METABOLIC AND

ENDOCRINE
DISORDERS
Prepared by: Emman M. Parangue, R.N.
 01
LIVER
DISORDERS
 LIVER
FUNCTIONS:
+ Glucose metabolism
- convert glucose to glycogen
- glycogen to glucose – glycogenolysis
- gluconeogenesis
+ Ammonia conversion
- converts metabolically generated ammonia into urea to
be excreted to the urine
+ Protein metabolism
 LIVER
+ Fat metabolism
- fatty acids are broken down for energy and ketone
bodies
+ Vitamin and iron storage
- vitamins A, B and B- complex vitamins and D
+ Bile formation
- bile salts with cholesterol and lecithin are required for
the emulsification of fats in the intestine which is
necessary for efficient digestion and absorption
 LIVER
Diagnostic examination
a. liver function test
- transaminase are sensitive indicator of injury to the
liver cells.

○ ALT – alanine aminotranferase

○ AST – aspartate aminotransferase

○ GGT - gamma-glutamyl transferase

b. Liver biopsy
 LIVER
Manifestation of Hepatic Dysfunction:
a. jaundice – clinically evident when serum bilirubin level
exceeds 2.5 mg/dl
b. portal hypertension
c. ascites
d. esophageal varices- varicosities that develop from elevated
pressure in the veins that drain into the portal system.
e. hepatic encephalopathy and coma
 Hepatitis

+ inflammation of the liver

Types:
1. Hepatitis A - Hepatitis A virus
• Transmission: fecal-oral route
- Virus is found in the stool 2 weeks before the
onset of signs and symptoms; one week before the
onset of jaundice.
 Hepatitis

+ Immunoglobulin M (IgM) appears in the serum as

the stool becomes negative for the virus (there is
no chronic carrier state of HAV)
 Hepatitis

2. Hepatitis B – HBV a DNA virus

Transmission:
○ Perinatal by infected mothers
○ Percutaneous ( IV, needle-stick punctures)
○ Exposure to contaminated blood and blood
products
○ Sexual transmission
(HBsAg – hepatitis B surface antigen is detected to
client who are HBV positive)
 Hepatitis

3. Hepatitis C – HVC is an RNA virus that is

transmitted percutaneously common method of
transmission is sharing of contaminated needles
and paraphernalia among drug users
 Hepatitis

4. Hepatitis D – Hepatitis D or delta hepatitis is a

defective single stranded RNA virus that cannot
survive on its own. HDV requires the helper function
of HBV to replicate
5. Hepatitis E – HEV is an RNA virus that is
transmitted by fecal-oral route. (drinking
contaminated water)
 Hepatitis
symptoms:
Acute phase:
+ malaise, anorexia, fatigue, nausea, occasional vomiting,
+ Abdominal pain (RUQ)
+ Liver enlargement
+ Jaundice when bilirubin diffuses into the tissues
 Hepatitis
+ Dark urine
+ Clay colored stool
+ Pruritus – due to accumulation of bile salts beneath the skin
 Hepatitis
Complications:
+ Hepatocellular carcinoma – chronic hepatitis B
+ Hepatic failure
+ Cirrhosis of the liver
 Hepatitis
Diagnostic studies
+ Hepatitis A:

○ anti-HAV IgM - acute infection

○ anti-HAV IgG - previous infection and long term

immunity or immunization
+ Hepatitis B: HBsAg ( hepatitis B surface antigen)- positive in
chronic carrier
 Hepatitis

