Upper GI - Pancreas disorders

Question 1

3 disorders of the pancreas

Answer 1

Acute pancreatitis
Chronic pancreatitis
Pancreatic cancer

Question 2

pancreas

Answer 2

Location: in epigastrum behind the stomach

Endocrine gland – release hormones into the blood
ex insulin from beta cells. Glucagon from alpha cells. Somatostatin produced in pancreas and inhibits pancreatic hormones

Exocrine – glands secrete into target tissue.
Ex digestive enzymes (amalyse, tripsin, lipase)

Main pancreatic duct empties into duodenum

Question 3

two types of pancreatitis

Answer 3

Acute and Chronic

Question 4

Acute pancreatitis

Answer 4

Acute caused by:

1. Blocked common bile duct by gallstones
2. Heavy Alcohol use 4-7 drinks/day. 3-4 for women

Acute can be hereditary, cystic fibrosis, certain meds like steroids, viruses, hypertriglyceridemia, trauma, abd sx, ulcers, smoking, high calcium levels

most common: alcohol consumption

def: An acute inflammation of the pancreas which varies from mild edema to severe hemorrhagic necrosis (cell death)

-Pathophysiology is auto digestion of the pancreas from blockage of panc. Enzymes are activated and eat the pancreas
“walking dead” in the pancreas

If auto digestion and hemorrhagic necrosis, pt can be acutely ill and at risk for:
1. Sepsis
2. hypovolemic shock, blood leaks into abd cavity (fluid shift, decreased blood volume)
3. fluid and electrolyte disturbances

Clinical Manifestations: Pancreatitis

PAIN
- (predominant symptom - Severe pain in LUQ, can radiate to the back because of the location of the pancreas

-Sudden onset, deep piercing and continuous.
-Aggravated 24 hours after eating or drinking alcohol
-Pain is worse when rercumbant (laying down)
-Pain not relieved by vomiting

-n,v
-abd can be rigid or board-like
-Low grade fever
-high WBC “leukocytosis”
-Bowel sounds may be decreased
-stools are bulky, pale, foul smelling, fat content 50-90% (normal is 20%)
-lung crackles - because chemicals create inflammation in whole body
-Ecchymosis (bruising) in the flank (Grey Turner’s Sign) or around the umbilicus (Cullen’s Sign) in severe cases
-Both septic and hypovolemic shock are possible outcomes in severe cases

Acute: Complications

Severe pancreatitis- complete enzymatic autodigestion of the gland
-Tissue becomes necrotic
-Damage extends into retroperitoneal tissues

local complication: pseudocyst develops
-accumulation of fluid/puss (enzymes, dead tissue
-Pancreatic abscess- a large collection of __puss_________ in the pancreas from pancreatic necrosis
-S/s- abd pain, palpable mass, n,v,a, high serum amylase,
-Must be drained promptly or can cause sepsis
-Most resolve on own
-Risk: rupture = peritonitis, would need to be drained in sx (suction out noxious fluid)

Systemic complications: x 3

1-pulmonary_____________ (pleural effusion, atelectasis, and pneumonia
-Passage of exudate that contains pancreatic enzymes from the peritoneal cavity travels thru transdiaphragmatic lymph channels = inflammation of diaphragm = lack of movement= atelectasis

2-CVS________ hypotension

3-tetany_________ caused by __decrease in Calcium (hypocalcemia)__________

more complications

Trypsin (panc ezyme)which is a ____ pancreatic enzyme ________can activate prothrombin and plasminogen increasing the risk of pulmonary embolism

Labs

Labs to order:

-serum amylase (elevated) but also raised in other conditions) -usually elevated early and remains so for 24 hours.

