Promotes synthesis of cholesterol into neutral

UP COLLEGE OF NURSING

fatstriglycerides

MEDICAL-SURGICAL NURSING
GIT, GUT, BURNS
Lecturer: Mr. Ferdinand B. Valdez

Liver cirrhosisno bile productionurine becomes tea colored

and stool is clay colored <DIET: low in protein>

LIVER
Largest gland of the body that occupies most of the
right hypochondriac region
Scarlet brown, transparent in appearance covered
by the Glissons capsule (fibrous covering)
Liver lobules are the functional unit of the liver

I.

A. FUNCTIONS
1. Production of bile which emulsifies fats
(composed of H20 and 95% bile salt) and is stored
in the gall bladder
Presence of gall stone (made up of cholesterolwhich is the
precursor bile salts) fat intoleranceeating of fatty foodpain

2. Detoxifies drug and chemical agents in the

blood
3. Promotes synthesis of fat soluble vitamins
(ADEK)

LIVER CIRRHOSIS (Laennecs cirrhosis)

Loss of architectural design of the liver
leading to fat necrosis and scarring
A. PREDISPOSING FACTORS
1. Alcoholismmajor cause (loss of VITAMIN
B1/THIAMINE and Vitamin B6/Pyrdoxine)
2. Malnutrition--#1 cause
3. Viruses
4. Toxicity
Carbon tetrachloride
5. Use of hepatotoxic agent
B. SIGNS AND SYMPTOMS
1. Early
Weakness and fatigue
Anorexia
Nausea and vomiting
Tea-colored urine, clay-colored stool
Decreased sexual urge
Amenorrhea
Dyspepsia indigestion
Hepatomegaly
Jaundice
Urticaria/pruritus
DIET: MODERATE PROTEIN
2. Late signs
Hematologic changes
Anemia
Leucopeniainfection
PANCYTOPENIA
Bleeding tendencies
Endocrine changes
Spider angiomas/ telangiectasis--NOSE
Caput medusae (loss of tortuosity of
the umbilicus)
Palmar erythema
Gynecomastia
GIT changes
Ascites
Bleeding esophageal varices d/t portal
HPN
Neuro changes
Hepatic encephalopathy
Early Asterixis (flapping hand
tremors)
Late headache, confusion,
irritability,
fetor
hepaticus,

Obstruction in Billiary tractbile cannot enter the intestinefat

soluble vitamins will not be reabsorbedBLEEDING (Vit.K)

Estrogensecondary sex characteristicsliver dysfunction

increase excess estrogen gynecomastia

4. Kills excess estrogen hormones

5. Metabolism of:
a. Carbohydrates
Glycogenesissynthesis of glycogen
Glucogenolysisbreakdown of glycogen
Gluconeogenesisformation of glucose
from non carbohydrate sources (fats and
protein)
b. Protein
It promotes synthesis of albumin and
globulins
Liver dysfunctiondecreased albumin synthesis(+) for ascites
and edemaAltered skin integrity

Promotes synthesis of fibrinogen and

prothrombinliver dysfunctionbleeding
Promotes conversion of ammonia to urea
Liver cirrhosisammonia reabsorbed in the bloodbrain
hepatic encephalopathy (ASTEREXIS) hepatic coma

c. Fats:
1

(ammonia breath) decreased LOC

hepatic coma

PANCREAS
Both an endocrine (islets of Langerhans) and exocrine
gland (Acinar cells)
Consists of pancreatic duct where pancreatic juices
pass

DIET: LOW IN PROTEIN

C. DIAGNOSTICS
1. Liver enzymes
SGPT (ALT) elevated
SGOT (AST) elevated
2. Serum cholesterol
Ammonia elevated
3. Indirect bilirubin / Unconjugated bilirubin
elevated
4. CBC low (pancytopenia)
5. PTT prolongedbleeding
6. Hepatic UTZ fat necrosis of liver lobules

