NCM 116 101 – Care of Clients with Problems in Nutrition and GI Metabolism and Endocrine, Perception

and Coordination
The Gastro-Intestinal System

ANATOMY AND PHYSIOLOGY

THE SEQUENCE
Hypothalamus
↓
Pituitary Gland (Hypophysis)
Anterior (Adenohypophysis)
Posterior (Neurohypophysis)
↓ ANTERIOR PITUITARY GLAND (ADENO
Target Glands HYPOPHYSIS)
 TSH (Thyroid Stimulating Hormone)
-target  thyroid gland
 T3, T4, (BMR)
 Calcitonin (calcium & phosphorus regulation)
osteoblast
 Parathyroid Gland
 Parathormone (calcium & phosphorus regulation)
osteoclast
 ACTH (Adrenocorticotropic Hormone)
-target  adrenal gland
 Cortex
 Aldosterone (Na reabsorption)
 Glucocorticoid (glucose)
 Androgen (sex hormones)
 Medulla (catecholamines) stress or sympa effect
 Epinephrine
 Nor-epinephrine
 ICSH (Interstitial Cell Stimulating Hormone)
- target testes (maturation of spermatozoa)
 Testes
- ICSH testosterone
 GH (Growth Hormone)
- target  epiphyseal plate (bone growth)
 FSH (Follicle Stimulating Hormone)
FUNCTIONS of Hypothalamus: target  ovary-estrogen (maturation of graafian
 Water balance follicles to release mature ovum)
 Ovary
 Uterine contraction and milk release
FSH maturation of graafian follicle, estrogen
 Growth, metabolism and tissue maturation LH maturation of ovum, progesterone
 Ion regulation  LH (Luteneizing hormone)
 Heart rate and blood pressure - target  graafian follicle (formation of corpus
 Blood glucose levels luteum to maturation of ova)
 Immune system regulation  MSH (Melanocyte Stimulating Hormone)
 Reproductive functions → skin (pigmentation)
  Pineal Gland thyroid – hypometabolism
Melatonin (decrease skin pigmentation, inhibit gonads – amenorrhea, impotence
gonadotropic hormone) adrenal glands - adrenal insufficiency
 PROLACTIN → (maturation of mammary gland and growth hormone – dwarfism, hypoglycemia
production of milk) • Hemianopsia and headache – (if due to tumor)
 Placenta • Increased ICP (if due to tumor)
HCG, estrogen, progesterone, human placental MANAGEMENT:
lactogen • Surgical removal of tumor
• Radiation
PANCREAS • HRT (hormonal replacement therapy)
• Islet of Langerhans
• Alpha – glucagon (hyperglycemia) 2. Hyperpituitarianism:
Beta – insulin (hypoglycemia)  Hyper-secretion of the gland
• Delta – somatostatin (GH)  Acromegaly -after 15-16 yo

POSTERIOR PITUITARY GLAND  Gigantism -before 15-16 yo

(NEUROHYPOPHYSIS)
• ADH (Anti – Diuretic Hormone) CAUSED BY:
- target kidney tubules (H2O reabsorption)  Trauma, congenital disorders
• OXYTOCIN
– uterine contraction and ejection of milk MANIFESTATIONS:
• Increase BP
ENDOCRINE GLANDS: • Arthritic changes
• Noted enlargement of hands and feet
• Adrenal Gland • Thickening and protrusion of the jaw
• Hypothalamus
• Ovaries MANAGEMENT:
• Pancreas • Hypophysectomy: surgical removal of the
• Parathyroid pituitary gland
• Pituitary
• Testes • Craniotomy
• Thyroid
• Supratentorial: above the tentorial cerebellum

• Post Op: Semi – fowlers

• Infratentorial: below the tentorial cerebellum

A. DISORDERS OF THE PITUITARY GLAND
1. Hypopituitarianism:
 Hypofunction of the pituitary gland
CAUSED BY:
• trauma, tumor at the hypothalamus or pituitary gland
• complication from radiation therapy (head and neck)
• Panhypopituitarism (Simmonds’ Disease) -total
absence of pituitary secretions
• Sheehan’s Syndrome – postpartum pituitary necrosis
(bleeding)
MANIFESTATIONS:
• Related to hypofunction of:
• Post Op: in flat of Bed
• Transphenoidal Hypophysectomy
– Oro –Labial
COMPLICATIONS OF HYPOPHYSECTOMY:
• Leakage of the CSF
• bleeding and hemorrhage
• Increase of ICP: flat on bed right after
Transsphenoidal Hypophysectomy and monitor for
blurring of vision
POST OP CARE: HYPOPHYSECTOMY:
• Head elevation for 2 weeks MANIFESTATIONS:
• Nasal packing • S – sign of fluid overload (crackles/ rales/
• Oral care edema
• No activity that will increase ICP • I – increase heart rate/ weight gain
• Watch out Diabetes Insipidus • A – anorexia/ nausea and vomiting
• Observe for CSF leakage • D – decrease in LOC/ DEMECLOCYCLINE

