ENDOCRINE

SYSTEM
By: MISS SHENELL A. DELFIN, RN
FUNCTION:
Endocrine system consist of a series of glands
that function individually or conjointly to
integrate and control innumerable metabolic
activities in the body.
These glands automatically regulate various body
processes by releasing chemical signals called
hormones.
FUNCTION:
Maintenance and regulation of vital functions.
 Response to stress or injury
 Growth and development
 Reproduction
 Fluids and electrolytes
 Acid base-balance
 Energy metabolism
ENDOCRINE GLANDS
ENDOCRINE HORMONES FUNCTIONS
GLAND
PITUITARY TSH Thyroid to release
hormones
ANTERIOR
LOBE ACTH Adrenal cortex to release
hormones
FSH,LH Growth, maturation &
function of sex organs
GH/ Growth of body tissues &
bones
SOMATOTROPIN
PROLACTIN/ Development of
mammary glands &
LTH lactation
 ENDOCRINE GLANDS
ENDOCRINE HORMONE FUNCTION
GLAND
PITUITARY ADH Regulates water metabolism

POSTERIOR
LOBE
OXYTOCIN Stimulate uterine contractions
release of milk

INTERME- MSH Affects skin pigmentation

DIATE LOBE
 ENDOCRINE GLANDS
ENDOCRINE HORMONES FUNCTION
GLAND
ADRENAL ALDOSTERONE Fluid & electrolyte balance;
Na reabsorption;
CORTEX
K excretion
CORTISOL Glycogenolysis;
Gluconeogenesis
Na & water reabsorption
Antiinflammatory
Stress hormone
SEX Slightly significant
HORMONES
ENDOCRINE GLANDS
ENDOCRINE HORMONE FUNCTION
GLAND
ADRENAL EPINEPHRINE Increase heart rate & BP
Bronchodilation,
MEDULLA NOR-
Glycogenolysis
EPINEPHRINE
Stress hormone
 ENDOCRINE GLANDS
ENDOCRINE HORMONE FUNCTION
GLAND
THYROID T3 & T4’ Regulate metabolic rate
Regulate physical & mental
growth & development

THYRO- Decrease serum Ca by

increasing bone deposition
CALCITONIN

PARA- PTH Increase serum calcium by

promoting bone decalcification
THYROID
 ENDOCRINE GLANDS
ENDOCRINE HORMONE FUNCTION
GLAND

PANCREAS INSULIN Decrease blood glucose by:

Glucose diffusion across cell
BETA membrane;
CELLS Converts glucose to
glycogen

ALPHA GLUCAGON Increase blood glucose by:

Gluconeogenesis
CELLS Glycogenolysis
 ENDOCRINE GLANDS
ENDOCRINE HORMONES FUNCTION
GLAND
•Development of secondary sex
OVARIES ESTROGEN &
charac in female
PROGES-
•Maturation of sex organs
TERONE •Sexual functioning
•Maintenance of pregnancy

TESTOS- •Development of secondary sex

TESTES
charac in male
TERONE
•Maturation of sex organs
•Sexual functioning
HORMONE REGULATION
NEGATIVE FEEDBACK MECHANISM

CHANGING OF BLOOD LEVELS OF

CERTAIN SUBSTANCES (e..g CALCIUM & GLUCOSE)

RHYTHMIC PATTERNS OF SECRETION

(e.g. CORTISOL, FEMALE REPRODUCTIVE HORMONES)

AUTONOMIC & C.N.S. CONTROL

(PITUITARY-HYPOTHALAMIC AXIS,
ADRENAL MEDULLA HORMONES)
 NEGATIVE FEEDBACK
MECHANISM
DECREASED HORMONE CONCENTRATION
IN THE BLOOD (e.g. Thyroxine)

PITUITARY GLAND RELEASE OF

STIMULATING HORMONE (e.g. TSH)

STIMULATION OF TARGET ORGANS TO

PRODUCE & RELEASE HORMONE
(e.g. Thyroid gland release of Thyroxine)

RETURN OF THE NORMAL

CONCENTRATION OF HORMONE
 NEGATIVE FEEDBACK
MECHANISM
INCREASED HORMONE CONCENTRATION
IN THE BLOOD (e.g. Thyroxine)

PITUITARY GLAND IS INHIBITED TO

RELEASE STIMULATING HORMONE (e.g. TSH)

DECREASED PRODUCTION & SECRETION

OF TARGET ORGAN OF THE HORMONE
(e.g. Thyroid gland release of Thyroxine)

RETURN OF THE NORMAL

CONCENTRATION OF HORMONE
Hypothyroidism
• underactive state of the thyroid gland  hyposecretion
of thyroid hormone
• most common in women, middle-age
• primary function is to control the level of cellular
metabolism by secreting thyroxin (T4) and
triiodothyronine (T3)
Causes :
• thyroidectomy
• pituitary / hypothalamic dysfunction
• iodine deficiency
• autoimmune thyroiditis (Hashimoto’s disease) –
immune system attacks the thyroid gland
• idiopathic (unknown)
DX: decreased T3, T4
Elevated TSH, cholesterol
Med. Mgt. – thyroid replacement therapy
• Levothyroxine (Synthyroid) , liothyronine
• Expected effects: diuresis, puffiness, improved
reflexes and muscle tone, PR
Nsg. Interventions
 provide a warm environment, conducive to rest
 avoid use of all sedatives
 assist client in choosing calorie,  cholesterol
diet
  fluid and fiber to relieve constipation
  physical activity and sensory stimulation
gradually as condition improves
 monitor cardiovascular response to increased
hormone levels carefully
 provide info. about prescribed medications (name,
dosage, side effects) and importance of lifelong
medical supervision
Hyperthyroidism

