ENDO SYSTEM

BY
KEHINDE AGBETAYO O.
 THE OVERVIEW ENDOCRINE SYSTEM
• MEDICAL SURGICAL NURSING

• AGBETAYO K.O (Rn)

• COLLEGE OF NURSING SCIENCES
• ADO EKITI
 Introduction
• The endocrine system is one of the regulating systems of
the body, the other being the nervous system.
• Endocrine system consists of endocrine glands that
secrete chemicals called hormones.
• Endocrine glands are ductless; that is, they do not have
ducts to take their secretions to specific sites.
• Instead, hormones are secreted directly into capillaries and
circulate in the blood throughout the body. Each hormone then
exerts very specific effects on certain organs, called target
organs or target tissues.
 Introduction
• Some hormones, such as insulin and thyroxine, have many
target organs.
• Other hormones, such as calcitonin and some pituitary
gland hormones, have only one or a few target organs.
• In general, the endocrine system and its hormones help
regulate growth, the use of foods to produce energy,
resistance to stress, the pH of body fluids and fluid balance,
and reproduction.
Introduction
• Endocrine glands are ductless glands that secrete
hormones into the blood. Hormones exert their effects
on target organs or tissues.
• Hormones are chemical messengers, transferring
information and instructions from one set of cells to
the other
 Introduction
• With respect to their chemical structure, hormones may be
classified into three groups: amines, proteins, and steroids.
• Amines: these simple hormones are structural variations of
the amino acid “tyrosine”. This group includes thyroxine from
the thyroid gland and epinephrine and norepinephrine from the
adrenal medulla.
• Proteins: these hormones are chains of amino acids. Insulin
from the pancreas, growth hormone from the anterior
 introduction
• gland, and calcitonin from the thyroid gland are all proteins.
Short chains of amino acids may be called peptides.
• Antidiuretic hormone and oxytocin, synthesized by the
hypothalamus, are peptide hormones.
• Steroids: cholesterol is the precursor for the steroid
hormones, which include cortisol and aldosterone from the
adrenal cortex, estrogen and progesterone from the ovaries,
and testosterone from the testes.
REGULATION OF HORMONE SECRETION
• Hormones are secreted when there is a need for their effects.

• Each hormone has a specific stimulus for secretion.

• T h e secretion of most hormones is regulated by negative.
feedback mechanisms:
• As the hormone exerts its effects, the stimulus for secretion
is reversed, and secretion of the hormone decreases.
ENDOCRINE GLANDS AND THEIR
HORMONES
• Hypothalamus
• T h e hypothalamus is composed of several groups of
nuclei which contain neurons that respond to either
neural inputs (stimuli) from widespread regions of the
nervous system or non-neural stimuli such as
changes in temperature and blood hormone level
Hypothalamus
• T h e hypothalamus is the principal visceral control
center of the brain and mediates a broad range of
functions via its connections with the endocrine,
autonomic (visceral motor), somatic motor, and limbic
systems, thereby maintaining a state of homeostasis.
hypothalamus secretes Releasing and Inhibiting
hormones
• Corticotrophin-releasing hormone
• Thyrotropin-releasing hormone
• Growth hormone-releasing hormone
• Gonadotropin-releasing hormone
• Somatostatin inhibits GH and TSH
 Pituitary Gland (Hypophysis)
• hangs from hypothalamus by the infundibulum; enclosed
by sella turcica of sphenoid bone.
• Posterior Pituitary (Neurohypophysis): stores
hormones produced by the hypothalamus
• ADH: increases water reabsorption by the kidneys,
decreases sweating, in large amounts causes
vasoconstriction. Result: decreases urinary output and
increases blood volume; increases BP. Stimulus: nerve
impulses from hypothalamus when body water decreases.
Posterior Pituitary
• Oxytocin: stimulates contraction of myometrium
of uterus during labor and release of milk from
mammary glands.
• Stimulus: nerve impulses from hypothalamus as
cervix is stretched or as infant sucks on nipple.
Anterior Pituitary
(Adenohypophysis)
• secretionsare regulated by releasing hormones from
the hypothalamus
• G H : through intermediary molecules, IGFs, GH
increases amino acid transport into cells and increases
protein synthesis;
• increases rate of mitosis; increases use of fats for
energy. Stimulus: GHRH from the hypothalamus.
