Disorders of the

Liver
 Cirrhosis
Definition
• Scarring of the liver tissue, which interferes with normal
liver function and results in structural changes within codes
of the liver
• End state of chronic liver disease
• Progressive and irreversible
• Tenth leading cause of death in U.S.

Pathophysiology
• Functional liver tissue gradually destroyed and replaced
with fibrous scar tissue
• As hepatocytes are destroyed, metabolic functions are lost
• Blood and bile flow within liver is disrupted
• Portal hypertension develops
– Portal vein receives blood from the intestines and
spleen, so as portal hypertension increases, the blood
flows back in the esophageal and umbilical veins
causing ascites as well as splenomegaly
Alcoholic cirrhosis (Laennec’s cirrhosis)
• Alcohol causes metabolic changes in liver
leading to fatty infiltration (stage in which
abstinence from alcohol could allow liver
to heal)
• With continued alcohol abuse,
inflammatory cells infiltrate liver causing
necrosis, fibrosis and destruction of liver
tissue
• Regenerative nodules form, liver shrinks
and is nodular
• Malnutrition commonly present
Biliary cirrhosis Post hepatic
• Bile flow is cirrhosis
obstructed and is
Chronic
retained within
liver causing
hepatitis B or C
inflammation, and unknown
fibrosis and cause leads to
regenerative liver shrinkage
nodules to form and nodule
• Increased skin formation with
pigmentation extensive liver
resembling a deep cell loss and
tan, jaundice and
fibrosis
Cardiac cirrhosis Manifestations
– Right sided CHF. • Early: liver
Liver is swollen, enlargement and
yet reversible if tenderness, dull
CHF is treated ache in RUQ, weight
loss, weakness,
fatigue, anorexia,
Nonspecific, diarrhea or
metabolic constipation
cirrhosis • Progresses to
– Metabolic impaired
problems, metabolism causing
infectious bleeding, ascites,
gynecomastia in
disease, men, infertility in
infiltrative women, jaundice,
disease, GI neurological
Complications
a. Portal hypertension
– shunting of blood to collateral blood vessels
leading to engorged veins in esophagus,
rectum and abdomen, ascites
– Pressures within the portal venous system
become elevated as liver damage obstructs
the free flow of blood through the organ
b. Splenomegaly: anemia, leucopenia,
thrombocytopenia
c. Ascites
– accumulation of abdominal fluid rich in
protein; hypoalbuminemia, sodium and water
retention
d. Esophageal varices: thin walled
dilated veins in esophagus which may
rupture leading to massive
hemorrhage
– Secondary to portal hypertension
– Bleeding may occur as a result of
mechanical trauma, ingestion of
coarse food
e. Hepatic f. Hepatorenal
encephalopathy syndrome: renal
• from accumulated failure with
neurotoxins in blood; azotemia
ammonia produced
in gut is not – Anorexia
converted to urea – Fatigue
which is normally
excreted and – Weakness
accumulates in – Fluid retention
blood and is trapped leads to
in the brain;
medications may not
hyponatremia
be metabolized and and fluid overload
add to mental – Needs
changes including hemodialysis for
personality changes,
Diagnostic Tests
• Liver function tests (ALT, AST, alkaline
phosphatase, GGT); elevated, but not as high as
with acute hepatitis
• CBC and platelets: anemia, leucopenia,
thrombocytopenia
• Prothrombin time: prolonged (impaired coagulation
due to lack of Vitamin K)
• Serum electrolytes: deficiencies in sodium,
potassium, phosphate, magnesium
• Bilirubin: elevated failing liver can’t bind bilirubin
• Serum albumin: hypoalbuminemia
• Serum ammonia: elevated
• Serum glucose and cholesterol
• Abdominal ultrasound: evaluation of liver size and
nodularity, ascites
• Upper endoscopy: diagnose and possibly treat
Medications
• Medications are used to treat complications
and effects of cirrhosis; all liver toxic drugs
(sedatives, hypnotics, acetaminophen) and
alcohol must be avoided
• Diuretics: spironolactone (Aldactone)
(works against increased aldosterone
levels), furosemide (Lasix)
• Medications to decrease manifestations of
hepatic encephalopathy by reducing
number of ammonia forming bacteria in
bowel and to convert ammonia to
ammonium which is excreted in stool;
• Beta-blocker nadolol (Corgard)
with isosorbide mononitrate
(Ismo, Imdur) used to prevent
esophageal varices from rebleeding
• Ferrous sulfate and folic acid to treat
anemia
• Vitamin K to reduce risk of bleeding
• Antacids to decrease risk of acute
gastritis
• oxazepam (Serax) benzodiazepine
antianxiety/sedative drug not
Collaborative Care
Holistic care to client and family addressing
physiologic, psychosocial, spiritual needs
Treatment
Dietary and fluid management
• Fluid and sodium restrictions based on
response to diuretic therapy, urine output,
electrolyte values
• Protein: 75 – 100 grams per day; unless
client has hepatic encephalopathy (elevated
ammonia levels),then 60 – 80 gm/day
• Diet high in carbohydrates, moderate in fats
or as total parenteral nutrition (TPN)
• Vitamin and mineral supplements;
Treatment
Complication management
• Ascites and associated respiratory distress;
Paracentesis
– Removal of 5 or more liters of fluid
• For bleeding esophageal varices
1. Restore hemodynamic stability with fluids,
blood transfusion and fresh frozen plasma
(contains clotting factors)
2. Control bleeding with vasoconstrictive
medications: somatostatin or octreotide,
vasopressin
3. Upper endoscopy to treat varices with
banding (variceal ligation or endoscopic
4. Balloon
tamponade, if
bleeding not
controlled or
endoscopy
unavailable as
short term
measure: multiple-
lumen naso-gastric
tube such as
Sengstaken-
Blakemore tube or
Minnesota tube
which have gastric Triple-lumen nasogastric
and esophageal tube
balloons to apply (Sengstaken-Blakemore)
continuation:
• Surgery: liver transplant; contraindications
include malignancy, active alcohol or drug
abuse, poor surgical risk

