Neurological disorders

1. Endocrine Disorders
By: Robera D. (BSc, MSc)
Department of Nursing
School of Nursing and Midwifery
Institute of Health Sciences
Wallaga University

2. Review of Anatomy
and Physiology
3

3. Learning objectives
Upon completion of this lesson, students will be able
to:
Identify major endocrine glands, their anatomic
location, and hormones they secrete
Summarize major action of hormones secreted from
each gland
Name disorders produced by over- and under-secretion
of hormones
4

4. Review of anatomy and physiology
Endocrine system (ES) is involved in regulating
metabolism, tissue function, reproduction, growth, and
development
Endocrine glands: pituitary, thyroid, parathyroids,
adrenals, pancreatic islets, ovaries, and testes
─They secrete their hormones into blood
Hormones: chemical messengers with specific target
tissue, where it impacts cells’ functions and reactions 5

5. Review of anatomy and physiology…
Hypothalamus is the link between NS and ES
─It controls pituitary
Hormone concentration in blood is maintained at a
relatively constant level according to need by negative
feedback mechanism
6

6. 7
Figure 1: Hypothalamic and pituitary hormones and their target organs

7. Glands of the Endocrine System
8

8. Pituitary gland
Located on the inferior aspect of the brain
Secretes hormones that control secretion of hormones
by other endocrine glands
GHRH, GnRH, TRH, CRH, oxytocin and
vasopressin
─produced and released by hypothalamus
─act on cells of the pituitary gland
9

9. Pituitary gland…
Anterior pituitary gland
1. Follicle-stimulating
hormone (FSH)
2. Luteinizing hormone (LH)
3. Adrenocorticotropic
hormone (ACTH)
4. Thyroid-stimulating
hormone (TSH)
5. Prolactin (PRL)
6. Growth hormone (GH)
Posterior pituitary
gland
1. Vasopressin (or
ADH)
2. Oxytocin
10

10. Thyroid gland
Butterfly-shaped organ located in lower neck, anterior
to trachea
Blood flow to the thyroid is very high (about 5 mL/min
per gram of thyroid tissue)
3 hormones:
1. Thyroxine (T4): controls cellular metabolic activity
2. Triiodothyronine (T3): controls cellular metabolic
activity
3. Calcitonin: reduces plasma level of calcium
11

11. Parathyroid Glands
12
Situated in the neck and
embedded in the posterior aspect
of the thyroid gland
Parathyroid hormone
─Lowers phosphorus and rises
calcium in blood

12. Adrenal Glands
13
There are two adrenal glands, one attached to the
upper portion of each kidney
ACTH stimulates adrenal cortex to secrete adrenal
hormones
Adrenal hormones: glucocorticoids,
mineralocorticoids, sex hormones
Adrenal medulla secretes catecholamines

13. Glucocorticoids (e.g. Cortisol)
Influence on glucose metabolism (↑BG) : Increased
cortisol secretion results in elevated blood glucose
Inhibit inflammatory response (powerful immune
suppressant)
14

14. Mineralocorticoids (e.g. Aldosterone)
Involved in electrolyte metabolism
Act principally on renal tubules and GI epithelium to
cause increased Na+ absorption in exchange for
excretion of K+ or H+
Aldosterone is the primary mineralocorticoid
It is primarily secreted in response to presence of
angiotensin II
15

15. Adrenal Sex Hormones
Androgens
─exert effects similar to those of male sex hormones
Female sex hormones
─Adrenal gland may also secrete small amounts of
some estrogens
16

16. Pancreatic Islets
Pancreas lies transversely in the upper
abdomen
Beta cells of pancreas secrete insulin,
Insulin facilitates glucose transport into cells
alpha cells of pancreatic islets secrete
glucagon when blood glucose level is low
Glucagon promotes gluconeogenesis to raise
glucose level
Delta cells secrete somatostatin
17

17. Assessment
Health history
Ask if they have experienced changes:
Energy level
Tolerance to heat or cold
Weight
Thirst
Frequency of urination
Bowel function
Fat and fluid distribution
Secondary sexual characteristics (e.g., loss or growth of hair)
Any enlargement of thyroid gland
18

18. Assessment…
Physical examination
Vital signs
Head-to-toe inspection
Palpation of skin, hair, and thyroid
Abnormal findings
─Facial hair in women, buffalo hump, vision changes,
thinning of the skin, obesity of the trunk
19

19. Inspect the neck for thyroid gland
Tilt patient’s head
slightly back
Using lighting directed
downward from the tip of
the patient’s chin, inspect
region below cricoid
cartilage to identify
contours of the gland
20

20. 21

21. Observe patient swallowing
Ask the patient to sip some water and to extend the neck
again and swallow.
Watch for upward movement of thyroid gland, noting its
contour and symmetry
Thyroid cartilage, cricoid cartilage, and thyroid gland all rise
with swallowing and then fall to their resting positions
With swallowing, lower border of this large gland rises and
looks less symmetric
22

22. Palpate thyroid gland
With the patient seating or standing
Stand behind the patient, ask the patient to flex the neck
slightly forward
Gently place fingers of both hands on patient’s neck so
that your index fingers are just below cricoid cartilage
Ask the patient to sip and swallow
Feel for the thyroid isthmus rising up under your finger
pads
23

23. Palpate thyroid gland…
Normal
─small, smooth, firm, nontender, free of nodules
Abnormal:
─soft in Graves disease
─firm in Hashimoto thyroiditis and malignancy
─tender in thyroiditis
24

24. Click here to see video
25

25. Diabetes
26

26. Learning objectives
At the end of this lesson, students will be able to:
Differentiate between type 1 and type 2 diabetes
Describe etiologic factors associated with diabetes
Explain diagnostic procedures of diabetes
Describe management strategies for diabetes
Differentiate between diabetic ketoacidosis and
hyperosmolar nonketotic syndrome
27

27. Definition
Diabetes is a group of metabolic diseases characterized
by hyperglycemia resulting from defects in insulin
secretion, insulin action, or both
It is a chronic illness that requires medical care and
patient self-management
Has physical, social, & economic consequences
28

28. Normal and abnormal blood glucose levels
29
2 hr post-load
glucose
FPG
0
7
0
-
-
10
0
12
6
-
Diabetes
Prediabete
s(IFG)
Normal
Hypoglycemi
a
-
14
0
20
0
-
Hypoglycemi
a
Normal
Diabetes
Prediabete
s (IGT)
RBS
Hypoglycemi
a
Normal
Diabetes

