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MAJOR DISORDERS

OF THE ENDOCRINE SYSTEM


Nio C. Noveno, RN, MAN
HORMONE REGULATION:
NEGATIVE FEEDBACK MECHANISM

If the client is healthy,


the concentration of hormones
is maintained at a constant level.

When the hormone concentration rises,


further production of that hormone is inhibited.

When the hormone concentration falls,


the rate of production of that hormone increases.
HORMONE REGULATION:
NEGATIVE FEEDBACK MECHANISM
DISORDERS OF THE ENDOCRINE
SYSTEM

Primary
Problem in the target gland; autonomous

Secondary
Problem in the pituitary

Tertiary
Problem in the hypothalamus
ANTERIOR PITUITARY
DISORDERS
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 Acromegaly
Prior to closure After closure
of the epiphyses; of the epiphyses;
proportional growth disproportional
growth
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
HYPERPITUITARISM:
MANAGEMENT

Medication Radiation
Bromocriptine- Indicated for larger
Cabergoline tumors
(dopamine agonists)
GH hypersecretion Surgery
and prolactinoma Trans-sphenoidal
hypophysectomy
Ocreotide
(somatostatin)
GH hypersecretion
TRANS-SPHENOIDAL
HYPOPHYSECTOMY
Post-surgery nursing care
 Semi- to high- Fowler’s position
 Protect from infection and stressful situations
 Hormone replacement
 Constant neurologic checks
 MIOW to check for DI
 WOF CSF leak
 Encourage deep-breathing, but not coughing
 Institute measures to prevent constipation
[straining increases ICP]
HYPOPITUITARISM

Deficiency of one or more


anterior pituitary hormones

Causes
Infections / Inflammatory disorders
Autoimmune diseases
Congenital absence
Tumor
Surgery / Radiation therapy
HYPOPITUITARISM
Simmonds' disease Sheehan’s syndrome
[Panhypopituitarism]
[Post-partum
Complete absence
pituitary necrosis]
of pituitary hormones
Cachexia: A complication
most prominent feature of delivery
Follows destruction Results from severe
of the pituitary blood loss and
by surgery, infection, hypovolemia
injury, or a tumor  Pituitary ischemia
HYPOPITUITARISM:
CLINICAL MANIFESTATIONS

Hypo -thermia, -glycemia, -tension

Loss of vision, strength, libido, &


secondary sexual characteristics
HYPOPITUITARISM:
MANAGEMENT

Medication Radiation
Hormonal substitution Indicated for larger
[maybe for life] tumors

Corticosteroids Surgery
Levothyroxine Trans-sphenoidal
Androgen / Estrogen hypophysectomy
Growth hormone
POSTERIOR PITUITARY
DISORDERS
DIABETES INSIPIDUS
Characterized by massive polyuria
due to either lack of ADH or renal insensitivity
Central DI
Due to a deficiency in ADH production
Nephrogenic DI
Due to a defect in the kidney tubules
that interferes with water absorption
Polyuria is unresponsive to ADH,
which is secreted normally.
DIABETES INSIPIDUS:
DIAGNOSTICS

Fluid deprivation test


Administration of desmopressin
24-hour urine collection
for volume, glucose, and creatinine
Serum for glucose, urea nitrogen,
calcium, uric acid, potassium,
sodium
DIABETES INSIPIDUS:
MANAGEMENT
Central DI:
Desmopressin, Lypressin [intranasal]
Vasopressin tannate in oil [IM]

Nephrogenic DI:
Indomethacin-
-hydrochlorothiazide
-desmopressin
-amiloride

Clofibrate, chlorpropamide
SYNDROME OF INAPPROPRIATE ADH
Disorder due to excessive ADH release

