Pancreas

- Located upper abdomen; behind the stomach; Below liver

- 2 parts : Exocrine & Endocrine
- Pancreatic enzyme secretion is normally 1500 to 3000 mL/day

Exocrine Pancreas (secreting externally, hormonal secretion from excretory ducts)

- secretion of enzymes into the GI through pancreatic duct
- secretion are collected in the pancreatic duct which joins the common bile duct and enters the duodenum at the
ampulla of Vater.
- Sphincter of Oddi, controls the rate which secretions from the pancreas and the gallbladder enter the duodenum.
- Secretions of the exocrine are DIGESTIVE ENZYMES high in protein content and electrolyte-rich fluid. They are
VERY ALKALINE because of their high concentration of sodium bicarbonate, which is capable of neutralizing highly
acid gastric juice that enters the duodenum.
ENZYMES: - stimulated by the GI hormones
AMYLASE – aids in the digestion of carbohydrates
TRYPSIN - digestion of proteins
LIPASE – digestion of fats
Secretin – a hormone which is a major stimulus for increase bicarbonate secretion from the pancreas.
Cholecystokinin – major stimulus for digestive enzyme secretion
Vagus nerve also influences exocrine pancreatic secretion

Endocrine Pancreas (Secreting internally, hormonal secretion of a ductless gland)

- secretions into the bloodstream
- Islet of Langerhans (endocrine part of the pancreas)
Insulin (beta cells)
- lower blood glucose by permitting entry of glucose into the cells of the liver, muscle, and other tissues, where it is
either stored as glycogen or used for energy.
- Promotes storage of fat in the adipose tissue and synthesis of proteins in various body tissues.
- Without insulin, glucose cannot enter cells and excreted in urine
- Diabetes: High level of glucose in the blood. Stored fats and protein are used – loss of body mass
Glucagon (alpha cells)
- It raise blood glucose by converting glycogen to glucose in the liver.
- It is secreted by the response when there is a decrease level of blood glucose in the body
Somatostatin (delta cells)
- Exerts a hypoglycemic effect by interfering with release of growth hormone from a pituitary and glucagon from the
pancreas; both of which tend to raise blood glucose level.
- Lows blood sugar

Hormones
> Insulin – lower blood glucose level
> Glucagon, epinephrine, adrenocorticosteroids, growth hormone, and thyroid hormone – Raise blood glucose level

ACUTE PANCREATITIS

Pathophysiology
- Alcohol ingestion (damage to acinar cells – produces enzymes)

- Spasms of sphincter of ODDI (backflow of enzymes)

- Increase pancreatic juice secretion
- Increase viscosity of pancreatic juice

- Leads to stone formation and protein plugs

- Blocked Pancreatic Ducts
- Increase pressure within the pancreas
- Pressure compresses blood vessels causing tissue ischemia
- activation of inactive enzymes digesting pancreatic tissue
(Disruption of calcium signaling – calcium plays a central role in controlling digestive enzyme secretion in pancreatic
acinar cells
(breakdown of trypsinogen to trypsin by the enzyme lysosomal hydrolase cathepsin-B or decreased activity of the
intracellular pancreatic trypsin inhibitor. Once activated trypsin in turn activates several pancreatic digestive
enzymes)
- Destruction of pancreatic parenchyma
- Attraction of inflammatory cells – release of cytokines – PANCREATIC INFLAMMATION

Hypocalcemia: lipase breaks down peripancreatic and mesenteric fat; → release of free fatty acids that bind calcium
→ hypocalcemia (fatty saponification)
Mesentery – attaches the intestines to the abdominal wall to keep your intestines in place and prevent it from
collapsing down to your pelvic are and helps STORE FATS. It also allows the blood and lymph vessels, as well as
the nerves, to supply the intestines.

