GASTROINTESTINAL DISORDERS

Diagnostic Tests
• Barium Swallow- pharynx and esophagus
- NPO, force fluids after
• Upper GI series- esophagus, stomach, duodenum and other portions of small bowel
- NPO, administer enemas, stool light colored, administer fluids and enemas after
• Lower GI series ( Barium enema)- large intestine
- NPO, administer laxatives/enema, force fluids after and administer enemas, monitor color and consistency
of stool
• Endoscopy- esophagus and stomach
- NPO, informed consent, baseline VS, administer sedatives.
- Assess gag and cough reflex
• Colonoscopy- large intestine
Before
- consent, clear liquid diet x 48hrs, bowel prep, explain that cramping/ sensation of needing to have BM
will be felt, use of air to distend the bowel lumen
After
- monitor for gross bleeding, colon perforation, NPO for 2hrs and check stool for blood if polyps removed

ORAL CANCER
- cancer of lips and pharynx, tongue and soft palate – ingestion of smoked meats, tobacco and alcohol
abuse
Squamous cell carcinoma- most common
TNM classification- Tumor, node and metastasis
Manifestations: non-healing blister (lips), painless sore that does not heal, tumors in tongue- dysphagia,
voice changes, weight loss, difficulty chewing and swallowing, enlarged cervical lymph nodes
Diagnostic Exams: CT scan, MRI, Biopsy
Interventions:
Radiotherapy; Chemotherapy
Surgery: Radical neck dissection
Maintain patent airway, oral hygiene, nutrition, ATB, emotional support

Radical Neck Dissection

Removal of all cervical lymph nodes from the mandible to the clavicle and removal of the
sternocleidomastoid muscle , internal jugular vein and spinal accessory muscle
Post-operative Care:
Maintain patent airway- assess for stridor, dyspnea and VS changes
Wound care and oral hygiene
Adequate nutrition
Observe for hemorrhage or nerve injury

PEPTIC ULCER DISEASE

Risk factors:
Tobacco use, H. Pylori, genetic predisposition, stress, food or drugs that injure or alter gastric mucosa or
increase HCL production ( ASA, steroids, caffeine and spicy foods) ,presence of diseases altering gastric
secretion
1) Gastric ulcers
injury in gastric mucosa due excess or imbalance of HCL to natural gastric barriers

2) Duodenal Ulcers
Increased rate in production of gastric secretions- increased # of parietal cells or 2ndary to vagal
stimulation that affects gastric release
3) Stress ulcers
- occurs after physiologically stressful events such as burns, shock, sepsis and trauma
- Upper GIB is the hallmark indicator
 - Usually preceded by shock- decreased gastric mucosal blood flow and reflux of duodenal
contents to stomach
- Large quantities of pepsin are released
- multiple ulcerations due to gastric ischemia
Cushing’s ulcers- deeper and more penetrating- brain trauma
Curling’s ulcers- after extensive burns
4) Drug-induced ulcers
-ulceration/ erosion of the gastric mucosa, duodenum, lower esophagus and jejunum- may extend
to the muscles or through the muscles to the peritoneum
Manifestations:
Bloating, belching, n/v, pain (burning, gnawing or aching) located in the upper abdomen and occuring
between mealtimes or at night, pain associated with ingestion of specific foods (spicy, fried, alcohol) and
ASA, relief of pain after administration of antacids and food
Diagnostics:
Barium swallow, fecal occult blood, Upper GI series, endoscopy shows location of the ulcer
Gastric analysis: Normal gastric acidity in gastric ulcers; increased in duodenal ulcers
Interventions for PUD
- Administer meds- neutralize stomach acid, decrease acid production, decrease vagal stimulation,
inhibit gastric acid secretion and provide protective coating over ulcerated site
- Avoid foods that provoke gastric acid secretions
- Stress reduction techniques; Rest
- Gastric decompression with NGT
- Endoscopic laser to control bleeding
- Prepare for gastric surgery (gastric resection, gastroduodenostomy, gastrojejunostomy), vagotomy
to eliminate acid secreting stimuli and pyloroplasty
- Saline lavage and blood transfusion
- Assess for signs of dehydration, hypovolemic shock and sepsis
- Maintain on NPO
Surgical Management for PUD
Gastroenterostomy- creates a passage between the body of the stomach and jejunum
Antrectomy- reduce the acid secreting portion of the stomach- cells that secrete gastrin are excised
Subtotal gastrectomy
- Gastroduodenostomy- Billroth I
- Gastrojejunostomy- Billroth II
Total gastrectomy

Post-operative Care after Gastric Resection

• pain management
- Maintain on fowler’s position for comfort and to promote drainage
- Gastric drainage system management- don’t reposition NGT
- Monitor dressings for drainage (bleeding)
- Assess bowel sounds; maintain on NPO
- Nutritional support
- Prevent dumping syndrome - rapid emptying of gastric contents into the small intestine which
has been anastomosed to the gastric stump
- Cause: Ingestion of food high in CHO and electrolytes, which must be diluted in the jejunum;
ingestion of fluid at mealtimes
- Sweating, weakness, nausea, flatulence and palpitations 30mins after a meal
- high fat diet of frequent small feedings, separate solid from liquids and avoidance of hyperosmolar
foods ; lie down after meals

APPENDICITIS
- ulceration of the mucosa or obstruction of the lumen
Causes: Barium ingestion, fecal mass, stricture, viral infection
S/Sx: Anorexia, gen. Abdominal pain that localizes in right lower abdomen (Mcburney’s point), n/v,
sudden cessation of pain (indicates rupture), low grade fever
Diagnostic findings- elevated WBC, abdominal X-ray
Treatment- Appendectomy, NPO, IV fluids
Post-operative Care:
- Assess GI status and pain
- Monitor VS, I&O, NPO till bowel sounds return then advance diet, monitor drainage and incision site,
assist with incentive spirometry
- If ruptured, will have penrose drain present- profuse drainage for 1st 12 hrs
- Position in right side lying position or low to semi-fowler’s position with legs flexed for comfort