Clinical Manifestations

Persistent excretion of concentrated urine


Signs of fluid overload
Hyponatremia
LOC changes
No edema
SIADH: DIAGNOSTICS
 Low serum sodium [<135 mEq/L]
 Low serum osmolality
 High urine osmolality [>100 mOsmol/kg]
 High urine sodium excretion [>20
mmol/L]
 Normal renal function: low BUN [<10
mg/dL]
SIADH: MANAGEMENT
Maintain fluid balance Maintain Na balance
 MIOW  Increased Na intake
 Fluid restriction  Emergency treatment
 Loop diuretic of 3% NaCl, followed
[If with evidence of by furosemide
fluid overload] [If serum Na <120, or if
patient is seizing]
 Lithium or
demeclocycline  Excessively rapid
correction of
[Chronic treatment] hyponatremia may
cause central pontine
myelinolysis!
THYROID DISORDERS
THYROID FUNCTION TESTS

Serum TSH
Single best screening test [high sensitivity]
0.38 – 6.15 mcU/mL
If TSH is normal, fT4 should be normal.
Screening required beginning 35 years,
then q 5 years thereafter
Also used for monitoring thyroid hormone
replacement therapy
THYROID FUNCTION TESTS

Serum fT4
A direct measurement of free
thyroxine,
the only metabolic fraction of T4
0.9 to 1.7 ng/L (11.5 to 21.8 pmol/L)
Used to confirm an abnormal TSH
THYROID FUNCTION TESTS

Total serum T3 and T4


T3 70 to 220 ng/dL (1.15 to 3.10 nmol/L)
T4 4.5 to 11.5 mcg/dL (58.5 to 150 nmol/L)

T3 levels appear to be a more accurate


indicator of hyperthyroidism.
THYROID FUNCTION TESTS

T3 resin uptake test


Indirect measurement of unsaturated
thyroid-binding globulin (TBG)
25 – 35% uptake
Thyroid antibodies
5 – 10% of the population
Grave’s: 80%
Hashimoto’s: 100%
THYROID FUNCTION TESTS

Thyroid scan / Radioscan / Scintiscan


Utilizes a gamma camera and
radioisotopes
123
I, thallium, americium,
technetium-99m [99m Tc] pertechnetate
Results
Hot areas: increased activity
Cold areas: decreased activity
THYROID FUNCTION TESTS

Radioactive iodine uptake (RAIU)


Measures the proportion of administered
tracer
dose of ¹²³I present in the thyroid gland
at a specific time after administration
Results
Hyper: high uptake
Hypo: low uptake
THYROID FUNCTION TESTS

Fine-needle aspiration biopsy


Sampling of thyroid tissue to detect malignancy
Initial test for evaluation of thyroid masses
Results
Negative [benign]
Positive [malignant]
Indeterminate [suspicious]
Inadequate [non-diagnostic]
THYROID FUNCTION TESTS

Nursing Implications
 Determine whether the patient has taken
medications or agents that contain iodine
[antiseptics, multivitamins, cough syrup, amiodarone]
because these may alter the test results.
 Assess for allergy to iodine or shellfish.
 For scans, tell patient that radiation is only
minimal.
HYPERTHYROIDISM

Increased basal metabolic rate (BMR)

Causes
Grave’s disease (autoimmune)
Initial manifestation of thyroiditis
TSH-screening pituitary tumor
Toxic adenoma
Factitious thyrotoxicosis
Amiodarone therapy
HYPERTHYROIDISM:
CLINICAL MANIFESTATIONS

GI hypermotility
Rapid weight loss
Apprehension
[tremors, tachycardia, palpitations]
Volume deficit; voracious appetite
Exophthalmos; erratic menses
Systolic BP elevated; sweating

