PO1 MARK KENNETH N. FERNANDEZ, RN, MAN

Pituitary gland

Adrenal gland

Thyroid gland

Parathyroid gland

Islets cells of the pancreas

Gonads

HORMONES- Natural chemicals that exert their effects of a specific tissue

TARGET TISSUE - usually located at a distance from the endocrine gland w/ no direct connection bet the endocrine gland & target tissue.

ENDOCRINE GLANDS - “ductless glands”

Hypothalamus & Pituitary. Together they control many

endocrine functions

Hypothalamus When stimulated by

feedback produces releasing factors (RF) that stimulates the pituitary to release hormones

Pituitary gland The master gland of the

body

The primary function of the endocrine glands is to regulation of overall body function.

The body must maintain a homoeostasis to respond to environmental changes. Temperature regulation Serum sodium levels

As hormones travel through the body, they can only recognize their target tissue. Each receptor site type is specific to only one hormone.

Only the correct hormone can connect to the correct receptor.

Once the hormone binds to the site the target tissue will change the tissues activity.

Disorders of the endocrine system are related to either excess or deficiency of a specific hormone or to a defect at its receptor site.

ONSET Slow or insidious Abrupt or life threatening

Endocrine Gland

Hormones Endocrine Disorders

Hyper Hypo

Anterior Pituitary

Growth Hormone Gigantism, acromegaly

Dwarfism

Thyroid Thyroxine (T4)Triodothronine T3)

ThyrotoxicosisGoitreExopthalmos

HypothroidismCretinismMyxoedemaGoitre

Parathyroid Parathormone OsteoporosisKidney stones

Kidney stonesTetany

Adrenal Cortex

Glucacorticoids Cushings syndrome

Addisons disease

Adrenal Medulla

Epinephrine Norepinephrine

Increased metabolismHypertension

Pancreatic Islets

Insulin Diabetes mellitus

Major endocrine conditions

THYMUS Thymosin

HYPOTHALAMUS

Corticotropin-releasing hormone Thyrotropin releasing hormone Gonadotropin releasing hormone Growth hormone releasing hormone Growth inhibiting hormone Prolactin inhibiting hormone Melanocyte inhibiting hormone

Principal hormones of the endocrine glands

Anterior & posterior pituitary gland

ANTERIOR PITUITARY

Thyroid stimulating hormone

Adrenocorticotropic hormone

Luteinizing hormone

Follicile stimulating hormone

Growth hormone

Melanocyte stimulating hormone

Principal hormones of the endocrine glands

Posterior pituitary Vasopressin Oxytocin Triiodothyronine

(T3) Thyroxine (T4) Calcitonin

Principal hormones of the endocrine glands

THYROID GLAND

Thyroxine (T4) –

precursor

Triiodothyronine (T3) –

active hormone

PARATHYROIDParathyoid hormone

ADRENAL GLANDS

The medulla secretesEpinephrineNorepinephrine

The cortex secretesGlucocorticoidsMineralocorticoidsAndrogens

OVARY

Estrogen Progesterone

TESTES

testosterone

PANCREAS

InsulinGlucagonsomatostatin

Hormone secretion is dependant on the need of the body for the final action of that hormone.

When the body moves away from homeostatis a specific change or action is required or a response is needed to correct the change.

Supply and demand

Blood sugar increase to above 120, hormone insulin is secreted

Insulin increases glucose uptake by the cells, causing a decrease in the blood glucose.

Main action-insulin decreased the elevated blood sugar.

HypothalamusSmall area of nerve and glandular tissue

located beneath the thalamus on each side of the third ventricle of the brain.

Shares a small closed circulatory system with the anterior pituitary

Known as the hypothalamic-hypophysial portal system

Hormones can travel directly to the anterior pituitary

PITUITARY GLANDThe hypothalamus and the pituitary work

together.

The hormones of posterior Pituitary are produced in the hypothalamus and are sent through the portal system

▪ The hormones are stored in the nerve endings of the posterior Pituitary and are released into the blood when needed.

The pituitary hormone is responsible for many hormones and subsequent target tissues and actions.

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GONADS

Male and female reproductive endocrine glands.

Male gonads are the testesFemale gonads are the ovariesThese glands are present at birth

but do not begin to function until puberty

ADRENAL GLANDS They are vascular and tent shaped

organs on top of the kidneys Outer portion-cortex Inner portion-medulla Each area works independently

Adrenal cortex is 90% of the adrenal gland.