29. Risk Factors
Family history (e.g., parents or siblings with diabetes
Obesity
Age >30 years for type 2 and <30 years for type 1
Previously identified impaired fasting glucose or
impaired glucose tolerance
Hypertension
High-density lipoprotein (HDL) cholesterol ≤35 mg/dL
and/or triglyceride level ≥250 mg/dL
History of gestational diabetes or delivery of a baby
over 9 lb
30

30. Classification
1. Type 1 diabetes (5 – 10% of all diabetes)
2. Type 2 diabetes (90 – 95% of all diabetes)
3. Gestational diabetes
4. Latent autoimmune diabetes of adult (LADA)
5. Diabetes associated with other conditions or
syndromes
31

31. Pathophysiology
Insulin controls blood glucose levels by regulating the
production, use, and storage of glucose.
In patients with diabetes, cells may respond
inadequately to insulin or the pancreas may decrease
insulin secretion or stop insulin production completely.
When person eats a meal, insulin secretion increases
and moves glucose from the blood into muscle, liver,
and fat cells. (in healthy person)
32

32. Pathophysiology…
During fasting periods, the pancreas continuously
releases a small amount of “basal” insulin
33

33. Pathophysiology…
If the blood sugar becomes too low, glucagon is
secreted
Glucagon stimulates liver to release stored glucose,
thereby increasing the blood sugar.
They work together to maintain a constant level of
glucose in the blood.
Liver assists with glucose control (glycogenolysis &
gluconeogenesis)
34

34. Pathophysiology…
Once inside the cells, insulin functions in the following ways:
─Transports and metabolizes glucose for energy
─Stimulates storage of glucose in the liver and muscle cells
─Signals liver cells to stop the release of glucose
─Enhances storage of dietary fat in adipose tissue
─Accelerates transport of amino acids into cells
─Facilitates the transport of potassium into the cells
─Inhibits the breakdown of stored glucose, protein, and fat
35

35. Type 1 Diabetes
It is often characterized by acute onset and most commonly
affects children and young adults, although it can occur at
any age
It is characterized by destruction of pancreatic beta cells
It develops as a result of autoimmunity against beta cells
It is believed that autoimmunity destruction is initiated by a
combination of genetic, immunologic, and environmental
factors
36

36. Type 1 Diabetes…
Although events are not fully understood, it is generally
accepted that genetic susceptibility is a common
underlying factor in the development of type 1 diabetes.
People do not inherit type 1 diabetes itself but rather a
genetic predisposition, or tendency, toward the
development of type 1 diabetes.
This genetic tendency has been found in people with
certain human leukocyte antigen types
37

37. Type 1 diabetes cont’d
Beta cell destruction
Decreased insulin production
Increased glucose production by the liver,
and fasting hyperglycaemia
Glucose from food cannot
be stored in the liver but instead
remains in the bloodstream and
contributes to postprandial
hyperglycemia
38

38. Type 1 diabetes…
If concentration of glucose in blood exceeds renal
threshold for glucose, kidneys may not reabsorb all of
filtered glucose; glycosuria occurs
As glucose is excreted in urine, water follows it
(osmotic diuresis)
Fat breakdown results in increased production of ketone
bodies (ketoacidosis)
39

39. Type 1 diabetes…
Increased blood
glucose level pulls
cellular water into
blood → cellular
dehydration→
polydipsia
Deficiency of insulin
Glucose will not be conveyed from
extracellular to intracellular
compartment
Cells become energy depleted
fat & protein will be
drawn from adipose
tissue & muscle & and
ketosis
↑sed appetite
(polyphagia)
40

40. Type 2 Diabetes
It occurs more commonly in who are >30yrs and obese
Characterized by insulin resistance, impaired insulin
secretion, and increased hepatic glucose production
Insulin resistance refers to ↓sed tissue sensitivity to insulin.
Exact mechanisms of insulin resistance and impaired
insulin secretion are unknown
Although increasing age, obesity, and lack of physical
exercise as well as genetic factors are thought to play a role
41

41. Type 2 diabetes…
Type 2 DM has a strong genetic component
 In early stages of type 2 diabetes, glucose tolerance
remains near-normal, despite insulin resistance, because
beta cells compensate by increasing insulin output
As insulin resistance and compensatory
hyperinsulinemia progress, pancreatic islets are unable
to sustain the hyperinsulinemic state
IGT then develops
42

42. Type 2 diabetes…
Further decline in insulin secretion and increase in
hepatic glucose production lead to overt diabetes
Glucagon is relatively overproduced and secreted,
further augmenting hepatic glucose production
There is enough insulin present to prevent the
breakdown of fat
Note: Impaired insulin secretion contribute to the pathogenesis of type 2 DM
43

43. 44

44. Gestational Diabetes (GD)
Glucose intolerance developing
during 2nd or 3rd trimester of
pregnancy
Hyperglycemia develops during
pregnancy because of secretion
of placental hormones, which
causes insulin resistance
45

45. Gestational diabetes cont’d
Most women with GD revert to normal glucose
tolerance postpartum but have a substantial risk (35–
60%) of developing diabetes in the next 10–20 yrs
Women with a history of GD should
─undergo lifelong screening for the development of
diabetes or prediabetes at least every 3 years.
─be counselled to maintain her ideal body weight and
to exercise regularly
46

46. Latent Autoimmune Diabetes of Adults
(LADA)
LADA is a subtype of diabetes in which the progression
of autoimmune beta cell destruction in the pancreas is
slower than in types 1 and 2 diabetes
Patients with LADA are not insulin-dependent in the
initial 6 months of disease onset.
Clinical manifestation of LADA shares the features of
types 1 and 2 diabetes
47

47. Clinical Manifestations
Classic clinical manifestations include the “3 Ps”: polyuria,
polydipsia, and polyphagia
Other symptoms include
Dehydration, weight loss, fatigue and weakness,
Vision changes
Tingling or numbness in hands or feet
Skin lesions, wounds that are slow to heal
Recurrent infections
48

48. Diagnosis
Abnormally high blood glucose level
The following may be used:
─Fasting plasma glucose (FPG)
─Random plasma glucose
─2-hour post-load glucose
49

49. ADA’s diagnostic criteria for diabetes
Symptoms of diabetes (polyuria, polydipsia, weight
loss) plus casual plasma glucose concentration ≥200
mg/dL (11.1 mmol/L).
Fasting plasma glucose ≥126 mg/dL (7.0 mmol/L).
Two-hour postload glucose ≥200 mg/dL (11.1 mmol/L)
Glycated haemoglobin A1C ≥6.5% (48 mmol/mol).
OR
OR
OR
50