TSH  in primary disease


 in secondary disease
HYPERTHYROIDISM:
CLINICAL MANIFESTATIONS
THYROID STORM / THYROTOXIC
CRISIS
Occurs in patients
with existing
Marked delirium
but unrecognized
Severe tachycardia
thyrotoxicosis,
Vomiting
stressful illness,
Diarrhea
thyroid surgery, RAI
Dehydration
High fever
Increased systemic
adrenergic activity:
Severe
hypermetabolism
HYPERTHYROIDISM:
MANAGEMENT
Anti-thyroid drugs
Propylthiouracil (PTU); methimazole
Blocks thyroid hormone (TH) synthesis
Used for pregnant women and patients
who have refused surgery or RAI treatment
During pregnancy, PTU is DOC.
1% of infants born to mothers on anti-
thyroid therapy will be hypothyroid.
WOF agranulocytosis.
HYPERTHYROIDISM:
MANAGEMENT

RAI (¹³¹I), K or Na iodide, SSKI (Lugol’s)


Adjunct to other anti-thyroid drugs
in preparation for thyroidectomy
Treatment for thyrotoxic crisis

Inhibit release and synthesis of TH


Decrease vascularity of the thyroid gland
Decrease thyroidal uptake of RAI
HYPERTHYROIDISM:
MANAGEMENT

Medications to relieve the symptoms


related to the increased metabolic rate:
Digitalis, propranolol (Inderal), phenobarbital

Well-balanced, high-calorie diet


with vitamin and mineral supplements

Subtotal or total thyroidectomy


RAI THERAPY:
NURSING IMPLICATIONS
 NPO post-midnight prior to administration
[Food may delay absorption]
 After initial dose:
Urine and saliva slightly radioactive x 24H
Vomitus highly radioactive x 6-8H
Institute full radiation precautions.
 Instruct the patient to use appropriate
disposal methods when coughing and
expectorating.
K OR NA IODIDE, SSKI (LUGOL’S):
NURSING IMPLICATIONS
 Dilute oral doses in water or fruit juice and
give with meals to prevent gastric irritation,
to hydrate the patient, and to mask the very
salty taste.
 Give iodides through a straw to avoid teeth
discoloration.
 Force fluids to prevent fluid volume deficit.
 Warn patient that sudden withdrawal may
precipitate a thyrotoxic crisis.
 Store in a light-resistant container.
HYPOTHYROIDISM
A state of low serum TH levels
or cellular resistance to TH

Iodine deficiency
Autoimmune Oncologic
Developmental Drugs
Dietary Iatrogenic
Non-thyroidal
Endocrine
HYPOTHYROIDISM
Causes
Chronic autoimmune [Hashimoto’s]
thyroiditis
Hypothalamic failure to produce TRH
Pituitary failure to produce TSH
Inborn errors of TH synthesis
Thyroidectomy / Radiation therapy
Anti-thyroid therapy
Iodine deficiency
HYPOTHYROIDISM
Classified according to the time of life in which it occurs
Cretinism
In infants and young children
Lymphocytic thyroiditis
Appears after 6 years of age
and peaks during adolescence; self-limiting
Hypothyroidism without myxedema
Mild thyroid failure in older children and adults
Hypothyroidism with myxedema
Severe thyroid failure in older individuals
HYPOTHYROIDISM:
CLINICAL MANIFESTATIONS

Dry, brittle hair; dry, coarse skin


Edema (periorbital)
Reduced BMR [bradycardia, bradypnea]
Apathy; anorexia; anemia
Increased weight; intolerance to cold
Lethargy; loss of libido
Enlarged tongue
Drooling
 in primary disease
TSH  in secondary disease
MYXEDEMA COMA

Hypotension
Precipitating Factors
Bradycardia
Acute illness
Hypothermia
Rapid withdrawal
of thyroid medication
Hyponatremia
Anesthesia / Surgery
Hypoglycemia
Respiratory failure
Hypothermia
Comause
Opioid
HYPOTHYROIDISM:
MANAGEMENT
Prevention
Prophylactic iodine supplements to decrease
the incidence of iodine-deficient goiter
Symptomatic cases
Hormonal replacement
Levothyroxine (Synthroid)
Liothyronine (Cytomel)
Liotrix (Thyrolar)
Dosage increased q 2-3 weeks
especially in elderly patients
HYPOTHYROIDISM:
MANAGEMENT

Tell patient to WOF:


Chest pain, palpitations, sweating,
nervousness, and other S/S of overdosage

Instruct the patient to take TH at the same time


each day to maintain constant hormone levels.
Suggest a morning dosage to prevent insomnia.