Capillary leakage: release of inflammatory cytokines and vascular injury by pancreatic enzymes → vasodilation and
increased vascular permeability → shift of fluid from the intravascular space into the interstitial space (third space
loss) → hypotension, tachycardia → distributive shock

Pancreatic necrosis: uncorrected hypotension and third space loss → decreased organ perfusion → multiorgan
dysfunction (mainly renal) and pancreatic necrosis

When the pancreas is damaged, free fatty acids are generated by the action of pancreatic lipase. Insoluble calcium
salts are present in the pancreas, and the free fatty acids avidly chelate the salts, resulting in calcium deposition in
the retroperitoneum.

In addition, hypoalbuminemia may be a part of the clinical picture, resulting in a reduction in total serum calcium.
- Hypoalbuminemia usually is accompanied by hypocalcemia (as reflected by measurement of serum total calcium
concentration) as a result of decreased protein binding of calcium.

In patients with concomitant alcohol abuse, a poor nutritional intake of calcium and vitamin D, as well as
accompanying hypomagnesemia, may predispose these patients to hypocalcemia. (ALCOHOL ABUSE – LOW
MAGNESIUM DUE TO ACLOHOL USE DISORDER)
- Magnesium is required for the production and release of parathyroid hormone, so when magnesium is too low,
insufficient parathyroid hormone is produced and blood calcium levels are also reduced (hypocalcemia).
Jaundice – When the bile ducts become blocked, bile builds up in the liver, and jaundice (yellow color of the skin)
develops due to the increasing level of bilirubin in the blood.

Grey Turner Sign = Enzymes leaks and damaged the surrounding tissues – Bleeding – Discoloration, Retroperitoneal
Hemorrhage = reddish-brown discoloration along the flanks resulting from retroperitoneal blood dissecting along
tissue planes

Pseudocysts form when the cells of the pancreas become inflamed or are injured and pancreatic enzymes start to
leak. Leaking of the enzymes harms the tissue of the pancreas. Pancreatic pseudocysts may start after an episode of
sudden (acute) pancreatitis
A large pseudocyst that ruptures can cause complications such as internal bleeding and infection. Infection. Acute
pancreatitis can make your pancreas vulnerable to bacteria and infection.
Pancreatitis occurs when there is inflammation of the pancreas. When the pancreas gets inflamed, it may leak
digestive enzymes. This damages the pancreas. This causes collections of fluid to form. These are called pancreatic
pseudocysts.

Why does pancreatitis cause fluid loss?

This is caused by release of cytokines and other pro inflammatory mediators. These further cause vasodilatation,
intravascular volume depletion, and end organ hypoperfusion. Patients of acute pancreatitis have significant fluid loss
in third space. This is evident by increased hematocrit.

Why does pancreatitis cause hypovolemia?

Hypovolemic shock
In severe cases, parts of the pancreas die, a condition referred to as necrotizing pancreatitis. This can cause
pancreatic fluid and blood to leak into the abdominal cavity, decreasing the blood volume and blood pressure. This
can lead to hypovolemic shock.
Hypoactive bowel sounds, accompanied by epigastric distention, may be caused by peripancreatic spread of the
inflammatory process that produces a generalized ileus, localized spread of the inflammation to the adjacent small
intestine that produces a sentinel loop, or localized spread of the inflammation to the adjacent transverse colon that
produces a colon cut-off sign. Tachycardia and mild hypotension may result from hypovolemia from sequestration of
fluid in the pancreatic bed. About 60% of patients develop low-grade pyrexia from peripancreatic inflammation
without evident infection. Patients may have shallow, rapid respirations from diaphragmatic inflammation, pleural
effusions, and respiratory compromise
LOW BP DUE TO VASODILATION – NAGDILATE ANG VESSEL SO TENDECY TAAS ANG HEART RATE TO
COMPENSATE PARA MORE BLOOD TO PUMP TO INCREASE BP

FLUIDS: WHY D5LR

Studies outside the pancreatitis field could also show that hyperchloremic acidosis induced by
infusion of large amounts of saline can lead to a worse outcome with an increased risk for kidney
injury, thus leaving normal saline to be only a second choice of fluids in critically ill patients (12).

Hyperchloremic acidosis – elimination of bicarbonate –

Studies show that acidosis enhances inflammation and necrosis in acute pancreatitis.