Mineralocorticoids are produced in the cortex

Adrenal steroids and corticosteriods are produced in the cortex

MINERALCORTICOIDS

Aldosterone-chief mineralocortoidMaintains extracellular fluid volmePromotes sodium and water reabsorption and potassium excretion

Aldosterone secretion is controlled by renin angiotensin system, ACTH, and potassium

GLUCOCORTICOIDS

Cortisol is secreter from the adrenal cortex

Cortisol affectsCarbohydrate, protein, and fat metabolism

Emotional stabilityImmune function

ADRENAL MEDULLA

Sympathetic nerve ganglion that has secretory cells.

Releases catacholamines including epinephrine and norepinephrine.

Not essential for life, however plays a role in stress response.

THYROID GLAND

Found in the anterior neck below the

cricoid cartilage.

Rich in blood supply

Produce hormones t3 and t4

Function of the thyroid gland

Fetal developmentControl metabolic rate of all cellsRegulate fat, carbohydrate, and protein

productionIncrease red blood cell productionProduces calcitonin-lowers calcium and

phosphorus levels by reducing bone breaksdown.

PARATHYROID GLAND Consists of four small glands located on

the back of the thyroid gland. Chief cell of this gland production and

secretion of PTH Regulates calcium and phosphorus

metabolism by acting on the bone, kidneys and intestinal tract.

Serum calcium is the major controlling factor of PTH.

PANCREAS

The Islets have three cell types.

Alpha-secrete glucagonBeta-secrete insulinDelta- secrete somatostatin

The main endorcrine function is to regulate blood sugar.

Glucagon is the hormone the increase blood sugars

The liver is the main target tissue for glucagon and it causes glycogenolysis-conversion of glycogen to glucose.

Gluconeogensis-conversion of amino acids to glucose. This enhances the transport of amino acids to the muscle.

Insulin

Anabolic hormone, promotes the movement and storage of carbohydrates, protein and fat.

Lowers blood glucose levels by enhancing glucose movement across the cell membrane.

HypopituitarismHyperpituitarism

Adenohypophysis-controls growth, metabolic activity and sexual development.

GH, PROLACTIN, TSH, AdrenoCorticoTropin (ACTH), FSH, LH, MSH

Disorders arise when the anterior pituitary does not work effectively or when the hypothalamus is not work effectively.

(Primary pituitary dysfunction vs. secondary pituitary dysfunction)

If a person has hypopitutarism, the patient will exhibit deficiencies in one or more hormones. In rare cases, panhypopituitarism is present.

(Decreased hormone production from the anterior pituitary)

Deficiencies in ACTH and TSH are the most life threatening as the correspond to vital hormones from the adrenal gland and thyroid gland. The other hormones from the gonads LH and FSH interfere with sexual reproduction.

GH deficiency changes tissue growth although it is indirect.

In GH deficiencies in adults Accelerate bone destruction and

osteoporosis In GH deficiencies in children

Small stature, growth retardation

Anorexia nervosaBenign or malignant tumors of

pituitaryPostpartum hemorrhageSheehan’s syndrome

GH Decreased bone density Fractures Decreased muscle strength

Gonatropins-women Amenorrhea Anovulation Low estrogen levels Breast atrophy Decreased libido

Gonatropins-male Decreased facial hair Reduced muscle mass Impotence Decreased body hair Loss of bone density

Thyroid stimulating hormone (TSH) Weight gain Intolerance to cold Menstrual abnormalities Slow cognition lethargy

Andrenocorticotropin-ACTH Decreased serum cortisol levels Pale sallow skin Headache Hypoglycemia hyponatremia

Stimulation test Usually involve injecting agents that are

known to stimulate secretion of specific pituitary hormones.

Skill x ray CT scan MRI

Replacement of defiecient hormone Androgens▪ Avoid in men with prostate cancer

▪ Women will be given a combination of estrogen and progesterone.▪ Gonadatropin releasing hormone and human

gonadatropin are used to stimulate ovulation

Oversecretion usually caused by pituitary tumor of hyperplasia

RareCan cause gigantism or acromegaly.