○ Anti-HBs (antibody to surface antigen)-marker of

response to vaccine
+ Hepatitis C: Anti-HCV (antibody to hepatitis C) – marker for
acute or chronic infection with HCV
+ Hepatitis D: anti-HDV, HDV Ag (hepatitis D antigen) –
infection with hepatitis D
+ Management:
(there is no specific treatment or therapy for acute viral
hepatitis)
 Hepatitis
Emphasis on management
+ Rest for liver to regenerate
+ Well-balanced diet –high calorie, high protein, high
carbohydrate, low fat
+ Avoid alcohol and drugs detoxified by the liver
+ Vitamin supplement
+ Drug therapy: (Supportive)
+ Antiemetics, benadryl - if client needs sedative
+ a- interferon - it has an effect on the viral replication cycle
 Hepatitis
Prevention:
+ Immunization for hepatitis A,B virus
+ Hepatitis B Immune globulin (HBIG)- given to exposed
persons to HBV who never had Hepatitis B and have never
received hepatitis B vaccine ( needlestick, transmucosal,
perinatal exposure(infants born to HBV-infected mothers)
 Hepatitis
+ Proper disposal of excreta
+ Water sanitation
+ Proper disposal of syringes and needles
+ Proper screening for blood donors
 Nonviral Hepatitis
A. TOXIC HEPATITIS
+ cause : - exposure to hepatotoxic chemicals,
medications, botanical agents
B. DRUG-INDUCED HEPATITIS
 FULMINANT HEPATIC FAILURE
+ is the clinical syndrome of sudden and severely impaired
liver function in a previously healthy person.
+ The generally accepted definition is that fulminant hepatic
failure develops within 8 weeks after the first symptoms of
jaundice.
 LIVER CIRRHOSIS
- chronic, progressive, irreversible, widespread destruction of
hepatic cells, with scar tissue replacing healthy tissue.
Forms:
a. Alcoholic (Laennec’s or portal) – results from malnutrition
especially protein malnutrition
b. postnecrotic cirrhosis – a complication of viral, toxic
hepatitis
c. biliary cirrhosis – scarring occurs in the liver around the bile
ducts
 LIVER CIRRHOSIS
Pathophysiology:
+ Hepatocyte necrosis leads to development of scar tissue
which in turn disrupts blood flow. This leads to an increase
in pressure in the portal circulatory system – portal
hypertension
 LIVER CIRRHOSIS
Symptoms:
+ Fatigue, weakness, decrease appetite, dull right upper
quadrant, pruritus, fetor hepaticus, asterixis
+ Jaundice, anemia, memory impairment
+ Testicular atrophy, menstrual irregularities
+ Peripheral neuropathies
 LIVER CIRRHOSIS
Complications:
a. Portal hypertension
- increase pressure throughout the portal venous
system that results from obstruction of blood flow into and
damage liver
 LIVER CIRRHOSIS
b. ascites
+ Portal hypertension and the resulting increase in capillary
pressure and obstruction of venous blood flow through the
damaged liver are contributing factors.
 LIVER CIRRHOSIS
Symptoms:
+ Increased abdominal girth
+ Rapid weight gain
+ Shortness of breath
+ Fluid waves on palpation
+ Distended veins visible over the abdominal wall
+ Fluid and electrolyte imbalance
 LIVER CIRRHOSIS
c. esophageal varices
- are varicosities that develop from elevated pressure in the
veins that drain into the portal system, found in the
submucosa of the lower esophagus.
 LIVER CIRRHOSIS
d. hepatic encephalopathy
- is the neuropsychiatric manifestation of hepatic failure
associated with portal hypertension and the shunting of blood
from the portal venous system into the systemic circulation.
(ammonia enters the brain and excites peripheral
benzodiazepine-type receptor and stimulate GABA. GABA
causes depression of the CNS producing sleep and behavioral
patterns)
 LIVER CIRRHOSIS
Symptoms:
+ Mental status changes – alteration in mood and sleep
+ disorientation
