INTENSIVE PHASE HANDOUT

ENDOCRINE
ISLETS OF LANGERHANS
Classified with cells:
 Alpha – 20%
- Glucagon – increases blood sugar (BS) level

 Beta – 70%
Insulin – decreases BS levels

 Delta – 10% - secretes somatostatin  (x) somatotropin

CALORI ENZYMES PROCESS PRODUCT

E
Carbohydrates 4 grams Amylase – salivary and Glucogenesis – Glucose
pancreatic formation of sugar
Protein 4 grams Pepsin (trypsin + Catabolism Amino acids
pepsinogen) Albumin
Globulin – transport
system of antibodies
Fats 9 grams Lipase / Bile - blood Emulsification Faty acids
(from liver)

Food
↓
Cell (insulin)
↓
Glycogen (glycogenesis by insulin)
↓ ↓
Liver muscles
↓
Less than 80 BS level (HYPOGLY)  alpha cells: glucagon (glycogenolysis)
↓
Glucose

INSULIN – to lower BS level

 By transporting glucose to the cell
 By converting excess to become glycogen

What is the cause of HYPOGLYCEMIA in liver problem?

- Loss of glycogen (not able to store glucagon)

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DIABETES MELLITUS
- Less or no insulin  HYPERGLYCEMIA (HALLMARK OF DM)
- Is the most common metabolic disorder

Exact cause: unknown

Predisposing Factor: Stress

Classifications:

A. Acquired
Type1 – IDDM (HRDM -heredity related) Type 2 – NIDDM (DRDM – dietary related)
- Heredity (3rd generation uplink) - Obesity
- Unstable - Stable
- Thin - Adult onset (>30)
- Zero insulin - ↓ insulin. Insulin resistance
- Child-onset or juvenile (<30) - HHNC: complication
- DKA: complication

B. Secondary
1. Gestational (PRDM – Pregnancy related)
- 3rd month of pregnancy: ↑ HCS (human chorionic somatomammotropin) – form of insulinase  will
decrease insulin  will increase BS level

2. Cushing’s-related (CRDM) – CHRONIC

- ↑ Glucocorticoids  Glucogenesis (formation of sugar from new sources)
- New sources: Fats and protein (converted by glucocorticoids)  Glucose  causing
Hyperglycemia

** PATHOGNOMONIC – unique

** HALLMARK – di pwede mawala

 Hallmark of SLE: (+) ANA/ antinuclear antibody

 Hallmark of asthma: wheezing
 Pathognomonic of Measles: Koplik’s
 Pathognomonic of Kawasaki disease – Strawberry tongue
 Pathognomonic sign of Pernicious – red beefy tongue
 Pathognomonic sign of Scarlet fever – raspberry tongue

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 (2) POLYDIPSIA

Movement of water
from A to B
(KIDNEYS)

(1) POLYURIA

Cellular starvation  profound weakness  Primary defense: HUNGER

SQ INSULIN  should be given within 30 mins – 3 hours

CELL
If NOT…

BLOOD Secondary Defense – GLUCOCORTICOIDS

_____________________
1. Protein – glucose (will aggravate hyperglycemia)
↑ Glucose 2. Fats – glucose (will aggravate hyperglycemia)
_____________________ ↓ ↓
Glucose Ketones

Acidosis (DKA)

Manifestations: TRIAD OF HYPERGLY

1. Polyuria
- excessive urination
- osmotic diuresis (glucosuria)

2. Polydipsia
- Excessive thirst
- Total DHN

3. Polyphagia
- Excessive hunger
- Cellular starvation

DKA
1. Abd pain
2. Weak and thready pulse
3. 3 Ps
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 4.Acetone or fruity breath
5.Kussmaul’s breathing  respiratory depression (EARLY)
6.Alter LOC – ketotic coma (LATE)
 MANAGEMENT FOR DKA – IV INSULIN (REGULAR INSULIN- CLEAR INSULIN WITH NO KNOWN
ALLERGIC REACTION)
 When giving insulin IV, WOF for: Hypoglycemia, Hypokalemia, Insulin edema
 Standby: D50W and Kcl