PERITONITIS
Manifestations:
- abdominal resonance and tympany on percussion, abdominal rigidity and distention, constant, diffuse
abdominal pain, decreased or absent bowel sounds, rebound tenderness, shallow respirations, weak, rapid
pulse, fever, decreased peristalsis (accumulation of gas and fluids), n/v, decreased urine output
Diagnostics:
Abdominal X-ray shows free air in the abdomen under the diaphragm; elevated WBC (20,000/mm³) and
neutrophils
Interventions:
-Maintain fluid and electrolyte balance- treat shock, IVF and NPO with NGT to reduce pressure
analgesics, paracentesis, monitor weight
TPN and Antibiotics
-Prepare for surgery- treat the cause- drains will be placed; ATB irrigation of peritoneum, wound care, pain
- Avoid lifting and straining of abdominal muscles x 6wks post-op

ULCERATIVE COLITIS
inflammatory process affecting mucosa and submucosa of colon and rectum
Characterized by exacerbations and remissions
Infection, genetic predisposition , stress, autoimmune
Manifestations: abdominal cramping, weight loss, hyperactive bowel sounds, bloody purulent, mucoid,
watery stools (15-20/day), n/v, fever, F&E imbalances, colicky pain in left lower quadrant
Interventions:
Steroids, Flagyl, antidiarrheal (Imodium, Psyllium and antispasmodic agents),
low residue, lacto-free diet, elemental type diet, TPN, monitor weights, I&O, stool specimens
prepare for bowel resection (administer antibiotic bowel prep- Neomycin)
After surgery: wound care, F&E, pain, bowel function (paralytic ileus) , manage ileostomy or colostomy,
emotional support

CROHN’S DISEASE
Chronic inflammatory bowel disease affecting segmental areas along the entire wall of the GIT- common in
terminal ileum
Manifestations: abdominal cramps and spasms after meals, chronic diarrhea (3-5) , fever, weight loss,
cramp-like pain in lower right quadrant after meals, foul smelling and fatty stools
Diagnostics: Abdominal x-ray shows thickened, fibrosed, narrowed intestinal wall, Ba enema shows
lesions in terminal ileum, Upper GI series shows classic string sign: segments of stricture separated by
normal bowel
Interventions:
ATB, diet therapy, vitamin supplements, stool specimens, F&E
Prepare for surgery if there is obstruction
Provide wound management with skin care; fistulas may require placement of drains, pouches, skin barriers

INTESTINAL OBSTRUCTION
CAUSES:
A. MECHANICAL- obstruction from causes that physically impede passage of intestinal contents.
1. Adhesions
2. neoplasms
3. Inflammatory Bowel Disease
4. Foreign Bodies (gallstones, worms, fruit pits)
5. Fecal Impaction
6. Congenital Strictures
7. Radiation strictures
8. Intussusception
9. Volvulus
10. Hernias
ASSESSMENT:
Small Bowel:
Non-fecal vomiting
Colicky, intermittent abdominal pain
Large Bowel:
-cramp-like abdominal pain
-occasional fecal-like vomitus
-(-) stool & flatus
-abdominal distention, cramping pain, diminished or absent bowel sounds, vomiting fecal material,
constipation
-Abdominal distention & rigidity
-Bowel sounds: high-pitched above obstruction
-decreased/absent distal to obstruction
Diagnostics:
Abdominal US and X-ray
Management:
Bowel resection with or without anastomosis
GI decompression using NGT, Miller Abbott tube or Cantor tube
NPO, F&E replacement
IVT to prevent dehydration and shock

COLORECTAL CANCER
-malignancy of small or large intestine (most common)- low fiber high fat diet
-Grows slowly (polyps); s/sx absent till extensive (anorexia, n/v, weight loss, anemia)
-Metastasis to peritoneum, lymphatics, liver and lungs
-Most common symptom is change in bowel habits, rectal bleeding; progressive constipation with change
in stool shape (flattened, ribbon shaped)
-Abdominal distention and pain as tumor grow
-If tumor obstructs bowel, fluid backs up causing abdominal distention, reduced or absent bowel sounds
and fecal smelling vomitus
Diagnostic Procedures;
Abdominal and rectal exam, occult blood test, barium enema, proctosigmoidoscopy and colonoscopy
Elevated CEA
Interventions:
-ATB, analgesics, antiemetics; chemotherapy; radiation therapy
-Small bowel resection- ileotransverse colostomy
-Colonic resection and anastomosis; temporary colostomy
-Nutritional support
-Emotional support
-Monitor for tumor re-occurrence
-Monitor for perforation and obstruction
Stoma Care
Assess stoma- red, slightly raised- can be cleaned with soap and water and dried well
Treat with skin barrier and apply new pouch, cut about 1/16 to 1/8 in larger than stoma
Change every 4-5 days; empty when half-full and clean the pouch
Stoma irrigation
- Use 500-1L of warm tap water, suspend container 18in above the stoma
 - Insert lubricated cone 2-4in into the stoma (never force) and allow solution to enter
- Instill all solution about 6-8 mins then allow stool to empty then close off the pouch
- Do not irrigate more than once a day, when diarrhea is present or use more than 1000ml a day
Minimize flatus
- Odor- proof pouches
- Diet- avoid gas-forming foods- nuts, legumes, corn, cabbage, broccoli, cauliflower
- Swallowing air by eating too fast, chewing gum and drinking carbonated beverages also
produces intestinal gas

