ENDOCRINE

SYSTEM AND MAJOR

DISORDERS
FUNCTION:
Endocrine system consist of a series of glands
ductless 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 messengers
called hormones.
OVERACTIVITY OR UNDERACTIVITY of any
one of them affects the whole system.
FUNCTION:
Control and coordination of the processes which
are wide spread in the body such as:
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 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
BETA cell membrane;
CELLS Converts glucose to
glycogen

ALPHA GLUCAGON Increase blood glucose by:

Gluconeogenesis
CELLS Glycogenolysis
 ENDOCRINE GLANDS
ENDOCRINE HORMONES FUNCTION
GLAND
OVARIES ESTROGEN & Development of secondary sex
charac in female
PROGES-
Maturation of sex organs
TERONE Sexual functioning
Maintenance of pregnancy
TESTES TESTOS- Development of secondary sex
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
 Endocrine
Disorders
If you can remember what each hormone does in
the body, it will be easier to remember what
results from imbalances of that hormone. Most
symptoms of hormone HYPERACTIVITY are the
opposite of symptoms of that hormones
HYPOACTIVITY.
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 Cushings dse
cortex
TSH Atrophy & Graves dse
depressed thyroid fxn
FSH Atrophy & infertility Exaggerated fxn of
sex organs
PROLACTIN Underdevelopment Decreased milk
of mammary glands production
Hyperpituitarism
May be due to overactivity of gland
or the result of an adenoma

Characterized by:
Excessive serum concentration
of pituitary hormones (GH, ACTH,
PRL)
Morphologic and functional changes
in the anterior pituitary
Growth Hormone Hypersecretion
GIGANTISM
Manifestations of acromegaly. Progressive alterations in
facial appearance include enlargement of the cheekbones
and jaw along with thickening of soft-tissue structures
such as the nose, lips, cheeks, and the flesh above the
brows. (Courtesy of Clinical Pathological Conference,
American Journal of Medicine.)
Hyperpituitarism:
Clinical Manifestations
Arthritis
Chest: barrel-shaped
Rough facial features
Odd sensations: hands and feet
Muscle weakness & fatigue
Enlargement of organs
Growth of coarse hair
Amenorrhea; breast milk production
Loss of vision; headaches
Impotence; increased perspiration
Snoring
Hyperpituitarism:
Clinical Manifestations
Hypopituitarism
Deficiency of one or more
anterior pituitary hormones

Causes
Infections / Inflammatory disorders
Autoimmune diseases
Congenital absence
Tumor
Surgery / Radiation therapy
Hypopituitarism:
Clinical Manifestations

Hypo -thermia, -glycemia, -tension

Loss of vision, strength, libido, &

secondary sexual characteristics
DWARFISM
MANAGEMENT
HYPOPITUITARISM
SURGICAL REMOVAL / IRRADIATION
REPLACEMENT THERAPY
THYROID HORMONES (Levothyroxine (Levoxyl,
Synthroid) -replaces deficient thyroid hormone due to
low deficient or TSH production
CORTICOSTEROIDS ( Hydrocortisone/Prednisone)-
replaces adrenal hormones-not produce due to ACTH
deficiency)
SEX & GROWTH HORMONES (testosterone in
men/hormone replacement for women)
GONADOTROPINS (restore fertility) SOMATROPIN-
growth hormone injection
HYPERPITUITARISM
SURGICAL REMOVAL / IRRADIATION
MONITOR FOR HYPERGLYCEMIA & CARDIOVASCULAR
PROBLEMS
Trans-sphenoidal hypophysectomy
is the surgical removal of the hypophysis
(pituitary gland). It is most commonly performed
to treat tumors, especially craniopharyngioma
tumors ...
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
2 groups
central diabetes insipidus insufficient
production or secretion of ADH; can be a
result of damage to the pituitary gland caused
by head injuries, genetic disorders, tumors,
surgery,and other diseases.
nephrogenic diabetes insipidus lack of kidney
response to normal levels of ADH: can be
caused by drugs or chronic disorders, such as
kidney failure, sickle cell disease, or polycystic
kidney disease.
DIABETES INSIPIDUS
ABSOLUTE / PARTIAL DEFICIENCY OF VASOPRESSIN

S/SX:
Common signs
POLYURIA
and symptoms:
15-29L/ DAY
POLYDIPSIA 1. excessive
thirst
SG OF URINE IS
2. excessive
<1.010 urine production
S/SX OF DHN 3. dehydration
SHOCK
 Causes of diabetes insipidus:

Diabetes insipidus can be caused by several conditions,

including the following:
malfunctioning hypothalamus
damage to hypothalamus or pituitary gland during surgery
brain injury
tumor
tuberculosis
blockage in the arteries leading to the brain
encephalitis
meningitis
sarcoidosis (a rare inflammation of the lymph nodes and other
tissues throughout the body)
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 + WEIGHT (MIOW)
MAINTAIN FLUID & ELECTROLYTE
BALANCE
 SYNDROME OF
INAPPROPRIATE ADH
(SIADH)
ELEVATED ADH
S/SX:
DECREASED SERUM SODIUM
CX IN LOC TO UNCONSCIOUSNESS
SEIZURES
WATER INTOXICATION
N/V
MENTAL CONFUSION
Persistent excretion of concentrated urine
Signs of fluid overload
Hyponatremia
 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
 THYROID
DISORDERS
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)

DX: decreased T3, T4

Elevated TSH, cholesterol
Hypothyroidism
A state of low serum TH levels
or cellular resistance to TH

Iodine deficiency
Autoimmune Oncologic
Developmental Drugs
Dietary Iatrogenic
Non-thyroidal
Endocrine
Pathophysiology
inadequate secretion of thyroid hormone general
slowing of all physical and mental process
metabolic rate
oxidation of nutrients for energy
heat production
Complications :
Cretinism severe physical and mental retardation
resulting from severe deficiency of thyroid function in
infancy or childhood (congenital hypothyroidism)
requires lifetime hormone replacement
Myxedema occur from prolonged severe disease
accelerated devt. of coronary artery disease
coma rapid devt. of impaired consciousness and
suppression of vital functions
MYXEDEMA COMA- a condition resulting from
persistent low thyroid production.
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, graves 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
Graves 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
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)
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
Do you take this woman as
your wife. In sickness and
in health

TAKE
ME!
TAKE
ME!!
Assessment
Findings:
Thyroid storm
Anxiety
Flushed, smooth skin
Heat intolerance
Mood swings
Diaphoresis
Tachycardia
Palpitations
Dyspnea
Delirium, coma
Heart failure
Med. Mgt.
Medications
Propylthiouracil (PTU) antithyroid drug
- blocks thyroid hormone production
- can cause agranulocytosis
- monitor pt. CBC
Methimazole (Tapazole) blocks TH prod.
Iodine preparations the size and
vascularity of the thyroid gland; inhibit release of
thyroid hormones
1.) Lugols solution
can be given with milk or fruit juice
should be taken with a straw may stain the teeth
complications : brassy taste in the mouth, sore teeth
and gums
2.) Saturated solution of potassium iodide (SSKI)
Med. Mgt.
Medications
Propanolal (Inderal) and other adrenergic blockers
relieve the adrenergic effects of excess thyroid
hormone (sweating, palpitations, tremors)

Radioactive iodine limits the secretion of the

hormone by damaging or destroying thyroid
tissue

Surgical intervention (performed only when pt. is

in a
euthyroid state)
subtotal thyroidectomy (large goiter)
total thyroidectomy (if carcinoma is present)
Nsg. Interventions:
Provide calm, restful envt.
1. physical comfort, cool envt. temp., bathe
frequently w/ cool water
2. provide adequate rest, avoid muscle fatigue
3. stressors in the envt. noise and lights
4. relaxation techniques
Provide adequate nutrients
1. calorie, protein, balanced diet (4,000-5,000
cal/day)
2. fluid intake
3. Restrict stimulants (tea, coffee, alcohol)
4. small, frequent feedings if hypermotility is
present
5. Daily wt.
Nsg. Interventions:

Provide emotional support

Provide eye care

1. eye drops, dark glasses, patch eyes if necessary
2. elevate head of bed for sleep
3. restrict dietary sodium
4. 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 patients 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
Chvosteks sign and Trousseaus 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
 PARATHYROID
GLAND DISORDERS
 Promotes
CALCIUM
Mobilization
CALCIUMof resorption of
Renal: increases
EXCRETION
calcium and
STAYS IN DEPOSITED
calcium from
calcium
phosphorous
INtoTHE
bone maintain OF CALCIUM
reabsorption and
THE
fromBONE
bone phosphate
normal serum
BONE
calcium levels
excretion

Hypoparathyroidism is
characterized by decrease in
the PTH level
PARATHYROID HORMONE

TINGLING OF FINGERS
Function of calcium:
CHVOSTEKS/
maintains N muscle
Promotes absorption of TROUSSEAUS
HYPOCALC
calcium in the GI tract
( by stimulating kidneys
and neuromuscular
FATIGUE, WEAKNESS
responses.
CARDIAC
Necessary component
EMIA
to convert vit.D to its
active form).
ARRHYTHMIAS
for blood coagulation
SEIZURE
mechanisms
BRONCHOSPASMto
Chvostek's sign is the twitching of the facial muscles in response
tapping over the area of the facial nerve.
Trousseau's sign is carpopedal spasm caused by inflating the blood-pressure
cuff to a level above systolic pressure for 3 minutes
TESTS USED TO ELICIT SIGNS OF CALCIUM
DEFICIENCY