II. PANCREATITIS an acute inflammation of the

pancreas leading to pancreatic edema, necrosis and
hemorrhage d/t AUTODIGESTION; idiopathic; TRYPSIN
kills pancreas
A. PREDISPOSING FACTORS
1. Chronic alcoholism
2 main factors
2. Hepatobiliary disorders
3. Drugs:
Thiazide diuretics - Etacrynic acid
OCPs
Pentamide HCl (Pentam) for AIDS
4. Metabolic disorders
Hyperlipidemia
Hyperparathyroidism
5. Obesity
6. Diet: high in saturated fats

D. NURSING MANAGEMENT
1. Enforce CBR
2. Monitor strictly VS and IO
3. Weigh pt daily and assess for pitting edema
4. Measure abdominal girth and notify physician
5. RESTRICT NA and fluids
6. EARLY--Diet high in CHO, moderate in protein,
decreased fat, increased vitamins and minerals
LATESame but decreased protein
7. Meticulous skin care
8. Prevent complications
Ascitesaccumulation of fluid in the
peritoneal cavity
Administer medications as ordered
Loop
diuretics
(Furosemide/Lasix)
Assist
in
abdominal
paracentesis/thoracentesis
(EMPTY THE BLADDER PRE-OP
because a distended bladder may
accidentally
be
punctured;
aspirates should not exceed 2-3
Lhypovolemic shock)
Bleeding esophageal varicesdilation of
esophageal veins d/t portal HTN
Administer meds as ordered
Vitamin K
Pitressin
/Vasopressin
(to
conserve fluids)
Institute NGT decompression by
gastric lavage (ice/cold saline
solution)
Assist in mechanical decompression
insertion of sengstaken-blakemore
catheter ( 3-lumen catheter)
Hepatic Encephalopathy
Assist in mechanical ventilation
Monitor VS, NVS
Maintain side rails
Administer medications as ordered
Lactulose for ammonia
excretion

B. S/Sx
1. Severe abdominal pain radiating from the back
(left upper quadrant), chest and flank area
accompanied by DOB and aggravated by
eating < GOALREST GIT BY PLACING PX ON
NPO;
DIETTPN
(Vamine glucose or
lipofundin; Nutripak); remember to keep all
lines securely taped to prevent embolism>
2. Shallow respirations
3. tachycardia and palpitations
4. anorexia, n&v, dyspepsia
5. decreased bowel sounds
6. (+) Cullens sign ecchymoses around
umbilicus and (+) Grey-turners spots
ecchymoses at the flank area; both are
indications of hemorrhage in the pancreas
C. DIAGNOSTICS
1. Serum amylase (very toxic to the body) and
lipase elevated
2. URINE AMYLASE INCREASED
3. Serum Ca low (hypocalcemia)
D. NURSING MANAGEMENT
1. Administer meds as ordered
Narcotic analgesics
Meperidine HCl (Demerol)
Respiratory Depression
DO NOT GIVE MORPHINE &
CODEINE can cause spasm of the
sphincter of Oddi
Smooth muscle relaxation
Papanarine HCl
Vasodilators
2

2.
3.

4.
5.

NTG
Antacids (Maalox)
Milk of Magnesiadiarrhea
Aluminum Hydroxideconstipation
Decrease pancreatic stimulation
H2 receptor antagonist
Ranitidine (Zantac)at bedtime
Decrease pancreatic stimulation
Calcium gluconate for decreased Ca
Phosphate binders
Amphogel
Withhold food and fluids (need to rest the GIT)
Assist in TPN on sub-clavian veinto the
stomach or hyperalimentation
Complications of TPN
Infection (maintain strict asepsis)
change dressing 2-3x a week or when
dressing is soiled
severely tape all connections drom the
system to prevent:
o Air embolism
o Hyperglycemia
o Hyponatremia
Instruct pt to assume comfortable position
Fetal position (knee-chest position)
Prevent complications
Chronic hemorrhagic pancreatitis
Shock
MORE ON RESPIRATORY D/T PANCREATIC

