CHOLECYSTITS
Bile stasis or the lack of gallbladder
- acute or chronic inflammation of the gallbladder.
CLASSIFICATION
There are two classifications of cholecystitis:
- Calculous cholecystitis. In calculous cholecystitis, a
gallbladder stone obstructs bile outflow.
- Acalculous cholecystitis. Acalculous cholecystitis
describes acute inflammation in the absence of
obstruction by gallstones.
PATHOPHYSIOLOGY
- Calculous and acalculous cholecystitis have
different origins.
- Obstruction. Calculous cholecystitis occurs when a
gallbladder stone obstructs the bile outflow.
- Chemical reaction. Bile remaining in the
gallbladder initiates a chemical reaction; autolysis
and edema occur.
- Compression. Blood vessels in the gallbladder
compressed, compromising its vascular supply.
STATISTICS AND INCIDENCES
Cholecystitis account for most patients requiring
gallbladder surgery.
- Although not all occurrences of cholecystitis are
related cholelithiasis, more than 90% of patients
with acute cholecystitis have gallstones.
- The acute form is most common during middle age.
- The chronic form usually occurs among elderly
patients.
CAUSES:
The causes of cholecystitis include:
- Gallbladder stone. Cholecystitis is usually
associated with gallstone impacted in the cystic
duct.
- Bacteria. Bacteria plays a minor role in
cholecystitis; however, secondary infection of bile
occurs in approximately 50% of cases.
- Alterations in fluids and electrolytes. Acalculous
cholecystitis is speculated to be caused by
alterations in fluids and electrolytes.
- Bile stasis.
contraction also play a role in the development of
cholecystitis.
CLINICAL MANIFESTATIONS
Cholecystitis causes a series of signs and symptoms:
- Pain. Right upper quadrant pain occurs with
cholecystitis.
- Leukocytosis. An increase in the WBC occurs
because of the bodys attempt to ward off
pathogens.
- Fever. Fever occurs in response to the infection
inside the body.
- Palpable gallbladder. The gallbladder becomes
edematous as infection progresses.
- Sepsis. Infection reaches the bloodstream and the
body undergoes sepsis.
COMPLICATIONS
Cholecystitis can progress to gallbladder complications,
such as:
- Empyema. An empyema of the bladder develops if
the gallbladder becomes filled with purulent fluid.
- Gangrene. Gangrene develops because the tissues
do not receive enough oxygen and nourishment at
all.
- Cholangitis. The infection progresses as it reaches
the bile duct.
ASSESSMENT AND DIAGNOSTIC FINDINGS
Studies used in the diagnosis of cholecystitis include:
- Biliary ultrasound: Reveals calculi, with gallbladder
and/or bile duct distension (frequently the initial
diagnostic procedure).
- Oral cholecystography (OCG): Preferred method of
visualizing general appearance and function of
gallbladder, including presence of filling defects,
structural defects, and/or stone in ducts/biliary
tree. Can be done IV (IVC) when nausea/vomiting
prevent oral intake, when the gallbladder cannot be
visualized during OCG, or when symptoms persist
following cholecystectomy. IVC may also be done
perioperatively to assess structure and function of
ducts, detect remaining stones after lithotripsy or
cholecystectomy, and/or to detect surgical
complications. Dye can also be injected via T-tube
drain postoperatively.
- Endoscopic retrograde cholangiopancreatography
(ERCP): Visualizes biliary tree by cannulation of the
common bile duct through the duodenum.
- Percutaneous transhepatic cholangiography (PTC):
Fluoroscopic imaging distinguishes between
gallbladder disease and cancer of the pancreas
(when jaundice is present); supports the diagnosis
of obstructive jaundice and reveals calculi in ducts.
- Cholecystograms (for chronic cholecystitis): Reveals
stones in the biliary system. Note:Contraindicated
in acute cholecystitis because patient is too ill to
take the dye by mouth.
- Nonnuclear CT scan: May reveal gallbladder cysts,
dilation of bile ducts, and distinguish between
obstructive/nonobstructive jaundice.
- Hepatobiliary (HIDA, PIPIDA) scan: May be done to
confirm diagnosis of cholecystitis, especially when
barium studies are contraindicated. Scan may be
combined with cholecystokinin injection to
demonstrate abnormal gallbladder ejection.
- Abdominal x-ray films (multipositional):
Radiopaque (calcified) gallstones present in 10%
15% of cases; calcification of the wall or
enlargement of the gallbladder.
- Chest x-ray: Rule out respiratory causes of referred
pain.
- CBC: Moderate leukocytosis (acute).
- Serum bilirubin and amylase: Elevated.
- Serum liver enzymesAST; ALT; ALP; LDH: Slight
elevation; alkaline phosphatase and 5-
nucleotidase are markedly elevated in biliary
obstruction.
- Prothrombin levels: Reduced when obstruction to
the flow of bile into the intestine decreases
absorption of vitamin K.
- Ultrasonography. Ultrasound is the preferred initial
imaging test for the diagnosis of acute cholecystitis;
scintigraphy is the preferred alternative.
- CT scan. CT scan is a secondary imaging test that
can identify extra-biliary disorders and acute
complications of cholecystitis.
- MRI. Magnetic resonance imaging is also a
possible secondary choice for confirming a
diagnosis of acute cholecystitis.
- Oral cholecystography. Preferred method of
visualizing general appearance and function of the
gallbladder.
- Cholecystogram. Cholecystography reveals stones
in the biliary system.
- Abdominal xray. Radiopaque or calcified gallstones
present in 10% to 15% of cases.
MEDICAL MANAGEMENT
Management may involve controlling the signs and
symptoms and the inflammation of the gallbladder.
- Fasting. The patient may not be allowed to drink or
eat at first in order to take the stress off the
inflamed gallbladder; IV fluids are prescribed to
provide temporary food for the cells.
- Supportive medical care. This may include
restoration pf hemodynamic stability and antibiotic
coverage for gram-negative enteric flora.
- Gallbladder stimulation. Daily stimulation of
gallbladder contraction with IV cholecystokinin may
help prevent the formation of gallbladder sludge in
patients receiving TPN.
PHARMACOLOGIC THERAPY
The following medications may be useful in patients with
cholecystitis:
- Antibiotic therapy. Levofloxacin and Metronidazole
for prophylactic antibiotic coverage against the
most common organisms.
- Promethazine or Prochlorperazine may control
nausea and prevent fluid and electrolyte disorders.
- Oxycodone or Acetaminophen may control
inflammatory signs and symptoms and reduce pain.
SURGICAL MANAGEMENT
Because cholecystitis frequently recurs, most people
with the condition eventually require gallbladder
removal.
- Cholecystectomy. Cholecystectomy is most
commonly performed by using a laparoscope and
removing the gallbladder.
- Endoscopic retrograde cholangiopancreatography
(ERCP). ERCP visualizes the biliary tree by
cannulation of the common bile duct through the
duodenum.
NURSING INTERVENTIONS
Treatment of cholecystitis depends on the severity of the
condition and the presence or absence of
complications.
- Pain assessment. Observe and document location,
severity (0-10 scale), and character of pain.
- Activity. Promote bedrest, allowing the patient to
assume a position of comfort.
- Diversion. Encourage use of relaxation techniques,
and provide diversional activities.
- Communication. Make time to listen and to
maintain frequent contact with the patient.
- Calories. Calculate caloric intake to identify
nutritional deficiencies or needs.
- Food planning. Consult the patient about likes and
dislikes, foods that cause distress, and preferred
meal schedules.
- Promote appetite. Provide a pleasant atmosphere
at mealtime and remove noxious stimuli.
- Laboratory studies. Monitor laboratory studies:
BUN, pre-albumin, albumin, total protein,
CLINICAL MANIFESTATIONS:
transferrin levels.
- Gallstones may be silent; no pain and only mild GI
CHOLELITHIASIS
symptoms.
- Calculi or gallstones usually form in the gallbladder - Can only be detected incidentally during surgery or
from the solid constituents of bile; they vary greatly evaluation of unrelated problems.
in size, shape and composition. - Gallbladder diseases resulting from gallstones, may
- Uncommon in children and young adults but develop two types of symptoms:
become more prevalent with increasing age. o Due to the disease of the gallbladder
o Due to obstruction of the bile passages by a
gallstone
PATHOPHYSIOLOGY: - May be acute or chronic
- Epigastric distress; fullness, abdominal distention
Two major types of gallstones: and vague pain in the right upper quadrant of the
1. Pigment Stones abdomen may occur. Usually following a meal rich
- Unconjugated pigments in the bile precipitate in fried or fatty foods.
to form stones; only 10 25% of cases
- Increased risk in patients with cirrhosis,
hemolysis, infections of the biliary tract Pain and Biliary Colic
- They cannot be dissolved and must be removed - Due to acute cholecystitis
surgically - Fever
2. Cholesterol Stones - Palpable abdominal mass
- Cholesterol is normal in bile and is insoluble in - Biliary colic with right abdominal pain that radiates
water; its solubility depends on bile acids and to back or right shoulder
lecithin (phospholipids) in the bile. - Nausea and vomiting; noticeable several hours after
- Decreased bile acid synthesis a heavy meal
- Increased cholesterol synthesis
- Bile becomes supersaturated in cholesterol Jaundice
which precipitates out to form stones
- Bile is no longer carried to the duodenum
- Acts as an irritant that produces inflammatory
- It is absorbed by the blood and gives the skin and
changes in the mucosa
mucous membrane a yellow color
- 75% of cases
- Frequently accompanied by pruritus

