Endocrine Disorders - H

( )
Wednesday, 23 February 2022 JWNLD_HKYE 1

Outlines of session
Objectives
Introduction
Anatomy and physiology of the endocrine system
Review of assessment of endocrine system
Common diagnostic investigations for endocrine disorders
Endocrine disorders(pituitary, thyroid, parathyroid, adrenal

gland disorders and disorder of islets of Langerhans(DM&its
complications)
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Objectives of the Session
At the end of this session, the students will able to:
Differentiate causative/risk/contributing factors of endocrine disorders.
Describe the clinical manifestations of patients with endocrine
disorders
Explain pathophysiologic process of endocrine disorders
Discuss diagnostic procedures/evaluations used in the diagnosis of
endocrine disorders
Explain the medical and/or surgical managements of patients with
endocrine disorders
Apply nursing process in managing nursing care of patients with
endocrine
Wednesday, 23disorders
February 2022 JWNLD_HKYE 3
Introduction
The body contains two kinds of glands: endocrine and
exocrine.
• Exocrine Glands: secrete their products through ducts into
body cavities or onto body surfaces.
• Exocrine glands include the sweat, sebaceous, and
mammary glands, salivary and the glands that secrete
digestive enzymes(pancreas).
Introduction Cont..
• Endocrine system is the second great controlling system of the
body.
• It works by means of chemical messengers called hormones.
• Unlike exocrine glands, endocrine glands releases their

hormones directly into the blood stream & carried to the tissue
that they affect, called Target tissues.
• It coordinate and direct the activities of the almost every cell,

organ, and function of the body, along with particularly nervous
system
Anatomy and physiology of
endocrine system
The endocrine glands include
The pituitary,
Thyroid,
Parathyroid,
Adrenal,
Pineal, and
Thymus glands .
Pancreas(islets of Langerhans) and
Gonads (ovaries and testes).JWNLD_HKYE
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Anatomy and physiology Cont..

Pituitary Gland
• Also known as hypophysis and called the master gland
• Approximately size of 1.2 to 1.5 cm across, & weighs 0.5gm
• Located on the ventral surface(base) of the brain, resting

with in the sella turcica of the sphenoid bone.
• Hangs from the inferior surface of hypothalamus by

infundibulum – stem-like stalk,
• It has two separate divisions called: Anterior and Posterior

pituitary gland
Infundibulum
•It is stem-like stalk
•It neural &vascular

connections between
pituitary and
hypothalamus,
•It plays a central role in

the integration of
neuroendocrine activity.
Pituitary Gland Cont..
A. Anterior pituitary (Adenohypophysis)
• It has no nerve connection to hypothalamus, but is

connected to it by complex of blood vessels called
hypothalamo-hypophyseal portal system
- w/c transports hypothalamic regulating hormones/factors

to the glandular cells of adenohypophysis to produce and
release its hormones.
- The Anterior lobe basically secrets six hormones

GH(Growth hormone) – stimulate growth of bones & muscles
TSH(Thyroid Stimulating Hormone) – stimulates thyroid gland
FSH(Follicle Stimulating Hormone) – Stimulate production of ova &

sperm
LH(Luteinizing Hormone) – Stimulates testosterone production in

males & estrogen in females, w/c is responsible for ovulation &
formation of corpus luteum.
ACTH (AdrenoCorticoTropic hormone) -Stimulate Adernal cortex
Prolactin(PRL): stimulates milk secretions in the breast of a lactating

mother
B. Posterior pituitary (Neurohypophysis)
• Release hormone made by the hypothalamus
• Nerve fibers arise from cell bodies in the hypothalamus &

end in the posterior lobe bundle – hypothalamohypophyseal
tract
• Serve as storage & release site for anti – diuretic hormone

(ADH) &
• Oxytocin (OT) in to blood stream, which is controlled by

nervous stimulation
Hormones
• ADH- prevent large
volume of urine
formation here by
helping the body
conserve water
• Oxitocin- Cause
milk ejection from
lactating mother
- Also
stimulate contraction
of uterine muscle
during child birth.

Thyroid Gland
• It is the largest endocrine gland
• blood supply by superior thyroid

artery & drained by superior
thyroid vein
• Situated at the base of the throat

just inferior to the Adam’s apple
• Has two lobes (right and left)

joined by the thyroid isthmus
Thyroid Gland Cont..
Hormones of thyroid gland
A. Thyroxine (T4) and Tri- iodothyronine(T3, )

Stimulate metabolism of all cells & cell growth (in
reproduction & nervous /mental development)
Control the rate at w/c glucose is burned or oxidized and

converted to body heat and chemical energy
Exert a wide spectrum of metabolic & physiologic actions

that affect virtually every tissue in the body.

Thyroid
Abnormal conditions
Gland Cont..
– Hyperthyroidism - ed TH
- Hypothyroidism -  ed TH
- Goiter – the condition in
w/c the thyroid gland is unable
to produce T4 & T3 due to low
level of TSH from pituitary to
stimulate T.G  the gland
becomes enlarged
B.Calcitonin –
enhance the
storage of calcium
in to bone cells by
then it decreases
blood calcium
level

Parathyroid Glands
• Usually four in number, are

embedded in the dorsal surface of the
thyroid gland
• Secret parathyroid, or
pararthormone (PTH) in response to
low plasma calcium
• Antagonist to calcitonin and acts to

maintain calcium homeostasis

Parathyroid Glands
PTH acts on bone & kidney
• Cause demineralization of bone to elevate
plasma calcium level.
• Cause absorption of calcium in kidney
• Cause phosphate to be secreted by urine
• Cause increased intestinal absorption of
calcium by stimulating the kidney to produce
active vitamin D, w/c increase calcium
Adrenal(Suprarenal) Glands
• Paired yellowish masses, situated at superior
poles of each kidney
• Each glands consisting of two distinct entities:

• Adrenal cortex – is an outer structure which is
composed of endocrine tissue.
• Structurally it is arranged into three zones;
• a thin outer zona glomerusa,
• a thick middle zona fasciculate, &
• an inner zona reticularis
Wednesday, 23 February 2022
bordering on the medulla.
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• Adrenal medulla – composed of neurosecretary tissue, that
secret the catecholamine hormones epinephrine(Adrenalin)
and norepinephrine(Noradrenalin).

