, leading to an increased risk of pyrosis.
• Symptoms of pyrosis may include:
✓ Burning sensation in the chest or throat (often described as a "burning" or "gnawing"
pain)
✓ Sour or bitter taste in the mouth ✓ Regurgitation of stomach contents into the mouth or
throat
✓ Difficulty swallowing or a sensation of food sticking in the chest
✓ Chronic cough or hoarseness
✓ Discomfort or pain that worsens when lying down or bending over
• Treatment
✓ lifestyle modifications –
▪ avoiding trigger foods
▪ eating smaller meal
▪ maintaining a healthy weight
▪ avoiding lying down immediately after eating
▪ quitting smoking
▪ elevating the head of the bed while sleeping.
✓ dietary changes
✓ medications - including nonsteroidal anti-inflammatory drugs (NSAIDs), aspirin, certain
antibiotics, and medications for high blood pressure, can irritate the esophageal lining or weaken
the LES, contributing to pyrosis.
5. Dyspepsia
• commonly known as indigestion, is a term used to describe a range of symptoms
related to the upper gastrointestinal tract.
• Symptoms may include:
✓ Pain or discomfort: Dyspepsia often presents as a feeling of discomfort or pain in the
upper abdomen. This discomfort may be described as burning, gnawing, or aching.
✓ Fullness or bloating: Individuals with dyspepsia may experience a sensation of
fullness or bloating in the upper abdomen, even after consuming a small amount of food.
• Early satiety: Dyspepsia can cause feelings of fullness or satiety shortly after beginning a
meal, leading to a reduced appetite.
• Nausea: Some individuals with dyspepsia may experience nausea or an uncomfortable
sensation in the stomach.
• Heartburn: While heartburn is often associated with gastroesophageal reflux disease (GERD),
it can also be a symptom of dyspepsia.
• Belching or flatulence: Excessive belching or passing of gas may occur in individuals with
dyspepsia.

• The exact cause of dyspepsia is often unclear, but it may be related to various factors,
including:
 ✓ Dietary habits: Consuming spicy, fatty, or acidic foods, as well as overeating or eating
too quickly, can contribute to dyspepsia symptoms.
✓ Helicobacter pylori infection: Infection with the bacterium Helicobacter pylori can
lead to inflammation of the stomach lining, causing dyspepsia symptoms
✓ Certain medications, such as nonsteroidal anti-inflammatory drugs (NSAIDs),
antibiotics, and bisphosphonates, may irritate the stomach lining and cause dyspepsia.
✓ Gastrointestinal disorders: Conditions such as gastroesophageal reflux disease
(GERD), peptic ulcers, gastritis, or gastroparesis can manifest with symptoms of
dyspepsia.
✓ Stress and anxiety: Psychological factors, including stress and anxiety, can exacerbate
symptoms of dyspepsia.

• Treatment aims to alleviate symptoms and address any underlying causes.

✓ This may involve lifestyle modifications
✓ dietary changes
✓ stress reduction techniques
✓ medications to reduce stomach acid,
✓ manage Helicobacter pylori infection, or alleviate symptoms. In some cases,
further investigation or diagnostic testing may be necessary to identify the
underlying cause of dyspepsia. Individuals experiencing persistent or severe
symptoms of dyspepsia should consult with a healthcare professional for
evaluation and appropriate management.
6. Anorexia
• in its broader sense, refers to a loss of appetite or reduced desire to eat. It can be a
symptom of various medical conditions, including infections, gastrointestinal disorders,
hormonal imbalances, psychological disorders, medications, and chronic illnesses.
Anorexia may lead to unintended weight loss, malnutrition, weakness, fatigue, and other
complications depending on the underlying cause.
7. Satiety
• refers to the feeling of fullness or satisfaction that occurs after eating, which leads to a
decreased desire to continue eating. It is an important aspect of regulating food intake and
maintaining a healthy body weight. Satiety is influenced by various factors, including the
volume and nutrient content of food, hormonal signals, psychological factors, and
individual differences in metabolism and sensitivity to food cues.
• Several mechanisms contribute to the sensation of satiety:
✓ Stretch receptors: When the stomach and intestines are filled with food, stretch
receptors in the gastrointestinal tract send signals to the brain indicating that the stomach
is full, which contributes to feelings of satiety.
 ✓ Hormonal signals: Hormones released from the gastrointestinal tract and adipose
tissue, such as leptin, ghrelin, peptide YY (PYY), and cholecystokinin (CCK), play a role
in regulating appetite and satiety. For example, leptin, often referred to as the "satiety
hormone," signals to the brain that energy stores are sufficient, reducing hunger and
promoting satiety
✓ Nutrient composition of food: Foods high in protein, fiber, and water content tend to
increase satiety and prolong feelings of fullness compared to foods high in refined
carbohydrates and fats, which are typically less satiating.

8. Nausea
• is a sensation of discomfort or unease in the stomach, often accompanied by an urge to
vomit.
• caused by various factors, including:
✓ Gastrointestinal Issues: Nausea can be a symptom of gastrointestinal disorders such
as gastroenteritis (stomach flu), food poisoning, gastritis (inflammation of the stomach
lining), peptic ulcers, or gastroesophageal reflux disease (GERD).
✓ Infections: Viral or bacterial infections, such as the flu, norovirus, or Helicobacter
pylori infection, can cause nausea and vomiting.
✓ Motion Sickness: Nausea and vomiting can occur in response to motion, such as
during car rides, boat trips, or amusement park rides.
✓ Medications: Some medications, including antibiotics, pain relievers, chemotherapy
drugs, and certain supplements, can cause nausea as a side effect.
✓ Pregnancy: Nausea and vomiting, often referred to as morning sickness, are common
symptoms during early pregnancy, typically occurring in the first trimester.
✓ Migraines: Nausea is a common symptom associated with migraines, often occurring
before or during a migraine headache.
✓ Anxiety or Stress: Emotional stress or anxiety can trigger nausea in some individuals.
✓ Dietary Factors: Certain foods or beverages, such as fatty or spicy foods, strong
odors, alcohol, or caffeine, can trigger nausea in susceptible individuals.
✓ Underlying Medical Conditions: Nausea can be a symptom of various medical
conditions, including kidney disease, liver disorders, pancreatitis, gallbladder disease, or
thyroid disorders.
• Treatment for nausea depends on the underlying cause and may include:
✓ Medications: Anti-nausea medications, such as ondansetron, promethazine, or
dimenhydrinate, may be prescribed to alleviate nausea and vomiting.
✓ Dietary Changes: Avoiding trigger foods or beverages and consuming bland, easily
digestible foods may help reduce nausea.
✓ Hydration: Drinking clear fluids, such as water, herbal tea, or electrolyte solutions,
can help prevent dehydration associated with vomiting.
 ✓ Ginger: Ginger supplements, tea, or ginger ale may help alleviate nausea in some
individuals
✓ Rest and Relaxation: Getting adequate rest and practicing relaxation techniques, such
as deep breathing or meditation, may help reduce nausea associated with stress or
anxiety.

9. Vomiting
• Vomiting, also known as emesis, is the forceful expulsion of stomach contents through
the mouth and sometimes the nose. It is a reflex action coordinated by the vomiting
center in the brainstem in response to various triggers.
• Vomiting can occur as a result of:
✓ Gastrointestinal Issues: Conditions affecting the stomach or intestines, such as
gastroenteritis (stomach flu), food poisoning, gastritis (inflammation of the stomach
lining), peptic ulcers, or gastroesophageal reflux disease (GERD), can lead to vomiting.
✓ Infections: Viral or bacterial infections, such as the flu, norovirus, or gastrointestinal
infections, can cause vomiting as the body's defense mechanism to expel pathogens.
✓ Motion Sickness: Vomiting can occur in response to motion, such as during car rides,
boat trips, or amusement park rides, due to conflicting signals between the inner ear and
the visual system.
✓ Medications: Some medications, including chemotherapy drugs, opioid pain relievers,
antibiotics, and certain supplements, can cause vomiting as a side effect.
✓ Pregnancy: Vomiting, often referred to as morning sickness, is a common symptom
during early pregnancy, typically occurring in the first trimester.
✓ Migraines: Vomiting is a common symptom associated with migraines, often
occurring before or during a migraine headache.
✓ Toxic Ingestion: Ingestion of toxins, such as alcohol, certain chemicals, or poisonous
plants, can trigger vomiting as the body attempts to rid itself of harmful substances.
✓ Psychological Factors: Emotional stress, anxiety, or psychological disorders, such as
eating disorders or bulimia nervosa, can lead to vomiting.
✓ Underlying Medical Conditions: Vomiting can be a symptom of various medical
conditions, including kidney disease, liver disorders, pancreatitis, gallbladder disease, or
intestinal obstruction.
✓ Surgical Procedures: Vomiting may occur as a side effect of anesthesia or as a post-
operative complication following certain surgical procedures.
• Treatment for vomiting depends on the underlying cause and may include:
✓ Fluid Replacement: Oral rehydration solutions or intravenous fluids may be
administered to prevent dehydration associated with vomiting.
✓ Medications: Antiemetic medications, such as ondansetron, promethazine, or
metoclopramide, may be prescribed to alleviate nausea and vomiting.
✓ Dietary Changes: Consuming bland, easily digestible foods and avoiding trigger
foods or beverages may help reduce vomiting.
 ✓ Rest and Recovery: Getting adequate rest and avoiding activities or triggers that
exacerbate vomiting can aid in recovery.
✓ Treatment of Underlying Conditions: Treating underlying medical conditions or
addressing any contributing factors may be necessary to prevent recurrent vomiting.