A metabolic acidosis can be caused by three major mechanisms: 1) increased acid production; 2)
bicarbonate loss; and 3) decreased renal acid excretion

In pancreatitis patients resuscitation with Ringers´ Lactate led to a significantly reduced rate of
acidosis with a reverse correlation of bicarbonate to CRP levels (29).

Lactate in Ringer's lactate is metabolized in the liver, which results in lower

metabolic acidosis and hence protective effects," Iqbal explained.
In addition, Ringer's lactate may directly decrease the inflammatory response

RBS – ELEVATED GLUCOSE SA BODY – INFLAMMED ANG PANCREAS SO DECREASE ANG PRODUCTION
OF HORMONES: INSULIN

Why does pancreatitis cause acute respiratory distress syndrome (ARDS)?

With severe pancreatitis there are a lot of inflammatory chemicals that are secreted into the blood stream. These
chemicals create inflammation throughout the body, including the lungs. As a result, a person may experience an
inflammatory type of reaction in the lungs called ARDS. Specifically, the small air sacs inside the lungs called the
alveoli can get inflamed and become filled with fluid causing acute respiratory distress

DIAGNOSTICS:
CBC
Hemoglobin and hematocrit levels are used to monitor the patient for bleeding.
WBC count is usually elevated.
PC – check for bleeding or thrombosis
DVT, PULMONARY EMBOLI AND DIC – DUE TO TRYPSIN WHICH ACTIVATES PROTHROMBIN & FIBRINOGEN
UA - Glucose, myoglobin, blood, and protein may be present.
CXR-PA - The doctor may order a chest X-ray to check for areas of collapsed lung tissue, or accumulation of fluid in
the chest cavity, CP clearance.
With severe pancreatitis there are a lot of inflammatory chemicals that are secreted into the blood stream. These
chemicals create inflammation throughout the body, including the lungs. As a result, a person may experience an
inflammatory type of reaction in the lungs called ARDS. Specifically, the small air sacs inside the lungs called the
alveoli can get inflamed and become filled with fluid causing acute respiratory distress

S. amylase – Elevated – Indication of pancreatitis

S. Lipase usually elevates along with amylase, but stays elevated longer.
Ca+ - prone for hypocalcemia
RBS – Glucose is elevated – Indication of Diabetes

Omeprazole
Proton pump inhibitors (PPIs) could inhibit the secretion of gastric acid. Meanwhile, it could also decrease the
secretion of other digestive glands besides gastric parietal cell.

MEPERIDINE
BRAND: Demetrol
Classification: Opioid analgesic
Indication: used to help relieve moderate to severe pain
When meperidine is injected into a vein, it is given very slowly to prevent serious side effects
: interrupted breathing during sleep (sleep apnea), mental/mood changes (such as agitation, confusion,
hallucinations), stomach/abdominal pain, difficulty urinating, slow/irregular/fast heartbeat, shaking (tremors), vision
changes, signs of your adrenal glands not working well (such as loss of appetite, unusual tiredness, weight loss).
: LEADS TO ADDICTION - ABUSE
MOA: Binds to the mu-opioid receptor, inhibits ascending pain pathways, thus altering response to pain
Mu and kappa receptors, which alters the perceptions of and emotional response to pain.
(ASCENDING PAIN PATHWAY)
BIND MU RECEPTOR – TO BLOCK PAIN MESSAGES - THROUGH THE SPINAL CORD TO BRAIN IN ORDER TO
ALTER PERCEPTION OF PAIN IN BRAIN AND NERVOUS SYSTEM.
Meperidine may produce less smooth muscle spasm (SPHINCTER OF ODI), Opioids also inhibit the release of
vasopressin, somatostatin, insulin and glucagon.
Contraindication: Hypersensitive, GI obstruction
Drug Interaction: MAOI’s
Benzodiazepines & Other CNS
- can increase the risk of hypotension, respiratory depression, profound sedation, coma, and death.
Muscle Relaxant
- Meperidine may enhance the neuromuscular blocking action of skeletal muscle relaxants and produce an increased
degree of respiratory depression.
Diuretics
- Opioids can reduce the efficacy of diuretics by inducing the release of antidiuretic hormone.
Anticholinergic
- increase risk of urinary retention and/or severe constipation, which may lead to paralytic ileus.
Side Effect: Nausea, vomiting, constipation, sweating, lightheadedness, dizziness, drowsiness, or pain/redness at the
injection site may occur.
Adverse Effect: slow heartrate, weak or shallow breathing, breathing that stops during sleep, Severe drowsiness,
lightheadedness, confusion, mood changes, severe constipation, tremors
Nursing Responsibility:
- CHECK VS especially RR AND BP since it could cause hypotension
- Monitor VS ,
- To reduce the risk of dizziness and lightheadedness, get up slowly when rising from a sitting or lying position.
- Not prescribed to those people who are driving or doing machineries
- Assess patency IV

