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

GLANDS - ductless

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

Major endocrine conditions

Endocrine
Gland

Hormones

Endocrine Disorders
Hyper

Hypo

Anterior
Pituitary

Growth Hormone

Gigantism,
acromegaly

Dwarfism

Thyroid

Thyroxine (T4)
Triodothronine T3)

Thyrotoxicosis
Goitre
Exopthalmos

Hypothroidism
Cretinism
Myxoedema
Goitre

Parathyroid Parathormone

Osteoporosis
Kidney stones

Kidney stones
Tetany

Adrenal
Cortex

Glucacorticoids

Cushings
syndrome

Addisons disease

Adrenal
Medulla

Epinephrine
Norepinephrine

Increased
metabolism
Hypertension

Pancreatic
Islets

Insulin

Diabetes mellitus

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
Anterior & posterior pituitary gland

the endocrine
glands

Principal
hormones of

ANTERIOR PITUITARY
Thyroid stimulating hormone

the endocrine
Adrenocorticotropic hormone
glands
Luteinizing hormone
Follicile stimulating hormone
Growth hormone
Melanocyte stimulating hormone

Principal hormones of
the
Posterior
endocrine glands
pituitary

Vasopressin
Oxytocin
Triiodothyronine

(T3)
Thyroxine (T4)
Calcitonin

 THYROID

GLAND

Thyroxine (T4)

precursor
Triiodothyronine (T3)

active hormone

 PARATHYROID

Parathyoid hormone

ADRENAL GLANDS

The medulla secretes

Epinephrine
Norepinephrine

The cortex secretes

Glucocorticoids
Mineralocorticoids
Androgens

 OVARY
Estrogen
Progesterone

 TESTES

testosterone

 PANCREAS
Insulin
Glucagon
somatostatin

 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.

 Hypothalamus
Small 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

GLAND
The 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 testes
Female gonads are the ovaries
These 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 mineralocortoid

Maintains extracellular fluid volme

Promotes 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 affects
Carbohydrate, protein, and fat
metabolism
Emotional stability
Immune 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 development
Control metabolic rate of all cells
Regulate fat, carbohydrate, and protein

production
Increase red blood cell production
Produces 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 glucagon
Beta-secrete insulin
Delta- 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 glycogenolysisconversion 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.

Hypopituitarism
Hyperpituitarism

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 nervosa
Benign or malignant

tumors of

pituitary
Postpartum hemorrhage
Sheehans 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
Rare
Can 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 abnormalities

Proganthism
Changes to vision
Organmegaly
Hypertension
Dysphagia
Deepened 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 substancehormone or protein
being produced in excess is under the
control of regulating or releasing factor

 Drug

therapy

Dopamine agonist

Parlodel
Dostinex

Both of these drugs stimulate the

Production of dopamine and inhibit
the release of GH and PRL

 Somatostatin

analogues
Octreotide-inhibits GH release
Somavert-growth hormone blocker

Radiation

therapy
Takes a long time to be effective
Not immediate is acute situations
Side effects
Optic nerve damage

 Preop

: Education, education, education

Operative
Use of a microscope
makes incision in upper lip
graft taken from thigh to prevent

CSF

leak in

Postoperative- Vital signs and:

Monitor neurologic status
Monitor fluid balance (transient diabetes

insipidus)
Instruct client not to sneeze, cough, blow
nose.
Encourage deep breathing exercises
Monitor pad for nasal drip
Instruct patient to use dental floss and oral
rinse. Brushing teeth is not permitted.ita

 Diabetes insipidus
Syndrome 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

 Hypotension
Decreased pulse pressure
Tachycardia
Increased Hbg,hct and BUN
Increased UOP
Poor skin turgor
Irritability
Decreased cognition
Hyperthermia
Lethargy leading to coma

 Primary

management is with
medications.
Lypressin
DDAVP
Pitressin
Diabinese

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 9.4
rbc 3.9
hgb 12.1
hct 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/hr
MSO4 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 theadrenal
glands ,
do no produce adequate amounts
ofsteroid
hormones, primarilycortisol, but may also
Include impairedaldosteroneproduction

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 common
Life threatening
Cortisol and aldosterone needs are
greater than the supply
Related 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
5.Give

kayexalate

diuretics

6.Monitor

I/O

7.Administer

IV glucose if warranted

 Complete
Urine
CT,

Metabolic panel

analysis

MRI, skull x ray

ACTH

stimulation (Cosyntropin test,

Tetracosactide test or Synacthen
test)

 Hydrocortisone
Corrects glucocorticoid

deficiency

Florinef , a mineralo-corticoid,
maintains electrolyte balance

 The

adrenal gland may oversecrete

one or more of the adrenal hormones

AKA

Cushings syndrome,
Cushing disease or
hyperaldosteronism - excessive
mineralocorticoid production

 s/s

Cushings 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 hyperplasia
Adenoma
Carcinomas
EXOGENOUS (Cushing Syndrome)
Asthma
Autoimmune disorders
Organ transplants
Cancer chemo
Allergic responses
Fibrosis

 Moon face
Buffalo hump
Weight gain
Hypertension
Muscle atrophy
Paper like skin
Hyperpigmentation
Increased risk for infection
Elevated blood sugars

Moon face

Exaggerated weight gain

Hyperpigmentation

Striae

Facial Phletora

 Patient

will have
Inc. BS
Dec. lymph count
Inc. sodium
Dec. calcium
Dec. potassium

How does this compare to

Addisons disease?

 Urine
CT,

analysis

MRI

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

testing

 Drug

therapy
Lysodren
Elipten
Radiation therapy

Treats pituitary adenomas

Surgery
Removal 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
Headache
Fatigue
Nocturia
Polydipsia
Polyuria
paresthesias

and elevated BP

 UA specific
BMP
CT
MRI

gravity

 Surgery
Drug

for early stage

therapy
Medication to increase K+ Potassium supplements

 Catecholamine

producing tumor that

arises in chromaffin cells.

Occurs

gland

in a single lesion on adrenal

Releases
Cause

epinephrine and norepinephrine

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
Severe headache
Sweating
Weight loss

HR

Other symptoms that can occur with

this
disease:
Hand tremor
Sleeping 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. (Gilberts syndrome,
Dubin-Johnson and Rotors 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 symptoms
Increased abdominal girth
Rapid weight gain
Shortness of breath
Adominal striae
Distended veins over the abdominal wall.

 Dietary modifications
Diuretics
Bed rest
Paracentesis
Transjugular 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 management
Manage 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 manifestations
Minor mental changes ( early phases)
Motor dysfunction
Alterations in mood and sleep
Asterixis( 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
Hep A
Hep B
Hep C
Hep D
Hep E
Hep G

amounts of hepatitis

Epidemiolog
y

Hepatitis A

Hepatitis B

Hepatitis C

Hepatitis D

Hepatitis E

Cause

Virus (HAV)

Virus (HBV)

Virus

Virus

Virus

(HCV)

(HDV)

(HEV)

Mode of
Transmis
sion

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
Rash
symptom
s

Rash

Rash joint
pain

Flu like
symptom
s, severe
in
pregnant
woment

 Bed rest during acute

Patient teaching
Prevention

stages

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 enlargement
Portal obstruction and
Infection
Peritonitis
Varies
Edema
Vitamin Deficiency
Mental deterioration

ascites

 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.