HEPATO-BILIARY DISEASES
LIVER
• Largest organ in the body
• Receives about 25% of the cardiac output
• Blood supply
- portal vein- unoxygenated blood from GIT; carries nutrients, metabolites and toxins from the GIT to the
liver for processing and detoxification
- hepatic artery
• Blood pressure in the hepatic sinuses is low- any process elevating the CVP- liver engorgement
• Any process impeding the blood flow through the liver causes engorgement of the of the vessels
draining the GIT
Diagnostic Tests
> Liver Biopsy (open or percutaneous)
- removal of sample living tissue for analysis
Pre: Explain, d/c ASA, NSAIDS, anticoagulants 2wks before the test, Blood clotting tests, liver enzymes,
H&H, NPO x 6hrs, Consent form
Procedure: Sedation, analgesia, position (supine or left lateral with R arm elevated)
- during insertion, have client exhale and hold breath on expiration for 5-10sec
Post: Apply direct pressure, position on right side, VS; Bedrest x 24hrs
Watch for shock, puncture of bile duct, peritonitis and pneumothorax; assess for respiratory difficulty
>Paracentesis (peritoneal tap)
Extract ascites in the peritoneum
Relieve intraabdominal pressure
Obtain fluid for culture
Procedure: Insertion of long aspirating needle to collect fluid; to drain ascitic fluid, a trocar is placed thru
small stab wound below umbilicus- allows fluid (liters) to drain slowly thru a catheter
Pre: Consent, void, position: sitting
Post: Monitor for hypovolemia, VS, shock

CIRRHOSIS
-irreversible chronic inflammatory disease- massive degeneration and destruction of hepatocytes resulting
in disorganized lobular pattern of regeneration
-Characterized by widespread fibrosis and nodule formation
Types:
Laennec’s cirrhosis, postnecrotic, biliary and cardiac
GI effects like anorexia, constipation or diarrhea, abdominal pain, flatulence, n/v, weight loss
Hepatic encephalopathy, anemia, thrombocytopenia, ascites, peripheral edema, petechiae, dry skin,
pruritus, asterixis (hand flapping tremor in hepatic coma), peripheral neuropathies
Jaundice, spider angiomas, bleeding esophageal varices, hemorrhoids
Interventions:
Assess for bleeding, impaired skin integrity
Monitor I&O, VS and lab results, daily weight and abdominal girth, administer meds (Vit K, diuretics,
vasopressin) , IV therapy using volume expanders
Gastric intubation and esophageal balloon tamponade for bleeding esophageal varices
Assess for breathing problems
Sclerotherapy if continued repeated hemorrhagic episodes
Paracentesis
Lactulose- hepatic encephalopathy- excreted in feces
High calorie diet, mod to high CHON, moderate to low fat and low Na diet
Interventions for Cirrhosis
• Bedrest, reposition every 2hrs
• Encourage deep breathing ad listen to breath sounds
• Perform oral hygiene to prevent stomatitis and remove characteristic fetid or ammonia like mouth
odor
• Meticulous skin care
• Avoid straining to lessen pressure on hemorrhoids
Management
Prevent bleeding if possible
Administer FFP aimed at increasing clotting time
Assist with insertion of Sengstaken-Blakemore tube- assess for esophageal necrosis ( release pressure
periodically)
- assess for aspiration pneumonia- suction prn
- prevent airway obstruction (gastric balloon deflation or breakage)- cut asap
Provide soft diet and adequate nutrition
Manage the patient’s symptoms; no treatment available for varices

BILIARY DISORDERS
1. CHOLECYSTITIS
- acute or chronic
- associated with gallstone or biliary obst.
- occurrence: women 40-50 y.o.
Sedentary
obese
manifestations:
Acute: -nausea & vomiting
-indigestion, belching, flatulence
-epigastric pain >>scapula 2-4 hrs after fatty meal & last 4-6 hrs
-pain localized in RUQ
-tachycardia, tachypnea, fever
-leukocytosis
-guarding, rigidity, rebound tenderness
-Murphy’s sign (can’t take deep breath when examiner’s fingers are passed below the hepatic margin)
-signs of dehydration
Chronic:
-preceded by several acute
- attacks & a history of learning to avoid fatty foods
Treatment:
- Surgery – to prevent rupture >> peritonitis
- Meds: Antibiotics, antiemetics, analgesics, antispasmodics
* Demerol - choice
- NPO till symptoms subside >> low fat, no gas formers, small feedings
- NG decompression
Prevention:
- control obesity
- avoid excess weight
- less fat intake; increase fluids
Manifestations:
- indigestion after fatty intake
- RUQ pain, Murphy’s sign
- gas eructations after eating
- biliary colic: RUQ—back—scapula—shoulder-
- nausea vomiting
- diaphoresis, tachycardia

*CHOLEDOCHOLITHIASIS:
- jaundice
- acholic stools
- increase urine bilirubin
- increase prothrombin time
Treatment:
- drugs: NTG, Atropine, Ca Gluconate
- NGT >> suction
- low fat diet
- after attack of pain: Save stools

Non-surgical Interventions:
1. Dissolution therapy:
Chenodeoxycholic acid (Chenodiol)
Ursodiol p.o.– decrease stone size or
dissolve the stones
2. ESWL followed by oral dissolution
-1500 shockwaves delivered in 1-2 hrs

SURGICAL:
- Cholecystectomy
- Choledochotomy
- Laparoscopic Cholecystectomy
- 4 small (5-10 mm) incisions
umbilicus, epigastric, RUQ-
midclavicular line, ant. Axillary line

Post-Op care:
- Monitor respiratory comp.
- Maintain respiratory function
- NPO, NGT>>suction
- Meds: antiemetics, analgesics
- T-Tube care

T-TUBE CARE:
- semi=fowler’s position
- monitor amount, color, consistency, odor
- report sudden increase in bile output
initial: 500-1000 ml/day
decrease after a few days
- anchor properly, maintain patency, keep below
level of gall bladder
- check stool, urine, skin color
- avoid irrigation, aspiration or clamping without
orders from MD
- evaluate response to before meal clamping of
t-tube. Unclamp if nausea & vomiting
occurs.