10. Abdominal cramping

• Abdominal cramping refers to pain or discomfort in the abdomen that is often described
as a sharp, stabbing, or cramping sensation. It can vary in intensity and duration and may
be accompanied by other symptoms such as bloating, gas, diarrhea, or constipation.
• Abdominal cramping can have numerous causes, including:
✓ Gastrointestinal Issues: Conditions affecting the digestive system, such as irritable
bowel syndrome (IBS), inflammatory bowel disease (IBD), gastroenteritis (stomach flu),
food poisoning, gastritis (inflammation of the stomach lining), or gastrointestinal
infections, can lead to abdominal cramping.
✓ Menstrual Cramps: Many menstruating individuals experience abdominal cramping,
known as dysmenorrhea, during their menstrual periods due to uterine contractions.
✓ Gas and Bloating: Excess gas or bloating in the digestive tract can cause abdominal
discomfort and cramping.
✓ Constipation: Difficulty passing stool or infrequent bowel movements can lead to
abdominal cramping and discomfort.
✓ Diarrhea: Rapid movement of stool through the intestines, as seen in diarrhea, can
cause cramping and abdominal pain.
✓ Food Intolerances or Sensitivities: Consuming foods that an individual is intolerant
or sensitive to, such as lactose or gluten, can lead to abdominal cramping and discomfort.
✓ Muscle Strain: Strain or injury to the abdominal muscles, such as during strenuous
exercise or lifting heavy objects, can cause cramping or soreness.
✓ Appendicitis: Inflammation of the appendix, known as appendicitis, can cause sudden
and severe abdominal pain and cramping, often requiring immediate medical attention.
✓ Kidney Stones: Passing kidney stones can cause intense abdominal or flank pain,
often described as cramping or sharp in nature.
✓ Gynecological Issues: Conditions affecting the reproductive organs, such as ovarian
cysts, endometriosis, or pelvic inflammatory disease (PID), can cause abdominal
cramping in women.
• Treatment for abdominal cramping depends on the underlying cause and may include:
✓ Pain Relief: Over-the-counter pain medications, such as ibuprofen or acetaminophen,
may help alleviate abdominal cramping.
✓ Hydration: Drinking plenty of fluids can help alleviate abdominal cramping
associated with dehydration or diarrhea.
✓ Dietary Changes: Avoiding trigger foods or beverages and consuming a balanced diet
rich in fiber may help alleviate abdominal cramping associated with digestive issues.
 ✓ Medications: Depending on the underlying cause, medications such as
antispasmodics, laxatives, or antibiotics may be prescribed.
✓ Heat Therapy: Applying a heating pad or warm compress to the abdomen may help
relax abdominal muscles and alleviate cramping.

11. Abdominal distention

• Abdominal distention, also known as bloating or swollen belly, refers to an abnormal
increase in the size or girth of the abdomen. It is characterized by a feeling of fullness,
tightness, or discomfort in the abdominal area.
• Abdominal distention can be caused by various factors, including:
✓ Gas: Excess gas in the digestive tract, often due to swallowing air while eating,
consuming gas-producing foods, or fermentation of undigested carbohydrates by gut
bacteria, can lead to abdominal distention and bloating.
✓ Constipation: Difficulty passing stool or infrequent bowel movements can cause stool
to accumulate in the colon, leading to abdominal distention and discomfort.
✓ Dietary Factors: Consuming certain foods or beverages, such as carbonated drinks,
beans, cruciferous vegetables (e.g., broccoli, cabbage), onions, or artificial sweeteners,
can contribute to abdominal bloating and distention in some individuals.
✓ Fluid Retention: Conditions such as heart failure, liver disease, kidney disease, or
hormonal imbalances can lead to fluid retention in the abdomen, causing abdominal
distention.
✓ Gastrointestinal Disorders: Conditions affecting the digestive system, such as
irritable bowel syndrome (IBS), inflammatory bowel disease (IBD), celiac disease, or
gastroparesis, can cause abdominal bloating and distention as a result of altered gut
motility or inflammation.
• Abdominal distention can have various causes, including:
▪ Irritable Bowel Syndrome (IBS): IBS is a gastrointestinal disorder characterized by
abdominal pain, bloating, and changes in bowel habits. Bloating and abdominal
distention are common symptoms, particularly after eating certain trigger foods or during
periods of stress.
▪ Inflammatory Bowel Disease (IBD): Conditions such as Crohn's disease and ulcerative
colitis can cause inflammation and swelling in the intestines, leading to abdominal
distention and discomfort.
▪ Food Intolerances or Sensitivities: Consuming foods that an individual is intolerant or
sensitive to, such as lactose or gluten, can lead to bloating and abdominal distention.
▪ Gastrointestinal Obstruction: Blockage or obstruction in the gastrointestinal tract,
such as from tumors, adhesions, hernias, or impacted stool, can cause abdominal
distention, nausea, and vomiting.
▪ Ascites: Ascites is a condition characterized by the accumulation of fluid in the
abdominal cavity, often seen in individuals with liver disease, cancer, or heart failure. It
can lead to significant abdominal distention and discomfort.
 ▪ Ovarian Cysts or Tumors: Ovarian cysts or tumors can cause abdominal distention,
particularly if they become large or produce excess fluid.
▪ Pregnancy: Abdominal distention is a common symptom of pregnancy, particularly as
the uterus expands to accommodate the growing fetus.
✓ Bile Acid Deficiency: Bile acids produced by the liver are essential for the absorption
of fats and fat-soluble vitamins in the small intestine. Conditions that disrupt bile acid
production or impair bile flow, such as liver disease or gallbladder dysfunction, can lead
to malabsorption of fats and fat-soluble vitamins.
✓ Short Bowel Syndrome: Short bowel syndrome occurs when a significant portion of
the small intestine is surgically removed or damaged, leading to malabsorption of
nutrients.
✓ Parasitic Infections: Certain parasitic infections, such as giardiasis or intestinal
worms, can damage the lining of the intestines and interfere with nutrient absorption.
✓ Medications: Some medications, including antibiotics, proton pump inhibitors (PPIs),
and certain anti-inflammatory drugs, can disrupt the balance of gut bacteria or impair the
absorption of specific nutrients.
Symptoms of malabsorption can vary depending on the underlying cause and the specific
nutrients affected but may include:
✓ Chronic diarrhea or loose stools
✓ Abdominal pain or cramping
✓ Bloating or gas
✓ Fatigue
✓ Weight loss
✓ Weakness
✓ Muscle cramps or spasms
✓ Nutrient deficiencies, such as iron deficiency anemia, vitamin D deficiency, or vitamin
B12 deficiency
• Treatment for malabsorption depends on the underlying cause and may include:
✓ Dietary modifications, such as avoiding trigger foods or following a specific diet to
manage symptoms and improve nutrient absorption.
✓ Nutritional supplementation to address specific nutrient deficiencies, such as vitamin
or mineral supplements.
✓ Medications to manage underlying conditions or symptoms, such as anti-inflammatory
drugs, antibiotics, or pancreatic enzyme replacement therapy.
✓ Lifestyle changes, such as quitting smoking or reducing alcohol intake, to improve
overall digestive health.
✓ In some cases, surgery may be necessary to address structural abnormalities or
complications associated with malabsorption
• Treatment for abdominal distention depends on the underlying cause and may include:
 ✓ Dietary Changes: Avoiding gas-producing foods, such as beans, broccoli, cabbage,
and carbonated beverages, may help alleviate bloating and abdominal distention.
✓ Medications: Over-the-counter remedies for gas relief, laxatives for constipation, or
medications to reduce fluid retention may be prescribed depending on the underlying
cause.
✓ Fluid Management: In cases of ascites or fluid retention, fluid restriction or
medications to reduce fluid buildup may be necessary.