TROUSSEAU'S SIGN CHVOSTEK'S SIGN

PARATHYROID DISORDERS
DIAGNOSTIC TESTS:
HEMATOLOGICAL
SERUM CALCIUM
SERUM PHOSPHORUS
SERUM ALKALINE PHOSPHATASE
URINARY STUDIES
URINARY CALCIUM
URINARY PHOSPHATE - TUBULAR
REABSORPTION OF PHOSPHATE
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
T
ETANY
AKE
RACHEOSTO
MY

C
ALCIUM

ARE
GLUCONATE

ALCIUM 8.6 10.6

mg / dL
 HYPERCALCEMIA,
CALCIUM of Promotes TUBULAR CALCIUM
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
PARATHYROID
characterized by excesssive
HORMONE
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
MALABSORPTION SYNDROME
OSTEOMALACIA
HYPERPARATHYROIDISM
MANAGEMENT:

TX OF CHOICE : SURGICAL REMOVAL OF

HYPERPLASTIC TISSUE
IV PNSS 5L/ DAY WITH DIURETICS
CRANBERRY JUICE (ACID-ASH)
LOW Ca
STRAIN URINEFOR STONES
CARE FOR PARATHYROIDECTOMY
DISORDERS OF
THE PANCREAS
DIABETES MELLITUS
(TYPE I, TYPE II)
TWO TYPES OF DIABETES
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
1.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
2.Non InsulinDependent 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
 olyuri
aolydipsi
a
olyph
agia
ruritu
aresthes
s
oor
ia
oor
healing
DIAGNOSTIC TEST FOR DM
1. Fasting Blood Sugar (FBS)
NPO for 12 hours
Normal value= 80-120 mg/dl
140 mg/dl or more diagnostic of DM
2. 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
Diagnostic Tests for DM
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
 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
Management of Hypoglycemia

1. Give simple sugar orally if pt. is conscious and can

swallow orange juice, candy, glucose tablets, lump of
sugar
2. Give Glucagon (SQ or IM) if pt. is unconscious or cannot
take sugar by mouth
3. As soon as pt. regains consciousness, he should be given
carbohydrate by mouth
4. 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.
Oral Antidiabetic Agents
Classification & Examples
Sulfonylureas
-Tolbutamide (Orinase)
- Chlorpropamide (Diabinese)
- Glipizide (Glucatrol)
- Glimepiride (Amaryl)
- Glibenclamide
Biguanides
- Metformin (Glucophage)
Alpha-Glucosidase Inhibitors
- Acarbose (Precose)
- Miglitol (Glyset)
Thiazolidinediones
- Rosiglitazone (Avandia)
Mechanism of Action
stimulate beta cells of the
pancreas to secrete insulin
improve binding bet. insulin and
insulin receptors
no. of insulin receptors
body tissues sensitivity to insulin
glucose uptake
inhibit glucose prod. by the liver
delay absorption of glucose in the
intestine
enhance insulin action at the
receptor sites
Oral Antidiabetic Agents
DIABETES
MILLETUS
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 DURATI
ON
Ultra rapid 15 mins. 2-4 hrs. 6-8 hrs.
acting
Insulin
analog
(Humalog)
Rapid acting: -1 hr 2-4 hrs. 6-8 hrs.
Regular
(Semilente)
Intermediate: 1-2 hrs. 7-12 24-30 hrs.
NPH hrs.
(Lente)
Long acting: 4-6 hrs. 18 + hrs 30-36 hrs.
Protamine
Zinc
(Ultralente)
DIABETES
MILLETUS
INSULIN THERAPY:
SITE OF INJECTION:
ABDOMEN
ANTERIOR THIGH
ARM
UPPER BACK
BUTTOCKS
B. Teach pt. on correct administration of insulin and other
hypoglycemic agents.
1. insulin in current use may be stored at room temp., all
others in ref. or cool area
2. avoid injecting cold insulin lead to tissue reaction
3. roll insulin vial to mix, do not shake, remove air bubbles
from syringe
4. press (do not rub) the site after injection (rubbing may
alter the rate of absorption of insulin)
5. avoid smoking for 30 mins. after injection (cigarette
smoking absorption)
6. 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
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
ACUTE COMPLICATIONS
OF DIABETES MILLETUS

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 (Kussmauls breathing)
acetone breath (fruity odor)
lethargy COMA
Blood glucose level > 250-350 mg/100 ml.
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:
KAUSMAULS BREATHING
ACETONE BREATH
METABOLIC ACIDOSIS
KETONURIA
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

1. Vascular Changes
a. ) 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!!
DISORDERS OF
THE ADRENAL
GLANDS
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 CORTEX
DISORERS
ADRENAL INSUFFICIENCY
( ADDISONS DSE)