C. DIAGNOSTICS
1. Gallbladder series (Oral cholecystogram)
confirm presence of gallstones
2. serum lipase elevated
3. indirect bilirubin elevated
D. NURSING MGT
1. Administer medications as ordered
Narcotic analgesics
Meperidine HCl (Demerol)
NO CODEINE AND MORPHINE

Anticholinergic agents/Anti-spasmodic
Atropine sulfate

Anti-emetics
Metoclopramide (Plasil)
Phenergan
2. Diet low in fat, moderate CHON and CHO
3. Meticulous skin care
4. Assist in surgery: Cholecystectomy
Post-op: MAINTAIN PATENCY OF TUBE
DRAIN DRY AND INTACT (prevents bile
from entering the peritoneal cavity)
STOMACH
J-shaped structure
Widest section of alimentary canal especially p.c.

SPASM

6.

A. Parts
1. antrummost common site of gastric ulcer
2. fundus
3. pylorus
Valves - prevents reflux
1. cardiac sphincter between esophagus and stomach
2. pyloric sphincter between stomach and duodenum
projectile vomitinginitial sign
olive shaped bellypathognomonic sign
Cells
1. Chief cells or zymogenic cellssecretes:
Gastric amylase digests CHO
Gastric lipase digests fats
Pepsin proteins
Rennin milk and milk products
2. Parietal/argentaffin/oxyntic cells
Produces intrinsic factors reabsorption of
B12 (cyanocobalamin) maturation of
RBCs
Gasterctomypernicous anemiainjection
of Vitamin B12 once a month
Produces HCl acid with pH of 1-2 aids in
digestion
3. Endocrine cells
Secretes gastrin stimulates HCl Acid
secretion

o Pneumonia
o Atelectasis
o Pleural effusion
Diet low in fathome management

III. CHOLECYSTITIS/CHOLELITHIASIS
inflammation of the gallbladder with gallstone
formation
A. PREDISPOSING FACTORS
1. High risk group: women, 40 y/o above
2. Obesity
3. Post-menopausal women undergoing estrogen
therapy
4. diet high in saturated fats
5. sedentary lifestyle
6. presence of tumor
B. SIGNS AND SYMPTOMS
1. Severe abdominal pain (RUQ) radiating from
the back and chest that USUALLY OCCURS AT
NIGHT

2.
3.
4.
5.
6.

PROPANTHELENE BROMIDE/
PROBANTHENE

Fatty intolerance (pain after ingestion of high

fat meals)
Anorexia, nausea and vomiting
easy bruising, jaundice, pruritus
tea-colored urine
steatorrhea, clay-colored stool
3

B. FUNCTIONS
1. Mechanical and chemical digestion
2. STORAGE OF FOOD

CHO AND CHON 1-2 HOURS

FATS 2-3 HOURS

IV. PEPTIC ULCER DISEASE erosion/excoriation of

submucosa/mucosal lining d/t
Hypersecretion of acid pepsin
Decreased resistance of mucosal barrier
secondary to HCl acid secretion
A. INCIDENCE RATE
1. men
2. AGGRESSIVE

Gastric
Duodenal90-95%; less Bicarbonate ions
and thin mucosal lining; most common

Differences
Location
Pain

Gastric Ulcer
Antrum
30 mins-1hour p.c.

Duodenal Ulcer
Duodenal bulb

Pain location
Pain character

Epigastrium
Gaseous and burning,
not relieved by food
and antacids
Normal

Mid-epigastrium
Cramping
and
burning, relieved by
food and antacids
Increased

Loss
Hematemesis
Hemorrhage, stomach
cancer
Elderly, 60 y.o above

Gain
Melena
Perforation

Gastric
acid
secretion
Weight
Hemorrhage
Complications

B. PREDISPOSING FACTORS
1. Heredity
2. Emotional stress
3. Smoking (NICOTINE) vasoconstriction
gastric ischemia
4. Alcoholism stimulates release of histamine
promotes parietal cells to secrete gastrin/
HCl acid
5. Irregular diet
6. Rapid eating
7. Ulcerogenic drugs
Aspirin
Ibuprofen
Indomethacin (CORNEAL CLOUDINESS)
ANNUAL EYE EXAMINATION; DOC for
PDA
Steroids
NSAIDs
8. foods or beverages rich in caffeine
9. gastrin producing tumors
gastrinoma