 Anterior Pituitary
(Adenohypophysis)
• TSH: increases secretion of thyroxine (T4) and
triiodothyronine (T3) by the thyroid. Stimulus: TRH from the
hypothalamus.
• ACTH: increases secretion of cortisol by the adrenal
cortex. Stimulus: CRH from the hypothalamus.
• Prolactin: initiatesand maintains milk production by the
• mammary glands. Stimulus: PRH from the hypothalamus.
 Anterior Pituitary (Adenohypophysis)
• FSH: In women: initiates development of ova in ovarian
follicles and secretion of estrogen by follicle cells.
• In men: initiates sperm development in the testes. Stimulus:
GnRH from the hypothalamus.
• L H : In women: stimulates ovulation, transforms mature
follicle into corpus luteum and stimulates secretion of
progesterone. In men: stimulates secretion of testosterone
by the testes. Stimulus: GnRH from the hypothalamus.
 Thyroid Gland
• Located on front and sides of trachea below the larynx
• Thyroxine (T4) and Triiodothyronine (T3): produced by
thyroid follicles. Increase use of all food types for energy and
increase protein synthesis. Necessary for normal physical,
mental, and sexual development. Stimulus: TSH from the
anterior pituitary.
• Calcitonin: produced by parafollicular cells.
Decreases reabsorption of calcium from bones and lowers
blood calcium level. Stimulus: hypercalcemia.
 Parathyroid Glands
• They are four in number; two on posterior surface of
each lobe of the thyroid.
• PTH: increases reabsorption of calcium and phosphate from
bones to the blood;
• increases absorption of calcium and phosphate by the
small intestine; increases reabsorption of calcium and
excretion of phosphate by the kidneys, and activates
vitamin D.
• Result: raises blood calcium and lowers blood phosphate
levels. Stimulus: hypocalcemia. Inhibitor: hypercalcemia.
Pancreas
• Extends from curve of duodenum to the spleen.
Islets of Langerhans contain alpha cells and beta cells.
• Glucagon: secreted by alpha cells. Stimulates liver to
change glycogen to glucose; increases use of fats and
amino acids for energy. Result: raises blood
glucose level. Stimulus: hypoglycemia.
 Pancreas
• Insulin: secreted by beta cells. Increases use of glucose by
cells to produce energy; stimulates liver and muscles to
change glucose to glycogen; increases cellular intake of fatty
acids and amino acids to use for synthesis of lipids and
proteins Result: lowers bloodglucose level. Stimulus:
hyperglycemia.
• Somatostatin: inhibits secretion of insulin and glucagon.
 Adrenal Glands
• one on top of each kidney; each has an inner
adrenal medulla and an outer adrenal cortex.
• Adrenal Medulla: produces catecholamine instress
situations.
• Norepinephrine: stimulates vasoconstriction and raises
blood pressure.
Adrenal Glands
• Epinephrine: increases heart rate and force, causes
vasoconstriction in skin and viscera and vasodilation
in skeletal muscles; dilates bronchioles;
• slows peristalsis; causes liver to change glycogen to
glucose; increases use of fats for energy;
• increases rate of cell respiration. Stimulus:
sympathetic impulses from the hypothalamus.
 Adrenal Cortex
• produces mineralocorticoids, glucocorticoids, and
very small amounts of sex hormones.
• Aldosterone: increases reabsorption of sodium and
excretion of potassium by the kidneys.
• Results: hydrogen ions are excreted in exchange for
sodium; chloride and bicarbonate ions and water
follow sodium back to the blood; maintains normal
blood pH, blood volume, and blood pressure.
Adrenal Cortex
• Stimulus: decreased blood sodium or elevated
blood potassium; decreased blood volume or
blood pressure (activates the renin-angiotensin
mechanism of the kidneys).
 Cortisol
• increases use of fats and amino acids for energy; decreases
use of glucose to conserve glucose for the brain; anti-
inflammatory effect:
• blocks effects of histamine and stabilizes lysosomes to
prevent excessive tissue damage.
