Endocrine dysfunction

1. Care of A Child with
Endocrine
Disorders
By
Abbaskha
n BSN, Dip
Peads, IP&C, CHPE
Lecturer KMU

2. Overview of Hypothalamus

3. Hormones by Pituitary Gland
1. Anterior Pituitary (Hormones) produce:
• Growth Hormone (GH)
• Lutenizing Hormone (LH)
• Follicle Stimulating Hormone (FSH)
• ACTH (Adenocorticotropic Hormone)
• TSH (Thyroid Stimulation Hormone)
• Prolactin Hormone (PL)

4. Hormones by Pituitary Gland
2. Posterior Pituitary (Hormones) produce:
The posterior gland produces oxytocin and
stores Vasopressin (ADH) antidiuretic
hormone (produced in hypothalamus)

6. Pituitary Disorders of
Growth & Development
• Gigantism- over secretion of somatotrophin,
causes overgrowth of skeleton and soft tissues.
• Acromegaly-Complication of gigantism
involving enlargement of the head, hands and
feet.
• Pituitary Dwarfism-caused by under
secretion of somatotrophin, causes stunting of
growth.

7. Disorders of Growth Hormone
Dwarfism
Gigantism
Acromegaly

8. Growth Hormone (GH):
⚫Growth hormone (GH) or
somatotropin
(STH) is a protein hormone.
⚫It is a 191-amino acid,
single chain polypeptide
hormone
⚫Synthesized, stored, and
secreted by the somatotroph
cells of the anterior pituitary
gland.

9. “Gigantism”

10. Pituitary Hyper Function
Definition:
Excess GH before the epiphysis fuse cause
“gigantism”
In children (over growth of long bones) if
hyper secretion of GH after epiphysis fusion.
Growth in transverse direction, producing a
condition known as “acromegaly in
adults”

11. ⚫Direct effects are the result of
growth hormone binding its receptor
on target cells
⚫Protein metabolism: the growth
hormone stimulates protein
anabolism in many tissues. This
means increased amino acid uptake,
increased protein synthesis and
decreased oxidation of proteins.
Physiologic Effects of Growth Hormone:

12. Physiologic Effects of Growth
Hormone:
• Fat metabolism: The growth hormone
increases the utilization of fat by stimulating
triglyceride breakdown and adipocytes
oxidation (fat cells).
• Carbohydrate metabolism: The growth
hormone is often said to have anti-insulin
activity, because it suppresses the ability of
insulin to stimulate glucose uptake in
peripheral tissues, and increases glucose
synthesis in the liver.

13. Physiologic Effects of Growth Hormone:
• Indirect effects are mediated primarily
by a insulin-like growth factor-I (IGF-I),
a hormone that is secreted from the liver
and other tissues in response to growth
hormone. A majority of the growth
promoting effects of growth hormone is
actually due to IGF-I acting on its target
cells.

15. GH deficiency
–Interferes with linear bone growth
–Results in short stature or dwarfism
GH excess
–Results in increased linear bone growth
–Gigantism
Growth Hormone in
Children:

16. • Most common cause (95%)
– Somatotrope adenoma
• Other causes (<5%)
– Excess secretion of GHRH by hypothalamic tumors
– Ectopic GHRH secretion by non-endocrine tumors
such as carcinoid tumors or small cell lung cancers
– Ectopic secretion of GH by non-endocrine tumors
Causes

17. Features that result from high level of GH or
expanding tumor include:
• Soft tissue swelling of the hands and feet
• Lower jaw protrusion
• Broad and bulbous nose
• Enlarging hands
• Enlarging feet
• Arthritis and carpal tunnel syndrome
• Teeth spacing increase
• Macroglossia [enlarged tongue]
• Heart failure
• Kidney failure
Clinical Manifestation