12. Malabsorption
• refers to a condition in which the body is unable to properly absorb nutrients from the
diet, leading to deficiencies in essential vitamins, minerals, fats, proteins, and
carbohydrates. Malabsorption can occur due to various factors that interfere with the
digestion and absorption process in the gastrointestinal tract.
• Causes of malabsorption include:
✓ Celiac Disease: Celiac disease is an autoimmune disorder characterized by an
abnormal immune response to gluten, a protein found in wheat, barley, and rye. In
individuals with celiac disease, consumption of gluten triggers damage to the lining of the
small intestine, leading to malabsorption of nutrients.
✓ Inflammatory Bowel Disease (IBD): Conditions such as Crohn's disease and ulcerative
colitis can cause inflammation and damage to the lining of the intestines, impairing the
absorption of nutrients.
✓ Pancreatic Insufficiency: The pancreas produces digestive enzymes necessary for
breaking down fats, proteins, and carbohydrates in the small intestine. Conditions such as
chronic pancreatitis, pancreatic cancer, or cystic fibrosis can impair pancreatic function,
leading to malabsorption of nutrients.
✓ Small Intestinal Bacterial Overgrowth (SIBO): SIBO occurs when an abnormal
overgrowth of bacteria in the small intestine can interfere with nutrient absorption and
lead to malabsorption.

12. Diarrhea
• is a common gastrointestinal condition characterized by frequent, loose, and watery
bowel movements. It occurs when the intestines fail to properly absorb water or when
they actively secrete fluids, resulting in an increased volume of stool.
• Diarrhea can have various causes, including:
✓ Infections: Viral, bacterial, or parasitic infections of the gastrointestinal tract are
among the most common causes of acute diarrhea. Common pathogens include
norovirus, rotavirus, Salmonella, Escherichia coli (E. coli), and Giardia lamblia.
✓ Food Poisoning: Ingestion of contaminated food or water, often due to improper
handling, storage, or preparation, can lead to acute diarrhea. Bacterial toxins, such as
those produced by Staphylococcus aureus or Clostridium perfringens, are common
culprits.
 ✓ Medications: Certain medications, including antibiotics, laxatives, antacids containing
magnesium, chemotherapy drugs, and some supplements, can cause diarrhea as a side
effect.
✓ Food Intolerances or Sensitivities: Consuming foods that an individual is intolerant
or sensitive to, such as lactose or gluten, can lead to diarrhea. Conditions such as lactose
intolerance, celiac disease, or non-celiac gluten sensitivity may cause diarrhea in
susceptible individuals.
✓ Inflammatory Bowel Disease (IBD): Conditions such as Crohn's disease and
ulcerative colitis are chronic inflammatory disorders of the gastrointestinal tract that can
cause diarrhea, abdominal pain, and other symptoms.
✓ Irritable Bowel Syndrome (IBS): IBS is a functional gastrointestinal disorder
characterized by recurrent abdominal pain or discomfort associated with changes in
bowel habits, including diarrhea, constipation, or alternating diarrhea and constipation.
✓ Traveler's Diarrhea: Traveler's diarrhea is a type of acute diarrhea that occurs when
individuals travel to regions with poor sanitation or contaminated water sources.
✓ Stress or Anxiety: Emotional stress or anxiety can sometimes trigger diarrhea or
exacerbate existing symptoms in susceptible individuals.
✓ Malabsorption: Conditions that interfere with nutrient absorption in the intestines,
such as celiac disease, pancreatic insufficiency, or bile acid malabsorption, can lead to
diarrhea.
• Symptoms of diarrhea may include:
✓ Frequent, loose, or watery bowel movements
✓ Urgency or inability to control bowel movements
✓ Abdominal cramps or pain ✓ Bloating or gas
✓ Nausea or vomiting
✓ Fever or bloody stools (in severe cases)
• Treatment for diarrhea depends on the underlying cause and severity of symptoms but
may include:
✓ Hydration: Drinking plenty of fluids, including water, clear broth, or oral rehydration
solutions, is essential to prevent dehydration associated with diarrhea.
✓ Dietary Modifications: Consuming bland, easily digestible foods such as rice,
bananas, applesauce, and toast (BRAT diet) may help alleviate symptoms and replenish
lost nutrients.
✓ Medications: Anti-diarrheal medications, such as loperamide (Imodium) or bismuth
subsalicylate (Pepto-Bismol), may be used to alleviate diarrhea symptoms. However,
these medications are not recommended for certain types of infections or in cases of
bloody diarrhea.
✓ Rest and Symptom Management: Getting adequate rest and avoiding triggers, such
as certain foods or stressors, may help manage diarrhea symptoms.
14. Constipation is a common digestive issue characterized by infrequent bowel movements,
difficulty passing stool, or the sensation of incomplete evacuation. It can have various causes and
contributing factors, including:
1. Low Fiber Diet: Diets low in fiber, such as those high in processed foods, refined
grains, and low in fruits and vegetables, can contribute to constipation. Fiber helps add
bulk to stool and promotes regular bowel movements.
2. Dehydration: Inadequate fluid intake can lead to dehydration, resulting in harder and
drier stool that is difficult to pass.
3. Lack of Physical Activity: A sedentary lifestyle or lack of physical activity can slow
own bowel motility and contribute to constipation.
4. Ignoring the Urge to Defecate: Ignoring the urge to have a bowel movement or
delaying bathroom trips can disrupt normal bowel function and lead to constipation.
5. Medications: Certain medications, including opioid pain medications, antidepressants,
antacids containing aluminum or calcium, diuretics, and some anticonvulsants, can cause
constipation as a side effect.
6. Medical Conditions: Various medical conditions can contribute to constipation,
including irritable bowel syndrome (IBS), hypothyroidism, diabetes, neurological
disorders (such as Parkinson's disease or multiple sclerosis), pelvic floor dysfunction,
and structural abnormalities in the colon or rectum.
7. Pregnancy: Hormonal changes during pregnancy, as well as the pressure exerted by the
growing uterus on the intestines, can lead to constipation in pregnant women.
8. Certain Diseases: Chronic conditions such as inflammatory bowel disease (IBD),
diverticulosis, or colorectal cancer can affect bowel habits and lead to constipation.
• Symptoms of constipation may include:
✓ Infrequent bowel movements (typically fewer than three per week)
✓ Difficulty passing stool or straining during bowel movements
✓ Hard, dry, or lumpy stool
✓ Feeling of incomplete evacuation after bowel movements
✓ Abdominal discomfort or bloating
✓ Rectal pain or discomfort
• Treatment for constipation often involves lifestyle modifications and dietary changes to
promote regular bowel movements.
• Some strategies include:
✓ Increasing Fiber Intake: Consuming a diet rich in fiber from fruits, vegetables, whole
grains, legumes, and nuts can help add bulk to stool and promote regular bowel
movements.
✓ Hydration: Drinking plenty of fluids, especially water, can help soften stool and
facilitate bowel movements.
✓ Regular Physical Activity: Engaging in regular exercise and physical activity can
stimulate bowel motility and help prevent constipation.
 ✓ Establishing Regular Bathroom Habits: Responding promptly to the urge to have a
bowel movement and establishing a regular bathroom routine can help regulate bowel
function.
✓ Over-the-Counter Remedies: In some cases, over-the-counter laxatives, stool
softeners, or fiber supplements may be used to alleviate constipation. However, it's
important to use these medications as directed and consult a healthcare professional if
constipation persists or worsens.
❖ Persistent or severe constipation that does not improve with lifestyle modifications or
over-the-counter remedies should be evaluated by a healthcare professional to identify
and address any underlying causes. Additionally, sudden onset of constipation
accompanied by other concerning symptoms such as severe abdominal pain, blood in
stool, or unintended weight loss may require prompt medical attention.