50. Medical Management
Diabetes management has five components:
1. Nutritional therapy
2. Exercise
3. Monitoring
4. Pharmacologic therapy
5. Education
51

51. Nutritional Therapy
Nutrition, weight control, and increased activity are the
foundation of diabetes management
Objectives
─control of total caloric intake to attain or maintain a
reasonable body weight,
─control of blood glucose levels, and
─normalization of lipids and blood pressure
52

52. Nutritional therapy…
For patients who require insulin:
Maintain as much consistency as possible in the amounts of
calories and carbohydrates ingested at each meal
Maintain consistency in the approximate time intervals
between meals, with the addition of snacks if necessary
For patients who are overweight and obese:
weight loss is an important part of treatment (weight loss of
>5% may improve BG levels)
53

53. Caloric Requirements and Distribution
Carbohydrates
─50% to 60% carbohydrates, 20% to 30% fat, and 10% to
20% protein
Fats
─reduce to less than 30% of total calories
─limit amount of saturated fats to10% of total calories.
─limit total intake of dietary cholesterol to <300 mg/day
54

54. Caloric Requirements…
Protein
─Use of some nonanimal sources of protein (e.g. legumes,
whole grains) to help reduce saturated fat and cholesterol
intake
Fiber
─Increased fiber in the diet may improve blood glucose levels
─At least 25 g of fiber should be ingested daily
Alcohol consumption
─moderate (1 bottle/day for women and 2 bottles/day for men)
55

55. Exercise
It lowers blood glucose and reduces CVD risk
It also alters blood lipid concentrations, increasing
levels of HDL and decreasing total cholesterol and TG
levels
Gradual increase in the exercise period is encouraged.
56

56. Exercise Recommendations
150 min/week (distributed over at least 3 days)
Exercise at the same time of day and for the same duration
each session
Use proper footwear
Avoid trauma to the lower extremities
Inspect feet daily after exercise
Avoid exercise in extreme heat or cold
Avoid exercise during periods of poor metabolic control
57

57. Exercise Precautions
Patients who require insulin should be taught to eat 15-
g carbohydrate snack or snack of complex
carbohydrates with protein before engaging in moderate
exercise
To avoid post-exercise hypoglycemia, especially after
strenuous or prolonged exercise, the patient may need to
eat snack at the end of the exercise session
Patients taking insulin and participating in extended
periods of exercise should test their BG before, during,
and after exercise period
58

58. Monitoring Glucose Levels
Self-monitoring of blood glucose (SMBG)
It is recommended that SMBG occurs when circumstances
call for it (e.g., before meals, snacks, and exercise)
Allows for detection and prevention of hypo/hyperglycemia
Every 6 to 12 months, patients should conduct a comparison
of their meter result with lab measured BG level
59

59. Frequency of SMBG
3 or more times daily for most patients who require
insulin,
At least 2 or 3 times per week for those not receiving
insulin
Whenever hypoglycemia or hyperglycemia is
suspected; with changes in medications, activity, or diet;
and with stress or illness
60

60. Pharmacologic Therapy
Insulin Therapy
In type I diabetes, exogenous insulin must be given
for life
In type 2 diabetes, insulin may be necessary on a long-
term basis to control BG if meal planning and oral
agents are ineffective or when insulin deficiency occurs
SMBG is a cornerstone of insulin therapy
61

61. Preparations of insulin
Based on the onset, peak, and duration of action
Rapid-acting insulins
More rapid effect and shorter duration of action
Patient should eat within 5 to 15 minutes of injection
Long-acting insulin (basal insulin) is required to
maintain glucose control
62

62. Preparations of insulin…
Short-acting insulins
called regular insulin (marked R on the bottle)
Regular insulin is a clear solution and is usually given
20 to 30 minutes before a meal
Can be given alone or with longer-acting insulin
63

63. Preparations of insulin…
Intermediate-acting insulins
called NPH insulin (neutral protamine Hagedorn) or Lente
insulin
Appear milky and cloudy
function as basal insulins but may have to be split into 2
injections to achieve 24-hour coverage.
If NPH or Lente insulin is taken alone, it is not crucial that it
be taken before a meal but patients should eat some food
around its time of onset and peak
64

64. Preparations of insulin…
Very long-acting insulins (basal insulin)
Absorbed very slowly over 24hrs and can be given once
a day
65

65. Preparations of insulin cont’d
66

66. Insulin Regimens
Conventional Regimen
One or more injections of a mixture of short and
intermediate-acting insulins per day
 Τ
𝟐
𝟑 of total dose in the morning (with Τ
𝟐
𝟑 long-acting
and Τ
𝟏
𝟑 short-acting insulin) and Τ
𝟏
𝟑 before the evening
meal (with Τ
𝟏
𝟐 long-acting and Τ
𝟏
𝟐 short-acting)
67

67. Conventional Regimen…
Total insulin dose per day
─Initiation: 0.2 - 0.4 units/kg/day
─Maintenance: roughly 0.6 - 0.7 units/kg/day
Regimen options commonly available in Ethiopian setting
NPH twice daily (before breakfast and at bed time) and
Regular insulin twice daily (before breakfast & before supper)
Premixed insulin (70% NPH & 30% regular) twice daily:
before breakfast and before supper
NPH twice daily: before breakfast and before bedtime
68

68. Intensive Regimen
3 or 4 injections of insulin per day
allows the patient more flexibility to change the insulin
doses from day to day
Intensive insulin therapy requires:
─Monitoring BG before breakfast, before lunch, before
dinner & before bed
─Adjusting insulin doses in response to given glucose
patterns
─Coordinating diet, exercise, and insulin therapy
69

69. Storing Insulin
All insulin, including spare pens and vials not in use,
should be refrigerated
Insulin pen or vial in use should be kept at room
temperature to reduce local irritation at injection site
Insulin can be kept at room temperature for 1 month
70

70. Preparing the Injection
Mixing Insulins
─Regular and NPH insulins can be mixed together in the
same syringe.
─NPH should be mixed carefully by rolling the vial gently.
─Regular insulin is drawn into syringe first, followed by
NPH
Premixed insulin in a vial or in a prefilled syringe can be
used
Premixed insulins: 70/30 (70% NPH and 30% regular
insulin), 50/50 71