Adrenal Glands Cont..
Adrenal cortex
• Produce three major groups of hormone collectively

referred to as corticosteroid
• These are
1. Mineralocorticoids,
2. Glucocorticoid
3. Sex hormone
1. Mineralocorticoids
Mainly Aldesterone secreted in zona glomerulosa & has the

following actions;
Regulate mineral (salt) content of the blood (Na+ & K+)
Regulate water & electrolyte imbalance
Increase Na+ reabsorption in the kidney
Increase water retention and promote the loss of potassium

& hydrogen ion
2. Glucocorticoid (cortisone and cortisol)
• w/c occurs in the zona fasciculate.
• Promote normal cell metabolism & help the body to resist
long term stressors
• It is said to be hyperglycemic hormone, b/c it promote the
break down of accumulated fat & proteins by body cells to
be converted to glucose
• Has anti inflammatory effect (decrease edema) & anti pain
effect by inhibiting pain causing molecules (PGs)
• Stimulates gastric acid & pepsin secretion & inhibit

protective mucus
Wednesday, 23 February 2022 secretion JWNLD_HKYE
in the stomach 25
3. Sex hormone
• Androgen (male)- secondary sex
characteristics
• Estrogen (female) -  deposition of protein
in muscle

Hormones of Adrenal medulla
• It releases two similar hormones collectively called
catecholamine (non-steroidals)
• Epinephrine / Adrenaline/, and
• Norepinephrine /Noradrenaline/ released by sympathetic neuron
• Both hormones bind to receptors of sympathetic effectors to

prolong and enhance the effects of sympathetic stimulation by the
ANS
When you feel threatened physically or emotionally SNS bring

about “fight or flight “ to cope the situation, it stimulate adrenal
medulla to23release
Wednesday, February 2022 hormone w/c prolong effect of SNS
JWNLD_HKYE 27
Functions of Catecholamine
• es Heart Rate & BP by constricting cutaneous & visceral

vasculatures
• es Blood glucose level by glycogenolysis in the liver &

muscle
• Relaxes respiratory smooth muscles
• Pupillary dilation(mydriasis)
• Inhibits GI motility
The Pancreas
• The pancreas is one of abdominal cavity organs, that lies behind the stomach
to the left lateral to duodenum
• It is composed of endocrine & exocrine tissues
- Exocrine tissue – secretes a serious containing fluid; digestive enzyme

(pancreatic juice), & releases through ducts w/c drain directly into part of small
intestine(duodenum)
- Endocrine tissue – contains four primary types of glands w/c secrets

hormones;
• Its endocrine functions is performed by the islets of langarhans(also called

Pancreatic islets),
• w/c are small, highly vascularized masses of scattered cells throughout the
pancreas.
The Pancreas Cont..
Four primary types of glands w/c secrets hormones;
• Alpha cells (A cells) – secrete glucagon -es blood glucose
• Beta cells (B cells) – secrete insulin - es blood glucose
• Delta cells (D cells) – secrete somatostatin – indirectly

inhibits digestion & absorption of nutrients
• Pancreatic poly peptide(PP) cells (F cells) – also influence

digestion & distribution of food molecule

Assessment and examination of
patient with endocrine disorder
Health history
• Fatigue and changes in usual energy level
• Heat and cold tolerance
• Changes in sexual function and secondary sex

characteristics
• Changes in mood, memory and ability to concentrate and

altered sleep pattern are some common changes in
endocrine disorders.
Assessment and examination Cont..
Past Medical History
• Hormone replacement therapy
• Surgeries, chemotherapy, radiation
• Family history: diabetes mellitus, diabetes insipidus, goiter,

obesity, Addison’s disease, infertility
• Sexual history: changes, characteristics, menstruation,

menopause

Physical Assessment
General appearance
• Vital signs, height, weight
Integumentary
• Skin color, temperature, texture, moisture
• Bruising, lesions, wound healing
• Hair and nail texture, hair growth

Face
• Shape, symmetry
• Eyes, visual acuity
• Wednesday,
Neck 23 February 2022 JWNLD_HKYE 34
Extremities
• Hand and feet size
• Trunk
• Muscle strength, deep tendon reflexes
• Sensation to hot and cold, vibration
• Extremity edema
Thorax
• Lung and heart sounds

Diagnostic Tests
The commonest diagnostic test for endocrine disorders
include:
GH: fasting, well rested, not physically stressed
T3/T4, TSH: no specific preparation
Serum calcium/phosphate: fasting may or may not be

required
Cortisol/aldosterone level
24 urine collection to measure the level of catacholamines

(epinephrine, norepinephrine, dopamine).
Disorders of Pituitary gland
Diabetes Insipidus
• It is a pathologic condition resulting from deficiency of ADH( normal serum
level 1 to 5 picogram/mL or 0.9 to 4.6 pmol/L), which result in excess
urine formation.
Causes
Brain( pituitary) tumors/trauma,
Infections of the CNS( Hypothalamus),
Surgical ablation or radiation(pituitary and Hypothalamus)
Failure of the renal tubules to respond to ADH(Nephrogenic) and
Drugs
- medications (lithium demeocycline

Disorders of PG Cont..
Pathophysiology
Insufficient ADH(<1pg/ml) secretion or failure of renal
tubules to respond to ADH
Kidneys Do Not Reabsorb Water
Diuresis 3-15 L per Day

Clinical manifestations
Dehydration Polyuria-
Hypovolemic Shock Polydipsia-
Decreased LOC Nocturia
Death Dilute Urine
Decreased skin turgor, Increase heart rate (Tachycardia)

Irritability
Dry mucous membrane

Diagnosis
Urine Specific Gravity <1.005
Plasma Osmolality Increased(>3oo mosmol/kg)
CT or MRI for Cause
ADH(<1 pg/ml)

Management
Hypotonic IV Fluids
Hypophysectomy If Tumor
IV or Sc Vasopressin
Thiazide Diuretics If Nephrogenic

T3 and T4
Thyroid is controlled by TSH
Cellular metabolism, brain development, normal growth,

affect every organ in the body
T3 is five times as potent as T4( T3=5x T4)
Is common among women

Hypothyroidism
 It is the condition in which the serum thyroid hormone level is below
normal value
Causes
 Hashimoto’s thyroiditis(autoimmune)
 Previously treated for hyperthyroidism
 Atrophy of gland with aging
 Medications like lithium, iodine compounds, anti thyroid meds
 Radiation treatments to head and neck
 Infiltrative diseases like amyloidosis, scleroderma
 Iodine deficiency
 Hypothalamic or2022pituitary abnormality,
Wednesday, 23 February JWNLD_HKYE lesion/congenital abnormality
43
Pathophysiology
Cause/risky factors
TH Deficiency
Metabolic Rate Reduced
Manifestations
Fatigue Dry Skin and Hair
Bradycardia
Weight Gain
Constipation
Heart Failure
Mental Dullness
Cold Intolerance
Hyper lipidemia
Hypoventilation Myxedema
Abnormal menstrual periods
and sub-fertility (in adult Hoarse voice, lethargy,
females)
Puffy face, pallor, slow pulse memory loss(dementia),
(usually <60 per minute)
Goitre may
Wednesday, be2022present
23 February
depressed reflexes,
JWNLD_HKYE 45
Diagnosis
T3 and T4 Low
TSH High in Primary
TSH Low in Secondary

oT3 -normal value- 100 to 200 nanograms per deciliter)and
oT4- normal value-5.0 to 12.0 μg/dL
oTSH- normal value- 0.4 to 4.0 mIU/L(average)

Management
Levothyroxine, oral, 25-200microgram daily (start with a
low dose and adjust according to TSH levels, maintain 0.1-
0.2 mg/d)

Hyperthyroidism
• It is the condition in which, there is excess thyroid hormone
in the blood.
Causes
Autoimmune (Grave’s Disease)
Multi nodular Goiter
Pituitary Tumor (Secondary)
Synthroid / levo thyroxine Overdose