• Insertion of transjugular intrahepatic

portosystemic shunt (TIPS),
– a short-term measure to control portal
hypertension (varices and ascites)
– using a stent to channel blood between
portal and hepatic vein and bypassing
liver (increases risk for hepatic
encephalopathy)
Tips pre Tips post
Nursing Diagnoses Nursing Care
• Excess Fluid Volume
• Disturbed Thought • Health promotion
Processes: Early includes education
identification of
encephalopathy and about relationship
appropriate of alcohol and drug
interventions, i.e. abuse with liver
client safety,
avoidance of disorders;
hepatoxic avoidance of viral
medications, low-
protein diet, hepatitis
medications to treat
• Home care
• Ineffective Protection:
Risks associated with includes teaching
impaired coagulation, family to
esophageal varices,
acute gastritis participate in
• Impaired Skin disease
 Hepatitis

Definition Pathophysiology
• inflammation of the • metabolic functions
liver due to virus, and bile
exposure to elimination
alcohol, drugs, functions of the
toxins; may be liver are disrupted
acute or chronic in by the
nature inflammation of the
liver.
Viral Hepatitis
1. Types (causative agents)
Hepatitis A virus (HAV) Infectious
hepatitis
4. Transmission: fecal-oral route, often
contaminated foods, water or direct
contact, blood transfusions,
contaminated equipment
5. Contagious through stool up to 2
weeks before symptoms occur;
abrupt onset
Prevention of Incidence
Hepatitis A – More common in
– Good fall and winter
handwashing months
– Good personal
– Usually found in
hygiene
children and
– Control and
screening of food young adults
handlers – Infectious for 3
– Passive weeks prior and
immunization 1 week after
developing
Incubation period jaundice
• 20-50 days (short
Hepatitis B virus (HBV)
Transmission
– infected blood and body fluids,
– parenteral route with infusion
– ingestion or inhalation of the blood of an
infected person
– Contaminated needles, syringes, dental
instruments
– Oral or sexual contact
– High risk individuals include homosexual, IV
drug abusers, persons with multiple sexual
partners, medical workers
• Liver cells damaged by immune response;
increased risk for primary liver cancer; causes
acute and chronic hepatitis, fulminant hepatitis
and carrier state
Prevention
Hepatitis C virus (HCV)
• Transmission: infected blood and
body fluids; injection drug use is
primary factor
• Initial manifestations are mild,
nonspecific
• Primary worldwide cause of chronic
hepatitis, cirrhosis, liver cancer
• Usual incubation period 7-8 weeks
Hepatitis B- Hepatitis E virus
associated delta (HEV)
virus (HDV) • Transmission:
• Transmission: infected fecal-oral route,
blood and body fluids; contaminated
causes infection in
water supplies in
people who are also
infected with hepatitis developing nations;
B rare in U.S.
• Causes: acute or • Affects young
chronic infection adults; fulminant in
• Hepatitis D pregnant women
– Transmitted
through oral-fecal
Disease Pattern Associated with
hepatitis (all types)
• Incubation Phase (period after
exposure to virus): no symptoms