71. Injection Site
72
Injection sites:
─abdomen,
─posterior surface of upper arms,
─anterior surface of the thighs
─flank area

72. Injection Site…
Use all available injection sites within one area rather
than randomly rotating sites from area to area
Or, always using the same area at the same time of day
(E.g. Morning into abdomen, evening into arms)
If patient plans to exercise, insulin should not be injected
into the limb that will be exercised → faster absorption
→hypoglycemia
73

73. Insulin Injection
Injection site is cleansed prior to insertion of needle
To inject insulin, the skin is gently pinched and needle
is inserted at 90-degree angle
─45-degree angle for patients with lower BMI
Injection sites should be at least 1 inch apart
Too deep or too shallow injection affects rate of
absorption
Note: Routine aspiration to assess blood is not necessary
74

74. Insulin Injection…
75
Self-injection of Insulin
1. With one hand, stabilize the skin by
spreading it or pinching up a large area
2. Pick up the syringe with the other hand and
hold it as you would a pencil. Insert the
needle straight into the skin
3. To inject the insulin, push in the plunger all
the way
4. Pull the needle straight out of the skin. Press
a cotton ball over the injection site for
several seconds
5. Use a disposable syringe only once and
discard it into a hard plastic container

75. Oral Antidiabetic Agents
1. Biguanides
2. Sulfonylureas
3. Alpha-glucosidase inhibitors
4. Nonsulfonylurea insulin secretagogues (meglitinides
and phenylalanine derivatives)
5. Thiazolidinediones (glitazones)
6. Dipeptidyl peptidase 4 (DPP-4) inhibitors
7. Glucagon-like peptide 1 (GLP-1) analogs
8. Sodium-glucose transporter 2 (SGLT-2) inhibitors
76

76. Biguanides: Metformin
Acts by decreasing hepatic production of glucose and
improves peripheral glucose utilization
Reduces fasting plasma glucose and insulin levels, and
promotes modest weight loss
As monotherapy and in combination with other oral
agents or with insulin
77

77. Sulfonylureas
Stimulate the pancreas directly to secrete insulin
A functioning pancreas is necessary
 Improve insulin action at the cellular level and also
may directly decrease hepatic glucose production
Most common side effect is hypoglycemia
Second-generation sulfonylureas (glipizide, glyburide,
glimepiride) are safer
78

78. Indications for insulin therapy in type 2
diabetes mellitus
Failure to control blood glucose with oral medicines
Temporary use for major stress, e.g. surgery, medical illness
Severe kidney or liver failure
Pregnancy
HbA1C >10%, FPG >250 mg/dl, RBS consistently >300
mg/dl, or ketonuria
When distinguishing type 1 from type 2 diabetes is difficult
82

79. Doses and contraindications
83
Drug Dose Contraindications
Metformin
 500mg PO daily with meals
 Titrate dose slowly based on BG
levels or HbA1C to a maximum dose
2000-2500mg
 Serum creatinine: >1.5
mg/dL (men), >1.4 mg/dL
(women),
 CHF, radiographic contrast
studies, seriously ill patients,
acidosis, hepatic failure
Glibenclamide
 2.5mg-5mg PO daily 30min before
breakfast
 Titrate dose slowly based on HbA1c
and/or FBG levels to 15mg daily
 When 7.5mg per day is needed,
divide total daily dose into 2, with
larger dose in the morning
 Elderly and patients with
renal impairment
Glimepiride
 1-2mg PO dailywith breakfast or the
first main meal
 Titrate dose slowly based on HbA1c
and/or FBG levels
 Maximum dose of 8mg once daily
 Hypersensitivity to sulfonyl
ureas or sulfonamides,
 breast feeding
 DKA

80. Insulin initiation and dose increment in type-2 diabetes
84
Regimen Insulin
type
Starting
dose
Increment Alternative
dosing
Add on-to
oral agent
NPH 10 units
before
bedtime
2–4 units
in 3-7
days
Higher dose may be
started in patients
with severe
hyperglycemia
Substitutio
n
Therapy
(Insulin
substitutin
g
all oral
agents)
NPH 15 units
• 10 units,
30min
Before
breakfast
• 5 units,
30min
before supper
4 units in
3-7 days
Higher dose may
be started in
patients with
severe
hyperglycemia

81. 85
Management of other cardiovascular risk factors
Drug Dose Indications
Aspirin
 75–162mg PO daily  Increased cardiovascular risk (10-year risk
>10%)
 Men >50years or women >60years with at
least one additional major risk factor
(hypertension, smoking, dyslipidemia,
albuminuria and family history of CVD)
Statins  Simvastatin, 10-40mg
PO daily
 Atorvastatin 10-
40mg PO daily
 Rosuvastatin 5-20mg
PO daily
 Lovastatin 20-80mg P
O daily
 Overt CVD
 >40 years of age and have one or more
other CVD risk factors
 Without CVD and <40 years- if LDL
cholesterol remains >100mg/dl or have
multiple CVD risk factors,

82. Sequential therapy in Type 2 Diabetes
86
Healthy eating, weight control, increased
physical activity
Metformin
Two medicine therapies
Glycemic targets not meet in 3 months
Metformin +
Sulfonylurea
Metformin +
Basal Insulin
Three medicine therapies
Metformin + Sulfonylurea + Basal
Insulin
Glycemic targets not meet in 3 months
Glycemic
targets
not
meet
in
3-6
months
Complex Insulin
regimens i.e.
Multiple insulin
injections per day

83. Education
Provide the patient with basic knowledge and skills for diabetes
management
Include the following:
─Simple pathophysiology
─Treatment modalities
─Recognition, treatment, and prevention of acute complications
Provide also the patient with detailed information to foster self-
reliance and independence for diabetes management at home
Educate on skills and information to improve lifestyle and
individualization of diabetes self-management
87

84. Glycemic Targets for Non-Pregnant Adults with
Diabetes
88
Fasting plasma glucose (capillary) 70-130 mg/dl
Postprandial (1–2 hrs after beginning of
meal) plasma glucose
< 180 mg/dl
Haemoglobin A1C < 7%

85. Acute complications
of diabetes
89

86. Acute complications of diabetes
1. Hypoglycemia (Insulin Reaction)
2. Diabetic ketoacidosis
3. Hyperglycemic hyperosmolar syndrome
90

