ENDOCRINE

Fx of endocrine – ductless gland

Main gland – Pituitary gland – located at base of brain of Stella Turcica
Master gland of body
Master clock of body

Anterior pituitary gland – adenohypophysis

Posterior pituitary gland – neurohypophysis

Posterior pituitary:
1.) Oxytocin – a.) Promotes uterine contraction preventing bleeding/ hemorrhage.
- Give after placental delivery to prevent uterine atony.
b.) Milk letdown reflex with help of prolactin.
2.) ADH – antidiuretic hormone – (vasopressin) -Prevents urination – conserve H2O

A. DIABETIS INSIPIDUS (DI- dalas ihi) – hyposecretion of ADH

Cause: idiopathic/ unknown
Predisposing factor:
1. Pituitary surgery
2. Trauma/ head injury
3. Tumor
4. Inflammation

* alcohol inhibits release of ADH

S & Sx: Dx Proc:

1. Polyuria 1. Decrease urine specific gravity- concentrated urine
2. Sx of dehydration N= 1.015 – 1.035
- (1st sx of dehydration in children-tachycardia) 2. Serum Na = increase (N=135 -145 meq/L) Hypernatremia
- Excessive thirst (adult)
- Agitation Mgt:
- Poor skin turgor 1. Force fluid 2,000 – 3,000ml/day
- Dry mucus membrane 2. Administer IV fluid replacement as ordered
3. Weakness & fatigue 3. Monitor VS, I&O
4. Hypotension – if left untreated - 4. Administer meds as ordered
5. Hypovolemic shock a.) Pitresin (vasopressin) IM
Anuria – late sign hypovolemic shock 5. Prevent complications
Most feared complication – Hypovolemic shock

B.) SIADH - Syndrome of Inappropriate Anti-Diuretic Hormone

- Increase ADH
- Idiopathic/ unknown

Predisposing factor
1. Head injury
2. Related to Bronchogenic cancer or lung caner-
Early Sign of Lung Ca - Cough –1. non productive 2. productive
3. Hyperplasia of Pit gland
Increase size of organ

S&Sx Nsg Mgt:

1. Fluid retention 1. Restrict fluid
2. Increase BP – HPN 2. Administer meds as ordered eg. Diuretics: Loop and
3. Edema Osmotic
4. Wt gain 3. Monitorstrictly V/S, I&O, neuro check – increase ICP
5. Danger of H2O intoxication –Complications: 1. cerebral 4. Weigh daily
edema – increase ICP – 2. seizure 5. Assess for presence edema
Dx Proc: 6. Provide meticulous skin care
1. Urine specific gravity increase – diluted urine 7. Prevent complications – increase ICP & seizures activity
2. Hyponatremia – Decreased Na

Anterior Pituitary Gland – adeno

1. Growth hormone (GH) (Somatotropic hormone)
Fx: Elongation of long bones
Decrease GH – dwarfismchildren
Increase GH – gigantism
Increase GH – acromegaly – adult
Puberty 9 yo – 21 yo
Epiphyseal plate closes at 21 yo

Square face
Square jaw
 Drug of choice in acromegaly: Ocreotide (Sandostatin) SE dizziness
- Somatostatin Hormone – antagonizes the release of of GH
2. Melanocytes stimulating hormone - MSH
- Skin pigmentation
3. Prolactin/luteotrpic hormone/ lactogenic hormone - Promotes development of mammary gland
(Oxytocin-Initiates milk letdown reflex)
4. Adrenocorticotropic hormone – ACTH - Development & maturation of adrenal cortex
5. Luteinizing hormone – produces progesterone.
6. FSH- produces estrogen

PINEAL GLAND
1. Secretes Melatonin – inhibits lutenizing hormone (LH) secretion

THYROID GLAND (TG)

Question: Normal physical finding on TG:
a. With tenderness – thyroid never tender
b. With nodular consistency- answer
c. Marked asymmetry – only 1 TG
d. Palpable upon swallowing - Normal TG never palpable unless with goiter

TG hormones:
T3 T4 Thyrocalcitonin
- Triodothyronine -Tetraiodothyronine/ Tyroxine FX – antagonizes effects of parathormone

- 3 molecules of iodine - 4 molecules of iodine

Metabolic hormone

Increase metabolism brain –inc cerebration, inc v/s all v/s down, constipation

Hypo T3 T4 - lethargy & memory impairment –

Hyper T3 T4 - agitation, restlessness, and hallucination
7. Increase VS, increase motility