• over-secretion of the thyroid gland

• also called thyrotoxicosis or graves disease, tissues
are stimulated by excessive thyroid hormone
• a recurrent syndrome, may appear after emotional
stress or infection
• occurs mostly in women 20-50 yrs old

Causes : adenoma, goiter, viral inflammation, auto-

immune glandular stimulation, grave’s disease - most
common cause
Hyperthyroidism (cont.)

DX: > elevated T3, T4 values

T4= 5-12mcg/dl , T3= 70-220 ng/dl , TSH= 0.2-5.4 mU/L
•abnormal findings in the thyroid scan

Goiter – enlargement of the thyroid gland

•due to  stimulation of the thyroid gland by TSH

Simple goiter – enlarged thyroid gland

•due to iodine deficiency, intake of goitrogenic foods 
cabbage, turnips, soybeans
•may be hereditary
Grave’s Disease
 disorder char. by one or more of the ff:
• diffuse goiter
• hyperthyroidism
• infiltrative opthalmopathy  exophthalmos
 seen in females under age 40
 result from stimulation of the thyroid gland by
thyroid-stimulating immunoglobulins (TSI)
 cause is unknown, may be hereditary, gender-related,
often occurs after severe emotional stress or
infection
Thyroid Storm or Crisis

• a medical emergency  pts. develop severe

manifestation of hyperthyroidism
•  temp., tachycardia, dysrhythmias
• worsening tremors, restlessness
• delirious or psychotic state or coma
• abdominal pain
•  BP and RR

• Precipitated by a major stressor:

• infection
• trauma or surgery (thyroidectomy)
• inadequate treatment
Complications :

• cardiovascular disease (HPN, Angina, CHF)

• Exophthalmos – abnormal protrusion of the eyeballs
- caused by abnormal deposits of fat and fluid in
the retroocular tissue
• Corneal abrasion
•Thyroid storm or crisis  life-threatening
hypermetabolism and excessive adrenergic
response (HR, RR, BP)
TAKE
ME!
TAKE
ME!!
Assessment
Findings
 Anxiety
 Flushed, smooth skin
 Heat intolerance
 Mood swings
 Diaphoresis
 Tachycardia
 Palpitations
 Dyspnea
 Weakness
 Wt. loss
Nsg. Interventions:
• Provide calm, restful envt.
• physical comfort, cool envt. temp., bathe
frequently w/ cool water
• provide adequate rest, avoid muscle fatigue
•  stressors in the envt.— noise and lights
• relaxation techniques
• Provide adequate nutrients
•  calorie,  protein, balanced diet (4,000-5,000
cal/day)
•  fluid intake
• Restrict stimulants (tea, coffee, alcohol)
• small, frequent feedings if hypermotility is
present
• Daily wt.
Nsg. Interventions:

• Provide emotional support

• Provide eye care

• eye drops, dark glasses, patch eyes if necessary
• elevate head of bed for sleep
• restrict dietary sodium
• assess adequacy of lid closure

•Be alert for complications

Post-op care after Thyroidectomy

 O2 therapy, suction secretions

 Monitor for signs of bleeding and excessive edema
 elevate head of bed 30o, support head and neck – to
avoid tension on sutures
check dressing frequently, check behind the neck for
bleeding
 assess for signs of resp. distress, hoarseness
(laryngeal edema or damage)
 keep tracheostomy set in patient’s room for
emergency
use
Post-op Complications: be alert for the possibility of:

1. Tetany (due to hypocalcemia caused by accidental

removal of parathyroid glands)
assess for numbness, tingling or muscle twitching
 Chvostek’s sign and Trousseau’s sign
 Ca+ gluconate IV

2. Hemorrhage
WOF: hypotension, tachycardia, other signs of
hypovolemia
WOF: irregular breathing, swelling, choking---
possible hemorrhage and tracheal compression
WOF: early signs of hemorrhage: repeated clearing
of the throat, difficulty swallowing
Post-op Complications: be alert for the possibility of:

3. Thyroid storm
- life-threatening
- sudden  release of thyroid hormone
- fever, tachycardia, increasing restlessness and
agitation, delirium

administer food and fluid with care (dysphagia is

common) encourage client to gradually  ROM of
neck
teach about medications, frequent follow-up
total thyroidectomy – life long replacement
medication (T3, T4)
subtotal thyroidectomy – careful monitoring of
return of thyroid function
(TYPE I, TYPE II)
Diabetes Mellitus