GENITOURINARY DISORDERS
Diagnostic Tests
• Urinalysis- exam of urine for color, SG, appearance, ph, ketones, RBC and WBC- screen for
urinary and systemic disorders
• Urine C&S- identifies infection and antibiotic
• Creatinine clearance- assess kidney function by clearing creatinine from the blood- over 24 hrs-
85-135ml/min
• Cystoscopy- remove tumors, stones- anesthesia, consent, sedatives
- after- sitz bath, fluids, mild hematuria, burning on urination
• Serum electrolytes- measures the ability of the kidneys to filter, reabsorb or secrete electrolytes
BUN- measures the nitrogen fraction of urea. It reflects the protein intake and renal excretory capacity- 8-
25mg/dl- evaluate renal function and assess hydration
- increased BUN- renal disease, burns, dehydration
- decreased BUN- malnutrition, hepatic damage
 Serum creatinine- more sensitive measure of renal damage- reflects ability of kidneys to excrete
creatinine- assess renal GFR and damage- 0.6-1.3mg/dl
 IVP- structure and excretory function of kidneys, ureters and bladder- NPO x 8, consent, allergies,
laxatives
- after- fluids
 Specific gravity- ability of kidneys to concentrate urine- 1.016-1.022
Causes of Renal Failure
• Pre-renal- renal blood supply- tumors, blood loss, shock
• Intra-renal- renal parenchyma damaged-actual renal tissue destroyed from a disease process-
diabetic nephropathy, HTN, AGN, nephrotoxic drugs, SLE, hypercalcemia
• Post-renal- obstructive uropathy- below the level of the kidneys affecting urine flow
- urine stays in the renal pelvis – hydronephrosis- renal stones, tumor, inflammation

ACUTE RENAL FAILURE

- sudden and complete loss of kidney function associated with azotemia
- Creatinine clearance- a measure of GF drops suddenly
- Diagnostic tests that uses dye may precipitate ARF since dye is nephrotoxic
3phases
- Oliguria/anuric phase- 8-15 days- output <400ml/day. Toxins accumulate- metabolic acidosis-
BUN,Crea,  K, decreased ph, bicarb, Na and Ca; azotemia (elevated serum levels of urea, creatinine and
uric acid)
- Early Diuretic phase- extends from the time daily output > 400ml/day- BUN stops UO >
3-5L/day, hyponatremia, hypokalemia, change in LOC
- Recovery- extends from 1st day BUN falls to the day it returns to normal
Signs and symptoms:
Inability to excrete nitrogenous waste products- elevated BUN and creatinine- n/v, confusion, drowsiness,
coma, asterixis
Decreased urine output- edema, HF, pulmonary edema, HTN
Inability to regulate electrolytes
- hyperkalemia- weakness,paralysis, peaked T-waves, cardiac arrhythmias
- hypernatremia- dyspnea, edema, anasarca
- hyponatremia- thirst, dry mouth, weakness, tachycardia
- hypokalemia- weakness, constipation, cardiac arrythmias
- hypocalcemia- tremors,seizures
Inability to maintain acid-base balance
- metabolic acidosis- hyperventilation, Kussmaul’s respirations
Uremic syndrome – altered platelet function
- anorexia, n/v, increased susceptibility to infection, dry itchy skin due to uremic frost
Anemia
GIB- urea broken down to ammonia by intestinal bacteria-mucosal irritant- ulceration and bleeding
ARF Interventions
Dialysis, monitor f&E, acids and bases observe for fluid overload
moderate protein restriction, high in calories, CHO, low K
Monitor cardiac status, I&O, weigh daily
Monitor creatinine and BUN
Fluid restriction
Diuretic therapy to treat oliguric phase
Sodium polystyrene sulfonate (Kayexalate)- hyperkalemia- to exchange Na for K ions in GIT
Monitor for patient’s response to medications
Monitor for infection and anemia

CHRONIC RENAL FAILURE

- slow and insidious and irreversible impairment of renal function- destroys nephrons
- Causes: glomerulonephritis, chronic infection, obstruction, nephrotoxic agents, endocrine disorder
3 stages
- Diminished renal reserve- renal function is reduced but no wastes accumulate- polyuria, nocturia,
no lab changes- 35-50%
- Renal insufficency- waste accumulates- decreased GFR- increased symptoms of RF- infection-
20-35%
- ESRD- excessive amount of wastes accumulate in blood- life-threatening condition- uremia-
<20%
Manifestations:
Azotemia, metabolic acidosis
Altered LOC due to accumulation of wastes
Irregular heart rate
Yellow bronze skin due to altered metabolic process
Dry, scaly skin and severe itching due to uremic frost
Proteinuria, glycosuria
Diminished erythropoetin secretion- anemia
Renal phosphate excretion and Vit D synthesis are diminished; K secretion increases
Heart failure, pulmonary edema
Kussmaul’s respirations
CRF Interventions
- Dialysis, monitor I&O, F&E, manage symptoms
- Kidney transplant
• Low CHON diet- limit accumulation of end products of CHON metabolism
• Fluid restrictions
• Monitor for fluid overload
• Antihypertensives, diuretics
• Epogen- stimulate bone marrow to produce RBCs
• Antipruritics; good skin care
• Dialysis for hyperkalemia and fluid imbalances
• Monitor for disequilibrium syndrome for patients receiving hemodialysis- n/v, HA, confusion,
restlessness, seizures- solutes are removed from the blood rapidly
• Assess for infection, cardiac arrhythmias