HYPOTHYROIDISM – all decreased except wt & menstruation, loss of appetite but with wt gain
menorrhagia – increase in mens
HYPERTHYROIDISM - Increase appetite – wt loss, amenorrhea

SIMPLE GOITER – enlarged thyroid gland - iodine deficiency

Predisposing factors
1. Goiter belt area - Place far from sea – no iodine. Seafood’s rich in iodine
2. Mountainous area – increase intake of goitrogenic foods (US: Midwest, NE, Salt Lake)
Cabbage – has progoitrin – an anti thyroid agent with no iodine
Example: Turnips (singkamas), radish, peas, strawberries, potato, beans, kamote, cassava (root crops), all nuts.
3. Goitrogenic drugs:
Anti thyroid agents :(PTU) prephyl thiupil
Lithium carbonate, Aspirin PASA
Cobalt, Phenyl butasone
Endemic goiter – cause # 1
Sporadic goiter – caused by #2 & 3

S & Sx – enlarged TG
Mild restlessness
Mild dysphagia Nsg Mgt Lugol’s sol – violet color
1. use straw – prevent staining teeth
Dx Proc. 2. Prophylaxis 2 -3 drops Treatment – 5 to 6 drops
1. Thyroid scan – reveals enlarged TG Use straw – to prevernt staining of teeth
2. Serum TSH – increase (confirmatory) 1. Lugol’s sol., 2. tetracycline 3. nitrofurantin (macrodantin)-
3. Serum T3, T4 – N or below N urinary anticeptic-pyelonephritis. 4. Iron solution.

Nsg Mgt: B. Thyroid h / Agents

1. Administer meds 1. Levothyroxine (Synthroid)
a.) Iodine solution – Logol’s solution or saturated 2. Liothyronine (cytomel)
sol of K iodide SSKI 3. Thyroid extract

Nsg Mgt: for TH/agents

1. Monitor vs. – HR due tachycardia & palpitation
2. Take it early AM – SE insomnia
3. Monitor s/e
Tachycardia, palpitations
Signs of insomnia
Hyperthyroidism restlessness agitation
 Heat intolerance
HPN

3. Encourage increase intake iodine – iodine is extracted from seaweeds (!)

Seafood- highest iodine content oysters, clams, crabs, lobster
Lowest iodine – shrimps
Iodized salt –easily destroyed by heat take it raw not cooked

4. Assist surgery- Sub total thyroidectomy-

Complication: 1. Tetany 2. laryngeal nerve damage 3.Hemorrhage-feeling of fullness at incision site.Check nape for wet blood.
4.Laryngeal spasm – DOB, SOB – trache set ready at bedside.

2.) HYPOTHYROIDISM – decrease secretion of T3, T4 – can lead to MI / Atherosclerosis

Adult – myxedema
Child- cretinism – only endocrine dis lead to mental retardation
Predisposing factor:
1. `Iatrogenic causes – caused by surgery
2. Atrophy of TG due to:
a. Irradiation
b. Trauma
c. Tumor, inflammation
3. Iodine def
4. Autoimmune – Hashimoto disease

S&Sx everything decreased except wt gain & mens increase)

Early signs – weakness and fatigue
Loss of appetite – increased lypolysis – breakdown of fats causing atherosclerosis = MI
Wt gain
Cold intolerance – myxedema - coma
Constipation
Late Sx – brittle hair/ nails
Non pitting edema due increase accumulation of mucopolysacharide in SQ tissue -Myxedema
Horseness voice
Decrease libido
Decrease VS – hypotension bradycardia, bradypnea, and hypothermia
Lethargy
Memory impairment leading to psychosis-forgetfulness
Menorrhagia

Dx:
1. Serum T3 T4 decrease
2. Serum cholesterol increase – can lead to MI
3. RA IU – radio iodine uptake – decrease

Nsg Mgt:
1. Monitor strictly V/S. I&O – to determine presence of myxedema coma!
Myxedema Coma - Severe form of hypothyroidism
Hypotension, hypoventilation, bradycardia, bradypnea, hyponatremia, hypoglycemia, hypothermia
Might lead to progressive stupor & coma
Impt mgt for Myxedema coma
1. Assist mech vent – priority a/w
2. Adm thyroid hormone
3. Adm IVF replacement – force fluid