• is a chronic disorder of carbohydrate, protein, and

fat metabolism resulting from insulin deficiency or
abnormality in the use of insulin
Predisposing factors:
 exact cause of diabetes mellitus remain unknown
 genetic / hereditary predisposition
 viruses
 pancreatitis
 pancreatic tumor
 autoimmune disorder
 obesity (overweight people require more insulin
to metabolize the food they eat or the number of
insulin receptor sites in cells is decreased)
Types
•Insulin – Dependent Diabetes Mellitus (IDDM) or Type I
 destruction of beta cells of the pancreas  little or no
insulin production
 requires daily insulin admin.
 may occur at any age, usually appears below age 15
•Non Insulin–Dependent Diabetes Mellitus (NIDDM) or Type
II
 probably caused by:
 disturbance in insulin reception in the cells
  number of insulin receptors
 loss of beta cell responsiveness to glucose leading to
slow or  insulin release by the pancreas
 occurs over age 40 but can occur in children
 common in overweight or obese
 w/ some circulating insulin present, often do not require
insulin
Clinical Manifestations ( Signs and Symptoms)

- Polyuria - weakness
- Polydipsia - fatigue
- Polyphagia -  blood sugar / glucose level
- weight loss - (+) glucose in urine (glycosuria)
- nausea / vomiting
- changes in LOC (severe hyperglycemia)
(sleepiness, drowsiness  coma)
- recurrent infection, prolonged wound healing
- altered immune and inflammatory response, prone to
infection (glucose inhibits the phagocytic action of WBC 
resistance)
- genital pruritus – (hyperglycemia and glycosuria favor fungal
growth : candidal infection – resulting in pruritus, common
presenting symptom in women)
1. Fasting Blood Sugar (FBS)
 NPO for 12 hours
 Normal value= 80-120 mg/dl
 140 mg/dl or more – diagnostic of DM
Postprandial blood sugar
 Blood is withdrawn 2 hrs. after a meal
 N value = < 120mg/dl
 200 mg/dl or more is diagnostic of DM
3. Oral Glucose Tolerance Test (OGTT)
 NPO 12 hrs, no smoking, coffee or tea, minimize
activity, minimize stress
 obtain FBS, administer 100 gm. Glucose by mouth
diluted in juice; obtain blood and urine specimen after
1, 2 and 3 hrs.
 N value = blood glucose rise to 140 mg/dl in the 1st hour
and returns to normal by 2nd and 3rd hrs.
 Abnormal = blood glucose does not return to normal by
2nd and 3rd hrs.; all urine specimen positive for glucose
4. Glycosylated hemoglobin
 Provides information about blood glucose level
during the previous 3 months
 bec. glucose in the bloodstream attaches to
some of the hemoglobin and stay attached
during the 120-day lifespan of the RBC
Interventions for Diabetes Mellitus
A.Dietary Management

1. Follow individualized meal plan and snacks as scheduled

 Balanced diabetic diet – 50% CHO, 30% fats, 20%
CHON, vitamins and minerals
 diet based on pts. size, wt., age, occupation and
activity
2. Pt. must have adequate CHO intake to correspond to the
time when insulin is most effective
• Routine blood glucose testing before each meal and at
bedtime is necessary during initial control, during illness
and in unstable pts.
• Do not skip meals
• Measure foods accurately, do not estimate
• Less added fat, fewer fatty foods and low-cholesterol
Interventions for Diabetes Mellitus
A.Dietary Management

• Advise use of complex

carbohydrates to help stabilize
blood sugar. Meal should include
more fiber and starch and fewer
simple or refined sugars.
• Avoid concentrated sweets, high in
sugar (jellies, jams, cakes, ice
cream)
• If taking insulin, eat extra food
before periods of vigorous exercise
• Avoid periods of fasting and
feasting
• Keep weight at normal level, obese
diabetics should be on a strict
weight control program and should
lose weight.
B. Teach pt. on correct administration of insulin and other
hypoglycemic agents.
• insulin in current use may be stored at room temp., all
others in ref. or cool area
• avoid injecting cold insulin  lead to tissue reaction
• roll insulin vial to mix, do not shake, remove air bubbles
from syringe
• press (do not rub) the site after injection (rubbing may
alter the rate of absorption of insulin)
• avoid smoking for 30 mins. after injection (cigarette
smoking absorption)
• Rotate sites
 Failure to rotate sites may lead to Lipodystrophy
 Lipodystrophy – localized disturbance of fat metabolism
 Ex. Lipohypertrophy – thickening of subcutaneous tissue
at injection site, feel lumpy or hard, spongy
 result to  absorption of insulin  making it
difficult to control the pt.’s blood glucose
Factors that influence the body’s need for insulin
 need : trauma, infection, fever, severe psychological or
physical stress, other illnesses
•  need : active exercise
Hypoglycemia
 low blood glucose (usually below 60mg/dl)
 results from too much insulin, not enough food, and/or
excessive physical activity
 may occur 1-3 hrs after regular insulin injection
S/Sx:
•Sweating, tremor, pallor, tachycardia, palpitations and
nervousness
1. caused by release of epinephrine from the CNS when
blood glucose falls rapidly
•Headache, light-headedness, confusion, numbness of lips and
tongue, slurred speech, drowsiness, convulsions and coma
• caused by depression of the CNS because of glucose
supply of brain cells
Management of Hypoglycemia

•Give simple sugar orally if pt. is conscious and can swallow

– orange juice, candy, glucose tablets, lump of sugar
•Give Glucagon (SQ or IM) if pt. is unconscious or cannot
take sugar by mouth
•As soon as pt. regains consciousness, he should be given
carbohydrate by mouth
•If pt. does not respond to the above measures, he is
given 50 ml of 50% glucose I.V. or 1000 ml of 5%-10%
glucose in water I.V.
Preventing Hypoglycemic Reactions Due to Insulin