Changes in Urine and Stool Color

RISK FACTORS:
- Urine very dark color; (+) bile
- Women 40 years and above, multiparous and obese - Feces gray or clay colored; (-) bile
- Women who use oral contraceptives (estrogen,
Vitamin Deficeiency
clofibrate; increases biliary cholesterol saturation)
- Interferes with the absorption of Vitamin ADEK
ASSESSMENT AND DIAGNOSTIC FINDINGS:
- Abdominal X-ray
- Ultrasonography
- Radionuclide Imaging or Cholescintigraphy
- Cholecystography
- Endoscopic Retrograde Cholangiopancreatography
(ERCP)
- Percutaneous Transhepatic Cholangipgraphy
MEDICAL MANGEMENT:
- Major objectives of medical therapy are to reduce
incidence of acute episodes of gallbladder pain and
cholecystitis by:
o Supportive and dietary management
o Remove the cause of cholecystitis by
pharmacologic therapy, endoscopic
procedures or surgical interventions
Nutritional and Supportive Therapy
- Low-fat liquids
o Powdered supplements high in protein and
carbohydrate stirred into skim milk
- Cooked fruits, rice or tapioca, lean meats, mashed
potatoes, non-gas forming vegetables, bread,
coffee or tea may be added as tolerated.
- AVOID: eggs, cream, pork, fried foods, cheese, rich
dressings, gas-forming vegetables and alcohol
PHARMACOLOGIC THERAPY:
- Ursodeoxycholic acid (UDCA) and
Chenodeoxycholic acid (Chenodiol); have been
used to dissolve small radiolucent gallstone
composed primarily of cholesterol.
- UDCA has fewer side effects than Chenodiol and
can be administered in smaller doses to achieve
same effect.
- Inhibits synthesis and secretion of cholesterol;
thereby desaturating bile.
- Treatment with UDCA can reduce the size of existing
stones, dissolve small stones, and prevent new
stones from forming
- 6 12 months of therapy is required in many
patients to dissolve stones, and monitoring of the
patient for recurrence of symptoms or the
occurrence of side effects.
- Indicated for patient who refuse surgery or for whom
surgery is contraindicated.
NON SURGICAL REMOVAL OF GALLSTONES
1. Dissolving of Gallstones
2. Stone Removal by Instrumentation
3. Intracorporeal Lithotripsy
4. Extracorporeal Shockwave Lithotripsy
SURGICAL MANAGEMENT
- Laparoscopic Cholecystectomy
- Cholecystectomy
- Small Incision Cholecystectomy
- Choledochostomy
- Surgical Cholecystostomy
- Percutaneous Cholecystostomy
ANATOMY AND PHYSIOLOGY OF THE PANCREAS
PANCREAS
- Located in the upper abdomen
EXOCRINE PANCREAS
- Secreting externally, hormonal secretions form
excretory ducts
- FUNCTION: secretion of pancreatic enzyme into the
gastrointestinal tract through the pancreatic duct
- PANCREATIC ENZYMES
o Amylase digestion of carbohydrates
o Trypsin aids in the digestion of protein
o Lipase digestion of fats
ENDOCRINE PANCREAS
- Secreting internally; hormonal secretion of a
ductless gland
- Secretion of insulin, glucagon and somatostatin
directly into the bloodstream
- Islet of Langerhans
- Compsed of:
o Alpha cells glucagon
o Beta cells insulin
o Delta cells somatostatin
Insulin
- Lowers blood glucose by permitting entry of glucose
into the cells of the liver, muscle and other tissues
- It is either stored as glycogen or used for energy
- Promotes the storage of fat in adipose tissue and
the synthesis of proteins in various body tissues
Glucagon
- Opposite effects from insulin
- Raises the blood glucose by converting glycogen to
glucose in the liver
- Secreted by the pancreas in response to a decrease
in the level of the blood glucose
Somatostatin
- Exerts a hypoglycemic effect by intefrerring with
release of growth hormone from the pituitary and
glucagon from the pancreas, both of which tend to
raise blood glucose levels.
ENDOCRINE CONTROL OF BLOOD GLUCOSE LEVELS
- GLUCONEOGENESIS the process by which the
glucose required for energy is derived by
metabolism of ingested carbohydrates and also
from proteins.
- The endocrine system controls the level of blood
glucose by regulating the rate which glucose is
synthesized, stored and moved to and from the
blood stream.
- Insulin is the primary hormone that lowers the blood
glucose levels.
- Hormones that raise blood glucose levels:
o Glucagon
o Epinephrine
o Adenocorticosteroids
o Growth hormone
o Thyroid hormone
- Pancreatic enzyme secretion = 1,500
3,000mL/day
PANCREATITIS
- Pancreatitis, which is the inflammation of the
pancreas, can be acute or chronic in nature. It may
be caused by edema, necrosis or hemorrhage. In
men, this disease is commonly associated to
alcoholism, peptic ulcer or trauma; in women, its
associated to biliary tract disease. Prognosis is
usually good when pancreatitis follows biliary tract
disease, but poor when the factor is alcoholism.
Mortality rate may go as high as 60% when the
disease is associated from necrosis and
hemorrhage. (Schilling McCann, 2009)
- Pancreatitis ranges from a mild, self-limited
disorder to a severe, rapidly fatal disease that does
not respond to any treatment.
- Pancreatitis is an inflammation of the pancreas and
is a serious disorder.
- Pancreatitis can be a medical emergency
associated with a high risk of life-threatening
complications and mortality.
- Pancreatitis is commonly described as
autodigestion of the pancreas.
CLASSIFICATION
The most basic classification system divides the
disorder into acute and chronic forms.
1. Acute Pancreatitis. Acute pancreatitis does not
usually lead to chronic pancreatitis unless
complications develop.
2. Chronic pancreatitis. Chronic pancreatitis is an
inflammatory disorder characterized by progressive
destruction of the pancreas.
PATHOPHYSIOLOGY
Self-digestion of the pancreas caused by its own
proteolytic enzymes, particularly trypsin, causes acute
pancreatitis.
- Entrapment. Gallstones enter the common bile duct
and lodge at the ampulla of Vater.
- Obstruction. The gallstones obstruct the flow of the
pancreatic juice or causing a reflux of bile from the
common bile duct into the pancreatic duct.
- Activation. The powerful enzymes within the
pancreas are activated.
- Inactivity. Normally, these enzymes remain in an
inactive form until the pancreatic secretions reach
the lumen of the duodenum.
- Enzyme activities. Activation of enzymes can lead to
vasodilation, increased vascular permeability,
necrosis, erosion, and hemorrhage.
- Reflux. These enzymes enter the bile duct, where
they are activated and together with bile, back up
into the pancreatic duct, causing pancreatitis.
CAUSES
Mechanisms causing pancreatitis are usually unknown
but it is commonly associated with autodigestion of the
pancreas.
- Alcohol abuse. Eighty percent of the patients with
pancreatitis have biliary tract disease or a history of
long term alcohol abuse.
- Bacterial or viral infection. Pancreatitis occasionally
develops as a complication of mumps virus.
- Duodenitis. Spasm and edema of the ampulla of
Vater can probably cause pancreatitis.
- Medications. The use of corticosteroids, thiazide
diuretics, oral contraceptives, and other
medications have been associated with increased
incidences of pancreatitis.
CLINICAL MANIFESTATIONS
The signs and symptoms of pancreatitis include:
- Severe abdominal pain. Abdominal pain is the
major symptom of pancreatitis that causes the
patient to seek medical care and this result from
irritation and edema of the inflamed pancreas.
