Professional Documents
Culture Documents
● Location. The C-shaped stomach is on the left side of the abdominal ● Location. The small intestine is a muscular tube extending from the
cavity, nearly hidden by the liver and the diaphragm. pyloric sphincter to the large intestine.
● Function. The stomach acts as a temporary “storage tank” for food as ● Size. It is the longest section of the alimentary tube, with an average
well as a site for food breakdown. length of 2.5 to 7 m (8 to 20 feet) in a living person.
○ Mixes saliva, food, and gastric juice to form chyme. ● Subdivisions. The small intestine has three subdivisions: the duodenum,
○ Serves as a reservoir for food before release into small intestine. the jejunum, and the ileum, which contribute 5 percent, nearly 40
○ Secretes gastric juice, which contains HCl, percent, and almost 60 percent of the small intestine, respectively.
pepsin, intrinsic factor, and gastric lipase . ● Ileocecal valve. The ileum meets the large intestine at the ileocecal
○ Secretes gastrin into blood. valve, which joins the large and small intestine.
● Cardiac region. The cardiac region surrounds the cardioesophageal ● Hepatopancreatic ampulla. The main pancreatic and bile ducts join at
sphincter, through which food enters the stomach from the esophagus. the duodenum to form the flasklike hepatopancreatic ampulla, literally,
● Fundus. The fundus is the expanded part of the stomach lateral to the the ” liver-pacreatic-enlargement”.
cardiac region. ● Duodenal papilla. From there, the bile and pancreatic juice travel
● Body. The body is the midportion, and as it narrows inferiorly, it becomes through the duodenal papilla and enter the duodenum together.
the pyloric antrum, and then the funnel-shaped pylorus. ● Microvilli. Microvilli are tiny projections of the plasma membrane of the
● Pylorus. The pylorus is the terminal part of the stomach and it is mucosa cells that give the cell surface a fuzzy appearance, sometimes
continuous with the small intestine through the pyloric sphincter or referred to as the brush border; the plasma membranes bear enzymes
valve. (brush border enzymes) that complete the digestion of proteins and
● Size. The stomach varies from 15 to 25 cm in length, but its diameter and carbohydrates in the small intestine.
volume depend on how much food it contains; when it is full, it can hold
PHASES OF DIGESTION
● During the cephalic phase of digestion, the smell, sight, thought, or initial
taste of food activates neural centers in the cerebral cortex,
hypothalamus, and brain stem. The brain stem then activates the facial
(VII), glossopharyngeal (IX), and vagus (X) nerves. The facial and
glossopharyngeal nerves stimulate the salivary glands to secrete saliva,
while the vagus nerves stimulate the gastric glands to secrete gastric
juice.
● The intestinal phase of digestion begins once food enters the small
intestine.
● The intestinal phase of digestion begins once food enters the small
intestine. Those occurring during the intestinal phase have inhibitory
effects that slow the exit of chyme from the stomach.
● Function. The teeth tear and grind the food, breaking it down into
smaller fragments.
● Deciduous teeth. The first set of teeth is the deciduous teeth, also called
baby teeth or milk teeth, and they begin to erupt around 6 months, and
a baby has a full set (20 teeth) by the age of 2 years.
● Permanent teeth. As the second set of teeth, the deeper permanent
teeth, enlarge and develop, the roots of the milk teeth are reabsorbed,
and between the ages of 6 to 12 years they loosen and fall out.
● Incisors. The chisel-shaped incisors are adapted for cutting. H. SALIVARY GLANDS
● Canines. The fanglike canines are for tearing and piercing. Three pairs of salivary glands empty their secretions into the mouth.
● Premolars and molars. Premolars (bicuspids) and molars have broad
crowns with round cusps (tips) and are best suited for grinding. ● Parotid glands. The large parotid glands lie anterior to the ears and
● Crown. The enamel-covered crown is the exposed part of the tooth empty their secretions into the mouth.
above the gingiva or gum. ● Submandibular and sublingual glands. The submandibular and
● Enamel. Enamel is the hardest substance in the body and is fairly brittle sublingual glands empty their secretions into the floor of the mouth
because it is heavily mineralized with calcium salts. through tiny ducts.
