Endocrine disorders power point for health science students.

1. Nursing Interventions of
patients
With Endocrine system
With Endocrine system
Disorders
1 7/30/2019
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2. Content outlines
Review of anatomy, physiology and assessment of the
endocrine system
Diabetes mellitus
Disorders of the thyroid gland
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Disorders of the thyroid gland
Disorders of the parathyroid glands
Disorders of the adrenal glands
Disorders of the pituitary gland
Disorders of the posterior pituitary gland 7/30/2019

3. Learning objectives
On completion of this unit, you will be able to:
1. Describe the functions of each of the endocrine glands and their
hormones
2. Compare & contrast type I & type II DM ,DKA & HHNKS with
their interventions
3. Compare hypothyroidism and hyperthyroidism: their causes,
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3. Compare hypothyroidism and hyperthyroidism: their causes,
clinical manifestations, management, and nursing interventions
4. Compare hyperparathyroidism and hypoparathyroidism: their
causes, clinical manifestations, management, and nursing
interventions
5. Compare Addison’s disease with Cushing’s syndrome: their
causes, clinical manifestations, management, and nursing
interventions
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4. Endocrine system
It is a chemical system which controls
communication and coordination of body functions.
Uses chemical signals called hormones for cell to
cell communication
Common anatomic features of endocrine glands
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Common anatomic features of endocrine glands
They are composed of secretary cells arranged in minute clusters
Have no ducts, but they have rich blood supply
Hormone concentration in the blood stream is regulated by feed
back control mechanism.
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6. Pituitary gland (Hypophysis)
Located at the base of the brain with oval shaped
Referred to as “Master gland”
–Secretes hormones that control functions of other glands
–Has two distinct lobes with specific functions
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–Has two distinct lobes with specific functions
1.Anterior lobe (Adeno-hypophysis)
2.Posterior lobe (Neuro-hypophysis)
–Controlled by the hypothalamus or other neural mechanisms
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7. Anterior pituitary gland(Adeno-hypophysis)
Hormones Target gland |tissue|
1.Thyroid stimulating hormone /TSH/ Thyroid gland
2. Adrenocorticotropic hormone /ACTH/ Adrenal cortex
3. Follicle stimulating hormone /FSH/ Ovaries & testes
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3. Follicle stimulating hormone /FSH/ Ovaries & testes
4. Luteinizing hormone /LH/ Ovaries & testes
5. Prolactin Breast
6. Growth hormone |GH| All tissues
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8. The anterior pituitary gland(Adeno-hypophysis)
→Secretes Thyroid-Stimulating Hormone (TSH)
Promotes and maintains normal growth and development
of the thyroid gland
Stimulates secretions of the thyroid hormones
→ Secretes Growth Hormone (GH)
Also called Somatotropic Hormone (STH)
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Also called Somatotropic Hormone (STH)
Regulates growth of bone, muscle, and other body
tissues
→ Secretes Adrenocorticotropic Hormone (ACTH)
Stimulates normal growth and development of adrenal
cortex and secretion of corticosteroids
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9. Anterior pituitary gland(Adeno-hypophysis)--
→Secretes Follicle-Stimulating Hormone (FSH)
Stimulates secretion of estrogen and production of eggs in the
female ovaries
Stimulates production of sperm in the male testes
→ Secretes Lactogenic Hormone (LTH)
Also called Prolactin
Promotes development of breasts during pregnancy
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Promotes development of breasts during pregnancy
Stimulates secretion of milk from breasts after delivery of baby
→ Secretes Luteinizing Hormone (LH)
Stimulates female ovulation and the secretion of testosterone in
the male
→ Melanocyte-Stimulating Hormone (MSH)
Controls intensity of pigmentation in pigmented cells of the skin
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10. 2. Posterior pituitary gland(Neuro-hypophysis)
→The posterior pituitary does not produce any hormones
of its own; instead, it stores and secretes two hormones
made in the hypothalamus.
Secretes Antidiuretic Hormone (ADH) /Vasopressin/
Increases re-absorption of water by the renal tubules
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Increases re-absorption of water by the renal tubules
Decreases excretion of large amounts of urine
→ Secretes Oxytocin
Stimulates contraction of the uterus during child birth
Stimulates release of milk from the breasts of lactating women
in response to the suckling reflex of the infant.
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11. Thyroid gland
Located: anteriorly in the neck directly below the cricoids cartilage
Shape = Butter fly shaped
Weight about 30 gm. has two lobes
It is an extremely vascular gland
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Blood supply = 5ml of blood/min per gm. of thyroid gland ( i.e,
about 5 times the blood flow to the liver)
Produce 3 different hormones
-Thyroxine/T4/ -Triadothyronin/T3/ &-Calcitonin
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13. Calcitonin
Involved in maintenance of blood calcium levels
Decrease Ca ++ level in the blood
When Ca++ levels rise, calcitonin is released
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Inhibits intestinal absorption of calcium
Inhibits reabsorption of calcium in kidneys
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14. Parathyroid gland
Consists of four tiny rounded bodies located on dorsal
aspect of thyroid gland
–Secrete Parathyroid Hormone (PTH= Parathormone)
Functions of PTH
Increases the re-absorption of calcium and phosphate
from bone to blood
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from bone to blood
Increases absorption of calcium and phosphate by the
small intestine
Increases the re-absorption of calcium and the excretion
of phosphate by the kidneys
Increase Ca++ level in the blood
Activates vitamin D
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15. Cont…
Net effect of PTH -↑Serum calcium
- ↓Serum phosphate
Low serum [Ca+2] = Increased PTH secretion
High serum [Ca+2] = Decreased PTH secretion
Role of Calcitriol (the active form of vitamin D, is formed in the
kidney or made in laboratory)
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kidney or made in laboratory)
Stimulates GI absorption of both calcium and phosphate
Stimulates renal re-absorption of both calcium and
phosphate
Stimulates bone resorption
Net effect of calcitriol =↑ serum calcium
=↑ serum phosphate
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16. Thymus gland
Single gland located in mediastinum near the middle of
the chest, just beneath sternum
Large in fetus and infants, shrinks with age
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Secretes thymosin and thymopoietin
Stimulates production of T cells that are involved in the
immune response.
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17. Adrenal glands (Suprarenal glands)
Located in the retroperitoneal space at the
superior poles of each kidney
Consists of an -- Outer portion –Cortex (90%)
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-- Inner portion –Medulla (10%)
Adrenal Cortex
Is essential for maintenance of life sustaining
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18. Adrenal cortex secretes corticosteroids
–Mineralocorticoids--Aldosterone
Regulate how mineral salts (electrolytes) are processed in the
body
–Glucocorticoids--Cortisol
Influence metabolism of carbohydrates, fats, and proteins in
the body.
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the body.
Have an anti-inflammatory effect on the body
Increase glucose available during “fight-or-flight” responses by
the body
–Gonadocorticoids
Sex hormones secreted in small amounts
Contribute to secondary sex characteristics
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19. Adrenal medulla
Functions as part of autonomic nervous system
Plays a role in the physiologic stress response
Secretes catecholamines
– Epinephrine = Adrenaline
Increases heart rate and force of heart muscle contraction
Dilates bronchioles in the lungs
Decreases peristalsis in the intestines
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Decreases peristalsis in the intestines
Raises blood glucose levels by causing the liver to convert
glycogen into glucose (Glycogenolysis)
Increase metabolic rate
– Norepinephrine = Noradrenaline
Produces a vasoconstrictor effect on the blood vessels,
thereby raising blood pressure.
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20. Pancreas
Located in left upper quadrant of the abdomen behind
the stomach
Has both exocrine & endocrine gland functions
Exocrine pancreas
Exocrine function is to secrete digestive enzymes into
duodenum.
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duodenum.
Secretions are digestive enzymes high in protein
content & electrolyte rich fluids.
The secretions are very alkaline
Digestive enzymes include amylase, triypsine, lipase.
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21. Endocrine pancreas
Islets of Langerhans are the cells involved in the endocrine
function.
-Alpha cells (15-20% of islet cells) secret -Glucagon
-Beta cells (65-80% of islet cells) secret -Insulin
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-Delta cells secret -Somatostatine
Somatostatine
-Decreases (inhibits) secretion of insulin and glucagon
-Slows absorption of nutrients
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22. Glucagon
Released when blood glucose level is low
Causes glycogen to be broken into glucose
Released during periods of sympathetic stress
Increase blood glucose levels by stimulating liver to release
glucose stores from glycogen (Glycogenolysis)
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Increases the use of excess amino acids and fats for energy
production = Gluconeogenesis
The overall effect of glucagon, therefore, is to raise the blood
glucose level and to make all types of food available for energy
production.
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23. Insulin
Released when blood glucose level is high
Transports and metabolizes glucose for energy
Accelerates transport of amino acids (derived from dietary protein)
into cells
Promotes transport of fatty acids in to cells
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Promotes transport of fatty acids in to cells
Facilitate movement of K+ from ECF to ICF
Stimulates storage of glucose in the liver, muscle and adipose
tissue (in the form of glycogen)
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24. Enhances storage of dietary fat in adipose tissue
Signals the liver to stop the release of glucose
Insulin also inhibits the breakdown of stored glucose,
protein, and fat.
Insulin…
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Insulin -is anabolic hormone bse it stimulate the synthesis of
glycogen, protein & lipid while it inhibits degradation of
these substances.
Result: Lowers blood glucose level.
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25. Insulin…
Effect on carbohydrate
Facilitates glucose uptake by the cell
Increases rate of glycogen synthesis in the liver &
muscles
Inhibit gluconeogenesis
Effect on protein
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Effect on protein
Facilitates amino acids transport in muscles and other
tissues
Stimulate protein synthesis
Inhibits protein degradation
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26. Effect on lipids
Promotes transport of fatty acids in to cells
Promotes synthesis of fatty acids and glycerol from glucose
Inhibits lipolysis
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Increases the synthesis of cholesterol in the liver
Without insulin, blood levels of lipids tend to rise and cells
accumulate excess fatty acids
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27. Insulin is a vital hormone; we cannot survive for very long
without it. A deficiency of insulin leads diabetes mellitus
Secretion of insulin is stimulated by hyperglycemia, a high
blood glucose level. This state occurs after eating, especially of
meals high in carbohydrates
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meals high in carbohydrates
As glucose is absorbed from the small intestine into the blood,
insulin is secreted to enable cells to use the glucose for
immediate energy. At the same time, any excess glucose will
be stored in the liver and muscles as glycogen