- Boardlike abdomen. A rigid or boardlike abdomen
may develop and cause abdominal guarding.
- Ecchymosis. Ecchymosis or bruising in the flank or
around the umbilicus may indicate severe
pancreatitis.
- Nausea and vomiting. Both are also common in
pancreatitis and the emesis is usually gastric in
origin but may also be bile stained.
- Hypotension. Hypotension is typical and reflects
hypovolemia and shock caused by the large
amounts of protein-rich fluid into the tissues and
peritoneal cavity.
COMPLICATIONS
Complications that arise in pancreatitis include the
following:
- Fluid and electrolyte disturbances. These are
common complications because of nausea,
vomiting, movement of fluid from the vascular
compartment to the peritoneal cavity, diaphoresis,
fever, and use of gastric suction.
- Pancreatic necrosis. This is a major cause of
morbidity and mortality in patients with pancreatitis
because of resulting hemorrhage, septic shock, and
multiple organ failure.
- Septic shock. Septic shock may occur with bacterial
infection of the pancreas.
ASSESSMENT AND DIAGNOSTIC FINDINGS
The diagnosis of pancreatitis is based on a history of
abdominal pain, the presence of known risk factors,
physical examination findings, and diagnostic findings.
- Serum amylase and lipase levels. These are used in
making diagnosis, although their elevation can be
attributed to many causes, and serum lipase remain
elevated for a longer period than amylase.
- WBC count. The WBC count is usually elevated.
- X-ray studies. X-ray studies of the abdomen and
chest may be obtained to differentiate pancreatitis
from other disorders that can cause similar
symptoms.
- Ultrasound. Ultrasound is used to identify an
increase in the diameter of the pancreas.
- Blood studies. Hemoglobin and hematocrit levels
are used to monitor the patient for bleeding.
- CT scan: Shows an enlarged pancreas, pancreatic
cysts and determines extent of edema and necrosis.
- Ultrasound of abdomen: May be used to identify
pancreatic inflammation, abscess, pseudocysts,
carcinoma, or obstruction of biliary tract
- Endoscopic retrograde cholangiopancreatography:
Useful to diagnose fistulas, obstructive biliary
disease, and pancreatic duct strictures/anomalies
(procedure is contraindicated in acute phase).
- CTguided needle aspiration: Done to determine
whether infection is present.
- Abdominal x-rays: May demonstrate dilated loop of
small bowel adjacent to pancreas or other intra-
abdominal precipitator of pancreatitis, presence of
free intraperitoneal air caused by perforation or
abscess formation, pancreatic calcification.
- Upper GI series: Frequently exhibits evidence of
pancreatic enlargement/inflammation.
- Serum amylase: Increased because of obstruction
of normal outflow of pancreatic enzymes (normal
level does not rule out disease). May be five or more
times normal level in acute pancreatitis.
- Serum lipase: usually elevates along with amylase,
but stays elevated longer.
- Serum bilirubin: Elevation is common (may be
caused by alcoholic liver disease or compression of
common bile duct).
- Alkaline phosphatase: Usually elevated if
pancreatitis is accompanied by biliary disease.
- Serum albumin and protein: May be decreased
(increased capillary permeability and transudation
of fluid into extracellular space).
- Serum calcium: Hypocalcemia may appear 23
days after onset of illness (usually indicates fat
necrosis and may accompany pancreatic necrosis).
- Potassium: Hypokalemia may occur because of
gastric losses; hyperkalemia may develop
secondary to tissue necrosis, acidosis, renal
insufficiency.
- Triglycerides: Levels may exceed 1700 mg/dL and
may be causative agent in acute pancreatitis.
- LDH/AST: May be elevated up to 15 times normal
because of biliary and liver involvement.
- CBC: WBC count of 10,00025,000 is present in
80% of patients. Hb may be lowered because of
bleeding. Hct is usually elevated
(hemoconcentration associated with vomiting or
from effusion of fluid into pancreas or
retroperitoneal area).
- Serum glucose: Transient elevations of more than
200 mg/dL are common, especially during
initial/acute attacks. Sustained hyperglycemia
reflects widespread cell damage and pancreatic
necrosis and is a poor prognostic sign.
- Partial thromboplastin time (PTT): Prolonged if
coagulopathy develops because of liver involvement
and fat necrosis.
- Urinalysis: Glucose, myoglobin, blood, and protein
may be present.
- Urine amylase: Can increase dramatically within 2
3 days after onset of attack.
- Stool: Increased fat content (steatorrhea) indicative
of insufficient digestion of fats and protein.
MEDICAL MANAGEMENT
Management of pancreatitis is directed towards
relieving symptoms and preventing or treating
complications.
- Pain management. Adequate administration of
analgesia (morphine, fentanyl, or hydromorphone)
is essential during the course of pancreatitis to
provide sufficient relief and to minimize
restlessness, which may stimulate pancreatic
secretion further.
- Intensive care. Correction of fluid and blood loss
and low albumin levels is necessary to maintain
fluid volume and prevent renal failure.
- Respiratory care. Aggressive respiratory care is
indicated because of the high risk elevation of the
diaphragm, pulmonary infiltrates and effusion, and
atelectasis.
- Biliary drainage. Placement of biliary drains (for
external drainage) and stents (indwelling tubes) in
the pancreatic duct through endoscopy has been
performed to reestablish drainage of the pancreas.
SURGICAL MANAGEMENT
There are several approaches available for surgery. The
major surgical procedures are the following:
- Side-to-side pancreaticojejunostomy (ductal
drainage). Indicated when dilation of pancreatic
ducts is associated with septa and calculi. This is
the most successful procedure with success rates
ranging from 60% to 90%.
- Caudal pancreaticojejunostomy (ductal drainage).
Indicated for uncommon causes of proximal
pancreatic ductal stenosis not involving the
ampulla.
- Pancreaticoduodenal (right-sided) resection
(ablative) (with preservation of the pylorus)
(Whipple procedure). Indicated when major
changes are confined to the head of the pancreas.
Preservation of the pylorus avoids usual sequelae of
gastric resection.
- Pancreatic surgery. A patient who undergoes
pancreatic surgery may have multiple drains in
place postoperatively, as well as a surgical incision
that is left open for irrigation and repacking every 2
to 3 days to remove necrotic debris.
NURSING INTERVENTIONS
Performing nursing interventions for a patient with
pancreatitis needs expertise and efficiency.
- Relieve pain and discomfort. The current
recommendation for pain management in this
population is parenteral opioids including
morphine, hydromorphone, or fentanyl via patient-
controlled analgesia or bolus.
- Improve breathing pattern. The nurse maintains the
patient in a semi-Fowlers position and encourages
frequent position changes.
- Improve nutritional status. The patient receives a
diet high in carbohydrates and low in fats and
proteins between acute attacks.
- Maintain skin integrity. The nurse carries out wound
care as prescribed and takes precautions to protect
intact skin from contact with drainage.

