Review Notes – GI/GU

Stomach (gastric) Cancer – pg 1028

• Adenocarcinomas primarily found in men in the LES (lower esophageal sphincter) and
upper part of stomach but can occur anywhere along the GI tract
• No S&S until disease is well progressed and the area is very vascular so metastasis is
common
• No single causative agent but increased with smoking and alcohol together, GERD, and
smoked, highly salted and spicy foods; other factors include gastritis, anemia, polyps,
and decreased stomach acid (achlorhydria)
• S&S – asymptomatic initially; weight loss without trying, anemia (fatigue, pale,
weakness), pain that is relieved by belching and antacids, dysphagia, constipation, N/V,
hematemesis
• Diagnostics – Endoscopy/biopsy (gold standard), upper GI series, CBC (anemia),
AST/ALT (liver), amylase (pancreas), UA, stool; tumor markers – CEA and CA
• Treatment – surgery; radiation and chemotherapy for palliative care and to give them
time
o Billroth I and II, and total gastrectomy
o Complications
 Afferent loop syndrome – with Billroth II; severe pain with eating and
vomiting large amounts of dark brown blood with undigested food
 Dumping syndrome – with Billroth II and total gastrectomy; rapid gastric
emptying causing hypovolemia, weakness, palpitations, decreased BP,
tachycardia, pale, clammy skin causing hypoglycemia
• Eat 6 small dry meals, fluids only in between meals, recline after
eating on right side

Peritonitis – pg 1049
• Localized or generalized inflammation of the peritoneum; happens in hours – kill you
quick
• Causes – blood borne pathogens (anywhere in the body), genital tract infections, UTI,
cirrhosis with ascites; any type of rupture, trauma, bowel obstruction, pancreatitis,
ulcer; infection in the gut
• S&S – high fever, hot abdomen, abdominal pain with rebound tenderness “emergency”,
rigid abdomen, tachycardia, tachypnea, N/V, hypovolemic shock and sepsis due to fluid
loss, abscess formation
• Diagnostics – CBC (WBC will be elevated), peritoneal aspiration (gold standard) to see
blood, bile, pus, bacteria, fungus, amylase content; x-ray, ultrasound, CT,
peritoneoscopy with biopsy
• Collaborative care – surgery, NPO, fluid replacement (replacement for NG tube
secretions), NG suction, antibiotics (gram positive and gram negative (Flagyl)),
analgesics (sparingly as it masks symptoms), semi-fowler’s position, TPN (sterile),
sedatives/narcotics

Portal Hypertension (PH) and Esophageal Varices – pg 1103

• PH is a major complication of cirrhosis and alcoholics
• PH is an obstruction of normal blood flow into the liver causing increased pressure
throughout the portal circulation; anything > 12
o Results in enlarged liver, splenomegaly, large collateral veins, ascites (from
albumin), and esophageal varices; blood backs up into right side of heart “blue
bloaters”
• Esophageal Varices
o Veins at LES are large, fragile, thin-walled and bleed easily; life threatening if
ruptured
o Risk factors – alcohol ingestion, swallowing poorly masticated food, ingestion of
course food, acid reflex, increased intra-abdominal pressure causing rupture
(vomiting, straining with elimination, coughing, sneezing, lifting heavy objects),
foods such as chocolate, mints, spicy foods
o S&S – GI bleeds, coffee ground emesis, red melena, increased ammonia levels
(causing confusion and neuro issues), hypovolemic shock, cool/clammy skin,
tachycardia, tachypnea, coma
o Treatment – stop bleeding, saline lavage, Sengstaken-Blakemore tube (doctor
must put in NG tubes), replace fluids/blood, endoscopy to cauterize ruptured
vessels
o Management – prevent bleeding, avoid alcohol, ASA, ibuprofen, irritating foods;
treat URI promptly, prophylactic drugs - Inderal (non-selective Beta Blocker)
o Transjugular intrahepatic portosystemic shunt (TIPS) – after second episode of
bleeding; shunt between the systemic and portal venous system to redirect
portal blood flood and decrease pressure; non-surgical through a catheter in the
jugular vein