● Root. The outer surface of the root is covered by a substance called ● Saliva. The product of the salivary glands, saliva, is a mixture of mucus
cementum, which attaches the tooth to the periodontal membrane and serous fluids.
(ligament). ● Salivary amylase. The clear serous portion contains an enzyme, salivary
● Dentin. Dentin, a bonelike material, underlies the enamel and forms the amylase, in a bicarbonate-rich juice that begins the process of starch
bulk of the tooth. digestion in the mouth.
● Pulp cavity. It surrounds a central pulp cavity, which contains a number
of structures (connective tissue, blood vessels, and nerve fibers)
collectively called the pulp.
● Root canal. Where the pulp cavity extends into the root, it becomes the
root canal, which provides a route for blood vessels, nerves, and other
pulp structures to enter the pulp cavity of the tooth
Study for Teeth
● Location. Located under the diaphragm, more to the right side of the
body, it overlies and almost completely covers the stomach.
● Falciform ligament. The liver has four lobes and is suspended from the
diaphragm and abdominal wall by a delicate mesentery cord, the
falciform ligament.
● Location. The pancreas is a soft, pink triangular gland that extends across ● Function. The liver’s digestive function is to produce bile.
the abdomen from the spleen to the duodenum; but most of the ○ Carbohydrate metabolism.
pancreas lies posterior to the parietal peritoneum, hence its location is ○ Lipid metabolism.
referred to as retroperitoneal. ○ Protein metabolism.
● Pancreatic enzymes. The pancreatic enzymes are secreted into the ○ Processing of drugs and hormones.
duodenum in an alkaline fluid that neutralizes the acidic chyme coming ○ Excretion of bilirubin.
in from the stomach. ○ Synthesis of bile salts.
● Endocrine function. The pancreas also has an endocrine function; it ○ Storage for certain vitamins (A, B12, D, E, and K) and minerals (iron
produces hormones insulin and glucagon. and copper)
○ Phagocytosis.
○ Activation of vitamin D.
● Bile. Bile is a yellow-to-green, watery solution containing bile salts, bile
pigments, cholesterol, phospholipids, and a variety of electrolytes.
● Bile salts. Bile does not contain enzymes but its bile salts emulsify fats by
physically breaking large fat globules into smaller ones, thus providing
more surface area for the fat-digesting enzymes to work on.
ROLE AND COMPOSITION OF BILE
● Indigestion can result from disturbed nervous system control of the IX. Diagnostic Evaluation
stomach or from a disorder in the GI tract or elsewhere in the body.
● Common blood tests include complete blood count (CBC),
INTESTINAL GAS carcinoembryonic antigen (CEA), liver function tests, serum cholesterol,
and triglycerides.
● The accumulation of gas in the GI tract may result in belching or ● General nursing interventions for the patient who is having GI diagnostic
flatulence. assessment include the following:
NAUSEA AND VOMITING ● Providing general information about a healthy diet and the nutritional
factors that can cause GI disturbances; after a diagnosis has been
● Vomiting is usually preceded by nausea, which can be triggered by odors, confirmed, the nurse provides information about specific nutrients that
activity, or food intake. should be included in the diet.
● When vomiting occurs soon after hemorrhage, the emesis is bright red. ● Providing needed information about the test and the activities required
● If blood has been retained in the stomach, it takes on a coffee-ground of the patient
appearance because of the action of the digestive enzymes. ● Providing instructions about post procedure care and activity restrictions
● Alleviating anxiety
BOWEL HABITS AND STOOL CHARACTERISTIC ● Helping the patient cope with discomfort
● Encouraging family members or others to offer emotional support to the
● Diarrhea commonly occurs when the contents move so rapidly through patient during the diagnostic testing
the intestine and colon that there is inadequate time for the GI secretions ● Assessing for adequate hydration before, during, and immediately after
to be absorbed. the procedure
● Constipation may be associated with anal discomfort and rectal
bleeding. STOOL TEST
● Blood in the stool can present in various ways and must be investigated.