DIABETES MELLITUS
The major sources of the glucose that circulates in the
blood are through the absorption of ingested food in the
gastrointestinal tract and formation of glucose by the
liver from food substances.
- Diabetes mellitus is a group of metabolic diseases
that occurs with increased levels of glucose in the
blood.
- Diabetes mellitus most often results in defects in
insulin secretion, insulin action, or even both.
CLASSIFICATION:
The classification system of diabetes mellitus is unique
because research findings suggest many differences
among individuals within each category, and patients
can even move from one category to another, except for
patients with type 1 diabetes.
- Diabetes has major classifications that include type
1 diabetes, type 2 diabetes, gestational diabetes,
and diabetes mellitus associated with other
conditions.
- The two types of diabetes mellitus are differentiated
based on their causative factors, clinical course,
and management.
PATHOPHYSIOLOGY:
ISLET OF LANGERHANS
1. Insulin is secreted by beta cells in the pancreas and
it is an anabolic hormone.
2. When we consume food, insulin moves glucose
from blood to muscle, liver, and fat cells as insulin
level increases.
3. The functions of insulin include the transport and
metabolism of glucose for energy, stimulation of
storage of glucose in the liver and muscle, serves as
the signal of the liver to stop releasing glucose,
enhancement of the storage of dietary fat in
adipose tissue, and acceleration of the transport of
amino acid into cells.
4. Insulin and glucagon maintain a constant level of
glucose in the blood by stimulating the release of
glucose from the liver.
TYPE 1 DIABETES MELLITUS
- Type 1 diabetes mellitus is characterized by
destruction of the pancreatic beta cells.
- A common underlying factor in the development of
type 1 diabetes is a genetic susceptibility.
- Destruction of beta cells leads to a decrease in
insulin production, unchecked glucose production
by the liver and fasting hyperglycemia.
- Glucose taken from food cannot be stored in the
liver anymore but remains in the blood stream.
- The kidneys will not reabsorb the glucose once it
has exceeded the renal threshold, so it will appear
in the urine and be called glycosuria.
- Excessive loss of fluids is accompanied by excessive
excretion of glucose in the urine leading to osmotic
diuresis.
- There is fat breakdown which results in ketone
production, the by-product of fat breakdown.
TYPE 2 DIABETES MELLITUS
Pathophysiology of Type 2 Diabetes Mellitus
- Type 2 diabetes mellitus has major problems of
insulin resistance and impaired insulin secretion.
- Insulin could not bind with the special receptors so
insulin becomes less effective at stimulating
glucose uptake and at regulating the glucose
release.
- There must be increased amounts of insulin to
maintain glucose level at a normal or slightly
elevated level.
- However, there is enough insulin to prevent the
breakdown of fats and production of ketones.
- Uncontrolled type 2 diabetes could lead to
hyperglycemic, hyperosmolar nonketotic syndrome.
- The usual symptoms that the patient may feel are
polyuria, polydipsia, polyphagia, and fatigue,
irritability, poorly healing skin wounds, vaginal
infections, or blurred vision.
GESTATIONAL DIABETES MELLITUS
- With gestational diabetes mellitus (GDM), the
pregnant woman experiences any degree of glucose
intolerance with the onset of pregnancy.
- The secretion of placental hormones causes insulin
resistance, leading to hyperglycemia.
- After delivery, blood glucose levels in women with
GDM usually return to normal or later on develop
type 2 diabetes.
CAUSES
The exact cause of diabetes mellitus is actually
unknown, yet there are factors that contribute to the
development of the disease.
Type 1 Diabetes Mellitus
- Genetics. Genetics may have played a role in the
destruction of the beta cells in type 1 DM.
- Environmental factors. Exposure to some
environmental factors like viruses can cause the
destruction of the beta cells.
Type 2 Diabetes Mellitus
- Weight. Excessive weight or obesity is one of the
factors that contribute to type 2 DM because it
causes insulin resistance.
- Inactivity. Lack of exercise and a sedentary lifestyle
can also cause insulin resistance and impaired
insulin secretion.
Gestational Diabetes Mellitus
- Weight. If you are overweight before pregnancy and
added extra weight, it makes it hard for the body to
use insulin.
- Genetics. If you have a parent or a sibling who has
type 2 DM, you are most likely predisposed to GDM.
CLINICAL MANIFESTATIONS
Clinical manifestations depend on the level of the
patients hyperglycemia.
- Polyuria or increased urination. Polyuria occurs
because the kidneys remove excess sugar from the
blood, resulting in a higher urine production.
- Polydipsia or increased thirst. Polydipsia is present
because the body loses more water as polyuria
happens, triggering an increase in the patients
thirst.
- Polyphagia or increased appetite. Although the
patient may consume a lot of food but glucose
could not enter the cells because of insulin
resistance or lack of insulin production.
- Fatigue and weakness. The body does not receive
enough energy from the food that the patient is
ingesting.
- Sudden vision changes. The body pulls away fluid
from the eye in an attempt to compensate the loss
of fluid in the blood, resulting in trouble in focusing
the vision.
- Tingling or numbness in hands or feet. Tingling and
numbness occur due to a decrease in glucose in the
cells.
- Dry skin. Because of polyuria, the skin becomes
dehydrated.