Pathophysiology
Cause/risky factors
TH Excess
Metabolic Rate and beta receptors Increased
Systemic Hyperthyroidism Manifestations

Hypermetabolic State Tachycardia, Palpitations
Heat Intolerance Tremor

Increased Appetite Heart Failure
Weight Loss Warm Smooth Skin
Frequent Stools Exophthalmoses' (Grave’s Disease)
Nervousness & Pretibial myxedema
irritability
Menstrual irregularity and sub-
Excessive sweating fertility
Exophthalmoses

Diagnosis
Elevated T3 and T4
TSH Low in Primary
TSH High in Secondary
TRH(thyroid releasing hormone) Stimulation Test
CT/MRI If Tumor Suspected

Complications
Thyrotoxic Crisis (Thyroid Storm)

Tachycardia, Hypertension
Fever, Dehydration
Coma
Death

Management
Non pharmacologic
Avoid stimulants e.g. Caffeine
Partial thyroidectomy –
 Is indicated in large goiters, those who cannot take anti

thyroid meds, or who need rapid normalization
 Should only be done after a state of euthyroidism is

achieved with medical therapy
Radioiodine ablation
Pharmacological management
Carbimazole, P.O., Initial dose 15-60mg/day divided in 2-3 doses until

euthyroid state is achieved.
Maintenance dosage, 5-15mg/day or
Propylthiouracil (PTU), Initial: 300 to 400mg/day in 3 divided doses ;

until euthyroid state is achieved.
Maintenance dosage,100-150mg/day for 1-2years or until surgery for goiter
Adjunct treatment(beta-blocker)
Propranolol, 20-40mg, P.O, 8 hourly or
Atenolol 25-100mg, P.O., daily or
Metoprolol 25-100mg, P.O,daily

Goiter
 It is Swelling of the neck due to enlargement of the thyroid
gland.
 All grades of goiter are encountered from that are barely

visible to those producing disfigurement.
 Some are symmetrical and diffuse others are nodular.
 Some are accompanied by hyperthyroidism in which case

they are described as toxic, others are associated with
euthyroid called non-toxicJWNLD_HKYE
goiter 56
• Endemic (iodine deficient) goiter is the most common type,
encountered in geographic regions which natural supply of iodine is
deficient
• It is the so called simple or colloid goiter.
• It may also be caused by an intake of large quantities of goitrogenic

substances.
• Simple goiter represents a compensatory hypertrophy of the thyroid

glands, presumably caused by stimulation by the pituitary glands.
• Such goiters usually cause no symptoms except for the swelling in the
neck which may result is tracheal compression when excessive
Causes
Enlarged Thyroid Gland(Hyperplasia)
Elevated TSH
Low TH
Iodine Deficiency
Virus
Genetic

Signs and Symptoms
Enlarged Thyroid
Hypo or Hyperthyroid, or Euthyroid
Dysphagia
Difficulty Breathing

Diagnosis
• Thyroid Scan
• TSH, T3, and T4

Management
• Treat Cause
• Thyroidectomy
• Monitor Breathing (Stridor)
• Monitor Swallowing?
• Avoid Goitrogens
• Treat Hypo or Hyperthyroidism

Preoperative care
Pharmacotherapy:- Medications may prolong clotting (e.g.
Aspirin) are stopped several weeks before surgery to
minimize the risk of postoperative bleeding
Anxiety reduction
Nutritional support (high daily caloric intake)
Preoperative preparations night's rest preceding surgery,

diagnostic tests)
Pt education
Post operative care
• Patient is moved and turned carefully to support the head
and avoid tension on the sutures
• The most comfortable position is the semi fowler's position

with the head elevated and supported by pillows.
• Analgesics
• Patient may receive humidified O2 to facilitate breathing
• Surgical dressing is assessed for bleeding

• Monitoring the v/sign (pulse & B/P) for any indication of
internal bleeding.
• Be alert for complaints sensation of pressure or fullness at

the incision site.
• Difficulty in respiration occurs as a result of edema of the

glottis, hematoma formation or an injury to the recurrent
laryngeal nerve this complication requires than an air way
be inserted.
• A well balanced, high calorie diet is prescribed

Complications of thyroidectomy
Hemorrhage
Hematoma formation
Edema of glottis
Injury to the recurrent laryngeal nerve.

Thyroiditis
• Thyroiditis is an inflammation of the thyroid gland.
• There are three types:

Acute,
Subacute, and
Chronic (Hashimoto’s disease)

Acute Thyroiditis
• Is a rare disorder caused by infection of the thyroid gland by
bacteria, fungi, mycobacteria, or parasites, Staphylococcus aureus
and other bacteria
• It is manifested by
Anterior neck pain and swelling,
Fever, dysphagia, and dysphonia.
Pharyngitis or pharyngeal pain is often present.
• P/Examination may reveal:
Warmth, erythema
Wednesday, 23 February 2022 (redness),JWNLD_HKYE
and tenderness of the thyroid gland.
67
Acute Thyroiditis
Treatment
• Antimicrobial and Antipain drugs
• Fluid replacement.
• Surgical incision may be indicated, if an abscess is present.

Subacute Thyroiditis
• This type of thyroiditis are may be granulomatous thyroiditis
or lymphocytic thyroiditis.
Subacute granulomatous thyroiditis
Is predominantly affects women between the ages of 40 and 50 years
Is usually associated with a viral respiratory infection
Has a summer peak incidence that coincides with coxsackievirus

groups A and B and echovirus infections.
Manifestations include a painful swelling in the anterior neck that lasts

1 to 2 months, fever, chills, dysphagia, and muscle and joint pain. Pain
can radiate to the ears and the jaw.
Subacute Thyroiditis Cont..
Manifestations of hyperthyroidism like Irritability, nervousness,
insomnia, and weight loss are common, but the some patients
may have signs of hypothyroidism rather than hyperthyroidism.
Thyroid function can remain normal, although hyperthyroidism
or hypothyroidism may develop.
Treatment includes NSAID, propranolol and corticosteroids
Subacute lymphocytic thyroiditis
Occurs in the postpartum period and is thought to be an
autoimmune process.
Symptoms of hyperthyroidism or hypothyroidism may present.
Treatment is directed
Wednesday, 23 February 2022 at symptoms
JWNLD_HKYE 70
Chronic Thyroiditis
• Are also known as Hashimoto’s disease, or chronic lymphocytic
thyroiditis
• Occurs most frequently in women between the ages of 30 and 50
years
• Unlike acute thyroiditis, the chronic forms usually are not
accompanied by pain, pressure symptoms, or fever
• Thyroid activity usually is normal or low rather than increased.
• Cell-mediated immunity and a genetic predisposition is
associated with pathogenesis of chronic thyroiditis.
• Diagnosis is based on the histologic appearance of the inflamed
thyroid gland.
Chronic Thyroiditis
• Patients with Hashimoto’s disease are 60-80 times more
likely to develop thyroid lymphoma than general
population.
• The treatment of chronic thyroiditis include thyroid

hormone therapy for hypothyroidism, and surgery may be
indicated if pressure symptoms persist.