• Stimulus: ACTH from hypothalamus during physiological
stress.
 Ovaries
• in pelvic cavity on either side of uterus.
• Estrogen: produced by follicle cells. Promotes maturation of
ovum; stimulates growth of blood vessels in endometrium;
stimulates development of secondary sex characteristics:
growth of duct system of mammary glands, growth of uterus,
fat deposition.
• Promotes closure of epiphyses of long bones; lowers blood
levels of cholesterol and triglycerides. Stimulus: FSH from
anterior pituitary.
Progesterone
• produced by the corpus luteum. Promotes
storage of glycogen and further growth of blood
vessels in the endometrium; promotes growth of
secretory cells of mammary glands.
• Stimulus: LH from anterior pituitary.
• Inhibin: inhibits secretion of FSH.
ADDITIONAL HORMONE SECRETING
ORGANS
• Other organs are not typically considered endocrine
glands, yet they secrete one or more hormones
among the other major functions that they perform.
For example:
• T h e atria of the heart secrete atrial natriuretic
peptide (ANP), a hormone that helps reduce blood
volume by promoting urinary excretion of sodium
 ADDITIONAL HORMONE SECRETING
ORGANS
• Conversely, the kidneys release renin, a hormone that
initiates the production of angiotensin and aldosterone to
increase blood pressure and blood volume.
• The kidneys also secrete erythropoietin, a substance that
promotes the maturation of red blood cells.
• During pregnancy, the placenta provides maternal
circulation to the developing fetus, but it also secretes
hormones such as estrogen; progesterone; corticotrophin-
ADDITIONAL HORMONE SECRETING
ORGANS
• releasing hormone (CRH), which determines the
length of gestation and the onset of labor; and
human chorionic gonadotropin.
• W h e n exposed to sunlight, epidermal skin cells
form a precursor of vitamin D;
• the liver continues the conversion, and the kidneys
complete the activation process
 Other Hormones
• Melatonin: secreted by the pineal gland during darkness;
brings on sleep.
• Prostaglandins: synthesized by cells fromthe
phospholipids of their cell membranes; exerttheir
effects locally. Are involved in inflammation and pain
reproduction, nutrient metabolism, changes in blood
vessels, blood clotting
 MECHANISMS OF HORMONE ACTION
• A hormone affects cells that have receptors for it. Receptors
are proteins that may be part of the cell membrane, or within
the cytoplasm or nucleus of the target cell.
• The two-messenger mechanism: a protein hormone (1st
messenger) bonds to a membrane receptor. The hormone-
receptor bonding activates the enzyme “adenyl cyclase” on the
inner surface of the cell membrane which in turn stimulates
the formation of cyclic adenosine monophosphate (cAMP) (2nd
messenger), which activates the cell’s enzymes to bring about
the cell’s characteristic response to the hormone.
MECHANISMS OF HORMONE ACTION
• Steroid hormones diffuse easily through cell
membranes and bond to cytoplasmic receptors.
• Steroid-protein complex enters the nucleus and
activates certain genes, which initiate protein
synthesis.
• The enzymes produced bring about the cell’s
characteristic response to the hormone
AGING AND THE ENDOCRINE
SYSTEM
• M o s t of the endocrine glands decrease their
secretions with age, but normal aging usually does
not lead to serious hormone deficiencies
• There are decreases in adrenocortical hormones,
for example, but the levels are usually sufficient to
maintain homeostasis of water, electrolytes, and
nutrients.
AGING AND THE ENDOCRINE
SYSTEM
• The decreased secretion of growth hormone leads to a
decrease in muscle mass and an increase in fat storage.
• A lower basal metabolic rate is common in elderly
people as the thyroid slows its secretion of thyroxine.
• Unless specific pathologies develop, however, the
endocrine system usually continues to function
adequately in old age.
ASSESSMENT OF THE ENDOCRINE SYSTEM
• Already Discussed in the previous class
 DIABETES MELLITUS
• World Health Organization defined Diabetes Mellitus (DM) as
a chronic, metabolic disease characterized by elevated levels
of blood glucose (or blood sugar), resulting from defects
in insulin secretion, insulin action, or both which leads
overtime to serious damage to the heart, blood vessels, eyes,
kidneys and nerves.