** ANY ACID CAN SEDATE YOUR BRAIN

** More CO2  can sedate your brain

 Primary Acid
- Carbonic acid (H2CO3): H2 + CO2

 Abnormal Acid
- Ketones (acidosis) – should flush out 600 cc
- Deep and fast breathing (Kussmaul’s breathing): to remove co2 – to balance H20 – to manage
ketoacidosis

Complications

a. Acute Complications:

CELL
I. DKA
- Cause: Cellular starvation
- Ketotic coma
- Management: IV insulin __________________________________

↑ Glucose  ↑ viscosity  ↑osmolarity

II. HHNC __________________________________
- Hyperglycemic (600 mg/dL)

- Hyperosmolar Dehydrated  brain cells (cerebral DHN)

- Non-ketotic

- Coma

- Cause: Cerebral DHN

- Management: Hypotonic solution

b. Chronic Complications

- Inc BS level  inc viscosity  sluggish blood flow

I. Hypertension

II. Atherosclerosis – CVA, CAD, PVD (peripheral vascular disorders)

III. Nephropathy

IV. Impotence

V. Foot ulcers  gangrene  Septicemia (Septic shock)

VI. Neuropathy  paresthesia

VII. Retinopathy (annual eye examination)

______________________

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↑Glucose Fats Proteins
______________________

ATHEROSCLEROSIS

***
# of cases: CANCERS (WHO)
1. Breast Ca
2. Lung Ca
3. Colon Ca

#1 Mortality:
- Lung Ca
Management: (DAM)

1. Diet
- ↓ caloric diet
- ↑fiber diet
- Complex carbohydrates
a. PRUDENT DIET: % distribution: Fats 30  Carbs 50  Protein
20
b. Caloric counting
c. Caloric substitution
d. Inverted pyramid

2. Activity
- Enhances CHO uptake by the cells
- Decreases insulin requirements
- Done 1 – 2 hours p.c.
- Regular pattern
- Other benefits
o Allows additional snacks
o Maintains
▪ IBW
▪ Serum glucose
▪ Serum lipids

** NOV 14 – diabetes awareness day

Nov – diabetes awareness month

3. Medications

a. Oral Hypoglycemic Agents

i. Stimulates beta cells to secrete insulin –↑ insulin
ii. Suppress Alpha cells - ↓ glucagon
iii. Corrects insulin resistance

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Examples:
- Diabenese
- Ordinase
- Tolinase
- Micronase
- Glucotrol
- Diamicron
- Glucophage (METFORMIN)

Side Effects
Observe for:
• G.I. Upset – SULFONYLUREA  Give during meals or with meals
• Hypoglycemia
 Gait disturbances
 Unusual perspiration
 Tachycardia
 Obvious tremors
 Moodiness or irritability
 MANAGEMENT FOR HYPOGLY – give oral glucose sources
** always choose the liquid form (orange juice)
a. Insulin

OBSERVE FOR HYPOGLYCEMIA – PEAK

Time Course Agent Onset Peak Duration Remarks

Rapid acting lispro (Humalog) 10-15 1 hour 2-4 hours • Used for rapid
mins. reduction of
aspart (NovoLog) 40-50 2-4 hours postprandial
glulisine (Apidra) 5-15 mins. hyperglycemia
2 hours
mins.
30-60
5-15 mins.
mins.
Short acting Regular (Humulin 30-60 2-3 4-6 hours. • 20-30 mins a.c.
(CLEAR) R, Novolin R, Iletin mins. hours
II Regular) • Given alone or
combination

Intermediate NPH (neutral 2-4 4-12 16-20 • Given p.c.

acting protamine hours hours hours
(CLOUDY) Hagedorn)
4-12 16-20
(Humulin N, Ileten 3-4
II Lente, Ileten II hours hours
hours
NPH, Novolin N)
Very long glargine (Lantus) 1 hour (Contin 24 hours • Used for basal dose
acting uous)
determir (Levemir) 24-36
(CLOUDY) 6 hours
Glargine (Toujeo) hours

