MS/Endocrine System/MJTayco/09 1

 Disorders of the Endocrine System 

Hypopituitarism Hyperpituitarism
Definition  Deficiency of one or more anterior  Excessive concentration of pituitary
pituitary hormones hormones (GH, ACTH, PRL) in the blood,
PANHYPOPITUITARISM or “SIMMONDS 
DISEASE”
“SHEEHAN’S SYNDROME”
 [Women with Severe Bleeding,
Hypovolemia, Hypotension – Delivery]
Etiology  Destruction of the anterior lobe of the  Benign Pituitary Adenoma
gland:  Hyperplasia of pituitary tissue
 Trauma (Surgery/Radiation) Prolactinomas
 Tumor/Vascular Lesion (Prolactin-secreting Tumors)
 Hemorrhage
Assessmen Vary with Target Organs Affected 2 Classifications of GH Overproduction
t  CNS:  Giantism:
[Hemianopsia/Headache  Acromegaly:
[Lethargy]  CNS:
[Visual disturbances] [Headaches]
 Integument: [Depression]
[Wt. Loss/Emaciation] [Hemianopsia or scotomas/blind]
[Hair Loss] [Somnolence]
[Tolerance for cold (Temp.)] [ICP]
 Repro: [Behavioral Changes, Seizures]
[Impotence] [Disturbances in Appetite, Sleep, Temp.,
[Amenorrhea] Emotion]
 CVS:  Endocrine:
[Postural Hypotension] [Irreg. Menses]
 Endocrine: [Infertility]
[Glycemia] [Galactorrhea]
[Hypometabolism (hypothyroidism)] [Libido]
[Adrenal Insufficiency] [Dyspareunia]
[Atrophy of Endocrine Glands & Hormones] [GH, ACTH, PRL]
[GH, ACTH, TSH, FSH, & LH] [Hyperthyroidism]
Diagnostic  X-Ray  X-Ray
Tests Long Bones Skull (Sella Turcica) Jaw Long Bones Skull (Sella Turcica) Jaw
 CT Scan  CT Scan
 MRI  MRI
Collaborati a. Surgery: a. Surgery:
ve Mgt.  Surgical Removal of Tumor  “Transphenoidal Hypophysectomy”
 “Transphenoidal Hypophysectomy”  Nsg. Intervention After:
 Nsg. Intervention After:  HOB 
 HOB   Nasal Packing
 Nasal Packing  Oral Care with Toothettes
 Oral Care with Toothettes  AVOID blowing the nose NO Bending
 AVOID blowing the nose  Care for client (Intracranial surgery):
 NO Bending  Neurologic assessments
 Report:  Specific gravity of urine,
 Output:  900 cc/H  I&O
 MS/Endocrine System/MJTayco/09 2
 Sp. Gr.  1.004 (D.I.)  Wt. (Daily)
 Note:  Check clear nasal drainage for
 Swallowing glucose to determine presence of
 Nasal Drip + CHON CSF
b. Pharmacotherapy:  Deep breathing, but not coughing
 HRT (Hormone Replacement Therapy)  Prevent constipation
 Thyroid replacement is not given Pharmacotherapy:
until (+) hypothyroidism  Somatostatin Analog Octreotide
 Vasopressin Testosterone (Sandostatin)
 Estrogen-progestin  Dopamine Agonist Bromocriptine
 Lifetime hormone therapy (Parlodel)
c. Radiation b. Radiation

Siadh
Diabetes insipidus (Syndrome of inappropriate anti-diuretic hormone)
Definition  Deficient production or secretion of the  Excessive ADH secretion  fluid
ADH (Posterior Pituitary Gland)   retention and dilutional Hyponatremia
reabsorption of H2O in nephron tubules
 NEUROGENIC DI:
Etiology  Familial  Head trauma
 Idiopathic  Tumors
 Secondary:  Infection
 Trauma; Surgery; Tumors; Infections
 Autoimmune disorders
 Neurogenic:
 Familial
 From renal disorders
 Primary Aldosteronism ( H2O intake)
(primary polydipsia)
 Results in impaired renal concentrating
ability
Assessment  Polydipsia (Craving for Cold H2O)  CNS:
 Polyuria (5 – 25 L/24H) [Fatigue] [Headache]
 DHN: [Change in Mental Status]
[Poor Skin Turgor] [Seizures] [Coma]
[Dry Mucous Membrane]  GIT:
[Temp.] [Anorexia] [Nausea]
 Renal:
[Urine Output]
 MuscSkeletal:
[DTRs]
 Fluid Retention:
[Wt.] [Crackles]
[Jugular Vein Distention]
Diagnostic  Sp. Gr. (1.001 – 1.005)  S. Na+ & Osmolality
Tests  S. Na+ & Osmolality
Collaborati a. Pharmacotherapy a. Fluid restriction
ve Mgt.  Vasopressin b. IV (Hypertonic)
 Lypressin (Diapid) c. Fluid & Electrolyte Status
 Desmopressin (DDAVP) d. Seizure precautions
 Vasopressin Tannate e. Supportive measures for related
 MS/Endocrine System/MJTayco/09 3
(Pitressin Tannate) disorders
[ADH Hormone Replacement]
b. Fluid: P.O/IV
c. Fluid & Electrolyte Status
d. I&O
e. Daily Wt.
f. Skin Turgor
g. Monitor response to ADH replacement
h. Teach:
 Long-Term Vasopressin Therapy
 Daily Wt. records
 Recognition of Polyuria
 Wearing a Medical Alert Bracelet
 Over dosage  SIADH H2O
retention and Na+
 AVOID alcohol
[Suppresses ADH secretion]
i. Treat Underlying Condition