Instruct the pt. as follows:

4.Hypoglycemia may be prevented by maintaining regular
exercise, diet and insulin
5.Early symptoms of hypoglycemia should by recognized
and treated
6.Carry at all times some form of simple carbohydrate
(orange juice, sugar, candy)
7.Extra food should be taken before unusual physical
activity or prolonged periods of exercise
8.Between-meal and bedtime snacks may be necessary
to maintain a normal glucose level.
 D-I-A-B-E-T-E-S
D- DIET: 50-60% CHO, 20-30% FATS,
10-20% CHON
I- INSULIN– TYPE 1
A- ANTIDIABETIC AGENTS– TYPE 2
B- BLOOD SUGAR MONITORING
E- EXERCISE
T- TRANSPLANT OF PANCREAS
E- ENSURE ADEQUATE FOOD INTAKE
S- SCRUPULOUS FOOT CARE
Oral Antidiabetic Agents
INSULIN THERAPY
DISPENSED IN “U”/ml : eg 100, 80
REFRIGERATE
GIVEN @ ROOM TEMP
GENTLY ROTATED, NOT SHAKEN
ROUTE : SQ ; IM OR IV
SYRINGE: 5/8 INCH ; SAME BRAND
 INSULIN ONSET PEAK DURATION

Ultra rapid acting 15 mins. 2-4 hrs. 6-8 hrs.

Insulin analog
(Humalog)
Rapid acting: ½-1 hr 2-4 hrs. 6-8 hrs.
Regular (Semilente)

Intermediate: 1-2 hrs. 7-12 hrs. 24-30 hrs.

NPH (Lente)

Long acting: 4-6 hrs. 18 + hrs 30-36 hrs.

Protamine Zinc
(Ultralente)
INSULIN THERAPY:
SITE OF INJECTION:
ABDOMEN
ANTERIOR THIGH
ARM
UPPER BACK
BUTTOCKS
LIPODYSTROPHY
CAUSE:
FAULTY TECHNIQUE
TRAUMA
INJECTION OF REFRIGERATED INSULIN
MANAGEMENT:
ROTATING SITES: 1 AREA IS NOT USED MORE
THAN ONCE EVERY 3 WKS
Teach pt. to estabilish and maintain a
pattern of regular exercise
Benefits of exercise :
• promotes use of CHO & enhances
action of insulin
  blood glucose levels
  need for insulin
  the no. of functioning receptor
sites for insulin
perform exercise after meals to ensure
an adequate level of blood glucose
carry a rapid-acting source of glucose
during exercise
excessive or unplanned exercise may
trigger hypoglycemia
take insulin and food before active
exercise
Teach pt. to practice good personal hygiene and positive
health promotion to avoid diabetic complications

•teach pt. about diabetic foot care

•teach pt. the adjustments that must be made in the event of
minor illness (e.g. colds, flu)
 continue taking insulin or oral hypoglycemic agents
 maintain fluid intake
  frequency of blood testing or urine testing
•help pt. identify stressful situations in lifestyle that might
interfere with good diabetic control
•encourage good daily hygiene
•advise regular eye exams
•teach aggressive care for minor skin cuts and abrasions
DIABETIC KETO-ACIDOSIS (DKA)

INSULIN SHOCK

HYPERGLYCEMIC, HYPEROSMOLAR,
NONKETOTIC (HHONK) COMA
Diabetic Ketoacidosis (DKA) Coma

S/Sx:
•polyuria, thirst
•nausea, vomiting, abdominal pain –-- due to acidosis
•weakness, headache, fatigue --- due to acidosis and F/E
imbalance
•dim vision
•dehydration, hypovolemic shock (PR, BP, dry skin, wt.
loss)
•hyperpnea (Kussmaul’s breathing)
•acetone breath (fruity odor)
•lethargy  COMA
•Blood glucose level > 250-350 mg/100 ml.
INSULIN SHOCK
LOW BLOOD SUGAR
CAUSE:
OVERDOSE OF EXOGENOUS INSULIN

EATING LESS

OVEREXERTION WITHOUT ADDITIONAL

CALORIE INTAKE
 INSULIN SHOCK
S/SX:
PARASYMPATHETIC SYMPATHETIC
HUNGER IRRITABILITY
NAUSEA SWEATING
HYPOTENSION TREMBLING
BRADYCARDIA TACHYCARDIA
CEREBRAL PALLOR
LETHARGY,
YAWNING
SENSORIUM CX
INSULIN SHOCK
CLINICAL FINDING :
BLOOD GLUCOSE BELOW 55-60 mg/DL

TREATMENT:
GLUCOSE PO ( SUGAR, ORANGE JUICE OR
CANDY) or IV
ADMINISTRATION OF GLUCAGON IM, IV
OR SQ
Hyperglycemic, Hyperosmolar, Non-Ketotic Coma
(HHNC)
• can occur when the action of insulin is severely
inhibited
• seen in pts. w/ NIDDM, elderly persons w/
NIDDM
Precipitating factors:
•infection, renal failure, MI, CVA, GI hemorrhage,
pancreatitis, CHF, TPN, surgery, dialysis, steroids