- Skin lesions or wounds that are slow to heal.
Instead of entering the cells, glucose crowds inside
blood vessels, hindering the passage of white blood
cells which are needed for wound healing.
- Recurrent infections. Due to the high concentration
of glucose, bacteria thrives easily.
PREVENTION
Appropriate management of lifestyle can effectively
prevent the development of diabetes mellitus.
- Standard lifestyle recommendations, metformin,
and placebo are given to people who are at high risk
for type 2 diabetes.
- The 16-lesson curriculum of the intensive program
of lifestyle modifications focused on weight
reduction of greater than 7% of initial body weight
and physical activity of moderate intensity.
- It also included behavior modification strategies
that can help patients achieve their weight
reduction goals and participate in exercise.
COMPLICATIONS
If diabetes mellitus is left untreated, several
complications may arise from the disease.
- Hypoglycemia. Hypoglycemia occurs when the
blood glucose falls to less than 50 to 60 mg/dL
because of too much insulin or oral hypoglycemic
agents, too little food, or excessive physical activity.
- Diabetic Ketoacidosis. DKA is caused by an
absence or markedly inadequate amounts of insulin
and has three major features of hyperglycemia,
dehydration and electrolyte loss, and acidosis.
- Hyperglycemic Hyperosmolar Nonketotic Syndrome.
HHNS is a serious condition in which
hyperosmolarity and hyperglycemia predominate
with alteration in the sense of awareness.
ASSESSMENT AND DIAGNOSTIC FINDING
Hypoglycemia may occur suddenly in a patient
considered hyperglycemic because their blood glucose
levels may fall rapidly to 120 mg/dL or even less.
- Serum glucose: Increased 2001000 mg/dL or
more.
- Serum acetone (ketones): Strongly positive.
- Fatty acids: Lipids, triglycerides, and cholesterol
level elevated.
- Serum osmolality: Elevated but usually less than
330 mOsm/L.
- Glucagon: Elevated level is associated with
conditions that produce (1) actual hypoglycemia,
(2) relative lack of glucose (e.g., trauma, infection),
or (3) lack of insulin. Therefore, glucagon may be
elevated with severe DKA despite hyperglycemia.
- Glycosylated hemoglobin (HbA1C): Evaluates
glucose control during past 812 wk with the
previous 2 wk most heavily weighted. Useful in
differentiating inadequate control versus incident-
related DKA (e.g., current upper respiratory
infection [URI]). A result greater than 8% represents
an average blood glucose of 200 mg/dL and
signals a need for changes in treatment.
- Serum insulin: May be decreased/absent (type 1)
or normal to high (type 2), indicating insulin
insufficiency/improper utilization
(endogenous/exogenous). Insulin resistance may
develop secondary to formation of antibodies.
- Electrolytes:
o Sodium: May be normal, elevated, or
decreased.
o Potassium: Normal or falsely elevated (cellular
shifts), then markedly decreased.
o Phosphorus: Frequently decreased.
- Arterial blood gases (ABGs): Usually reflects low pH
and decreased HCO3 (metabolic acidosis) with
compensatory respiratory alkalosis.
- CBC: Hct may be elevated (dehydration);
leukocytosis suggest hemoconcentration, response
to stress or infection.
- BUN: May be normal or elevated
(dehydration/decreased renal perfusion).
- Serum amylase: May be elevated, indicating acute - Other options for diabetes management. Diet
pancreatitis as cause of DKA. education, behavioral therapy, group support, and
- Thyroid function tests: Increased thyroid activity can ongoing nutritional counselling should be
increase blood glucose and insulin needs. encouraged.
- Urine: Positive for glucose and ketones; specific
gravity and osmolality may be elevated.
- Cultures and sensitivities: Possible UTI, respiratory Meal Planning
or wound infections.
- Criteria in meal planning. The meal plan must
consider the patients food preferences, lifestyle,
usual eating times, and ethnic and cultural
MEDICAL MANAGEMENT
background.
Here are some medical interventions that are performed - Managing hypoglycemia through meals. To help
to manage diabetes mellitus. prevent hypoglycemic reactions and maintain
overall blood glucose control, there should be
- Normalize insulin activity. This is the main goal of
consistency in the approximate time intervals
diabetes treatment normalization of blood
between meals with the addition of snacks as
glucose levels to reduce the development of
needed.
vascular and neuropathic complications.
- Assessment is still necessary. The patients diet
- Intensive treatment. Intensive treatment is three to
history should be thoroughly reviewed to identify his
four insulin injections per day or continuous
or her eating habits and lifestyle.
subcutaneous insulin infusion, insulin pump
- Educate the patient. Health education should
therapy plus frequent blood glucose monitoring and
include the importance of consistent eating habits,
weekly contacts with diabetes educators.
the relationship of food and insulin, and the
- Exercise caution with intensive treatment. Intensive
provision of an individualized meal plan.
therapy must be done with caution and must be
- The nurses role. The nurse plays an important role
accompanied by thorough education of the patient
in communicating pertinent information to the
and family and by responsible behavior of patient.
dietitian and reinforcing the patients for better
- Diabetes management has five components and
understanding.
involves constant assessment and modification of
the treatment plan by healthcare professionals and
daily adjustments in therapy by the patient.
Other Dietary Concerns