Addison’s disease Cushing’s SYNDROME

Definition  Hyposecretion of Adrenocortical H.  Hypersecretion of Adrenocortical H.
 ADDISONIAN CRISIS: Acute adrenal
insufficiency
Precipitated by Stresses:
[Pregnancy] [Surgery] [Infection] [DHN]
[Emotional Turmoil]
FATAL: if not treated
Etiology  Autoimmune Destruction of the Cortex  Hyperplasia
 Idiopathic Atrophy  Tumor of the Adrenal Cortex
 TB [However, the primary lesion may occur in the
 Fungal (KOH Smear) pituitary gland   production of ACTH]
 Administration of Glucocort. or ACTH
Assessment  NeuroMusc:  NeuroMusc: [Mood Swings] [Psychosis]
[Fatigue] [Weakness] [Weakness]
 Cardio:  Cardio: [BP]
[BP]  Repro: [Libido] [Amenorrhea]
Resp:  Physical:
[Weak Pulse] [Obese trunk] [Thin arms & legs]
 GIT: [Moon Face] [Buffalo Hump] [Acne]
[N/V] [Anorexia] [Diarrhea] [Hirsutism] [Ecchymotic areas]
 Integument: [Purple Striae on breast and abdomen]
[Bronze Pigmentation] Immune: [Susceptibility to Infection]
Diagnostic  S. CortisolGlucose; Na+  S. Cortisol; Glucose
Tests  17-ketosteroids & 17-hydroxysteroids  17-hydroxycorticosteroids &
[24-Hour Urine Collection] 17-ketosteroids
 P. ACTH; K+  K+
 X-Ray (Osteoporosis)
Collaborati a. Pharmacotherapy a. Pharmacotherapy
ve Mgt.  Hormone Replacement  Dosage of externally administered
 Glucocorticoids corticoids

[Correct Metabolic Imbalance & BP]
 Steroids as ordered
 Anti-emetics
[Prevent F&E loss by vomiting]
[Give with milk or an antacid to limit
ulcerogenic factor of the drug]
b. Correct F& E & Glucose Imbalances
c. Diet: CHO, CHON
d. VS
[Alert for Temp. (infection,
dehydration)]
[PR &Rhythm (hyperkalemia)]
[Alterations in BP]
e. Signs of Na+ & K+ imbalance
f. I&O, Daily WT.
g. Private room
[Prevent contact with clients having
infectious diseases]
h. Limit the number of visitors
i. Teach:
 Advise the client to avoid physical and
emotional stress
 Need for lifelong hormone replacement
with Dosage (stress)
 Review signs of adrenal hypofunction
or hyperfunction
[Client can recognize need for
adjustment of steroid dose]
 Wear medical alert band
MS/Endocrine System/MJTayco/09 4
 Adrenal enzyme inhibitors
 K+ Supplements
b. Surgery
 Adrenalectomy [Adrenal Gland Tumor]
(Surgical excision of the adrenal tumors)
 Hypophysectomy or irradiation of the
pituitary [Pituitary Gland Tumor]
[If Pituitary Lesion  Secretion
ACTH]
c. Diet
 CHON with Na+ Restriction
d. VS; Daily Wt; I&O; blood glucose, E.
e. Protect from exposure to infections
f. Encourage ventilation of feelings by the
client and spouse
[Changes in body image and sex drive can
alter marital support]
g. Attempt to  Stress in the environment
[Limiting visitors]
[Explaining procedures carefully]
h. Care for the client following bilateral
Adrenalectomy
i. Care for the client following a
Hypophysectomy