S/Sx:
polyuria  oliguria (renal insufficiency)
lethargy
temp, PR, BP, signs of severe fluid deficit
Confusion, seizure, coma
Blood glucose level > 600 mg/100 ml.
HHONK
S/SX:
S/SX OF DKA WITHOUT:
KAUSMAUL’S BREATHING
ACETONE BREATH
METABOLIC ACIDOSIS
KETONURIA
LACTIC ACIDOSIS
SEVERE TISSUE ANOXIA

LACTIC ACID PRODUCTION

AGGRAVATION OF EXISTING
METABOLIC ACIDOSIS
Interventions for DKA and Hyperosmolar Coma

• Regular insulin IV push or IV drip

• 0.9% NaCl IV – 1 L during the 1st hr, 2-8 L over 24 hrs.
• administer sodium bicarbonate IV to correct acidosis
• Monitor electrolyte levels, esp. serum K+ levels
• administer K+, monitor UO hourly (30ml/hr)
Long-term Complications of DM

3.Vascular Changes
•) Macroangiopathy – hardening and damage of the walls of
large arteries
• Coronary Artery Disease
• CVA (Stroke)
• Peripheral vascular disease – foot ulcers and gangrene
b. ) Microangiopathy – destruction of small blood vessels
• Retinopathy – damage to retinal capillaries; hemorrhage,
blindness
• Nephropathy – damage microcirculation of kidneys; CRF
2. Neuropathy
• Damage to the neurons caused by vascular insufficiency
and  blood glucose
• Sensory and motor impairment
• Numbness, tingling, pain in extremities
• Painless neuropathy
• Impotence!!
SURPRISE!!!
PARATHYROID GLAND
4 GLANDS
SECRETES PARATHORMONE (PTH) IN
RESPONSE TO SERUM Ca & Ph LEVELS
REGULATE CALCIUM & PHOSPHORUS
METABOLISM
ORGANS AFFECTED:
BONES - RESORPTION
KIDNEYS
Ca REABSORPTION
Ph EXCRETION
GIT – ENHANCES Ca ABSORPTION
 Promotes
CALCIUM
Mobilization
CALCIUMof Renal: increases
resorption of EXCRETION
calcium and
STAYS IN DEPOSITED
calcium from
calcium
phosphorous
THE INtoTHE
bone maintain OF CALCIUM
reabsorption and
fromBONE
bone phosphate
normal serum
BONE
calcium levels
excretion

Hypoparathyroidism is
characterized by decrease in
the PTH level
•TINGLING OF FINGERS
Function of calcium:
•CHVOSTEKS/
maintains N muscle
Promotes absorption of TROUSSEAU’S
HYPOCALC
calcium in the GI tract
( by stimulating kidneys
and neuromuscular
•FATIGUE, WEAKNESS
responses.
•CARDIAC ARRHYTHMIAS
Necessary component
EMIA
to convert vit.D to its
active form).
•SEIZURE
for blood coagulation
•BRONCHOSPASM
mechanisms
HYPOPARATHYROIDISM
DECREASED PTH PRODUCTION
HYPOCALCEMIA
CALCIUM IS:
DEPOSITED IN THE BONE
EXCRETED

CAUSE:
HEREDITARY
IDIOPATHIC
SURGICAL
PARATHYROID DISORDERS
DIAGNOSTIC TESTS:
HEMATOLOGICAL
SERUM CALCIUM
SERUM PHOSPHORUS
SERUM ALKALINE PHOSPHATASE
URINARY STUDIES
URINARY CALCIUM
URINARY PHOSPHATE - TUBULAR
REABSORPTION OF PHOSPHATE
HYPOPARATHYROIDISM
S/SX:
ACUTE HYPOCALCEMIA
TINGLING OF THE FINGERS
CHVOSTEK’S, TROUSSEAU’S
CHRONIC HYPOCALCEMIA
FATIGUE, WEAKNESS
PERSONALITY CHANGES
LOSS OF TOOTH ENAMEL, DRY SCALY SKIN
CARDIAC ARRHYTHMIA
CATARACT
HYPOPARATHYROIDISM
XRAY: INCREASED BONE DENSITY
MANAGEMENT:
Ca SUPPLEMENT
VIT D SUPPLEMENT – LIQ FORM: WITH WATER,
JUICE OR MILK, pc
SEIZURE prec
STRIDOR OR HOARSENESS
 LISTEN FOR

TRACHEOSTOMY SET @ BEDSIDE

CaGLUCONATE @ BEDSIDE
 HYPERCALCEMIA, TUBULAR CALCIUM
CALCIUM of Promotes
Mobilization LACK OF RESORPTION Renal: increases
DEPOSIT- KIDNEY
RELEASED INTO resorption of
calcium and OF CALCIUM INTO THE calcium
STONES, AZOTEMIA,
THE BLOOD calcium from
phosphorous
LEADS TO BONE BONE( BONE CYST reabsorption
HPN and
BY RF, RENAL
bone to maintain
from bone
DAMAGE AND PATHOLOGIC phosphate
FAILURE
normal serum
FRACTURE) excretion
calcium levels