87. Hypoglycemia
Blood glucose <70 mg/dL (3.9 mmol/L)
It can cause serious morbidity; if severe it can be fatal
Its incidence is lower in T2DM than in T1DM
It often occurs before meals (if meals are delayed/omitted)
Causes
─too much insulin or oral hypoglycemic agents,
─too little food, or
─ excessive physical activity
91

88. Hypoglycemia…
Hypoglycemia may be documented by Whipple’s
triad:
1. Symptoms consistent with hypoglycemia
2. Low plasma glucose concentration measured with a
precise method
3. Relief of symptoms after plasma glucose level is
raised
92

89. 93
Fig: Physiology of glucose counterregulation: Mechanisms that normally prevent or
rapidly correct hypoglycemia

90. 94

91. Clinical Manifestations
2 categories of symptoms:
─Autonomic nervous system (ANS) symptoms
─Central nervous system (CNS) symptoms
In mild hypoglycemia, ANS is stimulated
─Adrenergic symptoms: tachycardia, palpitations,
tremor, and anxiety
─Cholinergic symptoms: sweating, hunger, and
paresthesiae 95

92. C/M….
In moderate hypoglycemia
─inability to concentrate, headache, lightheadedness,
confusion, memory lapses, slurred speech, impaired
coordination, emotional changes, irrational or
combative behaviour
In severe hypoglycemia,
─disoriented behavior, seizures, difficulty arousing
from sleep, or loss of consciousness
96

93. C/M…
Hypoglycemia unawareness
Caused by attenuated sympathoadrenal response to
hypoglycemia
Loss of warning adrenergic and cholinergic symptoms
Occurs in some pts who have had diabetes for many
years
Affected pts must perform SMBG on frequent basis
97

94. Management
Giving carbohydrates (CHO)
─15 to 20 g of fast-acting concentrated source of
glucose orally
Sources of glucose for include:
─3 or 4 commercially prepared glucose tablets
─4 to 6 oz of fruit juice or regular soda
─6 to 10 hard candies
─2 to 3 teaspoons of sugar or honey
98

95. Management…
BG level should be retested in 15 minutes and retreated
with another 15 g if the patient is still hypoglycemic.
If symptoms persist for > 15minutes after initial
treatment, treatment is repeated even if BG testing is not
possible
Once BG has come to normal, snack or meal containing
protein and starch (e.g., milk or cheese) is
recommended to prevent recurrent hypoglycemia
99

96. Management…
25 to 50 mL D50W via IV push at a rate of 10 mL/min
Glucagon 1 mg IV or SC can be administered if
patient is unconscious or unable to swallow
100

97. Diabetic Ketoacidosis (DKA)
DKA is caused by absence or markedly inadequate
amount of insulin
3 main clinical features of DKA are:
─Hyperglycemia
─Dehydration and electrolyte loss
─Acidosis
101

98. DKA…
Causes of DKA
Insufficient or missed doses of insulin
Physical or emotional stress
Illness or infection
Undiagnosed and untreated diabetes
102

99. Pathophysiology
Insulin deficiency → reduced amount of glucose
entering the cells and increased hepatic glucose
production and release → hyperglycemia
Kidneys excrete excess glucose → osmotic diuresis →
dehydration and electrolytes loss
Hyperosmolality of blood → stimulation of thirst →
polydipsia and fluid shifting from intracellular to
extracellular space → low serum sodium level
103

100. Pathophysiology…
Insulin deficiency → breakdown of fat into free fatty acids
→ free fatty acids conversion into ketone
bodies→metabolic acidosis
Metabolic acidosis → respiratory system blows off
CO2→rapid deep respirations (Kussmaul respirations)
Ketones (volatile acid), as they are exhaled, they may
manifest as acetone breath that has a fruity odor similar to
overripe apples
104

101. Clinical manifestations
Polyuria, polydipsia, weakness, and malaise
Blurred vision → due to osmotic changes to lens
Orthostatic hypotension; warm, dry skin; decreased
skin turgor; flat neck veins; and dry mucous membranes
Weak, rapid pulse
Anorexia, nausea, vomiting, and abdominal pain
Acetone breath & Kussmaul respirations
105

102. Diagnostic findings
Blood glucose levels >250 mg/dL
Low serum pH (6.8 to 7.3)
Low serum bicarbonate (0 to 15 mEq/L)
Urine glucose (usually >3+), Urine ketone (usually >2+)
Abnormal levels of serum electrolytes (Na+, K+, and Cl-)
Increased creatinine, BUN, and Hematocrit may be seen with
dehydration
Others: CBC, Blood and urine culture, Blood film, Chest X-ray
106

103. Management of DKA
Rehydration
2 to 3 L of IV fluid (0.9% NaCl solution) at 0.5 -
1L/hr for 1-3 hours, but the patient may need as much
as 6 to 10 L
Use 0.45% NaCl solution for pts with hypertension or
hypernatremia
Change IV solution to D5W when BG level becomes
≤250mg/dL
107

104. Management of DKA…
Reversing acidosis
Administer short-acting regular insulin: 0.1 units/kg IV
bolus, then 0.1 units/kg/hour or 5 units/hour by continuous
IV infusion; increase 2 – 3 fold if no response by 2–4 h.
If initial serum potassium is <3.3 mEq/L, do not administer
insulin until it is corrected
Even if BG levels are decreasing, insulin drip must not be
stopped until SC insulin therapy has been started or until
serum bicarbonate level ≥15 mEq/L and anion gap is ≤12
─Instead, rate of D5W infusion can be increased
108

105. Management of DKA…
Restoring Electrolytes
Monitor serum K+ levels carefully during Rx of DKA
Insulin administration or rehydration will decrease serum K+
If initial serum potassium is >5.2 mEq/L, do not supplement K+
until it is corrected
Give 10mEq/h when plasma K+ <5.0–5.2 meq/L (or 20–30 meq/L
of infusion fluid), ECG normal, urine flow and normal creatinine
documented
Administer 40–80 meq/h when plasma K+ <3.5 meq/L or if
bicarbonate is given
If K+ determination is not possible delay initiation of K+
replacement until there is reasonable urine put(>50 ml/hr)
109

106. Management of DKA…
Assess patient for precipitating factors (noncompliance,
infection, trauma, pregnancy, infarction, cocaine).
Initiate appropriate investigation (cultures, CXR, ECG)
Measure BG every 1–2 h; measure electrolytes
(especially K+, bicarbonate, phosphate) and anion gap
every 4 h for first 24 h
Monitor blood pressure, pulse, respirations, mental
status, fluid I&O every 1–4 h
110