• The major classifications of diabetes are type 1 diabetes, type
2 diabetes
 DIABETES MELLITUS
• diabetes, gestational diabetes, & diabetes mellitus
associated with other conditions or syndromes. The types of
DM vary in cause, clinical course, & treatment:
• Type 1 DM: This is formerly called insulin-dependent
diabetes mellitus (IDDM). This type of DM is characterized
by destruction of the pancreatic beta cells. Combined
genetic, immunologic, and possibly environmental (e.g.
viral) factors are thought to contribute to beta cell
DIABETES MELLITUS
• destruction which is characterized by no insulin
production by the beta cells in the islets of Langerhans
of the pancreas.
• The onset of type 1 diabetes is more likely in
childhood and adolescence and this is why it is also
referred to as Juvenile Diabetes, but the disease can
occur at any age
 DIABETES MELLITUS
• Type 2 DM: This is formerly known as non–insulin-
dependent diabetes mellitus (NIDDM).
• It is characterized by insulin resistance or insufficient
insulin production.
• Type 2 diabetes is more common in aging and obese adults.
However, in 2007, slightly more than 50% of people with
newly diagnosed disease were in the 40- to 59-year age group
(CDC, 2008), and type 2 diabetes also is being detected in
obese children.
DIABETES MELLITUS
• The incidence of this form of diabetes now
accounts for 20% of all newly diagnosed cases.
• It is often preventable.
• Symptoms are always almost the same but milder/less
marked in this type than Type1.
• As a result, the disease may be diagnosed several
years after onset, after complications have already
arisen.
 DIABETES MELLITUS
• Gestational Diabetes Mellitus (GDM): This is any degree of
glucose intolerance with its onset during pregnancy.
• This is as a result of the secretion of placental hormones,
which causes insulin resistance.
• Gestational diabetes occurs in as many as 14% of pregnant
women and increases their risk for hypertensive
disorders during pregnancy.
• Women with gestational diabetes are at an increased risk of
complications during pregnancy and at delivery
 DIABETES MELLITUS
• These women and possibly their children are also at
increased risk of type 2 diabetes in the future.
• Gestational diabetes is diagnosed through prenatal screening,
rather than through reported symptoms.
• Impaired Glucose Tolerance and Impaired Fasting
Glycaemia: Impaired Glucose Tolerance (IGT) and Impaired
Fasting Glycaemia (IFG) are intermediate conditions in the
transition between normality and diabetes.
• People with IGT or IFG are at high risk of progressing to
type 2 diabetes, although this is not inevitable
 CAUSES/Risk Factors
• Modifiable Risk factors
• Physical inactivity
• Obesity
• Unhealthy diet
• High cholesterol level
• Inadequate Sleep
• Excess Alcohol Consumption
• Smoking
• Physical and/or EmotionalStress
• Non-Modifiable Risk Factors
• Family History
• Age
• Race
• Gestational Diabetes
DIFFERENCES BETWEEN TYPE 1 & TYPE 2 DM
 Signs and Symptoms
• Symptoms of diabetes may occur suddenly. However, in type
• 2 diabetes, the symptoms can be mild and may take many
years to be noticed. Manifestations of diabetes include:
• Polydipsia (Excessive thirst) Polyuria (Excessive Urination -
>3Ltrs of urine daily)
• Polyphagia (Excessive appetite)
• Glucosuria
• Blurred vision
Signs and Symptoms
• Feeling tired/Fatigue
• Unintentional loss of weight
• O v e r time, diabetes can damage blood vessels in the
heart, eyes, kidneys and nerves
 Pathophysiology
• Deficiency of or peripheral resistance to insulin leads to
increased level of glucose in the blood and subsequent
heamoconcentration.
• Polydipsia or increased thirst is due to high blood glucose that
raises the osmolarity of blood and makes it more
concentrated.
• Polyuria or increased frequency of urination is due to
excess fluid intake and glucose-induced urination.
• Weight loss occurs due to loss of calories in excess urine
 Pathophysiology
• Polyphagia due to loss or excess glucose in urine or
absence of adequate uptake of glucose from the blood
stream that leads the body to crave for more glucose.