Mgt myxedema coma

1. Monitor VS, I&O
2. Provide dietary intake low in calories – due to wt gain
3. Skin care due to dry skin
4. Comfortable & warm environment due to cold intolerance
5. Administer IVF replacements
6. Force fluid
7. Administer meds – take AM – SE insomia. Monitor HR.
Thyroid hormones
Levothyroxine(Synthroid), Liothyronine (cytomel)
Thyroid extracts
8. Health teaching & discharge plan
a. Avoidance precipitating factors leading to myxedema coma:
1. Exposure to cold environment
2. Stress 3. Infection
4. Use of sedative, narcotics, anesthetics not allowed – CNS depressants V/S already down

Complications:
9. Hypovolemic shock, myxedema coma
10. Hormonal replacement therapy - lifetime
11. Importance of follow up care
HYPERTHYROIDISM - Graves dse or thyrotoxicosis ( everything up except wt and mens)
-Increased T3 & T4
Predisposing factors:
1. Autoimmune disease – release of long acting thyroid stimulator (LATS)
Exopthalmos
Enopthalmos – severe dehydration depressed eye
2. Excessive iodine intake
3. Hyperplasia of TG

S&Sx:
1. Increase in appetite – hyperphagia – wt loss due to increase metabolism
2. Skin is moist - perspiration
3. Heat intolerance
4. Diarrhea – increase motility
5. All VS increase = HPN, tachycardia, tachypnea, hyperthermia
6. CNS changes
8. Irritability & agitation, restlessness, tremors, insomnia, hallucinations
7. Goiter
8. Exopthalmos – pathognomonic sx
9. Amenorrhea

Dx:
1. Serum T3 & T4 - increased
2. Radio iodine uptake – increase
3. Thyroid scan – reveals enlarged TG

Nsg Mgt:
1. Monitor VS & I & O – determine presence of thyroid storm or most feared complication: Thyrotoxicosis
2. Administer meds
a. Antithyroid agents
1. Prophylthiuracil (PTU)
2. Methymazole (Tapazole)
Most toxic s/e agranulocytosis- fever, sore throat, leukocytosis=inc wbc: check cbc and throat swab culture
Most feared complication : Thrombosis – stroke CVS

3. Diet – increase calorie – to correct wt loss

4. Skin care –
5. Comfy & cool environment
6. Maintain siderails- due agitation/restlessness
7. Provide bilateral eye patch – to prevent drying of eyes- exopthalmos
8. Assist in surgery – subtotal thyroidectomy

Nsg Mgt: pre-op

Adm Lugol’s solution (SSKI) K iodide
9. To decrease vascularity of TG
10. To prevent bleeding & hemorrhage
Mgt post op:
Complication: 1. Watch out for signs of thyroid storm or thyrotoxicosis
Triad signs of thyroidstorm;
a. Tachycardia /palpitation
b. Hyperthermia
c. Agitation

Nsg Mgt Thyroid Storm:

1. Monitor VS & neuro check
Agitated might decrease LOC
2. Antipyretic – fever
Tachycardia -  blockers (-lol)
3. Siderails – agitated

Comp 2. Watch for inadvertent (accidental) removal of parathyroid gland

Secretes Para hormone

If removed, hypocalcemia - classic sign tetany – 1. .(+) Trousseau sign/ 2. Chvosteck’s sign
Nsg Mgt:
Adm calcium gluconate slowly – to prevent arrhythmia
Ca gluconate toxicity – antidote – MgSO4
3.Laryngeal (voice box) nerve damage (accidental)
Sx: hoarseness of voice
***Encourage pt to talk or speak post operatively asap to determine laryngeal nerve damage
Notify physician!