Pheochromocytoma
Definition  Tumor that is usually benign
 Malignancy: 10% (Bilateral) 10% (Malignant)
Incidence  Age: 20 – 50 yrs. Old
Etiology  Originates from chromaffin cells of adrenal medulla
Pathophysiolo Stimulates Hypersecretion of catecholamines (epi. & norepi.)
gy 
Assessment SNS Over activity

Hypertension
Headache
Hyperhidrosis (Sweating)
Hypermetabolism
Hyperglycemia
Diagnostic  Vanillylmandelic Acid Test (VMA)
Studies  Total Plasma Catecholamine Concentration
 Clonidine Suppression Test
 CT Scan, MRI, & UTZ
Collaborative a. Pharmacotherapy
Mgt. i. Phentolamine (Regitine)
ii. Na Nitroprusside (Nipride) [ BP quickly]
 MS/Endocrine System/MJTayco/09 5
iii. Metyrapone [Dx adrenal gland dysfunction]
b. Surgery
i. Adrenalectomy
ii. Removal of single gland requires corticosteroid therapy for 1st few days/weeks
post-op
iii. Bilateral Removal requires lifetime corticosteroid therapy
c. Bed Rest, HOB elevated during BP, CR & anxiety [Provide orthostatic BP]

Hypothyroidism
Definition  Absence or  production of thyroid
hormone
Classified accdg. to time of life occurs:
1.CRETINISM
 Infants & young children
2.LYMPHOCYTIC THYROIDITIS
 After 6 y.o
 Peaks at Adolescence
 Self-limiting
3.HYPOTHYROIDISM (no MYXEDEMA)
 Mild degree of thyroid failure in older
children & adults
4.HYPOTHYROIDISM (w/ MYXEDEMA)
 Severe degree of thyroid failure in
older individuals
5.MYXEDEMA COMA
 Most Severe degree of hypothyroidism
 Potentially fatal endocrine emergency
 Precipitated by a severe physio. stress
 Temp., HR, Ventilation &
progressive LOC
 level of TH  interfere with
Erythropoiesis & Lipid Metabolism
Etiology  Primary Thyroid Disease
 Response to  TSH
 Effect of thyroid surgery
 Effect of radioactive iodine (RAI)
treatment
 AntiThyroid Drugs
 Hashimoto’s Thyroiditis
 An autoimmune disorder
 Most common
Assessment 3 Basic Concepts:
 MR [d/t Hyposecretion of T3]
 Body Heat [d/t Hyposecretion pf T4]
 Ca++ [d/t Hyposecretion of T,cal]
 CNS:
[Dull Mental Processes] [Apathy]
[Lethargy]
 Cardio: [PR]
Hyperthyroidism
 Excessive concentration of TH in the
blood
 Enlargement of the gland (Goiter)
“GRAVES’ DISEASE”
“THYROTOXICOSIS”
1. “Parry’s Disorder”
2. “Basedow’s Disorder”
3. “Exophthalmic Disorder”
4. Toxic Diffuse Disorder
 Thyroid disease or TSH
 Graves’ Disease
[Autoimmune process of impaired regulation
20 to other autoimmune disorders]
 Iodine intake with no  in secretion of
thyroid is present.
 Thyrotoxic crisis (Thyroid Storm)
[State of hypermetabolism]  H. Failure
[Precipitated by a period of severe
physiologic or psychological stress, thyroid
surgery, or radioactive iodine T.]
3 Basic Concepts:
 MR [d/t Hypersecretion of T3]
 Body Heat [d/t Hypersecretion T4]
 Ca++ [d/t Hypersecretion of T.cal]
 CNS: [Emotional Lability] [Apprehension]
[Insomnia]
 Cardio: [Systole] [Pulse]
 Resp: [RR]