18. • Compression of the optic chiasm leading to loss of
vision in the outer visual fields
• Compression of other pituitary structures can cause
secondary hypothyroidism hypogonadism & adrenal
insufficiency.
• Headache
• Impaired glucose tolerance lead to Diabetes mellitus
• Hypertension
• Enlarging heart
• Increased palmer sweating and sebum production over
the face (seborrhea)
• Cartilaginous structure of larynx and respiratory tract
also enlarged resulting deepening of voice and
bronchitis
• Kyphosis or hunchback

19. • Hormonal
– IGF1 provides the most sensitive and useful lab test for the
diagnosis of gigantism.
• Radiological
–An MRI of the brain focussing on the sella turcica for clear
demarcation of the pituitary and the hypothalamus and the
location of the tumor.
Diagnosis

20. • CT scan
• MRI
• Skull x-ray
• Blood work: Elevation in growth hormone
level.
Diagnostic Test

21. • Normalization of the GH to prevent or reverse
progression of the discorder
• Normalization of IGF-1 levels to age- and sex-
matched control levels
• Removal or reduction of the tumor mass
• Improvement of adverse clinical features
• Normalization of the mortality rate
Treatment Goals :

22. • Provide pain relief for joint pain
• Provide emotional support
• Irradiation of the tumor
• Life long hormone replacement
• Dopamine agonists
• Cryosurgery to destroy tissue
Treatment

23. • Medication for headache & joint pain
• Soft diet
• Encourage fluids
• Safety concerns due to possible visual
disturbances
• Self esteem issues
Educate that medication therapy is
lifelong
Nursing Interventions

24. • Short stature is a condition in which the attained
height is well below the fifth percentile or linear
growth is below normal for age and sex.
Dwarfism or Short stature :

25. Dwarfism

26. • Genetic short stature
• Chronic illness and malnutrition
- Renal failure
- Nutritional deprivation
• Functional endocrine disorders
- Psychological dwarfism
• Chromosomal disorders
- Turner’s syndrome
• Skeletal abnormalities
Causes of Short Stature:

27. • Primary GH deficiency
- Idiopathic GH deficiency
- Pituitary agenesis
(Panhypopituitarisim)
• Secondary GH deficiency
- Hypothalamic- pituitary tumor
- Head injuries, Brain
infection & hydrocephalus
• Biologically inactive GH production
• Hereditary defect in IGF receptor
• Hypothyroidism
• Diabetes mellitus in poor control
Causes cont…

29. • X ray of wrist to evaluate bone age
• Blood work indicates that growth hormone level is
decreased
• CT, MRI of the head
Diagnostics

30. • Pituitary Dwarfism: Removal of cause of
dysfunction (tumor, cyst)
• administration of steroids (growth hormones)
to promote growth and development.
Nursing intervention
•Accommodations for patients size must
be taken into consideration such as
commode, height of sink, etc.
Treatment

31. Pituitary Hypo Function
• Also known as underactive pituitary gland that
affects the anterior lobe of the pituitary gland
resulting in a partial or complete loss of
functioning
1 PANHYPOPITUITARISM
• In some cases, the production of all of the
pituitary hormones decreases or stops, usually
due to damage to the entire pituitary gland
• This condition is called Panhypopituitarism

32. Symptoms of PHP
Depending on what hormones are
insufficiently produced by Pituitary gland
• Insufficient gonadotropins production
• Insufficient growth hormone
• Insufficient prolactin production
• Insufficient thyroid stimulating
hormone production

33. Causes of Growth Hormone
Disorder
Several possible mechanisms that results in GHD
• Genetic defect, (gene present on chromosome
# 17)
• Tumor of hypothalamus or pituitary gland
• Disease of brain (tuberculosis)
• An autoimmune attack
• Idiopathic (unknown)
• Trauma

34. Diagnostic Evaluation GHD
• Family & Child history/ physical
examination
• Radiographic survey / Bone X-ray
(A child’s bone age is measured by taking
an X-ray of a child’s hand and wrist and
comparing it to standard X-ray findings
seen in children of the same age)
• Low level of IGF1

