THE METABOLIC AND ENDOCRINE SYSTEMS

Metabolism - sum total of all bodily reactions

 Anabolism – simple to complex (building)
 Catabolism – complex to simple (breakdown)

“ Regulation of the balance is dynamic and is one function of the endocrine and neuroendocrine system.
Metabolic processes affect ALL cells of the body and whole-body metabolic regulation involves
numerous endocrine structures, the liver, muscle and fat cells.”

STRUCTURES OF THE METABOLIC SYSTEMS

1. LIVER - largest gland about 2.5 of TBW; located in the RUQ ; lies under the R lung and above the
stomach and intestines. Liver flow represents about 20% of CO (1L/min)
a. Hepatic artery –supplies the liver about 1/3 of its blood, carries O2 blood
b. Portal vein – supplies the liver about 2/3 of its blood; carries deO2 blood; formed by the
junction of superior and inferior mesenteric veins and splenic veins which receive blood from
pancreas, spleen, stomach, intestines, and gallbladder; carries nutrients, metabolites and
toxins from digestive organs to liver for processing, detoxification or assimilation
c. BP in the liver is low hence and increase in CVP causes liver engorgement

 Lobule – fxn’l unit of the liver

 Hepatocytes – major cells
 Kupffer cells – MPS

Functions of the Liver

 Storage of glycogen
 Performs glycogenesis – glucose to glycogen
 Performs glycogenolysis – glycogen to glucose
 Performs gluconeogenesis – amino acid/fructose/galactose to glucose
 Formation of lipoproteins
 Cholesterol and phospholipid synthesis
 Fat synthesis from CHON and CHO
 Deamination of amino acids – degradation or catabolism of amino acids, removal of amino group
(NH2) to NH3 converted to urea and excreted by the kidneys
 Formation of urea
 Formation of plasma CHON (albumin, clotting proteins, etc)
 Biotransformation of hormones, drugs and other substances
 Reservoir of blood – contraction of hepatic venules and veins moving about 500ml into the
circulation
 Oxidation of fatty acids for energy – through splitting of glycerol and fatty acids

ENDOCRINE SYSTEM – secretes hormones that acts on target organs

a. Hypothalamus – regulates secretions of APG and PPG through the infundibulum; lies dorsal to the
pituitary gland.
b. Pituitary Gland – (hypophysis) a small extension on the dorsal surface of the hypothalamus
i. ANTERIOR PITUITARY GLAND - (adenphypophysis) a glandular tissue that consists a variety
of secretory cell types
1. Prolactin – promotes milk production
2. TSH – stimulates prdxn of thyroid hormone secretion
3. ACTH – stimulates release of adrenal hormones
4. Growth hormone - somatotropins
5. Gonadotropins – secondary sex characteristics
ii. POSTERIOR PITUITARY GLAND – (neurohypophysis) is a neural tissue that contains glial cells
and terminal axons from cells of the hypothalamus.
1. Anti-diuretic hormone – aka Vasopressin, inhibits diuresis
2. Oxytocin – formed primarily in the paraventricular nucleus of the hypothalamus,
promotes uterine contraction during parturition, causing milk let-down.

c. Thyroid Gland - Located in the neck, just below the cricoid , H-shaped
1. Triidothyronine (T3) – rapid effect on target tissue, 3 days for peak effect
2. Thyroxine (T4) – requires 11 days for peak effect
a. Requires Iodine for synthesis of thyroid hormones
b. Release is dependent on TSH via negative feedback
FUNCTIONS:
a. Increases metabolism
b. Promotes growth
c. Balance between CHON anabolism and catabolism
d. Assists in acclimitization to cold env’ts by the increasing metabolic rate (heat
pdxn is a by product of metabolism)
 e. Increases DNA translation and transcription

d. Pancreas
1. Insulin – Beta Cells
a. Enhance glucose transport into the cell. (adipose tissue formation)
b. Enhances amino acid transport into the cell
c. Works with growth hormone to promote cell hypertrophy and hyperplasia
2. Glucagon – alpha cells
a. Elevates plasma glucose when blood glucose levels drop below 90 mg/dl
3. Somatostatin –delta cells
a. Delay nutrient absorption at the GI tract
b. Regulates release of insulin and glucose

e. Adrenal Glands - Paired endocrine organs situated at the superior poles of the kidney
1. Cortex
a. Aldosterone – primary mineralocorticoid secreted by the adrenal cortex,
degraded in the liver and excreted by the as glucosonide or SO4, conserves
Na and excretes K
b. Cortisol – primary glucocorticoid, stress hormone
 Facilitates gluconeogenesis – increases plasma glucose
 Stimulates appetite – which leads to central deposition of fat
2. Medulla – postganglionic sympathetic nerve secreting catecolamines
a. Epinephrine – 80% of secretion, strong beta adrenergic effects, potent
stimulator of HR, contractility, increases met. Rate by 100%
b. Norepinephrine

f. Gonads – Males- androgens primarily testosterone (promotes CHON synthesis and musculoskeletal
growth), have a potent anabolic action; Females- estrogen estradiol, puberty related increase in
musculoskeletal growth

I. NURSING ASSESSMENT
a. History Taking
i. Biographic and Demographic Data
 Determine AGE, GENDER, ETHNIC BACKGROUND, GEOGRAPHICAL LOCATION
 As person ages, fewer hormones and metabolic secretions may be produced and their
effect on target organs may diminish.