Hyperparathyroidism is
characterized by excesssive
secretion of PTH

Function of calcium:
MUSCLE
 maintains N muscle
Promotes absorption of WEAKNESS
ANOREXIA
calcium in the GI tract
and neuromuscular
N/V kidneys PERSONALITY
responses.
( by stimulating Necessary component
CONSTIPATION
to convert vit.D to its CHANGES
for blood coagulation
PEPTIC
active ULCER DSE
form). CARDIAC
mechanisms
ARRHYTHMIAS
HYPERPARATHYROIDISM
INCREASED PTH PRODUCTION
HYPERCALCEMIA
HYPOPHOSPHATEMIA
PRIMARY – TUMOR OR HYPERPLASIA OF THE
PARATHYROID GLAND
SECONDARY – COMPENSATORY OVERSECRETION
OF PTH IN RESPONSE TO HYPOCALCEMIA FROM:
 CHRONIC RENAL DSE
 RICKETS
 MALABSORPTION SYNDROME
 OSTEOMALACIA
HYPERPARATHYROIDISM
S/SX:

BONE PAIN : ESP @ THE BACK, PATHOLOGIC

FRACTURES
TUBULAR CALCIUM DEPOSITS - KIDNEY
STONES, RENAL COLIC, POLYURIA,
POLYDIPSIA
MUSCLE WEAKNESS
PERSONALITY CX, DEPRESSION
CARDIAC ARRHYTHMIAS, HPN

XRAY: BONE DEMINERALIZATION

HYPERPARATHYROIDISM
MANAGEMENT:

TX OF CHOICE : SURGICAL REMOVAL OF

HYERPLASTIC TISSUE
IV PNSS 5L/ DAY WITH DIURETICS
CRANBERRY JUICE (ACID-ASH)
LOW Ca, HIGH Ph DIET
NO MILK, CAULIFLOWER & MOLASSES
FOR STONES
STRAIN URINE
CARE FOR PARATHYROIDECTOMY
ADRENAL GLAND
STIMULATED BY ACTH
ADRENAL MEDULLA- SECRETES
CATECOLAMINE, EPINEPHRINE, &
NOREPINEPHRINE.
ADRENAL CORTEX- MAIN BODY; RESP
FOR SECRETION OF GLUCO,MINERALO,
SEX HORMONES (ANDRO & ESTRO)
FUNCTION IS TO CONTROL THE (-)
FEEDBACK MECHANISMS REGULATING
HORMONE RELEASE
ADRENAL GLAND
HORMONE FUNCTION
ALDOSTERONE Renal : Na & Cl reabsorption; K
excretion
GI : Na absorption
GLUCO- • increase serum glucose by
CORTICOIDS gluconeogenesis & glycogenolysis esp
during STRESS
•Blocks inflammation
•Counteracts effect of histamine
SEX HORMONE Physiologically significant
Becomes useful during menopause in
women
SYMPTOMATOLOGY

ALDOSTERONE DEFICIENCY
DECREASE IN PLASMA VOLUME LEADING TO
DEHYDRATON
HYPOTENSION TO SHOCK
INCREASED K
METABOLIC ACIDOSIS
SYMPTOMATOLOGY
CORTISOL DEFICIENCY
ANOREXIA, N/V, ABDOMINAL PAIN, WT LOSS,
LETHARGY
HYPOGLYCEMIA
HYPOTENSION
INCREASED K, WEAK PULSE
PIGMENTATION
IMPAIRED STRESS TOLERANCE
SYMPTOMATOLOGY
SEX HORMONE DEFICIENCY

LOSS OF BODY HAIR

LOSS OF LIBIDO OR IMPOTENCE!
MENSTRUAL & FERTILITY DISORDER
ADRENAL CORTEX
DISORERS
ADRENAL INSUFFICIENCY

ADRENAL CRISIS

CUSHING’S SYNDROME

ALDOSTERONISM
 ADRENAL INSUFFICIENCY
ADDISON’S DISEASE
INCAPABILITY OF THE ADRENAL CORTEX TO
PRODUCE GLUCOCORTICOIDS IN
RESPONSE TO STRESS
 *Hyposecretion of the adrenal cortex hormones
Assessment:

Subjective:
• Muscle weakness, fatigue, lethargy, dizziness,
fainting, nausea, anorexia, abdominal pain/cramps.
Objective:
• V/S: decreased BP, orthostatic hypotension
• Pulse: increased, collapsing, irregular
• Subnormal temp.
• Vomiting, diarrhea, weight loss
• Tremors
• Skin: poor turgor excessive pigmentation (bronze
tone)
• Hyponatremia, hypoglycemia, hyperkalemia
ADRENAL CRISIS
ACUTE EPISODES FROM STRESS THAT
TAXES THE ADRENAL CORTICAL FUNCTION
BEYOND ITS CAPABILITIES

POSSIBLE COMPLICATION OF ADDISON’S

DISEASE
ADRENAL CRISIS
PRECIPITATING CAUSES:
ABDOMINAL DISCOMFORT
INFECTION
TRAUMA
HIGH TEMP
EMOTIONAL UPSET
ADRENAL CRISIS
S/SX:

HYPOTENSION
FLUID LOSS
HYPONATREMIA
ADRENAL CRISIS
LAB:
SERUM ELEC: DECREASED Na
INCREASED K
S. BUN :
S. GLUCOSE:
ADRENAL HORMONE ASSAY :
HYDROXYCORTICOID & 17 KETOSTEROID IN
24-HR URINE DET.
ADRENAL CRISIS
GOALS OF CARE:
TO REVERSE SHOCK