Rapid acting Afrezza <15 ~50 2-3 hours • Used as rapid-acting

inhaled mins. mins insulin
insulin

Nursing Management (insulin administration)

a. Route: SUBCUTANEOUS
• slow absorption
• less painful than ID
• Angle: 90° - to prevent inaccuracy
• Needle:
o thin: 3/8”  pinch
o obese: ½”, 5/8”  stretch
• IV – DKA
• Don’t massage site of injection
- Can predispose lipodystrophy
- Can have hypoglycemia
b. Refrigerate unused insulin
b. Never shake the vial  bubbles  difficult to aspirate insulin
● Roll at the palm of hands
d. Prevent lipodystrophy
 ● administer at room temperature
● rotate the site of injection

Side – effects:
Localized
● Induration or Redness  avoid using for 4-6 weeks
● Swelling
● Lesion at the site  abscess
● Lipodystrophy  invalid for injection of insulin
Generalized

● Edema
● Hypoglycemia
● Somogyi phenomenon
- ↑ Insulin
- Insulin + heavy activity
- AGLYCEMIA (no sugar)
- Release of Glucagon and Glucocorticoids
- Rebound Hyperglycemia (SOMOGYI PHENOMENON)
- MANAGEMENT: Tapered insulin

FOOT CARE
- Inspect the feet daily
- Wash feet with warm water and mild soap
- Wear comfy properly fitted pair of shoes
- Break in new pair of shoes (1-2 days)
- Use white cotton socs (males)
- Avoid going barefooted, trimming toenails laterally, wearing knee-high or stay up
stockings
- Applu lotion on feet
- Exercise or massage feet

For any s/sx of injury, consult a PODIATRIST

THYROID GLAND
- 2 lateral lobes
- Fixed to the anterior surface of the upper trachea

Hypothalamus – releases TRS (thyroid releasing hormone)

↓ - TRS stimulates APG to release TSH
APG (TSH)
↓TSH will stimulate TG to release t3, 34 and thyrocalcitonin
Thyroid gland
T3- triiodothyronine  overall body metabolism
T4  overall body heat production
Thyrocalcitonin  PTH regulator

** RICH IN IODINE
- Crabs
- Shrimp
** RICH IN CALCIUM
- Broccoli
- Milk

Calcium
↓
Blood ANIONIZED Calcium
Absorbed in the small intestines
 Lactose: hydrophilic (attracts water) IONIZED
 Pancreatic enzyme
Inc PTH – stress and steroids =
calcitonin (will inhibit the PTH to
Vit D
avoid calcitonin to go out to
prevent osteoporosis Small intestine
(calciferon)
↓
BONES Matrix formation and Mineralization Pancreatic
enzyme and
Lactose

Small intestine
Lactase
↓
Lactamase – enzymes that absorbs lactose (pulls calcium to help pancreatic enzyme to get
calcium)
↓
Lactose + H2O

THYROID CONDITIONS

HYPERTHYROIDISM

Kinds:
 Grave’s Disorder
 Parry’s Disorder
 Basedow’s Disorder
  Exophthalmic Goiter
- Because of too much t4
 Toxic Diffuse Goiter

3 Basic concepts
1. Increased metabolic rate – increase t3
2. Increased body heat production – increase t4
3. Hypocalcemia

Etiology and Incidence:

● Females, below 40 yrs.
● Severe emotional stress
● Autoimmune Disorder
 TSI – THYROID STIMULATING IMMUNOGLOBLULIN
 stimulates thyroid gland to release t3, t4 and thyrocalcitonin
 Highlands – less source of iodine (fuel of thyroid gland  iodine)
 COMPENSATE: will increase iodine  Enlarged thyroid gland

↓ ESTROGEN  ↓ THYROCALCITONIN  ↑ PTH (osteoporosis- common in women and elderly)

↑ T3  ↑ METABOLOISM  STRESS  SNS  ADRENAL MEDULLA (epi – increase HR / norepi –

increase BP)

Manifestations:

Thyroidal Disturbances
Cardiovascular
- Hypertension
- Tachycardia

CNS

- Restlessness
- Nervousness
- Irritability
- Agitation: with impaired judgment
 - Fine tremors