 Respi: [Drooling] [Hoarseness]
 GIT:
[Obesity] [Anorexia] [Constipation]
[Anemia]
 Integument: [Lack of Facial Expression]
[Temp.] [Dry, Brittle Hair & Nails]
[Dry, Coarse Skin] [Enlarged Tongue]
[Hair Loss]
 Sensory:
[Diminished Hearing] [Periorbital Edema]
 Endocrine:
[(T4) & (T3)]
[radioactive iodine uptake]
[Delayed or poor response to TSH
stimulation test]  20 hypothyroidism
[ in TSH]  10 hypothyroidism
Repro: [Irreg. Mens]
Collaborativ a. Pharmacotherapy:
e Mgt.  Thyroid Hormones
 Proloid (Thyroglobulin)
 Synthroid (Levothyroxine)
[Before Breakfast]
 Interacts with Synthroid:
i. Anticoagulant
ii. Oral AntiDM
iii. Digitalis
 Dessicated Thyroid Extract
 Cytomel (Liothyronine)
[BP, PR before admin.]
[Start with Low Dose, gradually ]
b. Monitor VS
 Alert:
i. Angina pectoris (chest pain,
indigestion)
ii. Cardiac failure (dyspnea,
palpitations)
c. Weigh daily
d. Diet [Caloric] [Fiber]
 Diet that Inhibit Thyroid Secretions
i. [Strawberry] [Cabbage] [Radishes]
e. Provide Warm Environment
[Cold Climate]
f. Explain  sensitivity to narcotic
analgesics and tranquilizers
necessitates dosage adjustment
[OTC drugs should be avoided unless
MS/Endocrine System/MJTayco/09 6
 GIT:
 [Polyphagia] [Wt.] [Loose Stools]
 Sensory/Integument:
[Heat Intolerance] [Diaphoresis] [Temp]
[Exopthalmos (accumulation of fluid at
fatpads behind eyeballs)]
[Corneal Laceration, Ophthalmitis, Blind]
Von Graefe’s Sign (LID LAG)
Long & deep palpebral fissure still evident
(looks down)
Jeffrey’s Sign
Forehead remains smooth (looks up)
Dalyrimple’s Sign (Thyroid Stare)
Bright-eyed stare, infrequent blinking
 MuscSkeletal:
[Tremors] [Hyperactive Reflexes]
 Endocrine:
[TSH, if Thyroid Disorder]
[TSH, if 20 to Pituitary Disorder]
[T3, T4] [CHON bound iodine]
[Long Acting Thyroid Stimulator]
[Radioactive Iodine Uptake]
a. Pharmacotherapy:
 PTU or Methimazole (Tapazole)
[Block the synthesis of thyroid hormone]
[ISOLATION: Private, aircon room]
[Note:Agranulocytosis/Neutropenia]
(Fever, Sore Throat, Skin Rashes)
 Anti Thyroid
 Iodine (Lugol’s solution or SSKI)
[To  vascularity of the thyroid gland]
[Mix with fruit juice with ice or glass of
H2O to improve palatability]
[Provide straw; to avoid teeth stain]
[Note: Allergy, Saliva, Coryza]
 Radio Active Iodine
[To destroy thyroid gland cells 
 production of thyroid hormone]
 Digitalis; Propranolol; Phenobarbital
[To relieve the symptoms r/t  M.R.]
[To control PR, HPN]
 Ca++ - Channel Blockers
 Dexamethasone
[Inhibit action of Thyroid Hormone]
b. Surgery
 Thyroidectomy (Subtotal or Total)
[5/6 of gland is removed]
 Before Thyroidectomy:
 Administer prescribed anti thyroid
medications [Euthyroid State]
 Administer Iodides

approved by the physician]
g. Moisturizers to skin
h. Myxedema Coma:
 IV Thyroid Hormones
 Correction of Hyperthermia
 Maintenance of Vital Functions
 Treat Precipitating Factors
 AVOID Sedatives or Hypnotics
[Unconsciousness]
i. Iodine-Based Chemo.
MS/Endocrine System/MJTayco/09 7
[Size & Vascularity of gland]
 Teach breathing exercises and use of
hands
[To support neck and to avoid strain on
suture line]
 Stable VS
 ECG [Cardiac Failure from HPN/CR]
 After Thyroidectomy:
 Signs of respiratory distress &
laryngeal stridor caused by tracheal
edema
[To speak qH]
[Keep tracheotomy set available]
(1st 48H)
[PT damage  Ca++  L. Spasm]
 Humidity with cold steam nebulizer
[To keep secretions moist when home]
 Bed (Semi Fowler’s elevated w/
pillow)
 Prevent Hemorrhage
 Ice collar over the neck
 Dressings at the operative site and
back of the neck and shoulders
 Signs of hemorrhage
 Signs of Thyroid Storm
 Temp, HR, irritability, delirium,
coma
[From manipulation of the gland during
surgery  releases TH  bloodstream]
 Measures to Temp.
 [TSB, Acetaminophen]
 Notify the physician immediately
 Signs of thyroid storm occur
 Propranolol (Inderal)] [Iodides] [PTU]
[Steroids]
 Signs of Tetany
 [Numbness or twitching of
extremities] [Spasm of the glottis]
 [Hypocalcemia]  [After accidental
trauma or removal of the parathyroid
g.]
 Monitor BP [Trousseau]
 If Tetany Occurs
 Ca++ Gluconate or Ca++ Cl (IV)
c. Well balanced, high calorie diet with
vitamin and mineral supplements
d. Stimulation, medications
e. Back rub
f. Protect the client from stress producing
situations
g. Keep the room cool
 MS/Endocrine System/MJTayco/09 8
h. Provide eye drops or patches prn
O2 prn