Types of Dialysis
1) Hemodialysis- used for patients who have abdominal surgery or abdominal adhesions, fluid
overload or hyperkalemia-removes wastes and fluids rapidly than PD
- removes toxic wastes and impurities from the blood. Blood removed from surgically created access site-
filtration unit- osmosis, diffusion and filtration
- uses semi-permeable membrane- pore size small enough to let small particles pass through
- dialysate bath-contains electrolytes and H2O
Nursing Responsibilities:
- monitor venous access site for bleeding
- Don’t use arm for BP, IVT or venipuncture
- Auscultate for bruits and palpate for thrills
- Weigh before and after the procedure
- Monitor for shock and hypovolemia
Types of Dialysis
2) Peritoneal dialysis- used for patients with cardiac instability, recent cerebral bleeding, GIB
- removes toxins from the blood- uses peritoneal membrane as a semi-permeable dialyzing membrane.
Hypertonic dialyzing solution is instilled thru a catheter- (diffusion) excessive concentrations of
electrolytes and uremic toxins move across the PM to the solution. (Osmosis) water in the blood does the
same.
Dwelling time- solution is drained taking toxins and wastes with it
NR: Weights daily, change dressing daily, calculate fluid balance after each session. Record all imbalances,
either + or - . Maintain sterile technique, warm dialysate, turn patient

UROLITHIASIS/ NEPHROLITHIASIS
-formation of stones in the urinary tract 2ndary to precipitates caused by Ca, stasis, altered purine
metabolism
Manifestations:
• Costovertebral angle tenderness- inflammation and edema
• Renal colic and ureteral colic
• Infection and fever- urinary stasis and retention
Interventions:
- Increase fluid intake to 3L/day
- Strain urine, encourage to ambulate, administer analgesics
- Acid ash diet for Ca/phosphate stones
- Alkaline ash- cystine and uric acid stones
- Low purine diet for uric acid stones
- Surgical removal of stone, lithotripsy

UTI
- Infections of the kidney, bladder and urethra
- Caused by bacteria- E.Coli- more common women
Manifestations:
- Chills, fever, dysuria, urinary frequency, cloudy, foul smelling urine, hematuria and pyuria
Interventions:
- Antimicrobials
- Hydration
- Good hygiene practices
- Maintain acid urine (5.5); acid ash diet

BENIGN PROSTATIC HYPERTROPHY

- slow enlargement of the prostate gland- 40 years and above
- Constriction of the urethra and interference in urination
Interventions:
- Relief of acute obstruction by insertion of indwelling or cystostomy catheter
- Administer Finasteride (Proscar)- reduce size of prostate
- Alpha-1 adrenergic receptor blocking agents- Terazosin- Hytrin- relax the muscles and promote
urination
- Urinary antiseptics and antibiotics to prevent infection from stasis if urine
Surgical Removal of Prostate
- TURP- resectoscope or laser inserted thru urethra
- Suprapubic- incision in abdomen and bladder
- Retropubic- abdominal incision
- Perineal- perineal incision- highest risk for incontinence, impotence and wound contamination
-CBI (continous bladder irrigation) after surgery to promote hemostasis and limit clots that block the
catheter
- Installation of sterile isotonic solution into the bladder using 3 lumen catheter- used to prevent
occlusion of catheter by clots or to administer direct antibiotic treatment to the bladder
Nursing Care:
- Connect catheter port to irrigant via IV tubing using sterile technique
- Set rate of infusion per MD order; usually to keep drainage reddish pink
- Maintain infusion continuously, observing color, clarity and amount of drainage
- Bladder spasms typical after TURP, notify patient

-Transurethral dilatation of prostrate- reduction of prostatic obstruction of urethra via balloon catheter, stent
or coils
Nursing Management:
- Encourage increased fluid intake
- Administer antiseptics and antibiotics as ordered
- Instruct to avoid anticholinergics and antihistamines
- Assist the pt to void prior to surgery- stand up; use moist heat or warm shower – Incontinence is
common
After surgery:
- Observe for signs of hemorrhage
- Maintain patency of catheter
- Monitor output
- Administer stool softeners to avoid straining and pressure on operative site
- Maintain suprapubic catheter after suprapubic prostatectomy; change dressigns frequently after
removal of catheter because of urine leakage
- Instruct to do perineal exercises to regain urinary control; dribbling after surgery common
- Encourage to express sexual concerns (Radical perineal resection)
-Tell patient to avoid prolonged sitting, vigorous exercise, heavy lifting and straining to decrease pressure
on the operative site and prevent bleeding
-Avoid constipation
-Discuss feelings about possible impotence and incontinence
-Encourage fluids to avoid straining during defecation

PROSTATE CANCER
- slow malignant change in the prostate gland that spreads by direct invasion of surrounding tissue
and can metastasize to bony pelvis and spine
- Increases with age and familial tendency
- Adenocarcinoma- typical type- posterior lobe
Manifestations include hard, fixed nodules palpated on rectal examination, frequency of urination,
urgency, difficulty initiating stream, back, groin or lower abdominal pain, decreased force of stream,
urinary retention
-Elevated serum acid phosphatase and serum PSA (prostatic specific antigen) and carcinoembryonic
antigen (CEA)
-Transurethral ultrasound (TRUS)- reveals mass, detects non-palpable masses- can stage extracapsular
extension
-Biopsy- reveals malignancy , MRI, CT
-If signs of urinary obstruction, tumor is large enough to metastasize
Interventions:
- Type of surgical intervention depends on the extent of the lesion, physical condition and
acceptance of outcome
- Radical prostatectomy- perineal or retropubic approach- remove the seminal vesicles and portion
of bladder neck
- Radiation alone or along with surgery- pre or post-op- reduce lesion, reduce metastasis
-Diethylstilbestrol (Estrogen)- reduce the size of an inoperable lesion or can be used post-op to limit
metastasis
-Orchiectomy- limit production of testosterone slowing the spread of the disease
Nursing Management
- Same care as with BPH
- Explain to pt that development of secondary female characteristics is due to estrogen
- Monitor for development of metastasis
- Provide care for patients receiving radiation
- Provide emotional support to patient and family
- *** advise men over age 40 to have digital rectal exam annually for early detection of prostate CA
-Discuss feelings and concerns about disease
-Evaluate response to pain medications
-Monitor for complications of chemotherapy and radiation therapy
-Promote adequate nutrition
-Maintain adequate urinary patterns

