ENDOCRINE

DISORDERS
Lecturer:
Christian John B. Timogan, RN, USRN
DIABETES MELLITUS
TYPE 1
INSULIN – DEPENDENT DIABETES MELLITUS
 DIABETES MELLITUS TYPE 1

I G
G I G I G
I
I G G
I
I G G
G G
G I I
I G
 DIABETES MELLITUS TYPE 1

I G
G I G I G
I
I G G
I
I G G
G G
G I I
I G
 DIABETES MELLITUS TYPE 1

PANCREAS
ALPHA BETA

GLUCAGON INSULIN
 DIABETES MELLITUS TYPE 1
F
G G G
G G
G G G G G
G G
G G
G G G G G
G G
G G G
G G
G G
G G
G G
 DIABETES MELLITUS TYPE 1
F
G G G
G G

K K
G G G G G
G G
G G
G G G G G
G G
G G G
G G
G G
G G
G G
 Failure of glucose transport to cells

HYPERGLYCEMIA Cellular starvation

Hemoconcentration Cell will use fats as energy source

Sluggish circulation Fluid Volume Deficit Increase Ketones WEIGHT

LOSS
Poor peripheral blood IC fluid shifts to IV Ketones will
flow enter the brain
HYPERTENSION
DELAYED WOUND DIABETIC
HEALING KETOACIDOSIS
 DIABETES MELLITUS TYPE 1
 Complication:
1. Diabetic Ketoacidosis
- Initial sign: Altered level of consciousness
- Manifestation:
• Severe 3Ps (Polyphagia, Polyuria, Polydipsia)
• Severe Fluid Volume Deficit
• Kausmaul’s Breathing
- Attempt to release excess glucose through
breathing
- Rapid deep breathing
- Acetone / Fruity breath
 Management: DKA
1. Fluids – 6 – 10L/day of Isotonic Solution
2. O2 therapy to neutralize acidic brain
3. IV Insulin – REGULAR INSULIN
DIABETES MELLITUS
TYPE 2
NON INSULIN – DEPENDENT DIABETES MELLITUS
 DIABETES MELLITUS TYPE 2

PANCREAS
ALPHA BETA

GLUCAGON LACKS INSULIN

INSULIN RESISTANCE
DIABETES MELLITUS TYPE 2

G
G I G I G

G G
I
G G
G G
I G G
DIABETES MELLITUS TYPE 2

G
G I G I G

G G
I
G G
G G
I G G
 DIABETES MELLITUS TYPE 2

I G
G I G I G
I
I G G
I
I G G
G G
G I I
I G
 DIABETES MELLITUS TYPE 2

I G
G I G I G
I
I G G
I
I G G
G G
G I I
I G
 DIABETES MELLITUS TYPE 2
RISK FACTORS: (Syndrome X)
• Pressure Increase (HPN)
• Hyperglycemia
• Increase Triglyceride
• Decrease High Density Lipoprotien
• Obesity
 DIABETES MELLITUS TYPE 2
COMPLICATION:
HYPERGLYCEMIC, HYPEROSMOLAR, NON-KETOTIC SYNDROME
- Extreme hyperglycemia (>800 mg/dL) without ketosis or acidosis
- Management:
1. PRIORITY: Fluid Therapy
2. Weight reduction and exercise
3. Oral Hypoglycemic Agents
 ORAL HYPOGLYCEMIC AGENTS

 For type II DM only

 Types of Oral Hypoglycemic Agents:

1. SULFONYLUREAS
 Glucotrol (Glipizide), Tolinaze (Tolazamide)
 MOA: Stimulates beta cells to secrete insulin and increases

its
sensitivity
 Should not be taken with alcohol
 ORAL HYPOGLYCEMIC AGENTS

2. NON SULFONYLUREAS
 BIGUANIDE – Metformin (Glucophage)
– Inhibits liver to produce glucose
– Caution with pts who are using dye!

 ALPHA – GLUCOSIDASE INHIBITORS

– Acarbose (Precose)
– Delays absorption of complex carbohydrates
 COLLABORATIVE DIAGNOSTICS OF DM
 Diagnostic:
1. Fasting Blood Sugar (FBS)
- N: 70-110 mg/dL
2. Glycosylated Hemoglobin (HbA1c)
- Test for compliance to treatment for the past 3 months
- N: <7.5% (>8% Poor Compliance)
3. Glucose Tolerance Test
- 8 hours pre-procedural fasting
- Intake of 75G glucose
- Patient will be taken a pre procedure and 2 hours post
intake HGT
- Prediabetes = 140 – 199 mg/dL
- (+) DM = >200 mg/dL
 DIABETES MELLITUS TYPE 1 & 2
 Signs & Symptoms:
1. 3P - Polyuria - To release excess glucose
- Polydipsia - Due to frequent urination
- Polyphagia - Due to cellular starvation
2. Hypokalemia - Due to polyuria
3. Unexplained fatigue / lethargy
4. Occasional enuresis – previously toilet-trained child
5. Vaginitis – Due to Candida Infection
 COLLABORATIVE COMPLICATIONS
 Complications:
1. Neurovascular complications due to sluggish circulation
• Retinopathy = Could lead to BLINDNESS
• Peripheral neuropathy
• Diabetic foot ulcer = Could lead to SEPSIS