Ceftriaxone:
Brand:
Classification: Third Generation Cephalosporin, Antibiotics
Indication: Prophylaxis to prevent pancreatic infection and decrease mortality since pancreatitis can lead to necrosis.
MOA: exerts antimicrobial effect by interfering with synthesis of peptidoglycan (major structural component of
bacterial cell wall) – bactericidal
Contraindication: Hypersensitive, hepatotoxicity
Drug Interaction:
Side Effect: Mild diarrhea, mild abdominal cramping, pain, warm, nausea
Adverse Effect: Allergic reaction (rash, pruritus, urticaria), thrombophlebitis (pain, redness and swelling)
Nursing Responsibility:
- Check for allergies
- Monitor stool consistency, and bowel pattern
- Assess oral thrush (antibiotics kill good bacteria, candida grow out of control)
- Monitor for superinfection: fever,vomiting, diarrhea, genital pruritus, mental changes
- Check IV PATENCY
- CHECK CULTURE AND SENSITIVITY

Tramadol
Brand: Tramal
Classification: Cyclohexanol, Opioid Analgesic
Indication: To relieve moderate to moderately
severe pain
MOA: Binds with mu receptors and inhibits the reuptake of norepinephrine and serotonin, which may account for
tramadol’s analgesic effect.
BIND MU RECEPTOR – TO BLOCK PAIN MESSAGES - THROUGH THE SPINAL CORD TO BRAIN IN ORDER TO
ALTER PERCEPTION OF PAIN IN BRAIN AND NERVOUS SYSTEM.

Opioids block pain messages sent from the body through the spinal cord to the brain. – TO ALTER BRAIN AND NS
in response to pain
Mu and kappa receptors, which alters the perceptions of and emotional response to pain.
Ads (antidepressant) can reduce levels of inflammatory cytokines
Contraindication: Hypersensitivity to tramadol or other opioid analgesics; patients on MAO inhibitors; patients acutely
intoxicated with alcohol, hypnotics, centrally acting analgesics, opioids, or psychotropic drugs; substance abuse;
patients on obstetric preoperative medication; abrupt discontinuation; alcohol intoxication; pregnancy
Drug Interaction:
Side Effect: Dizziness, Nausea, Drowsiness, Headache, Constipation
Adverse Effect: Seizure, serotonin syndrome (agitation, hallucinations, tachycardia, hyperreflexia), blurred vision,
rash, anorexia, respiratory depression
Nursing Responsibility:
•After patient receives first tramadol dose,watch for allergic reactions, including angioedema, bronchospasm,
pruritus, Stevens-Johnson syndrome, toxic epidermal necrolysis, and urticaria. Also watch for signs and symptoms of
anaphylaxis, such as dyspnea and hypotension.
If patient has respiratory depression, assess respiratory status often, and expect to givea nonopioid analgesic—not
tramadol.
• Reassess level of pain at least 30 mins after administration
• Monitory CV and respiratory status
• Monitor for risk of seizures
• Drug dependence
• Assess patency of IV
- raise side rails due to drowsiness and dizziness