• Prodromal Phase (preicteric – before

jaundice)
5. “Flu” symptoms: general malaise,
anorexia, fatigue, muscle and body
aches
6. Nausea, vomiting, diarrhea,
constipation, and mild RUQ
abdominal pain
Icteric (jaundiced) Convalescent
Phase Phase
– 5 – 10 days after
prodromal • In uncomplicated
symptoms cases, symptoms
– Jaundice of the improve and
sclera, skin and spontaneous
mucous recovery occurs
membranes
occurs within 2 weeks of
– Elevation of jaundice
serum bilirubin • Lasts several
– Pruritis weeks; continued
– Stool become improvement and
light brown or liver enzymes
clay colored
Chronic hepatitis
• chronic infection from viruses: HBV, HBC, HBD
1. Few symptoms (fatigue, malaise,
hepatomegaly)
2. Primary cause of cirrhosis, liver, cancer,
liver
transplants
3. Liver enzymes are elevated

Fulminant hepatitis
• rapidly progressive disease with liver failure
developing within 2 – 3 week of onset of
symptoms; rare, but usually due to HBV with
HBD infections

Toxic hepatitis
Diagnostic Tests
• Liver function tests
1. Alanine aminotransferase (ALT):
specific to liver
2. Aspartate aminotransferase (AST):
heart and liver
cells
3. Alkaline phosphatase (ALP): liver
and bone cells
4. Gamma-glutamyltransferase (GGT):
present in cell
membranes; rises with hepatitis and
obstructive
biliary disease
5. Lactic dehydrogenase (LDH):
• Lab tests for viral antigens and antibodies
associated with types of viral hepatitis
• Liver biopsy: tissue examined to detect
changes and make diagnosis
1. Preparation: signed consent; NPO 4 –
6 hours
before
2. Prothrombin time and platelet count
results; may need Vitamin K first to correct
3. Client voids prior to procedure, supine
position
4. Local anesthetic; client instructed to
hold breath during needle insertion
5. Direct pressure applied to site after
sample obtained; client placed on right side
to maintain site pressure
Medications for prevention of hepatitis
• Vaccines available for Hepatitis A and B
• Vaccine for Hepatitis B recommended for
high-risk groups
• Post exposure prophylaxis recommended for
household and sexual contacts of persons
with HAV or HBV
• Hepatitis A prophylaxis: single dose of
immune globulin within 2 weeks of exposure
• Hepatitis B prophylaxis: Hepatitis B immune
globulin (HBIG) for short-term immunity;
HBV vaccine may be given at the same time
Treatment
Medications
1. Medication for acute hepatitis C:
interferon alpha to prevent chronic
hepatitis
2. Chronic Hepatitis B: interferon alpha
intramuscular or subcutaneously or
lamivudine
3. Chronic Hepatitis C: interferon alpha with
ribavirin (Rebetol) oral antiviral drug
Acute hepatitis treatment
1. As needed bedrest
2. Adequate nutrition
3. Avoid substances toxic to the liver
especially alcohol
Collaborative Care Nursing Care
• Focus is on Teaching about
determination of prevention by
cause, treatment stressing
and support, and
prevention future • Hygiene
liver damage • Handwashing,
especially for food
• Home care must handlers
include proper • Blood and body
infection control fluids precautions
measures;
continuing medical • Vaccines for
care persons at high risk
• Restrict use of
alcohol
Nursing Diagnoses
• Risk for Infection
1. Standard precautions, proper hand
washing
at all times
2. Reporting of contagious disease to
health
department to control spread of
disease
• Fatigue
1. Scheduling planned rest periods
2. Gradual increase of activity with
improvement
• Imbalanced Nutrition: Less than body
requirements
Disorders of the
Gallbladder
 Cholelithiasis and
Cholecystitis
Definition
– Cholelithiasis: formation of stones