GI METABOLISM

- Increase appetite to eat

- Weight loss
- Diarrhea
- Amenorrhea
---- fats  emulsify to become fatty acids  fatty acids transports ADEK and
builds the adipose tissue and adrenal cortex
- Fine silky hair (less protein  proteins are used as energy source)
- Pliable nails (less protein  proteins are used as energy source)

OTHER SYMPTOMS

- Diaphoresis
- Heat intolerance

Opthalmopathy
Exophthalmos – Cystine Cells
 Corneal ulceration
 Ophthalmitis
 Blindness
Dalyrimple’s sign (Thyroid stare)

 Bright – eyed stare

 Infrequent blinking
Von Graefe’s sign (lid lag)
 Long and deep palpebral fissure when one looks down
Jeffroy’s sign
 Forehead remains smooth when one looks up

Management
1. Rest
● Non-stimulating, restful environment
2. Diet
● ↑ caloric (metabolism is x4 the normal)
● ↓ fiber
3. Promote safety
4. Protect the eyes
 ● artificial tears or NSS
● dark sunglasses or non-irritating tape
5. Replace fluid – electrolyte losses
6. Administer medications, as ordered:
- Beta – blockers: INDERAL
● To control tachycardia, HPN (Monitor HR)
- Ca – channel blockers (monitor BP)
- Potassium Iodides  suppress the blood supply of thyroid gland  to kill some cells
 reduce the size and vascularity of thyroid gland
● Lugol’s solution
● SSKI (saturated solution of K iodides – to suppress blood supply  dec
production of hormones)
o Mix with fruit juice with ice or glass of water
o Provide drinking straw  (x) staining tasting
o Side effects: allergic reaction, increased salivation, coryza
- Thioamides: Chemotherapeutic
● PTU (Propylthiouracil)
● Tapazole (Methimazole)
● Side effects: agranulocytosis
o Fever, Sore throat, Skin rashes (TRIAD OF
AGRANULOCYTOSIS)
- Dexamethasone

7. Radiation therapy (I123/Iodine 123) – Isolation for few days  kill cells without bone
marrow suppression
 RADIATION PROTOCOLS
- Isolation (3 days)
- ALLARRA – all are regarded radioactive
- Distance – 6 feet
- Time exposure – 30 mins q shift
- Wear lead shield
- ABSOLUTE CONTRAINDICATION  pregnant of any trimester, children below 12
(Philippines) below 16 (US)

8. Surgery: Subtotal Thyroidectomy (if there is altered trachea and thyroid crisis)

Preop Care
● Promote euthyroid state
● Administer Iodides as ordered
o to decrease the size & vascularity of thyroid gland  prevent hemorrhage,
thyroid crisis (exaggerated amount of hormones)
● Monitor ECG
 ● Postop Care
● Position: SEMI-FOWLERS with head, neck & shoulder erect  AVOID HYPERFLEXION
AND HYPEREXTENSION
● Prevent hemorrhage - Ice collar over the neck (assess for hemorrhage: NAPE
ASSESSMENT)
● Keep on bed side: (first 48o)
- Tracheostomy set  hypocalcemia  tetany
- SIGNS OF TETANY:
- (+) chovstek’s sign (facial spasms when tapping facial nerve)
- (+) trousseau’s sign (carpal spasms upon occluding bracial nerves)
- Laryngospasm  airway obstruction  TRACHEOSTOMY SET

● Calcium Gluconate (IONIZED) - WOF HYPORCALCEMIA

● Assess for laryngeal nerve damage
- Observe for hoarseness of voice
● Monitor:
o Temperature  HYPERTHERMIA IS THE FIRST SIGN OF THYROID CRISIS
o Monitor BP
● Steam inhalation to soothe irritated airways
● Observe for potential complications
o Hemorrhage: check the nape
o Tetany - airway obstruction
o Laryngeal nerve damage  WOF hoarseness of voice
o Thyroid crisis  Hyperthermia
o Myxedema  HYPOthyroidism (most common cause of hypothy: TEATMENTS
for hyperthy)
● Client Teaching
o ROM exercises of the neck 3 – 4 x / day after discharge
o Regular follow – up care (to know onset of hypothyroidism)