2. Kidney Failure – Due to high molecular weight filtration

3. Cardiac Disease
4. Erectile Dysfunction
 COLLABORATIVE MANAGEMENT OF DM 1 & DM 2

1. Diet: Well-Balanced Diet / “My plate diet”

 Dietary recommendation:

• HIGH FIBER – Fiber prevents glucose absorption

in the intestine
• LOW FRUITS – It contains natural sugar (Fructose)
• DECREASE LDL (Bad Cholesterol)
 Instruct to carry a source of glucose (candy / glucose

tablets)
 COLLABORATIVE MANAGEMENT OF DM 1 & DM 2
2. Regular Exercise: Moderate (<150 mins/week)
 Timing should be based on meal glucose’s peak time (NOT ON

INSULIN PEAK TIME)

 Check glucose level prior to exercise
• <100 mg/dL – Offer Snacks (15g Carbohydrates)
• >250 mg/dL – Rest until blood glucose becomes normal
 Weight modification:
• Target BMI: 18.5 – 24.9 kg/m2
• Waist circumference:
- Female = < 88 cm
- Male = < 102 cm
COLLABORATIVE MANAGEMENT OF DM 1 & DM 2

3. Management: Diabetic Foot Ulcer

1. Proper foot care – podiatrist to cut toe nails
2. Inspect daily
3. Notify AP if (+) skin damage to prevent gangrene
4. Thermal injuries must be avoided (No heating pads & hot water)
5. Wear well-fitted shoes and cotton socks
6. Avoid walking barefooted
7. Avoid smoking – Causes vasoconstriction
COLLABORATIVE MANAGEMENT OF DM 1 & DM 2
4. Insulin
 Rotate injection site to prevent lipodystrophy
 Storage:
• Used/Opened Insulin – Room Temperature
• Unused/Unopened Insulin – Refrigerator but

thaw first in room temp prior to administration

 Mixing: NR – RN Sequence
COLLABORATIVE MANAGEMENT OF DM 1 & DM 2

NPH REGULAR
(Cloudy) (Clear)
ORDER: 0.5 mL NPH + 0.5 mL Regular
 COLLABORATIVE MANAGEMENT OF DM 1 & DM 2
5. Insulin Phenomenon
Somogyi = Sobra ang Insulin
SOMOGYI PHENOMENON
 Cause: Increase dose in evening insulin

Becomes HYPOGLYCEMIC between 2 am – 4 am

Release of counter regulatory hormone (GLUCAGON)

Glucagon goes to liver to withdraw stored glucose

(Glycogenolysis)

MORNING HYPERGLYCEMIA
 Treatment: Bedtime snacks and decrease evening insulin
dose
 COLLABORATIVE MANAGEMENT OF DM 1 & DM 2
5. Insulin Phenomenons
Dawn = Decrease ang Insulin
DAWN PHENOMENON
 Cause: Decrease evening insulin dose

Ideally: Body releases a hormone surge between 2 am – 4 am

(Cortisol & Growth Hormone)

Cortisol stimulates liver to produce glucose from non

carbohydrate
sources (Gluconeogenesis)

MORNING HYPERGLYCEMIA
 Treatment: Increase evening dose of insulin
 INSULIN

ONSET PEAK DURATION

REGULAR 30 - 1 2- 4 3.5 - 7

INTERMEDIATE 1- 2 4-8 7 - 14

LONG - ACTING 14 - 28
2- 4 8 - 16
HYPOGLYCEMIA
 HYPOGLYCEMIA
 Glucose level: <70 mg / dL
 Causes:
• Too much insulin
• Too large amount of oral hypoglycemic agent
• Too little food
• Excessive activity
 HYPOGLYCEMIA
 Signs and Symptoms:
• Tremors
• Irritability
• Restlessness
• Easy fatigability
• Diaphoresis
 HYPOGLYCEMIA
 Management:
- If glucometer is available: Check blood glucose level
- If no glucometer and pt. experiences symptoms of hypoglycemia:
“Assume hypoglycemia and Treat accordingly”