4. Signs of bleeding post subtotal thyroidectomy

- “Feeling of fullness” at incision site
Nsg mgt:
 Check soiled dressing at nape area

5. Signs of laryngeal spasm

a. DOB
b. SOB
Prepare at bedside tracheostomy

6. Hormonal replacement therapy - lifetime

7. Importance of follow up care
(Liver cirrhosis – bedside scissor – if pt complaints of DOB)

(Cut cystachean tube to deflate balloon)

Parathyroid gland – pair of small nodules located behind the TG

11. Secrets parathyroid hormone – promotes Ca reabsorption

Thyrocalcitonin – antagonises secretion of parathyroid hormone

1. Hypoparthroidism – decrease of parathyroid hormone

2. Hyperparathroidsm

HYPOPARATHYROIDISM – decreased parathormone

Hypocalcemia Hyperphosphatemia
(Or tetany)

[If Ca decreases, phosphate increases]

A. Predisposing, factors:
1. Following subtotal thyroidectomy
2. Atrophy of parathyroid gland due to
a. Irradiation
b. Trauma

S&Sx:
1. Acute tetany
a. Tingling sensation
b. Paresthesia
c. Dysphagia
d. Laryngospasm
e. Bronchospasm

Pathognomonic Sign of tetany:

a. (+) Trousseau’s or carpopedial spasm
b. (+) Chvosteck’s sign

f. Seizure most feared complication

g. Arrhythmia

2. Chronic tetany
a. Loss of tooth enamel
b. Photophobia & cataract formation
c. GIT changes – anorexia, n/v, general body malaise
d. CNS changes – memory impairment, irritability

Dx:
1. Serum calcium – decrease (N 8.5 – 11 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

Nsg Mgt:
1. Administration of meds:
a.) Acute tetany –
Ca gluconate – IV, slowly
b.) Chronic tetany
1. Oral Ca supplements
Ex. Ca gluconate
Ca carbonate
Ca lactate
 Vit D (Cholecalceferol)

Drug diet sunlight

Cholecalceferol calcidiol calcitriol 7am – 9am

2. Phosphate binder
Alumminum DH gel (ampho gel)
SE constipation
Antacid
AAC MAD
Aluminum containing acids Mg containing antacids
Ex. Milk or magnesia
Aluminum OH gel Diarrhea

Constipation Maalox – magnesium & aluminum - Less s/e

2. Avoid precipitating stimulus such as bright lights & noise: photophobia leading to seizure
3. Diet – increase Ca & decrease phosphorus
- Don’t give milk – due to increase phosphorus
Good = anchovies – increase Ca, decrease phosphorus + inc uric acid. Tuna & green turnips- Inc Ca.
4. Bedside – tracheostomy set –due to laryngospasm
5. Encourage to breath with paper bag in order to produce mild respiratory acidosis – to promote increase ionized Ca levels
6. Most feared complication : Seizure & arrhythmia
7. Hormonal replacement therapy - lifetime
8. Important fallow up care

HYPERPARATHYROIDISM - increase parathormone. Complication: Renal failure

Hypercalcemia can lead to Hypophosphatemia

Bone dse - kidney stones

Mineralization

Leading to bone fracture

Ca – 99% bones
1% serum blood

Predisposing Factors:
1. Hyperplasia parathyroid gland (PTG)
2. Over compensation of PTG due to Vit D deficiency
Children – Rickets Vit D
Adults – Osteomalacia deficiency

Sippy’s diet – Vit D diet – not good for pt with ulcer

2 -4 cups of milk & butter
Karrel’s diet – Vit D diet – not good for pt with ulcer
6 cups of milk & whole cream

Food rich in CHON – eggnog – combination of egg & milk

S/Sx:
Bone fracture
1. Bone pain (especially at back), bone fracture
2. Kidney stone –
a. Renal colic
b. Cool moist skin
3. GIT changes – anorexia, n/v, ulcerations
4. CNS involvement– irritability, memory impairment

Dx Proc:
1. Serum Ca increase
2. Serum phosphorus decreases
3. X-ray long bones – reveals bone demineralization

Nsg Mgt: Kidney Stone

1. Force fluids – 2,000 – 3,000/day or 2-3L/day

2. Isotonic solution
3. Warm sitz bath – for comfort
4. Strain all urine with gauze pad
5. Acid ash diet – cranberry, plum, grapefruit, vit C, calamansi – to acidify urine
6. Adm meds
 a. Narcotic analgesic – Morphine SO4, Demerol (Meperidine Hcl)
S/E – resp depression. Monitor RR)
Narcan/ Naloxone – antidote
Naloxone toxicity – tremors
7. Siderails
8. Assist in ambulation
9. Diet – low in Ca, increase phosphorus lean meat
10. Prevent complication
Most feared – renal failure
11. Assist surgical procedure – parathyroidectomy
12. Impt ff up care
13. Hormonal replacement- lifetime