● Blood entering the lower portion of the GI tract or passing rapidly
through it will appear bright or dark red. ● Basic examination of the stool includes:
● Lower rectal or anal bleeding is suspected if there is streaking of ○ inspecting the specimen for consistency
blood on the surface of the stool. and color and testing for occult blood
● Other common abnormalities in stool characteristics include the ○ tests for fecal urobilinogen, fat, nitrogen,
following: ○ parasites, pathogens, food residues, and
○ Bulky, greasy, foamy stools that are foul in odor; stool color is gray, other substances
with a silvery sheen ● The most widely used occult blood test is the Hematest. False-positive
○ Light gray or clay-colored stool, caused by the absence of urobilin results may occur if the patient has eaten rare meat, liver, poultry,
○ Stool with mucus threads or pus that may be visible on gross turnips, broccoli, cauliflower, melons, salmon, sardines, or horseradish
inspection of the stool within 7 days before testing.
○ Small, dry, rock-hard masses called scybala; sometimes streaked ● Medications that can cause gastric irritation, such as aspirin, ibuprofen,
with blood from rectal trauma as they pass through the rectum indomethacin, colchicine, corticosteroids, cancer chemotherapeutic
○ Loose, watery stool that may or may not be streaked with blood agents, and anticoagulants, may also cause false-positive results.
● The patient lies supine with knees flexed slightly for inspection, ● The hydrogen breath test was developed to evaluate carbohydrate
auscultation, palpation, and percussion of the abdomen. absorption. It also is used to aid in the diagnosis of bacterial overgrowth
● The nurse performs inspection first, noting skin changes and scars from in the intestine and short bowel syndrome.
previous surgery. It also is important to note the contour and symmetry ● Urea breath tests detect the presence of Helicobacter pylori. The patient
of the abdomen, to identify any localized bulging, distention, or takes a capsule of carbon labeled urea and then provides a breath sample
peristaltic waves. 10 to 20 minutes later.
● Glucose Metabolism
○ The liver plays a major role in the metabolism of glucose
and the regulation of blood glucose concentration. After a
meal, glucose is taken up from the portal venous blood by
the liver and converted into glycogen, which is stored in the
hepatocytes.
● Ammonia Conversion
○ Use of amino acids from protein for gluconeogenesis
results in the formation of ammonia as a byproduct. The
liver converts this metabolically generated ammonia into ● Indigestion is present in varying degrees.
urea. Ammonia produced by bacteria in the intestines is ● Liver and spleen are often moderately enlarged for a few days after onset.
also removed from portal blood for urea synthesis. ● Patient may have an aversion to cigarette smoke and strong odors;
symptoms tend to clear when jaundice reaches its peak.
● Protein Metabolism ● Symptoms may be mild in children; in adults, they may be more severe,
○ The liver also plays an important role in protein metabolism. It and the course of the disease prolonged.
synthesizes almost all of the plasma proteins (except gamma- ASSESSMENT & DIAGNOSTIC METHODS
globulin), including albumin, alpha-globulins and beta-globulins, ● Stool analysis for hepatitis A antigen
● Serum hepatitis A virus antibodies; immunoglobulin
Hepatitis A
HEPATITIS E
HAV HepatItIs A virus; etiologic agent of hepatitis A formerly
● The hepatitis E virus is transmitted by the fecal-oral route, principally infectious hepatitis)
through contaminated water and poor sanitation.
● Incubation is variable and is estimated to range between 15 and 65 days.
In general, hepatitis E resembles hepatitis A. AntI-HAV Anybody to hepatitis A virus; appears in serum soon
● It has a self-limited course with an abrupt onset. Jaundice is almost always after onset of symptoms; disappears after 3-12 months
present. Chronic forms do not develop.
● The major method of prevention is avoiding contact with the virus IgM anti-HAV IgM antibody to HAV; indicates recent infection with
through hygiene (hand washing). The effectiveness of immune globulin in HAV; positive up to 6 months after infection
protecting against hepatitis E virus is uncertain.