15. Melena
• a medical term used to describe black, tarry stools that result from the presence of
digested blood in the gastrointestinal tract. It typically indicates bleeding in the upper
gastrointestinal tract, specifically in the esophagus, stomach, or duodenum.
• The dark color and characteristic tar-like consistency of melena occur because the blood
has been partially digested by stomach acids.
• Melena is often a sign of significant gastrointestinal bleeding and requires prompt
medical evaluation.
• Some common causes of melena include:
✓ Peptic Ulcers: Ulcers in the stomach lining or duodenum can cause bleeding, leading
to melena.
✓ Esophageal Varices: Enlarged and swollen veins in the esophagus, often associated
with liver cirrhosis, can rupture and cause severe bleeding, resulting in melena.
✓ Gastritis: Inflammation of the stomach lining, often caused by infection with
Helicobacter pylori bacteria or long-term use of nonsteroidal anti-inflammatory drugs
(NSAIDs), can lead to bleeding and melena.
✓ Esophagitis: Inflammation or irritation of the esophagus, commonly caused by
gastroesophageal reflux disease (GERD), infections, or ingestion of corrosive substances,
can result in bleeding and melena
✓ Mallory-Weiss Tears: Tears or lacerations in the mucous membrane lining of the
esophagus, typically caused by severe vomiting or retching, can lead to bleeding and
melena.
✓ Upper Gastrointestinal Cancers: Cancers of the esophagus, stomach, or duodenum
can cause bleeding and melena, particularly in advanced stages of the disease.
✓ Gastric Varices: Similar to esophageal varices, enlarged veins in the stomach can
rupture and cause significant bleeding, resulting in melena.
✓ Gastric Angiodysplasia: Abnormal blood vessels in the stomach can be prone to
bleeding, leading to melena.
• Diagnosis of melena typically involves a combination of medical history, physical examination,
and diagnostic tests, such as blood tests, upper gastrointestinal endoscopy
(esophagogastroduodenoscopy or EGD), and imaging studies. Treatment depends on the
underlying cause of the bleeding and may include medications to suppress acid production,
endoscopic procedures to stop bleeding (such as cautery or banding), blood transfusions, or
surgical intervention in severe cases.
• Melena should be considered a medical emergency, especially if accompanied by symptoms
such as dizziness, weakness, lightheadedness, fainting, or signs of shock. Prompt evaluation and
treatment are essential to identify and address the source of bleeding and prevent complications

16. Weight loss refers to a reduction in body weight, typically resulting from a decrease in body
fat, muscle mass, or fluid. It can occur intentionally through changes in diet, physical activity, or
lifestyle, or unintentionally due to underlying medical conditions or factors.
• Intentional weight loss is often pursued for health or aesthetic reasons and may involve
strategies such as:
✓ Dietary Modifications: Adopting a balanced and nutritious diet that is lower in
calories can promote weight loss. This may involve reducing portion sizes, choosing
foods that are high in fiber and protein, and limiting intake of processed or high-calorie
foods.
✓ Regular Exercise: Engaging in regular physical activity, including aerobic exercises,
strength training, and flexibility exercises, can help burn calories and promote weight
loss. Consistency and variety in exercise routines are important for maximizing results.
✓ Behavioral Changes: Adopting healthy behaviors such as mindful eating, keeping
food journals, setting realistic goals, and managing stress can support longterm weight
loss success.
✓ Medications: In some cases, prescription medications may be used to aid weight loss,
particularly for individuals with obesity or certain obesity-related health conditions.
These medications may work by suppressing appetite, reducing fat absorption, or
increasing calorie expenditure.
✓ Surgery: Bariatric surgery may be considered for individuals with severe obesity who
have not been successful with other weight loss methods. Procedures such as gastric
bypass, gastric sleeve, or gastric banding can lead to significant and sustained weight
loss, as well as improvement in obesity-related health conditions.
• Unintentional weight loss, on the other hand, may occur as a result of various underlying
medical conditions, including:
✓ Gastrointestinal Disorders: Conditions such as celiac disease, inflammatory bowel
disease (IBD), or gastrointestinal cancers can interfere with nutrient absorption and lead
to weight loss.
✓ Thyroid Disorders: Hyperthyroidism, characterized by an overactive thyroid gland
can increase metabolism and lead to unintentional weight loss.
✓ Diabetes: Uncontrolled diabetes, particularly type 1 diabetes, can lead to weight loss
due to the body's inability to properly utilize glucose for energy.
 ✓ Cancer: Certain types of cancer, particularly those affecting the digestive system can
cause weight loss due to metabolic changes, decreased appetite, or the presence of
tumors.
✓ Chronic Infections: Chronic infections such as tuberculosis, HIV/AIDS, or parasitic
infections can lead to weight loss due to increased metabolic demand and nutrient loss.
✓ Mental Health Disorders: Conditions such as depression, anxiety, or eating disorders
can affect appetite, eating habits, and weight regulation, leading to unintentional weight
loss.
✓ Medications: Certain medications, including chemotherapy drugs, antidepressants, or
medications that affect appetite or metabolism, can cause weight loss as a side effect.
❖ Unexplained or unintentional weight loss, particularly if it occurs rapidly or is accompanied
by other symptoms such as fatigue, weakness, or changes in appetite, should be evaluated by a
healthcare professional to identify and address any underlying medical conditions. Treatment for
unintentional weight loss depends on the underlying cause and may involve medical
management, dietary interventions, or addressing contributing factors such as medication side
effects or psychological issues

ASSESSMENT OF CLIENTS WITH GASTROINTESTINAL DISORDER

The GIT Physiology: LIVER

 Functions to store excess glucose, fats and amino acids
 Also stores the fat-soluble vitamins- A, D and the water soluble- Vitamin B12
 Produces the BILE for normal fat digestion
 The Von Kupffer cells remove bacteria in the portal blood
 Detoxifies ammonia into urea

The GIT anatomy: The gallbladder

 Located below the liver
 The cystic duct joins the hepatic duct to become the bile duct
 The common bile duct joins the pancreatic duct in the sphincter of Oddi in the first part
of the duodenum
Physiology
 Stores and concentrates bile
 Contracts during the digestion of fats to deliver the bile
 Cholecystokinin is released by the duodenal cells, causing the contraction of the
gallbladder and relaxation of the sphincter of Oddi

The pancreas
 A retroperitoneal gland
 Functions as an endocrine and exocrine gland
 The pancreatic duct (major) joins the common bile duct in the sphincter of Oddi
Physiology
 The exocrine function of the pancreas is the secretion of digestive enzymes for
carbohydrates, fats and proteins
 Pancreatic amylase→ carbohydrates
 Pancreatic lipase (steapsin)→ fats
 Trypsin, Chymotrypsin and Peptidases→ proteins
 Bicarbonate→ to neutralize the acidic chyme. Stimulated by SECRETIN

Gastrointestinal Assessment Laboratory Procedures

COMMON LABORATORY PROCEDURES

FECALYSIS: Occult Blood Testing

 Examination of stool consistency, color and the presence of occult blood.
 Special tests for fat, nitrogen, parasites, ova, pathogens and others
 Instruct the patient to adhere to a 3-day meatless diet
 No intake of NSAIDS, aspirin and anti-coagulant
 Screening test for colonic cancer

Upper GIT study: barium swallow

 Examines the upper GI tract
 Barium sulfate is usually used as contrast
 Pre-test: NPO post-midnight
 Post-test: Laxative is ordered, increase pt fluid intake, instruct that stools will turn
white, monitor for obstruction

Lower GIT study: barium enema

 Examines the lower GI tract
 Pre-test: Clear liquid diet and laxatives, NPO post-midnight, cleansing enema prior to
the test
 Post-test: Laxative is ordered, increase patient fluid intake, instruct that stools will turn
white, monitor for obstruction

Gastric analysis
 Aspiration of gastric juice to measure pH, appearance, volume and contents
 Pre-test: NPO 8 hours, avoidance of stimulants, drugs and smoking
 Post-test: resume normal activities

EGD (esophagogastroduodenoscopy)
 Visualization of the upper GIT by endoscope
 Pre-test: ensure consent, NPO 8 hours, pre-medications like atropine and anxiolytics
  Intra-test: position: LEFT lateral to facilitate salivary drainage and easy access
 Post-test: NPO until gag reflex returns, place patient in SIMS position until he awakens,
monitor for complications, saline gargles for mild oral discomfort

Lower GI- scopy

 Use of endoscope to visualize the anus, rectum, sigmoid and colon
 Pre-test: consent, NPO 8 hours, cleansing enema until return is clear
 Intra-test: position is LEFT lateral, right leg is bent and placed anteriorly
 Post-test: bed rest, monitor for complications like bleeding and perforation

Cholecystography
 Examination of the gallbladder to detect stones, its ability to concentrate, store and
release the bile
 Pre-test: ensure consent, ask allergies to iodine, seafood and dyes; contrast medium is
administered the night prior, NPO after contrast administration
 Post-test: Advise that dysuria is common as the dye is excreted in the urine, resume
normal activities

Paracentesis
 Removal of peritoneal fluid for analysis
 Pre-test: ensure consent, instruct to VOID and empty bladder, measure abdominal girt
 Intra-test: Upright on the edge of the bed, back supported and feet resting on a foot stool

Liver biopsy
 Pretest
o Consent
o NPO
o Check for the bleeding parameters
 Intratest
o Position: Semi fowler’s LEFT lateral to expose right side of abdomen
 Post-test: position on RIGHT lateral with pillow underneath, monitor VS and
complications like bleeding, perforation. Instruct to avoid lifting objects for 1 week

Assessment
 Health history Nursing History
 PE
 Laboratory procedures

The ABDOMINAL examination

The sequence to follow is:
  Inspection
 Auscultation
 Percussion
 Palpation

The ENDOCRINE SYSTEM

Anatomy and physiologic Overview

 Endocrines: Without ducts: Ductless glands.
 A group of glands all of which lack ducts or specific channels to release their secretions.
 All of them secrete or produce “Chemical Messengers” or Hormones.
 Hormones by definition bring metabolic changes in target tissues.
 The target tissues are usually far away from the endocrine glands.