ADRENAL GLAND
12. Atop of @ kidney
13. 2 parts
Adrenal cortex – outermost layer
Adrenal medulla - innermost layer
14. Secrets cathecolamines
a.) Epinephrine / Norephinephrine – potent vasoconstrictor – adrenaline=Increase BP

Adrenal Medulla’s only disease:

PHEOCHROMOCYTOMA- presence of tumor at adrenal medulla
-increase nor/epinephrine
-with HPN and resistant to drugs
-drug of choice: beta blockers
-complication: HPN crisis = lead to stroke
-no valsalva maneuver

Adrenal Cortex –
1. Zona fasiculata – secrets glucocorticoids
Ex. Cortisol - Controls glucose metabolism (SUGAR)
2. Zona reticularis – secrets traces of glucocorticoids & androgenic hormones
M – testosterone
F – estrogen & progesterone
Fx – promotes development of secondary sexual characteristics
3. Zona glomerulosa - secretes mineralcortisone
Ex. Aldosterone
Fx: promotes Na & H2O reabsorption & excretion of potassium (SALT)

ADDISON’S DISEASE – Steroids-lifetime

Decreased adrenocortical hormones leading to:
a.) Metabolic disturbances (sugar)
b.) F&E imbalances- Na, H2O, K
c.) Deficiency of neuromuscular function (salt & sex)

Predisposing Factors:
1. Atrophy of adrenal gland
2. Fungal infections
3. Tubercular infections

S/Sx:
1. Decrease sugar – Hypoglycemia – Decreased glucocorticoids - cortisol

T – tremors, tachycardia
I - irritability
R - restlessness
E – extreme fatigue
D – diaphoresis, depression

2. Decrease plasma cortisol

Decrease tolerance to stress – lead to Addisonian’s crisis

3. Decrease salt – Hyponatermia – Decreased mineralocorticoids - Aldosterone

Hypovolemia
a.) Hypotension
b.) Signs of dehydration – extreme thirst, agitation
c.) Wt loss
4. Hyperkalemia
a.) Irritability
b.) Diarrhea
c.) Arrhythmia
5. Decrease sexual urge or libido- Decreased Androgen
 6. Loss of pubic and axillary hair

To Prevent STD Local – practice monogamous relationship

CGFNS/NCLEX – condom
7. Pathognomonic sign– bronze like skin pigmentation due to decrease cortisol will stimulate pituitary gland to release melanocyte
stimulating hormone.

Dx Proc:
1. FBS – decrease FBS (N 80 – 120 mg/dL)
2. Plasma cortisol – decreased
Serum Na – decreased (N 135 – 145 meg/L)
3. Serum K – increased (N 3.5 – 5.5 meg/L)

Nsg Mgt:
1. Monitor VS, I&O – to determine presence of Addisonian crisis
15. Complication of Addison’s dse : Addisonian crisis
16. Results the acute exacerbation of Addison’s dse characterized by :
Hypotension, hypovolemia, hyponatremia, wt loss, arrhythmia
17. Lead to progressive stupor & coma

Nsg Mgt Addisonian Crisis (Coma)

1. Assist in mechanical ventilation
2. Adm steroids
3. Force fluids

2. Administer meds
a.) Corticosteroids - (Decadron) or Dexamethazone
- Hydrocortisone (cortisone)- Prednisone

Nsg Mgt with Steroids

1. Adm 2/3 dose in AM & 1/3 dose in PM in order to mimic the normal diurnal rhythm.
2. Taper the dose (w/draw, gradually from drug) – sudden withdrawal can lead to addisonian crisis
3. Monitor S/E (Cushing’s syndrome S/Sx)
a.) HPN
b.) Hirsutism
c.) Edema
d.) Moon face & buffalo hump
e.) Increase susceptibility to infection sue to steroids- reverse isolation

b.) Mineralocorticoids ex. Flourocortisone

3. Diet – increase calorie or CHO

Increase Na, Increase CHON, Decrease K
4. Force fluid
5. Administer isotonic fluid as ordered
6. Meticulous skin care – due to bronze like
7. HT & discharge planning
a) Avoid precipitating factors leading to Addisonian crisis
1. Sudden withdrawal crisis
2. Stress
3. Infection
b) Prevent complications
Addisonian crisis & Hypovolemic shock
8. Hormonal replacement therapy – lifetime
9. Important: follow up care