+ Asterixis – involuntary flapping of the hands
+ Hand writing becomes difficult
+ Constructional apraxia
+ Fetor hepaticus
+ Reflexes disappear
+ Flaccid extremities
+ coma
 LIVER CIRRHOSIS
Management:
a. portal hypertension
- shunt (portacaval shunt, transjugular intrahepatic
portosystemic shunt)
b. bleeding esophageal varices
- Blakemore Sengstaken tube (Balloon tamponade)
- sclerotherapy
- gastric lavage
-Endoscopic Variceal Ligation (Esophageal Banding Therapy)
- vasopressin injection
 LIVER CIRRHOSIS
c. ascites
+ Restriction of sodium and water
+ Diuretics and albumin
+ Paracentesis
+ Peritoneal venous shunt ( Le Veen shunt)
 LIVER CIRRHOSIS
d. hepatic encephalopathy
( ammonia is a CNS depressant)
+ Lactulose – bind with ammonia and excrete with the stool
+ Neomycin sulfate
+ Enema
+ Low protein diet
 LIVER CIRRHOSIS
+ Ammonia is produced in the GIT when protein is broken
down by bacteria.
+ Normally liver converts ammonia into glutamine which is
stored in the liver, and is converted to urea and excreted
through the kidney)
 LIVER CIRRHOSIS
Additional principles of management of hepatic encephalopathy
include the following:
+ Neurologic status is assessed frequently.
+ Mental status is monitored by keeping a daily record of
handwriting and arithmetic performance.
+ I&O and body weight are recorded each day.
+ Vital signs are measured and recorded every 4 hours.
+ Potential sites of infection (peritoneum, lungs) are assessed
frequently.
+ Serum ammonia level is monitored daily.
 02
GALLBLADDER
DISORDERS
 CHOLECYSTITIS
+ acute inflammation of the gallbladder
Causes:
+ Stone, bacteria, cystic duct obstruction, burns
+ distention and inflammation. Inflammation is sterile but
within 24 hours gut organism can be cultured from the
gallbladder.
Symptoms:
+ Pain, tenderness, rigidity of the right upper quadrant
+ Nausea, vomiting
 CHOLECYSTITIS
+ Bile remaining in the gallbladder initiates a chemical
reaction; autolysis and edema occur; and the blood vessels
in the gallbladder are compressed, compromising its
vascular supply.
+ Gangrene → perforation, may result.
+ Acalculous cholecystitis describes acute gallbladder
inflammation in the absence of obstruction by gallstones.
 CHOLELITHIASIS
+ presence of stone in the gallbladder
Types of Stones:
+ Cholesterol stone
+ Pigment stones
Symptoms:
+ Triad manifestations: Pain, jaundice, fever
+ Jaundice when there is obstruction of the common bile
duct
+ Dark colored urine, stool is clay colored or pale
 CHOLELITHIASIS
+ Steatorrhea , a tendency to bleed and juandice – when total
obstruction occurs.
+ Enlarged liver if obstruction lasts for more than few hours
 GALLBLADDER DISORDERS
Diagnosis:
+ Ultrasound examinations
+ CT scan to detect ductal stones
+ ERCP – endoscopic retrograde cholangiopancreatography
- visualization of the gallbladder, cystic duct, common
hepatic duct and common bile duct
 GALLBLADDER DISORDERS
Management:
+ ERCP
+ Cholecystectomy (laparoscopic or the traditional method)
+ Extracorporeal-shock wave lithotripsy
+ Pharmacologic agents:
○ UDCA and CDCA
○ Analgesic
○ Anticholinergic
○ Fat-soluble vitamins
○ Bile salts
 GALLBLADDER DISORDERS
Management:
+ Dietary management – low-fat diet
 03
PANCREATIC
DISORDER
 PANCREATITIS
+ inflammation of the pancreas, can be acute or
chronic
Causes:
+ Alcohol
+ Gallbladder disease
+ Viral infections, doudenal ulcer, pancreatic cancer
 PANCREATITIS
+ Acute Pancreatitis is caused by premature activation of
digestive enzyme, which leads to autodigestion of
surrounding tissues, resulting to severe edema, interstitial
hemorrhage and necrosis.
 PANCREATITIS
+ Two main types of Acute Pancreatitis:

○ Interstitial edematous pancreatitis- lack of pancreatic

or peripancreatic parenchymal necrosis with diffuse
enlargement of the gland due to inflammatory edema

○ Necrotizing pancreatitis- there is presence of tissue

necrosis in either the pancreatic parenchyma or in the
tissue surrounding the gland.
 PANCREATITIS
+ Self-digestion of the pancreas by its own proteolytic
enzymes, principally trypsin, causes acute pancreatitis.
+ Gallstone obstructs the flow of pancreatic juice→ reflux of
bile → pancreatic duct→ activates the pancreatic enzymes
+ Activation of the enzymes→ vasodilation→ increased
vascular permeability→ necrosis → erosion→ hemorrhage
 PANCREATITIS
Symptoms:
+ Abdominal pain at epigastrium , left upper quadrant with
possible radiation to the back. Pain is aggravated with
alcohol intake
+ Nausea , vomiting, low grade fever
+ Hypotension, tachycardia
+ Cullen’s sign – bluish discoloration of the periumbilical area
+ Grey Turner’s sign – bluish discoloration of the left flank.
 PANCREATITIS
Management:
+ Analgesia – morphine
+ Platelet activator agonist (Lexipafant) reduce mortality if
given in 48hrs
+ NPO, Correction of fluid and blood loss
+ Parenteral nutrition for patients with severe cases
+ Nasogastric suctioning to relieve nausea and vomiting,
abdominal distention
 PANCREATITIS
Management:
+ Histamine 2 antagonist (ranitidine) to decrease pancreatic
activity
+ Proton pump inhibitors for those who can not tolerate H2
antagonist
+ Respiratory care , oxygen inhalation therapy
 CHRONIC PANCREATITIS
+ progressive destruction of the pancreas, acinar atrophy, cells
are replaced by fibrous tissue resulting to obstruction of the
pancreatic and common bile ducts
Symptoms:
+ Recurring severe abdominal pain and back , vomiting
+ Weight loss
+ Malabsorption, impaired fat and protein digestion
+ Steatorrhae (stool with high fat content)
 CHRONIC PANCREATITIS
Diagnostic Examination:
+ ERCP – endoscopic retrograde cholangiopancreatography
+ MRI
+ Glucose tolerance test
+ Lundh test – measurement of trypsin and lipase; use to
investigate steatorrhea
 CHRONIC PANCREATITIS
Management:
+ Endoscopy – to drain cysts, remove pancreatic stones,
correct stricture
+ Surgery

○ Pancreaticojejunostomy ( Roux-en-Y) gastric bypass

○ Pancreaticoduodenectomy (Whipple resection)

 CHRONIC PANCREATITIS
Management:
+ Instruct client to avoid alcohol
+ Low fat diet
+ Treatment for DM
 04
ENDOCRINE
DISORDERS
 ENDOCRINE DISORDERS
Diabetes Mellitus
- a chronic multisystem disease related to abnormal
insulin production, impaired insulin utilization or both.
Causes:
+ Genetic
+ Auto immune
+ Viral
+ Environmental factors (stress)
 ENDOCRINE DISORDERS
Functions of Insulin:
+ Transports and metabolize glucose for energy
+ Stimulates the storage of glucose in the liver and muscle in
the form of glycogen
+ Signals the liver to stop the release of glucose
+ Enhances the storage of dietary fat in adipose tissue
+ Accelerate transport of amino acid into the cell
+ Inhibits the breakdown of stored glucose, protein, fats
 ENDOCRINE DISORDERS
Classification:
+ Type I (juvenile onset, insulin dependent diabetes
mellitus)
Causes:
+ Body’s own T cell attack and destroy pancreatic beta cells
+ Genetic susceptibility is polygenic
+ Environmental influences; infection with rubella and
coxsackie viruses in pregnancy
+ Early exposure to cow’s milk ( under investigation )
 ENDOCRINE DISORDERS
Risks Factors:
+ Family history of DM
+ Obesity (20% over the desired body wt)
+ Age 45 years old and above
+ Hypertension
+ Increase HDL and cholesterol level
+ History of gestational diabetes or delivery of a baby over 9
lbs
 ENDOCRINE DISORDERS
Manifestations
+ Polyuria – due to osmotic diuresis
+ Polydipsia – due to resulting loss of fluid and electrolyte
+ Polyphagia – a consequence of cellular malnourishment
when insulin deficiency prevents utilization of glucose for
energy
+ Weight loss due to fluid depletion and the accelerated
breakdown of fat and muscle due to insulin deficiency
 ENDOCRINE DISORDERS
Diagnostic Test:
+ Fasting bloodsugar ( 126mg/dl or 7.0 mmol/L)
+ Random blood sugar 200mg/dl or 11.1 mmol/L
+ Glycosylated hemoglobin ( hemoglobin AIC)