Gigantism-onset of GH hypersecretion occurs before puberty

Andre the GIANT stood 7 feet tall and died at 46. He did not treat his disease. Excessive secretion of GH occurs after puberty

Facial feature abnormalitiesProganthismChanges to visionOrganmegalyHypertensionDysphagiaDeepened voice

Laboratory - blood exam to determine which hormone is excessively secreting.

CT scan MRI Suppression test - eg, dexamethasone

suppression test, used to determine whether a substance–hormone or protein being produced in excess is under the control of regulating or releasing factor

Drug therapy

Dopamine agonist

ParlodelDostinex

Both of these drugs stimulate theProduction of dopamine and inhibit

the release of GH and PRL

Somatostatin analogues Octreotide-inhibits GH release Somavert-growth hormone blocker

Radiation therapyTakes a long time to be effectiveNot immediate is acute situationsSide effectsOptic nerve damage

Preop : Education, education, education

OperativeUse of a microscopemakes incision in upper lipgraft taken from thigh to prevent leak in

CSF

Postoperative- Vital signs and:

Monitor neurologic statusMonitor fluid balance (transient diabetes

insipidus)Instruct client not to sneeze, cough, blow

nose.Encourage deep breathing exercisesMonitor pad for nasal dripInstruct patient to use dental floss and oral

rinse. Brushing teeth is not permitted.ita

Diabetes insipidusSyndrome of Inappropriate

Antidiuretic hormone

DI- a water metabolism problem caused by the ADH inablilty to synthesize or the inability of the kidneys to act in response to ADH.

Characterized by excessive diuresis

1. Nephrogenic-inherited

2. Primary-defect in the hypothalamus or pituitary gland

3. Drug related- Lithium

HypotensionDecreased pulse pressureTachycardia Increased Hbg,hct and BUN Increased UOPPoor skin turgor IrritabilityDecreased cognitionHyperthermiaLethargy leading to coma

Primary management is with medications.

LypressinDDAVPPitressinDiabinese

Case study- 77 year old female is taken to the ER for a fall at home.

Assessment reveals: Awake, alert and oriented Complains of pain to right hip. She has a history of hypertension and

asthma. EKG shows NSR CBC

wbc 9.4rbc 3.9hgb 12.1hct 39.0

BMP Glucose 92 BUN 18 Cr 1.1 NA 130 K 4.2 CO2 37 Cl 97 Pulse ox 94% on RA VS 98.6, 84, 18, 156/93

Ms. Mills undergoes a THA without complications.

IV solution is D51/2NS at 100ml/hrMSO4 PCA basal 1mg/hr with

demand of 1mg every 10 minutes

Ms. Mills is lethargic and confused Nausea Up to chair times 1 IV solution in increased to 125ml/hr. Inspiratory and expiratory wheezes with

treatments that are not effective, O2 sats are 88 % on 2 Liters

Moved to ICU for observation of respiratory status.

What is Ms. Mills suffering from?

Explain the pathophysiology

Na 116 K 3.5 Cl 86 BUN 9 Cr .8 Glucose 126 Hgb 9.1 Hct 27 Serum Osmolality 243 Urine Osmolality 541

A Swan-Ganz catheter is inserted to measure fluid and electrolyte and cardiac status.

What is the role of ADH on water regulation?

What are the major effects on organs?

As the RN what would you expect the MD to change or modify for Ms. Mills medical management?

What is the purpose of the serum and urine osmolality tests?

Ms. Mills still remains confused but her respiratory status has improved.

Twenty four hours later her lab shows Na 132 K 3.2 Cl 98 Serum osmolality 275 Urine osmolality 400

At this time her IV solution is changed to D5 NS at 50 ml/hr. She is weaned off the oxygen and is alert awake and oriented.

Vitals show 99.2 100 20 130/78

What other orders would expect from the MD at this time?

Ms Mills was transferred to a rehab unit for physical therapy and eventually moved back home.

Discuss two other sodium disorders that must be differientaited from SIADH?

Why are elderly more prone?

What are factors that contributed to the development of SIADH in Ms. Mills

Fluid volume excess related to compromised regulatory mechanism and intravenous overload.

Altered though process related to cerebral edema

Acute adrenal insufficiency or Addisonian

insufficiency (or Hypocortisolism).