35. Assessment of GHD Child
• At birth, the infant Height and Weight are normal but
at 3-9 months growth rate reduced
• Height is below the 10 percentile
• Maturation of bone delays
• May have symptoms of hypoglycemia (paleness,
shaky, irritability etc)
• Delayed permanent teeth & sexual development
• Psychosocial problems

36. Therapeutic Management
• Synthetic Human Growth
(Hormone, Somatropin (hGh)
• 0.15-0.3 mg/kg/week subcutaneous till achieve
normal height

37. Nursing Support
• Education
• Help In diagnostic tests
• Help them, to set realistic expectations
• Assign age specific responsibilities
• Encourage child to participate in group
activities
• Psychological support
• Advise to wear a medical alert card
(hypoglycemia)

38. Hypothyroidism (T3,T4)
• Hypothyroidism is the condition in which
the thyroid is underactive and is
producing an insufficient amount of
thyroid hormones.
• Thyroxine (T4) and Triiodthyronine (T3)
• When the deficiency is present at birth
the condition is also known as
“Cretinism”.

39. Causes
• Congenital (hypoplastic,Aplasia)
• Ectopic Thyroid Gland (Moved towards Heart)
• Acquired (Cancer)
• Decreased Iodine intake
Clinical Manifestations
• Decreased growth
• Mental and Physical sluggishness
• Diminished physical activity
• Constipation protuberant abdomen

40. • Thick and large tongue
• Diminished voice of cry/ Hoarseness
• Bradycardia, decreased pulse pressure
• Hypothermia, Diminished sweating
• Short stature, infantile skeleton proportion
with short extremities
Diagnostic Evaluation
• Decreased T3,T4 level
• Elevated serum TSH
• Imaging: Skeleton maturation is delayed, Epiphseal disgenesis

41. Therapeutic Management
• Levothyroxine 75-100 microgram/Kg
• In newborn 10-12 microgram/Kg
• Screening program for neonatal
Levothyroxine
The treatment goal is to return the thyroid hormones to
normal levels. Patient teaching includes:
1. Thyroid medication must be taken for life
2. Take the medication on an empty stomach about 01
hour before meal

42. Levothyroxine
• Take the medication in morning
preferably before breakfast
• Blood levels of thyroid hormones
will need to be checked every 6-8
weeks until the TSH level is normal
• Do not switch brands of
levothyroxine without consulting a
health care provider

43. Nursing Consideration
(Hypothyroidism)
• Early detection and initiating therapy after the
first few weeks of life
• Watch for normal brain development
• Monitor height and weight
• Emphasize on compliance as treated for 2-3
years
• Over treated children shows abnormal brain
maturation, irritable poor weight gain

44. Nursing Consideration
(Hypothyroidism)
• Untreated deficiency can cause severe,
irreversible mental and physical
handicaps known as “Cretinism”
• Provide genetic counseling

45. Hypoparathyroidism
• Characterized by deficiency in the secretion of
parathyroid hormone (PTH)
• Function is maintenance of serum calcium
• The impaired secretion of PTH affects calcium
and phosphorus metabolism
• The PTH results in hypocalcaemia and
hyperphosphatemia

46. Sign and Symptoms
• Jittery movements
• Convulsions
• Apnea
• Lethargy, Poor eating
• Vomiting
• Stridor
• Chvostek’s sign (elicited by tapping the facial nerve , which
produce a facial spasm
• Tingling of hands or around the mouth
• Diarrhea
• Seizures
• In the growing children, permanent bone deformities & limited
growth

47. Treatment
• In case of seizure or tetany, includes giving
Intravenous calcium in form of calcium
gluconate
• The infusion should be given slowly, rapid
infusion may lead to dysrhythmias
(extravasations can cause severe tissue burn)
• Oral calcium gluconate
• Chronic hypocalcemia is treated with an active
metabolite of vitamin D, calcitriol