-Serum lipase (primarily raised by pancreatitis) more indicative of pancreatitis

WBC up
LFT up
Calcium down
Glucose up
Bilirubin up
Hematocrit, hgb decrease if bleeding (not a good sign)

dx

-Abdominal Ultrasound
-Abdominal CT with contrast (used to detect complications)
-MRCP

Question 5

Acute Pancreatitis Collaborative Care

Answer 5

Acute Pancreatitis Collaborative Care

Goals are:
1) Pain relief
- IV analgesics, narcotics ex Demerol because morphine can induce spasms

Other Meds:
Antiemetics
Antismapsmotics
Nitroglycerin – spasmolytic
PPI to neutralize acid

2) Prevention/ alleviation of shock
-Monitor for shock - HR increase, BP decrease, RR increase, fever possibly, output of 30cc/hr

3) Reduction of pancreatic secretions
-NPO ASAP – to reduce panc. Secretions

4) Control of fluid and electrolyte imbalances
-Fluid balance, make sure has adequate fluid
-Give ringers lactate
-May give albumin or dextrin to restore blood volume

5) Prevention/ treatment of infection
-Prevent infection – look at WBC, fever

Resp func- listen, RR, sp O2, ABGs, sit upright, supplement O2 if 95 or lower

Suction if v

Nutrition
-Initially NPO
-When food is allowed, the diet is usually high in carbs because they are the least stimulating
-Abstain from ___alcohol___________
————————————————————————–

Prevention and promotion:

-Avoid high fat foods, heavy meals, and alcohol
-Referral to home care if going home
-Referral to alcoholic support groups (ie. AA)

Question 6

Chronic Pancreatitis

Answer 6

def: An inflammatory disorder characterized by progressive anatomic and functional destruction of the pancreas.

Pancreatic cells are replaced by fibrous tissue with repeated attacks of pancreatitis.

Two types:

Obstructive: mechanical obstruction of pancreatic common bile duct, and the duodenum d/t biliary disease

Nonobstructive: associated with inflammation and sclerosis mainly in the head of the pancreas d/t alcoholism

Clinical Manifestations:

Like acute pancreatitis but recurring attacks are more severe, more frequent, and longer duration

Wt loss – experienced by 75% of pts (usually secondary to malabsorption);

problems with digestion of fats and proteins; steatorrhea, diabetes mellitus, constipation, mild jaundice w dark urine

Pain LUQ or epigastric, but heavy, gnawing feeling; burning; cramp like. Not relieved with food or antacids.

dx

labs:

serum amylase and lipase NOT elevated significantly like in acute

WBC up
liver ALP up
Serum bilirubin up

Stool +’ve for high fat content

Assessment and Dx: ERCP, MRI, CT, ultrasound,

Collaborative Care:

Non-surgical tx –
endoscopy (remove pancreatic duct stones);
same tx for acute pancreatitis;

Prevention of further attacks
-change diet, take enzyme replacements

Relief of pain

Control of pancreatic endocrine and exocrine insufficiency (diet, pancreatic enzyme replacement and control of diabetes)
-diabetes mellitus – diet, insulin, or oral
antidiabetic agents
-Enteric-coated enzymes given - small int
-Bile salts are given (to aid absorption of Vit A, D, E, K)

Surgical treatment:

-They are Poor candidates for surgery – anorexic, poor nutrition and physical condition

-pancreaticojejunostomy – joins pancreatic duct to jejunum to allow drainage of pancreatic duct (pain relief for 80% in 6 months)

-Insert stents in pancreas –to allow things to flow

Question 7

Pancreatic Cancer

Answer 7

Most commonly associated with a poor outcome

65-75 yrs

Mean survival: 5-12 mos from diagnosis

5 yr survival rate: 6%

primary risk factor: _cig smoking_____

Other causes: obesity, heavy alcohol use, BRCA 1 and 2 – causes breast and ovarian cancer also for pancreatic cancer

Clinical Manifestations:
-Rapid wt loss – first sign -Why- cancer cells proliferate which increases metabolism to rapidly produce cancer cells + not hungry = become malnourished

-Abd pain
-Anorexia
-Nausea
-Obstructive jaundice/ pruritus
——————————————————————

Diagnostic Studies:

CT Scan (initial dx): provides info on metastasis and vascular involvement

ERCP: allows for visualization of the pancreatic duct and biliary system

Tumour markers: used for dx and monitoring of response to treatment.

Collaborative Care:

-Surgical Treatment: Whipples resection (pancreaticoduodenectomy)

-Chemotherapy or radiotherapy: postoperatively

-Nursing Management: symptomatic and similar to the approach with pancreatitis