Monitor apical pulse and BP.


If pulse >100 bpm, withhold drug.
HYPOTHYROIDISM:
NURSING INTERVENTIONS
Diet: high-bulk, low-calorie
Encourage activity
Maintain warm environment Maintain patent airway
Administer cathartics Administer medications:
and stool softeners Synthroid, glucose,
To prevent corticosteroids
myxedema coma, IV fluid replacement
tell patient to continue Wrap patient in blanket
course of thyroid Treat infection
medication even if
or any underlying illness
symptoms subside.
PARATHYROID DISORDERS
HYPERPARATHYROIDISM
Primary
Single adenoma
Genetic disorders
Multiple endocrine neoplasias
Secondary
Rickets
Vitamin D deficiency
Chronic renal failure
Phenytoin or laxative abuse
HYPERPARATHYROIDISM:
CLINICAL MANIFESTATIONS

Constipation
Apathy
Lordosis
Cardiac dysrhythmias
Upset GIT
Low energylevels
Increased BP
PTH
 Calcium
Alkaline phospatase
 PO4
HYPERPARATHYROIDISM:
MANAGEMENT

Surgery to remove adenoma


Force fluids; limit dietary calcium intake
For life-threatening hypercalcemia:
Furosemide
Bisphosphonates
[Etidroanate (Didrodinel), pamidronate]
Calcitonin (Cibacalcin, Miacalcin)
Plicamycin (Mithracin) + glucocorticoid
Mithramycin
HYPOPARATHYROIDISM
Causes
Congenital absence
or malfunction of the parathyroids
Autoimmune destruction
Removal or injury to one or more
parathyroids during neck surgery
Massive thyroid radiation therapy
Ischemic parathyroid infarction during surgery
HYPOPARATHYROIDISM:
CLINICAL MANIFESTATIONS

Dyspnea; dysrhythmias
Extremities: tingling
Fotophobia
Increased bone density
Chvostek sign; cramps
Irritability
Trousseau sign; tetany
PTH
 Calcium
Alkaline phospatase
 PO4
HYPERTHYROIDISM:
MANAGEMENT
IV Ca chloride or gluconate [emergency treatment]
DOC post-thyroidectomy
Oral Ca salts (Ca carbonate or gluconate)
Vitamin D supplementation
Increase intestinal Ca absorption
Dihydrotachysterol, ergocalciferol
Trousseau’s &
E levated serum PO4; low
Chvostek’s
T
Caingling
2+
Alkalosis; Arrhythmias
Narrowing of airway
Irritability
Cramps
HYPOPARATHYROIDISM

Parathormone injections [in acute


attacks]
WOF allergies
Diet: High-calcium [spinach], low-
phosphate [milk, cheese, egg yolks]
Al(OH)2, Gelusil, Amphogel p.c.
Pentobarbital (Nembutal)
[calm environment]
T
ETANY
AKE
RACHEOSTO
MY

C
ALCIUM

ARE
GLUCONATE

ALCIUM 8.6 – 10.6


mg / dL
PHEOCHROMOCYTOMA
ADRENAL GLANDS
ADRENAL MEDULLA

 Release
cathecholamines
 Epinephrine
 Norephinephrine

 Released during
“fight or flight”
situations
(sympathetic effect)
PHEOCHROMOCYTOMA