Suspected Hypoglycemic Reaction

1. Give simple sugar – 15G carbohydrates (orange juice)
2. Recheck HGT after 15 minutes
(Repeat for a maximum of 2 cycles if still <70 mg/dL)

3. IV Dextrose 50% / IM Glucagon

4. After glucose has stabilized, give complex carbohydrates
THYROID PROBLEMS
 THYROID HORMONES
● T3 & T4 – Used for body’s metabolism
- Battery of our body

● Calcitonin – Transports calcium from

blood to bone
NEGATIVE FEEDBACK
LOOP
 HYPOTHALAMUS

TRH (Thyroid-Releasing Hormone)

ANTERIOR PITUITARY GLAND

TSH (Thyroid-Stimulating Hormone)

THYROID GLAND

T3 & T4 Release
GOITER
 Tumor / enlargement of the thyroid

 Classifications:
• Toxic Goiter – Accompanied by hyperthyroidism

• Non Toxic Goiter – Associated with euthyroid state

 Types of Goiter:
• Endemic Goiter

• Nodular Goiter

• Thyroid Cancer
ENDEMIC GOITER
 Most common type

 Caused by iodine deficiency

 Asymptomatic ; tracheal compression

when excessive
 Treatment:

• Supplementary iodine

• Iodized salt

• SSKI
NODULAR GOITER

 Areas of hyperplasia (Overgrowth)

 Slowly increasing in size
 Can cause local pressure symptoms
in the thorax
 Some are malignant or with
hyperthyroid state.
HYPERTHYROIDISM
 Increase secretion of thyroid hormone

 Common Cause:
• Autoimmune (Grave’s Disease)

• Tumor (Toxic Goiter)

 Labs and assessment:

• Increase T3 and T4 ; Decrease TSH

• Thrill and Bruit at the anterior neck

 Signs and Symptoms:

THYROTOXICOSIS
• Increase basal metabolic rate (Increase vital signs)

• Increase body heat production (Heat intolerance)

• Diaphoresis

EXOPHTHALMOS
• Bulging of eyes due to increase IOP

• Von Graefe’s Sign: Eyelid lag when looking downward

• Dalyrimple’s Sign: Upper eye lid retraction

 Signs and Symptoms:

THYROTOXICOSIS
• Increase basal metabolic rate (Increase vital signs)

• Increase body heat production (Heat intolerance)

• Diaphoresis

EXOPHTHALMOS
• Bulging of eyes due to increase IOP

• Von Graefe’s Sign: Eyelid lag when looking downward

• Dalyrimple’s Sign: Upper eye lid retraction

OTHER MANIFESTATIONS
• Swelling of thyroid gland (Goiter)

• Increased appetite

• Hypocalcemia

• Amenorrhea

• Insomnia

• Diarrhea

• Weight loss
 Management:

1. Priority: Fluid Replacement

2. Diet: Finger foods; Increase calories due to increase
body processes
3. Cold Environment
4. Cold milk for insomnia Due to HEAT INTOLERANCE
5. Cold baths
 HYPERTHYROIDISM
6. For exophthalmos:
• Night – Patch the eye
• Day – Remove patch
- Use dark glasses to prevent visual deprivation
- Artificial tears
7. Promote adequate rest periods
8. Medications:
Propylthiouracil (PTU)
Methimazole
Blocks thyroid hormones production
Effectivity: 2-3 weeks
2nd ChoiceAdverse
Drug Effect: Agranulocytosis 1st Choice Drug
2nd – 3rd Trimester 1st Trimester
 HYPERTHYROIDISM
• Saturated Solution of Potassium Iodide (SSKI) / Lugol’s Solution
 MOA: Decreases vascularity of thyroid therefore decrease in size
 Given prior to thyroidectomy
 Dilute in milk, water, or juice
 Take with straw
 Ask for sea foods allergy prior to administration
 WOF: Hyperkalemia

• Propanolol
 Betablockers to decrease HR and BP
 Contraindicated to patient with Asthma
 HYPERTHYROIDISM
• Radioactive Iodine (RAI) Therapy
 MOA: Thyroid gland utilizes RAI to produce hormones

Once RAI is on the thyroid gland

RAI destroys overactive thyroid cells

 Route: Oral / Intravenous
 Health teachings:
• Observe for thyroid storm
• Propanolol may be given to control
symptoms
• Contraindicated to pregnancy because it
crosses the placenta
and while breastfeeding.
HYPOTHYROIDISM
 HYPOTHYROIDISM
 Insufficient thyroid hormone production