48. Hyperthyroidis
m
• Abnormally increase the level of T3 and T4
which effect different system of the body

49. Hyperthyroidism
causes
– Graves disease (95 %)
– Subacute thyroiditis
– Autonomous functioning nodules
– Iodine Excess Supplementation after a period
of iodine deficiency
TSH induced
TSH producing adenoma
Thyroid cancer

50. Causes cont…
• Graves Disease (>95% of Cases)
– Relatively rare in children
– Incidence increases with puberty
– Female:Male (3-5:1)
• Neonatal Graves
– Transplacental Antibodies
• TSH receptor mutations (gain of function)
• Subacute Thyroiditis
• Exogenous thyroxine Exposure
• Thyroid adenoma

51. Sign and
symptoms
• Change in School Performance
• Insomnia
• Restlessness and Irritability
• Nocturia
• Bone age advancement
• Infants
– Premature birth, Poor feeding, Failure to Thrive
• Other classic signs
– Weight Loss, Polyphagia, Tachycardia, Increased Pulse
Pressure, Heat Intolerance, Diarrhea, Tremor, hyperactive,
mental excitement and excessive sweating

52. Diagnostic
tests
• Graves Disease: Diagnosis
• Suppressed TSH (Grave’s disease)
• Elevated T4, T3 levels
• Positive Thyroid Stimulating Antibodies
• Radiological assessment
• CT scan, MRI and ultrasound

53. Treatment
• Radioactive Iodine
• Thionamides (methimazole, neomarcazole)
• Surgical Thyroidectomy (partial or complete)

54. Addison’s disease
• In childhood is rare.
• Damage of adrenal glands (caused by
Tuberculosis, fungal infections, autoimmune
disease and HIV) results In decreased
production of adrenal steroids, cortisol and
aldosterone.
• Addison’s disease can also results from
dysfunction of the hypothalamus or pituitary
gland or from discontinuation of high levels of
glucocorticoids for the treatment of other
disease

55. Addison’s disease
• The decrease production of cortisol has an impact on
the metabolism of glucose, fat and protein.
• Aldosterone plays a primary role in sodium ad
potassium excretion. Therefore, a deficit of this
hormone has an impact on blood pressure and
electrolytes
SIGN & SYMPTOMS
Acute Phase: severe hypotension, shock,
electrolytes imbalance, dehydration, weakness,
CV changes, fever, mental status changes &
hypoglycemia

56. Addison’s Treatment
• Intravenous hydrocortisone (regular intervals)
• Intravenous hydration (to correct dehydration)
• Electrolytes replacement
• In chronic phase, oral hydrocortisone. Dose will need to be
increased with illness
• Surgery
• Achild and caregivers should be counseled on essential need
for life long treatment, with the information that untreated
Addison's disease can be life threatening
• Amedical identification should be worn by individual with
Addison's irrespective of age

57. Cushing’s Syndrome
• Cushing’s syndrome is
cluster of sign & symptoms
caused by hypercortisolism
or excessive circulating
free cortisol.
• Too much cortisol can alter the normal
function of energy, BP and the ability to fight
disease resulting in the symptoms of Cushing’s
Syndrome
• CS is rare, for every 1 million people 2.5 /year

58. Causes
• Causes of hypercortisolism/ Cushing
Syndrome in children is prolong or excessive
corticosteroid therapy.
• Adrenal tumor or pituitary tumor that
produces excessive ACTH
• Diagnose: physical exam
• Urine test (Corticosteroid level high)
• CRH stimulation test (would be decrease/low)
• CT, MRI, Chest X-rayss

59. Sign and Symptoms
• Tiredness & weakness
• Extreme weight gain, excess hair growth, high blood pressure
and skin problems
• Growth retardation
• Missed periods in teen age girls
• Decreased fertility in men
• Acne
• Reddish blue streaks on skin
• Muscle & bone weakness
• Moodiness, irritability
• High blood pressure
• Sleep disturbence