Thyroid Cancer
Assignment on types of Tca
Papillary carcinoma
Follicular carcinoma
Medullary carcinoma
Anaplastic carcinoma
Thyroid lymphoma
• N.B for each type of thyroid carcinoma, you should
include: description, risk factor/etiology, pathophysiology,
classifications, clinical manifestation, assessment and
diagnosis, management (medical, surgical and/or nursing)
and prevention, complications)

The common disorders of parathyroid gland are
include:
Hypoparathyroidism
Hyperparathyroidism
o Normal value-10-65pg/ml

Hyperparathyroidism
• It is a condition in which, there is overproduction of
parathyroid hormone by the parathyroid glands.
• It is characterized by bone decalcification(decreased
osteoblastic and increased osteoclastic activity), the
development of renal calculi (kidney stones) containing
calcium, hypercalcemia and hypophosphatemia
• The disorder affects females 2-4 times than males
• It affects the population age group that fall between 60-70

years
• It could be classified as primary and secondary

hyperparathyroidism
Hyperparathyroidism cont.…
Causes
Parathyroid congenital Hyperplasia
Benign Parathyroid Tumor

Parathyroid carcinoma
 Neck trauma or radiation
Vitamin D deficiency (normal V- 14-60 ng/mL )
Chronic kidney disease with hypocalcemia
Parathyroid hormone–secreting carcinomas of the
lung, kidney, or GI tract
Heredity
Signs and Symptoms
Fatigue Joint Pain
Depression Pathologic Fractures
Confusion Dysrhythmias
Nausea and Vomiting Coma
Kidney Stones Cardiac Arrest

Diagnosis
• Serum Calcium Elevated (normal V-9.0-10.5 mg/dl)
• Phosphate Decreased (normal V-3.0-4.5 mg/dl)
• PTH Elevated
• X-Rays for Bone Density
• Ultrasound, MRI and other imaging and pathologic

examinations(biopsy) may be used

Management of hyperparathyroidism
• Recommended treatment includes:
Parathyroidectomy-for primary hyperparathyroidism
Hydration therapy necessary to prevent renal calculi
Administering loop diuretics like furosemide (Lasix)
Administering exogenous calcitonin
Increase mobility to promote bone retention of calcium
Avoid restricted or excess calcium in the diet
Advising the patient to take fluids, prune juice and stool
softeners to prevent constipation
Hypoparathyroidism
• Is the disorder in which, there is secretion of low
parathyroid hormone by the parathyroid glands.
• It is characterized by:
Hypocalcaemia
Hyperphosphatemia
Decreased intestinal absorption of dietary calcium
Decreased resorption of calcium from bone and through the

renal tubules.
Hypoparathyroidism Cont..
Causes
Heredity
Accidental removal of Parathyroid glands during

thyroidectomy
Parathyroidectomy
Congenital dysgenesis
Idiopathic (autoimmune) hypoparathyroidism
Hypomagnesemia
Interruption of the blood supply to Parathyroid glands
Atrophy of the parathyroid glands

Clinical Manifestations
• Manifestations of hypoparathyroidism are associated with
hypocalcaemia, which cause irritability of neuromuscular
system that contribute to chief Sign hypoparathyroidism
called tetany
• In mild to moderate hypocalcaemia, the patient may have

the following latent tetany manifestations: numbness,
tingling of of fingers and perioral area, and cramps in the
extremities, and stiffness in the hands and feet.
• In sever hypocalcaemia, the patient may have the following
overt tetany manifestations: bronchospasm, laryngeal
spasm, carpopedal spasm, dysphagia, photophobia, cardiac
dysrhythmias, and seizures.
• Other symptoms include anxiety, irritability, depression,

delirium, ECG changes and hypotension

Diagnosis
Serum Mg, Calcium & PTH Low, Phosphate increased,
X-Rays for Bone Density
Ultrasound, MRI and other imaging and pathologic
examinations(biopsy) may be used
P/E
Positive Chvostek’s Sign- a sharp tapping over the facial nerve just in
front of the parotid gland and anterior to the ear causes spasm or
twitching of the mouth, nose, and eye.
Positive Trousseau’s Sign- carpopedal spasm is induced by occluding
the blood flow to the arm for 3 minutes with a blood pressure cuff
Management
The management of hypoparathyroidism includes:
Administration of IV calcium gluconate
Administration sedative agents (phenobarbital) particularly,
if the patient’s condition is not improved with IV calcium
gluconate
IV parathyroidhormone may be used for extreme situations.
However, it’s use is limited due to the probability of allergic
reactions.
Long Term
• Oral Calcium gluconate
• Oral Vitamin D
• Thiazide Diuretics-
Monitoring serum calcium level
Adminstration of Aluminum hydroxide gel or aluminum
carbonate after meal to bind phosphate and promote it’s
excretion through GIT.
Tracheostomy or mechanical ventilation and bronchodilators
may be helpful in treating patient with respiratory distress.
Advising the patient to take diet that high in Ca and low in
Phosphorus
Keeping the patient in environment that is free of noisy, bright
lights, or sudden movement.
Cushing syndrome
Addison’s diseases
Pheochromocytoma
Primary aldestronism
Adrenal gland hormones normal values
oCortisol- 6 AM to 8 AM: 5-23 mcg/dL or 138-635 SI units
(nmol/L) and 4 PM to 6 PM: 3-13 mcg/dL or 83-359 SI units
(nmol/L)
oAldosterone- 2-9 ng/dl with supine position and normal Na
level
Cushing syndrome
• Is a disorder resulting from excessive adrenocortical activity
(excessive adrenal cortex hormones).
Causes
Excessive use of corticosteroid medications
Hyperplasia of the adrenal cortex
Tumor of pituitary gland that producing ACTH
Ectopic production of ACTH by malignancies e.g. broncho

genic carcinoma, thyroid carcinoma
Signs and symptoms

Signs and symptoms cont..

Signs and symptoms cont..

Assessment and Diagnostic Findings
• An overnight dexamethasone suppression test is the most widely used
diagnosis
 Dexamethasone 1g administered orally at 11pm and cortisol level

checked at 8am. Suppression of cortisol to less than 5 mg/dL indicates
that the hypothalamic–pituitary–adrenal axis is functioning properly.
• Measurement of plasma ACTH (normal V-10-60 pg/ml) and cortisol
level to rule out whether the cause is from hypothalamus or pituitary or
adrenal gland
• MRI, CT and also help to detect tumors of adrenal or pituitary
• Increased sodium(normal V-136-145mEq/L) & blood glucose level
• Decreased lymphocyte count, serum calcium & potassium level
(normal V-3.5-5 mEq/L)
Medical management
• Treat the underlying causes:
Pituitary tumor-hypophysectomy or radiation
Adrenal hypertrophy or tumor - Adrenalectomy
• Symptom Control
• Low Sodium, High Potassium Diet