• P o o r wound healing, gum and other infections due to
increased blood glucose providing a good source of nutrition
to microbes and due to a diminished immunity
Pathophysiology
• Heart disease – this occurs due to changes in the
large blood vessels leading to coronary, cerebral, and
peripheral artery diseases, atherosclerosis,
dyslipidemia etc
• E y e damage – this is termed diabetic retinopathy
and occurs due to damage of the fine blood vessels of
the retina in the eye due to long term exposure to high
blood sugar.
 Pathophysiology
• Kidney damage – similar damage to small and large blood
vessels of the kidneys. Initially there is proteinuria or
increased outflow of protein and may lead to end stage
renal disease (ESRD).
• Nerve damage – this can affect the arms and legs and is
called stocking-glove numbness/tingling.
• It can also affect autonomic functions leading to
impotence, erectile dysfunction, difficulty in digestion or
gastroparesis etc.
Pathophysiology
• Diabetic foot – this occurs due to peripheral nerve
damage as well as blood vessel affliction due to long
term diabetes.
• Little trauma, sores and blisters go unnoticed due
to lack of sensation and peripheral vascular disease
impairs healing and allows infection.
 Pathophysiology
• Diabetic Ketoacidosis is caused in type 1 diabetes where there
is complete lack of insulin and reliance on fatty acids for
energy.
• This uncontrolled lipid breakdown leads to formation of ketones
and causes acidosis, ketonemia and ketonuria.
• This is a medical emergency.
 Pathophysiology
• Non-Ketotic Hyperosmolarity – this is caused due to
extreme rise of blood sugar.
• This is seen in type 2 diabetics. There is just enough insulin
to suppress ketone synthesis.
• The high blood sugar leads to excessive concentration or
osmolarity of blood which in turn leads to diuresis and
collapse of the blood vessels and cardiovascular shock.
• This is a medical emergency.
 Diagnostic Evaluation

• Health history/History taking

• Physical examination
• Fasting Blood Glucose (FBG)
• Random Blood Glucose (RBG)
• Glucose Tolerance Test
• Urinalysis
• HbA1C Test: AverageBlood Glucose over the past 2 or
3 months, Etc.
Medical Mgt./Chemotherapy
• Insulin
• Biguanides (e.g., metformin),
• Sulfonylureas (e.g., glimepiride),
• Meglitinides (e.g., repaglinide),
• Thiazolidinediones (e.g., pioglitazone)
• Dipeptidyl peptidase IV inhibitors (e.g.,sitagliptin),
• alpha-glucosidase inhibitors (e.g., acarbose)
Surgical Mgt.
• Bariatric (weight loss) surgery
• Islet cell transplantation (New procedure)
• NSG CARE
• TO BE DISCUSSED IN THE CLASS
 DIABETES INSIPIDUS
• Diabetes Insipidus (DI),otherwise called ”arginine vasopressin
deficiency (AVP-D) OR arginine vasopressin resistance
(AVP-R)”, is a condition characterized by large amounts of
dilute urine and increased thirst.
• It is an uncommon condition in which the kidneys are unable
to prevent the excretion of water. The amount of urine
produced can be nearly 20 liters per day.
• DI is not the same as diabetes mellitus type 1 and 2.
However, untreated, both DI and diabetes mellitus cause
constant thirst and frequent urination.
 DI
• Diabetes insipidus (DI) is defined as the passage of large
volumes (>3 L/24 hr) of dilute urine (< 300 mOsm/kg).
• The most common form is central DI after trauma or surgery to
the region of the pituitary and hypothalamus; this condition may
exhibit one of the following three patterns:
• Transient
• Permanent
• Triphasic (observed more often clinically)
 TYPES OF DI
• Neurogenic/Central DI (CDI): is due to a lack of
vasopressin (antidiuretic hormone) production. This can be due to
injury to the hypothalamus or pituitary gland or genetics and some
other causes.
• Central (neurogenic, pituitary, or neurohypophyseal) DI, characterized
by decreased secretion of antidiuretic hormone (ADH; also referred to
as arginine vasopressin [AVP])
• Nephrogenic DI (NDI): occurs when the kidneys do not respond
properly to vasopressin.