3. PITUITARY TUMORS (Declomycin, Declostatin and

BDF F FB Ledermycin): due to Hyponatremia.
WOF: hepatotoxic
CAUSED BY:
• H – hyponatremia
• Basophilic Tumors
MANAGEMENT:
• Cushing’s Syndrome
• FVE intervention
• Musculinization and amenorrhea (female)
• Stop vasopressin
• Chromophobic Tumors (COMMON)
• Surgery (tumor excision) 
• Destroy the rest of the pituitary gland
• No hormones except for prolactin (galactorrhea)
CRITICAL CONDITIONS:
• Blindness
• Pulmonary edema
• Increased ICP
• Cerebral edema
DIAGNOSTIC:
• Heart failure
• CT scan
• Hypertension
• MRI
• Renal Failure
MANAGEMENT:
2. Diabetes Insipidus (DI)
• Drug
Bromocriptine (Parlodel)
CAUSED BY:
– to lower GH and Prolactin
• Radiation
• trauma or injury to pituitary gland, resection of
• Surgery (transsphenoidal hypophysectomy)
hypophysis, insensitivity of kidney to ADH
Octreotide (Sandostatin) = pre-op drug to reduce
tumor
B. DISORDERS OF THE POSTERIOR PITUITARY MANIFESTATIONS:
GLAND P – polyuria/ polydipsia/ poor skin turgor/ HOPN
L – low specific gravity (diluted)
1. Syndrome of Inappropriate Anti Diuretic Hormone
(SIADH) U – undersecretion of ADH
I - inability to concentrate urine
D – diabetes/ DESMOPRESSIN: Sulfonylurea
CAUSED BY: (OHA) may have DISULFIRAM like reaction
Side Effects: hypoglycaemia, mild D.I.
• over medication of vasopressin and benign pituitary S – signs of DHN
tumor
• Increased secretion of ADH
• Increased tubular reabsorption MANAGEMENT:
=increased blood volume • FVE intervention
(low Hct, hypoosmolality, edema) • Stop vasopressin
• Decreased urine output • Surgery (tumor excision) 
= concentrated urine
(high S.G., dark urine) CRITICAL CONDITIONS:
• Watch out for manifestations of Fluid Volume Excess • Pulmonary edema
• Cerebral edema
• Heart failure
 • Hypertension • Cerebral edema
• Renal Failure • Heart failure
• Hypertension
2. Cushings’s Disease:
 Over secretion of the Adeno – Cortical Hormone

PREDISPOSING FACTORS:

• Hyperplasia of the adrenal gland

• Tubular infection
• Iatrogenic cause: prolonged used of corticosteroids

MANIFESTATIONS:

• Hyperglycemia:
MANAGEMENT: - Polyuria
- Polyphagia
• FVD intervention - Polydipsia
• Synthetic ADH administration (vasopressin) Complication: Diabetes Mellitus
Desmopressin (DDAVP) spray intranasal OD or BID • Increase susceptibility to infection
• Vasopressin tannate in oil = IM OD or every 4 days • Hypernatremia:
CRITICAL CONDITIONS: - HPN
• Thrombosis – thromboembolism – pulmonary - Edema
embolism - Weight gain
• Ischemia • Moon face appearance
• Infarction - buffalo humps
• Necrosis (CVA, MI, RF) - obese trunks
C. DISORDERS OF THE ADRENAL GLAND - pendulous abdomen CLASSIC SIGNS
1. Conn’s Disease or Primary Hyperaldosteronism - thin extremities
• Hypokalemia
CAUSED BY: - weakness and fatigue
- constipation
• tumor and trauma of the adrenal cortex - U wave with the ECG tracing
MANIFESTATIONS: • Hirsutism
• Adrenal cortex disorder • Acne and striae
• Over secretion of aldosterone or mineralocorticoid • Increase masculinity in females
• Increased Na and H2O reabsorption=FVE • Irritability/ depression/ frequent mood swings
• Increased K urinary excretion=hypokalemia • Osteoporosis
• Watch out for manifestations of: • Thin and fragile skin
• SIADH
• Hypervolemia or FVE DIAGNOSTIC PROCEDURE:
• Hypokalemia (arrhythmias) • Increase FBS
MANAGEMENT: • Hypernatremia
• FVE intervention • Hypokalemia
• Stop sodium intake • Increased in Cortisol
• Critical conditions:
• Arrhythmias
• Hypertension
• Same with SIADH MANAGEMENT:
CRITICAL CONDITIONS:  Monitor IO and VS
• Pulmonary edema Renal Failure  Restrict Na and fluids
 Weight patient daily and assess for edema  Decrease plasma cortisol: Decrease tolerance to
 Measure abdominal girth daily stress – lead to Addisonian’s crisis
 Diet: Increased CHON, Increased K, Decreased  Decrease salt
CHO, Decreased Calorie -Hyponatremia – Decreased mineralocorticoids and
 Administration of Medications: Aldosterone
Potassium Sparring Diuretics: Spironolactone/  Hypovolemia
Aldactone -Hypotension
 Prevent complication: DM -Signs of dehydration – extreme thirst, agitation
 Assist in surgical procedure: Adrenalectomy -Wt loss
Adrenalectomy:  Hyperkalemia
 UNILATERAL: HRT for 6 – 12 months -Irritability
 BILATERAL: HRT lifetime -Diarrhea
 Hormonal Replacement Therapy -Arrhythmia
• Decrease sexual urge or libido:Decreased
 Importance of follow up care
Androgen
3. ADDISONS DISEASE: • Loss of pubic and axillary hair
 Decreased adrenocortical hormones leading to: • Hallmark Sign: bronze like skin pigmentation due
 Metabolic disturbances (sugar) to decrease cortisol will stimulate pituitary gland to
 F&E imbalances- Na, H2O, K release melanocyte stimulating hormone.
 Deficiency of neuromuscular function (salt & sex)
DIAGNOSTIC PROCEDURE:
PREDISPOSING FACTORS: • FBS – decrease FBS (N 80 – 120 mg/dL)
 Atrophy of adrenal gland • Plasma cortisol – decreased
 Fungal infections • Serum Na – decreased (N 135 – 145 meg/L)
• Serum K – increased (N 3.5 – 5.1 meg/L)
 Tubercular infections
MANAGEMENT:
 Monitor VS, I&O: to determine presence of
MANIFESTATIONS: Addisonian crisis
WOF: Complication of Addison’s dse :
 Decrease sugar
Addisonian crisis
 Hypoglycemia  Results the acute exacerbation of Addison’s dse
characterized by:
 Decreased glucocorticoids – corti
-Hypotension
-Hypovolemia
-Hyponatremia
-wt los
-arrhythmia
 Lead to progressive stupor & coma

SIGNS OF HYPOGLYCEMIA: MANAGEMENT FOR ADDISONIAN CRISIS (COMA)

T – tremors, tachycardia
I - irritability  Assist in mechanical ventilation
R - restlessness
 Administer steroids
E – extreme fatigue
 Force fluids
D – diaphoresis, depression
 Administer meds
 Corticosteroids - (Decadron) or Dexamethasone
 Hydrocortisone (cortisone)- Prednisone • Palpitations
 Mineralocorticoids (Flourocortisone) • Flushing and profuse diaphoresis
• Pain in the chest or abdomen with nausea and
ADMINISTRATION OF STEROIDS vomiting
 Administer 2/3 dose in AM & 1/3 dose in PM in order • Heat intolerance
to mimic the normal diurnal rhythm. • Weight loss
 Best time to give between 7-8 AM (active gland) to • Tremors
prevent side effects • Hyperglycemia
 Wear the Medic Alert Bracelet
 Taper the dose (w/draw, gradually from drug) – DIAGNOSTIC PROCEDURE:
sudden withdrawal can lead to addisonian crisis
 Monitor S/E (Cushing’s syndrome S/Sx) • Plasma levels of catecholamine: The Normal
-HPN range of urinary catecholamine is 14 mcg/100 ml
-Hirsutism of urine
-Edema • Urinary Vanillyl Mandelic Acid Test: confirmatory
-Moon face & buffalo hump test for Pheochromocytoma through 24-hour
-Increase susceptibility to infection due to steroids: urine collection
reverse isolation • Presence of tumor on x – ray
 Diet – increase calorie or CHO, Increase Na,
Increase CHON, Decrease K Management:
 Force fluid
1. Monitor the V/S
 Administer isotonic fluid as ordered
2. Administer Medications such as:
 Meticulous skin care – due to bronze like (Increased Beta Blockers
in MSH) DOC: Regetine
 HT & discharge planning 3. Enforce complete bed rest and avoid stressful stimuli
4. Monitor urine test for glucose and acetone
Avoid precipitating factors leading to Addisonian 5. Diet: Increase in calorie, well balanced diet. Avoid
crisis stimulant such as coffee and tea
6. Assist in surgical procedure: Adrenalectomy
S - udden withdrawal crisis
S – tress D. DISORDERS OF THE THYROID GLAND
I – nfection
P - revent complications: 1. Simple Goiter:
Addisonian crisis & Hypovolemic shock
 enlarged thyroid gland - iodine deficiency
 Hormonal replacement therapy – lifetime
 Important: follow up care PREDISPOSING FACTORS