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28. Stimuli for insulin secretion
Rise in plasma glucose level (Hyperglycemia)
Rise in plasma amino acids
Parasympathetic stimulation
Factors that inhibit insulin secretion are
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Factors that inhibit insulin secretion are
Hypoglycemia
Sympathetic stimulation
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29. Gonads
Ovaries (Estrogen) = Sex characteristics
Maturity and coordination
Testes (Testosterone) = Sex characteristics
Muscle development and maturity
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Muscle development and maturity
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30. Ovaries
Female sex glands = female gonads
Pair of almond shaped glands
Located in upper pelvic cavity, on either side of
lateral wall of uterus
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lateral wall of uterus
Near fimbriated ends of the fallopian tubes
Responsible for producing mature ova and releasing
them at monthly intervals during ovulation
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31. Hormones secreted by the ovaries
Estrogen
Promotes maturation of ovum in the ovary
Stimulates vascularization of uterine lining each month
to prepare for implantation of a fertilized egg
Contributes to secondary sex chx changes in female
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Contributes to secondary sex chx changes in female
Progesterone
Primarily responsible for changes within the uterus in
anticipation of a fertilized ovum
Responsible for development of maternal placenta after
implantation of a fertilized ovum
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32. Testes
Testes = male gonads = Testicles
Two small ovoid glands located in scrotum
Primary organs of male reproductive system
Responsible for production of sperm
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Secrete testosterone
Responsible for secondary sex characteristic
changes in male
Responsible for maturation of sperm
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33. Assessment of the endocrine system
History
Changes in energy level
Tolerance to heat or cold
Weight
Fat and fluid distribution
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Fat and fluid distribution
Secondary sexual characteristics
Sexual dysfunction
Concentration
Sleep patterns
Stature
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34. The health history information should include:
1. The severity of these changes
2. The length of time the patient has experienced
these changes
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3. The way in which these changes have affected
patient’s ability to carry out daily living activity
4. The effect of the changes on the patient’s daily
activities
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35. Physical Exam
Vital signs
Visual head-to-toe assessment
Tactile examination
Appearance of facial hair in women
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“moon face,”
“buffalo hump,”
Exophthalmos
Slow wound healing
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36. Edema
Thinning of the skin
Obesity of the trunk
Thinness of the extremities
Physical Exam
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Increased size of the feet and hands
Elevated/Decreased blood pressure
Behavioral changes such as agitation, nervousness, or a
lack of concern about personal appearance
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37. Diabetes Mellitus
DM is a group of metabolic diseases characterized by
elevated levels of glucose in the blood (hyperglycemia)
resulting from:
Defects in insulin secretion
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Defects in insulin secretion
Insulin actions
Both
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38. Risk factors
Family history of diabetes
Obesity (BMI > 27 kg/m2)
Race ethnicity
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Age ≥ 45 years
Previously identified impaired fasting glucose or
impaired glucose tolerance
Hypertension (≥ 140/90mmhg)
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39. DM Classification
1. Type 1 diabetes (previously referred to as insulin
dependent diabetes (IDDM)
LADA (Latent Autoimmune Diabetes in Adults)
2. Type 2 diabetes (previously referred to as non-insulin
dependent diabetes (NIDDM)
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dependent diabetes (NIDDM)
MODY (Maturity-Onset Diabetes of Youth)
3. Gestational diabetes
4. Diabetes mellitus associated with other conditions or
syndrome
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40. Type 1 Diabetes (T1D)
Affects approximately 5% to 10% of people
characterized by destruction of pancreatic beta cells
Factors contributing to beta cell destruction:
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Genetic (common)
Immunologic
Environmental (e.g., viral)
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41. Physiologic responses to insufficient insulin:
Glycogenolysis
Decreased glycogenesis
Gluconeogenesis
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Increased lipolysis Hyperglycemia
Proteolysis
Increased ketogenesis
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42. Pathophysiology
Destruction of the beta cells
Decreased insulin production
Unchecked glucose production and fasting hyperglycemia
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Postprandial hyperglycemia
Blood glucose level exceeds the renal threshold for glucose,
usually 180 to 200mg/dL, the kidneys may not reabsorb all of the
filtered glucose
Glucosuria Osmotic diuresis
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43. Type 2 Diabetes (T2D)
Accounts approximately 90 to 95% of cases
Results from decreased sensitivity of tissues to insulin
(called insulin resistance) & impaired β-cell functioning
Obesity appears to play a major role in T2D by down
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Obesity appears to play a major role in T2D by down
regulating insulin receptors in skeletal muscle and fat cells
Stimulates increased insulin production as a compensatory
response, which may also predispose the patient to weight
gain.
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44. The exact mechanisms that lead to insulin resistance and
impaired insulin secretion in T2D are unknown.
Prevalence of diabetes increases with age, with about half
of cases in people older than 55
Despite the impaired insulin secretion that is characteristic
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Despite the impaired insulin secretion that is characteristic
of T2D, there is enough endogenous insulin present, to
prevent lipolysis and production of ketene bodies
Therefore, diabetic ketoacidosis (DKA) does not typically
occur in T2D
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45. Pathophysiologic factors that have been identified in T2D
include:
Decreased tissue (e.g. fat, muscle) responsiveness to insulin as
a result of receptor or post receptor defects
Over production of insulin in the early phase
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Over production of insulin in the early phase
Abnormal hepatic glucose regulation
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46. Because it is associated with a slow (over years),
progressive glucose intolerance, the onset of T2D may go
undetected for many years
For approximately 75% of patients, T2D is detected
incidentally
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incidentally
Long term diabetes complications may have
developed before the actual DX of diabetes is
made.
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47. Type1 vs type2 DM
Type 1
Juvenile
Thin at diagnosis
Abrupt onset
Family history
Autoimmune
Type 2
Older age
Obese at diagnosis
Slow onset
Family history
Not autoimmune
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Autoimmune
Ketones typically present
Total insulin defect
Insulin dependent
Not autoimmune
No ketone bodies
Partial insulin
defect/resistance
Insulin requiring
Diet/Oral hypoglycemic
agent
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48. Gestational Diabetes Mellitus (GDM)
Glucose intolerance diagnosed in women during pregnancy
Occurs in approximately 14% of all pregnancies
Pancreas can't provide enough insulin during pregnancy
During pregnancy, gestational diabetes requires treatment
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During pregnancy, gestational diabetes requires treatment
to normalize maternal blood glucose levels to avoid
complications in the infant.
After pregnancy, 5% -10% of women with gestational
diabetes are found to have type II diabetes.
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49. ♣ An abundance of glucose causes excessive insulin production
by the fetus, which, if left uncontrolled, can lead to the
development of an abnormally large fetus.
♣ Infant hypoglycemia at delivery and complications associated
with delivery of a large baby also may occur when blood
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with delivery of a large baby also may occur when blood
glucose levels are not controlled adequately
♣ Gestational diabetes, however, usually does not cause birth
defects.
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50. All women should be screened with an oral glucose
tolerance test (OGTT) between 24-28 weeks of gestation
Any woman diagnosed with GDM should be retested at 6
weeks postpartum
If the fasting plasma glucose (FPG) level is normal, then
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If the fasting plasma glucose (FPG) level is normal, then
reassessment for DM should occur every 3 years
Family planning for subsequent pregnancies should be
discussed and monitoring for development of symptoms
Pregnancy = Normal blood sugar 60-95 mg/dl (or 70-85)
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51. Secondary DM
Account for 1-5% of all diagnosed cases of diabetes
Secondary causes of diabetes mellitus include:
Acromegaly
Cushing syndrome
Thyrotoxicosis
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Thyrotoxicosis
Pheochromocytoma
Chronic pancreatitis
Cancer
Surgery, malnutrition, infections, other illnesses
Drugs etc
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52. Drug induced hyperglycemia
Beta-blockers-Inhibit insulin secretion
Calcium channel blockers -Inhibits secretion of insulin by
interfering with cytosolic calcium release
Corticosteroids-Cause peripheral insulin resistance and
gluconeogenesis
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gluconeogenesis
Fluoroquinolones-Inhibits insulin secretion by blocking ATP
sensitive potassium channels
Phenothiazines-Inhibit insulin secretion
Thiazide diuretics -Inhibit insulin secretion due to hypokalemia.
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53. Clinical manifestation
Hallmark symptoms of all types of DM are the 3Ps:
Polyuria
Polydipsia
Polyphagia
Other symptoms include:
Fatigue and weakness
Sudden vision changes
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Sudden vision changes
Tingling or numbness in hands or feet
Skin lesions or wounds that are slow to heal
Recurrent infections
Sudden weight loss, vomiting, or abdominal pains, fruity breath if
DKA has developed
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54. Diagnosis
History- personal, family, symptoms
Physical examination
Neurology examination
Lab tests
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Lab tests
Gestational DM: OGTT >155 mg/dl -----(best)
FBS >105 mg/dl
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55. Diagnosis…
Sign and Symptoms of diabetes plus RBS ≥ 200 mg/dL
The classic symptoms of diabetes include the 3Ps and
unexplained weight loss
OR
Fasting plasma glucose ≥ 126 mg/dL
Fasting is defined as no caloric intake for at least 8 hours
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OR
2-hour post load glucose ≥ 200mg/dL during an oral glucose
tolerance test.
The test should be performed using a glucose load containing
the equivalent of 75g glucose dissolved in water
Note- Each test must be confirmed, on a subsequent day, under
similar circumstances
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56. Additional diagnostic studies
Serum acetone (ketones)
Serum osmolality
Glucagon
Electrolytes
Arterial blood gases (ABGs)
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Arterial blood gases (ABGs)
CBC
RFT
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57. Diabetes Management
The main goal of diabetes treatment is to
normalize insulin activity and blood glucose
levels
To reduce the development of complications
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To reduce the development of complications
There are five components of diabetes
management