Acute Pancreatitis – pg 1118

• Pancreas has endocrine and exocrine functions; acute deals mostly with exocrine
function
• Acute inflammatory process with mild edema up to severe hemorrhagic necrosis
• Primary factors – alcohol and biliary disease; can also be caused by trauma, infection,
CF, HIV and drugs
• S&S – abdominal pain in LUQ that radiates to back/shoulder (referred pain), N/V,
dyspnea, cyanosis, flushing; will prefer fetal position to relieve pain
o Other S&S – fever, increased WBC, hypotension, tachycardia (shock/septic),
jaundice, abdominal tenderness, ileus (hyperactive bowel sounds above
obstruction and hypoactive bowel sounds below); Grey Turner’s sign (bluish flank
discoloration), Cullen’s sign (periumbilical discoloration)
• Pancreatic abscess – fluid cavity in the pancreas due to extensive necrosis in pancreas;
must drain
• Complications – pleural effusion, atelectasis, pneumonia, hypotension, tetany due to
hypocalcemia (Trousseau sign (BP cuff on arm) and Chvostek’s sign (facial nerve))
• Diagnostic – amylase (primary – elevated for 24-72 hours), lipase (to rule out other
causes), glucose (hyperglycemia), WBC (hyperlipidemia), ultrasound, x-ray, CT, ERCP
endoscope with biopsy
• Collaborative care – pain medication (Demerol – stays in system), NPO, NG tube, IV
fluids, monitor blood sugar, F&E labs

Pancreatic Cancer – pg 1125

• Tumors in head of pancreas with jaundice as first sign; prognosis is poor
• Risk factors – smoking, high-fat diet, diabetes, exposure to chemicals, drugs, eating
lots of meat
• S&S – recurrent episodes with chronic pancreatitis, rapid weight loss, dull abdominal
pain that radiates to back and associated with eating and occurs at night, jaundice,
nausea
• Diagnostic – ERCP endoscope with biopsy, ultrasound, CT, tumor markers – CEA and CA
Whipple Procedure – pg 1126
• Radical pancreaticoduodenectomy – resection of pancreas, duodenum stomach and
bile duct
• Most effective treatment for pancreatic cancer to remove tumor

Total Parenteral Nutrition (TPN) – pg 965

• Used to give nutrients when the GI track cannot be used; administered via the blood
stream
• Must use central line or PICC; PICC only good if dextrose is 10% or less
• Composition – water, dextrose (10 to 50%), protein/amino acids, electrolytes, vitamins
and minerals; hypertonic solution
• Must be ordered and mixed every day based on order sheet; must do daily F&E lab
work and finger sticks
• Indications – chronic diarrhea/vomiting, complicated surgery/trauma, GI obstructions,
fistulas, sepsis, burns, pancreatitis, anorexia, short gut syndrome
• Fats – lipids (10, 20 or 30%) in glass bottle with special tubing and vent; piggyback into
TPN at port closest to patient and below filter
• Administration – peripheral lines for up to 10% dextrose solutions, central lines for >
10%
o Prepared by pharmacists, keep refrigerated, verify with 2 RNs
o Do not increase rate or stop flow; must start slow and wean off TPN
o Use smallest lumen in central line; sterile dressing changes every week; flush
with saline or heparin
o New tubing with filter with every new bag; use pump; acu-checks every 6 hours
o Vital signs Q4 for infections, daily weights, I/O, monitor labs every day
Renal Artery Stenosis – pg 1175
• Occlusion of renal arteries due to atherosclerotic narrowing or fibromuscular
hyperplasia
• S&S – abrupt HTN in those under 30 or over 50
• Diagnosis – renal arteriogram
• Treatment – renal angioplasty or surgical revascularization