WHY ENDOCRINE SYSTEM?

4 MOST IMPORTANT PURPOSES
1. HOMEOSTASIS.
2. COMBATING STRESS.
3. GROWTH & DEVELOPMENT.
4. REPRODUCTION.

ENDOCRINES ARE USEFUL FOR…

1. HOMEOSTASIS
 Endocrines help us in maintaining the homeostasis of:
o Temperature: Thermoregulation or thermostasis.
o Metabolism
o Nutrition: Glucostasis
o Acid Base Balance

2. COMBATING STRESS
 INFECTION
 TRAUMA
 SHOCK

3. GROWTH & DEVELOPMENT

 Increase in the cell number: Hyperplasia
 Increase in cell SIZE: Hypertrophy.

4. REPRODUCTION
 The Male and female Gonads secrete:
o Sex Hormones
  These sex hormones cause the development of
o Primary sex organs
o Secondary sexual characteristics.

HORMONES
 It is important in regulation of the internal environment of the body and effect every
aspect of life.
 Natural chemicals that exert their effects on specific tissues known as
 target tissues
 The mechanism for regulating hormone in the blood stream is called negative feedback

Target Tissues
 usually located some distance from endocrine glands with no direct
 physical connection between the endocrine glands and its target tissue

Glands Of The Endocrine System

1. Pituitary glands
2. Thyroid glands
3. Parathyroid glands
4. Pancreatic islets
5. Ovaries
6. Testes
7. Adrenal glands

CLASSICAL ENDOCRINE GLANDS IN THE BODY

 HORMONES PRODUCED IN THE BODY

 HYPOTHALAMUS:
o CRH, TRH, GHRH, GHIH, GnRH, PIH.
 ANTERIOR PITUITARY GLAND:
o GH, ACTH, TSH, FSH, LH, Prolactin.
 POSTERIOR PITUITARY GLAND:
o ADH, & Oxytocin.
 THYROID GLAND:
o Thyroxin, T3, Calcitonin.
 ADRENAL CORTEX:
o Aldosterone, Cortisol, Sex steroids.
 ADRENAL MEDULLA:
o Epinephrine, Norepinephrine, Dopamine.
 ENDOCRINE PANCREAS:
o Glucagon, Insulin, Somatostatin, Pan polypeptide.
 TESTES:
o Testosterone, Estrogen, Inhibin.
 OVARY:
o Estrogens, Progesterone, Relaxin.
 PLACENTA:
o Estrogens, Progesterone, HCG, HPL.
 THYMUS:
o Thymosin.
 PINEAL GLAND:
o Melatonin

HYPERSECRETION:
 Excessive Production of hormones due to:
o Tumors in the gland.
o Excess tropic influence.
  Results in:
o Clinical syndromes with signs/symptoms due to:
 Increased blood levels of the hormone
 Example: Hyperthyroidism: ⮅Thyroxin levels
 Clinical features: Fine tremor, Anxiety, PR⭡, ⭡BMR
 Acromegaly: ⮅ Growth Hormone.

HYPOSECRETION:
 Drop in the production of hormones due to:
o Excision of gland: Eg: Parathyroids.
o Hypofunctioning of gland cells: Eg: Diabetes mellitus.
o Decreased tropic influence.
 Results in:
o Clinical features/ syndromes due to
o ⮇ blood levels of the hormone

HORMONE REGULATION:
NEGATIVE FEEDBACK MECHANISM
 If the client is healthy, the concentration of hormones is maintained at a constant level.
 When the hormone concentration rises, further production of that hormone is inhibited.
 When the hormone concentration falls, the rate of production of that hormone increases.

ENDOCRINE DISORDERS

Thyroid Hyperfunction Disorder

1. Graves disease: immunological factors, genetic predisposition, infection, stress,
excessive intake of thyroid medication; occurs 8 times more frequently in females
2. Goiter: inadequate intake of iodine, increase in thyroid demand
3. Thyroid storm: Stress, injury, infection, surgery
Causes of Hyperthyroid Disorder
 Autoimmune response
 Neoplasm
 Excessive intake of thyroid medication
 Excess secretion of TSH from the anterior pituitary glands

Pathophysiology
THYROID HYPERFUNCTION DISORDERS
1. Production of thyroid hormone (TH) is dependent on adequate secretion of thyroid
stimulating hormone (TSH) from the anterior pituitary gland; The hypothalamus
regulates pituitary secretion of TSH by negative feedback

Hyperthyroidism
 Hyper function of the thyroid gland
 Leads to an excess of thyroid hormone in the body
 The presence of excess TH leads to hyper metabolic state
 Which causes increase in metabolic function
 Increase in oxygen consumption by tissue,
 And heat production

Graves’ Disease
 The most common cause of hyperthyroidism, is seen most often in woman under age of
40.
 The exact cause is unknown, it is considered an autoimmune disorder to stimulation of
the thyroid gland from a long acting thyroid stimulator (LATS)
 The result in an excess production of TH, Which leads to hypermetabolic state

GOITER
 It is describes the enlargement or hypertropy of the thyroid gland in attempt to
compensate for inadequate TH
 It may be present in hyperthyroidism or hypothyroidism
 Goiter may be result of response to excess TSH stimulation, excess –growth stimulating
immunoglobulins, or presence of substance that inhibit thyroid hormone synthesis
 The goiter may become enlarge that compress the neck and chest
 Toxic Multinodular Goiter
 It exist when small, independently functioning nodules in the thyroid gland tissue are
present and secrete TH hormone
 The nodule may be benign or malignant
 The manifestation developed more slowly than graves’ disease.
 Toxic goiter is most often seen in woman age 60 or older who had goiter for several
years.
Thyroid Storm
 Also known as thyroid crisis or thyrotoxicosis
 It is life threatening condition which describes an extreme state of hyperthyroidism
 The presence of excessive TH causes a rapid increase in metabolic rate
 Immediate treatment is necessary to avoid death

THYROID STORM / THYROTOXIC CRISIS

 Occurs in patients with existing but unrecognized thyrotoxicosis, stressful illness, thyroid
surgery, RAI
 Increased systemic adrenergic activity: Severe hypermetabolism

HYPERTHYROIDISM: CLINICAL MANIFESTATIONS

 Gi hypermotility
 Rapid weight loss
 Apprehension [tremors, tachycardia, palpitations]
 Volume deficit; voracious appetite
 Exophthalmos; erratic menses
 Systolic BP elevated; sweating

TSH

 ↓in primary disease

 ↑in secondary disease

Nursing assessment for Hyperthyroidism

1. eyes, vital sign, cardiac monitor for rhythm changes, sign of congestive heart failure,
nutritional assessment, complaints of GI distress, muscle strength and appearance,
presence of goiter, reproductive history, integument assessment, weight, fluid status
2. Assessment findings for thyroid storm include elevated temperature, symptoms of pain,
bowel/GI complaints, neurological, development of seizures, changes in VS, respiratory
status

Nursing management for Hyperthyroidism

1. Medication
A. Antithyroid medication to reduce TH production
i. Methimazole (Tapazole)
ii. Propylthioracil (PTU, Propyl-Thracil)
B. Propanolol (Inderal) to treat dysrhythmias
C. Glucocorticoids: interfere with conversion of T3 and T4
D. Lugol’s Solution (iodine) to decrease vascularity and size of thyroid
E. Antipyretic if needed

2. Educate the client that it may take several weeks before the therapeutic effects of
antithyroid medications are noticed
a. Instruct to take medication as prescribe and not abruptly discontinue medication
b. Educate about the signs of hypothyroidism, which may occur if to much medicine is
taken or dose needs adjusting
3. Monitor for cardiac dysthythmias
4. Implement antipyretic measures
5. Elevate head of the bed to decrease eye pressure
6. Teach eye care and monitor for vision changes if exophthalmos occurs, since it will not
change even after medication have been started.
7. Monitor dietary intake: Client may require up to 4,000 to 5,000 calories a day during
hypermetabolic state
 8. Monitor intake and output
9. Monitor weight
10. Keep the environment cool and quiet because of the symptoms
11. Radioactive therapy may be recommended to destroy thyroid cells in order to reduce
production of TH
A. Give radioactive iodine orally; expect result in 6 to 8 weeks
B. Does not require hospitalization or radiation precaution
C. Contraindicated in pregnant woman
D. Monitor for sign and symptoms of hyperthyroidism
12. Preoperative and postoperative care for surgical intervention to remove all or part of the
thyroid (thyroidectomy)
A. subtotal thyroidectomy leaves part of the thyroid gland intact in order to produce
adequate amounts of TH
B. For total thyroidectomy life long thyroid hormone replacement is necessary; educate
for strict compliance with medication regimen
C. Preoperative care include administering antithyroid medications to promote euthyroid
state, and iodine preparation to decrease vascularity of the glands. Teach the client
how to support the neck to reduce strain in the suture line
 Post operative care includes monitoring for complication of hemorrhage, respiratory
distress, laryngeal nerve damage, and tetany
13. Priority nursing diagnosis for thyroid hyperfunction disorders: Activity intolerance;
altered nutrition; hyperthermia; risk for injury

HYPERTHYROIDISM: MANAGEMENT Anti-thyroid drugs

 Propylthiouracil (PTU); methimazole

 Blocks thyroid hormone (TH) synthesis
 Used for pregnant women and patients who have refused surgery or RAl treatment
 During pregnancy, PTU is DOC.
 1% of infants born to mothers on anti-thyroid therapy will be hypothyroid.
 WOF agranulocytosis.