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59. 1. Nutritional therapy
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60. Nutrition, meal planning, and weight control are the foundation
of diabetes management
The goals of nutritional management include:
Providing all the essential food constituents
Meeting energy needs
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Meeting energy needs
Achieving and maintaining reasonable weight
Preventing wide daily fluctuations in blood glucose levels
Decreasing serum lipid levels, if elevated
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61. For obese diabetic patients (especially with T2D) weight
loss is the key to treatment
In general – overweight is considered to be a BMI of 25-29
Obesity is defined BMI equal to or greater than 30
The use of fiber diets:
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The use of fiber diets:
Soluble (legumes, fruits) and
Insoluble (whole grain breads and serials) plays a role in
lowering total cholesterol and low density lipoprotein
cholesterol in the blood
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62. Balanced diet with controlled carbohydrates &
adequate protein & fat
Dietary fat 25-35% of total intake of calories
Cholesterol consumption should be restricted and limited to
300 mg or less daily
Protein(animal and vegetable sources )intake can range
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Protein(animal and vegetable sources )intake can range
between 10-15% total. Requirements increase for children
and during pregnancy
Carbohydrates (complex and high in fiber ) 50-60%
Excessive salt intake is to be avoided. It should be
particularly restricted in people with hypertension and those
with nephropathy
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63. 2. Exercises
Exercise is extremely important in managing diabetes because it
lowers the BGL by:
Increasing the up take of glucose by body mussels
Improving insulin utilization
Exercise recommendations
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People with diabetes should exercise at the same time
(preferably when blood glucose levels are at their peak) and in
the same amount each day
A slow, gradual increase in the exercise period is encouraged
For many patients, walking is a safe and beneficial form of
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64. Who can exercise ?
Those with;
1. Blood glucose less than 250 mg/dl
2. No symptoms of retinopathy
3. No neuropathy
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4. No Nephropathy
5. No cardiovascular problems such as angina,
embolism, or aneurysm
6. No other condition that makes exercise
inadvisable
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65. General precautions for exercise in Diabetes
Use proper foot wear and if appropriate, other
protective equipment
Avoid exercise in extreme cold or heat
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Avoid exercise in extreme cold or heat
Inspect feet daily after exercise
Avoid exercise during periods of poor metabolic
control
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66. 3. Monitoring Glucose levels & ketenes
Blood glucose monitoring is a cornerstone of diabetes
management
Ketones in the urine signal that there is a deficiency of insulin and
control of type 1 diabetes is deteriorating.
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control of type 1 diabetes is deteriorating.
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67. 4. PharmacologicTherapy
Includes treatment with insulin or oral anti- diabetic agents
Decisions in drug treatment should be based primarily on the
type of diabetes and the goals for glycolic control
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Administration of insulin: since it is protein ,it is degraded in the GI
if taken orally. So it should be taken parenterally.
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68. Insulin Therapy and Preparations
Because the body losses the ability to produce insulin in T1D, exogenous
insulin must be administered for life.
In T2D, insulin may be necessary: On a long term basis to control glucose
levels if diet and oral agents fail
For some patients in whom T2D is usually controlled by diet alone or by
diet and oral agents. patients may require insulin temporary during:
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diet and oral agents. patients may require insulin temporary during:
Illness
Infection
Pregnancy
Surgery
Some other stress-full events.
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69. Short-term use
Acute illness, surgery, stress and emergencies
Pregnancy & Breast-feeding
Insulin may be used as initial therapy in type 2 diabetes
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In marked hyper glycaemia
Severe metabolic decompensation (diabetic ketoacidosis,
hyperosmolar non-ketotic coma, lactic acidosis, severe
hypertriglyceridemia)
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70. Long-term use
If targets have not been reached after optimal dose of
combination therapy
A number of insulin preparations are available. They vary
according to three (3) main characteristics:
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according to three (3) main characteristics:
1. Time course of action
2. Species (source)
3. Manufacturer
Reading assignment! Preparations or types.
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71. Insulin injection sites
The four main areas for injection sites are the abdomen, arms
(posterior surface), thigh s(anterior surface), and hips
The speed of absorption is greatest in the abdomen and decreases
progressively in the arm, thigh, and hip
Administering each injection 1.5 –2.5 cm away from the previous injection
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A few general principles apply to all injection rotation patterns. First, patients
should try not to use the same site more than once in 2 to 3 weeks
In addition, if the patient is planning to exercise, insulin should not be injected
into the limb that will be exercised, because it will be absorbed faster, and this
may result in hypoglycemia
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72. Route of insulin injection: Subcutaneous
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73. Complications of insulin therapy
Local allergic reactions : In duration of 2-4 cm may appear at the
injection site 1 to 2 hours after the insulin administration
Systemic allergic reactions: Systemic allergic reactions to insulin
are rare
Insulin lipodystrophy
–Lipoatrophy:-loss of subcutaneous fat appears as a slight dimpling
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–Lipohypertrophy:-development of fibro fatty masses at injection site
Insulin resistance (with obesity, antibodies)
Hypoglycemia:↑ dose, insufficient food income, interaction
with alcohol
Morning hyperglycemia, hypokalemia
Weight gain
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74. Oral Anti-diabetic Agents
May be effective for patients who have T2D that cannot be
treated by diet and exercise alone
Cannot be used during pregnancy
May also be used with insulin in the management of T2D and
Use with insulin may decrease the insulin dosage
Generally oral hypoglycemic have the following effects
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Generally oral hypoglycemic have the following effects
Stimulation of insulin secretion by B cell
Increase cell sensitivity towards insulin
Decrease glucose absorption from GI
Decrease hepatic glucose output & gluconeogenesis
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75. Types of oral hypoglycemic agents
I. Sulphonylureas
Stimulating the beta cells of the pancreas to release insulin
First generation sulfonylureas: chlorpropamide, tolazamide, & tolbutamide
Second and third generations: glimepiride, glipizide, and Glibenclamide
II. Meglitinides
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Stimulates the release of insulin from the pancreas
e.g., ◦Nateglinide, Repaglinide
III. Biguanides
Reduce hepatic glucose production and increasing insulin sensitivity in
muscle and fat cells
e.g., Metformin
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76. IV. Alpha-glycosidase inhibitors
Lower blood sugar by delaying the digestion of carbohydrates
and absorption of carbohydrates in the intestine
e.g., acarbose and miglitol
V. Thiazolidinediones (TZDs)
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V. Thiazolidinediones (TZDs)
Decrease hepatic gluconeogenesis and increasing insulin
dependent muscle glucose uptake
e.g., Rosiglitazone, Pioglitazone
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77. 5. Patient Education
Nutrition
Medication effects and side effects
Exercise
Disease progression
Prevention strategies: blood glucose monitoring techniques,
and medication adjustment
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and medication adjustment
Basic definitions of insulin
Treatment modalities
Recognition, treatment, and prevention of acute
complications
Preventive measures of long term complications
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78. Teaching patients to self administer insulin
Storing insulin
Selecting syringes
Preparing the injection mixing insulin
With drawing insulin
Selecting and rotating the injection site
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Selecting and rotating the injection site
Preparing the skin. Alcohol is not recommended for
cleansing
Inserting the needle
Aspiration is generally not recommended
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79. Acute Complications of Diabetes
Major acute complications of diabetes related to short-term
imbalances in blood glucose levels:
A. Hypoglycemia
B. Diabetic ketoacidosis/DKA
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B. Diabetic ketoacidosis/DKA
C. Hyperglycemic hyperosmolar non-ketotic
syndrome/HHNKS, which is also called hyperglycemic
hyperosmolar syndrome or state
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80. 1. Hypoglycemia (Insulin Reactions)
Occurs when the BGLs falls to < 60mg/dL
Causes
Too much insulin or OHAs
Too little food
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Too little food
Excessive physical activity
Often occurs before meals, especially if meals are delayed
or snacks are omitted
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81. The Clinical manifestations are because of:
1.Adrenergic stimulation
2.Effect of hypoglycemia on CNS
I .Mild hypoglycemia
Stimulation of sympathetic nervous system resulting in a
surge of epinephrine and norepinephrine; in turn results in:
• Sweating
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• Sweating
• Tremor
• Tachycardia
• Palpitation
• Nervousness
• Hunger
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82. II. Moderate hypoglycemia
Drop in BGL deprives the brain cells of needed fuel
for functioning
Signs of impaired function of the CNS may include:
Inability to concentrate
Headache, Light headiness, Adrenergic symptoms:
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Headache, Light headiness,
Confusion, Memory loses,
Slurred speech,
Double vision
Drowsiness,
Numbness of the lips and tongue
Adrenergic symptoms:
Sweating
Tremor
Tachycardia
Palpitation
Nervousness
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83. III. Sever hypoglycemia
Results in:
Impaired CNS functions
Disoriented behavior
Seizures
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Seizures
Difficulty arousing from sleep
Loss of consciousness
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84. Managements of hypoglycemia
A. Immediate treatment with carbohydrate
The usual recommendation is for 15 g of a fast-acting concentrated
source of carbohydrate such as the following, given orally:
A. Three or four commercially prepared glucose tablets
B.100-150 ml of fruit juice or regular soda
C.6 to 10 hard candies
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C.6 to 10 hard candies
D. 2 to 3 teaspoons of sugar or honey
Nursing Alert: To prevent sharp increase in BGL, it is not
necessary to add sugar to juice, even if it is labeled as
unsweetened juice: the fruit sugar in juice contains enough
carbohydrate to raise the BGL
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85. Immediate treatment with carbohydrate…
The BGL should be retested in 15 minutes and
retreated if it is less than 70 to 75 mg/dL
If the symptoms persist for longer than 10 to 15
minutes after initial treatment, the treatment is repeated
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minutes after initial treatment, the treatment is repeated
Once the symptoms resolve, a snack containing protein
and starch (eg, milk or cheese and bananas/crackers) is
recommended unless the patient plans to eat a regular
meal or snack within 30 to 60 minutes
7/30/2019