(calculi) within the gallbladder or
biliary duct system
– Cholecystitis: inflammation of gall
bladder
– Cholangitis: inflammation of the
biliary ducts
Pathophysiology
a. Gallstones form due to
1.Abnormal bile composition
2.Biliary stasis
3.Inflammation of gallbladder
b. Most gallstones are composed
primarily of bile (80%); remainder are
composed of a mixture of bile
components
c. Excess cholesterol in bile is
associated with obesity, high-
cholesterol diet and drugs that lower
d. If stones from gallbladder lodge in the
cystic duct
1. There can be reflux of bile into the
gallbladder and
liver
2. Gallbladder has increased pressure
leading to
ischemia and inflammation
3. Severe ischemia can lead to necrosis of
the gall
bladder
4. If the common bile duct is obstructed,
pancreatitis
 Gall Stones
Common locations of
gallstones
Risk factors for cholelithiasis
• Age
• Family history, also Native Americans
and persons of northern European
heritage
• Obesity, hyperlipidemia
• Females, use of oral contraceptives
• Conditions which lead to biliary stasis:
pregnancy, fasting, prolonged
parenteral nutrition
• Diseases including cirrhosis, ileal
disease or resection, sickle-cell
anemia, glucose intolerance
Manifestations of
cholelithiasis
• Many persons are
asymptomatic
• Early symptoms are • Episode of biliary
epigastic fullness after
meals or mild distress
after eating a fatty
meal
• Biliary colic (if stone is
blocking cystic or
common bile duct):
steady pain in
epigastric or RUQ of
abdomen lasting up to
5 hours with nausea • Anorexia, nausea,
and vomiting
• Jaundice may occur if
Manifestations of
acute
cholecystitis
colic involving RUQ
pain radiating to
back, right scapula,
or shoulder; the
pain may be
aggravated by
movement, or deep
breathing and may
last 12 – 18 hours
and vomiting
Complications of Collaborative Care
cholecystitis • Treatment depends
• Chronic cholecystitis on the acuity of
occurs after repeated symptoms and
attacks of acute client’s health
cholecystitis; often status
asymptomatic
• Clients
• Empyema: collection experiencing
of infected fluid within symptoms are
gallbladder usually treated
• Gangrene of gall with surgical
bladder with removal of the
perforation leading to stones and
peritonitis, abscess gallbladder
formation
• Pancreatitis, liver
damage, intestinal
Diagnostic Tests
• Serum bilirubin: conjugated bilirubin
is elevated with bile duct obstruction
• CBC reveals elevation in the WBC as
with infection and inflammation
• Serum amylase and lipase are
elevated, if obstruction of the
common bile duct has caused
pancreatitis
• Ultrasound of gallbladder: identifies
presence of gallstones
• Other tests may include flat plate of
the abdomen, oral cholecytogram,
Treatment Laparoscopic
• Treatment of cholecystectomy
choice is • Minimally invasive
laparoscopic
cholecystectomy procedure with low
• If surgery is risk of
inappropriate due complications;
to client condition required hospital
1.May attempt to stay< 24 hours.
dissolve the • Learning needs of
gallstones with
medications client and
2.Medications are family/caregiver
costly, long include pain
duration control, deep
3.Stones reoccur breathing,
when treatment is mobilization,
Some clients require a surgical laparotomy (incision
inside the abdomen) to remove gall bladder

• client will have nasogastric tube in place post-

operatively and require several days of
hospitalization
• If exploration of the common bile duct is done
with the cholecystectomy, the client may have a
T-tube inserted which promotes bile passage to
the outside as area heals