Renal Vein Thrombosis – pg 1175

• A clot obstructing the renal vein related to trauma, compression, tumor, pregnancy,
contraceptive use or nephrotic syndrome
• S&S – flank pain, hematuria, fever, nephrotic syndrome (proteinuria, edema, low
albumin, high cholesterol)
• Increased risk of pulmonary emboli
• Treatment – anticoagulant therapy (heparin, Coumadin) to prevent clots and
thrombectomy

Renal Trauma – pg 1175

• Blunt (car accidents, falls) or penetrating (GSW, stabbing) trauma to the kidneys
• S&S – contusions, hematuria, pain at site, signs of shock as kidneys are very vascular -
20% of cardiac output
• Diagnosis – urinalysis, IVP with cystography (uses dyes), ultrasound, renal
arteriography with dye, CT, MRI
• Treatment – bed rest and fluids for blunt traumas that can heal spontaneously; surgical
exploration and repair or nephrectomy for penetrating traumas; stay away from
contrast dyes if possible
o Follow-up care should be done for 18 months after injury
• Nephroptosis – floating kidney; kidney ripped from its location and drops down into the
abdomen
o Causes ureter to kink and leads to obstruction; hydronephrosis
o Treatment – nephropexy to surgically tack kidney back; keep patient in modified
Trendelenburg position to maintain position of kidney for healing to occur

Kidney Cancer – pg 1177

• Tumors in the cortex or pelvis and calyces
• Risk factors – smoking, obesity, exposure to asbestos, cadmium and gasoline
• S&S – intermittent and painless gross hematuria, late signs include flank pain and
palpable mass
• Metastasis to the lungs, liver, long bones (thigh pain), extension into vena cava
• Diagnosis – IVP with nephrotomography with contrast dye (kidneys, ureter and
bladder), ultrasound (to differentiate between a tumor (solid) and a cyst (fluid
filled/hollow)), angiography with contrast dye, percutaneous needle aspiration for
biopsy (get CBC and PTT first), CT, MRI
o Ask about iodine allergies and get BUN and creatinine values before doing tests
with contrast dyes – may have to use Mucomyst to get rid of dye in the kidneys
• Treatment – Radical nephrectomy (removal of kidney, adrenal gland, soft tissue, part of
ureter, lymph nodes), radiation therapy to shrink (for inoperable tumors); no effective
chemotherapy
o Nephrectomy – surgery to remove kidney or polycystic kidneys
 Lateral lithotomy incision – large incision near diaphragm; monitor for
respiratory issues and abdominal distention for paralytic ileus
 Laparoscopic – shorter healing time and fewer complications