RESTORE BLOOD CIRCULATION

REPLENISH NEEDED STEROID

ADRENAL CRISIS
TREATMENT:
D5NSS
ADRENAL CORTICAL HORMONE
REPLACEMENT: INJECTABLE
NEOSYNEPHRINE - SHOCK
HIGH SALT DIET
ANTIBIOTICS
CUSHING’S
SYNDROME
CAUSE:
SUSTAINED OVER-PRODUCTION OF
GLUCOCORTICOIDS BY ADRENAL GLAND FROM

ACTH BY PITUITARY TUMOR

EXCESSIVE GLUCORTICOID
ADMINISTRATION
CUSHING’S
SYNDROME
S/SX:
TRUNCAL OBESITY
BUFFALO HUMP
MOON-FACE
WT GAIN
SODIUM RETENTION
THINNING OF EXTREMITIES – FROM LOSS OF
MUSCLE TISSUE DUE TO PROTEIN CATABOLISM
CUSHING’S
SYNDROME
PURPLE STRIAE – FROM THINNING OF SKIN
ECHYMOSIS FROM SLIGHT TRAUMA
ANDROGENIC EFFECTS:
OLIGOMENORRHEA
HIRSUTISM
GYNECOMASTIA
HYPERTENSION FROM S. Na
CUSHING’S
SYNDROME
TREATMENT & NURSING CARE:

PSYCHOLOGICAL SUPPORT
PREVENT INFECTION – INFLAM & IMMUNE
RESPONSE ARE SUPPRESSED
PROMOTE SAFETY
SURGERY – SUB/TOTAL ADRENALECTOMY
ALDOSTERONISM
HYPERSECRETION OF ALDOSTERONE

PRIMARY – CONN’S SYNDROME

SECONDARY
CONN’S SYNDROME
PRIMARY ALDOSTERONISM
CAUSE:
ADRENAL ADENOMA
S/SX:
HYPOKALEMIA
FATIGUE
HYPERNATREMIA, HPN, TETANY
MANAGEMENT:
SURGERY
ALDACTONE – ALDOSTERONE ANTAGONIST
SECONDARY
ALDOSTERONISM
THE PROBLEM IS OUTSIDE THE ADRENAL
GLAND:

e.g. RENIN – ANGIOTENSIN SYSTEM

ADRENAL MEDULLA
HORMONES : EPINEPHRINE
NOREPINEPHRINE EFFECTS
PHEOCHROMOCYTOMA
 TUMOR OF ADRENAL MEDULLA SECRETES INCREASED
AMOUNT OF CATECHOLAMINES

A small tumor in the adrenal gland that secretes

large amounts of epinephrine and norepinephrine.
S/SX:
HPN
HYPERGLYCEMIA
CARDIAC ARRHYTHMIA & CHF
DIAGNOSTIC TEST :
VMA IN 24H URINE- VANILLYMANDALIC
ACID
VMA IN 24H URINE
END PRODUCT OF CATECHOLAMINE
METABOLISM
DRUGS & FOOD TO BE WITHHELD 24H B4 THE
TEST:
COFFEE & TEA
BANANA
VANILLA
CHOCOLATES
PHEOCHROMOCYTOMA
MANAGEMENT:
SURGERY
MEDICAL : ADRENERGIC BLOCKING
AGENTS: PHENTOLAMINE

NURSING CARE:
MONITOR BP IN SUPINE & STANDING
MONITOR URINE FOR GLUCOSE &
ACETONE
ANTERIOR PITUITARY
DISTURBANCES

HYPOPITUITARISM

HYPERPITUITARISM
PITUITARY ANTERIOR LOBE
HORMONE HYPO FXN HYPER FXN

GH Dwarfism – young Gigantism – young

Cachexia - adult Acromegaly - adult
ACTH Atrophy of adrenal Cushing’s dse
cortex
TSH Atrophy & Grave’s dse
depressed thyroid fxn
FSH Atrophy & infertility Exaggerated fxn of
sex organs
PROLACTIN Underdevelopment Decreased milk
of mammary glands production
MANAGEMENT
HYPOPITUITARISM
SURGICAL REMOVAL / IRRADIATION
REPLACEMENT THERAPY
 THYROID HORMONES

 STEROIDS

 SEX HORMONES

 GONADOTROPINS (restore fertility)

HYPERPITUITARISM
SURGICAL REMOVAL / IRRADIATION
MONITOR FOR HYPERGLYCEMIA &
CARDIOVASCULAR PROBLEMS
POSTERIOR PITUITARY
DISTURBANCES
DIABETES INSIPIDUS

SYNDROME OF INAPPROPRIATE
ANTIDIURETIC HORMONE
FUNCTION:
WHEN THERE IS A OF SERUM
OSMOLALITY, THE NORMAL BODY RESPONSE
IS TO THE SECRETION OF ADH.
WHEN THE NORMAL FEEDBACK MECHANISM
FOR ADH IS SUSTAINED, THERE IS
EXCESSIVE WATER RETENTION IN THE BODY
WHEN THERE IS OR INADEQUATE
AMOUNT OF ADH, THE BODY IS UNABLE TO
CONCENTRATE URINE, & EXCESSIVE H2O
LOSS OCCURS
DIABETES INSIPIDUS
CHARACTERIZED BY A DEFICIENCY OF ADH.
WHEN IT OCCURS, IT IS MOST OFTEN
ASSOCIATED WITH :
NEUROLOGICAL CONDITIONS,
SURGERY,
TUMORS,
HEAD INJURY,
OR INFLAMMATORY PROBLEMS
DIABETES INSIPIDUS ABSOLUTE
/ PARTIAL DEFICIENCY OF VASOPRESSIN