• Nephrogenic DI, characterized by decreased ability to concentrate urine
because of resistance to ADH action in the kidney
 TYPES OF DI
• Dipsogenic DI: is a result of excessive fluid intake due to damage
to the hypothalamic thirst mechanism. It occurs more often in
those with certain psychiatric disorders or on certain medications.
• Gestational DI: occurs only during pregnancy and the postpartum
period. During pregnancy, women produce ”vasopressinase” in
the placenta, which breaks down antidiuretic hormone (ADH).
Gestational DI is thought to occur with excessive production and/or
impaired clearance of vasopressinase
Causes/Risk factors
• Idiopathic
• Genetic problems
• H e a d injury (common cause)
• Infection and tumors of the brain
• Problem with the ADH-producing autoimmune
disease
Causes/Risk factors
• L o s s of blood supply to the pituitary gland
• Surgery in the area of the pituitary gland or
hypothalamus (most common cause)
• Certain medicines, such as lithium
• High level of calcium in the body (hypercalceamia)
• Kidney disease, such as polycystic kidney disease
Signs and symptoms of diabetes
insipidus
• The predominant manifestations of DI are as follow
• Polyuria - The daily urine volume is relatively constant
for each patient but is highly variable between patients
(3-20 L)
• Polydipsia
• Nocturia
Signs and symptoms of diabetes
insipidus
• In infants with DI, the most apparent signs may be the
following:
• Crying
• Irritability
• Growth retardation
• Hyperthermia
• Weight loss
Signs and symptoms of diabetes
insipidus
• In children, the following manifestations typically
predominate:
• Enuresis
• Anorexia
• Linear growth defects
• Fatigability
 Signs and symptoms of diabetes
insipidus
• If the condition that caused DI also damaged the anterior
pituitary or hypothalamic centers that produce releasing factors,
patients may present with the following:
• Excessive fatigue
• Diminished libido or erectile dysfunction
• Headache
• Dry skin
• Hair loss
Pathophysiology
• A D H is also called vasopressin. ADH is produced in
a part of the brain called the hypothalamus.
• It is then stored and released from the pituitary gland.
This is a small gland just below the base of the brain.
• T h e amount of water excreted in the urine is
controlled by antidiuretic hormone (ADH).
Pathophysiology
• DI caused by a lack of ADH is called Central
Diabetes Insipidus. When DI is caused by a failure of
the kidneys to respond to ADH, the condition
is called Nephrogenic Diabetes Insipidus.
Nephrogenic means related to the kidney.
• During the day, your kidneys filter all your blood
many times. Normally, most of the water is reabsorbed,
and only a small amount of concentrated urine is excreted
 Pathophysiology
• DI occurs when the kidneys cannot concentrate the
urine normally, and a large amount of dilute urine is
excreted alongside loss of electrolyte.
• This may lead to severe electrolyte
derangement, dehydration, and generalized body
weakness.
• Severe dehydration leads to falling of cardiac output or
what may otherwise be referred to as hypovolemia
(shock).
 Pathophysiology
• A s cardiac output falls, the body’s cells become deprived of
oxygen and switch from aerobic metabolism to the less
efficient anaerobic metabolism.
• Anaerobic metabolism results in an accumulation of lactic
acid, which lowers blood pH and can eventually cause
metabolic acidosis.
• Hypovolemia is multi-systemic in manifestation e.g.
reduce perfusion of the brain cells leads to irrational talks,
blurry vision and even loss of consciousness.
Diagnostic evaluation
• Inadequate renal tissue perfusion eventually results
to oliguria, renal injury and possible renal shutdown
etc.
• Diagnostic evaluation
• A 24-hour urine collection for determination of urine
volume
• Serum electrolyte concentrations and glucose level
• Urinary specific gravity
• Simultaneous plasma and urinary osmolality
• Plasma ADH leve
 MGT
• The cause of the underlying condition wil be treate when
possible.
• Central DI may be controlled with vasopressin
(desmopressin,)Youtake vasopressin as an Injection,
injection, a nasal spray, or tablets.
• If nephrogenic DI is caused by medicine, stopping
the medicine may help restore normal kidney function. But
after many years of use of some medicines, such as
lithium, nephrogenic DI can be permanent.