• For Adrenalectomy
Preoperative Care
• Monitor Electrolytes, Glucose
• Preoperative Teaching
Postoperative Care
• Monitor for Adrenal Crisis
• Lifelong Hormone Replacement
Addison’s diseases
• Is the a disorder in which, there is inadequate adrenocortical
hormone to meet the patient’s need for cortical hormones.
Causes
• Autoimmune or idiopathic atrophy of the adrenal glands
• Surgical removal of both adrenal glands and infection of the

adrenal glands
• Tuberculosis and histoplasmosis
• Inadequate secretion of ACTH from the pituitary gland
• Sudden cessation of exogenous adrenocortical hormonal therapy

Signs and symptoms
• The common features of hypofunction of adrenal cortex
includes:-

Diagnosis
• Skull x-rays, CT, MRI, and arteriography may help
determine the cause of pituitary problems
• Serum and Urine Cortisol Level
• Blood Glucose
• Electrolytes
• BUN/HCT
• ACTH Stimulation Test

Medical Management
Hormone Replacement
• Start rapid infusion of normal saline or dextrose 5% in normal
saline.
• Initial dose of hydrocortisone sodium succinate (Solu-Cortef) is

100 to 300 mg or dexamethasone 4 to 12 mg as an IV bolus.
• Infuse additional 100 mg of hydrocortisone sodium succinate by

continuous IV drip over the next 8 hours.
• Give hydrocortisone 50 mg IM concomitantly every 12 hours.
• Initiate an H2 histamine blocker (e.g., ranitidine) IV for ulcer
prevention.
Medical Management cont..
Hyperkalemia Management
• Administer insulin (20 to 50 units) with dextrose (20 to 50

mg) in normal saline to shift potassium into cells.
• Give loop or thiazide diuretics.
• Avoid potassium-sparing diuretics, as prescribed.
• Initiate potassium restriction.
• Monitor intake and output.
• Monitor heart rate, rhythm, and ECG

Medical Management cont..
Hypoglycemia Management
• Administer IV glucose, as prescribed.
• Administer glucagon, as needed and prescribed.
• Maintain IV access.
• Monitor blood glucose level hourly.

Nursing interventions
Assessing the Patient
Monitoring and Managing Addisonian Crisis
Restoring Fluid Balance
Teaching Patients Self-Care

Primary aldestronism
• It is a disorder in which results from excessive secretion of aldosterone
with mineralocorticoid from one or both adrenal glands
• Increased aldosterone levels affect the kidney tubules and cause
sodium retention with potassium and hydrogen ion excretion.
• Hypernatremia, hypokalemia, and metabolic alkalosis result. Sodium
retention increases blood volume, which raises blood pressure but
usually does not cause peripheral edema.
• The elevated blood pressure may cause strokes, heart attacks, and
kidney damage.
Causes
Benign adrenal adenoma
High levels of angiotensin II that are stimulated by high plasma renin

levels caused by kidney hypoxemia and the use of thiazide diuretics
Signs and Symptoms
Hypernatremia (Hypertension(elevated BP), polyuria,
nocturia, polydipsia, fatigue, headache)
Hypokalemia (Muscle weakness, cramping, and fatigue)
Hypocalcaemia (tetany and paresthesias,Trousseau’s and

Chvostek’s signs )
Metabolic alkalosis(↑PH)
Low urine specific gravity (normal V- 1.005 to 1.030)

Diagnosis
X-rays , and imaging with CT or MRI
Serum electrolyte test(K, Na, and Ca)
Serum hormone tests (renin and aldestrone)

Management
Surgical removal of one or both adrenal gland that have
tumor is the most common treatment for primary
aldestronism
Monitoring for manifestations of hyponatremia post-op
Administration of potassium-sparing diuretic

(spironolactone)
Diet high in potassium
Glucocorticoid replacement

Pheochromocytoma
• Is a benign tumor that originates mainly from the chromaffin cells
of the adrenal medulla. Secretes extra-Epinephrine and
Norepinephrine
• In 10% of patients, the tumor arises from chromaffin cells found

in or near the aorta, ovaries, spleen, or other organs
• It can occur in any age, but usually between 40-50 years old
• Can be familial and affects both sexes equally

• 10% are malignant
• May be associated with thyroid carcinoma or parathyroid
hyperplasia or tumor
• Cause is 23unknown
Wednesday, February 2022 JWNLD_HKYE 105
Signs and Symptoms
Fight or Flight(ANS-
• Hyperglycemia
sympathetic activity)
• Headache
• Hypertension (most
common ) • Vision Changes
• Tachycardia • Risk for Stroke
• Palpitations • Risk for Organ Damage

• Tremor • BPs exceeding 250/150
• Diaphoresis have occurred
• Wednesday,
Anxiety 23 February 2022 JWNLD_HKYE 106
Assessment and Diagnostic Findings
Signs of pheochromocytoma is associated with the 5 H’s—
hypertension, headache, hyperhidrosis/ excessive sweating,
hypermetabolism and hyperglycemia
Clonidine suppression test—in normal individual, would block
catecholamine release
Serum epinephrine (normal v-100 pg/mL) and norepinephrine
(normal v-100-550 pg/mL) levels will be elevated
Imaging studies such as CT, MRI, and ultrasonography to
localize tumor
Collecting urine specimen for 24 hrs (urine test for free
catecholamine's)
Management
Management of pheochromocytoma are more of symptomatic, which
includes:
Hypertension
Beta Blockers (Propranolol [Inderal])
Alpha Blockers (Phenoxybenzamine [Dibenzyline])
Calcium channel blockers
Tumor
Adrenalectomy
Steroid therapy if adrenalectomy performed
Monitoring the patient for hypotension and hypoglycemia
postoperatively
BedWednesday,
rest 23 February 2022 JWNLD_HKYE 108
normal V-50 to 100 pg/mL
normal fating insulin level- 2 to 20 mIU/mL

• Is defines as a group of metabolic diseases
characterized by elevated levels of glucose in the
blood (hyperglycemia) resulting from defects in:
 Insulin secretion
 Insulin action or both.
• Is a disorder characterized by metabolic abnormality in

carbohydrate, protein and fat
• The exact cause of DM is unknown

Predisposing factors for diabetic mellitus
Family hx of diabetic mellitus
Obesity (i.e.>over desired body out or BMI> 27kg/m2
Race /ethnicity and age > 45 years
Previously identified impaired fasting glucose or impaired

glucose tolerance
Hypertension (>140/90 MM Hg)
HDL cholesterol level (<35 mg/dl) or (0.90 mmol/L)
Hx Gestational diabetes/delivery of babies > 4 kg

The major classification includes:-
• Type 1 diabetes (insulin dependent/juvenile)
• Type 2 diabetes (non-insulin dependent/adult onset)
• GDM(Gestational DM)-pregnant mother

Type-1 diabetes
Is characterized by destruction of the pancreatic
Beta -cells.
 Causes-unknown
 Contributing factors:-
• Genetic related immunologic (associated to autoimmune
response)
• Environmental (eg.viral or toxin)