Thyroid Hypofunction Disorder

1. Hypofunction of the thyroid glands leads to an insufficient amount of thyroid hormone
(TH), a condition known as hypothyroidism
2. Decrease TH result in a hypometabolic state manifested by a decrease in metabolic
function, a decrease in oxygen consumption by tissue, and decrease in heat production

Thyroid hypofunction Disorder

A. Hypothyroidism
B. Myxedema
C. Myxedema coma
 HYPOTHYROIDISM
 A state of low serum TH levels or cellular resistance to TH
o Autoimmune
o Developmental
o Dietary
o Iodine deficiency
o Oncologic
o Drugs
o Latrogenic
o Non-thyroidal
o Endocrine

 Causes
o Chronic autoimmune (Hashimoto’s) thyroiditis
o Hypothalamic failure to produce TRH
o Pituitary failure to produce TSH
o Inborn errors of TH synthesis
o Thyroidectomy / Radiation therapy
o Anti-thyroid therapy
o Iodine deficiency

 CLINICAL MANIFESTATIONS
o Dry, brittle hair; dry, coarse skin
o Edema (periorbital)
o Reduced BMR [bradycardia, bradypneal
o Apathy; anorexia; anemia
o Increased weight; intolerance to cold
o Lethargy; loss of libido
o Enlarged tongue
o Drooling

TSH:

o High in primary disease

o Low in secondary disease

MYXEDEMA
 HYPOTHYROIDISM

Classified as primary and secondary

A. Causes of primary hypothyroidism include congenital defects, loss of thyroid tissue from
surgery or radiation, antithyroid medication, endemic iodine deficiency, or thyroiditis
B. Causes of secondary hyperthyroidism include peripheral resistance to TH or pituitary
TSH deficiency

Pathophysiology
1. Hypothyroidism describe an insufficient amount of TH which leads to a decrease in
metabolic rate; manifestation developed slowly over months or years
2. Myxedema describes a generalized hypometabolic state occurring with untreated
hypothyroidism
A. Accumulation of proteins in the interstitial space result in an increase of interstitial
fluid, causing mucinous edema, (myxedema)
B. This non-pitting edema is most commonly found in the pretibial and facial area

Pathophysiology of Myxedema coma

 Also known as hypothyroid crisis
 It is the result of extreme or prolonged hypothyroidism; though rare, it is life threatening
condition
  Characterized by severe metabolic state: lactic acid acidosis, hypoglycemia,
hyponatremia, hypotension, bradycardia, cardiovascular collapse, hypothermia,
hypoventilation, coma
 Precipitated by inadequate thyroid replacement, infection, trauma, exposure to cold
temperature, CNS depressant

Iodine deficiency: iodine is necessary for TH synthesis and secretion

A. Iodine deficiency occurs as a result of antithyroid drugs, and lithium or iodine intake
B. In US , thyroid deficiency because of in adequate iodine intake is rare with the use of
iodized salt

Myxedema Coma
Signs and symptoms:
 Hypothermia
 Cardiovascular collapse
 Coma
 Hyponatremia
 Hypoglycemia
 Lactic acidosis

Nursing Assessment
1. Assessment of hypothyroidism include neurological assessment, presence of periorbital
edema, presence of goiter, reproductive history, fluid status, weight, activity tolerance,
respiratory status
2. Assessment in myxedema coma include cardiac assessment, and other assessment
performed for hypothyroidism

HYPOTHYROIDISM: MANAGEMENT

 Prevention
o Prophylactic iodine supplements to decrease the incidence of iodine-deficient
goiter
 Symptomatic cases
o Hormonal replacement
o Levothyroxine (Synthroid)
o Liothyronine (Cytomel)
o Liotrix (Thyrolar)
o Dosage increased q 2-3 weeks especially in elderly patients

HYPOTHYROIDISM: NURSING INTERVENTIONS

 Diet: high-bulk, low-calorie Encourage activity

 Maintain warm environment
 Administer cathartics and stool softeners To prevent myxedema coma, tell patient to continue
course of thyroid medication even if symptoms subside.
 Maintain patent airway
 Administer medications: Synthroid, glucose, corticosteroids IV fluid replacement
 Wrap patient in blanket
 Treat infection or any underlying illness

Priority nursing diagnosis for thyroid hypofunction disorder

 Activity intolerance
 Altered nutrition
 Decrease Cardiac output
 Hypothermia
 Risk for skin integrity
 Risk for injury

Parathyroid disorder
1. The parathyroid glands are located posterior to the thyroid glands
a. Their major function is to maintain normal serum calcium levels by secreting TH,
which increases bone reabsorption of calcium
b. PTH respond to decrease calcium levels by increasing calcium absorption from bone,
kidneys, and intestine

Hyperparathyroidism
 It is an Increase in PTH, which leads to hypercalcemia, hyperposphatemia, bone damage,
and renal damage

HYPERPARATHYROIDISM
Primary

 Single adenoma
 Genetic disorders
 Multiple endocrine neoplasias

Secondary

 Rickets
 Vitamin D deficiency
 Chronic renal failure
 Phenytoin or laxative abuse

HYPERPARATHYROIDISM: CLINICAL MANIFESTATIONS

 Constipation
 Apathy
 Lordosis
 Cardiac dysrhythmias
 Upset GIT
 Low energylevels
 Increased BP

HIGH

 PTH
 Calcium
 Alkaline phospatase

LOW
 PO4
Nursing assessment for Hyperparathyroidism
1. Includes neurological assessment including LOC, VS , heart rhythm, GI assessment,
complain of pain, muscle strength, weight , I and O

HYPERPARATHYROIDISM: MANAGEMENT

 Surgery to remove adenoma

 Force fluids; limit dietary calcium intake
 For life-threatening hypercalcemia:
o Furosemide
o Bisphosphonates
o [Etidroanate (Didrodinel), pamidronate] Calcitonin (Cibacalcin, Miacalcin)
Plicamytin (Mithracin) + glucocorticoid Mithramycin

HYPOPARATHYROIDISM
  It is a decrease in PTH, Which leads to hypocalcemia, hyperreflexia, and altered
sensorium
 The most common cause of hypoparathyroidism is damage or removal of the parathyroid
gland during surgery

Causes

 Congenital absence or malfunction of the parathyroids

 Autoimmune destruction
 Removal or injury to one or more parathyroids during neck surgery
 Massive thyroid radiation therapy
 Ischemic parathyroid infarction during surgery

CLINICAL MANIFESTATIONS

 Dyspnea; dysrhythmias
 Extremities: tingling
 Fotophobia
 Increased bone density
 Chvostek sign; cramps
 Irritability
 Trousseau sign; tetany

LOW

 PTH

 Calcium
 Alkaline phospatase

HIGH
 РО4

Priority nursing diagnosis for parathyroid disorder

 Impaired physical mobility
 Risk for injury
 Altered urinary elimination
 Altered nutrition

Adrenal Cortex Hyperfunction Disorder

1. The adrenal glands are located superior to each kidney and composed of the adrenal medulla
(the inner layer of adrenal gland) and the adrenal cortex (the outer layer of adrenal gland
a. The adrenal medulla secretes the catecholomines: epinephrine, norepinephrine and
dopamine
b. The adrenal cortex secretes mineralcorticoids (aldosterone), glucocorticoids (cortisol,
androgen, andestrogens (sex hormone)
2. The function of epinephrine and norepinephrine (catecholamines) include increasing
metabolic rate, increasing alertness, increasing insulin levels and the “fight or flight response
3. The functions of glucocorticoids (cortisol) includes assisting the body’s response to stress,
suppression of inflammation, increasing serum glucose by acting as insulin antagonist, it
regulates CHO, fat’ and protein metabolism, enhancing protein synthesis, and increasing
breakdown of protein and fatty acid