HEPATITIS G Hepatitis B
ASSESSMENT FINDINGS: HBcAg Hepatitis B core antigen: found in liver cells: not
Preicteric stage (prodromal phase) = 1 week
- Anorexia (major manifestation), N&V, fatigue, constipation or easily detected in serum
diarrhea, weight loss
- RUQ discomfort, hepatomegaly, splenomegaly, lymphadenopathy Anti-HBc Antibody to hepatitis B core antigen; most sensitive
Icteric stage indicator of hepatitis B; appears late in the acute phase
- Fatigue, weight loss, light-colored stools, dark urine of the diseasel indicates infection of HBV at some time in
- Continued hepatomegaly with tenderness, lymphadenopathy, the past
splenomegaly
- Jaundice, pruritus
Posticteric stage IgM anti-HBc IgM antibody to HBcAg; present for up to 6 months after
- Fatigue, but an increased sense of well-being, hepatomegaly HBV infection
gradually decreasing
COLLABORATIVE MANAGEMENT
● Promotion of rest to relieve fatigue
Hepatitis D
Hepatitis E
Types
● Laênnec’s cirrhosis - associated with alcohol abuse and malnutrition;
HEV Hepatitis E virus; etiologic agent of hepatitis E characterized by an accumulation of fat in the liver cells, progressing to
widespread scar formation.
Hepatitis G ● Postnecrotic cirrhosis - results in severe inflammation with massive
necrosis as a complication of viral hepatitis.
● Cardiac cirrhosis - occurs as a consequence of RSHF; manifested by
hepatomegaly with some fibrosis.
HGV Hepatitis G virus; also known as GB virus C or GB-C ● Biliary cirrhosis - associated with biliary obstruction, usually in the
common bile duct; results in chronic impairment of bile excretion
ASSESSMENT:
● Anorexia, weakness, weight loss (liver is unable to metabolize nutrients
and store fat-soluble vitamins)
● Fever (in response to tissue injury)
● Jaundice, pruritus, tea colored urine (due to bilirubin in the blood)
- remember!!! bilirubin is conjugated initially before excretion
● Increased Bleeding tendencies. (liver is unable to store Vit. K.) There is
also impaired production of clotting factors)
● Portal HPN
PATHOLOGY
● In portal hypertension
Chronic, progressive disease characterized by inflammation, fibrosis, and - plasma shift into interstitial spaces within the liver due to the
degeneration of the liver parenchymal cells increase pressure. The collection of fluids shifts out of the Glisson’s
capsule and accumulate in the peritoneal cavity
● The liver is unable to metabolize protein, thereby hypoalbuminemia
occurs
- result to decreased oncotic pressure, fluids shift out of the IVC, and
accumulate in the peritoneal cavity.
● The liver is unable to excrete adrenal cortex hormone, one of which is
aldosterone
- Hyperaldosteronism leads to retention of sodium and water
● Esophageal varices = 2° to backpressure
● Internal hemorrhoids, leg varicosities, and dependent edema
- due to venous stasis, increasing hydrostatic pressure. This leads to
shifting of plasma into interstitial space
● Consequences of Portal HPN:
- Hepatomegaly= initially, then the liver shrinks in size as fibrosis
replaces the liver parenchyma
- Splenomegaly= due to increased backpressure of the blood
CLINICAL MANIFESTATIONS
● May be silent, producing no pain and only mild GI symptoms
● May be acute or chronic with epigastric distress (fullness, abdominal
distention, and vague upper right quadrant pain); may follow a meal rich
in fried or fatty foods
● If the cystic duct is obstructed, the gallbladder becomes distended,
inflamed, and eventually infected; fever and palpable abdominal mass;
biliary colic with excruciating upper right abdominal pain, radiating to
back or right shoulder with nausea and vomiting several hours after a
heavy meal; restlessness and constant or colicky pain
● Jaundice, accompanied by marked itching, with obstruction of the
common bile duct, in a small percentage of patients
● Very dark urine; grayish or clay-colored stool
● Deficiencies of vitamins A, D, E, and K (fat-soluble vitamins)
ASSESSMENT FINDINGS
● Cholecystitis, an acute complication of cholelithiasis, is an acute infection ● Most patients are asymptomatic.