86. B. Initiating Emergency Measures
Glucagon
Has an onset of 8 to 10 minutes, and its action lasts 12 to
27 minutes
For adults who are unconscious and cannot swallow,
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For adults who are unconscious and cannot swallow,
glucagon 1mg can be administered either subcutaneously
or intramuscularly
After injection of glucagon, the patient may take as long
as 20 minutes to regain consciousness
7/30/2019

87. A concentrated source of carbohydrate:
Should be given to the patient on awakening to prevent
recurrence of hypoglycemia followed by a snack
50%/40% Dextrose in water (D50W/D40W)
For patients who are unconscious or cannot swallow
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For patients who are unconscious or cannot swallow
25 to 50 mL of 50%/40% dextrose in water may be
administered IV
The effect is usually seen within minutes
7/30/2019

88. C. Providing Patient Education
Consistent pattern of eating, administering insulin, and
exercising
Between-meal and bedtime snacks may be needed to
counteract the maximum insulin effect
The patient should cover the time of peak activity of insulin
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The patient should cover the time of peak activity of insulin
by eating a snack and by taking additional food when
physical activity is increased
Routine blood glucose tests to anticipate change insulin
requirements and to adjust the dosage
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89. To prevent unexpected hypoglycemia all patients treated with
insulin should wear an identification bracelet or tag stating that
they have diabetes
Symptoms of hypoglycemia
Patients with diabetes, especially those receiving insulin, learn to
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carry some form of simple sugar with them at all times
Advising to refrain from eating high-calorie, high-fat dessert
foods (eg, cookies, cakes, ice cream) to treat hypoglycemia
because their high fat content may slow the absorption of the
glucose and resolution of the hypoglycemic symptoms
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90. 2. Diabetic Ketoacidosis (DKA)
DKA is a metabolic imbalance in T1D that is caused by an
absence or markedly inadequate amount of insulin
Insulin deficiency results in disorders in the metabolism of
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carbohydrate, protein, and fat
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91. Three main causes:
1. Decreased or missed dose or deficiency of
insulin caused by:
An insufficient dosage of insulin prescribed
An insufficient insulin being administered by the patient
Patient error in drawing up or injecting insulin
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Patient error in drawing up or injecting insulin
Intentional skipping of insulin doses
Equipment problems
2. Illness or infection
3. Undiagnosed and untreated diabetes
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92. Illnesses and infections are associated with insulin resistance
In response to physical (and emotional) stressors, there is an
increase in the level of “stress” hormones:
Glucagon,
Epinephrine, norepinephrine,
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Cortisol
Growth hormone
These hormones promote glucose production by the liver and
interfere with glucose utilization by muscle and fat tissue
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93. The three main clinical features of DKA are:
1.Hyperglycemia
2.Dehydration and electrolyte loss
3.Acidosis
DKA: Diagnosis
BGLs may vary from 300 to 800mg/dL
Serum Bicarbonate 0-15mq/L
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Serum Bicarbonate 0-15mq/L
PH 6.8-7.3
PaCO2 10-30mmHg – Respiratory compensation
Increased creatinine
Increased BUN
Increased hematocrite
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94. DKA: Prevention
If DKA is related to illness, teach the patient about “Sick
day” rules for managing their diabetes when ill
Assess diabetic self management skills including blood
glucose testing and insulin administration
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If insulin dose is intentionally altered, psychological
counseling is recommended for patients and family members
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95. DKA Medical management
Treatment Goals:
1.Treating hyperglycemia
2.Correcting dehydration
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2.Correcting dehydration
3.Maintaining electrolyte balance
4.Reversing acidosis
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96. 1. Rehydration
Is important for maintaining tissue perfusion and to enhance
exertion of excessive glucose by the kidney
Patients may need up to 6-10 liters of IV fluid per day
Initially 0.9% NaCl – 0.5 to 1L per hour for 2 to 3hrs.
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Initially 0.9% NaCl – 0.5 to 1L per hour for 2 to 3hrs.
Use 0.45% NaCl for the patients with hypertension or
hypernatremia or those at risk for heart failure
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97. After the first few hours, 0.45% NaCl (200 to 500ml/hr) if
blood pressure is stable and the serum sodium level is not
low.
When the BGL reaches 300 mg/dL or less, the IV fluid may
be changed to D5W to prevent a precipitous decline in the
BGL.
Monitoring fluid volume status
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Monitoring fluid volume status
Vital Signs- orthostatic changes in BP and PR
Lung assessment
Intake and out put
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98. 2. Restoring Electrolytes
The major electrolyte of concern during treatment of DKA is K+
Some cause of Hypokalemia in DKA treatment include:
Rehydration (decreased plasma volume, decreased serum K+
concentration)
Increased urinary excretion of potassium
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Increased urinary excretion of potassium
Insulin administration(movement of potassium from ECF in to the
cells )
NURSING ALERT Because a patient’s serum potassium level
may drop quickly as a result of rehydration and insulin treatment,
potassium replacement must begin once potassium levels drop to
normal 7/30/2019