○ indicates the overall glucose control for the previous 90

to 120 days.
+ Urine test for glucose
 ENDOCRINE DISORDERS
Management:
+ Insulin therapy for type I DM
Types of Insulin:
+ a. rapid acting –

○ lispro (Humolog), clear- peak 1 hr

○ aspart (Novolog), clear- peak 40-50 min

○ glusiline (Apidra), clear-peak 30-60 min

 ENDOCRINE DISORDERS
+ b. short-acting – regular insulin ( humulin R, Novolin R),clear
+ c. intermediate-acting

○ NPH (Humulin N, Novolin N, ReliOn N), cloudy

○ (neutral protamine Hagedorn), isophane insulin

+ d. Long-acting

○ Glargine (lantus), clear

○ Detemir (Levemir), clear

 ENDOCRINE DISORDERS
+ e. combination (premixed)

○ NPH/regular 70/30 (Humulin 70/30), cloudy

○ NPH/regular 50/50 (Humulin 50/50), cloudy

○ Lispro protamine/lispro 75/25 (Humalog Mix 75/25),

cloudy

○ Aspart protamine/aspart 70/30 (Novolog mix 70/30),

cloudy
 ENDOCRINE DISORDERS
+ TECHNIQUE FOR INSULIN:
 ENDOCRINE DISORDERS
Administration:
+ Subcutaneous
+ Insulin pump
+ Inhaled insulin (Exubera) powder form by a designed
inhaler
+ Insulin pens – use small (150-300 units) prefilled insulin
cartridges that are loaded into a penlike holder. A
disposable needle is attached to the device for insulin
injection.
 ENDOCRINE DISORDERS
+ absorption is more rapid from the abdomen, and slowest
from the thigh.
+ site should be changed regularly to prevent lipodystrophy
Complication of insulin therapy:
+ Insulin resistance
+ Weight gain for clients who are non-compliant with their
diet
+ Hypoglycemia
+ Lipodystrophy
 ENDOCRINE DISORDERS
Storing Insulin
+ Insulin preparation, vials not in use, including spare vials or
pens should be refrigerated.
+ Insulin should not be allowed to freeze and should not be
kept in direct sunlight or in a hot car.
+ Cloudy insulin should be thoroughly mixed by gently
inverting the vial or rolling it between the hands before
drawing the solution into the syringe.
 ENDOCRINE DISORDERS
Storing Insulin
+ Pay attention to expiration date on any type of insulin
+ Bottles of intermediate acting insulin should be inspected
for flocculation- a frosted, whitish coating inside the bottle.
This makes insulin inactive and should be used.
 ENDOCRINE DISORDERS
Oral Hypoglycemics
+ ( stimulate the pancreas to secrete insulin)
+ Sulfonylureas – glucotrol, micronase, diabeta, amyrel
+ Meglitinides – prandin, starlix
+ Biguanides – metformin ( glucophage)
+ alpha-Glucosidase inhibitors – acarbose ( precose), miglitol
(glycer)
 ENDOCRINE DISORDERS
Oral Hypoglycemics
+ Dipeptidyl peptidase-4 (DPP-4) inhibitor, vildagliptin
(galvus)

+ Nutritional Therapy – meal planning, wt control (wt. loss is

the key to treatment)
+ Transplantation of pancreatic cells
 ENDOCRINE DISORDERS
Exercise
Benefits:
+ Lowers blood glucose by increasing the uptake of glucose
by body muscle
+ Improve insulin utilization
+ Improves circulation and muscle tone
+ Reduce cardiovascular risk
+ Increase HDL and decrease total cholesterol and triglyceride
level.
 ENDOCRINE DISORDERS
Acute Complications of Diabetes Mellitus
a. hypoglycemia
cause: too little food, too much insulin
symptoms
. Sweating . Trembling . Blurred vision
. Extreme tiredness and paleness
. Headache . Hunger . Dizziness
 ENDOCRINE DISORDERS
Acute Complications of Diabetes Mellitus
a. hypoglycemia
management:
- give 10-15 g fast acting simple carbohydrate ( 4-6 oz of
fruit juice/regular soft drink, or 4-6 hard candies
 ENDOCRINE DISORDERS
For Unconscious Client:
+ place corn syrup, icing, honey on the client’s buccal pouch
+ IV of 50% dextrose solution
+ HYPOGLYCEMIA is preventable: client’s with DM should
always carry a simple sugar with them and have
identification confirming their diagnosis.
 ENDOCRINE DISORDERS
+ b. Diabetic ketoacidosis – is a state of uncontrolled
catabolism associated with insulin deficiency, fluid depletion
and counter- regulatory hormone excess.
+ Clinical feature – hyperglycemia, dehydration and acidosis
 Increase glucose Increase ketones