4. Pheochromocytoma: • Goiter belt area - Place far from sea

– no iodine. Seafood’s rich in iodine
 the only disorder in the Adrenal Medulla due to • Mountainous area – increase intake of goitrogenic
hypersecretion of the hormone foods (US: Midwest, NE, Salt Lake)
PREDISPOSING FACTORS: • Cabbage – has progoitrin – an anti-thyroid agent with
no iodine
• Hereditary
• Neoplasms/ tumors Example: Turnips (singkamas), radish, peas,
strawberries, potato, beans, kamote, cassava (root
MANIFESTATIONS: crops), all nuts.

• Paroxysmal or sustained hypertension • Goitrogenic drugs:

• Severe headaches • Anti-thyroid agents :(PTU) Propylthiouracil
• Lithium carbonate, Aspirin PASA
• Cobalt, Phenylbutazone
• Endemic goiter – Place far from sea
• Sporadic goiter – Increase intake of goitrogenic foods
Iodine solution – Lugol’s solution or saturated
sol of K iodide SSKI
Lugol’s sol – violet color
use straw – prevent staining teeth
Prophylaxis 2 -3 drops /Treatment – 5 to 6

MANIFESTATIONS: Use straw – to prevent staining of teeth

– Enlarged TG • Lugol’s solution
– Mild restlessness
– Mild dysphagia • tetracycline
DIAGNOSTIC PROCEDURE: • nitrofurantoin (macrodontia)-urinary antiseptic-
pyelonephritis.
• Thyroid scan – reveals enlarged TG
• Iron solution
A – a radioisotope of iodine or technetium is
given THYROID HORMONE/ AGENTS
B – be sure the client did not receive
radiographic agents for the past 3 months 1. Levothyroxine (Synthroid): monitor for manifestations
C – check with the MD the need to discontinue of hyperthyroidism, presence of sore throat
the thyroid medications for 14 days before
the test
Pedia Complication: Cretinism: only endocrine disorder
D – diet NPO, if iodine is used additional 45
which can lead to Mental Retardation
minutes
D – diet NPO, if iodine is used additional 45
Adult Complication: Myxedema Coma: severe form of
minutes
Hypothyroidism
Serum TSH – increase (confirmatory) H –hypotension
H – hypothermia
Normal TSH: 0.2 – 5.4 microunits/ml H – hyponatremia
H – hypoglycaemia
Serum T3, T4 – N or below N B - bradycardia
Normal T3: 80 – 230 mg/dl Priority: airway
Normal T4: 5 – 12 mcg/dl 2. Liothyronine (Cytomel)
Radioactive Iodine Uptake: small dose of 3. Thyroid extract
Radioactive Iodine is given PO or IV then
measured in 2 – 4 hours and at 24 hours MANAGEMENT FOR THYROID AGENTS:
Normal 2 – 4 hours: 3% to 10% • Monitor vs. – HR due tachycardia & palpitation
• Take it early AM – SE insomnia
Normal 24 hours: 5% to 30% • Monitor s/e of hyperthyroidism
• - insomnia, restlessness, agitation, Heat
intolerance, HPN
• Encourage increase intake iodine – iodine is
MANAGEMENT: extracted from seaweeds (!)