ii. Chief Complaint – take note of the onset, duration, intensity, characteristic manifestations
and alterations in growth patterns esp. changes in weight, height or hand, foot, or head size.
1. Integumentary manifestations
a. Non – inflammatory blisters on the dorsum of the hand - common among patients w/
Hepa C virus
b. Jaundice – viral hepatitis, cirrhosis, obstructive or cholestatic liver
c. Unexplained punctured holes – route for entry of hepa virus
d. Spider Angiomas – liver cirrhosis
e. Dilated abdominal veins (caput medusa) – liver cirrhosis
f. Skin lesions that do not heal – pancreatic dysfunction, DM
g. Changes in pigmentation – hyperpigmentation in addison’s dse, hypopigmentation such
as vitiligo (patches) and albinism (general hypopigmentation)
h. Hard, non pitting edema – hypothyroidism (myxedema)
i. Changes in appearance of hands, head, feet and face – acromegaly produces
enlargement of head, hands and feet, coarsening of facial features; cushing’s
syndrome moonlike face, thin extremities and truncal obesity
j. Growth – stunted growth (dwarfism); excessive (gigantism), inappropriate (acromegaly)
k. Hair distribution, amount and texture – hirsutism (excessive hair may indicate ovarian or
adrenocortical d/o; loss of pubic and ancillary hair (pituitary problem); dry brittle hair
(hypothyroidism); soft silky (hyperthyroidism)
l. Diaphoresis – hyperthyroidism and pheochromocytoma

2. Cardiovascular manifestations
a. Epistaxis - problem w/ liver decreases ability to produce clotting factors
b. Hemorrhoids – indicative of hepatic disorder in which fluid overload results from the
liver’s improper functioning and metabolism of hormones and ADH
c. Changes in V/S – elevated in hyperthyroidism and pheochromocytoma
d. Hypertension – portal HPN in liver dse.
e. Elevated HR, flushing - elevated in hyperthyroidism and pheochromocytoma
f. Kussmaul’s Respiration - DKA
g. Tolerance to heat/ cold – heat intolerance in hyperthyroidism; cold intolerance in
hypothyroidism
 3. Neurologic Manifestations
a. Weakness –late manifestation of DM, liver and pancreatic dses.
b. Depression – pancreatic cancer or endocrine disorder (decrease cortisol-decrease
endorphins)
c. Changes in mental status or mood – diabetic neuropathy, hepatic encephalopathy
d. Emotional lability - diabetic neuropathy, hepatic encephalopathy
e. Pain – radiating to the back  pancreatic, gallbladder or biliary tract d/o
f. Tremors – hyperthyroidism – increased calcitonin decreases serum calcium
g. Muscle weakness- DM due to muscle wasting; hypothyroidism decreased calcitonin
increases serum calcium
h. Loss of sensation – DM neuropathy

4. Ophthalmic Manifestations
a. Exophthalmos - hyperthyroidism
b. Diminished/ blurring of vision - DM retinopathy or pituitary tumor

5. GIT
a. Glossitis – enlarged red tongue in severe DM and acromegaly
b. Changes in weight – decreased in hypothyroidism and increased in hypothyroidism
c. Anorexia – liver d/o
d. Polydipsia - DM
e. Nausea and Vomiting – pancreatitis and hepatobiliary obstruction
f. RUQ Pain – gallbladder and liver dse.
g. Fatty food intolerance – hepatobiliary dse and pancreatitis
h. Belching (excessive eructation or aerophagia) – gall bladder dse and pancreatitis
because of fat malabsorption and reflux of bile and acid
i. Heartburn – gall bladder dse and pancreatitis because of fat malabsorption and reflux of
bile and acid
j. Changes in bowel habits – diarrhea in hyperthyroidism, constipation in hypothyroidism
k. Constipation/ diarrhea
l. Changes in stool appearance – acholic stool in hepatobiliary obstruction, steatorrhea in
pancreatitis

6. GUT
a. Tea – colored urine - hepatobiliary obstruction
b. Frequent urination - DM
c. Menstrual cycle irregularities – endocrine d/o
d. Calcium stones – hypothyroidism or hyperparathyroidism

iii. Past Health History

 Childhood / Infectious Diseases – ask client and family members about episodes of
endocrine and metabolic d/o that client may have experience as a child or adolescent
 Immunizations – Hepa Vaccines
 Major Illnesses and Hospitalizations – head trauma (hypopituitarism), break in the skin
(hepa B or C)
 Medications
• Use of hormones and steroids
• Over the counter medications – hepatotoxic drugs (Acetaminophen, INH,
sulfonamides, arsenic, thiazide diuretics, antineoplastic drugs, oral contraceptives,
anesthetics, antipsychotics)
• Allergies

iv. Family Health History

 Any family member with a similar disorder?
 Family history of diabetes mellitus
 Any family member with cancer?
 OBESITY, GOITER, HYPOTHYROIDISM, HYPERTHYROIDISM, HPN, low BP, DM, Diabetes
Insipidus, Addison’s insipidus, addison’s dse, pheochromocytoma

v. Psychosocial History
 Stress and patient’s coping mechanisms – stress can increase the severity of DM
 Work environment – job related stressors, exposure to hepatotoxic chemicals such as lead,
anesthethic agents such as nitrous oxides
 Physical activity – balance in activity and rest promotes utilization of glucose in DM
 Sleep and rest patterns
 Nutrition
• Food preferences – Laennec’s cirrhosis in alcoholism
• Eating patterns
 • Meal preparation – Hepa A
 Travel in areas where hepa/pancreatitis is endemic
 Eating raw or steamed selfish (oysters, clams, scallops) from polluted H2O
 Swimming or bathing in polluted water
 Any known contact w/ hepa infected host

b. Physical Assessment
i. General Appearance and Nutritional Status
 Level of consciousness – client’s mood, affect, orientation, alertness, verbal and nonverbal
memory, speech patterns
 Appearance
 Obtain the weight

ii. Vital Signs

iii. Integument
 Hair texture and distribution
 Skin color
 Palpate skin for texture, moisture

iv. Head
 Symmetry of facial features

v. Eyes
 Position, symmetry, shape, eyelid lag
 Visual acuity and Extraocular movements