- Alcohol consumption. Patients with diabetes do not

Nutritional Management need to give up alcoholic beverages entirely, but
they must be aware of the potential adverse of
- The foundations. Nutrition, meal planning, and
alcohol specific to diabetes.
weight control are the foundations of diabetes
- If a patient with diabetes consumes alcohol on an
management.
empty stomach, there is an increased likelihood of
- Consult a professional. A registered dietitian who
hypoglycemia.
understands diabetes management has the major
- Reducing hypoglycemia. The patient must be
responsibility for designing and teaching this
cautioned to consume food along with alcohol,
aspect of the therapeutic plan.
however, carbohydrate consumed with alcohol may
- Healthcare team should have the knowledge.
raise blood glucose.
Nurses and other health care members of the team
- How much alcohol intake? Moderate intake is
must be knowledgeable about nutritional therapy
considered to be one alcoholic beverage per day for
and supportive of patients who need to implement
women and two alcoholic beverages per day for
nutritional and lifestyle changes.
men.
- Weight loss. This is the key treatment for obese
- Artificial sweeteners. Use of artificial sweeteners is
patients with type 2 diabetes.
acceptable, and there are two types of sweeteners:
- How much weight to lose? A weight loss of as small
nutritive and nonnutritive.
as 5% to 10% of the total body weight may
- Types of sweeteners. Nutritive sweeteners include
significantly improve blood glucose levels.
all of which provides calories in amounts similar to
 sucrose while nonnutritive have minimal or no
calories.
- Exercise. Exercise lowers blood glucose levels by
increasing the uptake of glucose by body muscles
and by improving insulin utilization.
- A person with diabetes should exercise at the same
time and for the same amount each day or regularly.
- A slow, gradual increase in the exercise period is
encouraged.
Using a Continuous Glucose Monitoring System
- A continuous glucose monitoring system is inserted
subcutaneously in the abdomen and connected to
the device worn on a belt.
- This can be used to determine whether treatment is
adequate over a 24-hour period.
- Blood glucose readings are analyzed after 72 hours
when the data has been downloaded from the
device.
Testing for Glycated Hemoglobin
- Glycated hemoglobin or glycosylated hemoglobin,
HgbA1C, or A1C reflects the average blood glucose
levels over a period of approximately 2 to 3 months.
- The longer the amount of glucose in the blood
remains above normal, the more glucose binds to
hemoglobin and the higher the glycated
hemoglobin becomes.
- Normal values typically range from 4% to 6% and
indicate consistently near-normal blood glucose
concentrations.
Pharmacologic Therapy
- Exogenous insulin. In type 1 diabetes, exogenous
insulin must be administered for life because the
body loses the ability to produce insulin.
- Insulin in type 2 diabetes. In type 2 diabetes,
insulin may be necessary on a long-term basis to
control glucose levels if meal planning and oral
agents are ineffective.
- Self-Monitoring Blood Glucose (SMBG). This is the
cornerstone of insulin therapy because accurate
monitoring is essential.
- Human insulin. Human insulin preparations have a
shorter duration of action because the presence of
animal proteins triggers an immune response that
results in the binding of animal insulin.
- Rapid-acting insulin. Rapid-acting insulins produce
a more rapid effect that is of shorter duration than
regular insulin.
- Short-acting insulin. Short-acting insulins or regular
insulin should be administered 20-30 minutes
before a meal, either alone or in combination with a
longer-acting insulin.
- Intermediate-acting insulin. Intermediate-acting
insulins or NPH or Lente insulin appear white and
cloudy and should be administered with food
around the time of the onset and peak of these
insulins.
- The rapid-acting and short-acting insulins are
expected to cover the increase in blood glucose
levels after meals; immediately after the injection.
- Intermediate-acting insulins are expected to cover
subsequent meals, and long-acting insulins provide
a relatively constant level of insulin and act as a
basal insulin.
- Approaches to insulin therapy. There are two
general approaches to insulin therapy: conventional
and intensive.
- Conventional regimen. Conventional regimen is a
simplified regimen wherein the patient should not
vary meal patterns and activity levels.
- Intensive regimen. Intensive regimen uses a more
complex insulin regimen to achieve as much control
over blood glucose levels as is safe and practical.
- A more complex insulin regimen allows the patient
more flexibility to change the insulin doses from day
to day in accordance with changes in eating and
activity patterns.
- Methods of insulin delivery. Methods of insulin
delivery include traditional subcutaneous
injections, insulin pens, jet injectors, and insulin
pumps.
- Insulin pens use small prefilled insulin cartridges
that are loaded into a pen-like holder.
- Insulin is delivered by dialing in a dose or pushing a
button for every 1- or 2-unit increment
administered.
- Jet injectors deliver insulin through the skin under
pressure in an extremely fine stream.
- Insulin pumps involve continuous subcutaneous
insulin infusion with the use of small, externally
worn devices that closely mimic the function of the
pancreas.
- Oral antidiabetic agents may be effective for
patients who have type 2 diabetes that cannot be
treated by MNT and exercise alone.
- Oral antidiabetic agents. Oral antidiabetic agents
include sulfonylureas, biguanides, alpha-
glucosidase inhibitors, thiazolidinediones, and
dipeptidyl-peptidase-4.
- Half of all the patients who used oral antidiabetic
agents eventually require insulin, and this is called
secondary failure.
- Primary failure occurs when the blood glucose level
remains high 1 month after initial medication use.