Adrenal tumor

Increased Epi and NEpi

Heredity
PHEOCHROMOCYTOMA

Headache
Anxiety
Nausea
Eye disturbances
Severe hypertension
PHEOCHROMOCYTOMA

BP
HR
Diaphoresis
BMR
VMA
Glucose
PHEOCHROMOCYTOMA
Adrenalectomy

Steroid treatment

Antihypertensive and
antidysrhythmic
nitroprusside (Nipride)
propranolol (Inderal)
phentolamine (Regitine)
PHEOCHROMOCYTOMA
MBP / MIO
Fluid replacements
Decrease environmental stimulation
Maintenance doses of steroids
Follow-up check up
24-hour urine specimens
[VMA and catecholamine studies]
Avoid: coffee, chocolate, beer, wine, citrus
fruit, bananas, and vanilla 24h before
test
ADDISON'S DISEASE
ADRENAL CORTEX HORMONES
 Glucocorticoids
Cortisol, corticosterone
Increase blood glucose levels by
increasing rate of gluconeogenesis
Increase protein catabolism
Increase mobilization of fatty acids
Promote sodium and water retention
Anti-inflammatory effect
Aid the body in coping with stress
ADRENAL CORTEX HORMONES
 Mineralocorticoids
Aldosterone, Corticosterone,
Deoxycorticosterone
Regulate fluid and electrolyte balance
Stimulate reabsorption of sodium, chloride
and water
Stimulate potassium excretion
 Underthe control of Renin-Angiotensin-
Aldosterone system (RAAS)
ADRENAL CORTEX HORMONES

Sex hormones
Androgens, Estrogens
Influences the development of
sexual characteristics
ADDISON'S DISEASE

Hyposecretion of adrenocortical
hormones

Destruction of the cortex

Idiopathic atrophy
ADDISON'S DISEASE

Weakness
Excess stress
A/N/V/D
K & ACTH elevation; Low Na,
BP, cortisol, glucose
ADDISON'S DISEASE

Replacement of hormones
Hydrocortisone; Fludrocortisone
PNSS (0.9 NaCl)
Dextrose
Diet:
High-CHO & CHON
Low potassium, high sodium
ADDISON'S DISEASE

VS, weight, and serum glucose


level
24-hour urine specimens
[LOW 17- hydroxycorticosteroids &
17-ketosteroids]
Electrolyte levels: K; Na
Bronze-skin
Changes in energy or activity
ADDISON’S DISEASE
ADDISON'S DISEASE

MVS [4x / day]


Infection, Addisonian crisis,
dehydration
MIOW / MBP / MBG
Give steroids with milk or an antacid
Avoid: Contacts & Stress
CUSHING'S SYNDROME
CUSHING'S DISEASE

Adrenal hyperplasia /
tumor
Cushing’s disease
Tumor-secreting ACTH
Hypothalamic
Buffalo hump
Unusual behavior (depression, personality
changes, fatigability)
Facial features (moonface, hirsutism in
women)
Fat (truncal obesity)
ACTH and cortisol in blood
elevated;
Loss of muscle mass
Overextended skin (abdominal
striae with easy bruisability)
Hypertension, hyperglycemia,
hypernatremia
Urinary cortisol elevated
Menstrual irregularities
Porosity of bones
(osteoporosis)
CUSHING’S SYNDROME
CUSHING'S SYNDROME

Remove exogenous steroids

Hypophysectomy or irradiation

Adrenalectomy
CUSHING'S SYNDROME

Cyproheptadine (Periactin)
Metyrapone
Mitotane (Lysodren)
Aminoglutethamide (Cytadren)
Potassium supplements
High-CHON; Low Na
CUSHING'S SYNDROME
MVS, MIOW, MBP, MBG
Electrolyte levels: Na & K
Urine specimens
[LOW 17- hydroxycorticosteroids & 17-
ketosteroids]
Physical appearance
Changes in coping & sexuality
[verbalization]
Stress reduction
DIABETES MELLITUS
DIABETES MELLITUS

Insulin resistance [GDM, age]