99. Cautious but timely K+ replacement is vital to avoid
dysrhythmias that may occur with hypokalemia
As much as 40 mEq/h may be needed for several hours
Frequent (every 2 to 4 hours initially) ECGs and
laboratory measurements of K+ are necessary during the
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laboratory measurements of K+ are necessary during the
first 8 hours of treatment.
K+ replacement is withheld only if hyperkalemia is
present or if the patient is not urinating.
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100. Potassium replacement
Should be according to serum potassium values.
10 meq/h when plasma K+ < 5.5 meq/L, ECG
normal, urine flow and normal creatinine 40–80
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meq/h when plasma K+ <3.5 meq/L
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101. 3. Reversing Acidosis
Acidosis is reversed with insulin to inhibit fat break down,
there by stopping acid build up
Insulin:
20 units of regular insulin (10 units IM, 10 units IV),
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followed by 5 units IM every hour in adults
Blood glucose should be checked every 1-2 hours.
If after the 1st two hours the blood glucose level has not
fallen significantly, dose of IM insulin can be doubled.
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102. When the patient is completely out of ketoacidosis,
regular insulin is given 4 hourly subcutaneously
according to the random blood sugar (RBG) level as
follows:
If RBG > 250mg/dl 12 Units
If RBG - 180-250mg/dl 8 Units
If RBG - 120-180mg/dl 4 Units
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If RBG - 120-180mg/dl 4 Units
If RBG < 120 mg/dl 0 Units
IV fluid solutions with higher concentrations of glucose
such as D5NS or (D50 0.45NS) are administered when
BGLs reach 250-300 mg/dL to avoid too rapid drop in the
BGL.
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103. Insulin must be infused continuously until subcutaneous
administration of insulin resumes
BGLs are usually corrected before acidosis is corrected.
Thus, IV insulin may be continued for 12-24 hrs until
the serum HCO3- level improves to at least 15 to 18
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the serum HCO3- level improves to at least 15 to 18
mEq/L and until the patient can eat
NURSING ALERT
Bicarbonate should be avoided, because of precipitation of
sudden hypokalemia
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104. DKA: Nursing Management
Monitoring fluid and electrolyte status, BGLs, ECG, V/S, ABGs and other
clinical findings
Administering fluids, insulin
Prevent other complications such as fluid over load
As DKA resolved and potassium replacement rate is decreased, the nurse
makes sure that:
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There are no signs of hyperkalemia on the electrocardiogram (tall, peaked or
tented T-waves)
The laboratory, values of potassium are normal or low
The patient is urinating (i.e. no renal shut down)
As the patient recovers, the nurse reassess the factors that may have led to
DKA and teach the patient and family
7/30/2019

105. Hyperglycemic hyperosmolar
non-ketotic syndrome (HHNKS)
Is a metabolic disorder of T2D resulting from a relative
effective insulin deficiency (i.e., Insulin resistance) initiated
by an inter-current illness that raises the demand for insulin,
associated with polyuria and sever dehydration.
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associated with polyuria and sever dehydration.
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
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106. Hyper osmolality and hyperglycemia are predominant
The patient’s persistent hyperglycemia causes osmotic
diuresis, resulting in losses of water and electrolytes.
Because of water shifts from ICF space to ECF space the
patient may present with neurologic abnormalities such as:
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coma
Seizures
Hemiparesis
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107. HHNKS: Diagnosis
History
Physical Examination
BGL 600 to 1200mg/dL
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Electrolytes
BUN
Serum osmolality >350 mosm/kg
ABG analysis – PH normal
7/30/2019

108. HHNKS: Medical Management
The overall approach to the treatment of HHNKS is
similar to that of DKA:
Fluid replacement
Correction of electrolyte imbalances
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Insulin administration
Fluid replacement is started with 0.9% or 0.45% NS,
depending on the patient’s sodium level and the severity
of sodium depletion.
Extremely elevated BGLs drop as the patient is rehydrated
7/30/2019

109. Chronic complications of diabetes
•Affect almost every organ system of the body; Categorized in to:
Macro vascular complications
Coronary artery disease
Cerebrovascular disease
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Cerebrovascular disease
Peripheral vascular disease
Micro vascular complications
Diabetic retinopathy
Nephropathy
Neuropathies 7/30/2019

110. Diabetic retinopathy
Retinopathy has three main stages:
Non proliferative (background),
Pre proliferative, and
Proliferative
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Proliferative
widespread vascular changes (proliferation of new blood
vessels growing from the retina into the vitreous) and
loss of nerve fibers
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111. Retinopathy-Management
Patient education
Controlling BGL
Control of Hypertension
Cessation of smoking
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Cessation of smoking
Vitrectomy: vitreous humor filled with blood or fibrous
tissue is removed and replaced with saline or another
liquid
7/30/2019

112. Diabetic neuropathy
Refers to a group of diseases that affect all types of nerves,
including peripheral (sensorimotor), autonomic, and spinal
nerves
Prevalence increases with the age of the patient and the
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duration of the disease
Etiology of neuropathy may involve elevated BGL over a
period of years
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113. A. Sensory neuropathy leads to loss of pain and pressure
sensation
B. Autonomic neuropathy leads to increased dryness and
fissuring of the skin (secondary to decreased sweating).
C. Motor neuropathy results in muscular atrophy, which may
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C. Motor neuropathy results in muscular atrophy, which may
lead to changes in the shape of the foot.
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114. Nephropathy
The change that damages the kidneys glomeruli
leads the hallmark feature of albuminuria
As progress, glomerular filtration barrier
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As progress, glomerular filtration barrier
damages
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115. Peripheral vascular disease
Poor circulation of the lower extremities contributes to
poor wound healing and the development of gangrene
Immunocompromise
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Hyperglycemia impairs the ability of specialized
leukocytes to destroy bacteria
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116. Foot and Leg problems
Between 50% and 75% of lower extremity amputations are
performed on people with diabetes in USA
More than 50% of these amputations are thought to be
preventable
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preventable
Complications of diabetes that contribute to the increased
risk of foot problems and infections
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117. Foot Care: Patient Education
Take care of your diabetes
Inspect your feet every day
Wash your feet every day
Keep the skin soft and smooth
Smooth corns gently
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Smooth corns gently
Wear shoes and socks at all times
Protect your feet from hot and cold
Keep the blood flowing to your feet
Check with your health care provider
7/30/2019

118. Disorders of the Thyroid Gland
Thyroid gland produces 3 hormones:
A.Thyroxine (T4)
B.Triiodothyronine (T3)
C.Calcitonin
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C.Calcitonin
T3+T4= Iodine molecule + tyrosine (amino acid)
The major use of iodine in the body is by the
thyroid gland
7/30/2019

119. Function of Thyroid Hormone
A. The primary function is to control cellular metabolic activity
T4
Relatively weak hormone
Stored form, not active
Maintains body metabolism in a steady state
T3
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T3
Is about five times as potent as T4
Not stored, active
Has a more rapid metabolic action
B. Influence cell replication and are important in brain development.
C. Necessary for normal growth
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120. Definition of terms
Euthyroid: normal thyroid hormone production
Thyroid storm: severe life-threatening hyperthyroidism
precipitated by stress; characterized by high fever, extreme
tachycardia, and altered mental state.
Thyrotoxicosis: condition produced by excessive endogenous
or exogenous thyroid hormone.
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or exogenous thyroid hormone.
Myxedema: sever form of hypothyroidism characterized by
an accumulation of mucopolysaccharides in subcutaneous and
other interstitial tissues; mask like expression, puffy eyelids,
hair loss in the eyebrows, thick lips and a broad tongue.
Myxedema coma: The most extreme, sever stage of
hypothyroidism. 7/30/2019

121. Hypothyroidism
Results from suboptimal levels of thyroid hormone
During fetal and neonatal development, it results in
stunted physical and mental growth (cretinism)
because of general depression of metabolic activity
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In adults, may result in:
Lethargy,
Slow mentation,
Generalized slowing of body functions.
7/30/2019

122. Causes
Primary causes
1. Decreased thyroid tissue
Autoimmune thyroiditis: Hashimoto’s disease most common
Thyroidectomy, Radiation, Cancer
Congenital thyroid agenesis (failure to develop)
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Congenital thyroid agenesis (failure to develop)
2. Decreased synthesis of TH
Endemic iodine deficiency
Anti-thyroid medications
Radioiodine, Methimazole
7/30/2019

123. Secondary causes
Inadequate production of TSH
Pituitary or hypothalamic tumors, infection, or infarction
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Pituitary or hypothalamic tumors, infection, or infarction
Congenital pituitary defects
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124. Ayelign M.
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125. Clinical manifestations
Fatigue
Hoarseness
Weight gain
Hypothermia
Loss of outer third of
eyebrow ,hair loss
Constipation
Cool, rough, dry skin
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Hypothermia
Cold intolerance
Peri-orbital puffiness
Depression
Cool, rough, dry skin
Bradycardia
Peripheral neuropathy
7/30/2019

126. Diagnosis
History
Physical Examination
Lab:
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Serum TSH
high – when the defect is in the thyroid
low – when the defect is in the pituitary or hypothalamus
Serum T3 and T4
7/30/2019