Pathophysiology
• If the concentration of glucose in the blood exceeds the renal
threshold for glucose(180-200mg/dl), the kidneys may not
reabsorb all of the filtered glucose glucose then
appears in the urine (glucosuria)
• Excess glucose is excreted in the urine, it is accompanied by

excess loss of fluids and electrolytes
Osmotic dieresis(polyuria)
Pathophysiology cont..
• This can further lead to excessive hungry & thirst
(polyphagia &polydipsia) and glycogenolysis,
glueconeogenesis and breakdown of fat substance due to
insulin deficiency
• Hyperglycemia and increased production of free fat acids

like ketone bodies appearance of sever
manifestations hyperglycemia & ketone bodies

Type II DM
• The main problems in this type of DM are:
- Insulin resistance from peripheral body tissue(receptors)
- Impaired insulin secretion (less than normal level)
• Insulin resistance: -causes insulin, less effective at

stimulating glucose uptake by the tissue & regulating
glucose by the liver.
• It is common in obese people older than 30 year (b/s insulin

resistance is associated with obesity).
No Feature Type 1 Type 2
.
1 Synonyms *IDDM(insulin,dependent), * NIDDM, adult or maturity onset diabetes,
juvenile diabetes, labile, brittle mild diabetes
diabetes
2 Age at onset * Usually before age 30 but may * Usually after age 30 yrs but can occur in
occur at any age children
3 Incidence * 5-10% or ~ 10% * 90-95% or ~ 90%
4 Type of onset * Sudden with rapid onset of * Insidious, may be a symptomatic, body
hyperglycemia adapts to slow onset of hyperglycemia
5 Endogenous insulin * Little or none Below normal or above normal

production
6 Body weight at onset thin Obese
7 Ketosis * Prone to ketosis * Resistant to ketosis

8 Manifestations * Polyuria, polydipsia, polyphagia, Frequently,none,mild manifestations of
fatigue hyperglycemia
9 Dietary management * Essential * Essential
10 Exercise management * Essential * Essential
11 Exogenous insulin * Dependent on insulin for survival 20% - 30% of clients may require insulin
administration
12 Oral hypoglycemic * Not effective * Effective

13 Teaching needs * At diagnosis & ongoing * At diagnosis & ongoing
Clinical Manifestation
Fatigue & weakness Numbness tingling in
Irritability hands or feet
Polyuria Blurred vision (if
Polydipsia glucose level is very high
Polyphagia Skin wound or lesions
Hyperglycemia Sudden wt loss &

N/vomiting or abdominal
Glucose uria
pains if DKA has
Ketoacidosis (type I
developed ( type I DM)
DM)
Diagnostic evaluation
On at least two occasions (WHO diagnosis
criteria)
Random plasma glucose > 200mg/dl
Fasting plasma glucose > 126 mg/ dl
2-hour sample during 75gm OGTT (oral
glucose tolerance test) > 200mg /dl
Haemoglobin A1C >6.5%

Management
There are five components for the MX for diabetes
Diet
Exercise
Monitoring
Mediation (as needed)
Education

Management cont..
Diet/nutritional therapy
• Avoid refined sugars as in soft drinks, or adding to their teas/other drinks.
• Be encouraged to have complex carbohydrates
• Low in animal fat and alcohol
• Increase in the amount of fibre e.g. vegetables, fruits and cereals
• If patient can able to adjust his/her daily nutritional requirement, it is

recommended to take:
A diet containing 45% to 65% of calories from carbohydrate,
with a minimum intake of 130 g carbohydrate/day.
15% to 20% of total daily calories from protein and
The rest % from fat with limited saturated fat and dietary cholesterol.
Management cont..
Exercise
• Lowers blood glucose levels by increasing the uptake of glucose by
body muscles and by improving insulin utilization.
• It also reduces the risk of cardiovascular complications & promote
weight lose by improving circulation and muscle tone.
• Recommended the patient to have regular physical activity for at least
30 minutes at least 5 days a week or at least 150 min/week.
• Encourage resistance training/ vigorous exercise three times per week

Management cont..
General Precautions for Exercise
• Use proper footwear and, if appropriate, other protective

equipment.
• Avoid exercise in extreme heat or cold.
• Inspect feet daily after exercise
• Patients blood glucose level(before, during & after exercise) .
• Avoid exercise during periods of poor metabolic control(blood

glucose levels exceeding 250 mg/dL (14 mmol/L, below 80-
100mg/dl(5.6mmol/L)
and ptJWNLD_HKYE
have ketones). 123
Management cont..
• Warn the patient not to exercise within 1 hour of insulin injection
or near the time of peak insulin action.
• Teach patients how to prevent hypoglycemia during exercise
• Have a carbohydrate snack before exercising if 1 hour has passed
since the last meal or if the planned exercise is high intensity.
• Carry a simple sugar to eat during exercise if symptoms of
hypoglycemia occur.
• Ensure that identification information about diabetes is carried
during exercise.
• Remind the patient to check blood glucose levels more frequently
on days in which exercise is performed and that extra
carbohydrate and less insulin may be needed during the 24-hour
period after
Wednesday, extensive
23 February 2022 exercise.
JWNLD_HKYE 124
Management cont..
Self-monitoring of blood glucose
• Blood glucose monitoring is a cornerstone of diabetes
management
• It is useful for all diabetic patients, but is a key component of
patients who are on insulin therapy(2-4 times per day,
usually before the meal and at bed time)
• It involves pricking of fingertip and applying the blood on
strip of meter machine and allowing it to stay for 5 to 30
seconds.

Management cont..
Self-monitoring of blood glucose (SMBG) is recommended
for:
• Unstable diabetes (severe swings from very high to very low

blood glucose levels within a 24-hour day)
• A tendency to develop severe ketosis or hypoglycemia
• Hypoglycemia without warning symptoms

Management cont..
Mediation
I. Exogenous Insulin therapy
• Insulin lower blood glucose after meal by facilitating the uptake
of utilized glucose by muscles, fat & liver cells.
• In type I diabetes, the body loses the ability to produce insulin.

Thus, exogenous insulin must be administered indefinitely .
• In type II diabetes insulin may be necessary on a long term basic

to control glucose levels if diet, exercise and oral agents, have
failed or during illness, infection, pregnancy, surgery, or some
other stressful event.
Management cont..
Insulin preparations
• There are a number of insulin preparations that vary
according to :
Time course of action(onset, peak, and duration of action)
Species (source), and
Manufacturer

Based on time course of action

Management cont..
Insulin Regimens
• Vary from one to four injections per day.
• Usually there is a combination of a short acting insulin and a longer-acting insulin.
• There are two general approaches to insulin therapy:
Conventional approaches(CA):
• To simplify the insulin regimen as much as possible, with the aim of
avoiding the acute complications of diabetes (hypoglycemia and symptomatic
hyperglycemia).
• One or two injections of a mixture of short acting(R) and intermediate-acting

(NPH)insulins per day
• The simplified regimen would be appropriate for the: terminally ill, the frail
elderly with limited self-care abilities, or patients who are completely
unwilling
Wednesday,or unable
23 February 2022to engage in the self-management activities
JWNLD_HKYE 130
Management cont..
Intensive approaches
• Is a complex insulin regimens require a strong level of

commitment, intensive education, and close followup by the
health care team
• To achieve as much control over blood glucose levels as is safe

and practical.
• This regimen allows the patient more flexibility to change the

insulin doses from day to day in accordance with eating and
activity patterns.
• Three or 23four
Wednesday, injections
February 2022 of insulin per day
JWNLD_HKYE 131
Management cont..
Methods of Insulin Delivery
• Includes: traditional subcutaneous injections, insulin pens, jet injectors,
and insulin pumps
Teaching Patients to Self-Administer Insulin
 Insulin injections are administered in to the sc tissue with the use of

special insulin syringes.
Before use of insulin, the patient have to store insulin in refrigerator

and avoid extreme temperature or at room temperature
Wash hand & mix insulin or shake the insulin vial if it looks cloudy
Select appropriate syringe(U-100 or U-5oo) based on ordered insulin

unitWednesday, 23 February 2022 JWNLD_HKYE 132
Management cont..
Mix insulin in one syringe if needed or if the mixed
preparation is not present (e.g, R &NPH)
Withdraw correct amount of insulin from its vial and select

appropriate site for injection from the four common
sites(abdomen-posterior surface arm/deltoid-thigh-
hip/buttock)
Swab the area with alcohol socked cotton/ gauze and follow
the following steps.