Functions
4. The function of adrenocorticotropic hormone is for growth and development
5. The function mineralcorticoids (aldosterone) includes sodium (Na) and water retention and
potassium excretion
6. Androgens and estrogens contribute to growth and development

ADRENAL CORTEX HYPERFUNCTION DISORDER

 Cushing’s Syndrome or hypercortisolism result in excess production of cortisol
(glucocorticoids).
 Conn’s Syndrome or Hyperaldosteronism result in excess production of aldosterone

Cause of Hypercortisolism
( Cushing’s syndrome)
 Include Adrenal tumors
 Adrenal hyperplasia
 Or exogenous glucocorticoids

Causes of hyperaldosteronism
( conn’s syndrome)
 Include adrenal lesion
 Or condition that stimulate overproduction of aldosterone: heart failure, cirrhosis of liver,
dehydration, renal disease

CUSHING’S DISEASE
 Adrenal hyperplasia / tumor
 Cushing’s disease
 Tumor - secreting ACTH
 Hypothalamic
Buffalo hump
Unusual behavior (depression, personality changes, fatigability)
Facial features (moonface, hirsutism in women)
Fat (truncal obesity)
ACTH and cortisol in blood elevated;
Loss of muscle mass
Overextended skin (abdominal striae with easy bruisability)
Hypertension, hyperglycemia, hypernatremia
Urinary cortisol elevated
Menstrual irregularities
Porosity of bone (osteoporosis)
CUSHING’S SYNDROME

Pathophysiology of Hypercortisolism
A. The functions of glucocorticoids (cortisol, ACTH) include promoting gluconeogenesis,
maintaining serum glucose levels, adaptation to stress, and augmenting release of
catelectomines to increase blood pressure

S/S of Hypersecretion of cortisol

Nursing management for Cushing’s Syndrome

 Includes vital sign: increase BP/ arrhythmias
 Neurological assessment
 History of GI, renal, and reproductive problem
 Muscle strength
 Integument assessment
  Weight ; presence of edema, I and O

Nursing management for Cushing’s syndrome

 Remove exogenous steroids
 Hypophysectomy or irradiation
 Adrenalectomy
 Cyproheptadine (Periactin)
 Metyrapone
 Mitotane (Lysodren)
 Aminoglutethamide (Cytadren)
 Potassium Supplements
 High-CHON; Low Na

B. Preoperative and postoperative care is for adrenalectomy if performed

C. Assist in monitoring effects of radiation if performed
D. Monitor for addisonian crisis cause by drug therapy

Priority Nursing diagnosis for Cushing’s Syndrome

 Fluid volume in excess
 Risk for infection
 Activity intolerance
 anxiety
 Knowledge deficit
 Risk for impaired skin integrity

CONN’S SYNDROME/
HYPERALDOSTERONISM

Causes of Conn’s Syndrome or Hyperaldosteronism

 Adrenal lesion
 Any condition that stimulates overproduction of aldosterone: heart failure, cirrhosis of
liver, dehydration, renal disease.

Pathophysiology of Conn’s syndrome

a. Role of aldosterone ( a mineralcorticoid) is soduim and water retention
b. Aldosterone affects tubular reabsorption of sodium and water also has role in excretion of
potassium and hydrogen ions

S/S for Conn’s Syndrome

 In secondary hyperaldosteronism hypertension is uncommon
 Visual disturbance
  Paresthesia
 Dysarrythmias
 Fluid retention, renal damage, polyuria
 Muscle weakness, tetany
 Electrolyte and acid-base imbalance

Nursing management for Conn’s Syndrome

A. Medication
1. Spironolactone (aldactone) to treat hypertension and hypokalemia for clients who will
not treat surgically
2. Amiloride (midamor) for those clients unable to tolerate aldactone
3. Administer glucocorticoids preoperatively as prescribed to prevent adrenal
hyperfunction
B. Preoperative and postoperative care for adrenalectomy
C. If bilateral adrenalectomy is performed, life time replacement of glucocorticoid is necessary
D. Monitor BP, Urine output, electrolytes
E. Low sodium diet
F. Teach side effects of medications

Priority nursing diagnosis for Conn’s syndrome

 Altered urinary elimination
 Fluid volume in excess
 Risk for injury

ADDISON’S DISEASE
 Hyposecretion of adrenocortical hormones
 Destruction of the cortex
 Idiopathis atrophy

Addison’s Crisis
 It can occur, which is an acute insufficiency of adenocortical hormone from lack of cortisol
during stress , such as surgery or pregnancy, or exogenous corticosteroid therapy is abruptly
discontinue
 If not treated immediately, circulatory collapse, shock, and death may occur
Nursing Management
1. Medication
A. Addison’s Disease: administer cortisone, prednisone, fludcortisone acetate (florinef)
asprescribe
B. Addisonian Crisis, immediate intravenous glucocticoid replacement and fluids with
sodium

Anterior Pituitary Disorder

1. The pituitary gland referred to as master gland is located at the base of the brain adjacent to
hypothalamus, it is responsible for regulating endocrine function by producing hormone that
affect body system and stimulating other endocrine glands to secrete hormone

2. Hormones Secreted By the Pituitary glands

a. Growth Hormone (GH)
b. Thyroid stimulating hormone (TSH)
c. Adenocorticotropic hormone (ACTH)
d. FSH
e. LH
f. Prolactin (PRL)
3. Disorder of the anterior pituitary gland result in excessive or insufficient pituitary hormone
disorder are as not common than other endocrine disorder
4. Growth hormone is the hormone necessary for growth that regulates cell division and the
synthesis of protein, exerts other metabolic effects on endocrine organs, skin. Skeletal muscle,
cardiac muscle, and connective issue

Hyperfunction of the Anterior Pituitary (Hyperpituitarism)

 It is the result of excess production and secretion of one or more hormones: (GH), FSH,
TSH, LH, ACTH: Leading to Tissue over growth.
 The most comm0n cause of hyperpituitarism is benign adenoma
Hypofunction of the Pituitary Gland (hypopituitarism)
1. It is aresult in a deficiency of one or more pituitary hormones: GH, follicle stimulating
hormone (FSH), TSH, LH, ACTH
2. Causes include surgical removal of the pituitary gland, pituitary tumors, infection, trauma,
congenital defects, radiation

Common Disorder
a. Hyperpituitarism ; Giantism and acromegaly
b. Hyporpituitarism: dwarfism

Pathophysiology of Giantism
A. Giantism is the result of growth hormone hypersecretion that begins before the closure of the
epiphysicial plates
1. This hypersecretion leads the person to become abnormally tall reaching 7 to 8 ft. in height
2. The body proportion are generally normal
3. Early detection, diagnosis, and treatment has made this disorder rare in occurrence
4. Common cause is tumor

Acromegaly
 It is the result of GH over secretion during continue to grow, leading to adulthood, bone
connective tissue continue to grow , leading to disproportionate enlargement of tissue.
 Most common cause is tumor
 S/S include large hands and feet, protrusion of the lower jaw, coarse facial features, sign of
osteoporosis, change in hand and shoe and glove size that slowly progress; systemic
symptoms hypertension, CAD, CHF, enlarge adrenal gland, thyroid and parathyroid gland

Dwarfism
 Result from deficient secretion of anterior pituitary hormones
 Inadequate secretion of these hormones leads to growth retardation and accompanying
metabolic disorder
 S/S include short stature, obesity, short pitch voice, slow measuring skeletal system ,
hyperlipidemia, hypercholesteremia

Nursing assessment
a. Assessment of gigantism includes growth chart for height and weight by age and visual
exam.
b. Assessment of acromegaly includes VS, Visual disturbances, S/S of CHF or diabetes,
growth and development, symptoms and analysis of pain
c. Assessment for dwarfism include growth chart and development of sex organ
d. Diagnostic test : bone scan, cholesterol, lipid funnel , hormone levels

TRANSSPHENOIDAL HYPOPHYSECTOMY
Nursing Diagnosis
 Activity intolerance, body image disturbance, sexual dysfunction, anticipatory grieving,
ineffective individual coping; altered growth and development

HYPOPITUITARISM
 Deficiency of one or more anterior pituitary hormones

Causes
 Infections / Inflammatory disorders
 Autoimmune diseases
 Congenital absence
 Tumor
 Surgery / Radiation therapy

Posterior pituitary disorder

1. The posterior pituitary gland secrete hormones oxytoxin and antidiuretic hormone
(vasopressin), the purpose of antidiuretic hormone is to control serum osmolarity
 Disorder of the posterior pituitary gland are primarily result of excessive or deficient
ADH secretion