127. Thyroid Function tests
Serum T3 70-200 ng/dl
Serum T4 4.0-12.0 mcg/dl
TSH 0.25-4.30 micro units/ml
ECG –Sinus bradycardia, flat or inverted T waves
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ECG –Sinus bradycardia, flat or inverted T waves
Use of aspirin, corticosteroids, phenytoin sodium may
cause a false decrease in serum thyroid hormone levels
7/30/2019

128. Management
Objective – restoring normal metabolic state
A. Pharmacologic Therapy
Synthetic levothyroxine (Synthroid, Levothroid)
Treatment begins slowly and the dosage increases
every 2 to 3 weeks until the desired response is
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every 2 to 3 weeks until the desired response is
obtained
If replacement therapy is adequate, the symptoms of
myxedema disappear and normal metabolic activity is
resumed 7/30/2019

129. B. Supportive Therapy
In severe hypothyroidism and myxedema coma, management
includes maintaining vital functions.
Use of assisted ventilation to combat hypoventilation based
on ABGs result
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on ABGs result
Treating hypoglycemia if occurred
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130. Myxedema coma
This serious condition may occur gradually (over years) or
more acutely in response to a precipitating factors such as
exposure to cold, infection, stress, hypoglycemia, respiratory
depressants, allergic reactions, CHF
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Usually occur in individuals with long-standing
hypothyroidism
More common in elderly women with under-diagnosed or
under-treated hypothyroidism
7/30/2019

131. Treatment
Admit patient to a monitored setting
L-thyroxin (T4) 500 µg is given as IV bolus slowly, followed
by oral L-thyroxin 100 µg QID
L-triiodothyronine(T3) 25 µg IV or PO TID
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L-triiodothyronine(T3) 25 µg IV or PO TID
Hypoglycemia –Dextrose-containing IV fluids (monitoring)
Hypothermia and heat loss should be avoided
7/30/2019

132. Hyperthyroidism
• Is the second most prevalent endocrine disorder after DM.
Excess synthesis and secretion of thyroid hormones by the
thyroid gland, which results in accelerated metabolism.
Causes
Graves’ disease is the most common cause
Is an autoimmune syndrome that includes hyperthyroidism,
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Is an autoimmune syndrome that includes hyperthyroidism,
diffuse goiter, ophthalmopathic changes (exophtalmia) and skin
findings (local dermopathy)
Thyroiditis
After an emotional shock, stress, or infection
Excessive ingestion of thyroid hormones
7/30/2019

133. Clinical manifestations
Nervousness
Emotionally hyper excitable, irritability
They cannot sit quietly
Heat intolerance
Unusual perspiration
Palpitation
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Palpitation
Increased sweating
PR 90-160 beats/min
Myocardial hypertrophy
heart failure
7/30/2019

134. Clinical manifestations…
Increased appetite and progressive weight loss
Elevated BP
Warm, moist skin
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Exophthalmos
Dyspnea
Increased gastrointestinal motility
7/30/2019

135. Diagnosis
History
Physical Exam
Enlarged thyroid gland to some extent
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Lab tests
Increased T3 and T4
7/30/2019

136. Mgt
Objective reducing thyroid hyperactivity
A. Pharmacologic therapy
Irradiation by radioisotope I123 or I131 , causes a decrease
in function and size of the thyroid gland in 6-12 weeks
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Propylthiouracil 100–200 mg Qid or Tid and
methimazole 10–20 mg Tid or Bid
Propranolol 80-160 mg every 6hr,to control the
sympathetic nervous system effects of hyperthyroidism
7/30/2019

137. B. Surgical management- total or subtotal thyroidectomy
C. Adjutant therapy
Strong iodine (Lugol’s ) solution reduce the activity of TH
(Suppresses release of thyroid hormone) and the vascularity
of the thyroid gland making the surgical procedure safer
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of the thyroid gland making the surgical procedure safer
7/30/2019

138. Thyroid Tumors
If the enlargement of thyroid gland is sufficient to
cause a visible swelling in the neck, the tumor is
referred to as a goiter
Some goiters are:-
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Symmetric and diffuse
Accompanied by hyperthyroidism (toxic goiter)
Accompanied by euthyroidism (non-toxic goiter)
Accompanied by hypothyroidism
7/30/2019

139. Endemic (Iodine Deficient) Goiter
Is the most common type of goiter, encountered briefly
in geographic regions when the natural supply of
iodine is deficient
Is also called simple or colloidal goiter
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Is also called simple or colloidal goiter
Cause
geographically iodine deficiency
large intake of goiterogenic substances in patients with
unusually susceptible gland
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140. Ayelign M.
140 7/30/2019

141. Clinical Manifestation
Usually no symptoms except for the enlargement in the
neck, which may result in tracheal compression when
excess
Diagnosis
TSH and serum T4 are measured to determine whether a
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TSH and serum T4 are measured to determine whether a
goiter is associated with hyperthyroidism,
hypothyroidism
Provision of iodized salt has been the single most
effective means of preventing goiter in at risk
populations
7/30/2019

142. Disorders of the parathyroid gland
Hypoparathyroidism
This is a diminished functioning of the parathyroid
glands leading to low levels of PTH.
This causes hypocalcemia.
This causes hypocalcemia.
The primary cause is destruction of the glands by an
autoimmune rxn.
Occasionally the glands may be accidentally
removed during thyroidectomy.
7/30/2019
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143. Clinical Manifestation
Tetany due to abnormal levels of calcium
Tingling of periorbital area, hands and feet from
abnormal calcium levels.
Lethargy due to low levels of parathyroid hormone
Lethargy due to low levels of parathyroid hormone
Convulsions due to acute low calcium levels
7/30/2019
143
143 Ayelign M. 7/30/2019

144. Diagnosis
Decreased serum Calcium due to low levels of PTH.
Increased serum phosphate due to low levels of PTH.
Decreased urinary calcium from diminished PTH.
Trousseau’s sign is positive when carpopedal spasm is
induced by occluding the blood flow to the arm for 3
minutes with a blood pressure cuff (20mmhg above
minutes with a blood pressure cuff (20mmhg above
Normal systole).
Chvostek’s sign is positive when 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.
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144
144 Ayelign M. 7/30/2019

145. Positive Trousseau’s Sign
145 Ayelign M. 7/30/2019

146. Positive Chvostek’s Sign
146 Ayelign M. 7/30/2019

147. Diagnosis…
Normal serum values
Ca ++= 8.5 -10.2 mg/dl
Phosphorus = 2.0 -4.3 mg/dl
PTH = 10 -60 pg/ml
147 Ayelign M. 7/30/2019

148. Treatment
Initiate seizure precaution
Administer calcium gluconate by slow IV drip for acute
hypocalcemia
Oral calcium carbonate
Large doses of vitamin D (calciferol) to help absorption of calcium.
For Tetany administer calcium gluconate 2-3gm over 10minutes
intravenously.
Diet rich in Ca++ (Oats, beans, green leafy vegetables,
cereals, diary products, Juices)
7/30/2019
148
148 Ayelign M. 7/30/2019

149. Hyperparathyroidism
Hyperparathyroidism, is overproduction of parathyroid hormone
by the parathyroid glands; is characterized by bone decalcification
and the development of renal calculi (kidney stones).
Cause:- Tumor
Excess calcium is reabsorbed by the kidneys and may result in
kidney stones.
Parathyroid tumors are usually benign.
Patients can expect a normal life span once the parathyroid tumor
is removed
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149 Ayelign M. 7/30/2019

150. Sign/Symptoms
Asymptomatic usualy
Increased serum calcium level
Bone pain or fracture
Kidney stones
Kidney stones
Frequent urination as a result of hypercalciuria
Osteoporosis, abdominal pain and other GI symptoms, such
as anorexia, constipation, nausea, and vomiting; muscle
weakness, particularly in legs; and lethargy.
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150 Ayelign M. 7/30/2019

151. DIAGNOSTIC TEST RESULTS
Increased serum calcium.
Increased serum PTH.
Decreased serum phosphate
Increased urine calcium
Parathyroid tumor seen on ultrasound
Fine needle biopsy of the parathyroid tumor
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151 Ayelign M. 7/30/2019

152. MANAGEMENT
Surgical removal of the parathyroid tumor.
Administer biphosphonates to lower serum calcium by increasing
calcium absorption in the bone.
IV normal saline to dilute serum calcium.
Diuretic such as furosemide to excrete excess calcium in the urine
Hydration therapy with a fluid intake of 2,000 mL or more is
encouraged to help prevent calculus formation.
Dialysis for renal failure
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152 Ayelign M. 7/30/2019

153. DISORDERS OF ADRENAL GLANDS
Cushing’s disease/syndrome (over secretion
of adrenal cortex)
Addison’s disease(adrenal hypofunction)
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153
Addison’s disease(adrenal hypofunction)
Pheochromocytoma
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154. 154 Ayelign M. 7/30/2019