Zollinger-Ellisons
Syndrome
10. MICROBIAL
INVASION
(HELICOBACTER

CVA/Stroke increased vagal

stimulation hyperacidity
ulceration

High risk

2-3 HOURS P.C.

12MN-3AM PAIN

20 y.o above

D. DIAGNOSTICS
1. Endoscopy
2. Stool occult blood
3. Gastric analysis reveals
Normal gastric acid secretion if gastric
Increased gastric acid secretion
duodenal
4. UPPER GI SERIESCONFIRMS PRESENCE

if
OF

ULCER

E. NURSING MANAGEMENT (Diet, Drugs,

Surgery)
1. Bland diet non-irritating, non-spicy
Avoid beverages and foods high in
caffeine or milk and milk containing
products
No to Sippys diet2 cups of milk
and butter
No to Karrels diet4-6 cups of milk
and whole cream
2. Admin meds as ordered
Antacids
ACA aluminum containing antacids
Aluminum OH gel (Ampho gel)
Phosphate binder
SE: constipation
MAD magnesium containing
antacids
Milk of magnesia/Maalox
SE: diarrhea
Mg + Al preparations (Maalox)
less SE
H2 receptor antagonists
Cimetidine (Tagamet): SMOKING

PYLORI)MOST COMMON CAUSE OF ULCER

C. TYPES
1. Severity
Acute ulcers submucosal
Chronic ulcers deeper underlying
tissues; (+) scar formation
Can heal because gastric cells are labile
2. Location
Stress (Critically-ill patients)
Curlings ulcer
Burns
and
trauma

hypovolemia GIT ischemia

decreased resistance of mucosal
barrier to HCl acid secretion
DOC: H2 receptor antagonists
(Ranitidine/ Zantac)
Cushings ulcer
Head trauma

DECREASES EFFECT

Ranitidine (Zantac)
4

 Famotidine (Pepsic)
Give antacids and Cimetidine ONE
HOUR APART decreased each
others absorption
Instruct client to avoid smoking
because it decreases effectiveness of
drug
Cytoprotective agents
Sucralfate (Carafate) provides a
PASTE-LIKE SUBSTANCE that coats the
mucosal lining
Cytotec/Mesoprostol

causes
severe spasm (ABORTIFACIENT)
Anticholinergic/Anti-spasmodic agents
Atropine
Probanthelene sulfate (Probanthin)
Sedatives, tranquilizers
3. Assist in surgical procedure: subtotal
gastrectomy
Billroth I
Gastroduodenostomy removal of
part of a stomachgastric stump to
the duodenum
Billroth II
Gastrojejunostomy gastric stump
to jejunum
Removal of to of the stomach,
duodenal valve and anastomosis of
gastric valve to jejunum
Before Billroth 1&2: VAGOTOMY (severe
vagus nerve) to decrease HCl acid
secretion and prevent hemorrhage and
PYLOROPLASTY for drainage
Decrease vagal stimulation
decrease HCl acid secretion
prevent hemorrhage
Post-operative care
1. Monitor NGT output that includes:
Immediately after post-op bright red
6-8 hours greenish in color
24h dark red because of influence of
HCl acid
2. Administer medications as ordered
Antimicrobials
Narcotic analgesics
Anti-emetics
3. Maintain a patent IV line
4. Monitor VS, IO, Bowel Sounds
5. Prevent complication
Hemorrhage shock
Paralytic Ileus most common type of
complication in all abdominal surgery
caused by trauma
Peritonitis
Septicemia
Hypokalemia
PERNICIOUS ANEMIA