ENDOCRINE DISORDERS
Diagnostic Examinations
* FBS- measure plasma glucose- 12-14hrs fast
* Glycosylated Hgb-(HbA1c) info about average BG levels during 2-3 mos- evaluate effectiveness of
diabetic therapy
* Thyroid uptake- RAIU- measure the amount of iodine taken up by the thyroid gland in 24hrs- determine
the thyroid function
- Don’t ingest iodine rich foods x 24hrs
- discontinue all thyroid and cough meds 7-10 days prior to exam
* Serum T4 and T3
* TSH- determines primary from 2ndary hypothyroidism

HYPERTHYROIDISM
>oversecretion of thyroid hormone
>Causes:Graves disease ( toxic diffuse goiter), thyroid cancer, toxic multinodular goiter
>Hypermetabolism results with increased SNS activity
>Heart- increased HR and SV- increased CO and peripheral blood flow
>CHON, CHO and fat and vitamin metabolism increased
>Peristaltic activity- diarrhea
>Appetite- increased metabolism- weight loss
>Excessive sweating, heat intolerance and flushing
>Hair fine and brittle, nails grow away from nail bed
>CNS- agitation, nervousness, insomnia
>Exophthalmos and edema of orbital structures
>Menstrual irregularities
Thyroid storm- thyrotoxicosis- tachycardia, HTN and heat intolerance becomes life-threatening. Maybe
due to lack of meds, induced by stress
Diagnostics: T4, T3, RAIU, TSH
Nursing Interventions:
- Antithyroid meds -(I131) single dose
* PTU and Methimazole- monitor for leukopenia, agranulocytosis and thrombocytopenia. Take with meals.
Avoid OTC cough syrups
* Propanolol (Inderal)- manage tachycardia- monitor for hypotension
* Iodides- Lugol’s solution or SSKI- reduce size and vascularity of thyroid gland- administer with meals
and sip thru straw
- Monitor CV status
- Cool environment and cold fluids
- Keep HOB elevated to increased eye pressure
- Evaluate nutritional status and improve it
- Monitor CV status- hypertension, cardiac arrythmias and temperature
- Encourage bedrest
THYROIDECTOMY
- check for respiratory distress- Tracheostomy set
 - watch for hemorrhage into the neck- tight dressing with no blood.
- Monitor for signs of hypocalcemia (calcium gluconate)

HYPOTHYROIDISM
- insufficient secretion of thyroid hormone or person does not ingest enough substances necessary for
production of thyroid hormones
Primary
* congenital defects- Cretinism, thyroiditis and Hashimoto’s
disease
2ndary/central-failure of pituitary or hypothalamus or both= suppression of TSH
* Post-thyroidectomy patients- inadequate thyroid medications
Myxedema – accumulation of polyssacharides in subcutaneous and other
interstitial tissues ; used to describe extreme symptoms of severe
hypothyroidism
>Low T3 and T4, Increased TSH
>Decreased metabolism- stimulate the hypothalamus
>TSH elevated leading to goiter
>Decreased Basal metabolism- cellular energy decreased and metabolites build up (glycosaminoglycans)-
build up in the cells- cellular edema and changes organ texture
>Mucinous edema not just water (myxedema)
Manifestations:
-Nonpitting edema (eyes, hands, feet, shoulder blades)
-Tongue thickens, edema in larynx (husky voice)
-bradycardia with reduced blood flow to organs, cardiomegaly, constipation, cold intolerance, reduced
sweat gland secretion, low energy, weight gain, dry skin, dry hair, lethargy
-Severe cases-↓ LOC, BP, RR (Myxedema coma)- decreased perfusion to important organs

HYPERPITUITARISM
chronic disease marked by excess GH and tissue overgrowth
2 forms: Gigantism/ Acromegaly
Gigantism- excess of GH before puberty and char by excessive skeletal growth (rapid)
Acromegaly- adults after epiphyseal fusion. GH cant stimulate skeletal growth (slow)
Cause: Anterior pituitary adenoma
Acromegaly
-local expansion of adenoma causes both neurologic (increased ICP, HA, visual changes) and secretory
effects (endocrine)
-Optic and trigeminal nerve involvement causes visual disturbances
- Skeletal growth is not possible so the soft tissues are influenced by the excess GH
Clinical manifestations:
- Hands, feet, face and skull enlarge from GH. Slanting of forehead, protrusion of jaw ( ) and widening of
teeth also present.
-Soft tissue changes increases the size of every body organ (heart and liver)
-Increased glucose (GH- insulin antagonist) , hypertension, oily skin, weight gain, menstrual irregularities,
bone thinning, degeneration of joint cartilage
Interventions:
-Counseling re changed body image
-Visual disturbances
Octreotide – Somatostatin - GH analogue that suppresses GH production
bromocriptine (Parlodel) – dopamine agonists -inhibit GH synthesis
Tumor removal by cranial or transsphenoidal hypophysectomy
or pituitary radiation therapy
Hypophysectomy
Transphenoidal, subfrontal or cranial
Transphenoidal- incision made in upper lip thru the sphenoid sinus
Muscle graft taken from thigh to support the area and prevent leakage of CSF
Nasal packing with mustache dressing (drip pad)
Do not brush teeth, sneeze, cough, blow the nose or bend forward after surgery
Monitor for CSF leakage
Provide mouth care