of the gallbladder. Most patients with cholecystitis have gallstones ● When symptomatic; PAIN in RUQ and epigastric pain lasting
(calculous cholecystitis). A gallstone obstructs bile outflow and bile in the approximately 30 min.
gallbladder initiates a chemical reaction, resulting in edema, compromise ● Fever & leukocytosis (WBC)
of the vascular supply, and gangrene. In the absence of gallstones, ● Charcot triad
cholecystitis (acalculous) may occur after surgery, severe trauma, or - fever, jaundice, pain in RUQ pain (ascending cholangitis)
burns, or with torsion, cystic duct obstruction, multiple blood ● Intolerance for fatty foods (steatorrhea, N&V, sensation of fullness)
transfusions, and primary bacterial infections of the gallbladder. ● Pruritus, easy bruising, dark amber urine
● Infection causes pain, tenderness, and rigidity of the upper right DIAGNOSTIC TESTS
abdomen and is associated with nausea and vomiting and the usual signs ● Direct bilirubin transaminase, alkaline phosphatase, WBC, amylase,
of inflammation. lipase: all increased
● Purulent fluid inside the gallbladder indicates an empyema of the ● Oral cholecystogram (gallbladder series): positive for gallstone
gallbladder. ASSESSMENT & DIAGNOSTIC METHODS
● Cholecystogram, cholangiogram; celiac axis arteriography
● Laparoscopy
● Ultrasonography; EUS
● Helical CT scans and MRI; ERCP
● Serum alkaline phosphatase; gamma-glutamyl (GGT), gamma-glutamyl
transpeptidase (GGTP), LDH
● Cholesterol levels
GERONTOLOGIC CONSIDERATIONS
● Surgical intervention for disease of the biliary tract is the most common
operation performed in the elderly.
● Biliary disease may be accompanied or preceded by symptoms of septic
shock: oliguria, hypotension, mental changes, tachycardia, and
tachypnea.
● Cholecystectomy is usually well tolerated and carries a low risk if expert
assessment and care are provided before, during, and after surgery.
● Mortality from serious complications is high. Risk of complications and
shorter hospital stays make it essential that older patients and their
family members receive specific information about signs and symptoms
of complications and measures to prevent them.
NURSING INTERVENTION
● Administer pain medications as ordered and monitor for effects.
● Administer IV fluids as ordered.
● Provide small, frequent meals of modified diet, low fat (if oral intake
allowed)
● Provide care to relieve pruritus
● Provide care for the client with a cholecystectomy or choledochostomy
MEDICAL MANAGEMENT
● Major objectives of medical therapy are to reduce the incidence of acute
episodes of gallbladder pain and cholecystitis by supportive and dietary
management and, if possible, to remove the cause by pharmacotherapy,
endoscopic procedures, or surgical intervention
● Supportive treatment: NPO with NG intubation and IV fluids
● Diet modification with administration of fat- soluble vitamins
V. Adrenal Glands
- Although the adrenal gland looks like a single organ, it is structurally
and functionally two endocrine organs in one.
Hormones of the Anterior Pituitary Hormones of the Adrenal Cortex
There are several hormones of the anterior pituitary hormones that affect - The adrenal cortex produces three major groups of steroid
many body organs hormones, which are collectively called corticosteroids–
● Growth hormone (GH). Growth hormone is a general metabolic mineralocorticoids, glucocorticoids, and sex hormones.
hormone, however, its major effects are directed to the growth of ● Mineralocorticoids. The mineralocorticoids, primarily aldosterone, are
skeletal muscles and long bones of the body; it is a protein- sparing produced by the outermost adrenal cortex cell layer; mineralocorticoids
and anabolic hormone that causes amino acids to be built into proteins are important in regulating the mineral (or salt) content of the blood,
and stimulates most target cells to grow in size and divide. particularly the concentrations of sodium and potassium ions and
● Prolactin (PRL). Prolactin is a protein hormone structurally similar they also help in regulating the water and electrolyte balance in the
to growth hormone; its only known target in humans is the breast body.
because, after childbirth, it stimulates and maintains milk production ● Renin. Renin, am enzyme produced by the kidneys when the blood
by the mother’s breast. pressure drops, also cause the release of aldosterone by triggering a
● Adrenocorticotropic hormone (ACTH). ACTH regulates the endocrine series of reactions that form angiotensin II, a potent stimulator of
activity of the cortex portion of the adrenal gland. aldosterone release.