107. Management of DKA…
Continue above Rx until patient is stable, glucose goal is
150–200 mg/dL, and acidosis is resolved. Insulin infusion
may be decreased to 0.02–0.1 units/kg per hour.
Administer long-acting insulin as soon as patient is eating
Allow for a 2–4 hour overlap in insulin infusion and SC
long-acting insulin injection
Blood glucose usually improves at a rate of 50 to
100mg/dL/hr
111

108. Management…
Patient education about symptoms of DKA, its precipitating
factors, and management of diabetes during concurrent illness
During illness or when oral intake is compromised, pts should:
─Frequently measure capillary blood glucose
─Measure urinary ketones when serum glucose is >250 mg/dL
─Drink fluids to maintain hydration
─Continue or increase insulin
─Seek medical attention if dehydration, persistent vomiting, or
uncontrolled hyperglycemia develop
112

109. Hyperglycemic Hyperosmolar
Syndrome (HHS)
 HHS is a serious life-threatening condition characterized by
hyperosmolality (≥350 mOsm/L) and hyperglycemia (≥600
mg/dL) with alterations in level of consciousness
Results from relative insulin deficiency initiated by illness
and inadequate fluid intake
Hyperglycemia induces osmotic diuresis that leads to
intravascular volume depletion, which is exacerbated by
inadequate fluid replacement
113

110. HHS cont’d
HHS occurs most often in older people (b/n 50 & 70 yrs) with
no known history of diabetes or who have type 2 diabetes
Ketosis and acidosis is usually minimal or absent
HHS often can be precipitated by:
─Infection, acute or chronic illness (e.g, pneumonia, sepsis)
─Stroke or dementia
─Medications that exacerbate hyperglycemia (e.g thiazides)
─Therapeutic procedures, such as surgery or dialysis
114

111. Clinical Manifestations
Hypotension, tachycardia, and altered mental status
Profound dehydration (dry MM, poor skin turgor)
Variable neurologic signs secondary to cerebral
dehydration
─alteration of sensorium, seizures, hemiparesis
Nausea, vomiting, abdominal pain, and Kussmaul
respirations are absent
115

112. Diagnostic findings
Blood glucose, serum osmolality
─BG level is usually 600 to 1200 mg/dL
─Osmolality exceeds 350 mOsm/kg
ABG analysis
BUN, Electrolyte
CBC
116

113. Management of HHS
Overall approach to treatment is similar to that of DKA
Fluid replacement
1–3L of 0.9% NS over the first 2–3 h. If the serum sodium
is >150 mEq/L, 0.45% saline should be used
Change to D5W when BG decreases to 250 to 300 mg/dL
After hemodynamic stability is achieved, give hypotonic
fluids (0.45% saline initially, then D5W) over the next 1–2
days at rates of 200–300 mL/h
117

114. Management of HHS…
Insulin administration
IV insulin bolus of 0.1 unit/kg followed by IV insulin at a
constant infusion rate of 0.1 unit/kg/hr
If BG does not fall, increase insulin infusion rate by two fold
Insulin infusion should be continued until pt has resumed
eating and can be transferred to SC insulin regimen
Correction of electrolyte imbalances
K+ repletion is usually necessary depending on serum K+
level
118

115. 119

116. Diabetes Insipidus
120

117. Learning objectives
At the end of this lesson, students will be able to:
Define diabetes insipidus
Describe etiologic factors of diabetes insipidus
Explain clinical manifestations of diabetes insipidus
Discuss management strategies of diabetes insipidus
121

118. Diabetes insipidus (DI)
DI is a disorder of posterior lobe of pituitary gland
characterized by deficiency of ADH
It is characterized by polydipsia and large volumes of
dilute urine
Types
Neurogenic DI: results from destruction of posterior
pituitary gland, resulting in lack of vasopressin
Nephrogenic DI: results from drug-related damage to
renal tubules, resulting in inability to conserve water
Psychogenic DI: caused by excessive water intake
122

119. Risk factors
Head trauma, brain tumor
Surgical ablation or irradiation of pituitary gland
CNS infections
Failure of renal tubules to respond to ADH
─Due to hypokalemia, hypercalcemia, and
medications (e.g., lithium, demeclocycline)
123

120. Clinical Manifestations
Very dilute urine (3 to 20 L) with nocturia
Frequency of urination
Specific gravity of 1.001 to 1.005
Signs and symptoms of fluid volume deficit including:
─Weight loss
─Poor skin turgor
─Dry mucous membranes
─Hypotension, increased heart rate
Patient tends to drink 2 to 20 L of fluid daily
124

121. Diagnosis
24-hour urine collection to measure volume and
creatinine
Plasma levels of ADH (normal: 1.3-4.1pg/mL)
Plasma and urine osmolality
Fluid deprivation test
Vasopressin challenge test
─Desmopressin is administered IV
125

122. Medical Management
Objectives
─To replace ADH (usually a long-term therapeutic program)
─To ensure adequate fluid replacement
─To identify and correct the underlying pathology
Medications
─Desmopressin/DDAVP (synthetic vasopressin)
─Other: chlorpropamide, thiazide diuretics, and/or
prostaglandin inhibitors (e.g., ibuprofen, indomethacin, and
aspirin)
126

123. Nursing management
Educate patient, family, and other caregivers about follow-up
care, prevention of complications, and emergency measures
Instruct about dose, actions, side effects, & administration of
all medications and signs and symptoms of hyponatremia
Demonstrate and observe return demonstration of medication
administration to ensure patient received prescribed dosage
Advise to wear medical identification bracelet and carry
required medication and information about DI at all times
127

124. Disorders of
Thyroid Gland
128

125. Learning objectives
At the end of this lesson, students will be able to:
Differentiate between hypothyroidism and hyperthyroidism
Describe causes of hypothyroidism and hyperthyroidism
Describe diagnostic methods used for hypothyroidism and
hyperthyroidism
Describe management of hypothyroidism and
hyperthyroidism
129

126. Hypothyroidism
Results from suboptimal levels of thyroid hormone
It can range from mild, subclinical forms to myxedema
(severe deficiency)
Primary or thyroidal hypothyroidism
Central hypothyroidism
─Pituitary or secondary hypothyroidism
─Hypothalamic or tertiary hypothyroidism
Neonatal hypothyroidism: present at birth
130