NOSE – assess mucosa for swelling and color; listen for noisy breathing
MOUTH – note size and shape of the jaw. Inspect the color of the oral mucosa and the condition of
client’s teeth. Note malocclusion. Observe tongue size, activity and fasciculations

vi. Neck
 Inspect for symmetry, alignment, bulging over the thyroid gland
 Palpate thyroid gland in two ways
• Anterior
o Stand in front of the client.
o To palpate the thyroid gland’s right lobe, flex the client’s head toward the right to
relax the neck muscles on that side.
o Use the fingers of your right hand to displace the trachea slightly to the client’s
right.
o Ask the client to swallow while you palpate the right lobe of the thyroid with the
fingers of examiner’s left hand.
o Repeat with the left lobe.
o *** the nurse can also palpate for enlargement by palpating deep on each side of
the sternocleidomastoid muscles.

• Posterior approach
o Stand behind the client.
o Ask the client to lower the chin to relax the neck muscles.
o Tilt the head slightly to the right to examine the right lobe of the thyroid.
o Use the fingers of your left hand to displace the trachea and the slightly to the
right. This moves the thyroid laterally.
o Palpate between the trachea and the sternocleidomastoid for the right lobe with
the fingers of the right hand.
o Ask the client to swallow while you palpate; doing so will cause the gland to rise
in the neck.
o Repeat for the left lobe by reversing hand placement and positioning the client
toward the left.

 Observe for difficulty in swallowing

 Observe for hoarseness or huskiness – deepening of voice in hyperthyroidism

THORAX – inspect for gynecomastia in males because of decrease metabolism of estrogen

Extremities – examine for size, shape, symmetry, and proportionality to the trunk; note for
peripheral edema, palpate for peripheral pulses, DTR
UPPER EXTREMITIES
 Ask the client to extend the hand w/ palms down, observe for fine tremors and for
reddened palms
 Note the size of the client’s hand in proportion to the rest of the body
 Assess grip strength and muscle strength
LOWER EXTREMITIES
  Note the color and distribution of hair
 Assess the size of the client’s feet in proportion to the rest of the body
 Inspect for corns and calluses
 Palpate and note pedal pulses
 Assess leg for muscle weakness

vii. Abdomen

Inspection
 Observe for distention with tight and shiny skin.
 Take note of distended veins
 Obtain abdominal girth if ascites is present. Measure weight.

Auscultation
 Hum
 Friction rub
 Systolic bruit

Percussion
 Size
• Right Midclavicular line
• Begin at 3rd ICS
• Percuss downwards until the sound changes from resonant to dull.
• Mark.
• Inferiorly, percuss from the typanic area and progress upward until the sound changes
to dull.
• Mark
• LIVER SPAN:
• 6 – 12 cm.
• Midsternal Line
• Percuss upward from above the umbilicus from tympany to DULL.
• Mark.
• Superiorly, percuss down the sternum until the percussion note changes.
• Mark.
• Liver span: 4 – 8 cm.
 Liver span may increase more than 12 cm, more than slightly tender, rigid
• Liver Descent
• Mark the distance of liver descent by:
• Ask your patient to inhale deeply and hold it.
• Percuss the lower border of the liver from right midclavicular line.
• Mark and measure.
• Normal: 2 – 3 cm descent

 Test for shifting dullness

• To assess fluid level in ascites:
• To lower abdomen when standing.
• To flanks when supine
• To dependent side while lying on one side
 Fluid wave test
• 2 Nurses participate
• 1 stabilizes the abdominal wall by placing her hand on one side of the client’s
abdomen while briskly tapping the opposite side of the abdomen with the other hand.
• 2nd nurse feels for the movement of fluid wave against the palpating hand opposite
the side

Palpation
 Assess muscle guarding and tenderness
 RUQ/ Epigastric Pain
 WOF Rebound Tenderness
 LIVER
• Left hand of the examiner under the right posterior thorax (11th and 12th ribs).
• Push thorax upwards.
• Right hand over the previously marked level of liver descent.
• Examiner’s fingers are pushed up as the client takes a deep breath using the
abdominal muscles.
• Feel for the firm, sharp, smooth and regular border of the
 SPLEEN – located by percussion of LMAL bet 6th to 10th ribs; Normal: 2 ½ to 3 inches
• Do not palpate if enlarged (ruptured spleen)
 • If no enlargement, ask client to turn into the right side allowing gravity to bring the
spleen forward and down, closer to the abdominal wall.
• Normal spleen is not palpable
• Enlargement in portal HPN

c. Diagnostic Tests
i. Tests for Endocrine Pancreas Function
1. Fasting Blood Glucose (FBS)
• Patient to be on NPO for 8 hours