Hyperglycemia, glycosuria Acidosis

Osmotic Diuresis
Vomiting

Fluid and Electrolyte Depletion

Renal hypoperfusion

Impaired excretion of ketones and

hydrogen ions
 ENDOCRINE DISORDERS
Clinical Manifestations:
+ Blurred vision + Kussmaul respiration
+ Weakness + Marked dehydration
+ Headache + Anorexia, nausea, vomiting,
+ Orthostatic hypotension abdominal pain
+ Acetone breath
+ Hyperventilation
+ Mental changes
 ENDOCRINE DISORDERS
Management:
+ Insulin

○ (regular insulin the only one approved for IV use)

+ IV therapy for rehydration, and electrolyte losses
+ Restore acid-base balance
+ Monitor blood glucose level
+ 5% dextrose containing potassium chloride
 ENDOCRINE DISORDERS
Problems of Management:
+ Hypotension
+ Coma
+ Cerebral edema
+ Hypothermia
 ENDOCRINE DISORDERS
3. hyperosmolar, hyperglycemic nonketotic syndrome
HHNK
+ includes hyperglycemia, dhydration and hyperosmolality of
the plasma with the absence of ketones in the urine.
+ A metabolic disorder of type 2 DM resulting from a relative
insulin deficiency initiated by an illness that raises demand
for insulin.
 ENDOCRINE DISORDERS
Symptoms:
+ Hypotension , profound dehydration, tachycardia with
variable neurologic symptoms
Management:
+ Insulin IV
+ Fluid replacement - Normal saline solution
 ENDOCRINE DISORDERS
Patients with HHS are older clients management include
+ Monitoring of volume and electrolyte status to prevent fluid
overload, heart failure and cardiac dysrhythmia
+ Fluid treatment to start – 0.9%NS or .45% NS
+ Potassium is added to IV fluid if urinary output is adequate
 ENDOCRINE DISORDERS
Chronic complications of DM
a. retinopathy – client has an increased risk for cataract and
open angle galucoma
b. nephropathy – accounts for 36% of end stage renal disease
with characteristic lesions in the glomerulos
c. neuropathy – sensory disturbances, paresthesia
d. Peripheral polyneuropathy – real danger is- patient
cannot feel pain
 ENDOCRINE DISORDERS
Chronic complications of DM
e. infections
+ Persistent glycosuria encourages bladder infection
+ There is a defect in the mobilization of inflammatory cells
and an impairment of WBC in phagocytosis.
f. diabetic foot
+ Main threats: infection, ischemia
+ Management: foot care
 PITUITARY DISORDERS
Acromegaly – hypersecretion of growth hormone after
maturity
Assessment:
+ Body size enlarged – feet, hands
+ Flat bones enlarged
+ Prognathism
+ Poor coordination
+ Visual field changes
 PITUITARY DISORDERS
Diagnosis:
+ Growth hormone measured in blood plasma
Management:
+ Provide safety due to poor coordination
+ Provide emotional support
+ Surgery – hypophysectomy
Post op care:
+ Elevate head
+ Check neurological status
+ Monitor vital signs
+ Monitor intake and output
+ Provide cortisone replacement therapy
 PITUITARY DISORDERS
Dwarfism
hyposecretion of growth hormone before maturity
Causes:
+ Pituitary tumors
+ Idiopathic hyperplasia
Assessment:
+ Height below normal, body proportion normal
+ Bone/tooth development retarded
+ Delayed sexual maturity
+ Features delicate
 PITUITARY DISORDERS
Management:
+ Monitor growth and development
+ Assess body image
+ Refer for psychological counseling as needed
Hormone replacement
+ thyroid hormone
+ human growth hormone
+ testosterone
 PITUITARY DISORDERS
Hyperthyroidism
+ hypersecretion of thyroid hormone
Causes:
+ Thyroid –secreting tumors
+ Iatrogenic-overtreatment for hypothyroid
+ Pituitary hyperactivity
+ Severe stress
 PITUITARY DISORDERS
Diagnostic Tests:
+ TSH,T3,T4,
+ Protein bound iodine
+ increase basal metabolic rate
 PITUITARY DISORDERS
Symptoms: .
+ Frequent mood swings + Fine , soft hair
+ Frequent mood swing + Heat intolerance
+ Nervous, jittery + Weight loss
+ Increase perception of + Exophthalmus
stimuli + Fine, soft hair
+ Sleep and rest deprivation
+ Diarrhea
 PITUITARY DISORDERS
Management:
+ Surgery