Dumping syndrome rapid emptying of

hypertonic food solutions; chyme food
and HCl acid from stomach to jejunum
with resultant hypokalemia dizziness,
DIAPHORESIS, PALPITATION , tachycardia,
DIARRHEA
DIET: AVOID SUGAR

Nursing management for dumping

syndrome:
Avoid fluids/chilled solutions
(Give solutions before meals)
Provide a small frequent feeding
or 4-6 equal divided feeding
Diet low in CHO and sugar
moderate CHON and fats
INSTRUCT PT TO LIE FLAT ON
BED 15-30 MINUTES AFTER EACH
FEEDING

OVERVIEW OF THE STRUCTURE AND FUNCTION

OF THE GENITO-URINARY TRACT
- Promotes excretion of nitrogenous waste products
- Maintain fluid electrolytes and acid-base balance
I.

Kidneys
A. Location a pair of bean shaped organs located
retroperitoneally (behind peritoneum) on either side
of the verbral column
B. Structure
1. Renal pelvis
2. Renal colic
3. Renal medulla
C. Nephron basic living unit. Each nephron consists
of glomerulus network of capillaries responsible
for filtering the blood going to kidneys.
D. Functions
1. Urine formation
(Normal GFR: 125 ml of blood is filtered in the
glomerulus per minute)
Filtration of total cardiac output is
received by the kidney each minute. 125
ml of blood is filtered by glomerulus per
minute.
Tubular Reabsorption 124 ml of
ultrafiltrates are reabsorbed back into the
blood
Tubular Secretion 1 ml excreted in the
urine; of total cardiac output is received
by kidneys each minute. 125 ml of blood
is filtered by glomerulus per minute.
2. Regulates BP

eg in CS: there is excessive blood loss

hemorrhage leads to hypovolemia
decrease BP will stimulate the kidney
to secrete renin ( hydrodrolytic enzymes)
released in juxtaglomerular apparatus
Angiotensin I mild vasoconstrictor

Angiotensin II potent vasoconstrictor.

Angiotensin III 3X more potent than II

5.
6.

Stimulates adrenal cortex to secrete

aldosterone (promotes Na and water
reabsorption) increased water and Na
hypovolemia increased cardiac
output increased BP (within 24 36
hours)

Burning upon urination

Late sign - Hematuria

C. DX
1. Urine culture and sensitivity
(+) E. Coli 90%
2. Urinalysis
Increased WBC
Increased CHON
Increased pus cells
D. NSG MGMT
1. Forced fluids (2-3 L/d)
2. Provide warm sitz bath to promote comfort
3. Provide acid-ash diet
Cranberry and prune juices to acidify urine
4. Monitor for gross hematuria
5. Administer meds as ordered
systemic antibiotics
penicillins
cephalosporins
sulfonamides
Co-trimoxazole (Bactrim)
Gantricin
Urinary analgesic
Pyridium
Urinary antiseptics
Nitrofurantoin (Macrodantin)

increased cardiac output

increased
peripheral
resistance
resulting to increase BP

II. Ureters 20-30 mm long serves as a passageway of

urine. capable of peristalsis
hydroureters-dilation of ureters
III. Bladder
A. Located behind the symphysis pubis
B. Made up of muscular and elastic tissues
distensible reservoir of urine
C. Max: 1, 200 -1,800 ml of urine
D. Initiates urination: 250-500 cc ml
E. Normal urine:
1. amber, aromatic, turbid/clear, pH 4-8
2. spec gravity: 1.015-1.030
3. WBC, CHON none
4. (-) E. coli
5. mucus threads few
6. (-) amorphous urates

SE: GIT DISTURBANCES, STAINING OF TEETH

GIVE STRAW

6.

IV. Urethra
A. Serves as a passageway for urine, vaginal/seminal
fluids
B. Length
1. F: 3-5 cm or 1-1/2 inches
2. M: 20 cm or 8 inches
C. Catheter
1. pedia: 8-10 fr
2. F: 12-14 fr
3. M: 16-18 fr

7.