< 110 mg/ dl Normal FBS

110 – 126 mg/ dl Impaired Fasting Glucose(IFG)
> 126 mg/dl Dx of Diabetes

2. Glycosylated Hemoglobin (HBA1C) – glucose normally attaches itself to the hgb molecules
once attached, it cannot dissociate; stated in percentage and is useful in evaluating long
term glycemic control
• Average blood glucose measured over the previous 3 months
• Normal 6-7%
3. Oral Glucose Tolerance Test (OGTT) – unnecessary if FBS > 140 mg/dl; bedrest, infection,
trauma, medications and stress can alter result
• Diet of at least 150 g of CHO/ day for 3 days
• Blood sample withdrawn for FBS
• Client drinks 75 g of glucose in water
• Blood samples are obtained in between regular intervals (at 1 and 2 hours)
• Client cannot consume any food or fluid other than water between glucose load
ingestion and the end of the test

<140 mg/dl Normal glucose tolerance

140 – 200 mg/dl Impaired Fasting Glucose
>200 mg/dl Dx of Diabetes

ii. Tests of Thyroid Function

1. TSH Assay - measurement of the basal serum TSH concentration is useful in differentiating
primary and secondary hypothyroidism
Primary hypothyroidism– increase
Secondary hyperthyroidism - increase
2. Serum Thyroxine levels
 T4 is transported in blood largely bound to thyroxine binding globulin and is an
effective indicator of thyroid fxn
 Increase – hyperthyroidism, viral hepa, pregnancy, oral contraceptives
 Decrease – hypothyroidism, strenous exercise, heparin and lithium
3. Serum Triiodothyronine levels (same as above)
 BMR – calculated by measuring the amount of O2 that the body consumes when in a
state of complete mental and physical relaxation
4. Radioiodine Uptake
• Determines metabolic activity of the thyroid gland through measurement of iodine
radioisotopes
• Client is NPO 6 – 8 hrs prior to the test
• Assess: Have you taken any iodine containing meds? Are you taking estrogens? Eaten
seafoods?
• PO or IV radioactive iodine is administered (123I, 125I, 131I)
• 24 hr urine collection is begun after tracer dose is given.
• Scanning of thyroid q 2 – 4 hrs and 24 – hour intervals.

5. Adrenal Tendon Reflexes - Achilles Tendon Reflex test measures the amplitude and duration
of the ankle jerk and special instrument, which is used to tap the strong tendon at the back
of the heel. Hyperactive in hyperthyroidism.

iii. Liver Enzyme Test

1. Aspartate Aminotransferase (AST) – 35 units/l
• Blood in drawn without special preparation, venous blood is taken daily for 3 days.
• Increased in liver disease, hepatitis, hepatic cirrhosis, hepatic surgery, acute
pancreatitis.
• Decreased in acute renal disease

2. Alanine Aminotransferase (ALT) – 4 – 36 units/ L

• No fasting required, collect 7-10 ml of blood
• Marked increase in hepatitis, hepatic necrosis, ischemia, obstructive jaundice
 3. Lactate Dehydrogenase (LDH)
• LDH 5- marked increase in hepatic disorders, venous blood collected 7-10 ml, no
fasting required.

4. Serum Bilirubin - tests liver function and evaluate hemolytic anemia.

• Direct (Conjugated) 0.1-0.3 mg/dl – increased in galistones, extrahepatic duct

obstruction, liver metasis
• Indirect (inconjugated) – 0.2-0.8 mg/dl – increased in hepatitis, anemia, BT reaction,
cirrhosis
• Total Bilirubin- 0.3-1 mg/dl measures direct and indirect together; used to evaluate
liver function; Client on NPO after midnight, 5-7 ml of blood is collected
5. Urine Bilirubin – 0- 0.2 MG/ DL
• 0-Suggests decrease affecting bilirubin metabolism after conjugation or defects in
excretion.
• Increased in liver metastasis and extrahepatic duct obstruction

Test for Metabolic Organ Functions

A. PERITONEOSCOPY- insertion of a peritoneoscope through an abdominal stab wound permits direct

visualization of the liver and peritoneum, The examiner may take a photograph and perform biopsy.
Relatively safe and simple; obesity and ascites can interfere w/ results

PROCEDURE:
1. Obtain a written signed consent
2. Check Lab records to see if the client has a normal or adequate clotting factors
3. Prepare skin and administer preprocedural meds
4. Instruct client to be on NPO status and to empty bladder and bowel before the procedure
5. Instruct client to expect difficult breathing when air is placed in the abdominal activity,
Instruct client to hold on breath to protect major organs during needle insertion

POSTPROCEDURE:
1. Bed rest for 24 hours if ever the biopsy is done, If not, client can resume normal activity after recovery
from effects of the medication
COMMON COMPLICATIONS: Pneumothorax, subcutaneous emphysema, air embolism, bile
peritonitis, shoulder or abdominal pain
B. PORTAL PRESSURE MEASUREMENT – N: 5-10mmHg
a. Diagnose portal hypertension
b. Indicate severity of portal hypertension
c. Guide decisions about appropriate intervention

MAJOR PORTAL PRESSURE MEASUREMENTS:

1. WEDGED HEPATIC VENOUS PRESSURE- pressure is obtained indirectly by percutaneous
hepatic vein catheterization. The examiner uses either an arm or vein or a famoral vein.
2. UMBILICAL VEIN CATHERIZATION- allows direct measurement of portal pressure
3. SPLENIC PULP MANOMETRY- involves the insertion of a needle between 2 of the lower ribs
and inserts a manometer into the spleen. Client instructed to hold her breath during
needle insertion
OTHER PROCEDURES:

A. URINE UROBILINOGEN (0.3 – 3.5 mg/dl in random test; 0.05 – 2.5 in 24 hour test); test done after 2
hours or 24 hour afternoon collection placed in brown refrigerated bottle w/ NaHCO3 preservative
o Bilirubin is transformed in to urobilinogen by the action of bacteria in the bowel
o Increased in erythrocyte hemolysis and certain drug liver and toxic hepatitis
o Decreased billary obstruction or liver damage
B. FECAL UROBILINOGEN- -75- 275 EU/100 g,
o Results from the breakdown of direct bilirubin to fecal urobilinogen by the action of
bacteria in the bowel.
o Increased in erythrocyte hemolysis
o Decreased in billary obstruction

C. ALPHA PHETO PROTEIN- < 40 mg/ml or < 40 mg/dl, Used as tumor marker to identify cancers such
as hepatomas. No fasting required ; 7-10 ml of blood is sent to the lab

D. IMMUNOGLOBULIN (electrophoresis)
o Used to assist in diagnosis and monitoring of therapeutic response in many disease status
such as liver disorders.
o 1 gG- 565- 1765 mg/dl- increased in chronic liver disease
o 1 gA- 85-385 mg/dl- increased in chronic liver disease
o 1 gM-55-375 mg/dl- increased in chronic liver dysfunction, hepatitis, billary cirrhosis
o No fasting is required, venous blood is taken 7-10 ml is sent to the lab
 o Note drugs that can increase Ig (INH, Phenytoin, Contraceptives, steroids, tetanus toxoid,
ATS)

Imaging Studies

1. ABDOMINAL ULTRASOUND- visualizes abdominal organs. A transducer is passed over the organ

Reminders:
1. Client may or may not fast
2. Assure that procedures is relatively painless and safe, and may take 20 minutes only

2. RADIOGRAPHY- shows diaphragm elevation caused by nepatic enlargement or calcification in the

abdominal organs

3. COMPUTED TOMOGRAPHY- identifies and evaluates liver, billary tract, gallbladder and pancreatic
disorders. Useful in distinguishing cysts or tumors and differentiating obstructive from non-obstructive
jaundice.
PREPROCEDURE:
a. NPO 4 hours before tests; except water
b. Contrast dye is used. Note for allergy to iodine

4. ANGIOGRAPHY- Allows visualization of the hepatic, billary, and pancreatic arterial vessels after
administration of contrast medium. Injection of contrast medium through femoral artery than a
catheter is placed in the cliac/mesenteric artery afterwards series of x-ray will be done

5. BIOPSY – single-most valuable diagnostic study

OPEN- needs general anesthetic and a major abdominal incision
CLOSED- aspirate a core of tissue via needle for histologic study; blind procedure under local
anesthesia
C/I: Severe thrombocytopenia, local infection, prolonged PT, peritonitis, massive ascites,
uncooperative client
PREPROCEDURE:
1. 2 weeks before the test, no aspirin, NSAIDs, and anticoagulants should be taken.
2. Blood clotting test shoul be normal
3. NPO for 6 hours

4. Client needs sedation or anesthesia with midazolam or diazepam to help allay client’s fears
and make him comfortable during the procedure.
5. Place in a supine or left latest position with the right arm elevated
6. Instruct client to exhale during the insertion of the needle and to hold his breath on
expiration for 5-10 seconds to avoid puncture of the diaphragm

POSTPROCEDURE:
1. Monitor V/S q 15 minutes for 2 hours, every 30 minutes q 2 hours q 1 hour for 4 hours
2. Assess Tachycardia, Hypotension
3. Check puncture sites and observe crepitus, hematoma formation
4. Observe pain in the RUQ of abdomen caused by subcapsular accumulation of bid or bile or
at the rt. Shoulder as a result of bid on the undersurface of the diaphragm.
5. Beginning after 2 hours posttest, elevate head at 30 degrees. After 2 hours, 45 degrees
6. Maintain bed rest for 24 hours
7. Lying on the rt side for the 1st 1-2 hours decreases the risj of hemorrhage and bile leakage
8. Vit. K if prescribed
9. Observe for dyspnea

COMPLICATION – Hemorrhage within 24 hours is the most serious complication

6. CT PICTOGRAM- provide accurate picture of the liver when a small tumors are suspected. Helpful to
surgeon contemplating live resection, NPO for 2-4 hours before the test. Contrast dye is injected through a
catheter positioned I the splenic artery using CT Scan.