S/SX:
POLYURIA
15-29L/ DAY
POLYDIPSIA
SG OF URINE IS
<1.010
S/SX OF DHN
SHOCK
DIABETES INSIPIDUS
ABSOLUTE / PARTIAL DEFICIENCY OF VASOPRESSIN

MANAGEMENT
HORMONAL REPLACEMENT – FOR LIFE
 VASOPRESSIN (PITRESSIN TANNATE IN OIL) – IM
OR NASAL SPRAY
NON-HORMONAL THERAPY
 CHLORPROPRAMIDE – INCREASE RESPONSE OF THE
BODY TO DECREASED VASOPRESSIN
INCREASE FLUIDS
MONITOR I&O
MAINTAIN FLUID & ELECTROLYTE
BALANCE
 SYNDROME OF
INAPPROPRIATE ADH
(SIADH)
ELEVATED ADH
CAUSES:
BRONCHOGENIC CA
NONENDOCRINE TUMORS
S/SX:
DECREASED SERUM SODIUM
 CX IN LOC TO UNCONSCIOUSNESS
 SEIZURES
WATER INTOXICATION
 N/V
 MENTAL CONFUSION
 SYNDROME OF
INAPPROPRIATE ADH
MANAGEMENT:
WATER INTAKE RESTRICTION
ADMINISTER AS ORDERED:
NaCl
Diuretics
Demeclocycline (declamycin) – a tetracycline
analogue that interferes with the action of ADH
on the collecting tubules
RECAP:
ANTERIOR PITUITARY:
GIANTISM,
ACROMEGALLY,
DWARFISM

POSTERIOR PITUITARY:
DIABETES INSIPIDUS,
SIADH
LOCATION: BASE OF THE BRAIN
RECAP
ADRENAL GLAND:
ADDISON’S DSE
CUSHING SYNDROME

ADRENAL MEDULLA:
PHEOCHROMOCYTOMA
PRIMARY ALDOSTERONISM

LOCATION: ON TOP OF THE KIDNEY

RECAP
PANCREAS:
DM
LOCATION: POSTERIOR TO LIVER

PARATHYROID:
HYPORATHYROIDISM
HYPERPARATHYROIDISM
LOCATION: NEAR THYROID
RECAP
THYROID:
GOITER
CRETINISM
MYXEDEMA
HYPERTHYROIDISM (GRAVE’S DSE)

LOCATION: ANTERIOIR PART OF NECK

QUESTION NO. 1
A CLIENT IS FOUND TO BE COMATOSE &
HYPOGLYCEMIC W/ A BLOOD SUGAR OF 50
MG/DL. WHAT NURSING ACTION IS
IMPLEMENTED FIRST?
B.INFUSE 1L OF D5W OVER A 12 HR PERIOD.
C.ADMIN. 50% GLUCOSE IV
D.CHECK THE CLIENT’S URINE FOR THE
PRESENCE OF SUGAR AND ACETONE
E.ENCOURAGE THE CLIENT TO DRINK ORANGE
JUICE W/ ADDED SUGAR
QUESTION NO.2
WHAT IS THE PRIMARY ACTION OF INSULIN
IN THE BODY?
B.ENHANCES THE TRANSPORT OF GLUCOSE
ACROSS THE CELL WALLS
C.AIDS IN THE PROCESS OF
GLUCONEOGENESIS
D.STIMULATES THE PANCREATIC BETA CELLS
E.DECREASE THE INTESTINAL ABSORPTION OF
GLUCOSE
QUESTION NO.3
POSTOPERATIVE THYROIDECTOMY NURSING
CARE INCLUDES WHICH MEASURES?
B.HAVE CLIENT SPEAK EVERY 5-10 MINUTES IF
HOARSENESS IS PRESENT
C.PROVIDE LOW-CALCIUM DIET TO PREVENT
HYPERCALCEMIA
D.CHECK THE DRESSING AT THE BACK OF THE
NECK FOR BLEEDING
E.APPLY SOFT CERVICAL COLLAR TO RESTRICT
MOVEMENT
HOW TO HAVE GOOD
STUDY HABITS:
Use of memory aids, mind mapping and
mnemonics.
Review class notes the next day.
- very effective study habit
- spend an hour a day reviewing
Correlate the notes and the visual aids the
instructor presented
Plan your study time when you are most
receptive to learning
Set a study goal
- for 2 days I will finish endocrine
system…..
GROUP STUDY
- limit 4-5 person’s
- group members should be mature
and serious about studying
- group studying is very effective with
the exchange of ideas thru interaction
but with the right mix of participants
“Only in this life, you can do
good, what awaits you in the
next life is not to do
better, but the reward for
having done your best
today.”
Always remember…
“…..the last few miles of a
journey are always tough,
but if you keep going you’ll
see that the last few steps
are the most fulfilling…..”
THANK YOU…
………Let us see the good, the true, and the
beautiful in life.
Hope I can guide you with every step you
make, steps that we ascend the stairs of
your journey to your Nursing life.
GOD BLESS