Mgt

• Hereditary nephrogenic DI and lithium-induced

nephrogenic DI are treated by drinking enough
fluids to match urine output. Medicines that lower
urine output also need to be taken.
• Nephrogenic DI is treated with anti-inflammatory
medicines and diuretics (water pills).
 Mgt
Desmopressin (drug of choice for central DI )
• Synthetic vasopressin
• Chlorpropamide
• Carbamazepine (rarely used; employed only when all other
measures prove unsatisfactory)
• Clofibrate
• Thiazides
• Nonsteroidal anti-inflammatory drugs (NSAIDs), such as
indomethacin (may be used in nephrogenic DI, but only when no
better options exist
Prognosis: Outcome depends on the underlying disorder. If treated,
DI does not cause severe problems or result in early death.
Differences between Diabetes Mellitus and Diabetes Insipidus
 HYPOGLYCAEMIA
• Hypoglycemia is a condition in which the blood sugar
(glucose) level is lower than the standard range. Glucose is the
body's main energy source
• Hypoglycemia is often related to diabetes treatment. But other
drugs and a variety of conditions (many rare e.g. Addison’s
disease) - can cause low blood sugar in people who don't have
diabetes mellitus
• Hypoglycemia is a medical emergency and thus needs
immediate treatment. For many people, a fasting blood sugar
of 70 milligrams per deciliter (mg/dL), or 3.9 millimoles per
liter (mmol/L), or below should serve as an alert for hypoglycemia
Signs and Symptoms
• Looking pale
• Hydrophoresis (Sweating), Headache
• Hunger, Nausea
• A n irregular or fast heartbeat, Fatigue
• Irritability or anxiety, Difficulty concentrating
• Dizziness or lightheadedness
• Tingling or numbness of the lips, tongue or cheek
Signs and Symptoms
• Confusion, unusual behavior or both, such as the
inability to complete routine tasks
• L o s s of coordination
• Slurred speech
• Blurry vision
• Nightmares, if asleep
Risk Factors
• People using insulin and OHAs especially the
Sulfonylureas, such as glipizide, glimepiride or
glyburide.
• Young children and older adults and the alcoholics
• Those with impaired liver or kidney function
• People who've had diabetes for a long time
• Those taking multiple medications
Causes
• Taking too much insulin or diabetes medication
• Not eating enough and Drinking alcohol
• Postponing or skipping a meal or snack
• Increasing exercise or physical activity without
eating more or adjusting medications
 Prevention
• Monitor blood sugar.
• Meals or snacks should not be skipped or delayed
• Medications should be measured carefully and taken on time.
• Medications should be adjusted or eat additionalsnacks if
there is increased physical activity.
• Record your low glucose reactions.
• Diabetes identification/tag should be carried in
case of an emergency.
Management
• Don't inject insulin or give Plasma expander e.g.
Normal Saline, as this will cause blood sugar levels
to drop even further.
• Give glucagon by injection or a nasal spray
• Administer 50% Dextrose in H2O in double dilution
(1:1)
Complications

Unresponsiveness (Loss of consciousness-LOC)

• Seizures
• Death
 Diabetic ketoacidosis (DKA)
• Diabetic ketoacidosis (DKA) is a serious complication of
diabetes that can be life-threatening.
• DKA is most common among people with type 1 diabetes,
however, people with type 2 diabetes can also develop DKA.
Diabetic ketoacidosis (DKA)
• DKA develops when the body doesn’t have enough
insulin to allow blood sugar into the cells for use
as energy.
• Instead, the liver breaks down fat for fuel, a process
that produces acids called “ketones”.
• When too many ketones are produced too fast, they
can build up to dangerous levels in the body.
Causes
• Very high blood sugar and low insulin levels lead to
DKA. The two most common causes are:
• Illness. Inability to eat or drink as much as usual in
cases of illness, which can make blood sugar levels
hard to manage
• Missing insulin shots, or the wrong insulin dose.
Other causes of DKA include
• Heart attack or stroke.
• Physical injury, such as from a car accident.
• Alcohol or drug use.
• Certain medicines, such as some diuretics (water pills)
and corticosteroids (used to treat inflammation in the
body).