• Administer meds
 Seafood- highest iodine content oysters, clams, 2. Administer thyroid hormone
crabs, lobster
3. Administer IVF replacement – force fluid
Lowest iodine – shrimps
MANAGEMENT FOR MYXEDEMA COMA
Iodized salt –easily destroyed by heat take it raw not
cooked 1. Monitor VS, I&O
2. Provide dietary intake low in calories – due to wt gain
• Assist surgery- Subtotal thyroidectomy- 3. Skin care due to dry skin
4. Comfortable & warm environment due to cold
COMPLICATION: intolerance
5. Administer IVF replacements
1. Tetany 6. Force fluid
7. Administer meds – take AM – SE insomia.
2. Laryngeal nerve damage

3. Hemorrhage-feeling of fullness at incision site. Check

nape for wet blood. Monitor HR.
Thyroid hormones
4. Laryngeal spasm – DOB, -tracheostomy set ready at
bedside - Levothyroxine (Synthroid)

2. Hypothyroidism - Liothyronine (Cytomel)

CAUSED BY: - Thyroid extracts

• Autoimmune Disease (Hashimoto’s Thyroiditis) 8. Health teaching & discharge plan

• Use of radioactive iodine
• Destruction or removal of thyroid tissue a. Avoidance precipitating factors leading to
• Dietary iodide deficiency myxedema coma:
• Overtreatment of antithyroid drug
- Exposure to cold environment
MANIFESTATIONS: - Stress
- Infection
A – aches of muscle -Use of sedative, narcotics, anesthetics not
B – bradycardia allowed – CNS depressants V/S already down
C – constipation/ cold intolerance
D – dry skin/ hair WOF COMPLICATIONS:
E – edema around the eyes/ face
F – forgetfulness 9. Hypovolemic shock, myxedema coma
G – gain of weight
10. Hormonal replacement therapy - lifetime
MANAGEMENT:
11. Importance of follow up care
• Monitor strictly V/S. I&O – to determine presence of
myxedema coma  3. Hyperthyroidism

IMPORTANT MANAGEMENT FOR MYXEDEMA COMA

1. Assist mechanical vent – priority airway CAUSED BY:

• Grave’s Disease
– TSAd thyroid stimulating antibody duplicate
– TSH, which increases thyroid hormone sec.
• Toxic nodular goiter (benign, hot spot)
• Overmedication of thyroid hormone
8. Assist in surgery – subtotal thyroidectomy
Management: pre-op
Administer Lugol’s solution (SSKI) K iodide

9. To decrease vascularity of TG

MANIFESTATIONS: 10. To prevent bleeding & hemorrhage

D – diarrhea/ diaphoresis POST OPERATIVE MANAGEMENT:

E – enlarged thyroid gland, eyeball protrusions WOF: signs of thyroid storm or thyrotoxicosis

P – palpitations, personality changes Triad signs of thyroidstorm

H – HPN, heat intolerance a. H – yperthermia

S - smooth, soft skin and shiny hair b. A – gitation

I- irritability and tremors c. T - achycardia

MANAGEMENT: Monitor VS & neuro check, agitated might

decrease LOC
1. Monitor VS & I & O – determine presence of thyroid
storm or most feared complication: Thyrotoxicosis Antipyretic – fever

2. Administer medications: Tachycardia - beta blockers (-lol)

a. Antithyroid agents Siderails – agitated

- Propylthiouracil (PTU) OTHER COMPLICATIONS:

- Methimazole (Tapazole) • Accidental removal of the parathyroid gland

• Laryngeal Nerve Damage: hoarseness of voice
Most toxic side effects are agranulocytosis: • Bleeding/ Hemorrhage
• Laryngeal Spasm
Fever, sore throat, leukocytosis: increase wbc: check
cbc and throat swab culture

3. Diet – increase calorie – to correct wt loss

4. Skin care

5. Comfy & cool environment

6. Maintain siderails- due agitation/restlessness E. DISORDERS OF THE PARATHYROID GLAND

7. Provide bilateral eye patch – to prevent drying of eyes- 1. Hypoparathyroidism:

exophthalmos’s
 CAUSED: 5. Encourage to breath with paper bag in order to
produce mild respiratory acidosis – to promote
• Accidental removal or destruction of parathyroid increase ionized Ca levels
gland 6. Most feared complication: Seizure & arrhythmia
• Thyroidectomy 7. Hormonal replacement therapy - lifetime
• Radical neck dissection 8. Important fallow up care
• Idiopathic
• Autoimmune