CLINICAL MANIFESTATIONS
● Polyuria: Enormous daily output of very dilute urine (specific gravity 1.001
to 1.005). Primary diabetes insipidus may have an abrupt onset or an
insidious onset in adults.
● Polydipsia: Patient experiences intense thirst, drinking 2 to 20 L of fluid
daily, with a special craving for cold water.
Polyuria continues even without fluid replacement.
● If diabetes insipidus is inherited, the primary symptoms may begin at
birth; in adults, onset may be insidious or abrupt.
ASSESSMENT & DIAGNOSTIC FINDINGS
● Fluid deprivation test: Fluids are withheld for 8 to 12 hours until 3% to 5%
of the body weight is lost.
● Inability to increase specific gravity and osmolality of the urine during test
is characteristic of diabetes insipidus. ● A butterfly-shaped organ, the thyroid gland is located anterior to the
● Other diagnostic procedures include concurrent measurements of trachea, just inferior to the larynx. The medial region, called the isthmus,
plasma levels of ADH and plasma and urine osmolality as well as a trial of is flanked by wing-shaped left and right lobes. Each of the thyroid lobes
desmopressin (synthetic vasopressin) therapy and intravenous (IV) are embedded with parathyroid glands, primarily on their posterior
infusion of hypertonic saline solution. surfaces.
MEDICAL MANAGEMENT ● The tissue of the thyroid gland is composed mostly of thyroid follicles.
● The objectives of therapy are (1) to replace ADH (which is usually a long- The follicles are made up of a central cavity filled with a sticky fluid called
term therapeutic program), (2) to ensure adequate fluid replacement, colloid. Surrounded by a wall of epithelial follicle cells, the colloid is the
and (3) to identify and correct the underlying intracranial pathology. center of thyroid hormone production, and that production is dependent
Nephrogenic causes require different management approaches on the hormones' essential and unique component: iodine.
PHARMACOLOGIC THERAPY ● The thyroid gland is located in the neck where it wraps around the
● Desmopressin (DDAVP), administered intranasally, one or two trachea. (a) Anterior view of the thyroid gland. (b) Posterior view of the
administrations daily to control symptoms. thyroid gland. (c) The glandular tissue is composed primarily of thyroid
● Intramuscular administration of ADH (vasopressin tannate in oil) every 24 follicles. The larger parafollicular cells often appear within the matrix of
to 96 hours to reduce urinary volume (shake vigorously or warm; follicle cells.
● Hormones are produced in the colloid when atoms of the mineral iodine
attach to a glycoprotein, called thyroglobulin, that is secreted into the
colloid by the follicle cells. The following steps outline the hormones'
assembly:
1. Binding of TSH to its receptors in the follicle Left inferior thyroid
cells of the thyroid gland causes the cells to artery actively
transport iodide ions (I-) across their cell membrane. from the
bloodstream into the Fromleftsubclaviar cytosol. As a result, the
concentration of iodide ions "trapped" in the follicular cells is many
times higher than the concentration in the bloodstream.
2. Iodide ions then move to the lumen of the follicle cells that border
the colloid. There, the ions undergo oxidation (their negatively
charged electrons are removed). The oxidation of two iodide ions
(2 I-) results in iodine (12), which passes through the follicle cell
membrane into the colloid.
3. In the colloid, peroxidase enzymes link the iodine to the tyrosine
amino acids in thyroglobulin to produce two intermediaries: a
tyrosine attached to one iodine and a tyrosine attached to two
iodines. When one of each of these intermediaries is linked by
covalent bonds, the resulting compound is triiodothyronine (T3), a
thyroid hormone with three iodines. Much more commonly, two
copies of the second intermediary bond, forming
tetraiodothyronine, also known as thyroxine (T4), a thyroid
hormone with four iodines.