 Signs and Symptoms
• DKA usually develops slowly.
• Being very thirsty, polyuria
• Fast, deep breathing,
• D r y skin and mouth, acetone breathe
• Flushed face, Stomach pain, Fruity-smelling breath
• Headache, Muscle stiffness or aches
• Being very tired, Nausea and vomiting
• Sometimes DKA is the first sign of diabetes in people who
haven’t yet been diagnosed
 Treatment
• Diabetic Ketoacidosis is a medical emergency:
• Replacing lost fluids through frequent urination and to help
dilute excess sugar in the blood.
• Replacing electrolytes (minerals in the body that help the
nerves, muscles, heart, and brain work the way they
should). Too little insulin can lower the electrolyte levels.
• Administration of insulin. Insulin reverses the conditions
that cause DKA.
• Treatment of any underlying illness that caused DKA, such as
antibiotics for an infection etc.
 Acromegaly
• Acromegaly is a rare condition where the body produces too
much growth hormone,
• thereby causing body tissues and bones to grow more
quickly and this over time leads to abnormally large hands
and feet, and a wide range of other symptoms.
• Acromegaly is usually diagnosed in adults aged 30 to 50, but
it can affect people of any age.
• When it develops before the end of puberty, it's known as
"gigantism".
 Causes/Risk factors
• The most common cause of acromegaly is a tumor in the
pituitary gland called a ”pituitary adenoma” that causes the
pituitary gland to release excess growth hormone (GH).
• Risk factors to the development of acromegaly includes:
Family history of pituitary adenoma
• MacCun Albright syndrome
• Lung cancers
• Adrenal tumors
Signs & Symptoms
• In adults, acromegaly affects the body’s bones and
tissues and causes them to grow in irregular ways.
Adults with acromegaly may experience the
following symptoms:
• Enlarged hands or feet
• Changes in the face shape, including a more
prominent jaw and/or forehead
• Increase in size of your lips, nose and/or tongue
Signs & Symptoms
• Excessive sweating or oily skin
• Deepening of the voice
• Organomegaly
• Headaches, Joint pain
• Vision changes
• Sleep apnea
• Numbness of hands and feet
• Increase in the number of skin tags
• Carpal tunnel syndrome or spinal cord issues
Acromegaly and Gigantism
• Acromegaly and gigantism are both conditions that
result from excess growth hormone (GH).
• Acromegaly is usually diagnosed in adults aged 30 to
50, but it can affect people of any age. When it develops
before the end of puberty, it's known as "gigantism".
• In children, gigantism occurs when they experience excess
GH before the growth plates in their bones fuse (before the
end of puberty). This causes them to grow very tall.
Acromegaly and Gigantism
• Gigantism is more rare than acromegaly.
• Some healthcare providers refer to gigantism as
pediatric acromegaly
Pathophysiology
• Acromegaly is a condition in which GH is over-
secreted after the epiphyses of the long bones have
sealed.
• GH is overproduced when the pituitary gland is
insensitive to feedback inhibiting hormones such as
somatostatin, a hypothalamic hormone, and insulin-
like growth factor 1 (IGF-1).
• I G F - 1, a hormone released by the liver, stimulates
the growth of bones and tissue.
 Pathophysiology
• Unchecked GH allows sustained production of IGF-1,
increased blood glucose levels leading to lengthening and
widening of bones, organ enlargement and hyperlipidemia.
• Hypersecretion results from hyperplasia (increased
numbers of cells), which in the majority of cases is caused by
an adenoma, a benign tumor. As with other cranial
tumors, a benign pituitary tumor becomes a space-occupying
lesion and can affect other cerebral structures
 Diagnostic Evaluation
• Skull X-ray, MRI, and CT reveal pituitary enlargement.
• B o n e X-ray show thickened long bones and skull bones.
• Glucose tolerance test & GH measurement is the most
reliable method of confirming acromegaly. (Ingestion of a
bolus of glucose should lower GH levels, but GH levels
remain elevated in persons with acromegaly).
• Increased blood levels of IGF-1 can also indicate
acromegaly in non-pregnant women (there is typically high
IGF-1 levels two to three times higher than normal in
pregnant women).