CUSHINGS SYNDROME
 ADRENAL INSUFFICIENCY
ADDISONS DISEASE

INCAPABILITY OF THE
ADRENAL CORTEX TO
PRODUCE
GLUCOCORTICOIDS IN
RESPONSE TO
STRESS
Addison's Disease
Replacement of hormones
Hydrocortisone; Fludrocortisone
PNSS (0.9 NaCl)
Dextrose
Diet:
High-CHO & CHON
Low potassium, high sodium
Addisons disease
Addison's Disease
Monitor VS [4x / day]
Infection, Addisonian crisis,
dehydration
MIOW / MBP / MBloodGlucose
Give steroids with milk or an antacid
Avoid: Contacts & Stress
CUSHINGS
SYNDROME
CAUSE:
SUSTAINED OVER-PRODUCTION OF
GLUCOCORTICOIDS BY ADRENAL GLAND FROM

ACTH BY PITUITARY TUMOR

EXCESSIVE GLUCORTICOID
ADMINISTRATION
CUSHINGS
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
CUSHINGS
SYNDROME
PURPLE STRIAE FROM THINNING OF SKIN
ECHYMOSIS FROM SLIGHT TRAUMA
ANDROGENIC EFFECTS:
OLIGOMENORRHEA
HIRSUTISM
GYNECOMASTIA
HYPERTENSION FROM S. Na
CUSHINGS
SYNDROME
TREATMENT & NURSING CARE:

PSYCHOLOGICAL SUPPORT
PREVENT INFECTION INFLAM & IMMUNE
RESPONSE ARE SUPPRESSED
PROMOTE SAFETY
SURGERY SUB/TOTAL ADRENALECTOMY
Treat HPN
ALDOSTERONISM

HYPERSECRETION OF ALDOSTERONE

CONNS SYNDROME
CONNS SYNDROME
PRIMARY ALDOSTERONISM
CAUSE:
ADRENAL ADENOMA
S/SX:
HYPOKALEMIA
FATIGUE
HYPERNATREMIA, HPN
MANAGEMENT:
SURGERY
ALDACTONE ALDOSTERONE ANTAGONIST
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- VANILLY MANDALIC
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
 DECREASE
BMR & ENERGY
DECREASE
IN TSH,TH
& INSULIN
DECREASE
THE AGING GLUCOSE
EFFECTS OF TOLERANCE
ENDOCRINE
SYSTEM
DECREASE IN
DECREASE MUSCLE MASS
IN GH & INCREASE
FAT STORAGE
RECAP:
ANTERIOR PITUITARY:
GIGANTISM,
ACROMEGALLY,
DWARFISM

POSTERIOR PITUITARY:
DIABETES INSIPIDUS,
SIADH
LOCATION: BASE OF THE BRAIN
RECAP
ADRENAL GLAND:
ADDISONS DSE
CUSHING SYNDROME
ALADOSTERONISM

ADRENAL MEDULLA:
PHEOCHROMOCYTOMA

LOCATION: ON TOP OF THE KIDNEY

RECAP

PANCREAS:
DM
LOCATION: POSTERIOR TO LIVER

PARATHYROID:
HYPORATHYROIDISM
HYPERPARATHYROIDISM
LOCATION: NEAR THYROID
RECAP

THYROID:
HYPOTHYROIDISM
CRETINISM
MYXEDEMA
HYPERTHYROIDISM (GRAVES DSE)

LOCATION: ANTERIOR 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?
A. INFUSE 1L OF D5W OVER A 12 HR PERIOD.
B. ADMIN. 50% GLUCOSE IV
C. CHECK THE CLIENTS URINE FOR THE
PRESENCE OF SUGAR AND ACETONE
D. ENCOURAGE THE CLIENT TO DRINK ORANGE
JUICE W/ ADDED SUGAR
QUESTION NO.2
WHAT IS THE PRIMARY ACTION OF INSULIN
IN THE BODY?
A. ENHANCES THE TRANSPORT OF GLUCOSE
ACROSS THE CELL WALLS
B. AIDS IN THE PROCESS OF
GLUCONEOGENESIS
C. STIMULATES THE PANCREATIC BETA CELLS
D. DECREASE THE INTESTINAL ABSORPTION
OF GLUCOSE
QUESTION NO.3
POSTOPERATIVE THYROIDECTOMY NURSING
CARE INCLUDES WHICH MEASURES?
A. HAVE CLIENT SPEAK EVERY 5-10 MINUTES
IF HOARSENESS IS PRESENT
B. PROVIDE LOW-CALCIUM DIET TO PREVENT
HYPERCALCEMIA
C. CHECK THE DRESSING AT THE BACK OF THE
NECK FOR BLEEDING
D. APPLY SOFT CERVICAL COLLAR TO RESTRICT
MOVEMENT