DEF: a condition in which the adrenal glands ,

do no produce adequate amounts of steroid

hormones , primarily cortisol, but may alsoInclude impaired aldosterone production

Hypothalamic-pituitary-adrenal axis. (CRH = corticotropin-releasing hormone; ACTH = adrenocorticotropin hormone)

Acute adrenal insufficiency or Addisonian

insufficiency (or Hypocortisolism)Craving for salt or salty foods due to the

urinary losses of sodium is commonLife threateningCortisol and aldosterone needs are

greater than the supplyRelated to stress, trauma, severe

infection

Usually occurs with progressive destruction of the adrenal

gland. Classic symptoms are weakness, fatigue, anorexia

with nausea vomiting, and diarrhea. ETIOLOGY: Autoimmune disease Tuberculosis, Fungal lesions, AIDS Hemorrhage (Adrenal) Adrenalectomy Radiation

usually occurs when there is a glucocortioid deficiency and a result of hypothalamic-pituitary-adrenal axis. It is associated with reduced amounts of ACTH

ETIOLOGY Pituitary hormones Hypophysectomy High dose pituitary radiation Brain radiation

(3) MAIN GOALS:

1.Hormone replacement

2.Hyperkalemia management

3.Hypoglycemia management

1.Replacement of fluid volume and correction of electrolytes.

2.Hyperkalemia responds to volume expansion and glucocortroid replacement. Decadron or solucortef

3.Give D50 and insulin to shift potassium back into cells

4.Administer kayexalate

5.Give diuretics

6.Monitor I/O

7.Administer IV glucose if warranted

Complete Metabolic panel

Urine analysis

CT, MRI, skull x ray

ACTH stimulation (Cosyntropin test, Tetracosactide test or Synacthen test)

HydrocortisoneCorrects glucocorticoid deficiency

Florinef , a mineralo-corticoid, maintains electrolyte balance

The adrenal gland may oversecrete one or more of the adrenal hormones

AKA Cushing’s syndrome, Cushing disease or hyperaldosteronism - excessive mineralocorticoid production

s/s Cushing’s disease (hypercortisolism)

Problems with nitrogen, carbohydrate and mineral metabolism.

Slow turnover is of plasma fatty acids“Buffalo hump”High levels of corticosteroids decrease

immunity by destroying lymphocytes.Increased androgen production causes

hirutism

HIRSUTISM

ENDOGENOUS (Cushing disease)Adrenal hyperplasiaAdenomaCarcinomas

EXOGENOUS (Cushing Syndrome)AsthmaAutoimmune disordersOrgan transplantsCancer chemoAllergic responsesFibrosis

Moon faceBuffalo humpWeight gainHypertensionMuscle atrophyPaper like skinHyperpigmentation Increased risk for infectionElevated blood sugars

Moon face

Exaggerated weight gain

Hyperpigmentation Striae

Facial Phletora

Patient will haveInc. BSDec. lymph countInc. sodiumDec. calciumDec. potassium

How does this compare to Addison’s disease?

Urine analysis

CT, MRI

Overnight dexamethasone testing3 day low dose testing.8 day high dose testing

Drug therapy Lysodren Elipten

Radiation therapyTreats pituitary adenomas

SurgeryRemoval of tumor or pituitary itself

Increased secretion of aldosterone which results in mineralcorticoid excess

Most often caused by adrenal adenoma (primary hyperaldosteronism)

Elevated levels of angiotensin II are seen in secondary hyperaldosteronism

A steroid hormone produced exclusively in the zona glomerulosa of the adrenal cortex.

The major circulating mineralocorticoid in humans.

Principal regulators of its synthesis and secretion are the renin-angiotensin system and potassium ion concentrations.

Minor regulators: ACTH from the pituitary, atrial natriuretic peptide from the heart, & local adrenal secretion of dopamine

Hypokalemia and elevated BPHeadacheFatigueNocturiaPolydipsiaPolyuriaparesthesias

UA specific gravityBMPCTMRI

Surgery for early stage

Drug therapy Medication to increase K+ -

Potassium supplements

Catecholamine producing tumor that arises in chromaffin cells.

Occurs in a single lesion on adrenal gland

Releases epinephrine and norepinephrine

Cause is unknown occur more in women then men.

Could be inherited

Symptoms

Intermittent HPN- classic sign

Abdominal pain Chest pain Irritability, Nervousness Pallor palpitation , rapid HR Severe headache Sweating Weight loss

Other symptoms that can occur with this

disease:

Hand tremorSleeping difficulty

Drugs may induce hypertensive crisis

24-hr UA to test for VMA (vanillylmandelic acid) a production of catecholamine metabolism)

CT

MRI

Surgery- one or both of the adrenal glands are removed.