155. Cushing’s Syndrome
• A state of chronic glucocorticoid excess leading to
constellation of symptoms and signs of hypercortisolism
regardless of the cause.
• It is characterized by adrenal glands hyper functioning as
• It is characterized by adrenal glands hyper functioning as
a result of an excessive amount of cortisol or ACTH
circulating in blood
• High levels of cortisol reduce lymphocyte activity which
creates immunosuppression.
155 Ayelign M. 7/30/2019

156. Cause
Use of corticosteroid medications
Excessive corticosteroid production secondary
to hyperplasia of the adrenal cortex
Overproduction of endogenous corticosteroids
Tumor of the pituitary gland that produces ACTH
and stimulates the adrenal cortex
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157. Signs and Symptoms
• S/S are primarily a result of over secretion of
glucocorticoids and androgens.
• S/S include:
Central-type obesity
Central-type obesity
Fatty “buffalo hump” in the neck
A heavy trunk
Relatively thin extremities.
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158. Thin, fragile, easily traumatized skin; ecchymosis and striae
Weakness
Sleep disturbance
Excessive protein catabolism:
Muscle wasting and osteoporosis
Muscle wasting and osteoporosis
Moon-faced” appearance
Increased oiliness of the skin and acne
Hyperglycemia
Weight gain
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159. Diagnosis
• Elevated Plasma cortisol levels
• Overnight dexamethasone suppression test
Dexamethasone (1 mg) is administered orally at 11 PM,
Plasma cortisol level is obtained at 8 AM next morning
Plasma cortisol level is obtained at 8 AM next morning
Suppression of cortisol to less than 5mg/dL indicates
that the hypothalamic–pituitary–adrenal axis is
functioning properly.
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160. • Measurement of plasma ACTH: Elevation of both ACTH and
cortisol indicates pituitary or hypothalamic disease.
• A low ACTH with a high cortisol level indicates adrenal disease
• CT, ultrasound, or MRI: to localize adrenal tissue and detect
tumors of the adrenal gland.
• Serum glucose level: Increased
• Serum potassium and calcium levels: Decreased
• Serum sodium level: Increased
160 Ayelign M. 7/30/2019

161. Mgt
If caused by pituitary tumors:
• Surgical removal of the pituitary gland (has 80% success rate)
• Radiation of the pituitary gland
• Adrenalectomy if primary adrenal hypertrophy
• Adrenalectomy if primary adrenal hypertrophy
• Post-operatively: Temporary replacement therapy with
hydrocortisone for several months.
• Lifetime replacement of adrenal cortex hormones in case of
bilateral adrenalectomy.
161 Ayelign M. 7/30/2019

162. Addison’s disease
• Life-threatening disease process due to failure of the
adrenal cortex to secrete adequate mineralocorticoids and
glucocorticoids.
• Resulting from an autoimmune dysfunction, neoplasm,
infarctions, infections (TB, fungal infections, and
infarctions, infections (TB, fungal infections, and
HIV/AIDS, or a hemorrhage in the gland)
Primary adrenal insufficiency
Hypocortisolism
Hypoaldosteronism
162 Ayelign M. 7/30/2019