 Causes:
• Tumor

• Decrease Iodine Intake

• Autoimmune (Hashimoto’s Disease)

 Labs:
• Decrease T3 and T4 ; Increase TSH
 HYPOTHYROIDISM
 Signs and Symptoms:
• Decrease basal metabolic rate (Decrease vital signs)

• Decrease body heat production (Cold intolerance)

• Hypercalcemia

• Constipation

• Weight Gain

 Complication: Myxedema Coma – Severe Hypothyroidism

 HYPOTHYROIDISM
 Management:
1. Priority: Maintain normal temperature
2. Diet: Regular diet
3. Room temp environment Due to COLD INTOLERANCE
4. Warm baths
 HYPOTHYROIDISM
 Medication:
• Levothyroxine (Synthroid)

- MOA: Increases metabolism

- LIFETIME TREATMENT
- Give in morning due to its insomnia effect
- If HR >100 bpm, hold the drug
- Can be given to pregnant
- Sign of effectivity: Diuresis
PARATHYROID
PROBLEMS
 PARATHYROID HORMONE

● Parathormone
– Transport calcium from bone to blood
 HYPER
PARATHYROIDISM
 HYPER PARATHYROIDISM
 Overproduction of parathormone

 Manifestations:
• Hypercalcemia
• Cardiac Dysrhythmias
• Renal Stones
• Skeletal Pain
• Pathologic fractures
• Shortening of body structures
 HYPER PARATHYROIDISM
 Diagnostic:
• Elevated Calcium level
• Elevated parathormone concentration
• X-ray for bone changes

 Management:
1. Increase fluid intake (2L/day)
2. Assist in mobility (Walker / Cane)
3. Decrease calcium intake
4. Regular exercise
 HYPO
PARATHYROIDISM
 HYPO PARATHYROIDISM
 Inadequate secretion of parathormone

 Manifestations:
• Hypocalcemia
• Cardiac Dysrhythmias
• Tetany
• Laryngeal spasm
• Chvostek / Trousseau Sign
• Seizure
 HYPO PARATHYROIDISM
 Diagnostic:
• Decrease Calcium level
• Elevated phosphate level
• X-ray for bone calcification

 Management:
1. IV calcium gluconate
2. Aluminum carbonate – Phosphate binder
3. Vitamin D – For calcium administration
4. Regular exercise
5. Initiate seizure precaution
6. Increase calcium intake
DIABETES INSIPIDUS
 DIABETES INSIPIDUS

DECREASE ADH Production

ADH – Reabsorbs H2O in the kidney

Possible cause:
○ Stroke
○ Trauma
○ Surgery
○ Idiopathic
 DIABETES INSIPIDUS

2 Types:
• CENTRAL
- Dec. ADH Production
• NEPHROGENIC
- Adequate ADH
Production
- Kidneys do not respond
 NORMAL
H20
H20 H20 H20
H20
H20 H20
ADH H20 H20
H20
H20
ADH
H20
H20
H20
 NORMAL
H20
H20 H20 H20
H20
H20 H20

ADH H20 H20

H20
H20
ADH
H20
H20
H20
 DIABETES INSIPIDUS
H20
H20 H20 H20
H20
H20 H20

H20 H20

H20
H20
H20
H20
H20
 DIABETES INSIPIDUS
 Pathophysiology:
Decrease ADH Production / Unresponsive Kidney
Decrease H20 reabsorption in the kidneys
• Decrease urine specific
gravity
POLYURIA
• Electrolyte imbalance:
Hypernatremia,
DEHYDRATION Hypokalemia
• Decrease Central Venous Pressure
• Flat neck vein
• Sunken fontanels
• Increase HCT
• Weight loss
 DIABETES INSIPIDUS
 Management:
1. Goal: To stop the urination
2. Increase fluid intake
3. Meds:
• Desmopressin IM – synthetic vasopressin
• Thiazide Diuretics – To excrete excess Sodium
4. Fluid Resuscitation: Isotonic Solution
SYMPTOMS OF INAPPROPRIATE
ANTI DIURETIC HORMONE
 SIADH

Increase ADH Production

Common cause:
• Small cell lung cancer
• Severe pneumonia
• Pneumothorax
• Trauma
• Stroke
• Stress
 SIADH
H20
H20 H20 H20
H20
H20 H20
ADH H20 H20
ADH
H20
H20
ADH
ADH H20
H20
ADH H20
ADH
ADH
ADH
ADH
 SIADH
H20
H20 H20 H20
H20
H20 H20