Monitor BP and treat if hypertensive crisis

Hydrate

Most common liver function tests are ALT GGT AST Globulins Ammonia Cholesterol

Bilirubin concentration in the blood is abnormally elevated, all the tissues become yellow, green in color.

Becomes clinically evident with serum bilirubin levels above 2.3mg/dl

Hemolytic jaundice- increased destruction of the red blood cells

Found in pts with hemolytic transfusion reactions,

Hepatocellular jaundice- inability of damaged liver cells to clear normal amounts of bilirubin from the blood. Usually caused by hepatitis disease, yellow disease or Mononucleosis.

Patients with Hepatocellular jaundice may be mildly ill or severely ill.

Patient presents with lack of appetite, nausea, fatigue, weakness, and weight loss.

Obstructive jaundice- extrahepatic obstruction caused by an occlusion to the bile duct from a gall stone, tumor, or inflammatory process.

Hereditary hyperbilirubinemia- increased serum bilirubin levels resulting from inherited disorders. (Gilbert’s syndrome, Dubin-Johnson and Rotor’s syndrome).

Obstructed blood flow through the damaged liver results in increased pressure throughout the portal venous system.

Associated with hepatic cirrohosis

The pathophysiology of ascites is not clear. As a result of liver damage, large amounts of albumin rich fluid accumulate in the peritoneal cavity.

Clinical symptomsIncreased abdominal girthRapid weight gainShortness of breathAdominal striaeDistended veins over the abdominal wall.

Dietary modificationsDiureticsBed restParacentesisTransjugular intrahepatic

protosystemic shunt

Dilated vein that are found in the submucosa of the lover esophagus or extend into to the stomach.

Clinical manifestations Bleeding▪ Hemataemesis▪ Melena▪ Signs and symptoms of hypovolemic

shock

• Upper endoscopy• Portal Hypertension measurements• Laboratory tests

• Medical managementManage bleeding

Balloon tamponade

Sclerotherapy

Pharmacological intervention Vasopressin with nitroglycerin Inderal Corgard

Esophageal banding therapy-the varies are banded by using a modified endoscope loaded with elastic rubber band that is slipped over the varies.

Transjugular intrahepatic portosystemic shunting- TIPS

A life threatening complications of liver disease occuring with profound liver failure and results in high levels of ammonia circulating in the blood.

Clinical manifestationsMinor mental changes ( early phases)Motor dysfunctionAlterations in mood and sleepAsterixis( flapping tremor to hands)

EEG to determine level of brain waves

Patient are usually referred for aliver transplant after their first episode of encephalopathy.

Medical management Lactulose-reduce the amount of

ammomina in body.

Numerous amounts of hepatitisHep AHep BHep CHep DHep EHep G

Epidemiology

Hepatitis A Hepatitis B Hepatitis C Hepatitis D Hepatitis E

Cause Virus (HAV) Virus (HBV) Virus Virus Virus

(HCV) (HDV) (HEV)

Mode of Transmission

Fecal Oral Route

Parenterally Blood Parenterally Fecal Oral Route

Incubation 15-50 days 28-160 days 15-160 days 21-140 days 15-65 days

S/S Flu like symptoms

Rash Rash Rash joint pain

Flu like symptoms, severe in pregnant woment

Bed rest during acute stagesPatient teachingPrevention

A chronic disease characterized by repacement of normal liver tissue with diffuse fibrosis that destroy the structure and function of the liver.

Types of cirrhosis Alcoholic cirrhosis Postnecrotic cirrhosis Biliary cirrhosis

Liver enlargementPortal obstruction and ascites Infection PeritonitisVariesEdemaVitamin DeficiencyMental deterioration

Known as a solid organ liver transplant (OLTX).

Used as last resort to treat end stage liver disease

Immunosuppression is required for lifetime Prograf, Imuran, OKT3, cyclosporine

Can take from 5-10 hours due to the large amount of ligation to venous collateral vessels.

Blood loss can be great

Straight to ICU with hemodynamic monitoring.

Complications Bleeding Rejection Infection

Few hospitals in United States are sites for OLTX,UNMC, UCLA, Univ of Pittsburgh, Duke are noted as the best in the nation.