● These hormones remain in the colloid center of the thyroid follicles until
TSH stimulates endocytosis of colloid back into the follicle cells. There,
lysosomal enzymes break apart the thyroglobulin colloid, releasing free
T3 and Ta, which diffuse across the follicle cell membrane and enter the
bloodstream.
● In the bloodstream, less than one percent of the circulating T3 and Ta
remains unbound. This free Ts and T4 can cross the lipid bilayer of cell
membranes and be taken up by cells. The remaining 99 percent of
circulating T3 and T4 is bound to specialized transport proteins called ● Interrelationship with reproductive hormones, and deficiencies can
thyroxine-binding globulins (TBGs), to albumin, or to other plasma
proteins. This "packaging" prevents their free diffusion into body cells. influence libido, fertility, and other aspects of reproductive function. Finally,
When blood levels of T3 and T4 begin to decline, bound T3 and T4 are thyroid hormones increase the body's sensitivity to catecholamines
released from these plasma proteins and readily cross the membrane of (epinephrine and norepinephrine) from the adrenal medulla by
target cells. T is more potent than T4, and many cells convert T4 to T3
upregulation of receptors in the blood vessels. When levels of T3 and T4
through the removal of an iodine atom.
hormones are excessive, this effect accelerates the heart rate, strengthens
REGULATION OF TH SYNTHESIS the heartbeat, and increases blood pressure. Because thyroid hormones
regulate metabolism, heat production, protein synthesis, and many other
● The release of T3 and T4 from the thyroid gland is regulated by thyroid-
body functions, thyroid disorders can have severe and widespread
stimulating hormone (TSH). As shown in Figure 2, low blood levels of T3 and
consequences.
T4 stimulate the release of thyrotropin-releasing hormone (TRH) from the
hypothalamus, which triggers secretion of TSH from the anterior pituitary. HYPERTHYROIDISM
In turn, TSH stimulates the thyroid gland to secrete T3 and T4. The levels of
TRH, TSH, T, and T4 are regulated by a negative feedback system in which
increasing levels of Ts and T4 decrease the production and secretion of TSH.
Diagnostic Tests:
● T3/ T4 levels
- ↑ level: hyperthyroidism
- ↓ level: hypothyroidism
● PBI (Protein-bound Iodine) GOITER
﹘ Preparation:
○ No foods, drugs, test dyes with iodine 7-10 days before the ● Enlargement of the thyroid gland associated with hyperthyroidism,
test hypothyroidism or euthyroidism
● RAIU (Radioactive Iodine Uptake) ● A hyperthyroid goiter is called toxic goiter
﹘ Tracer dose of I131 is used P.O. & at 2°, 6°, and 24° exposure to
scintillation camera is done
﹘ No foods, drugs, test dyes with iodine 7-10 days before the test,
temporarily discontinue contraceptive pills (these may metabolic
rate)
﹘ Result:
○ ↑ iodine uptake: hyperthyroidism
○ ↓ iodine uptake: hypothyroidism
Hyperthyroidism (Thyrotoxicosis)
- Dexamethasone
○ inhibit the action of thyroid hormones
○ prevent the conversion of T4 to T3 in the peripheral tissues
● Hyperthyroidism: Management
- Rest (non-stimulating cool environment)
- Diet
○ HIGH Calorie, HIGH protein; vitamin and mineral supplement
○ Increased fluid intake (if with diarrhea)
○ Replace F&E losses
○ Avoid stimulants like coffee, tea and nicotine
- Promote safety
- Protect the eyes - Radiation therapy (Iodine131)
○ Artificial tears at regular intervals ○ Need isolation for few days; body secretions are radioactive
○ Wear dark sunglasses when going out under the sun contaminated
● Pharmacotherapy ○ NOT recommended in pregnant women because of potential
- ß-blockers: Propranolol teratogenic effects. Pregnancy should be delayed for 6
- Ca++ channel blockers months after therapy
○ These drugs are given to control tachycardia and HPN - Surgery
○ Subtotal Thyroidectomy- Usually about 5/6 of the gland is
removed
Hypothyroidism
- Paracetamol for fever
○ Aspirin must be avoided because it can displace the T3/T4 - results from deficiency of thyroid hormones
from the albumin in the plasma causing increased
manifestations