○ thyroidectomy
Complications:
+ Hypocalcemia
+ Laryngeal nerve injury
+ Hemorrahge
+ Respiratory distress
+ tetany
 PITUITARY DISORDERS
Management:
Drug therapy
+ Antithyroid drugs – PTU ( propylthiouracil), tapazole
(methimazole)
+ Iodine – SSKI saturated solution of potassium iodide, Lugol’s
solution inhibits synthesis of T3,T4
+ B-adrenergic blocking agent – propranolol
+ Radioactive iodine for nonpregnant women
 PITUITARY DISORDERS
Hypothyroidism:
+ hyposecretion of thyroid hormone
Types:
a. cretinism
- hypothyroidism in infants and young children
b. myxedema
- hypothyroidism in adult
 PITUITARY DISORDERS
Causes:
+ Thyroidectomy, irradiation of the thyroid
+ Overtreatment with antithyroid
+ Pituitary deficiencies
+ Inflammation of the thyroid gland
+ Iodine deficiency
 PITUITARY DISORDERS
Clinical Manifestations: + Sparse hair, thick brittle
+ Fatigue, lethargy nails
+ Forgetfulness + Sensitivity to cold
+ Low exercise tolerance + Bradycardia
+ Weight gain, obesity
+ Bradycardia
+ Constipation
+ Cool, dry, flaky skin
 PITUITARY DISORDERS
Management:
+ hormone replacement: synthroid, levothyroid
Nursing care:
+ Encourages wt loss with high bulk, low calorie diet
+ Encourages activity balanced with rest
+ Administer laxatives/stool softeners when needed
 PITUITARY DISORDERS
+ Allow client extra time to think, speak, act
+ Provide extra clothing and bedding
+ Restrict use of soap and apply lanolin or creams to skin
 PITUITARY DISORDERS
Adrenal Medulla:
+ Epinephrine and norepinephrine

○ raise blood glucose level, increase rate of metabolism,

constrict certain blood vessels
 PITUITARY DISORDERS
Adrenal Cortex:
+ Glucocorticoids

○ increase blood glucose

+ Mineralocorticoids

○ promote reabsorption of sodium and excretion of

potassium in kidneys
 PITUITARY DISORDERS
Addison’s Disease
+ adrenocortical insufficiency, hyposecretion of adrenal
hormones (mineralocorticoids, glucocorticoids, androgens)
Cause:
+ Autoimmune response
+ TB
+ Infarction of the adrenal gland
+ AIDS
+ Metastatic CA
+ Surgical removal of the adrenal gland
 PITUITARY DISORDERS
Signs and Symptoms:
+ Progressive weakness, fatigue, weight loss and anorexia as
primary features
+ Skin hyperpigmentation seen in sun-exposed areas of the
body, pressure points, over joints, in palmar creases