CUSHING’S SYNDROME – increase secretion of adrenocortical hormone

Predisposing Factors:
1. Hyperplasia of adrenal gland
2. Tubercular infection – milliary TB
S/Sx
1. Increase sugar – Hyperglycemia
3 P’s
1. Polyuria
2. Polydipsia – increase thirst
3. Polyphagia – increase appetite
Classic Sx of DM – 3 P’s & glycosuria + wt loss
2. Increase susceptibility to infection – due to increased corticosteroid
3. Hypernatrermia
a. HPN
b. Edema
c. Wt gain
d. Moon face
Buffalo hump
Obese trunk classic signs
Pendulous abdomen
Thin extremities
4. Hypokalemia
 a. Weakness & fatigue
b. Constipation
c. ECG – (+) “U” wave
5. Hirsutism – increase sex
6. Acne & striae
7. Increase muscularity of female
Dx:
1. FBS – increase↑ (N: 80-120mg/dL)
2. Plasma cortisol increase
3. Na – increase (135-145 meq/L)
4. K- decrease (3.5-5.5 meq/L)

Nsg Mgt:
1. Monitor VS, I&O
2. Administer meds
a. K- sparing diuretics (Aldactone) Spironolactone
- promotes excretion of NA while conserving potassium

Not lasix due to S/E hypoK & Hyperglycemia!

3. Restrict Na
4. Provide Dietary intake – low in CHO, low in Na & fats
High in CHON & K
5. Weigh pt daily & assess presence of edema- measure abdominal girth- notify doc.
6. Reverse isolation
7. Skin care – due acne & striae
8. Prevent complication
- Most feared – arrhythmia & DM
(Endocrine disorder lead to MI – Hypothyroidism & DM)
9. Surgical bilateral Adrenolectomy
10. Hormonal replacement therapy – lifetime due to adrenal gland removal- no more corticosteroid!

PANCREAS – behind the stomach, mixed gland – both endocrine and exocrine gland

Acinar cells (exocrine gland) Islets of Langerhans (endocrine gland ductless)

Secrete pancreatic juices at pancreatic ducts.  cells

Aids in digestion (in stomach) secrets glucagon

Fxn: hyperglycemia (high glucose)

 Cells

Secrets insulin

Fxn: hypoglycemia

Delta Cells

Secrets somatostatin

Fxn: antagonizes growth hormone

3 disorders of the Pancreas

1. DM
2. Pancreatic Cancer
3. Pancreatitis

Overview only:
PANCREATITIS (check page 72)– acute inflammation of pancreas leading to pancreatic edema, hemorrhage & necrosis due to
Autodigestion – self-digestion
Cause: unknown/idiopathic
18. Or alcoholism

Pathognomonic sign- (+) Cullen’s sign - Ecchymosis of umbilicus (bluish color)- pasa
(+) Grey turner’s sign – ecchymosis of flank area

Both sx means hemorrhage

CHRONIC HEMORRHAGIC PANCREATITIS- “bangugot”

Predisposing factors - unknown
Risk factor:
1. History of hepatobiliary disorder
2. Alcohol
3. Drugs – thiazide diuretics, oral contraceptives, aspirin, penthan
4. Obesity
5. Hyperlipidemia
6. Hyperthyroidism
7. High intake of fatty food – saturated fats

DIABETES MELLITUS - metabolic disorder characterized by non utilization of CHO, CHON,& fat metabolism

Classification:
I. Type I DM (IDDM) – “Juvenile “ onset, common in children, non-obese “brittle dse”
-Insulin dependent diabetes mellitus
Incidence rate
1.) 10% of population with DM have Type I
Predisposing Factor:
1. 90% hereditary – total destruction of pancreatic dells
2. Virus
3. Toxicity to carbon tetrachloride
4. Drugs – Steroids both cause hyperglycemia
Lasix - loop diuretics

S/Sx:
3 P’S + G
1.) Polyuria
2.) Poydipsia
3.) Polyphagia
4.) Glycosuria
5.) Weight loss
6.) Anorexia
7.) N/V
8.) Blurring of vision
9.) Increase susceptibility to infection
10.) Delayed/ poor wound healing

Mgt:
1. Insulin Therapy
Diet
Exercise

Complications – Diabetic Ketoacidosis (DKA)

Diabetic Ketoacidosis (DKA) – due to increase fat catabolism or breakdown of fats

DKA –(+) fruity or acetone breath odor

Kassmaul’s respiration – rapid, shallow breathing

Diabetic coma (needs oxygen)

II. Type II DM – (NIDDM)

Adult/ maturity onset type – age 40 & above, obese
Incidence Rate
1. 90% of pop with DM have Type II
Mid 1980’s marked increase in type II because of increase proliferation of fast food chains!