127. Causes
Autoimmune disease (Hashimoto thyroiditis)
Iodine deficiency
Therapy for hyperthyroidism
─Radioactive iodine, thyroidectomy
─Antithyroid medications
Atrophy of thyroid gland with aging
Radiation to head and neck
131

128. Pathophysiology
Decreased T4 leads to stimulation of TSH in the
pituitary gland
TSH stimulates secretion of T3 to increase production
of T4, leading to hypertrophy of thyroid gland
Laboratory findings
─Decreased T3 (normal: 260-480pg/dl)
─Decreased T4 (normal: 5.4-11.5mcg/dl)
─Increased TSH (normal: 0-15mIU/L)
132

129. Clinical Manifestations
Extreme fatigue, air loss, brittle nails, and dry and thick skin
Numbness and tingling of the fingers
Voice may become husky, and hoarseness
Menorrhagia, amenorrhea, loss of libido
Respiratory muscle weakness, Inadequate ventilation, and
sleep apnea
Elevated serum cholesterol, atherosclerosis, CAD, poor left
ventricular function, and pericardial effusion
133

130. Clinical Manifestations…
Face becomes expressionless and masklike
Subnormal body temperature and pulse rate
Weight gain even without increase in food intake
Irritability, fatigue, constipation, mental processes
become dulled
Speech is slow, tongue enlarges, hands and feet
increase in size, and deafness
134

131. Medical Management
Objectives
─To restore normal metabolic state
─To prevent disease progression and complications
Pharmacologic Therapy
─Synthetic levothyroxine (75 to 150 mcg per day)
─IV administration of T4 and T3 for myxedema coma
until the patient is safe to take oral form
135

132. Nursing Management
Monitor patient’s vital signs and cognitive level closely
Maintain vital functions, such as managing
cardiopulmonary status, hyponatremia, and
hypoglycemia
Monitor blood glucose levels closely
Take precautions during course of therapy because of
interaction of thyroid hormones with other medications
136

133. Hyperthyroidism
It is the 2nd most prevalent endocrine disorder, after
diabetes
It results of overproduction of T3, T4, or both
It is manifested by a greatly increased metabolic rate
Usually oversecretion of T3 and T4 is associated with
enlarged thyroid gland
Most common causes: Graves disease, toxic
multinodular goiter, and toxic adenoma
137

134. Hyperthyroidism…
Graves disease
Autoimmune disorder resulting from excessive output
of thyroid hormones caused by abnormal stimulation of
thyroid gland
Affects women eight times more frequently than men
138

135. Clinical Manifestations
Nervousness, emotionally hyperexcitable, irritable, and
apprehensive
Inability to sit quietly
Heat intolerance, perspiration
Skin appears flushed and feels warm, soft, and moist
Increased appetite and dietary intake
Weight loss, fatigability and weakness
139

136. Clinical Manifestations…
Ophthalmopathy (eg. Exophthalmo)
Amenorrhea and changes in bowel function
Palpitations, increased pulse
Atrial fibrillation, sinus tachycardia or dysrhythmias,
increased pulse pressure
Myocardial hypertrophy and heart failure if left
untreated
140

137. Diagnosis
P/E: thyroid gland is enlarged, feels soft, and may
pulsate; often thrill can be palpated, and bruit is heard
over thyroid arteries
─signs of increased blood flow through thyroid gland
ECG
↓sed serum TSH, ↑sed T3 and T4, and ↑se in radioactive
iodine uptake
141

138. Management
Aims: To reduce thyroid hyperactivity, relieve symptoms,
and prevent complications
Treatment consists of combination of radioactive iodine,
antithyroid agents, and surgery
Radioactive iodine 131 therapy
─Destroys the overactive thyroid cells
─Almost all body’s iodine are concentrated in thyroid
gland
142

139. Management…
Antithyroid drugs
Inhibits one or more stages in thyroid hormone synthesis or
release
Most commonly, propylthiouracil (PTU) or methimazole
(Tapazole) is used until the patient is euthyroid.
─These medications block the conversion of T4 to T3
Adjunctive Therapy to antithyroid drugs
Propranolol: to control nervousness, tachycardia, tremor,
anxiety, and heat intolerance
143

140. Management…
Thyroidectomy
Indications: pregnant women allergic to antithyroid drugs,
patients with large goiters, or patients unable to take
antithyroid drugs
Performed soon after thyroid function has returned to
normal (4 to 6 weeks)
Surgical removal of about five sixths of thyroid tissue
(subtotal thyroidectomy) reliably results in a prolonged
remission in most patients with exophthalmic goiter
144

141. 145

142. Disorders of
parathyroid gland
146

143. Learning objectives
At the end of this lesson, students will be able to:
Differentiate between hypoparathyroidism and
hyperparathyroidism
Describe causes of hypothyroidism and hyperthyroidism
Describe diagnostic methods used for hypoparathyroidism
and hyperparathyroidism
Describe management of hypoparathyroidism and
hyperparathyroidism
147

144. Hyperparathyroidism
It is caused by overproduction of parathormone
It is characterized by bone decalcification and
development of renal stone
Primary hyperparathyroidism
It occurs 2 to 4 times more often in women than in men
It is most common b/n 60 and 70 years of age
148

145. Hyperparathyroidism
Secondary hyperparathyroidism
It occurs in patients who have chronic kidney failure
and so-called renal rickets as a result of phosphorus
retention, increased stimulation of parathyroid glands,
and increased parathormone secretion
149

146. Clinical Manifestations
Patient may have no symptoms or may experience signs
and symptoms
Apathy, fatigue, muscle weakness, nausea, vomiting,
constipation, hypertension, and cardiac dysrhythmias
Irritability, neurosis, psychoses caused by the direct
action of calcium on the brain and nervous system
Decrease in excitation potential of nerve and muscle
tissue
150

147. Clinical Manifestations…
Nephrolithiasis, pyelonephritis, and kidney injury
Skeletal pain and tenderness
Pain on weight bearin
Pathologic fractures
Deformities, shortening of body stature
Peptic ulcer and pancreatitis
151

148. Diagnosis
Elevation of serum Ca++ levels and parathormone
Radioimmunoassays for parathormone
Bone changes may be detected on x-ray or bone scans
Double-antibody parathyroid hormone test is used to
distinguish between primary hyperparathyroidism and
malignancy
Ultrasound, MRI, thallium scan,and fine-needle biopsy
152

149. Management
Parathyroidectomy: surgical removal of abnormal
tissue
Daily fluid intake of 2,000 mL or more to prevent renal
stone formation
Thiazide diuretics are avoided
Patient is advised to avoid a diet with calcium
Monitor the patient to detect symptoms of tetany
closely
153