Management cont..
Problems with insulin
The common problems with insulin therapy includes:
Local allergic Rxns (Redness, swelling, tenderness)
Systemic allergic Rxns (rare)-urticaria(hives) , edema&

anaphylaxis
Insulin Lipodystrophy (disturbance of localized fat

metabolism)
Lipo atrophy:- (loss of sc fat appears as a slight dimpling)
Lipo hypertrophy:- dev't of fibro fatty masses at the injection site
Insulin
Wednesday,resistance
23 February 2022 (e.g. obesity)
JWNLD_HKYE 136
Management cont..
II .Oral anti diabetic Agents
• Are used to treat type II diabetic patients who can not be treated by diet
and exercise alone
• They can not be used during pregnancy.
• The most common diabetic agents that are available in our country are:
Sulfonylurea: exert their 10 function by directly stimulating the
pancreases to secrete insulin also they improve insulin action at the
cellular lever.
( e. g. Dymelor, Diabinese, Tolazamide, Glibenclamide )
Biguanides:- Facilitate insulin action on the peripheral receptor sites.
There fore it can be used only in the presence of insulin( e.g. Metforming)
Management cont..
Patient education
Diabetic patient education should address the following areas:
Basic definition of diabetes (having a high blood glucose level)
Normal blood glucose ranges and target blood glucose levels
Effect of insulin and exercise (decrease glucose)
Effect of food and stress, including illness and infections

(increase glucose)
Basic treatment approaches

Management cont..
Treatment modalities
a. Administration of insulin and oral antidiabetic medications
b. Meal planning (food groups, timing of meals)
c. Monitoring of blood glucose and urine ketones
Recognition, treatment, and prevention of acute and chronic
complications
a. Hypoglycemia
b. Hyperglycemia
Pragmatic information
a. Where to buy and store insulin, syringes, and glucose
monitoring supplies
b. When and
Wednesday, how
23 February 2022 to contact JWNLD_HKYE
the physician 139
Complication of DM
Diabetic complications are classified as:
Acute complications
A. Hypoglycemia
B. Diabetic ketoacidosis(DKA)
C. Hyperglycaemic hyperosmolar non ketotic
syndrome(HHNS)
Chronic complications
i. Macro vascular
ii. Microvascular

Acute complications
A. Hypoglycemia
• Are also known as insulin reaction
• Occurs when the blood glucose falls to less than 50 to 60 mg/dL (2.7 to 3.3
mmol/L)
Cause
Too much insulin or oral hypoglycemic agents,
Too little food, or excessive physical activity.
Delayed or omitted meals.
Wrong type of insulin injected at the wrong time
Decrease liver glucose production after alcohol ingestion
Decreased insulin clearance from progressive

Wednesday, 23 February 2022 JWNLD_HKYE
kidney failure 141
Acute complications cont..


Assessment and Diagnosis
Hypoglycemic signs & symptoms
RBG of less than 70 mg/dl
Immediate recovery after administration of glucose
Management
Immediate treatment recommendation for hypoglycemia is
administration/giving 15 g of a fast acting carbohydrate or
6 to 10 hard candies or ½ cup of fruit juice or soft drink
2 to 3 teaspoons of sugar or honey
The blood glucose level should be retested in 15 minutes and retreated
if it is less than 70 to 75 mg/dL (3.8 to 4 mmol/L) or If the symptoms
persist for longer than 10 to 15 minutes after initial treatment.
For unconscious patients:
Glucagon 1g IM or SC followed by oral carbohydrate diet

after patient become conscious or
25-50 ml of 50% dextrose in water (D50W) may be

administered IV
Teach your patient on preventive strategies

B. Diabetic ketoacidosis(DKA)
• It is an acute complication of diabetes that are characterized by
uncontrolled hyperglycemia, metabolic acidosis, and dehydration and
electrolyte loss
• Occurs most often in patients with type 1 DM, but may occur with
type 2 in sever stressful condition.
Causes
An absence or markedly inadequate amount of insulin.
Stress, infection, trauma, surgery(↑BG) by increasing counter
regulatory hormone release( glucagon, cortisol, GH & catecholamine
hormones )
Undiagnosed and
Wednesday, 23 February 2022 untreated diabetes
JWNLD_HKYE 146

Clinical Manifestations
Excessive urination Dehydration with dry skin,
Excessive thirst and drinking reduced skin turgor or sunken
of water eyes
Nausea, vomiting , blurred Deep and fast breathing
vision (Kussmaul respirations)
Abdominal pain, anorexia Low blood pressure
Alteration in sensorium or Fast and weak pulse
collapse 'Fruity' breath (smell of acetone)
Symptoms of infection or Confusion, stupor or
other underlying condition unconsciousness
Evidence of infection(illness),
recent surgery, stroke etc 148
JWNLD_HKYE
Diagnosis
 signs and symptom
Random blood glucose (usually >300mg/dl)

Urine glucose (usually >3+)
Urine ketones (usually >2+)
BUN and Creatinine ↑
Electrolytes ↓ or normal
Low serum bicarbonate (0 to 15 mEq/L) and low pH (6.8 to 7.3) values.
A low partial pressure of carbon dioxide (PCO2; 10 to 30 mm Hg) reflects
respiratory compensation (Kussmaul respirations) for the metabolic
acidosis.
Management
None pharmacological
• Admit to intensive care unit or a ward patient can be very closely

observed
• Closely monitor fluid input and urine output
Pharmacological
Replace fluids:
• 2–3L of 0.9% NS in 1–3 hrs; the reduce to 250–500 mL/h;
change to 5% glucose(D5W) when plasma glucose reaches 250
mg/dl in DKA and 300mg/dl in HHS.
• HHS requires more fluid. Assess hydration status, BP and urine
output frequently
Administer short-acting insulin: to reverse acidosis
Regular Insulin 10units IV and 10 units IM, stat, then 0.1 units/kg per
hour by continuous IV infusion OR 5 units, I.V boluses every hour.
If serum glucose does not fall by 50 to 70 mg/dL from the initial value
in the 2-3 hours, the insulin infusion rate should be doubled every hour
until a steady decline in serum glucose is achieved
Electrolyte replacement (Potassium)
All patients with DKA have potassium depletion irrespective of the
serum K+ level:-
If the initial serum K+ is <3.3 mmol/L, do not administer insulin until
the K+ is corrected.
If the initial serum K + is >5.3 mmol/L, do not supplement K+ until the
level reaches < 5.3.
If K+ determination is not possible delay intiation of K+ replacement
until there is a reasonable urine put(>50 ml/hr)
The serum potassium should be maintained between 4.0 and 5.0 meq/l
• Add 40–60 meq/l of IV fluid when serum K+ < 3.7 meq/L
• Add 20-40meq/l of IV fluid when serum K+ < 3.8-5.2 meq/l
• Treat underlying causes
• Monitor Blood glucose every 1–2hrs, Urine ketones every
4hr,electrolytes (especially K+) every 6 h for first 24 h.
• Continue the above treatment until the patient is stable,

ketone free.