○ due to increase secretion of beta-lipoprotein which

contain MSH melanin stimulating hormone.
 PITUITARY DISORDERS
Signs and Symptoms:
+ Orthostatic hypotension
+ Hyponatremia
+ Nausea and vomiting; diarrhea
+ Irritability and depression
+ Weak irregular pulse .
+ Poor coordination
+ Fasting hypoglycemia
+ Craving for salty foods
+ Amenorrhea (women)
 PITUITARY DISORDERS
Diagnosis:
+ Plasma cortisol
+ Urinary 17-hydroxycorticosteroids and 17-ketosteroids
Treatment:
+ Hormone replacement
 PITUITARY DISORDERS
Addisonian Crisis
+ a life-threatening emergency caused by insufficient or a
sudden sharp decrease in adrenocortical hormones.
Triggering Factors:
+ Infection, surgery, trauma, hemorrhage, psychologic stress
Symptoms:
. Hypotension . Dehydration
. Tachycardia . Hyponatremia, hyperkalemia
. Hypoglycemia . Fever, confusion
 PITUITARY DISORDERS
+ Circulatory collapse which is unresponsive to the usual
treatment (fluid replacement and vasopressors
Management:
+ Glucocorticoid (hydrocortisone) replacement
+ Vital signs monitoring for volume depletion and
hypotension
+ Monitor for electrolytes
+ Monitor blood glucose level as steroid replacement may
alter insulin requirements.
 PITUITARY DISORDERS
Cushing’s Syndrome:
+ result from excessive adrenocortical activity
Cause:
+ Increase ACTH production
+ Oversecretion of glucocorticoids and androgens
 PITUITARY DISORDERS
Symptoms:
+ (arrest of growth, obesity and musculo skeletal changes
+ along with glucose intolerance)
+ Buffalo hump
+ Heavy trunk with thin extremities
+ Skin is fragile- bruises, striae develop
+ Excessive protein catabolism – muscle wasting,osteoporosis,
kyphosis
+ Retention of sodium and water – hypertension, wt. gain.
 PITUITARY DISORDERS
+ Moon-faced appearance
+ Hyperglycemia due to glucose intolerance and increase
gluconeogenesis by the liver
+ Virilization in women – masculine traits and recession o
feminine traits, menses cease, clitoris enlarges, breast
atrophy
+ Hirsutism – excessive growth of hair that of men
 PITUITARY DISORDERS
The First Indication of Cushing Syndrome
+ Centripetal obesity (truncal obesity)
+ Moon facies (fullness of the face)
+ Purplish red striae
Method of Diagnosis
+ 24 hour collection test for free cortisol
+ Dexamethasone suppression test
+ Plasma cortisol test
+ CT scan and angiography for localize adrenal tumors
+ CT scan , MRI of the head for pituitary tumors
 PITUITARY DISORDERS
Management:
+ Surgical removal of tumor- transphenoidal n,
hypophysectomy for pituitary tumors.
+ Adrenalectomy
+ Amignoglutethimide, etomidate, trilostane – if tumor is
inoperable
 PITUITARY DISORDERS
PHEOCHROMOCYTOMA -
+ an adrenal medullary tumor that secretes
additional amount of epinephrine and
norepinephrine.
 PITUITARY DISORDERS
Assessment Findings:
+ Persistent hypertension
+ Hyperglycemia, glucosuria, polyuria
+ Diaphoresis, pallor. Tremor, nervousness
+ Pounding headache, weakness
Diagnostic Tests:
+ Histamine test – drop in blood pressure
+ Regitine test - done if BP is 170/110 mmHg
- phentolamine (regitine) is given IV
 PITUITARY DISORDERS
+ Urinary vanillylmandelic acid test (VMA) test

○ collect 24 hour urine, urine collected on ice or

refrigerated with preservative

○ normal result (1-5mg.), positive for tumor if significantly

higher foods affecting VMA excretion excluded 3 days
before the test:

○ Coffee ,Tea, Bananas

○ Vanilla, Chocolate
 PITUITARY DISORDERS
Management:
+ Avoid physical and emotional stress
+ Encourage rest
+ Ample diet due to increased metabolic demand
+ Antihypertensive drugs
+ Surgery - adrenalectomy
Thank you! God
Bless ☺