Predisposing Factor:
1. Obesity – obese people lack insulin receptors binding site
2. Hereditary

S/Sx:
1. Asymptomatic
2. 3 P’s and 1G

Tx:
1. Oral Hypoglycemic Agents (OHA)
2. Diet
3. Exercise

Complication: HONKC
H – hyper
O – osmolar
N – non
 K – ketotic
C – coma

III. GESTATIONAL DM – occurs during pregnancy & terminates upon delivery of child

Predisposing Factors:
1. Unknown/ idiopathic
2. Influence of maternal hormones
S/Sx :
Same as type II –
1. Asymptomatic
2. 3 P’s & 1G

Type of delivery – CS – due to large baby

Sx of hypoglycemia on infant
1. High pitched shrill cry
2. Poor sucking reflex
IV. DM ASSOCIATED WITH OTHER DISORDER
a.) Pancreatic tumor
b.) Cancer
c.) Cushing’s syndrome

3 MAIN FOOD GROUPS

Anabolism Catabolism
1. CHON glucose glycogen
2. CHON amino acids nitrogen
3. Fats fatty acids free fatty acids (FFA) – Cholesterol & Ketones

Pancreas → glucose → ATP (Main fuel/energy of cell )

Reserve glucose – glycogen
Liver will undergo – glucogenesis – synthesis of glucagons
& Glycogenolysis – breakdown of glucagons
& Gluconeogenesis – formation of glucose form CHO sources – CHON & fats

Hyperglycemia – pancreas will not release insulin. Glucose can’t go to cell, stays at circulation causing hyperglycemia.
increase osmotic diuresis – glycosuria
Lead to cellular starvation

Lead to wt loss stimulates the appetite/ satiety center polyuria

(Hypothalamus)
Cellular dehydration
Polyphagia
Stimulates thirst center (hypothalamus)

Polydipsia

Increased CHON catabolism

Lead to (-) nitrogen balance

Tissue wasting (cachexia)

Increase fat catabolism

Free fatty acids

Cholesterol ketones DKA

Atherosclerosis coma

HPN death

MI stroke

DIABETIC KETOACIDOSIS (DKA)

- Acute complication of Type I DM due to severe hyperglycemia leading to CNS depression & Coma.
- Ketones- a CNS depressant

Predisposing factor:
1. Stress – between stress and infection, stress causes DKA more.
2. Hyperglycemia
 3. Infection

S/Sx: 3 P’s & 1G

1. Polyuria
2. Polydipsia
3. Polyphagia
4. Glycosuria
5. Wt loss
6. Anorexia, N/V
7. (+) Acetone breath odor- fruity odor pathognomonic DKA
8. Kussmaul's resp-rapid shallow respiration
9. CNS depression
10. Coma

Dx Proc:
1. FBS increase, Hct – increase (compensate due to dehydration)
N =BUN – 10 -20 mg/100ml -- increased due to severe dehydration
Crea - .8 – 1 mg/100ml

Hct 42% (should be 3x high)-nto hgb

Nsg Mgt:
1. Can lead to coma – assist mechanical ventilation
2. Administer .9NaCl – isotonic solution
Followed by .45NaCl hypotonic solution
To counteract dehydration.
3. Monitor VS, I&O, blood sugar levels
4. Administer meds as ordered:
a.) Insulin therapy – IV push
Regular Acting Insulin – clear (2-4hrs, peak action)
b.) To counteract acidosis – Na HCO3
c.) Antibiotic to prevent infection

Insulin Therapy
A. Sources:
1. Animal source – beef/ pork-rarely used. Causes severe allergic reaction.
2. Human – has less antigenecity property
Cause less allergic reaction. Humulin

If kid is allergic to chicken – don’t give measles vaccine due it comes from chicken embryo.
3. Artificially compound

B. Types of Insulin
1. Rapid Acting Insulin - Ex. Regular acting I
2. Intermediate acting I - Ex. NPH (non-protamine Hagedorn I)
3. Long acting I - Ex. Ultra lente