HYPOTHYROIDISM

● Myxedema (Adult)  may lead to myxedema coma

● Cretinism- associated with intellectual disability (Children)

● Causes
o Surgery
o Radiation therapy
o Antithyroid drugs
o Autoimmune
o Thyroiditis
3 Basic concepts:
1. decreased metabolic rate  < T3
2. Decreased body heat production  < T4
3. Hypercalcemia  < TC

Assessment:
● Slowed physical, mental reactions
● Dull look
● Anorexia
● Obesity  slow metabolism  x6 slower metabolism
● Bradycardia  atherosclerosis  stroke, MI, angina, PVD
● Hyperlipidemia  atherosclerosis  stroke, MI, angina, PVD

● Cold intolerance
● Constipation
● Coarse, dry, sparse hair
● Brittle nails
● Irregular menstruation  menorrhagia

Management:
1. Monitor VS. Be alert for signs and symptoms of CV disorders
2. Diet
● ↓ caloric
● ↑ fiber
3. Provide warm environment during cold climate.

4. Pharmacotherapy
● Proloid (Thyroglobulin)
● Synthroid (Levothyroxine) - DOC: HOGHEST ABSORPTION RATE
● Dessicated Thyroid Extract
● Cytomel (Liothyronine)
o Check BP, PR before administration
o Start with low dose, gradually increase
 ADRENAL GLAND CONDITIONS

ADRENAL GLANDS

- Located on the top of the kidneys

- Consists of an outer cortex and an inner medulla

Hypothalamus - ACTHRH

APG - ACTH

ADRENAL Cortex

- NATURAL STEROIDS:
Glucocorticoids (cortisol) – Glucogeogenesis and fat distribution

Mineralocorticoids (aldosterone)- Na retention and K excretion

Sex hormones – androgen, progesterone and estrogen (secondary sex characteristics)

PHEOCHROMOCYROMA

- Benign tumor in the adrenal medulla (ADENOMA – type of tumor that increases the
number of cells  increases hormones  too much epi (HR) and norepi (VC))
- Main problem: hypertensive crisis: sudden elevation in BP  180/120 or higher
- DOC: Phentolamine Mesylate (Regitine)  fast acting vasodilator given via IV
- Monitor: BP q 15mins
- Antidote: DOPAMINE

CUSHING’S DISORDERS

Description:
● Hypersecretion of adrenal hormones  DISEASE (Unknown Cause)
● Abrupt steroids withdrawal  SYNDROME (Preventable)

Manifestations
 ↑ Glucocorticoids
- Can alter hypothalamus being an emotional center
1. Labile moods – similar to borderline personality disorder
2. Hyperglycemia  signs of DM
3. Fat misdistribution
a. Thinning of arms and legs
b. Buffalo humps
c. Frontal or truncal obesity  femoral congestion  thrombophlebitis (risk: embolism)

HEART

Internal – myosin/actin

External – K+

 Contract  asynchronous contraction

↑ Mineralocorticoids – salt

1. ↓ K  flaccid heart  prominent u waves  cardiac arrest

2. ↑ Na  FVE (1 cc of H2O = 1gram of weight)
a. Anasarca (moon face)
b. Obesity
c. Skin thinning/stretching  easy bruising
3. Complications:
- HTN
- CHF
- Possible pulmonary edema

↑ Androgens – hirsutism

↑ Natural Steroids
a. ↑ PTH – osteoporosis
b. Can cause immunosuppression – risk for infection and poor wound healing

Management:
1. Monitor:
● vital signs
● fluid balance
o edema
 o intake and output
o urine specific gravity (INCREASE Na – retain water – less urine – increase
concentration - increase specific gravity)
● hyperglycemia
o fingersticks
o urine glucose and ketones
● laboratory studies  monitor for Na (135-145meq/L) and K+ (3.5-5.5meq/L)
2. Apply antiembolism stockings  before arising
3. Diet: low caloric, low Na, high K, limit water intake
4. Maintain standard precautions  because of risk for infection
5. Prevent skin breakdown
6. Weigh the patient daily  1 cc = 1 gram of weight
7. Allow ventilation of feelings
8. Provide rest periods to prevent fatigue