NURSING INTERVENTIONS

The healthcare team must establish cooperation in

implementing the following interventions.

- Educate about home glucose monitoring. Discuss ANATOMY AND PHYSIOLOGY OF THE ENDOCRINE
glucose monitoring at home with the patient SYSTEM
according to individual parameters to identify and
manage glucose variations.
- Review factors in glucose instability. Review clients
common situations that contribute to glucose
instability because there are multiple factors that
can play a role at any time like missing meals,
infection, or other illnesses.
- Encourage client to read labels. The client must
choose foods described as having a low glycemic
index, higher fiber, and low-fat content.
- Discuss how clients antidiabetic medications work.
Educate client on the functions of his or her
medications because there are combinations of
drugs that work in different ways with different
blood glucose control and side effects.
- Check viability of insulin. Emphasize the
importance of checking expiration dates of
medications, inspecting insulin for cloudiness if it is
normally clear, and monitoring proper storage and
preparation because these affect insulin
absorbability. FUNCTIONS OF THE ENDOCRINE SYSTEM
Review type of insulin used. Note the type of insulin to Despite the huge variety of hormones, there are really
be administered together with the method of delivery only two mechanisms by which hormones trigger
and time of administration. This affects timing of effects changes in cells.
and provides clues to potential timing of glucose
instability. - Water equilibrium. The endocrine system controls
water equilibrium by regulating the solute
Check injection sites periodically. Insulin absorption can concentration of the blood.
vary day to day in healthy sites and is less absorbable in - Growth, metabolism, and tissue maturation. The
lipohypertrophic tissues. endocrine system controls the growth of many
tissues, like the bone and muscle, and the degree
of metabolism of various tissues, which aids in the
maintenance of the normal body temperature and
normal mental functions. Maturation of tissues,
which appears in the development of adult features
and adult behavior, are also determined by the
endocrine system.
- Heart rate and blood pressure management. The
endocrine system assists in managing the heart
 rate and blood pressure and aids in preparing the
body for physical motion.
- Immune system control. The endocrine system
helps regulate the production and functions of
immune cells.
- Reproductive function controls. The endocrine
system regulates the development and the
functions of the reproductive systems in males and
females.
- Uterine contractions and milk release. The
endocrine system controls uterine contractions
throughout the delivery of the newborn and
stimulates milk release from the breasts in lactating
females.
- Ion management. The endocrine system regulates
Na+, K+, and Ca2+ concentrations in the blood.
- Blood glucose regulator. The endocrine system
controls blood glucose levels and other nutrient
levels in the blood.
- Direct gene activation. Being lipid-soluble
molecules, the steroid hormones can diffuse
through plasma membranes of their target cells;
once inside, the steroid hormone enters the nucleus
and binds to a specific receptor protein there; then,
the hormone-receptor complex binds to specific
sites on the cells DNA, activating certain genes to
transcribe messenger RNA; the mRNA then is
translated in the cytoplasm, resulting in the
synthesis of new proteins.
- Second messenger system. Water-soluble,
nonsteroidal hormones-protein, and peptide
hormones- are unable to enter the target cells, so
instead, they bind to receptors situated on the
target cells plasma membrane and utilize a second
messenger system.
HYPOTHALAMUS
The major endocrine organs of the body include the
pituitary, thyroid, parathyroid, adrenal, pineal and
thymus glands, the pancreas, and the gonads.
- Hypothalamus. The hypothalamus, which is part of
the nervous system, is also considered as a major
endocrine organ because it produces several
hormones. It is an important autonomic nervous
system and endocrine control center of the brain
located inferior to the thalamus.
- Mixed functions. Although the function of some
hormone-producing glands is purely endocrine, the
function of others (pancreas and gonads) is mixed-
both endocrine and exocrine.
PITUITARY GLAND
The pituitary gland is approximately the size of a pea.
- Location. The pituitary gland hangs by a stalk from
the inferior surface of the hypothalamus of the
brain, where it is snugly surrounded by the Turks
saddle of the sphenoid bone.
- Lobes. It has two functional lobes- the anterior
pituitary (glandular tissue) and the posterior
pituitary (nervous tissue).
Hormones of the Anterior Pituitary
There are several hormones of the anterior pituitary
hormones that affect many body organs.
- Growth hormone (GH). Growth hormone is a general
metabolic hormone, however, its major effects are
directed to the growth of skeletal muscles and long
bones of the body; it is a protein-sparing and
anabolic hormone that causes amino acids to be
built into proteins and stimulates most target cells
to grow in size and divide.
- Prolactin (PRL). Prolactin is a protein hormone
structurally similar to growth hormone; its only
known target in humans is the breast because, after
childbirth, it stimulates and maintains milk
production by the mothers breast.
- Adrenocorticotropic hormone (ACTH). ACTH
regulates the endocrine activity of the cortex portion
of the adrenal gland.
- Thyroid-stimulating hormone (TSH). TSH, also called
thyrotropin hormone influences the growth and
activity of the thyroid gland.
- Gonadotropic hormones. The gonadotropic
hormones regulate the hormonal activity of gonads
(ovaries and testes).
- Follicles-stimulating hormone (FSH). FSH
stimulates follicle development in the ovaries; as
the follicles mature, they produce estrogen and
eggs that are readied for ovulation; in men, FSH
stimulates sperm development by the testes.
- Luteinizing hormone (LH). LH triggers ovulation of
an egg from the ovary and causes the ruptured
follicle to produce progesterone and some
estrogen; in men, LH stimulates testosterone
production by the interstitial cells of the testes.
Hormones of the Posterior Pituitary
The posterior pituitary is not an endocrine gland in the
strict sense because it does not make the peptide
hormones it releases, but it simply acts as a storage levels, thus it is said to be a hyperglycemic
area for hormones made by hypothalamic neurons. hormone; it also reduce pain and inflammation by
inhibiting some pain-causing molecules called
- Oxytocin. Oxytocin is released in significant amount
prostaglandins.
only during childbirth and in nursing women; it
- Sex hormones. Both male and female sex hormones
stimulates powerful contractions of the uterine
are produced by the adrenal cortex throughout life
muscle during labor, during sexual relations, and
in relatively small amounts; although the bulk of sex
during breastfeeding and also causes milk ejection
hormones produced by the innermost cortex layer
(let-down reflex) in a nursing woman.
are androgens (male sex hormones), some
- Antidiuretic hormone (ADH). ADH causes the
estrogens (female sex hormones), are also formed.
kidneys to reabsorb more water from the forming of
urine; as a result, urine volume decreases and
blood volume increases; in larger amounts, ADH
Hormones of the Adrenal Medulla
also increases blood pressure by causing
constriction of the arterioles, so it is sometimes The adrenal medulla, like the posterior pituitary,
referred to as vasopressin. develops from a knot of nervous tissue.