60. Symptoms of Excess
Cortisol
• Truncal obesity
• Moon face
• Fat deposits supraclavicular fossa and
posterior neck- buffalo hump
• HTN
• Hirsutism
• Amenorrhea or impotence
• Depression
• Thin skin
• Easy bruising
• Purplish abdominal striae
• Proximal muscle weakness
• Osteoporosis
• Diabetes Mellitus
• Avascular necrosis
• Wound healing impaired
• Pysch symptoms
• Hyperpigmentation
• Hypokalemic alkalosis

61. Treatment
• If the body produce too much cortisol
treatment may include:
• Oral medication
• Radiation
• Surgery to remove a tumor
• A combination of treatment

62. Diabetes Mellitus in children

63. Diabetes Mellitus
Definition: metabolic disorder characterized by
hyperglycemia due to an absolute or relative
lack of insulin or to a cellular resistance to
insulin
Major classifications
• 1. Type 1 Diabetes
• 2. Type 2 Diabetes

64. Diabetes Mellitus
Diabetes Type 1
Definition
• 1. Metabolic condition in which the beta cells of pancreas
no longer produce insulin; characterized by hyperglycemia,
breakdown of body fats and protein and development of
ketosis
• 2. Accounts for 5 – 10 % of cases of diabetes; most often
occurs in childhood or adolescence
• 3. Formerly called Juvenile-onset diabetes or insulin-
dependent diabetes (IDDM)

65. Diabetes Mellitus
Pathophysiology
• 1. Autoimmune reaction in which the beta cells that
produce insulin are destroyed
• 2. Alpha cells produce excess glucagons causing
hyperglycemia
Risk Factors
• 1. Genetic predisposition for increased susceptibility; HLA
linkage
• 2. Environmental triggers stimulate an autoimmune
response
• a. Viral infections (mumps, rubella, coxsackievirus B4)
• b. Chemical toxins

66. Diabetes Mellitus
2. Hyperglycemia leads to
• a. Polyuria (hyperglycemia acts as osmotic diuretic)
• b. Glycosuria (renal threshold for glucose: 180 mg/dL)
• c. Polydipsia (thirst from dehydration from polyuria)
• d. Polyphagia (hunger and eats more since cell cannot
utilize glucose)
• e. Weight loss (body breaking down fat and protein to
restore energy source
• f. Malaise and fatigue (from decrease in energy)
• g. Blurred vision (swelling of lenses from osmotic effects)

67. Diabetes Mellitus
• Diagnosis
– Patient is symptomatic plus
• RBS >200 mg/dl OR
• Fasting plasma glucose of >126 mg/dl
• Two hour plasma glucose level of 200 mg/dl or greater
during an oral glucose tolerance test

68. Diabetes Mellitus
Diabetic Ketoacidosis (DKA)
1. Results from breakdown of fat and overproduction of
ketones by the liver and loss of bicarbonate
2. Occurs when Diabetes Type 1 is undiagnosed or known
diabetic has increased energy needs, when under physical
or emotional stress or fails to take insulin
1. Mortality as high as 14%
3. Pathophysiology
• a. Hypersomolarity (hyperglycemia, dehydration)
• b. Metabolic acidosis (accumulation of ketones)
• c. Fluid and electrolyte imbalance (from osmotic diuresis)

69. Diabetes Mellitus
Diagnostic tests
• a. Blood glucose greater than 250 mg/dL
• b. Blood pH less than 7.3
• c. Blood bicarbonate less than 15 mEq/L
• d. Ketones present in blood
• e. Ketones and glucose present in urine
• f. Electrolyte abnormalities (Na, K, Cl)

70. Diabetes Mellitus
• DKA
– Signs and symptoms
• Kussmauls respirations
– Blow off carbon dioxide to reverse acidosis
• Fruity breath
• Nausea/ abdominal pain
• Dehydration
• Lethargy
• Coma
• Polydipsia, polyuria, polyphagia