163. Clinical manifestations
Hyponatremia
Hyperkalemia
Hypotension
Hypoglycemia
Weakness/fatigue
Hypercalcemia
Dizziness with orthostatic
Dehaydration
Nausea and vomiting
Weight loss
Dizziness with orthostatic
hypotension
Bronzing of the skin due to
hyper pigmentation from the
autoimmune disease
163
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164. Diagnosis
• Serum electrolytes: increased K+ & Ca++
• Decreased Na+
• ECG: Dysrhythmias
• Serum glucose: Decreased
• Serum glucose: Decreased
• Serum cortisol: Decreased
Positive ACTH stimulation test; ACTH acts on the adrenal
cortex to stimulate adrenal hormone secretion.
An infusion of ACTH is given and the test is positive if the
infusion fails to raise the cortisol level.
164
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165. General management
Restore circulatory status—fluids, steroids
May need antibiotics if infection precipitated crisis
May need lifelong steroid therapy and
mineralocorticoid therapy
May need additional salt intake
Daily weights
Aware that stressors can precipitate crises
165
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166. General management…
IV glucose and insulin (treats both hypoglycemia and
hyperkalemia)
IV hydrocortisone or fludrocortisone
Use stress reducing behavior and adjust medications
Monitor for and treat hypoglycemia: Perform frequent
checks of the client’s neurologic status and monitor for
signs and symptoms of hypoglycemia.
166
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167. Disorder of the pituitary Glands
167
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168. 168
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169. Disorders of the Pituitary gland
Abnormalities of the pituitary gland result from:
Over-secretion or under-secretion
Over-secretion most commonly involves ACTH leading
to Cushing's syndrome, or GH leading to acromegaly.
Acromegaly-an excess of growth hormone in adults,
results in bone and soft tissue deformities and
enlargement of the viscera without an increase in height.
Gigantism- over-secretion of growth hormone in
children.
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170. Cont…
Insufficient secretion of growth hormone during childhood
results in generalized limited growth and dwarfism.
Under-secretion commonly involves all of the anterior
pituitary hormones.
In this condition, the thyroid gland, the adrenal cortex, and
In this condition, the thyroid gland, the adrenal cortex, and
the gonads atrophy (shrink).
Pan hypopituitarism is total absence of all pituitary
secretions and it is rare.
The most common disorder related to posterior lobe
dysfunction is diabetes insipidus.
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171. ↑GH as Juvenile ↓GH = pituitary
dwarfism
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172. Diabetes Insipidus (DI)
Is a disorder of the posterior lobe of the pituitary
gland that is characterized by a deficiency of
ADH (vasopressin).
172
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173. DI: Types
There are three types of diabetes insipidus:
A. Neurogenic diabetes insipidus
A deficiency with ADH (antidiuretic hormone)
B. Nephrogenic diabetes insipidus
Insensitivity of the kidneys to ADH
C. Gestational diabetes insipidus
In very rare cases DI may also occur during pregnancy
173
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174. DI Causes
A. Central DI (cranial diabetes insipidus)
Damage to the hypothalamus or the pituitary glands which
result in disruption of ADH production, storage and release.
This may be caused by:
– Head trauma,
– Brain tumor
– Surgical ablation or irradiation of the pituitary gland
– Infections of the central nervous system (meningitis, encephalitis,
tuberculosis)
174
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175. Cont…
B. Nephrogenic DI
• Caused when kidneys do not respond properly to ADH
which may be caused by:
– Congenital problem (inherited disorder) or
– Some chronic (long-term) kidney disorder
– Lithium, tetracycline and some other medications
C. Gestational DI
• Occurs during pregnancy.
• An enzyme produced by the placenta may destroy ADH in the
mother.
175
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176. DI: C/Ms
• Enormous daily output of very dilute Water like urine
• Urine specific gravity of 1.001 to 1.005 (normal urine SG
1.010 to 1.025 )
• Urine contains no abnormal substances such as glucose
or albumin
• Intense thirst: the patient tends to drink 2 to 20 L of fluid
daily and craves cold water.
• DI cannot be controlled by limiting fluid intake
• Signs of dehydration in some individuals
176
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177. DI: Diagnosis
Fluid deprivation test:
Carried out by withholding fluids for 8 to 12 hours or
until 3% to 5% of the body weight is lost.
The patient is weighed frequently during the test
The patient is weighed frequently during the test
Plasma and urine osmolality studies are performed at
the beginning and end of the test
The inability to increase the specific gravity and
osmolality of the urine is characteristic of DI.
177
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178. Fluid deprivation test cont…
• The patient continues to excrete large volumes of
urine:
Low specific gravity
Experiences weight loss
Increasing serum osmolality
Increasing serum osmolality
Elevated serum sodium levels
The test should be terminated if tachycardia,
excessive weight loss, or hypotension develops.
• Plasma levels of ADH
• Plasma and urine osmolality
178
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179. DI: Medical Management
The objectives of therapy are:
To replace ADH (which is usually a long-term
therapeutic program)
therapeutic program)
To ensure adequate fluid replacement
To identify and correct the underlying
intracranial pathology or Nephrogenic causes.
179
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180. DI: Medical Management…
• Pharmacologic Therapy
• Desmopressin (DDAVP), a synthetic
vasopressin without the vascular effects of
natural ADH.
• Treat cause
180
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181. Syndrome of Inappropriate Antidiuretic
Hormone Secretion (SIADH)
• Includes excessive ADH secretion from the
pituitary gland even in the face of subnormal
serum osmolality
serum osmolality
• Patients cannot excrete a dilute urine, retain
fluids, and develop a sodium deficiency:
dilutional hyponatremia
181
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182. SIADH: Causes
• When the level of ADH increased, SIADH will
occur
• S sign of infection
• I intoxication
• A altered LOC
• D delusional hyponatremia
• D delusional hyponatremia
• H hypervolumia ,HTN
Disorders of CNS that cause direct stimulation of
the pituitary gland:
– Head injury
– Brain surgery or tumor
– Infection
182
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183. SIADH: Signs & symptoms
Decreased / Low urine output
Symptoms of hyponatremia
Lethargy, apathy, disorientation, muscle cramps, anorexia,
agitation.
agitation.
Symptoms of water toxicity
Nausea, vomiting, personality changes, confusion
If Na < 110 mEq/L
seizures, hypothermia, stupor, coma
183
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184. SIADH: Diagnosis
Serum Na < 135 (Na is diluted by excessive free water
re-absorption)
Serum osmolality low (normal 280 to 300 mOsm/kg)
Urine Na is inappropriately high, >20 mmol/L (actually
Urine Na is inappropriately high, >20 mmol/L (actually
losing Na in urine instead of retaining it)
Normal: 25-250 mmol/L
Urine osmolality is inappropriately high, can range
between 300-1400 mosm/l (normal: 200 to 800
mOsm/kg)
184
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185. SIADH: Diagnosis…
Imaging studies
CT scan of the head
Evidence of cerebral edema
Identify a CNS disorder responsible for SIADH (e.g, Brain
tumor)
Rule out other causes of acute changes in neurological status
185
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186. SIADH: Management
• Elimination of the underlying cause
• Restricting fluid intake
• Demeclocycline
Can be used in chronic situations when fluid
restrictions are difficult to maintain
restrictions are difficult to maintain
Is the most potent inhibitor of Vasopressin
(ADH/AVP) action
• Diuretics such as furosemide (Lasix) may be used
• Close monitoring of fluid intake and output, daily
weight, urine and blood chemistries, and neurologic
status
186
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187. PHEOCHROMOCYTOMA
Pheochromocytoma is a tumor that is usually benign and
originates from the chromaffin cells of the adrenal
medulla.
• In 80% to 90% of patients the tumor arises in the medulla;
in the remaining patients, it occurs in the extra-adrenal
chromaffin tissue located in or near the aorta, ovaries,
spleen, or other organs.
• Pheochromocytoma may occur at any age, but its peak
incidence is between ages 40 and 50 years.
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188. CON…
• Ten percent of the tumors are bilateral, and 10%
are malignant.
• Pheochromocytoma is the cause of high blood
pressure in 0.2% of patients with new onset of
hypertension.
hypertension.
• Although it is uncommon, it is one form of
hypertension that is usually cured by surgery;
without detection and treatment, it is usually
fatal.
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189. Clinical Manifestations
• The nature and severity of symptoms depend on the relative
proportions of epinephrine and nor-epinephrine secretion.
• The typical triad of symptoms comprises headache, diaphoresis,
and palpitations.
• Hypertension and other cardiovascular disturbances are common.
• Hypertension and other cardiovascular disturbances are common.
• Other symptoms may include tremor, headache, flushing, and
anxiety.
• Hyperglycemia may result from conversion of liver and muscle
glycogen to glucose by epinephrine secretion.
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190. Con…
• The clinical picture in the paroxysmal form of
pheochromocytoma is usually characterized by acute,
unpredictable attacks lasting seconds or several hours.
• During these attacks, the patient is extremely anxious,
tremulous, and weak.
• The patient may experience headache, vertigo, blurring of
vision, tinnitus, air hunger, and dyspnea.
vision, tinnitus, air hunger, and dyspnea.
• Other symptoms include polyuria, nausea, vomiting,
diarrhea, abdominal pain, and a feeling of impending
doom.
• Blood pressures exceeding 250/150 mm Hg have been
recorded.
• Postural hypotension occurs in 70% of patients with
untreated pheochromocytoma.
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191. Assessment and Diagnostic Findings
• Pheochromocytoma is suspected if signs of sympathetic nervous system
over-activity occur in association with marked elevation of blood
pressure.
• These signs can be associated with the “five Hs”: hypertension,
headache, hyperhidrosis (excessive sweating), hypermetabolism, and
hyperglycemia.
hyperglycemia.
• The presence of these signs has a 93.8% specificity and a 90.9%
sensitivity for Pheochromocytoma.
• Absence of hypertension excludes pheochromocytoma with a 99%
certainty.
• Paroxysmal symptoms of pheochromocytoma commonly develop in the
fifth decade of life.
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192. Con …
• Measurements of urine and plasma levels of catecholamine's are
the most direct and conclusive tests for overactivity of the adrenal
medulla.
• Measurements of urinary catecholamine metabolites
(metanephrines [MN] and vanillylmandelic acid[VMA]) or free
catecholamines are the standard diagnostic tests used in the
diagnosis of pheochromocytoma.
diagnosis of pheochromocytoma.
• Levels can be as high as three times normal limits.
• A 24-hour specimen of urine is collected for determining free
catecholamines, MN, and VMA; the use of combined tests
increases the diagnostic accuracy of testing.
• A number of medications and foods (eg, coffee, tea, bananas,
chocolate, vanilla, aspirin) may alter the results of these tests;
• Therefore, careful instructions to avoid restricted items must be
given to the patient.
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193. CONT…
• Normal plasma values of epinephrine are 100 pg/Ml (590
pmol/L); normal values of norepinephrine are generally less than
100 to 550 pg/mL (590 to 3,240 pmol/L).
• Values of epinephrine greater than 400 pg/mL (2,180 pmol/L) or
• Values of epinephrine greater than 400 pg/mL (2,180 pmol/L) or
norepinephrine values greater than 2,000 pg/mL (11,800 pmol/L)
are considered diagnostic of pheochromocytoma.
• Values that fall between normal values and those diagnostic of
pheochromocytoma indicate the need for further testing.
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194. CONT…
• A clonidine suppression test may be performed if the results of
plasma and urine tests of catecholamines are inconclusive.
• Clonidine is a centrally acting, antiadrenergic medication that
suppresses the release of neurogenically mediated
catecholamines.
• The suppression test is based on the principle that catecholamine
• The suppression test is based on the principle that catecholamine
levels are normally increased through the activity of the
sympathetic nervous system.
• In pheochromocytoma, increased catecholamine levels result
from the diffusion of excess catecholamines into the circulation,
bypassing normal storage and release mechanisms.
• Therefore, in patients with pheochromocytoma, clonidine does
not suppress the release of catecholamines.
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195. CONT…
• The results of the test are considered normal if 2 to 3 hours
after a single oral dose of clonidine, the total plasma
catecholamine value decreases at least 40% from baseline.
• Patients with pheochromocytoma exhibit no change in
catecholamine levels. False-positive results, however, may
occur in patients with primary hypertension.
• Imaging studies, such as CT scans, MRI, and ultrasound, may
also be carried out to localize the pheochromocytoma and to
determine whether more than one tumor is present.
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196. Medical Management
• During an episode or attack of hypertension, tachycardia, anxiety,
and the other symptoms of pheochromocytoma, the patient is
placed on bed rest with the head of the bed elevated to promote an
orthostatic decrease in blood pressure.
PHARMACOLOGIC THERAPY
PHARMACOLOGIC THERAPY
• The patient may be moved to the intensive care unit for close
monitoring of ECG changes and careful administration of alpha-
adrenergic blocking agents (eg, phentolamine or smooth muscle
relaxants (eg, sodium nitroprusside to lower the blood pressure
quickly.
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197. Con…
• Oral preparations of corticosteroids (prednisone) will be
prescribed after the acute stress of surgery diminishes.
• Beta-adrenergic blocking agents, such as propranolol
may be used in patients with cardiac dysrhythmias or
those not responsive to alpha-blockers.
those not responsive to alpha-blockers.
• Alphaadrenergic and beta-adrenergic blocking agents
must be used with caution because patients with
pheochromocytoma may have increased sensitivity to
them.
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198. SURGICAL MANAGEMENT
• The definitive treatment of pheochromocytoma is surgical removal
of the tumor, usually with adrenalectomy.
• Bilateral adrenalectomy may be necessary if tumors are present in
both adrenal glands.
• Patient preparation includes control of blood pressure and blood
• Patient preparation includes control of blood pressure and blood
volumes; usually this is carried out over 7 to 10 days.
• Phentolamine or phenoxybenzamine may be used safely without
causing undue hypotension.
• Other medications (metyrosine and prazosin have been used to
treat pheochromocytoma).
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199. Cont…
• Manipulation of the tumor during surgical excision may cause
release of stored epinephrine and norepinephrine, with marked
increases in blood pressure and changes in heart rate.
• Therefore, use of sodium nitroprusside (Nipride) and alpha-
adrenergic blocking agents may be required during and after
surgery.
surgery.
• Corticosteroid replacement is required if bilateral adrenalectomy
has been necessary.
• Corticosteroids may also be necessary for the first few days or
weeks after removal of a single adrenal gland.
• Intravenous administration of corticosteroids
(methylprednisolone sodium succinate [Solu-Medrol]) may
begin the
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200. Thank You Very
Much
For Your Attention!!!
For Your Attention!!!
200
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