Hypoparathyroidism Hyperparathyroidism
Definition  Hyposecretion of PTH  Hypersecretion of PTH
 Absorption of Ca++ & excretion of P by the
kidneys is 
If dietary intake is not enough to meet Ca+
+ levels demanded by high levels of
parathormone

Demineralization of the bone occurs
Etiology  Thyroid Surgery  Adenoma
 Parathyroid Surgery  Hypertrophy & hyperplasia of the glands
 Radiation Therapy of the Neck
 Idiopathic Hypoparathyroidism (Rare)
Assessment  CNS:  CNS:
[Trousseau’s Sign] [Chvostek’s Sign] [Apathy] [Fatigue] [Irritability]
[Irritability] [Tremors] [Convulsion]  Cardio: [Dysrrhythmias]
 Cardio: [Dysrrhythmias]  GIT:
 Resp: [Anorexia] [N/V] [Constipation]
[Dyspnea] [Wheezing (Laryngeal Spasm)]  Renal:
 MuscSkeletal: [Renal Calculi] [Pyelonephritis]
[Muscle Cramps] [Tingling of Extremities] [Renal Damage] [Polyuria]
[Bone Density]  MuscSkeletal:
 Sensory: [Weakness]
[Photophobia] [Deep Bone Pain  Demineralization]
 Endocrine: [Bone Cysts] [Pathologic Fractures]
[S. Ca++] [PTH] [S. PO4]  Endocrine:
[S.Ca++] [PTH] [S. Phosphorus]
Collaborativ a. Pharmacotherapy a. Pharmacotherapy
e Mgt.  Ca++ Cl or Ca++ Gluconate IV  Furosemide (Lasix)
[Emergency Tx. = Overt Tetany] [Renal Excretion of Ca++]
 Ca++ Salts P.O  Galium Nitrate; Calcitonin; Plicamycin
Ca++ CO3 or Ca++ Gluconate with Glucocorticoid
 Vit. D [Ca++ Level]
 Dihydrotachysterol b. Surgery
 Ergocalciferol  Excision of Parathyroid Gland
[Absorption of Ca++ from GIT]  Care same as Thyroidectomy
 PTH Injections c. Ca++ Intake Restricted
 AL OH d. Strain the urine [Calculi]
[Absorption of P from GIT] e. Encourage fluid intake
 Ca++; PO4 (Diet) f. Ambulating
b. Check: Respiratory Distress [To help prevent demineralization] [Avoid high
[Have emergency equipment available for impact activities]
tracheostomy & mechanical ventilation] g. I&O
c. Seizure precautions h. Fiber in diet [Constipation]
 Environmental stimuli i. Limit intake of foods  Ca++
d. Elimination of milk, cheese and egg [Milk products]
yolks [Phosphorus] j. Cardiac Monitoring
 MS/Endocrine System/MJTayco/09 9
e. Teach Sx. of Hypo/Hypercalcemia [Hypercalcemia is Severe]
[Instruct client to contact physician
immediately if either should occur]

DIABETES MELLITUS
 A Chronic Systemic disease characterized by disorder of CHO, Fat, & CHON Metabolism
 Etiology
 Unknown
 Occurs when there is insufficient supply of insulin and/ or cells become insulin resistant ; may result
from:
1. Failure in body’s production
2. Blockage of insulin supply
3. Autoimmune response wherein the insulin may bind to an immune serum globulin fraction,
4. preventing use
5. Excess body fat, which alters glucose metabolism
6. Glucose level in the blood remains high
7. Body attempts to rid itself of excess glucose by excreting some via kidneys
8. Osmotic force is created within the kidneys because of glucose excretion, and body fluid is
9. lost
10. Body is unable to use carbohydrates properly, and fat is oxidized as a compensatory
11. mechanism; oxidation of fats gives off ketone bodies
 Insulin
 Hormone produced & secreted by beta cells in the islets of Langerhans in the pancreas.
 It stimulates the active transport of glucose into muscle & adipose tissue cells, making it available for cell
use.
 How Insulin Works:
When we eat, food is broken down into chemicals & glucose  Bloodstream

Beta Cells of Pancreas Secrete Insulin Bloodstream [In response to S. Glucose]

Insulin combines with Insulin Receptors on Cell Wall (Activating Glucose Transporters)
Allowing Glucose to Enter Cell
 Predisposing Factors
1. Stress  Secretion of Epinephrine, Norepinephrine, & Glucocorticoids  S. CHO
2. Heredity (Type 1 DM)
3. Obesity (Adipose tissue are resistant to Insulin  Glucose Uptake (cells) Poor)
4. Viral Infection (Risk to Autoimmune Disorders)
5. Women (Multigravida with Large Babies)