71. Diabetes Mellitus
Treatment
• a. Requires immediate medical attention and usually
admission to hospital
• B .Frequent measurement of blood glucose and treat
according to glucose levels with regular insulin (mild ketosis,
subcutaneous route; severe ketosis with intravenous insulin
administration)
• c. Restore fluid balance: initially 0.9% saline at 500 – 1000
mL/hr.; regulate fluids according to client status; when blood
glucose is 250 mg/dL add dextrose to intravenous solutions

72. Diabetes Mellitus
• DKA
– d.Correct electrolyte imbalance: client often is initially
hyperkalemic
• As patient is rehydrated and potassium in pushed back into the
cell they become hypokalemic
• Monitor K levels
– e. Monitor cardiac rhythm since hypokalemia puts client
at risk for dysrrhythmias
– f. Treat underlying condition precipitating DKA
– G. Acidosis is corrected with fluid and insulin therapy and
rarely needs bicarb

73. Diabetes Mellitus
Diabetes Type 2
• A. Definition: condition of fasting
hyperglycemia occurring despite availability
of body’s own insulin
• B. Was known as non-insulin dependent
diabetes or adult onset diabetes
– Both are misnomers, it can be found in children
and type II DM may require insulin

74. Diabetes Mellitus
Pathophysiology
• 1. Sufficient insulin production to prevent
DKA; but insufficient to lower blood glucose
through uptake of glucose by muscle and fat
cells
• 2. Cellular resistance to insulin increased by
obesity, inactivity, illness, age, some
medications

75. Diabetes Mellitus
Risk Factors
• 1. History of diabetes in parents or siblings; no HLA
• 2. Obesity (especially of upper body)
• 3. Physical inactivity
• 4. Race/ethnicity
• 6. Clients with hypertension and > cholesterol .

76. Diabetes Mellitus
Manifestations
1. Client usually unaware of diabetes
• a. Discovers diabetes when seeking health care for
another concern
• b. Most cases aren’t diagnosed for 5-6 years after the
development of the disease
• c. Usually does not experience weight loss

77. Diabetes Mellitus
2. Possible symptoms or concerns
• a. Hyperglycemia (not as severe as with Type 1)
• b. Polyuria
• c. Polydipsia
• d. Blurred vision
• e. Fatigue
• f. Paresthesias (numbness in extremities)
• g. Skin Infections

78. Diabetes Mellitus
Diagnostic tests to monitor diabetes management
1. Fasting Blood Glucose (normal: 70 – 110 mg/dL)
2. Glycosylated hemoglobin (c) (Hemoglobin A1C)
• a. Considered elevated if values above 7%

79. Diabetes Mellitus
• 3. Urine glucose and ketone levels (part of
routine urinalysis)
4. Urine albumin (part of routine urinalysis)
• a. If albumin present, indicates need for workup
for nephropathy
• b. Typical order is creatinine clearance testing

80. Diabetes Mellitus
Medications
A. Insulin
• 1. Sources: standard practice is use of human insulin prepared by
alteration of pork insulin or recombinant DNA therapy
2. Clients who need insulin as therapy:
• a. All type 1 diabetics since their bodies essentially no longer produce
insulin
• b. Some Type 2 diabetics, if oral medications are not adequate for
control (both oral medications and insulin may be needed)
• c. Diabetics enduring stressor situations such as surgery,
corticosteroid therapy, infections, treatment for DKA,
• e. Some clients receiving high caloric feedings including tube feedings
or parenteral nutrition

81. Diabetes Mellitus
Oral Hypoglycemic Agents
• 1. Used to treat Diabetes Type 2
• 2. Client must also maintain prescribed diet and exercise
program; monitor blood glucose levels
• 3. Several different oral hypoglycemic agents and insulin
may be prescribed for the client
• 4. Must have some functioning beta cells