DIABETES INSIPIDUS
- permanent or transient disorder of the posterior lobe of the pituitary gland characterized by deficiency in
ADH/vasopressin ; results in large volume excretion of dilute urine & polydipsia
Cause: head trauma, tumor, surgical ablation or irradiation, infections
- Without ADH, distal kidney tubules and collecting ducts remain impermeable to water. Water is excreted
rather than reabsorbed- polyuria
- Leads to dehydration which stimulates the osmoreceptors to relay sensation of thirst- increase fluid intake
- Patient tends to drink 2-20 liters of fluid daily; craves cold water
- Can’t concentrate urine so large volumes of diluted urine excreted- SG 1.001 to 1.005
- Cannot be controlled by limiting fluid intake
Manifestations
-mostly related to dehydration
-hypotension, tachycardia, weak pulse, hemoconcentration, increased BUN, dry mucous membranes, poor
skin turgor
-Urine output between 4-30L/day
Diagnostic exams:
- fluid deprivation test – withholding fluids for 8-12 hours until 3-5% of the body weight is lost
- specific gravity, serum osmolality, serum sodium
Medical management:
- vasopressin replacement:
desmopressin (DDAVP) – 10mcg/metered dose intranasally- 1-2x/day
vasopressin tannate in oil – IM
- clofibrate
- clorpropamide (Diabinese)- increases the action of ADH
- thiazide diuretic
Nursing management:
- encourage/provide support
- instruct patient about follow-up; wear medic alert ID
- proper administration and monitoring of side effects of drugs
- weigh daily

SIADH – SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE

• Involves continuous secretion of ADH even when plasma osmolarity is low; cannot excrete or
dilute urine; opposite of DI
• Results from CNS disorder and drugs, Lung Ca (bronchogenic)
• Causes excessive water reabsorption
• Most common cause of hyponatremia (dilutional hyponatremia)
• Dilutes plasma- ↓Na = water intoxication
• Weight gain, no peripheral edema, urine SG>1.012
Thirst, anorexia, fatigue, intestinal cramps, n/v, decreased urine output
Nursing Interventions:
- Geared towards restricting fluid intake, excretion of water, replacing lost Na and interfere with action of
ADH
- Assess for s/sx of water intoxication
- fluid limitations (500ml-1L)
- weights, monitor VS and breath sounds, monitor for lethargy
- Diuretics
- Hypertonic saline given (3%NaCl)

HYPERPARATHYROIDISM
• Excess PTH secretion; when glands do not respond to normal feedback of Ca and secrete
autonomously
• Hypercalcemia and bone demineralizaton occurs> bone pain
• Increased serum Ca can cause hypercalciuria and kidney stones
• Hypophosphatemia can also occur
• N/v, anorexia, constipation, epigastric pain, weight loss
• Complication: hypercalcemic crisis- serum Ca> 12mg/dL- psychosis with mental confusion
Hyperparathyroidism
Interventions:
monitor for cardiac arrhythmias and ↓CO
Monitor Ca levels, fluids, acid ash juices
Protect against complications of hypercalcemia
Hydration and Lasix (increases urinary excretion of Ca)
Phosphates- orally given to inhibit bone resorption and interfere with Ca absorption
Calcitonin- decreases the release of skeletal Ca and increases renal excretion of Ca
Calcium chelators- Mithramycin- binds the Ca- cytotoxic agent

HYPOPARATHYROIDISM
• deficient PTH secretion or ↓effectiveness of PTH on target tissues (small intestines/kidney)
• Damage to parathyroid glands due to thyroid surgery
• Lack of PTH- hypocalcemia, increase phosphate
• Chief symptom - Tetany
(+ ) chvostek’s sign and Trosseau’s sign
• Spasms, hyperreflexia, altered sensorium, cramps
• Bands or pits encircling the teeth
Interventions:
• Administer Ca supplements
• Monitor Ca and phosphorous levels
• Calcium gluconate over 10mins
• Vit D
• Avoid milk,yogurt and processed cheese
Cushing’s Disease
• Excess secretion of cortisol results in Cushing's Syndrome.
• Cortisol is essentially catabolic, promoting the breakdown of most energy stores including protein
and fat. The symptoms of Cushing's Syndrome include the following:
• Wasting of muscles- weakness
• Thin skin- easy bruisability
• Poor wound healing
• Fat deposits in cheeks, resulting in "moon face"
• Fat deposits in abdomen, resulting in obesity
• Depression

CUSHING’S DISEASE
Cushing’s Disease and Syndrome
-Hypersecretion of adrenal hormones due to ACTH excess by pituitary gland or extrapituitary tumors
- Syndrome is due to the disease or administration of steroids
- Causes: Adrenal gland neoplasms and other tumors
- ↑levels of cortisol and steroid hormones
- Steroids antagonize insulin- ↑glucose
- Fat metabolism affected- adipose tissue accumulates in the abdomen, neck and behind the
shoulders (supraclavicular)- Buffalo hump
- Accelerated CHON metabolism leads to muscle wasting
- CHON loss- osteoporosis, edema, thinning of skin, moon face, changes in skin pigmentation
- “salt, sugar, sick, sad (mood elevation)”
-Na and water retention- weight gain, HTN
-Increased body and facial hair in women
-“salt, sugar (increased glycogenesis), sad (mood elevation), sick”
Interventions:
Monitor VS and labs
Antihypertensive drugs
Warn about sudden withdrawal from steroids (adrenal crisis)
Adjust insulin for diabetics
Protect from infection
Emotional support
Low calorie diet, high CHON
Monitor I&O
Medical Management
- Pituitary tumors- remove by hypophysectomy
- Adrenal cortex tumors- removed
- Radiation
Post-op management:
- Monitor for adrenal insufficiency- 12-48hrs after surgery- give hydrocortisone
- Bilateral adrenalectomy- lifetime replacement
- Tapering the dosage of corticosteroids- allow the adrenal glands to respond better to ACTH