C. Hyperglycaemic hyperosmolar syndrome(HHS/HHNS)
• Is a serious condition in which hyperglycemia and hyperosmolarity are
predominate.
• HHNS occurs most often in older people (50 to 70 years of age) who
have no known history of diabetes or who have type 2 diabetes.
Causes
Similar to DKA, which include
• an acute illness (eg, pneumonia, cerebrovascular accident [CVA]),
• Medications that exacerbate hyperglycemia (eg, thiazides),
• Treatments such as dialysis

Comparison between DKA & HHNS
• Both HHS and diabetic ketoacidosis (DKA) are caused by
hyperglycemia and dehydration.
• In HHS ketosis and acidosis generally do not occur, partly
because of differences in insulin levels
• In DKA no insulin is present, and this promotes the breakdown of
stored glucose, protein, and fat, which leads to the production of
ketone bodies and ketoacidosis.
• However, in HHNS the insulin level is too low to prevent
hyperglycemia (and subsequent osmotic diuresis), but it is high
enough to prevent fat breakdown.
• HHNS do not have the ketosis related gastrointestinal symptoms
that lead them to seek medical attention.
• So that, due to delays in therapy, hyperglycemia, dehydration, and
hyperosmolarity
Wednesday, 23 February 2022may be more severe in HHNS.
JWNLD_HKYE 154
Comparison of HHS & DKA

Pathophysiology

Chronic complications
• The chronic complications of DM are resulted from thickening of
basement membranes of vessels and chronic glucose irritation of
vessels associated chronic hyperglycemia
I. Macro vascular complications
• Result from changes in the medium to large blood vessels.
• The three main types of macrovascular complications that occur
frequently in the diabetic population includes:
Coronary artery disease(CAD)- account for 50% to 60% of all
deaths among patients with diabetes.
Cerebrovascular disease(CVD), and
Peripheral vascular disease(PVD)
Prevention and treatment -diet &exercise, BG control, rx HTN,
rx hyperlipidaemia,
Wednesday, 23 February 2022 wt reduction, smoke cessation
JWNLD_HKYE 157
Chronic complications
II. Microvascular complications –
cont..
• Results from thickening of capillary basement membrane(small
vessels). It includes:
Nephropathy(kidney dysfunction)- a long-term complication of
diabetes in which the kidney cells are damaged; characterized by
microalbuminuria in early stages and progressing to end-stage
renal disease
Neuropathy(nerve cell dysfunction)- a long-term complication
of diabetes resulting from damage to the nerve cell
Retinopathy(visual impairment)- a long-term complication of
diabetes in which the microvascular system of the eye is damaged
• Occur in almost all type 1 DM patients & more than 60% of type
2 after 20 years
Foot ulcer -About 50-75% of lower extremity amputation are
performed on people
Wednesday, 23 February 2022 with diabetes
JWNLD_HKYE 158
Chronic complications cont..
Foot ulcer

Chronic complications cont..
Foot care
1.Properly bathing, drying and lubricating feet
2.Apply lotion to entire foot except between toes
3.Inspect feet (using a mirror if necessary to see bottom of
foot), including inspection of cracks between toes.
4. Instruct patients to:
• Wear shoes at all times
• Avoiding using of heating a feet
• Wearing cotton socks
• Avoiding constrictive shoes
• Interior surfaces of shoes should be inspected for any rough sport
or foreign objects.

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Endocrine Disorders - H

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Wednesday, 23 February 2022 JWNLD_HKYE 1

Anatomy and physiology of the endocrine system

Review of assessment of endocrine system

Common diagnostic investigations for endocrine disorders

Endocrine disorders(pituitary, thyroid, parathyroid, adrenal

• Exocrine Glands: secrete their products through ducts into

body cavities or onto body surfaces.

• Exocrine glands include the sweat, sebaceous, and

mammary glands, salivary and the glands that secrete

• It works by means of chemical messengers called hormones.

• Unlike exocrine glands, endocrine glands releases their

• It coordinate and direct the activities of the almost every cell,

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• Approximately size of 1.2 to 1.5 cm across, & weighs 0.5gm

• Located on the ventral surface(base) of the brain, resting

• Hangs from the inferior surface of hypothalamus by

• It has two separate divisions called: Anterior and Posterior

•It neural &vascular

•It plays a central role in

• It has no nerve connection to hypothalamus, but is

- w/c transports hypothalamic regulating hormones/factors

- The Anterior lobe basically secrets six hormones

TSH(Thyroid Stimulating Hormone) – stimulates thyroid gland

FSH(Follicle Stimulating Hormone) – Stimulate production of ova &

LH(Luteinizing Hormone) – Stimulates testosterone production in

ACTH (AdrenoCorticoTropic hormone) -Stimulate Adernal cortex

Prolactin(PRL): stimulates milk secretions in the breast of a lactating

• Release hormone made by the hypothalamus

• Nerve fibers arise from cell bodies in the hypothalamus &

• Serve as storage & release site for anti – diuretic hormone

• Oxytocin (OT) in to blood stream, which is controlled by

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• It is the largest endocrine gland

• blood supply by superior thyroid

• Situated at the base of the throat

• Has two lobes (right and left)

A. Thyroxine (T4) and Tri- iodothyronine(T3, )

Control the rate at w/c glucose is burned or oxidized and

Exert a wide spectrum of metabolic & physiologic actions

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- Goiter – the condition in

w/c the thyroid gland is unable

to produce T4 & T3 due to low

level of TSH from pituitary to

stimulate T.G  the gland

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• Usually four in number, are

• Antagonist to calcitonin and acts to

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• Each glands consisting of two distinct entities:

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• Produce three major groups of hormone collectively

Mainly Aldesterone secreted in zona glomerulosa & has the

Regulate mineral (salt) content of the blood (Na+ & K+)

Regulate water & electrolyte imbalance

Increase Na+ reabsorption in the kidney

Increase water retention and promote the loss of potassium

• Stimulates gastric acid & pepsin secretion & inhibit

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• Norepinephrine /Noradrenaline/ released by sympathetic neuron

• Both hormones bind to receptors of sympathetic effectors to

When you feel threatened physically or emotionally SNS bring