7. GALLIUM SCAN- low level of gallium uptake esp. in the liver and spleen. Used when WBC tend to
aggregate; gallium has high affinity to infectious cells, inflammation and tumor cells

8. MRI- evaluate liver structure

9. PARACENTESIS- peritoneal tap

E. extracts fluid accumulation in the peritoneum
F. relieve intraabdominal tension which can impair respiratory function
G. obtain fluid for culture
 PRETEST:
 Instruct client to void
 Client sits upright w/ feet resting on a stool and
back well supported
  POSTTEST:
 Watch out for hypovolemia
 Monitor VS
 Check for bleeding and infection

Hepatic System
IV. Risk Factors in the development of metabolic d/o
• Diet/ hygiene (poor)
• Hepatitis
Hep A – infected H2O, milk, raw food, shellfish from contaminated H2O
- crowding/ poor sanitation
Hep B – health workers in contact with blood or carriers multiple blood transfusion/ analysis
- homosexual (men), morticians
- Tatorin; IV drug user, saliva and serum of carriers
Hep C – parenterally by blood
Hep D- blood contact (blood products)
- IV drug user/ people with hemophilia
Hep E- travel to counters with incidence of Hep E consuming food and H 2O contaminated with
virus
Cirrhosis- alcohol ingestion especially in the absence of proper nutrition use

Parathyroid Hormone Test

Definition

The parathyroid hormone (PTH) test is a blood test performed to determine the serum levels of a
hormone secreted by the parathyroid gland. The parathyroid glands are small paired glands located
near the thyroid gland at the base of the neck. Most people have four glands, two on each side of the
neck. PTH regulates calcium and phosphorus levels in the body. It is secreted in response to low blood
ionized calcium levels, causing bone to release calcium into the blood stream. In addition, it promotes the
renal reabsorption of calcium and excretion of phosphorus.

Purpose

The PTH level is measured to evaluate the cause of an abnormal serum or plasma calcium. It is routinely
monitored in patients with a kidney disorder called chronic renal failure (CRF). These patients lose calcium
via the kidneys which stimulates release of PTH. This can lead to bone demineralization. The PTH test is
also used to distinguish between primary hyperthyroidism and malignancies that result in high ionized
calcium via secretion of a protein called parathyroid hormone-related protein. This stimulates the PTH
receptor of bone causing increased plasma ionized calcium. PTH is also used to distinguish between
hypoparathyroidism and a condition called pseudohypoparathyroidism, which results from a poor renal
response to the hormone. Persons with primary hypoparathyroidism have a low ionized calcium because
the parathyroid glands fail to produce enough PTH. Persons with pseudohypoparathyroidism have a low
ioninzed calcium but have a normal or elevated level of PTH.

Description

Measurement of PTH is used for the differential diagnosis of hyperparathyroidism. Primary

hyperparathyroidism is most often caused by a benign tumor (adenoma) in one or more of the parathyroid
glands. It is rarely caused by parathyroid malignancy. Patients with this condition have high plasma PTH
and ionized calcium levels and low plasma inorganic phosphorus. Primary hyperparathyroidism is treated
by surgical removal of the tumor(s). The PTH test is used to measure the plasma hormone level during
surgery. Complete removal of the tumor is signaled by a return to normal plasma PTH levels.
Secondary hyperparathyroidism is often seen in patients with chronic renal failure (CRF). The kidneys fail
to excrete sufficient phosphate and do not reabsorb calcium. The parathyroid gland secretes PTH in an
effort to raise the plasma ionized calcium level. Because of the constant stimulation of the parathyroid,
CRF patients have high PTH and normal or slightly low calcium levels.

Tertiary hyperparathyroidism occurs when CRF causes proliferation of the parathyroids that does not
respond to normal suppression by ionized calcium. Patients with this condition have high plasma PTH and
calcium levels and low plasma inorganic phosphorus.

Specific PTH assays

Some PTH is split into peptide fragments by enzymes in the parathyroid gland prior to being released into
the blood. Therefore, in addition to intact PTH, three smaller fragments are also present, an amino or N-
terminal fragment, a midregion fragment, and a carboxy or C-terminal fragment. Only the intact hormone
and fragments containing the amino terminal end of the molecule are physiologically active. A two-site
enzyme immunoassay was recently developed to measure PTH. This method measures only the intact PTH
and active fragments and is preferred over other assays that detect the inactive fragments.

Precautions

Drug interactions

Some prescription drugs affect the results of PTH tests. Drugs that increase PTH levels include
phosphates, anticonvulsants, steroids, isoniazid, lithium, and rifampin. Drugs that decreasePTH include
cimetidine and propranolol.

Timing

PTH levels are subject to diurnal variation. The plasma level peaks at around 2:00 A.M. and is lowest
around 2:00 P.M. Specimens are usually drawn at 8:00 A.M. The laboratory should be notified if the
patient works the night shift so that this difference in biological rhythm can be taken into account.

Related blood tests

Due to the relationship between PTH and calcium, ionized calcium and inorganic phosphorus levels should
be tested at the same time as PTH. In addition, creatinine and other tests of renal function are helpful in
identifying those patients who have secondary hyperparathyroidism caused by renal loss of calcium.

Preparation

The PTH test is performed on a sample of the patient's blood, withdrawn from a vein. The procedure,
which is called a venipuncture, takes about five minutes. When performing this procedure, the nurse or
phlebotomist should follow universal precautions for the prevention of transmission of bloodborne
pathogens. The patient should have nothing to eat or drink starting at midnight of the day of the test.

KEY TERMS

Assay—An analysis of the chemical composition or strength of a substance.

Hypercalcemia—Abnormally high levels of blood calcium.

Hyperparathyroidism—Overactivity of the parathyroid glands. Symptoms include generalized aches and

pains, depression, and abdominal pain.

Hypoparathyroidism—Insufficient production of parathyroid hormone, which results in low levels of

blood calcium.

Complications

Risks for this test are minimal, but may include slight bleeding from the puncture site, a small bruise or
swelling in the area, or fainting or feeling lightheaded.