ADH H20 H20

ADH
H20
H20
ADH
ADH H20
H20
ADH H20
ADH
ADH
ADH
ADH
 SIADH
 Pathophysiology:
Increase ADH Production
Increase H20 reabsorption in the kidneys
• Increase urine specific
gravity
OLIGURIA
• Electrolyte imbalance:
Hyponatremia, Hyperkalemia
OVERHYDRATION
• Increase Central Venous Pressure
• Distended neck vein
• Bulging fontanels
• Decrease HCT
• Weight gain
 SIADH
 Management:
1. Goal: To promote the urination
2. Meds:
• Diuretics – Furosemide (Lasix)
• Democycline – To make kidneys less sensitive
to ADH
3. Fluid Restriction
4. Seizure precaution due to risk of Cerebral Edema
 DI SIADH
Hemoconcentration Distended Jugular Vein Hyperkalemia
Hypernatremia Weight loss Xerostomia
Sunken Fontanel Edema Increase CVP
ADRENAL GLAND
PROBLEMS
 ADRENAL GLANDS PROBLEMS
 Common Cause:
• Autoimmune
• Tumor formation
 Adrenal Cortex Hormones:
• Glucocorticoids – Promotes gluconeogenesis in the liver
• Mineralocorticoids – Reabsorbs sodium (Water will follow)
- “Aldosterone”
• Sex Hormones – Androgen and Estrogen
 Adrenal Medulla Hormones:
• Epinephrine – Increases heart rate
• Norepinephrine – Increases blood pressure
ADDISONS DISEASE
 ADDISONS DISEASE
 Decrease Adrenal Function
 Pathophysiology: Autoimmune Attack
Targets Adrenal Glands
Decrease Adrenal Glands function
Decrease Adrenal Cortex Decrease Adrenal Medulla
 Decrease Adrenal Cortex Decrease Adrenal Medulla
Dec. Glucocorticoids Dec. Mineralocorticoids Dec. Catecholamine
HYPOGLYCEMIA Dec. Na and H20 reabsorption HYPOTENSION
TACHYCARDIA
HYPONATREMIA TACHYPNEA
Dec. Immune System
HYPERKALEMIA
RISK FOR INFECTION POLYURIA SHOCK
DEHYDRATION
 ADDISONS DISEASE
 Diet: Increase Sodium ; Decrease Potassium
 Activities:
1. Offer relaxation
2. Avoid crowded place
 Medication:
1. Steroids
- Give with foods
- WOF: Agranulocytosis
 Fluid Management:
1. Isotonic Solution
- To correct dehydration
CUSHINGS DISEASE
 CUSHINGS DISEASE
 Decrease Adrenal Function

Pathophysiology: Autoimmune Attack / Tumor formation
Targets Adrenal Glands
Increase Testosterone
Increase Adrenal Glands function • Hirsutism
• Acne
Increase Adrenal Cortex Increase Adrenal Medulla
 Increase Adrenal Cortex Increase Adrenal Medulla
Inc. Glucocorticoids Inc. Mineralocorticoids Inc. Catecholamine
HYPERGLYCEMIA Inc. Na and H20 reabsorption HYPERTENSION
TACHYCARDIA
HYPERNATREMIA TACHYPNEA
HYPOKALEMIA
OLIGURIA RISK FOR CVA
Edema Formation
• Moon Face
• Buffalo Hump
• Truncal Obesity
 CUSHINGS DISEASE
 Diet: Decrease Sodium ; Increase Potassium
 Medication:
1. Steroids
- Give with foods
- WOF: Agranulocytosis
2. Chemo Drugs (For tumor cause)
 Limit fluid intake
 Surgical Management: Adrenalectomy
- WOF: ADDISONIAN CRISIS
• Profound fatigue
• Shock
- Management: Give high dose hydrocortisone
PHEOCHROMOCYTOMA
 PHEOCHROMOCYTOMA
 Tumor formation in Adrenal Medulla
 Pathophysiology: Presence of Tumor cells in Adrenal Medulla
Severe increase in Catecholamine
Increase Vital Signs
Hypertensive Crisis
Palpitation
 PHEOCHROMOCYTOMA
 Diagnostic Test:
VMA – Vanillylmandelic Acid Test
- Measures the amount of VMA that is passed into the
urine over 24 hour period
- 24 hour urine collection (Discard the first collection)
- Avoid stimulants while on test
 PHEOCHROMOCYTOMA
 Diet: Increase calories, vitamins, and minerals
 Medication:
1. Hydralazine (Diuretics)
2. Sodium Nitroprusside (Vasodilator)
3. Phentolamine (Alpha-Adrenergic Blocker)
 Avoid stimuli; provide calm environment
 Avoid palpation, heating pads, & strenuous activity
 Surgical Management: Adrenalectomy