Clients with cholelithiasis and cholecystitis prior to

Nursing Diagnoses
surgery can avoid future attacks by limiting fat
intake
• Pain
• Imbalanced Nutrition: Less than
body requirements
• Risk for Infection
T-tube placement in the common bile duct
Disorders of the
Pancreas
 Pancreas
Pancreas
– Secretes pancreatic enzymes that break
down carbohydrates, proteins and fats
– Pancreatic duct runs from tail to the head
– Joins with the common bile duct at the
ampulla of Vater which empties into the
duodenum
– Trypsin, Cymotrypsin, Elastase,
Phospholipase and Lipase are all
pancreatic enzymes
 When they come into contact with the
pancreas they result in vasodilation,
increased vascular permeability,
 Pancreatitis
Definition
• Inflammation of pancreas characterized by
release of pancreatic enzymes into
pancreatic tissue itself leading to
hemorrhage and necrosis
• Mortality rate is 10%;
• Occurs as acute or chronic in form
Risk factors
• Alcoholism
• Gallstones
Pathophysiology
• Interstitial pancreatitis: milder form leading
to inflammation and edema of pancreatic
tissue; often self-limiting
• Necrotizing pancreatitis: inflammation,
hemorrhage, and necrosis of pancreatic
tissue
• Exact cause is unknown; gallstones can
cause bile reflux activating pancreatic
enzymes; alcohol causes duodenal edema,
obstructing pancreatic outflow
• Other factors are trauma, surgery, tumors,
infectious agents
• With pancreatitis, large volume of fluid shifts
from circulation into retroperitoneal space,
peripancreatic space, abdominal cavity
Manifestations
2. Abrupt onset of continuous severe epigastric
and abdominal pain especially around the
umbilicus, radiating to back and relieved
somewhat by sitting up and leaning forward;
initiated by fatty meal or alcohol intake
3. Nausea and vomiting
4. Abdominal distention and rigidity, fatty
stools (steatorrhea)
5. Decreased bowel sounds
6. Hypotension
7. Fever, cold and clammy skin
8. 24 hours later: jaundice;
9. 3 – to 6 days: retroperitoneal bleeding,
bruising in flanks (Turner sign) or around
 RANSON’S CRITERIA
• At admission or diagnosis
– Age over 65
– WBC over 16,000/mm3
– Glucose over 200mg/dl
– LDH over 350 iu/liter
– Aspartate aminotransferase level above 250
units/liter
• After 48 hours
– HCT drop >10
– Increase in BUN.5 mg/dl
– Calcium < 8mg/dl
– Base deficit > 4 meq/liter
– Estimated fluid sequestration >6 liters
– PaO2 < 60 mm Hg
• Each criterion worth 1 point: Mortality rates 1-2
points 1%, 3-4 points 16%, 5-6 points 40%, 7 or
Complications
Intravascular volume depletion leads
to
3. Acute tubular necrosis and renal
failure: 24 hours post
4. Acute respiratory distress syndrome
(ARDS): 3 – 7 days post, atelectasis,
pneumonia, pleural effusion
5. Local complications of pancreatic
necrosis, abscess, pseudocysts,
pancreatic ascites
Collaborative Care
B. Acute pancreatitis is usually a mild,
self-limiting disease with care
focused on eliminating causative
factors, reducing pancreatic
secretions, supportive care
C. Severe necrotizing pancreatitis
requires intensive care management
D. Chronic pancreatitis focuses on pain
management and treatment of
malabsorption and malnutrition
Diagnostic Tests
• Laboratory tests
3. Serum amylase: 2 -3 times normal in 2 – 12
hours with acute; returns to normal in 3 – 4
days
4. Serum lipase: rises and remains elevated 7 –
14 days
5. Serum trypsinogen: elevated with acute;
decreased with chronic
6. Urine amylase: rises with acute
7. Serum glucose: transient elevation with acute
8. Serum bilirubin and alkaline phosphatase: may
be increased with compression of common bile
duct with acute
9. Serum calcium: hypocalcemia with acute,
binds with fatty acids during tissue necrosis
continuation:
• Ultrasounds to diagnose gallstones,
pancreatic mass, pseudocyst
• CT scan to identify pancreatic
enlargement, fluid collections, areas
of necrosis
• Endoscopic retrograde
cholangiopancreatography (ERCP)
diagnose chronic pancreatitis (acute
pancreatitis can occur after this
procedure)
• Endoscopic ultrasound
• Percutaneous fine-needle aspiration
Treatment
• Acute pancreatitis is supportive and
includes hydration, pain control, and
antibiotics, oxygenation
• Chronic pancreatitis includes pain
management without causing drug
dependence
• Medications may include
1. Pancreatic enzyme supplements to
reduce steatorrhea
2. H2 blockers or proton pump inhibitors
to decrease gastric secretions
3. Octreotide (sandostatin) to suppress
pancreatic secretion
Fluid and dietary Surgeries include
management
2. Blocked
2. Initially client is
NPO usually with gallstones may be
nasogastric removed
suction, endoscopically
intravenous fluids
and possibly total 3. Cholecystectomy
parenteral for cholelithiasis
nutrition 4. Drainage
3. Oral food and procedures or
fluids begun as
condition resolves resection of
4. Low fat diet and pancreas may be
no alcohol needed
Nursing Diagnoses
a. Pain
b. Impaired Nutrition: Less than body
requirements
c. Risk for Deficient Fluid Volume