MANIFESTATION: 2. Hyperparathyroidism

• Hypocalcemia CAUSED BY:

• Tetany
Numbness of fingers • Hyperplasia parathyroid gland (PTG)
Chvostek’s sign • Over compensation of PTG due to Vit D
Trousseau’s sign deficiency

Laryngeal spasm Children – Rickets Vitamin D

• Severe anxiety and apprehension
Adults – Osteomalacia deficiency
DIAGNOSTIC:

1. Serum calcium – decrease (N 8.6 – 10

mg/100ml)
2. Serum phosphate increase (N 2.5 – 4.5
mg/100ml)
3. X-ray of long bone – decrease bone density
4. CT Scan – reveals degeneration of basal ganglia MANIFESTATION:

MANAGEMENT: • Hypercalcemia
• Decalcification of bone
1. Administration of meds: • Fracture
a. Acute tetany –Ca gluconate – IV, slowly • Deep bone pain
b. Chronic tetany • Depression of neuromuscular function
• Generalized fatigue
Oral Ca supplements • Memory loss
Ex. Ca gluconate, Ca carbonate, Ca lactate • Dec LOC, stupor coma
2. Avoid precipitating stimulus such as bright lights DIAGNOSTIC:
& noise: photophobia leading to seizure
3. Diet – increase Ca & decrease phosphorus 1. Serum Ca increase
a. Don’t give milk – due to increase
phosphorus 2. Serum phosphorus decreases
Good = anchovies – increase Ca, decrease 3. X-ray long bones – reveals bone demineralization
phosphorus + inc uric acid. Tuna & green
turnips- Inc Ca. MANAGEMENT:
4. Bedside – tracheostomy set – due to • Treat the cause
laryngospasm • Hydration (IV saline) and Increase OFI
• Diuretics (Ca excretion)
• Strain the urine with the gauze • Insufficient insulin
• Calcitonin (inhibits bone resorption)
• Dietary Ca restriction • Beta cells cannot release Insulin
• Give Acid Ash foods
• Avoid thiazide and vit D (may increase Ca)
• Dialysis
• Digitalis is withdrawn (may increase Ca) TYPE 2 Non – Insulin Diabetes Mellitus
• Prevent Complication: renal failure
• Insulin resistance due to obesity
F. DISORDER OF THE PANCREAS
• Polyuria: due to hyperosmolarity
1. Diabetes Mellitus
• Polydipsia: due to excessive thirst
Glucose Tolerance Test:
• Polyphagia: due to cell retardation
• Avoid strenuous activities for 8 hours prior the test

• Be sure to withhold medications, caffeine products

• Diet (adequate CHO for 3 days before the test)

• Educate

• Most definitive for pregnant

Diabetes Mellitus
Glycosylated Hgb Test:
IDDM NIDDM
 Goal for client with DM is 7.5% ONSET JUVENILE ADULT
BODY WEIGHT NORMAL OBESE
 For client without DM is 4 %– 6% KETOACIDOSIS COMMON RARE

 No fasting required
ASSESSMENT AND DIAGNOSTIC FINDINGS
 Most definitive for general client
• 3 P’s- polyuria, polydipsia, polyphagia
• Fasting Plasma Glucose > 126 mg/dL
• Random Plasma Glucose > 200 mg/dL
• 2-hour Postload Glucose > 200 mg/dL
Glycosylated Hgb Test:

• Goal for client with DM is 7.5% DIET:

• For client without DM is 4 %– 6% CHO – 50%

CHON – 30%
• No fasting required FATS – 20%
• Exercise: if blood glucose is greater than 250 mg/dl
• Most definitive for general client or ketonuria
• OHA

TYPE 1 Insulin Dependent Diabetes mellitus (IDDM)

 Sulfonylureas: stimulates Beta Cell to produce
Insulin
A – cetohexamide
C - hlorpropramide
INSULIN SPECIAL INSTRUCTIONS:

A – avoid extreme temperature

-Within 1 month can place in a room

temperature
- Beyond 1 month: refrigerate

B – be sure mixing is done accurately

Non – Sulfonylureas: for Hepatitis and G. I. Glucose: -AIR ASPIRATION

Alpha Glucoside Inhibitors N 1ST R 2ND R 1ST N 2ND
- administer insulin within 5 to 15 minutes
A - carbose
C – check site/ no scars/ systematic rotation
B - iguanide
D – dosage error should prevent
M - etformin
E – ensure proper administration
M - eglitinide
Types of Hypoglycemia:
T - hiozolidinedione
1. Mild Hypoglycemia:
PROBLEMS ASSOCIATED: - 60mg/dl
- Headaches, palpitations and tremors
1. Local Allergic Reaction: - Admi. 10-15 g. Of fast acting sugar

-May 1 – 2 hours after administration 2. Moderate Hypoglycemia:

-MD may prescribe anti – histamine to be -40mg/dl
taken one hour before injection -Confusion, drowsiness, numbness of the
lips, combative behaviour
-Admi. 15-30 g of sugar
2. Insulin Lipodystrophy:
-Loss of SQ fats
-Rotate injection sites at once every 2 to 3 3. Severe Hypoglycemia:
weeks -Loss of consciousness
3. Insulin resistance: -Admi. Glucagon – SQ
-Do not get any response to insulin therapy
4. Dawn’s Phenomenon:
-Pre – break hyperglycemia usually 5am to
8am
5. Insulin Waning:
-Persistent increase in blood glucose
6. Somogyi Phenomena:
2 -3 am hypoglycemia at 7am hyperglycemia
Rebound
DIABETIC KETOACIDOSIS:
K – Kussmauls Respiration Types of Insulin Color & Peak
E – excessive urination consistency
T – tension HYPO Rapid clear 2-4h
O – odor of breath is fruity/ acetone Intermediate cloudy 6-12h
N – noted changes in CNS Long acting cloudy 12-24h
E – excessive thirst Glargine, Lantus continuous
S – saline treatment HYPER OSMOLAR NON KETOTIC COMA
MANAGEMENT:
1. Can lead to coma – assist mechanical ventilation - H – hyperglycemia occurs without acidosis
- H – hypotension
2. Administer .9NaCl – isotonic solution - N – neurological deficit
- C – coma (headache, restlessness, seizure,
Followed by .45NaCl hypotonic solution decrease LOC)
To counteract dehydration. MANAGEMENT:
3. Monitor VS, I&O, blood sugar levels 1. Can lead to coma – assist mechanical ventilation
2. Administer .9NaCl – isotonic solution
4. Administer meds as ordered: -Followed by .45NaCl hypotonic solution
-To counteract dehydration.
a.) Insulin therapy – IV push 3. Monitor VS, I&O, blood sugar levels
4. Administer meds
Regular Acting Insulin – clear (2-4hrs, a. Insulin therapy – IV
peak action) b. Antibiotic to prevent infection
c. OHA- Administer with meals – to lessen GIT
b.) To counteract acidosis – Na HCO3 irritation & prevent hypoglycemia
- Avoid alcohol (alcohol + OHA = severe
c.) Antibiotic to prevent infection hypoglycemic reaction=CNS depression=coma)
MANAGEMENT FOR DM
1. Monitor for PEAK action of OHA & insulin
2. Monitor VS, I&O, neurocheck, blood sugar levels.
3. Administer insulin & OHA therapy as ordered.
4. Monitor signs of hyper & hypoglycemia.
5. Provide nutritional intake of diabetic diet
6. Exercise – after meals when blood glucose is
Types of Insulin rising.
7. Monitor complications of DM
1. Rapid Acting Insulin – a. Atherosclerosis – HPN, MI, CVA
b. Microangiopathy – small blood vessels
Ex. Regular acting I Eyes – diabetic retinopathy, premature
cataract & blindness
2. Intermediate acting I – Kidneys – recurrent pyelonephritis &
Renal Failure
Ex. NPH (non-protamine Hagedorn I) (2 common causes of Renal Failure: DM & HPN)
c. Gangrene formation
3. Long acting I – d. Peripheral neuropathy
e. Shock due to cellular dehydration
Ex. Ultra lente 8. Foot care mgt
a. Avoid waking barefooted
b. Cut toe nails straight
c. Apply lanolin lotion – prevent skin
 breakdown
d. Avoid wearing constrictive garments
9. Annual eye & kidney exam
10. Monitor urinalysis for presence of ketones
Blood or serum – more accurate
11. Assist in surgical wound debridement
12. Monitor signs or DKA & HONKC
13. Assist surgical procedure: BKA or above
knee amputation