ADDISON’S DISEASE

May be:
● Primary – adrenal cortex
● Secondary – APG problem
● Tertiary – hypothalamic type

Etiology:
Tumor
Infection
Trauma
Autoimmune or atrophy

Pathophysiology:

↓ GC – fasting hypoglycemia – profound weakness (1)

↓ MC - ↑ K – spastic heart  cardiogenic shock (tall, peaked T waves in ECG)
- ↓ Na – FVD – hypovolemic shock
Cardiogenic and hypovolemic shock  irreversible shock (2)

↓ Androgen – bronze skin

↓ Steroids – severe inflammation – infection, pain (3)

(1,2,3)  Addisonian Crisis

 Management:
1. Administer:
● IVF – to prevent irreversible shock
o I.V. hydrocortisone
o NSS
2. Monitor and record:
● vital signs
● fluids balance
o intake and output
o urine specific gravity
o weight
● laboratory studies
3. Diet: ↑ calorie, ↑ Na, ↓ K
4. Advise the patient to gradually change positions
5. Encourage fluid intake
6. Assist with ADL
7. Maintain a quiet and calm environment

PITUITARY CONDITIONS

PITUITARY GLAND

- A small pea-shaped gland

- Connected to the hypothalamus
- 2 lobes: anterior and posterior

GH is the only hormone that cannot be manipulated by hypothalamus

POSTERIOR PG – STORAGE only
(produced by hypothalamus)

1. OXYTOCIN
- Contraction of the uterus
- Stimulates milk ejection
2. Antidiuretic hormone (ADH, vasopressin)
- Promotes water retention

HYPERPITUITARISM

Description:
● Chronic, progressive disease
● Excessive growth hormone (GH) secretion and tissue over-growth
● Appears as:
o Gigantism
o Acromegaly – hands and feet only

Etiology:
- An anterior pituitary adenoma

Pathophysiology:
● Overgrowth of tissues leads to problems on:
o Neurologic – optic (blurry vision) and trigeminal nerve involvement
----- trigeminal nerve
1. Ophthalmic: No peripheral vision
2. Maxillary: large jaws
3. Mandibular: difficulty in chewing

o Motor
o Secretory
● Motor – failure on range of motion
● Secretory

Nursing Interventions:
1. Counseling to deal with feelings about change body image.
2. Assist with ROM to maximize joint movement.
3. Monitor for visual disturbances.
4. Prepare the patient for surgery, if indicated  surgery will only prevent further growth
DOC: Sandostatin (Ocreotide)  suppress growth hormone

HYPOPITUITARISM

ADH-RELATED PROBLEMS

Syndrome of Inappropriate ADH (SIADH)

- Hypersecretion problem
● Involves continuous secretion of ADH
● Is one of the most common causes of hyponatremia

Characteristics:
● Edema
● Weight gain
● Hypertension
● Hyponatremia
 ↓
Hyponatremia (DILUTIONAL HYPONAT)
↓
Dec osmolarity
↓
Water intoxication

HYPOTHALAMUS – ADH
↓
PPG – no feedback mechanism  continuous production of ADH by
hypothalamus
Diabetes Insipidus (most dangerous endocrine disorder)

● A permanent or transient deficiency in ADH  WATER LOSS

Characteristics:
● Inability of the renal tubules to retain water
- Polyuria (20 L/day)  HALLMARK
- Dehydration
- Constipation
- Dilute, water-like urine (↓ specific gravity)  Normal: 1.010-1.025

Etiology:
- Tumor
- Intection
- Trauma
 Management:
1. Monitor
● Fluid balance
● I&O
● Specific gravity
● Weight
● VS
● Skin turgor
2. Maintain adequate hydration  MAIN THERAPY
3. Administer medications, as ordered  TAKEN FOR LIFETIME
a. Aqueous vasopressin (SC)
b. Desmopression acetate (intranasal) – long-acting  DOC: longer half-life,
longer effect
a. Lypressin (intranasal) – short- acting  for emergency