Results

Reference ranges for PTH tests vary somewhat depending on the specificity of the antibodies used in the
assay to detect the hormone. Results should always be interpreted in association with calcium results. The
following ranges are typical:

• intact PTH: 10–65 pg/mL

• PTH N-terminal (includes intact PTH): 8–24 pg/mL
• PTH C-terminal (includes C-terminal, intact PTH, and midmolecule): 50–330 pg/mL

Abnormally high PTH values may indicate primary, secondary, or tertiary hyperparathyroidism. Causes of
secondary hyperparathyroidism include chronic renal failure, malabsorption syndrome, and vitamin
D deficiency. Abnormally low PTH levels indicate primary hypoparathyroidism or hypercalcemia. Primary
hypoparathyroidism is less common than hyperthyroidism and may result from surgical removal of the
glands (during thyroidectomy) or chronic inflammatory (autoimmune) disease. Malignancies producing
parathyroid hormone-related protein are common causes of low PTH induced by high ionized calcium.

Health care team roles

This test is ordered by a physician. The blood sample is collected by a nurse or phlebotomist. PTH levels
are usually analyzed by clinical laboratory scientists/medical technologists. If abnormal results occur, the
patient is usually referred to an endocrinologist for further evaluation and treatment.

Adrenocortical Hormone Test

Adrenocortical hormone tests measure levels of aldosterone and cortisol (also known as hydrocortisone)
in blood and urine. These hormones are synthesized from cholesterol by the action of several enzymes.
The cells responsible are located in the outer part (cortex) of theadrenal glands, two small organs, one
sitting just above each kidney. As steroid hormones, they are an important part of the body's endocrine
system and help to regulate body functions. The adrenal cortex also produces many other steroid
hormones including androgens, primarily dehydroepiandrosterone (DHEA) and androstenedione, that are
converted to testosterone and dihydrotestosterone.
Aldosterone, a mineralcorticoid, helps regulate the amounts of sodium and potassium in the blood and,
because fluid follows sodium, helps maintain fluid balance and blood volume, which, in turn, affect blood
pressure.

Cortisol, a glucocorticoid, helps regulate the metabolism of proteins, fats, andcarbohydrates,

especially glucose (sugar). Specifically, cortisol helps convert amino acids (subunits of proteins) into
glucose within the liver. It raises blood sugar levels by stimulating the release of glucose from cellular
glucose stores and simultaneously acts to inhibit insulin, which moderates glucose transport into the cells.
Cortisol also has a number of anti-inflammatory effects, including suppressing the immune system and
reducing fever.

Purpose

Aldosterone measurement is used to detect aldosteronism (hyperaldosteronism), which is the excess

secretion of the hormone by the adrenal glands. It is also used to detect those cases of hypoaldosteronism
that occur in the absence of a low cortisol.

The cortisol test is performed on patients who are suspected to have malfunctioning adrenal glands. It is
considered to be the best indicator of adrenal activity. Blood and urine cortisol measurements, together
with the determination of ACTH levels, are the three most important tests in the investigation of Cushing's
syndrome (overproduction of cortisol) and Addison's disease (underproduction of cortisol). Additional tests
called simulation and suppression tests may be needed to detect disease in difficult cases, or to
distinguish between the causes.

Precautions

Adrenocorticol function tests may be done on serum or urine. The nurse or phletotomist performing
venipuncture should observe universal precautions for the prevention of transmission of bloodborne
pathogens. Cortisol levels in blood are subject to diurnal variation. Test results must be evaluated with
regard to the time of day the blood was collected. Physicians will determine if patients whose fluid balance
may already be compromised by illness can undergo 24-hour urine tests. Physicians will also determine if
patients can discontinue taking drugs that control sodium and potassium levels and fluid balance prior to
testing. These tests are sometimes performed by a method called radioimmunoassay (RIA) that tags test
reagents with radioactive iodide. RIA based tests may be contraindicated for patients who have had recent
procedures using radiation or who have had radioactive drugs administered, because results may be
altered and unreliable.

Description

Aldosterone

Aldosterone is produced by the outer area of the adrenal cortex called the zona glomerulosa.
Aldosteronism, an increased secretion of aldosterone, can be primary (a malfunction in the adrenal glands
or in aldosterone secretion itself) or secondary (caused by another condition). Excessive aldosterone
production results in the retention of sodium, and subsequently in fluid retention and high blood pressure
(hypertension). Because potassium can be lost in this process, muscle weakness is also a frequent
symptom. Primary aldosteronism is most often caused by an adrenal tumor (adenoma) a condition
referred to as Conn's syndrome. Primary aldosteronism can also be idiopathic (of unknown origin) or
congenital. Secondary aldosteronism is more common and occurs as a consequence of non-adrenal
conditions characterized by severe imbalances in sodium and potassium with resulting fluid imbalance,
such as congestive heart failure, cirrhosis (liver disease) with fluid in the abdominal cavity (ascites),
certain kidney diseases, excess potassium (hyperkalemia), a sodium-depleted diet, and the toxemia
of pregnancy. To differentiate primary aldosteronism from secondary aldosteronism, a plasma renin test
should be performed at the same time as the aldosterone assay. Renin, an enzyme produced in
the kidneys, is typically elevated in secondary aldosteronism and reduced in primary aldosteronism.