82. Diabetes Mellitus
Classifications and action
a.Sulfonylureas
• 1. Action: Stimulates pancreatic cells to
secrete more insulin and increases sensitivity
of peripheral tissues to insulin
• 2. Used: to treat non-obese Type 2 diabetics
• 3. Example: Glipizide (Glucotrol),
Chlorpropamide (Diabinese), Tolazamide
(Tolinase)

83. Diabetes Mellitus
b. Meglitinides
• 1. Action: stimulates pancreatic cells to secret
more insulin
• 2. Taken just before meals, rapid onset, limited
duration of action
• 3. Major adverse effects is hypoglycemia
• 4. Used in non-obese diabetics
• 5. Example: Repaglinide (Prandin), Nateglinide
(Starlix)

84. Diabetes Mellitus
c. Biguanides
• 1. Action: decreases overproduction of
glucose by liver and makes insulin more
effective in peripheral tissues
• 2. Used in obese diabetics
• 3. Does not stimulate insulin release
• 4. Metabolized by the kidney, do not use
with renal patients
• 5. Example: Metformin (Glucophage

85. Diabetes Mellitus
d.Alpha-glucoside Inhibitors
• 1. Action: Slow carbohydrate digestion and
delay rate of glucose absorption
• 2. Take with first bite of the meal or 15 min.
after
• 3. Adjunct to diet to decrease blood glucose
levels
• 4. Example: Acarbose (Precose), Miglitol
(Glyset)

86. Diabetes Mellitus
Thizaolidinediones (Glitazones)
• 1. Action: Sensitizes peripheral tissues to
insulin
• 2. Used in obese diabetics
• 3. Inhibits glucose production
• 4. Improves sensitivity to insulin in muscle,
and fat tissue
• 5. Example: Rosiglitazone (Avandia),
Pioglitazone (Actos)

87. Diabetes Mellitus
• Patients with Type 2 DM who are thin do not
produce enough insulin, they are not insulin
resistant
– Need sulfonylurea agents like Diabinese,
Tolinase, Glucotrol, Diabeta

88. Diabetes Mellitus
Role of Diet in Diabetic Management
A. Goals for diabetic therapy include
• 1. Maintain as near-normal blood glucose
levels as possible with balance of food with
medications
• 2.
• 3.
Obtain optimal serum lipid levels
Provide adequate calories to attain or
maintain reasonable weight

89. Diabetes Mellitus
Nursing Care
• A. Assessment, planning, implementation with client
according to type and stage of diabetes
• B. Prevention, assessment and treatment of complications
through client self-management and keeping appointments
for medical care
• C. Client and family teaching for diabetes management
• D. Health promotion includes education of healthy life
style, lowering risks for developing diabetes for all clients
• E. Blood glucose screening at 3 year intervals starting at
age 45 for persons in high risk groups

90. Diabetes Mellitus
1. Daily inspection of feet
2. Checking temperature of any water before washing feet
3. Need for lubricating cream after drying but not between toes
4. Patients should be followed by a podiatrist
5. Early reporting of any wounds or blisters
Common Nursing Diagnoses and Specific Teaching Interventions
A. Risk for impaired skin integrity: Proper foot care
•
•
•
•
•
B. Risk for infection
• 1. Frequent hand washing
• 2. Early recognition of signs of infection and seeking treatment
• 3. Meticulous skin care
• 4. Regular dental examinations and consistent oral hygiene care

91. Diabetes Mellitus
C. Risk for injury: Prevention of accidents, falls and
burns
D.Sexual dysfunction
• 1. Effects of high blood sugar on sexual
functioning,
• 2. Resources for treatment of impotence, sexual
dysfunction
E. Ineffective coping
• 1. Assisting clients with problem-solving strategies
for specific concerns

92. Diabetes Mellitus
• 2. Providing information about diabetic
resources, community education programs,
and support groups
• 3. Utilizing any client contact as opportunity
to review coping status and reinforce proper
diabetes management and complication
prevention