Perineal hygiene
Importance of hydration
Void after sexual intercourse
Instruct female client to:
Front to back cleaning
Avoid tissue use
Bubble bath
(-) talcum powder
Prevent complications
Pyelonephritis

II. PYELONEPHRITIS acute or chronic inflammation

of renal pelvis leading to tubular destruction, intestinal
abscesses and renal failure

Disorders of the Urinary Tract

CYSTITIS - inflammation of the bladder
I.
A. PREDISPOSING FACTORS
1. Microbial Invasion (E. Coli, 95% cause)
2. Increased estrogen levels
3. Hereditary
4. Women
5. Urinary stagnation ( esp after sexual
intercourse)
6. Poor perineal hygiene
B. S/SX
1. Early sign - Urinary frequency and urgency
2. Hypogastric pain
3. Fever, chills, anorexia, nausea and vomiting
4. Dysuria

A. PREDISPOSING FACTORS
1. Microbial invasion
E. coli
Streptococcus
2. Urinary retention
3. pregnancy
4. DM
5. Exposure to renal toxins
B. S/SX
1. Acute Pyelonephritis
Urinary frequency and urgency
Costovertebral angle pain and tenderness
Fevers and chills, anorexia
Burning upon urination
6

III.

Dysuria, nocturia, hematuria

2. Chronic Pyelonephritis
Weight loss
Polyuria
Polydypsia
HPN
C. DIAGNOSTICS
1. Urine CS: (+) cultured microorganisms
2. Urinalysis: elevated WBC, CHON, pus cells
3. Cystoscopic exam: (+) urinary obstruction
D. NURSING MANAGEMENT
1. Provide CBR especially during acute attack
2. Forced fluids
3. Provide an acid ash in the diet
4. Provide warm sitz bath
5. Administer medications as ordered
Nitrofurantoin
SE: GIT irritation, give with food,
peripheral neuropathy, hemolytic
anemia (INITIAL SX: FEVER, STOP &
NOTIFY PHYSICIAN), discoloration of
teeth
Urinary antiseptics
Peridium
6. prevent complications
renal failure
BENIGN
PROSTATIC
HYPERPLASIA

enlargement of the prostate gland which encircles the

neck of the bladder back flow of urine
hydroureters renal pelvis (hydronephrosis)
kidney stones renal failure
A. PREDISPOSING FACTORS
1. high risk group: male >50 yo
2. influence of male hormones
3. TRAUMA
B. S/SX
1.

6.

7.

8.

SE:
headache,
orthostatic
hypotension
Finasteride (Prescar) atrophy of the
prostate gland
SE: allergic reaction and neuro
toxicity: headache and dizziness
Assist in surgery prostatectomy
TURP (Trans Urethral Resection of
Prostate) will cut the prostate gland into
pieces.
Assist in continuous bladder irrigation
cystoclysis
Nursing management:
Monitor for sx of gross bleeding
within 24 48 (Normal)
Monitor for sign of infection
Maintain patency of drainage to
flush out clots and to prevent
bladder spasm
Complications of TURP
infection
hemorrhage
urethral stricture
erectile dysfunction

IV. NEPHROLITHIASIS/UROLITHIASIS formation

of stones elsewhere in the urinary tract
A. TYPES OF STONES
1. calcium
2. oxalate
3. uric acid
B. PREDISPOSING FACTORS
1. diet high in calcium and oxalate
2. hereditary (like gout)
3. hyperparathyroidism (Hypercalcemia)
4. obesity
5. sedentary lifestyle
C. S/SX
1. Renal colic - pain
2. Cool, moist skin
3. Burning upon urination
4. Dysuria
5. Hematuria
D. DIAGNOSTICS
1. KUB: reveals site or location of stones
2. Stone analysis: reveals composition of stone
3. Cystoscopic exam: urinary obstruction
4. IVP: reveals obstruction
E. NURSING MANAGEMENT
1. Forced fluids
2. Administer isotonic fluids as ordered
3. Strain all urine using gauze pad to filter for
stone analysis
4. Warm sitz bath for comfort
5. Meds as ordered
Narcotic analgesics morphine
Allopurinol (zyloprim) for gout
SE: allergic reaction manifested by rashes