 Diagnostic Tests
A. FBS
B. 20 PPBS
C. OGTT/GTT (Oral Glucose Tolerance Test)
D. Glycosylated Hgb
 Classification
Type 1 Type 2
Definition: Definition:
 Onset: Juvenile (Rapid)  Onset: Maturity (Gradual)
 Unstable DM  Stable DM
 Brittle DM  Ketosis – Resistant DM
 Age Onset: 30 yrs.  Age Onset: 40 yrs.
 Absolute Insulin Deficiency  With Insulin but Demands are
[Pancreas do not have Islets of 
 MS/Endocrine System/MJTayco/09 10
Langerhans]  Obese People
 Thin People  Prone to HHNC
 Prone to DKA (Hyperglycemic, Hyperosmolar,
(Diabetic Ketoacidosis) Non-Ketotic Coma)
Mgt: Mgt:
 Diet  Diet
 Activity/Exercise  Activity/Exercise
 Insulin  OHA [If hyperglycemia is
uncontrolled]
 Insulin [In case of Stress,
Surgery, Infection, Pregnancy]
A. Gestational:
 Onset: 2nd or 3rd trimester of pregnancy
 May or may not resolve after pregnancy
B. Secondary:
 Associated with Cushing’s disease, pancreatic disease, & glucocorticoid medications
 Pathophysiology:
Insulin Deficiency

Hyperglycemia

A. Blood Osmolarity

ICF DHN

B. Glycosuria
[Glucose Level Exceeds Renal Threshold (180mg/dL)]

C. Polyuria

Glucose exerts  Osmotic Pressure within the Renal Tubules

Osmotic Diuresis

Hypovolemia

ECF DHN

D. Polydipsia
[ECF/ICF DHN]

E. Blood Viscosity

Sluggish Circulation

Proliferation of Microorganism

Infections
[Periodontal]
[UTI]
[Vasculitis] [Cellulitis] [Vaginitis]
[Furuncles]
[Carbuncles]
[Retarded Wound Healing]

F. Polyphagia (Cells are Starved)
 MS/Endocrine System/MJTayco/09 11

Lipolysis

A. Hyperlipidemia

Atherosclerosis

1. Macroangiopathy
Brain: CVA
Heart: MI
Peri. Arteries: PVDs
2. Microangiopathy
Kidneys: RF
Eyes: Retinopathy/Cataract
3. Neuropathy
Spinal Cord/ANS
Paralysis
Gastroparesis
Neurogenic Bladder
Libido
Peri. Neuropathy; Numbness
B. Ketonemia
[Acetone, Aceto-acetic acid, Beta-hydroxy-butyric acid]

Blood ph Ketoacidosis
Ketonuria

CHON Breakdown

 (-) Nitrogen Balance
 BUN. S. Crea
 Tissue Wasting
 Wt.
 Debilitation
 Complications:
A. Insulin Therapy
 Hypoglycemia, hyperglycemia, lipodystrophy, erratic insulin action, insulin allergy, insulin resistance
B. Acute Complications of Diabetes
 Hypoglycemia/insulin reaction (below 50-60 mg/dl)
 Diabetic Ketoacidosis (DKA)
C. Chronic complications:
 Vascular degenerative changes: Atherosclerotic changes ( CAD, CVD, PVD)
 Neuropathies: DM affects nerves, decreased sensation of pain and temperature, unsteady gait, CV
changes, delayed gastric emptying, neurogenic bladder, sexual dysfunction
 Ocular Disturbances: diabetic retinopathy, blindness
 Microvascular changes: kidneys, ESRD
 Foot and Leg Problems: neuropathy, PVD, amputation