Home Care
Client and family teaching to include
prevention of future attacks including
abstinence from alcohol and smoking;
low fat diet; monitoring for signs of
infection (as with abscess formation
 Pancreatic Cancer
Definition
a.Accounts for 2% of cancers; most are
adenocarcinoma; most common site is head
of the pancreas
b.Very lethal death within 1 – 3 years after
diagnosis
c.Incidence increases after age 50; slightly
higher in females; and slightly higher African
Americans

Risk Factors
a.Smoking
b.Other factors include chemical or
Manifestations
• Usually nonspecific; up to 85%
persons seek health care with
advanced case
• Slow onset: anorexia, nausea, weight
loss, flatulence, dull epigastic pain
• Cancer in head of pancreas causes
bile obstruction resulting in jaundice,
clay colored stools, dark urine,
pruritus
• Late: palpable mass and ascites
Treatment
• Surgery is indicated in early cancers
• Pancreatoduodenectomy
(Whipple’s procedure)
 Removal of the proximal head of the
pancreas, the duodenum, a portion
of the jejunum, the stomach and the
gall bladder
 Pancreatic duct, common bile duct
and the stomach are attached to
the jejunum
Whipple Procedure
 Diabetes Mellitus
•chronic systemic disease
characterized by either a
deficiency of insulin or a
decreased ability of the body to
use insulin causing an increase
amount of glucose in the blood.
 CAUSES:

• GENETIC DEFECTS
• HORMONES
• RACE
• AGE
• OBESITY
• FAMILY HISTORY
 THREE
GENERAL
TYPES OF
DIABETES:
Destruction of beta cells in the pancreas

Failure to produce insulin

Elevated blood glucose

Increased osmolarity due to glucose

POLYDIPSIA POLYURIA POLYPHAGIA

WEIGHT LOSS
 Gestational diabetes
• develops in some women in the late
stages of their pregnancy or by lack
of insulin deficiency.
• Usually resolves after the baby is
born.
• Women who get GDM have a higher
risk of developing type 2 Diabetes
later in her life.
 DISTINGUISHING FEATURES OF TYPE 1 AND
TYPE 2 DM

FEATURE TYPE 1 TYPE 2

Synonym IDDM, juvenile diabetes, labile NIDDM, adult or maturity
or brittle onset diabetes, mild
diabetes
Age at onset Before age 30, but may After age 30, but may
occur at any age occur in children.

Type of onset Usually abrupt, wt rapid Insidious, maybe

onset of hyperglycemia asymptomatic, slow
hyperglycemia
Insulin Little or none Below normal, normal or
production above normal

Body weight Ideal body weight or thin 85% are obese, maybe
onset ideal body weight
Ketosis Prone to ketosis, Resistant to ketosis,
usually present at can occur with
onset, present during infection
poor control
Manifestations Polyuria, Frequently none but,
polydipsia,polyphagia, may be mild
fatigue manifestation of
hyperglycemia

Exogenous insulin Dependent on insulin 20% to 30% of clients

administration may require insulin

Oral hypoglycemic Not effective Effective

agents

Teaching needs At diagnosis and At diagnosis and

ongoing ongoing
 CLINICAL MANIFESTATIONS
OF DM AT DIGNOSIS
CLINICAL MANIFESTATIONS TYPE1 TYPE 2

POLYURIA ++ +
POLYDIPSIA ++ +

POLYPHAGIA ++ +

WEIGHT LOSS ++ +

RECURRENT BLURRED VISSION + ++

PRURITIS, SKIN INFECTIONS, VAGINITIS + ++

KETONURIA ++ -

WEAKNESS AND FATIGUE, DIZZINESS ++ +

OFTEN ASYMPTOMATIC - ++
 Stages of Diabetes:
PRE-DIABETES (POTENTIAL)-time period from conception to the
evidence of glucose metabolism alteration