- Catecholamines. When the medulla is stimulated by

sympathetic nervous system neurons, its cells
release two similar hormones, epinephrine, also
ADRENAL GLAND called adrenaline, and norepinephrine
(noradrenaline), into the bloodstream; collectively,
Although the adrenal gland looks like a single organ, it
these hormones are referred to as catecholamines.
is structurally and functionally two endocrine organs in
- Function. Basically, the Catecholamines increase
one.
heart rate, blood pressure, and blood glucose levels
and dilate the small passageways of the lungs; the
catecholamines of the adrenal medulla prepare the
Hormones of the Adrenal Cortex body to cope with a brief or short-term stressful
The adrenal cortex produces three major groups of situation and cause the so-called alarm stage of the
steroid hormones, which are collectively called stress response.
corticosteroids mineralocorticoids, glucocorticoids,
and sex hormones.
THYROID GLAND
- Mineralocorticoids. The mineralocorticoids,
primarily aldosterone, are produced by the The thyroid gland is a hormone-producing gland that is
outermost adrenal cortex cell layer; familiar to most people primarily because many obese
mineralocorticoids are important in regulating the individuals blame their overweight condition on their
mineral (or salt) content of the blood, particularly glands (thyroid).
the concentrations of sodium and potassium ions
- Location. The thyroid gland is located at the base of
and they also help in regulating the water and
the throat, just inferior to the Adams apple, where
electrolyte balance in the body.
it is easily palpated during a physical examination.
- Renin. Renin, am enzyme produced by the kidneys
- Lobes. It is a fairly large gland consisting of two
when the blood pressure drops, also cause the
lobes joined by a central mass, or isthmus.
release of aldosterone by triggering a series of
- Composition. Internally, the thyroid gland is
reactions that form angiotensin II, a potent
composed of hollow structures called follicles,
stimulator of aldosterone release.
which store a sticky colloidal material.
- Atrial natriuretic peptide (ANP). ANP prevents
- Types of thyroid hormones. Thyroid hormone often
aldosterone release, its goal being to reduce blood
referred to as the bodys major metabolic hormone,
volume and blood pressure.
is actually two active, iodine-containing hormones,
- Glucocorticoids. The middle cortical layer mainly
thyroxine or T4, and triiodothyronine or T3.
produces glucocorticoids, which include cortisone
- Thyroxine. Thyroxine is the major hormone secreted
and cortisol; glucocorticoids promote normal cell
by the thyroid follicles.
metabolism and help the body to resist long-term
stressors, primarily by increasing blood glucose
- Triiodothyronine. Most triiodothyronine is formed at
the target tissues by conversion of the thyroxine to
triiodothyronine.
- Function. Thyroid hormone controls the rate at
which glucose is burned oxidized, and converted
to body heat and chemical energy; it is also
important for normal tissue growth and
development.
- Calcitonin. Calcitonin decreases blood calcium
levels by causing calcium to be deposited in the
bones; calcitonin is made by the so-called
parafollicular cells found in the connective tissues
between the follicles.

PARATHYROID GLANDS

The parathyroid glands are mostly tiny masses of

glandular tissue.

- Location. The parathyroid glands are located on the

posterior surface of the thyroid gland.
- Parathormone. The parathyroids secrete
parathyroid hormone (PTH) or parathormone, which
is the most important regulator of calcium ion
homeostasis of the blood; PTH is a hypercalcemic
hormone (that is, it acts to increase blood levels of
calcium), whereas calcitonin is a hypocalcemic
hormone.; PTH also stimulates the kidneys and
intestines to absorb more calcium.