ADDISON’S DISEASE
-insufficient hormone secretion due to adrenal gland abnormality. Adrenal cortex destroyed-
↓gluco/mineralocorticoids
- Primary- Addison’s disease or 2ndary
Causes:
- Atrophy of adrenal cortex, tumors, rapid withdrawal of long term steroids, insufficient
ACTH stimulation, tuberculosis, histoplasmosis
- 2 hormones are deficient (aldosterone/cortisol)
- ↓levels of Na- hypovolemia and hypotension
- Because K moves opposite direction of Na, Na excretion results in hyperkalemia
- Can be life-threatening
- “salt, sugar and sad (mood disturbances)”
Addisonian crisis : cyanosis, and circulatory shock (pallor, apprehension, rapid and weak pulse, ↑RR, ↓BP
)
Interventions:
- Administer steroid replacements as needed
- Restrict to low K, high Na
- Prepare for surgery if tumor present
- Monitor VS
- Can be fatal because vascular collapse and hypotension are severe conditions
- I&O, high CHON, Na diet

DIABETES MELLITUS
• Chronic systemic disease that alters CHO, CHON and fat metabolism
• Types:
- Type I (IDDM)
- Type II (NIDDM)
- Gestational DM
- Other types related to disorder or use of drug or chemicals
Absence of Insulin
• Without insulin, glucose builds up in the blood, causing HYPERGLYCEMIA
• Polyuria- osmotic diuresis due to excessive glucose in the urine
- Na, Cl and K excreted with water loss > Dehydration
• Polydipsia
• Polyphagia- because cells receive no glucose > cell starvation results

Absence of Insulin
• With insulin deficiency, fats break down, releasing fatty acids. Conversion of fatty acids to ketone
bodies provides backup energy
• Metabolic acidosis results due to the accumulation of ketone bodies
• Excess acids caused by insulin increase H and CO2 levels in the blood- triggers the respiratory
centers of the brain to increase rate and depth of respirations- Kussmaul’s respirations
• Acetone is exhaled- fruity odor- low ph
• Insulin lack causes K depletion however, high K levels may occur in acidosis because of the shift
of potassium to the blood.
Nursing Responsibilities
- Monitor blood glucose
- Prevent complications such as ketoacidosis
- Dietary and lifestyle changes
• Instruct on weight loss and exercise (increases insulin sensitivity)
• Individualized meal planning to meet nutritional needs, control BS levels and reach and maintain
appropriate body weight
• Self- monitoring of blood glucose and instruct on medication administration esp insulin
• Instruct on how to recognize signs of DKA, HHNC and hypoglycemia
• Foot care and Avoid infection
• Monitor for complications
COMPLICATIONS
High plasma glucose caused by DM may damage small and large blood vessels and nerves.
- retinopathy- blurring of vision- 85%- leading cause of blindness- tx is photocoagulation
- nephropathy- ESRD- 35% of IDDM- HTN must be treated aggressively
- neuropathy- tingling and numbness and pain
- PVD, arteriosclerosis, CAD, CVD
• Lowers the body’s ability to fight infection-wounds heal slowly due to damaged vascular system
which cannot carry sufficient oxygen, WBC, nutrients and antibodies to the site
- increases the need for insulin
Diabetic Foot Ulcers
- 2ndary to diabetic neuropathy- sensory deficit- vascular disease contributes to the problem
- Ill-fitting shoes, cuts, punctures from foreign objects
- Prevent injury to feet. Inspect feet regularly, consult podiatrist for any callouses or corns;
- Do not go barefoot, wear shoes.
- Do not expose feet to heat sources
- Inspect, bathe and dry
Diabetic Ketoacidosis
- acute insulin deficiency- metabolic acidosis from ketone bodies- associated with Type I DM- 600-
800mg/dl
- Inadequate secretion of insulin, insufficient exogenous insulin, insulin needs or meds that
interfere with insulin secretion
- Insulin breaks down glucose- not metabolized properly – hyperglycemia. Exogenous insulin is
only way to metabolize glucose. Body uses fat- ketone bodies (ketosis). Acidosis results.
- Polyuria, polydipsia, hypokalemia, Kussmaul’s respirations, ketonuria, dizziness, metabolic
acidosis
- Interventions:
- Administer insulin, monitor blood glucose, monitor K levels, replace fluids and K, monitor
respirations and blood gases
Hyperglycemic Hyperosmolar Nonketotic Coma
- severe hyperglycemia and hypertonic dehydration without KA- reactive insulin deficiency- Type
II DM
- Inadequate insulin secretion, insulin needs; from TPN, meds like thiazides, glucocorticoids,
phenytoin
- Serum glucose levels rise- some insulin present but not enough to use glucose properly
- Acidosis absent since there is still some insulin
- The reason for the absence of ketoacidosis in NIDDM is unknown
- Hyperglycemia, glycosuria, polyuria
Interventions:
- Monitor for rapid thready pulse, VS, blood glucose, F&E, administer insulin and replace fluids
Hypoglycemia
• Excess insulin or OHA; too little food, too much exercise
• Cold, clammy skin, hunger, disorientation, pallor, nervousness, coma and death
• 10-15g of simple sugar followed by complex CHO and CHON
• Administration of D50
• If unconscious, glucagon injection to stimulate glycogenolysis
Anti-Diabetics
Insulin
- facilitates transports of glucose into the cells and promotes glycogenesis
- Available in 3 forms: human, beef and pork; administered parenterally
Oral antidiabetics
- require some functioning beta cells
- Lower serum glucose in variety of ways depending on the drug

Insulin
 Rapid acting: Lispro (humalog)- 10-15mins, 1 hour peak; duration 3hrs
 Short acting: Regular
 Intermediate acting: NPH and Lente
 Long acting: Ultralente
 Glargine (Lantus)- slow, prolonged absorption leads to relatively constant concentration over
24hrs without peaks
 Combination: Humulin 70/30
• Insulin adjusted considering the physical and emotional stresses of a person
• Administer all insulin SQ; only regular for IV
• Regular first when drawing insulin
• Rotate sites of injection preferred abdomen
• Dosage adjustments will be necessary for NPO status and when ill