Types of Insulin color & consistency onset peak duration

1. Rapid clear - 2-4h -
2. Intermediate cloudy - 6-12h -
3. Long acting cloudy - 12-24h -

Ex. 5am Hemoglucose test (HGT)

250 mg/dl
Adm 5 units of RA I
Peak 7-9am – monitor hypoglycemic reaction at this time- TIRED

Nsg Mgt: upon injection of insulin:

1.Administer insulin at room temp! – To prevent lipodystrophy = atrophy/ hypertrophy of SQ tissues
2. Insulin is only refrigerated once opened!
3. Gently roll vial bet palms. Avoid shaking to prevent formation of bubbles.
4. Use gauge 25 – 26needle – tuberculin syringe
5. Administer insulin at either 45(for skinny pt) or 90 (taba pt)depending on the client tissue deposit.
6. Don’t aspirate after injection
7. Rotate injection site to prevent lipodystrophy
8. Most accessible site – abdomen
9. When mixing 2 types of insulin, aspirate
1st regular/ clear – before cloudy to prevent contaminating clear insulin & to promote accurate calibration.
10. Monitor signs of complications:
a. Allergic reactions – lipodystrophy
b. Somogyi’s phenomenon – hypoglycemia followed by periods of hyperglycemia or rebound effect of insulin.
11. 1ml or cc of tuberculin = 100 units of insulin
 - - 1 cc = 100 units

- - .5cc = 50 units

- - .1 cc = 10 units

6 units RA

Most Feared Complication of Type II DM

Hyper ↑ osmolarity = severe dehydration
Osmolar
Non - absence of lipolysis
Ketotic - no ketone formation
Coma – S/Sx: headache, restlessness, seizure, decrease LOC = coma

Nsg Mgt; - same as DKA except don’t give NaHCO3!

1.Can lead to coma – assist mechanical ventilation

2. Administer .9NaCl – isotonic solution
Followed by .45NaCl hypotonic solution
To counteract dehydration.
3.Monitor VS, I&O, blood sugar levels
4.Administer meds
a.) Insulin therapy – IV
b.) Antibiotic to prevent infection
Tx:
O ral
H ypoglycemic
A gents
19. Stimulates pancreas to secrete insulin

Classifications of OHA
1. First generation Sulfonylurear
a. Chlorpropamide (diabenase)
b. Tolbutamide (orinase)
c. Tolazamide (tolinase)

2. 2nd generation sulfonylurear

a. Diabeta (Micronase)
b. Glipside (Glucotrol)

Nsg Mgt or OHA

1. Administer with meals – to lessen GIT irritation & prevent hypoglycemia
2. Avoid alcohol (alcohol + OHA = severe hypoglycemic reaction=CNS depression=coma) Antabuse-Disufram

Dx for DM
1. FBS – N 80 – 120 mg/dl = Increased for 3 consecutive times=confirms DM!!
+ 3 P’s & 1G
2. Oral glucose tolerance (OGTT) - Most sensitive test
3. Random blood sugar – increased
4. Alpha Glucosylated Hgb – elevated

Nsg Mgt;
1. Monitor for PEAK action of OHA & insulin
Notify Doc
2. Monitor VS, I&O, neurocheck, blood sugar levels.
3. Administer insulin & OHA therapy as ordered.
4. Monitor signs of hyper & hypoglycemia.

Pt DM –“ hinimatay”
20. You don’t know if hypo or hyperglycemia.
Give simple sugar
(Brain can tolerate high sugar, but brain can’t tolerate low sugar!)
Cold, clammy skin – hypo – Orange Juice or simple sugar / warm to touch – hyper – adm insulin
5. Provide nutritional intake of diabetic diet:
CHO – 50%
CHON – 30%
Fats – 20%
-Or offer alternative food products or beverage.
-Glass of orange juice.
6. Exercise – after meals when blood glucose is rising.
7. Monitor complications of DM
a. Atherosclerosis – HPN, MI, CVA
b. Microangiopathy – small blood vessels
Eyes – diabetic retinopathy , premature cataract & blindness
 Kidneys – recurrent pyelonephritis & Renal Failure
(2 common causes of Renal Failure : DM & HPN)
c. Gangrene formation
d. Peripheral neuropathy
1. Diarrhea/ constipation
2. Sexual impotence
e. Shock due to cellular dehydration
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