150. Hypoparathyroidism
It results from hyposecretion of parathyroid glands,
Leads to low levels of PTH that eventually results in
hypocalcemia and hyperphosphatemia
The most common cause is surgical removal of
parathyroid gland tissue during thyroidectomy,
parathyroidectomy, or radical neck dissection
154

151. Hypoparathyroidism…
In the absence of parathormone, there is decreased
intestinal absorption of dietary calcium and decreased
resorption of calcium from bone and through renal
tubules
Decreased renal excretion of phosphate causes
hypophosphaturia, and low serum calcium levels result
in hypocalciuria
155

152. Clinical Manifestations
Irritability of neuromuscular system and tetany
Symptoms of latent tetany: numbness, tingling, and
cramps in extremities, and stiffness in the hands and feet
Signs of overt tetany: bronchospasm, laryngeal spasm,
carpopedal spasm (flexion of the elbows and wrists and
extension of the carpophalangeal joints and dorsiflexion
of the feet), dysphagia, photophobia, cardiac
dysrhythmias, and seizures
Anxiety, irritability, depression, delirium
ECG changes and hypotension
156

153. Diagnostic Findings
Positive Chvostek sign or a positive Trousseau sign
suggests latent tetany
Chvostek sign is positive when sharp tapping over the facial
nerve just in front of parotid gland and anterior to ear causes
spasm or twitching of mouth, nose, and eye
Trousseau sign is positive when carpopedal spasm is
induced by occluding the blood flow to arm for 3 minutes
with a blood pressure cuff
Serum calcium & phosphate levels, x-rays of bone
157

154. Medical Management
Administer 10% calcium gluconate intravenously
If this does not decrease neuromuscular irritability and
seizure activity immediately, sedative agents, such as
pentobarbital, may be administered.
Parenteral PTH to treat acute hypoparathyroidism
with tetany
Diet high in calcium and low in phosphorus
158

155. Medical Management…
Aluminum hydroxide gel or aluminum carbonate
may be used after meals to bind phosphate and promote
its excretion through the GI tract
Vitamin D
─Dihydrotachysterol, ergocalciferol, or
cholecalciferol
─Enhances calcium absorption from the GI tract
159

156. Nursing Management
Keep calcium gluconate at the bedside in a locked
container or in a place where it is readily available
along with equipment necessary for IV administration.
Continuous cardiac monitoring and careful assessment
Educate patient about medications and diet therapy
Teach patient to contact the primary care provider if
these symptoms occur
160

157. Cushing syndrome
161

158. Learning objectives
At the end of this lesson, students will be able to:
Define Cushing syndrome
Describe causes of Cushing syndrome
Describe management Cushing syndrome
Describe diagnostic methods used for Cushing
syndrome
162

159. Cushing syndrome
It is a rare disorder characterized by high levels of
serum cortisol
3 causes of Cushing syndrome:
Pituitary tumor that overproduces ACTH
Adrenal tumor that overproduces ACTH
Long-term glucocorticoid therapy
163

160. Cushing syndrome…
It more frequently affects women,
Ectopic ACTH syndrome is more frequently identified
in men
Only 10% of patients with Cushing’s syndrome have
primary, adrenal cause
Use of glucocorticoids is the most common cause
164

161. Clinical Manifestations
C/Ms are primarily due to oversecretion of
glucocorticoids and androgens
Upregulation of gluconeogenesis, lipolysis, and protein
catabolism
Arrest of height, hypertension, hirsutism, and
depression
Thin, fragile, and easily traumatized skin
Ecchymoses, purple striae
165

162. Clinical Manifestations…
Muscle weakness, wasting, and thin extremities
Increased susceptibility to infection
Slow healing of minor cuts
Disturbed sleep
Osteoporosis, kyphosis, backache, and compression
fractures of vertebrae
166

163. Clinical Manifestations…
Altered fat metabolism results in a classic picture of
Cushing syndrome in the adult:
─Central obesity
─Protruding abdomen
─Fatty “buffalo hump” in the neck and
supraclavicular areas
─ “moon-faced” appearance
167

164. 168
Buffalo hump
Facial hair
Moon face

165. Clinical Manifest…cont’d
Virilization in females
─Hirsutism, breasts atrophy, menses cease, clitoris
enlarges, and voice deepens
Libido is lost in men and women
169

166. 170

167. 171

168. Diagnosis
Serum cortisol
Urinary cortisol
Low-dose dexamethasone suppression tests
─1 mg of dexamethasone is administered orally at 11:00 PM,
and plasma cortisol level is obtained at 8:00 AM the next
morning
─Suppression of cortisol to <5mg/dL indicates hypothalamic–
pituitary–adrenal axis is functioning properly
CT, ultrasound, or MRI is performed to localize adrenal tissue and
detect tumors of adrenal gland
172

169. Management
If cause is pituitary tumors,
─surgical removal of tumor by transsphenoidal
hypophysectomy
─Radiation of the pituitary gland
Adrenalectomy in patients with unilateral primary
adrenal hypertrophy
Medical management for bilateral adrenal dysplasia
173

170. Management…
Temporary replacement therapy with hydrocortisone
may be necessary for several months, until the adrenal
glands begin to respond normally to the body’s needs.
Lifetime replacement of adrenal cortex hormones if
bilateral adrenalectomy is performed
174

171. Management…
If cause is ectopic ACTH secretion
─Adrenal enzyme inhibitors to reduce hyperadrenalism
─Metyrapone, aminoglutethimide, mitotane, and
ketoconazole
If cause is administration of corticosteroids
─Reduce or taper medication to the minimum dosage
─Alternate-day therapy decreases the symptoms of
Cushing syndrome and allows recovery of the adrenal
glands’ responsiveness to ACTH
175

172. Nursing Management
Establish a protective environment to prevent falls, fractures, and
other injuries to bones and soft tissues
Encourage foods high in protein, calcium, and vitamin D to
minimize muscle wasting and osteoporosis.
Assess pt frequently for subtle signs of infection because anti-
inflammatory effects of corticosteroids may mask the common
signs of inflammation and infection.
Assess skin and bony prominences frequently and encourage and
assist pt to change positions frequently to prevent skin breakdown
176

173. Reading assignment
Iodine deficiency related goiter
Thyroiditis (acute and chronic)
Thyroid Cancer
Addison’s diseases
177

174. Thank you
178