Hypoglycemia Hyperglycemia
Definition “INSULIN SHOCK” “DKA” [Type 1 DM]
 No or very little insulin 
Hyperglycemia
 MS/Endocrine System/MJTayco/09 12
 Cells need energy from CHO but with
deranged CHO metabolism
 Body breaks down fats for energy into
free fatty acids & glycerol
 Converted to ketone bodies in the liver
 Accumulates in the blood (Ketosis)
 Accumulates in the urine (Ketonuria)
Etiology  Omission of meals  Infections
 Overdose of Insulin  Overeating
 Strenuous Exercises  Under dose of Insulin
 GI Upset  Stress (Surgery)
DKA
 Absence of CHO
 Incomplete Lipid Metabolism
 DHN (Na+ & K+) (Crea, BUN, Hgb.,
Hct.)
 Lactic Acidosis
Assessmen  Restlessness  Polyuria*
t  Hunger Pangs  Polydipsia*
 Yawning  Polyphagia*
 Weakness  Warm, Flushed Dry Skin
 Tremors  Soft Eyeballs
 Pallor  PR
 Diaphoresis  N/V*
 Cold, Clammy Skin  Abdominal Pain*
 H/A  Kussmaul’s Breathing*
 Dizziness; Faintness  Fruity Odor Breath*
 PR  Urine (+) CHO; Ketones
 Abdominal Pain  Altered LOC
 Blurred Vision  DHN*
 Slurred Speech
 Urine (-) CHO; Ketones
 Altered LOC
Diagnostic  S. Glucose  (800 – 100 mg/dL)
Studies  S. HCO3; pH; K+
 S. Ketones (+) Urine
Collaborati a. Simple Sugars P.O a. NSS + Regular Insulin [IV]
ve Mgt i. 3 -4 oz. regular Softdrink b. D10W [once S.CHO 250mg/dL]
ii. 8 oz. Fruit Juice [Prevent Hypoglycemia]
iii. 5 – 7 pcs. Lifesaver’s Candies c. KCl (Slow IV Drip)
iv. 3 – 4 pcs. Hard Candies [Urine Output is adequate]
v. 1Tbsp. Sugar d. Plasma Expanders [BP]
vi. 5 mL. Pure Honey/Karo syrup e. Initially with rapid administration of
10 -15 g. CHO normal saline at 500- 1000 ml in 2-3
b. D50W 20 – 50 mL. (IV Push) hours, then 0.45 normal saline to
c. Monitor Blood Sugar continue rehydration [DHN d/t
d. Teaching: polyuria, RR, V, diarrhea]
 Causes f. VS; I&O; F&E;ECG
 S/Sx g. Patent Airway
 Prevention h. O2 Therapy
 Mgt i. Monitor Blood Sugar
 MS/Endocrine System/MJTayco/09 13
j. Teaching:
 Causes
 S/Sx
 Prevention
 Mgt

HHNKS
[Type 2 DM]
Definition  Hyperglycemia & hyperosmolarity with a lack of effective insulin
&  DHN, Na+, osmolarity
Etiology  Occurs in older adults after an illness or as a result of taking medications
that cause insulin dependency
Assessment  BP; PR
 Polyuria
 Polydipsia
 DHN
 Neurological Changes
Diagnostic  S. Glucose (600 – 1200 mg/dL)
Tests  S. Osmolality (350 mOsm/kg)
 BUN
 S. Na+ & S. K+
Collaborati a. Same as DKA although insulin does not play a critical role since client is not
ve Mgt in acidosis
b. Neurologic manifestations take 3-5 days to clear
 Collaborative Managements:
a. FOOT CARE
1. Inspect Feet Daily
2. Wash Feet with Warm H2O & Mild Soap
3. Pat Dry the Feet [Do not Rub]
4. Wear comfortable properly – fitted pair of Shoes (Leather/Canvass)
5. Use White Cotton Socks [Males]
6. DO NOT Go BAREFOOTED
7. Trim the toenails Straight Across. [DO NOT CUT at LATERAL EDGES  Ingrowns]
8. Apply Lotion on the feet [NOT INTERDIGITAL]
9. Exercise or Massage Feet
10. PODIATRIST  any S/Sx of Injury