Hypoaldosteronism is characterized by low serum sodium, dehydration, and high serum potassium
(hyperkalemia). Hypoaldosteronism can occur in Addison's disease, which usually is caused by
autoimmune damage to the adrenal cortex. Addison's disease is marked by decreased glucocorticoids and
is detected by tests for deficient cortisol production. However, hypoaldosteronism may also occur in the
absence of low glucocorticoids. This condition may result from decreased renin production by the kidney,
heparin treatment, and a deficiency of an enzyme needed to produce aldosterone. In such cases, serum
aldosterone and plasma renin activity must be measured to establish the diagnosis.

Cortisol

Cortisol and the other glucocorticoid hormones are produced in the zona fasciculata and reticularis of the
cortex. Overproduction of glucocorticoids (cortisol) by the adrenal cortex is called Cushing's syndrome.
Excessive cortisol production leads to high blood glucose levels, sodium retention, obesity, and excessive
hair growth. Because cortisol production can suppress the immune system, excess levels may also cause
chronic infection in some patients.

The release of cortisol is controlled by circulating levels of a pituitary hormone, adrenocorticotropic

hormone (ACTH). In a complex process, the hypothalamus manufactures corticotropin-releasing hormone
(CRH), which, in turn, stimulates the pituitary gland to produce ACTH. While ACTH stimulates the
adrenal glands to produce cortisol, rising levels of cortisol act by negative feedback to inhibit further
production of CRH and ACTH. Disturbances in this elaborate feedback mechanism can be caused by
certain types of stress, such as physical trauma, infection, extreme heat or cold, exhaustion from
strenuous exercise, and extreme anxiety. When normal feedback becomes uncoordinated as a result of
one of these conditions, excessive amounts of ACTH and, in turn, cortisol will be released. For this reason,
cortisol levels in blood can vary considerably with time, a phenomenon called pulse variation.

Cushing's syndrome has four causes. The majority of cases result from the use of cortisol and related
compounds for immunosuppression and treatment of inflammatory diseases. This is called iatrogenic
hypercortisolism. The next most prevalent cause is Cushing's disease, also called pituitary Cushing's. This
results from adenomas of the pituitary gland that secrete ACTH. Less commonly, Cushing's syndrome is
caused by adrenal adenoma or carcinoma or by ACTH secreting tumors located outside the pituitary
(ectopic ACTH).

Primary Addison's disease results from damage to the adrenal cortex. The most common causes are
autoimmune disease and infection. Secondary Addison's disease is caused by a pituitary deficiency of
ACTH. These two conditions can often be differentiated by measuring both cortisol and ACTH. In primary
Addison's disease the ACTH will usually be increased because the functional pituitary gland is responding
to low blood levels of cortisol. In secondary Addison's disease, both cortisol and ACTH levels will be low.

Measurement

Cortisol is routinely measured by most laboratories. The most common method used is enzyme
immunoassay. Aldosterone levels are far lower and require a more sensitive method, typically
chemiluminescent immunoassay or radioimmunoassay. Measurement of cortisol intermediates such as 11-
dexoycortisol and 17-hydroxyprogesterone are used in conjunction with cortisol for the diagnosis of
congenital adrenal hyperplasia. In this condition, an enzyme deficiency in the synthetic pathway of cortisol
leads to low cortisol and accumulation of one or more steroid intermediates above the block. These
compounds are measured by RIA. ACTH is typically measured by RIA because of its low concentration in
plasma. Plasma renin is usually measured by determining the activity of the enzyme (renin activity) rather
than by immunoassay of the hormone mass because the latter method measures both the active and
inactive forms. In the assay, renin acts on angiotensinogen to produce angiotensin I, which is then
measured by RIA.

Adrenocortical hormone tests are typically performed on blood plasma or 24-hour urine samples. When
performed on blood, physicians may request that tests be performed on two samples, each drawn at a
different time, to account for fluctuations in hormone levels at different times during the day (diurnal
variation).

Tests for aldosterone are performed on blood plasma or on a 24-hour urine specimen. Levels of
aldosterone peak in early morning and are at half that level by afternoon, making the time of drawing a
blood sample significant. To help ensure a more reliable evaluation, two samples may be drawn for
testing, one in early morning (8 AM) and one mid-afternoon (4 PM). Diet and posture (upright or lying
down) may also cause aldosterone levels to fluctuate, so that a single blood sample may miss increased or
decreased levels and may not accurately reflect hormone production. Because a 24-hour urine specimen
reflects hormone production over an entire day, it will usually provide a more reliable aldosterone
measurement. Elevated blood levels should ideally be confirmed with a 24-hour urine test.

Since posture and body position affect aldosterone production, hospitalized patients should remain in an
upright position (at least sitting) for two hours before blood is drawn. Occasionally blood will be drawn
before

Normal findings for aldosterone assay

SOURCE: Pagana, K.D. and T.J. Pagana. Mosby's Diagnostic and Laboratory Test Reference. 3rd ed. St. Louis: Mosby, 1997.

Blood test

Supine Upright 3–10 ng/dl (0.08–0.30 nmol/L)

Adult female 5–30 ng/dl (0.14–0.80 nmol/L)

Adult male 6–22 ng/dl (0.17–0.61 nmol/L)

Newborn 5–60 ng/dl

1 week–1 year 1–160 ng dl

1–3 years 5–60 ng/dl

 Normal findings for aldosterone assay

3–5 years <5–80 ng/dl

5–7 years 5–70 ng/dl

7–11 years <5–50 ng/dl

11–15 years <5–50 ng/dl

24-hour urine test 2–80 μ g/24 hr (5.5–72.0 nmol/24 hr)