Failure in production
Blockage of insulin supply
Autoimmune response
Excess body fat
Heredity
DIABETES MELLITUS
Type I [juvenile ]/IDDM

Type II [adult- onset type]/


NIDDM
gradual onset
diet and exercise obesity

Pancreatectomy, Cushing's
syndrome, drugs
DIABETES MELLITUS

Low insulin leads to:


to

Hyperglycemia
Glucosuria
Polyuria
Gluconeogenesis
DIABETES MELLITUS

Complications
Microvascular
Retinopathy & Renal failure
Macrovascular
CV and PVD
Peripheral neuropathy
olyuri
aolydipsi
a
olyph
agia
ruritu
aresthes
s
oor
ia
oor
healing
Normal Impaired DM

FBS <110mg/dl 110-125mg/dl ≥126mg/dl

2H <140mg/dl ≥140; ≥ 200


OGTT <200mg/dl mg/dl
DIABETES MELLITUS

Diet
complex CHO [50% to 60%]
water-soluble fiber
oat, bran, peas, beans, pectin-rich
FV
CHON [12% to 20%]
60 and 85 g
CHOO [<30%]
70 to 90 g/day / MUFA
DIABETES MELLITUS

Insulin dose adjustments depend on:


physical and emotional
stresses
specific type of insulin
condition and needs of the
client
Insulin Onset Peak Duration

Ultra rapid acting 10-15 min 1H 3H


insulin analog
(humalog)

SAI (humulin regular) ½-1H 2-4 H 4-6 (8) H

IAI (humulin lente, 3-4 H 4-12 H 16-20 H


Humulin NPH)

LAI (Protamine zinc, 6-8 H 12-16 H 20-30 H


humulin ultralente)

Premixed insulin ½-1 H 2-12 H 18-24 hrs


(NPH-regular
[80-20, 70-30, 50-50])

Insulin glargine Slower than No Peak 24 H


(Lantus )
NPH
DIABETES MELLITUS

Somogyi effect
Epinephrine & Glucagon
Glycogenolysis
[iatrogenically-induced hyperglycemia]
Lowering insulin dosage at night
MBG
DIABETES MELLITUS
Insulin pump
1) Basal doses of regular insulin delivered
every few minutes bolus doses delivered
pc

2) Appropriate amount of insulin for 24


hours plus priming is drawn into syringe

3) The administration set is primed and


needle inserted aseptically, usually into
abdomen
DIABETES MELLITUS

Client teaching points:


1. Proper insulin preparation using
aseptic technique
2. When to remove the pump
(e.g., before showering or
sexual relations)
3. MBG at home
INSULIN ADMINISTRATION
Increases the hypoglycemic effects of insulin
Aspirin, alcohol, oral anticoagulants, oral
hypoglycemics, beta blockers, tricyclic
antidepressants, tetracycline, MAOIs
Increases blood glucose levels
Glucocorticoids, thiazide diuretics, thyroid
agents, oral contraceptives
Increase the need for increased insulin dose
Illness, infection, and stress
ORAL HYPOGLYCEMIC AGENTS
Sulfonylureas
Promotes increase insulin secretion from pancreatic
beta cells through direct stimulation
First Generation Agents:
Acetohexamide
Tolbutamide (Orinase)
Tolzamide (Tolinase)
Chlorpropamide (Diabenese)
Second Generation Agents:
Glipizide (Minidiab, Glucotrol)
Glyburide (DiaBeta, Glynase, Micronase)
Glimepiride (Amaryl)
ORAL HYPOGLYCEMICS

Biguanides
Reduces hepatic production of glucose
by inhibiting glycogenolysis
Decrease the intestinal absorption of
glucose and improving lipid profile
Agents:
Phenformin
Metformin (Glucophage, Glucophage XR)
Buformin
ORAL HYPOGLYCEMICS
Alpha-glucosidase inhibitors
Inhibits alpha-glucosidase enzymes in
the small intestine and alpha
amylase in the pancreas
Decreases rate of complex
carbohydrate metabolism resulting
to a reduced rate postprandially
Agents:
Acarbose (Precose, Gluconase, Glucobay)
Miglitol (Glyset)
ORAL HYPOGLYCEMICS