DISORDER OF THE POSTERIOR PITUITARY GLAND

A. DIABETES INSIPIDUS (DI) is the result of ADH insufficiency, resulting to excessive fluid
excretion
B. SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE SECRETION
(SIADH) is the result of excessive secretion of ADH and water retention

CAUSES
 Diabetes Insipidus: unknown etiology in most cases, head trauma with damage to the
pituitary or tumor
  SIADH: occurs most often as the result of ectopic production of ADH by malignant
tumors, but may also occur as the result of pituitary surgery, head injury, or medications
such as diuretics, anesthetics and barbiturates

Nursing assessment for DI

 I and O
 Complain of thirst
 Dry skin
 Sunken eyeball weakness,
 Decreased urinary output
 Dry mucous membrane

S/S of DI
 Polyuria
 Excessive Thirst
 Polydipsia
 Dehydration in event the client is unable to replace fluid loss

DI and its classification

 ADH insufficiency leads to the excretion of large amount of urine (polyuria), up to 12
L/day
 Neurogenic DI occurs when there is a decrease in the synthesis and excretion of ADH :
may be idiopathic, or may result from trauma or dysfunction of the hypothalamus or
pituitary gland
 Nephrogenic DI occurs when the renal tubules is not sensitive to ADH

Nursing Management For DI

 Medications include vasopressin (pitressin, pressyn) for treatment of nuerogenic DI
 Administration of hypotonic solution
 Increase fluid intake
 Treatment is life long for chronic DI
 Monitor daily weigh
 Low NA diet and to avoid caffeine since this increases urine output
 Educate client for medic alert bracelet

Syndrome of Inappropriate ADH

 Disorder due to excessive ADH release

S/S of (SIADH)
 Lethargy
 Confusion
 Changes in neurological status
  Cerebral edema
 Muscle cramps weakness, decrease urine output, fluid retention, weight gain

Assessment of SIADH
 Assess for nuerological indicator like LOC
 I and O
 weight

Nursing Management For (SIADH)

 Medications include diuretics, demeclocycline (declomycin)
 Administration of hypertonic saline fluids
 Oral fluid restriction
 I and O and daily weight
 Monitor for neurological changes and water retention

Nursing Diagnosis for disorder of posterior pituitary disorder

 Fluid volume in excess
 Fluid volume deficit
 Altered urinary elimination
 Risk for Injury
 Knowledge deficit

DIABETES MELLITUS
 Insulin resistance (GDM, age)
 Failure in production
 Blockage of insulin supply
 Autoimmune response
 Excess body fat
 Heredity

CAUSES OF DM
 Type 1 DM: occurs as a result of genetic, environmental or immunological factors that
may damage the pancreatic beta cells
 Type 2 DM Etiology is unknown: however, obesity is the single most important risk
factor

S/S of DM
 Early manifestation of type 1 DM; polyuria, polydispia, polypaghia, glycosuria, fatigue,
weight loss, nausea, vomiting, abdominal pain
 Early manifestation ofin type 2 Dm : polyuria, polydipsia, blurring of vision, weight gain
General multisystem findings
1. Sensory/ neurological: diabetic retinopathy, cataracts, glaucoma, paresthesias, loss of
sensation, peripheral neuropathy
2. Cardiovascular assessment: coronary artery disease, peripheral vascular disease,
hypertension
3. G I: constipation or diarrhea
4. Musculoskeletal : contractures
5. Integumentary : atrophy, foot ulcer, poor wound healing, chronic skin infections
6. Renal: edema, chronic renal failure, albuminuria, UTI
7. Reproductive assessment: Sexual dysfunction, Vaginitis
8. Metabolic: hypergycemia, hypokalemia, metabolic acidosis

Symptoms of DKA
 Abdominal pain , nausea and vomiting
 Metabolic acidosis
 Fruity breath odor
 Kaussmaul’s respiration
 Altered LOC
 Coma and death if not untreated

Complication of DKA
 Hypoglycemia
 Atherosclerosis
 CVA, PVD
 Retinopathy
 Paresthesia (especially feet)
 Renal failure
 Carpal tunnel syndrome,
 Peridontal disease
 Gangrene, amputation, inability to heal

Diagnostic test for DM

 Serum fasting sugar Increase (hyperglycemia) increase to 126 mg/dl
 Serum glycosylated hemoglobin levels; increase to 7 percent
 Urine for glucose, and ketones positive
 Urine for protein is positive
 Serum potassium is decrease
 2- hours plasma glucose (after meal) is increase to 200 mg/ dl
 Cholesterol and triglyceride levels is elevated

Nursing management for DM

1. Medication include insulin and hypoglycemic agent
a. Type 1 diabetes: regular insulin, NPH insulin such as 70/30
b. Type 2 diabetes: oral agents such as glipizide (glocotrol), glyburide (micronase), tolazamide
(tolomide), Metformin (glucophage) etc.
2. Monitor I and O, serum glucose, electrolytes

Client education for DM

A. Teach sign and symptoms of hypoglycemia (irritability, fatigue, weakness, tremors,
headache, possible coma) and hyperglycemia with appropriate interventions
B. Teach for self administration of insulin or hypoglycemic agent

Insulin therapy and insulin preparation

 In type I DM exogenous insulin must be administered for life because the body loses the
ability to produce insulin
 Reaction time of most common insulin preparation
 Rapid-acting insulin
 Short acting insulin
 Intermediate- acting
 Long acting insulin
 Very long acting insulin

Categories of insulin preparation

 Rapid acting it is indicated for rapid reduction of glucose level, to treat postprandial
hyperglycemia, and/or to prevent nocturnal hyperglycemia
 Agent: lispro (humalog)- onset 10-15 min, peak 1 hour, duration 2-4 hours
 Apart (novolog) – onset 5 to 15 min, peak 40-50 min duration 2-4 hours
 Short acting usually administered 20-30 min before meal; may be taken alone or in
combination with long acting insulin
 Agent : Regular (humalog R), Novolin R, Iletin II regular)
 Onset – ½ -1 hours, peak 1 hour, duration 4-6 hours
 Intermediate Acting it is usually taken after food
 Agent: NPH( neutral protamine hagadorn)
 Onset: 2-4 hours, peak: 4-12 hours, Duration 16 to 20 hours
 Agent: Humalin N, Iletin II lente, Iletin II NPH, Novolin L (lente) , Iletin II (NPH),
Novolin Lente, Novolin (NPH)
 Onset: 3-4 hours , Peak: 4-12 hours, Duration:16 -20 Hours
 Long Acting Insulin it is used to control fasting glucose level
 Agent: Ultra lente ( “UL”)
 Onset: 6-8 h, Peak:12-16 h, Duration: 20-30 h
 Very Long Acting it is used for basal dose (“Peakless”) that is the insulin is absorbed
slowly for 24 hours and can be given once a day and given HS originally, however it is
now approved to be given once a day at any time of the day but at same time to prevent
overlap of action. It should not mix with other insulin preparation to avoid precipitation
because of each PH of 4
Complication of insulin therapy
 Local allergic reaction ( readiness, swelling , tenderness and indurations or 2-4 cm wheal)
may appear at the injection site
 Systemic allergic reaction it is rare, when occur there is local skin reaction that gradually
spreads to generalized urticaria, treatment desensitization.
 Insulin lipodystrophy it refers to a localized reaction in form of lipoatrophy or
lipohypertrophy at the injection site
 Resistance to insulin injection.
 Morning hyperglycemia
a. Insulin Wanning it is progressive rise in blood glucose from bedtime to morning
b. Dawn Phenomenom it is relatively normal blood glucose until about 3 Am, when the
levels begins to rise
c. Somogyi Effect it is normal or elevated blood glucose at bedtime, a decrease at 2-3 AM
to hypoglycemic levels, and a subsequent increase cause by the production of
counterregulatory hormones

Patient Education
Self injection of insulin
 Insulin injection are self administered into subcutaneous tissue with the use of special
insulin syringe.
Self Injection
1. With on hand , stabilize the skin by spreading it or pinching large area
2. Pick up syringe with the other hand and hold it as you would a pencil. Insert needle straight
into the skin.
3. To inject the insulin, push the plunger all way in
4. Pull needle straight out of skin. Press cotton ball over the injection site for several seconds
5. Use disposable syringe only once and discard into hard plastic container (with a tight-fitting
top) such as empty bleach container. Follow state regulations for disposal of needle

Selecting and Rotating the injection site

Four main areas for injection
1. Abdomen
2. Upper arms (posterior surface)
3. Thighs (anterior surface)
4. Hips
Note: The speed of absorption is greatest in the abdomen and decreases progressively in the
arm, thigh and hip respectively

Patient Education
 Teach the patient how to get CBG or self monitoring glucose
 Teach the client about proper dietary management for diabetes
 Teach proper diabetic foot care and wound care
 Teach for proper exercise for diabetes