Bladder Cancer – pg 1178

• Multiple tumors commonly found in the trigone region of the bladder
• Risk factors – smoking, exposure to dyes in textile, rubber and cable industries
• S&S - intermittent and painless gross hematuria, bladder irritability, dysuria, frequency,
urgency, polyps (are pre-cancerous and should be removed)
• Diagnosis – UA for cytology, IVP, ultrasound, CT, MRI, cystoscopy with biopsy
• Treatment – chemotherapy instilled into the bladder
Acute Renal Failure (ARF) – pg 1197
• Rapid loss of renal function; must have early recognition and treatment before loss of
function
• Most common reason for death is from septic infections
• Effects every body system as toxins are passed throughout the entire body
• Signs and Symptoms
o Progressive azotemia – accumulation of nitrogenous waste products; a byproduct
of protein metabolism; will see an increase in BUN and creatinine
o Uremia – decline in renal function where symptoms develop in multiple body
systems
o Oliguria – decrease in urine output; less than 400 ml/day
o Develops over hours or days with progressive elevation in BUN, creatinine and
potassium
o ARF follows a hypo-perfusion event; hypotension, hypovolemia, nephrotoxic
drugs, obstruction
• Prerenal causes (above the kidneys)
o Due to factors external to the kidneys that reduce renal blood flow and lead to
decreased glomerular perfusion and filtration
 o Such as hypovolemia, decreased cardiac output, decreased peripheral vascular
resistance
o Can lead to intrarenal disease if renal ischemia is prolonged
• Intrarenal causes (the kidneys themselves)
o Due to direct damage to the renal tissue (parenchyma) resulting in impaired
nephron function
o Such as prolonged ischemia, nephrotoxin (aminoglycoside antibiotics like
tobramycin and gentamicin, contrast media), hemolyzed RBCs with released
hemoglobin or myoglobin (hemolytic anemias, large muscle injury); large protein
hard to filter through the kidneys that are damaged, and renal diseases (APSGN
and SLE-lupus)
 Pre and post levels are done with aminoglycoside drugs; should be 10 to
20
o Acute tubular necrosis (ATN) – caused by ischemia, nephrotoxins or pigments;
disruption in the basement membrane that slough off cells and plug the tubules
o Most common causes are ischemia and nephrotoxic injury
• Post renal causes (below the kidneys)
o Due to mechanical obstruction of urinary outflow with urine backflow into the
renal pelvis; increased pressure in the renal system leading to necrosis
o Such as BPH, prostate cancer, calculi, trauma, external tumors
• Four phases of progression
o Initiating phase – begins at time of insult and continues until S&S appear (can
last hours or days)
o Oliguric phase – oliguria that occurs within 1 to 7 days after causative event
(lasts 10 to 14 days)
 Urinary changes – output decreases to < 400 ml/day, UA shows casts,
RBCs, WBCs, specific gravity fixed at 1.010 that indicate tubular damage
 Fluid volume excess – fluid retention, JVD, edema, HTN, CHF, PE, pleural
and cardiac effusions
 Metabolic acidosis – kidneys cannot synthesize ammonia, Kussmaul
respirations, lethargy
 Potassium excess – greater than 6; avoid ACE inhibitors “pril”, arrhythmias
are common; will see tall, peaked “T” waves on EKG
• Lowing potassium levels – IV insulin (to change it quick - but watch
out for hypoglycemia); also can use Kayexalate, sodium
bicarbonate, calcium gluconate and dialysis
 Hematologic disorders – anemia related to impaired erythropoietin
production and decreased profusion; platelet abnormalities leading to
bleeding, altered WBCs and infection
 Waste product accumulation – elevated BUN (protein breakdown) and
creatinine (muscle metabolism) via 24 hour urine; creatine is true marker
of kidney damage
 Neurologic disorders – from elevated waste products in the brain; fatigue,
difficulty concentrating, seizure, stupor, coma
 o Diuretic phase – gradual increase in urine (lasts 1 to 3 weeks)
 Output can be 1 to 3 liters per day up to 5 liters per day
 Output is increasing but nephrons are still not fully functional
 Kidneys can now excrete wastes but cannot concentrate the urine
 Monitor for hyponatremia, hypokalemia and dehydration; also monitor for
hypovolemia and hypotension
o Recovery phase – begins when the GFR increases
 BUN and creatinine levels begin to decrease
 Improvement occurs within 1 to 2 weeks, but takes up to a year to fully
recover
• Diagnostics – BUN, creatinine, electrolytes, UA, renal ultrasound, renal scan, CT, MRI,
retrograde pyelogram, renal biopsy
• Collaborative care – eliminate the cause, manage the S&S and prevent complications
during recovery
o Fluid restrictions – calculated based on previous days output
o Nutritional therapy – restrict protein, TPN
o Potassium – use measures to lower potassium and monitor for dysrhythmias
o Dialysis – for volume overload, elevated potassium, metabolic acidosis
o Assessment – vital signs, I/O, daily weight, monitor lab and UA studies, assess
dialysis site, assess mental status and general appearance
o Hold ACE inhibitors – they decrease pressure and elevate potassium