b. LIFESTYLE CHANGES
1. Weight control: Obesity leads to insulin resistance; this can be reversed by weight loss
2. Exercise: insulin sensitivity but must be regular; brisk walking, swimming & bicycling are
recommended
3. Diet: (Current Recommendations Include)
i. Caloric control [To maintain ideal body weight]
ii. CHO: Complex CHO: (50 – 60%)
iii. Fiber foods rich in water soluble fiber (oat bran, peas, all forms of beans, pectin rich fruits &
vegetables)
iv. Foods with a Glycemic index should be AVOIDED
[Glycemic index refers to effect of particular foods on blood glucose]
v. CHON: Consistent with the dietary guidelines (usually between 60 & 85 grams):12 – 20%
vi. FAT: 20 – 20%; Not To Exceed 30% of daily calories (70-90 grams/day)
[Saturated Fat (Mono- and polyunsaturated fats)]
vii. Dietary ratio: CHO:CHON:FAT (5:1:2)
 MS/Endocrine System/MJTayco/09 14
viii.
Distribute food fairly evenly throughout the day in 3 or 4 meals, with snacks added between & at
bedtime as needed in accordance with total food allowance & therapy (insulin or oral hypoglycemics)
ix. Basic tools for planning diet: food composition tables showing nutrient content of foods; glycemic
index of foods
4. Exercise
i. Need for exercise
ii. activity insulin needs
5. Caution: Overexercise may cause hypoglycemia
i. Carry rapid acting glucose
ii. Exercise is less than usual, lighter diet or more insulin
iii. Exercise is more then usual, more food or less insulin
6. Blood Glucose Monitoring
i. Frequency depends on many variables
ii. If prone to frequent glycosuria or continual hyperglycemia, perform urine testing for ketonuria with
dip sticks.
c. INSULIN THERAPY
1. May be given depending on blood glucose monitoring results
2. Clients with type 1 DM taking insulin who are NPO for diagnostic examinations or surgery will have the
insulin dosage changed but not eliminated.
3. Adjusted after considering the client’s physical & emotional stresses; a specific type of insulin &
schedule is prescribed
4. Nursing Responsibilities
 Route
1. SC (Slow Absorption) (Less painful)
 90 Degrees; Thin 3/8”; Obese ½ “ or 5/8”
 DO NOT MASSAGE SITE OF INJECTION
2. IV (DKA) (Emergency)
 Administer at Room Temp
 Cold Insulin  LIPODYSTROPHY
 Rotate site
 Store vial at room temp; other vials should be refrigerated
 Gently roll vial in between palms to redistribute insulin particles
 DO NOT SHAKE [Bubbles make it difficult to aspirate exact amount]
 Observe for Side Effects
1. Localized
i. Induration of redness
ii. Swelling
iii. Lesion at the site
iv. Lipodystrophy
2. Generalized
i. Edema: Sudden resolution of hyperglycemia  Retention of H2O
ii. Hypoglycemia
iii. SOMOGYI EFFECT:
 Insulin-Induced Hypoglycemia Rebounds to Hyperglycemia
 Epinephrine & Glucagon (Released in response to Hypoglycemia)
 These reactions cause mobilization of the liver’s stored glucose & Iatrogenically Induce
Hyperglycemia
Doses of Insulin Therapy

S. CHO

 MS/Endocrine System/MJTayco/09 15
Stress Responses are triggered

Counterregulatory hormones are secreted

(EPI, NE, Glucocorticoid)  Rebound Hyperglycemia

iv. DAWN’S PHENOMENON
Normoglycemia during the night

12MN – 3 AM
GH Secretion

Hyperglycemia
(6 – 8 AM)

 Treatment: Gradually  Insulin Dosage while Monitoring BS

 Particularly during the night (when hypoglycemia is most likely to occur)
 Insulin Pump
 External battery-operated device that delivers insulin through a needle inserted SQ
 Small (basal) doses (regular insulin): computer-programmed delivered every few minutes; bolus
doses (extra preset amounts): delivered before meals
 Improves glucose control for clients with wide variations in insulin need as a result of irregular
schedules, pregnancy, or growth requirements
 A prescribed amount of insulin for 24 hours plus priming is drawn into syringe
 The administration set is primed & needle inserted aseptically, usually into subcutaneous tissue of
abdomen.
 Types of Insulin
Type Agent Onset Peak Duration
Rapid Acting Humalog 10 - 15 1 hr 3 hrs
min
Short Acting Humulin R ½ - 1 Hr 2 - 3 hrs 4 - 6 hrs
Intermediate Humulin N 3 - 4 hrs 4 - 12 hrs 16 - 24
Acting hrs
Long Acting Ultralente 6 - 8 hrs 12 - 16 hrs 20 - 30
hrs
Very Long Lantus 1 hr Continuous 24 hrs
Acting
Insulin Mixtures Humulin ½ - 1 hr 2 - 12 hrs 18 - 24
70/30 hrs
d. OHA
 Sulfonylureas, Biguanides, Alpha Glucosidase Inhibitors, Thiazolidinediones, Meglitinides
 Stimulate Islets of Langerhans to secrete insulin
 DM2 taking OHA may need insulin during periods of stress
 Oral anti diabetics for certain clients with NIDDM who cannot be managed with lifestyle changes alone;
must have some functioning beta cells in the islets of Langerhans
 Types of OHAs
SULFONYLUREAS AGENTS
First Generation Tolbutamide
Acetohexamide
Tolazamide
Chlorpropamide
Second Generation Glipizide
Glyburide
 MS/Endocrine System/MJTayco/09 16
Glimepride
NONSULFONYLUREAS AGENTS
Biguanides Metformin
Alphaglucosidase Inhibitors Acarbose
Thiazolininediones Rosiglitazone
Meglitinides Repaglinide

e. Other Therapies
1. Pancreatic Islet Cell Grafts
2. Pancreas Transplants
3. Implantable Insulin Pumps: Continually monitor blood glucose & release insulin
4. Cyclosporin Therapy [To prevent beta cell destruction in Insulin dependent diabetes]