• Impaired Fasting Glucose (IFG) A person has impaired

fasting glucose (IFG) when fasting plasma glucose is 100 to
125 mg/dL. This level is higher than normal but less than the
level indicating a diagnosis of diabetes.
2. Impaired Glucose Tolerance (IGT) Impaired glucose
tolerance (IGT) means that blood glucose during the oral
glucose tolerance test (OGTT) is higher than normal but not
high enough for a diagnosis of diabetes. IGT is diagnosed
when the glucose level is 140 to 199 mg/dL 2 hours after a
person drinks a liquid containing 75 grams of glucose.
SUSPECTED (SUBCLINICAL, LATENT)-
becomes overt only during times of unusual
stress such as during acute illness, in
normal pregnancy or when person takes
drugs that increase carbohydrate tolerance.

CHEMICAL- same as above but differs in

that the standard GTT is abnormal with
borderline or below abnormal values.

CLINICAL OR OVERT- increase FBS and

signs and symptoms of metabolic alteration,
vascular change or neural change.
 Diagnosis of Diabetes

1.FBS (Fasting blood Sugar)

• Measuring blood glucose levels
• Values between 110-125 indicate IFG
• No nutrients ingestion other than water for 8-
12 hours

2. RBG
• Blood sample maybe drawn anytime
• Results should be within normal limits
3. POSTPRANDIAL BLOOD GLUCOSE
• After a meal
• Glucose samples are drawn 2 hours
after a standard meal.
• consider aging, smoking, drinking
coffee, strenuous activity.

4. GLYCOSYLATED HEMOGLOBIN
• The higher the BGL, the higher the
levels of glycosylated hemoglobin.
• The results show the average BGL over
the previous 3 months.
• Drawn anytime during the day
5. CONNECTING PEPTIDE
• Proinsulin insulin
C-peptide
• This test indicate the amount of insulin production

6. ORAL GLUCOSE TOLERANCE TEST

• Above 140mg/dL
• Bed rest, medication, trauma and stress can alter
the results.
• Diet that offers 150g of carbohydrates/day for 3
day
• The sample is drawn and the patient is given 75 g
of glucose in water to drink.
• Blood samples are taken at intervals
KETONURIA (presence of Ketones in the
urine
• Urine will be tested for the presence of Ketones,
by use of dip-strips
• Indicates that the body is using fat as a major
source of energy, which may result to
KETOACIDOSIS

PROTEINURIA (presence of protein in the urine)

• A routine urinalysis tests the sample for protein
• Manifestation of neuropathy
 COMPLICATIONS OF DM

1. ACUTE
a) DIABETIC ACIDOSIS
b) HYPOGLYCEMIA
c) HYPERGLYCEMIA, HYPEROSMOLAR
NONKETONIC COMA (HHNK)
d) LACTIC ACIDOSIS
e) SOMOGYI EFFECT AND DRAWN
PHENOMENON
 2.CHRONIC COMPLICATIONS

A. DEGENERATIVE CHANGES IN
THE VASCULAR SYSTEM
B. NEUROPATHY
C. EYE COMPLICATIONS
D. NEUROPATHY
E. HEART DISEASE
F. SKIN CHANGES
G. LIVER
 Diabetic Ketoacidosis

• Disturbances of CHO, fat & protein metabolism

• Body depends on fat for energy
• Ketones are formed
• If inadequate CHO more ketones
• Acetoacetate & beta-hydroxybutyrate used for
energy
• Liver releases ketone bodies into blood
• Brain still needs some glucose
• Level of ketone bodies gets too high
• Blow off acetone in breath
• Ketonuria
• Renal threshold 70 mg/dl
 Implementation:

• Clients and family education

• Pathophysiology of DM
• Complications
• Exercise regimen
• Diet teaching
• Foot care
• Teach about hypoglycemia and
hyperglycemia
• Encourage to express feelings
• Help patient to achieve self care competency