Thiazolidinediones
Enhances insulin action at the cell and post-
receptor site and decreasing insulin
resistance
Agents:
Pioglitazone (Actos)
Rosiglitazone (Avandia)
Rosiglitazone + Metformin
(Avandamet)
DIABETES MELLITUS

Other therapies include:


1. pancreas islet cell grafts
2. pancreas transplants
3. implantable insulin pumps
4. cyclosporin [Sandimmune,
Neoral]
DIABETES MELLITUS

MBG [done pc and hs] +


HbA1C
MBP + weight
Renal function + MIO
Eye examination
GLYCOSYLATED HEMOGLOBIN
(HBA1C )

Reflects
effectiveness of
treatment
< 7.5% (good control)
7.6% - 8.9% (fair control)
> 9% (poor control)
DIABETES MELLITUS

diet & weight


ketonuria
note infection
legs / feet / toenails check
[keep in between toes dry]
acceptance & understanding
DIABETES MELLITUS

Administer insulin
sterile technique
rotating injection sites
dosage / types / strengths / peak
CHO source
Avoid:
Avoid tight shoes; smoking;
heat
DIABETES MELLITUS

hypoglycemia
Headache
Nervousness
Diaphoresis
Rapid, thready pulse
Slurred speech
THE CLIENT IS TIRED!

Tremors
achycardia Hypoglycemia: <50 mg/dL
Irritability Causes:

Restlessnes
 Overtreated hyperglycemia

 Increased exercise
sxcessive hunger β-blockers
E xcitability  Gastric paresis

 Alcohol intake

D iaphoresis  Erratic insulin absorption


Mild: Rx:
Shakiness 10-15 gm carbohydrate
Tremors 2 oz. (1 small tube of) cake
Excessive icing
4 oz. orange juice
hunger 6 oz. regular soda
Paresthesias 6-8 oz 2% skim milk
Pallor (4 to) 10 pieces of hard
candy
Diaphoresis
Moderate:
Drowsiness
Impaired judgment
Rx:
Double or blurred vision

Headache 20-30 gm
Inability to concentrate carbohydrate

Mood swings
Irritability
Glucagon 1 mg
Slurred speech SQ/IM
Severe:
Rx:
Seizures
Unconsciousnes 25 gm D dextrose IV
50
s
Disorientation Glucagon 1 mg IM/IV
DIABETES MELLITUS

diabetic coma
Restlessness
Hot, dry, flushed skin
Thirst
Rapid pulse
Nausea
Fruity odor to breath
Ketoacidosis
Urinary changes
Rx:
Sunken eyeballs Regular insulin drip
Skin is warm &  0.9% or 0.45% NSS
flushed  1:1 [100U:100cc]
Membranes are dry Nursing care:
 Check glucose
Arrhythmias
 250-300 mg/dL
Upset GI system [q30-60mins]
Low BP  250 mg/dL
Saline solution  DC the drip
NON
Ketosis is absent
Electrolyte imbalance [K+
decrease]
Thirst
Obtundation
Treat with regular insulin
drip
Initiate diet
Correct hyperglycemia
Normal creatinine?
Erythrocyte sedimentation rate [ESR: 0-20
mm/hr]
Poor glycemic control
Hemodialysis
Restrict: Na+, CHON, K+, weight
Output & input (MIO)
No symptoms
Reduced O2 in the eye
Elevated sugar & BP
Tension is high in the retina
Increased lens opacity
NO eyesight
Annual eye exam [every 6-12
months]
MAJOR DISORDERS
OF THE ENDOCRINE
SYSTEM
THANK YOU!

Nio C. Noveno, RN, MAN