EARLY SIGN - NOCTURIA

2.

urinary hesitancy with decreased force of

urinary stream
3. terminal dribbling
4. back ache
5. compression of sciatic nerve
6. burning upon urination
7. dysuria
C. DIAGNOSTICS
1. Digital rectal exam enlarged prostate gland
2. Intravenous pyelography urinary obstruction
3. Cystoscopic exam urinary obstruction
4. Urinalysis elevated chon, wbc, pus cells
D. NURSING MANAGEMENT
1. Instruct pt to do prostate massage to promote
evacuation of prostatic fluid ( dr should extract
4 drops of prostatic fluid)
2. Limit fluid intake
3. Provide catheterization
4. Acid ash diet
5. Administer medications as ordered
Terazosin (Hytrin) relaxes smooth
muscles of urinary sphincter
7

6.

7.

8.

Provide dietary intake:

If (+) to ca stones: acid ash
If (+) to oxalate stones: alkaline ash
(milk, tea, vegetables)
If (+) to uric acid: avoid purine rich
food like anchovies, legumes, organ
meat, nuts
Assist in surgical procedure
Litholapoxy surgical removal of 2/3
stone
Nephrectomy removal of kidney
Lithotripsy

(
non
invasive)
extracorporeal shockwave
Too costly
Stones can recur
Prevent complications renal failure

2. HPN
3. recurrent pyelonephritis
4. exposure to renal toxins
B. STAGES
1. renal insufficiency
2. diminished renal reserve volume
3. end-stage renal disease (ESRD)
C. S/SX
1. Uro/Nephro
Azotemia (elevated BUN and creatinine)
Oliguria
Nocturia
Hematuria
Dysuria
2. Neuro
Lethargy
Disorientation and confusion
Memory impairment
Decreased LOC
3. Resp
Depressed cough reflex
Kausmauls respirations
4. Hema
Anemia
Leucopenia
Bleeding tendencies (thrombocytopenia)
5. CV changes
Pulmo HPN
CHF
Pericarditis
6. GIT distress
Anorexia
N&V
Stomatitis
Uremic breath
7. Integumentary
Pruritus
Uremic frost deposition of urea in the
skin
8. Metabolic/Electrolyte imbalance
Hyperkalemia
Hyperphosphatemia
Metabolic acidosis
D. NURSING MANAGEMENT
1. Enforce CBR
2. High CHO diet low CHON, fats, High vit and
minerals
3. Meds as ordered
anti-HPN agents
hydralazine
NaHCO3hyperkalemia
(corrects
acidosis)
Kayexelate enema
Hamtinics
Supplementary vitamins and minerals
Phosphate binders
Calcium gluconate

V. ACUTE RENAL FAILURE (ARF) sudden inability

of the kidneys to excrete nitrogenous waste products
A. PREDISPOSING FACTORS
1. Pre-renal : involves decrease in GFR
Hemorrhage
Shock
Chronic diarrhea (dehydration)
CHF
Hypotension
2. Intrarenal involves renal pathology
Pyelonephritis
DM
AGN
ATN
3. Post-renal (+) mechanical obstruction
BPH
Nephro/urolithiasis
Tumor
Urinary strictures
B. STAGES
1. Oliguric phase passage of urine (1-2
weeks)
Hyperkalemia
Hypernatremia
Hyperphosphatemia
HYPOCALCEMIA
Hypermagnesemia
Metabolic acidosis
Elevated BUN, Creatinine
2. Diuretic Phase (2-3 weeks)
Hyperkalemia
Hyponatremia
Metabolic acidosis
3. Convalescent phase (3-12 months)
Characterized by complete diuresis

VI. CHRONIC RENAL FAILURE (CRF) irreversible

loss of kidney function
A. PREDISPOSING FACTORS
1. DM
8

4.

5.

Assist in hemodialysis
Secure consent and explain procedure to
client
Obtain baseline data
VS
Wt
Blood exams
I/O
Inform pt about bleeding (blood is
heparinized)
Monitor for signs of complications
Bleeding
Embolism ( prepare bulldog clips at
bedside)
Septicemia
Shock
hepatitis
DISEQUILIBRIUM SYNDROME
results from rapid loss of
nitrogenous waste products
HPN
Disorientation
Headache
Paresthesia
Numbness
Avoid BP taking, phlebotomy, IV meds at
the site of fistula to prevent compression
Maintain patency of fistula by:
Prepare at bedside bulldog clips to
prevent embolism
Auscultate for bruits and palpate for
thrills (if (+) patent)
Most common dialysate: Infersol
Complication of peritoneal dialysis:
Shock
Peritonitis- cloudy urine
output
Assist in surgical procedure: KIDNEY

I.

TRANSPLANTATION

6.

Most feared complication: REJECTION

Meds:
steroids
immunosuppressants
anti
lymphocyte globulin (lifetime)
acute rejection 6 mos 1 yr
sign: oliguria,
chronic rejection sign 4 10 yrs
sign: headache, dizziness, decreased LOC,
sensorium that can lead to coma.
BURNS
- direct tissue injury d/t:
o thermal: scald, hot grease, sunburn,
contact with flames
o electrical
o chemical
o smoke inhalation: fumes, gasses, smoke
9

TYPES
A. Full thickness
1. first degree burns (superficial)
epidermis
common cause is thermal burn
(+) blanching upon pressure and erythema
(+) pain
Prioritize fluid and electrolyte
2. second degree burns (deep burn)
chemical
(+) very painful
(+) erythema or fluid filled blisters
B. Partial thickness
1. third to fourth degree burns
affect all layers of skin, muscle and bones
electrical burns
less painful than 1st and 2nd degree burns
dry, thick, leathery texture
eschar devitalized tissue
C. STAGES
1. Emergent removal of client from source of
burn
Chemical flush
Thermal wrap it
Electrical determine the source and
location then establish safety, ABC
2. Shock phase (24-48 hours) shifting of fluids
from
intravascular
to
interstitial

hypovolemia decreased circulating blood

volume
Elevated HCT
Tachycardia
Metabolic acidosis
Low serum sodium
Low serum potassium
Hypotension
Low urine output
3. Diuresis Phase/Fluid remobilization phase
(3-6 days) characterized by the return of fluids
from interstitial to intravascular
4. Covalescent/Recovery phase characterized
by continuous wound healing
Healing starts immediately after injury
D. ASSESSMENT FINDINGS
1. Rule of 9s
Head and neck = 9
Anterior chest = 18
Posterior chest = 18
Upper extremity = 9 x 2
Lower extremity = 18 x 2
Genital = 1
E. NURSING MANAGEMENT
1. administer medications as ordered
Tetanus toxoid
Burn surface area is a good source of
microbial growth
CLOSTRIDIUM TETANY

2.
3.
4.
5.
6.
7.
8.

9.

Tetanospain
Tatanolysin
Narcotic analgesics morphine sulfate
Systemic antibiotics
Cephalosporins
Penicillin
Tetracyclines
Topical antibiotics
Silver sulfadiazide
Silver nitrate
Povidone iodine
administer isotonic fluid solutions and postreplacement as ordered
maintain strict aseptic technique
diet high in CHO, CHON, vit C
if (+) to burn of the head and neck and face
assist in intubation
assist in hydrotherapy
assist in surgical wound debridement
administer analgesics 15 30 mins before
debridement
Prevent complications
Infections
Septicemia
Paralytic ileus
Curlings ulcers
H2 receptor antagonists
Zantac at bedtime to prevent Hcl
secretion at night
Assist in surgical procedure
Skin grafting

10