Endocrine disorders

1. Hakim Shah
RN, BSN, MSN, PhD (Scholar)
September 06 & 07, 2022
1
Required Reading Book:
Carol, Porth M. (2014). Pathophysiology concept of altered health states (9th Ed). Philadelphia: J. B. Lippincott
Chaper-48 (Page# 1264), Chapet-50 (Page# 1303)

2. Class Agenda
 Review the hypothalamic pituitary control
mechanism of hormone secretions in the body.
 Differentiate between hypo & hyper function of
the endocrine glands.
 Review of Anatomy & Physiology of endocrine
pancreas.
 Briefly discuss the classification of diabetes
mellitus (DM)
 Discuss etiology, pathophysiology, and clinical
manifestations of Type-1 DM & Type-2 DM.
 Identify the main differences between Type-1 &
Type-2 DM.
2

3. Review of Endocrine System
Gland of Endocrine system
 Hypothalamus
 Posterior Pituitary
 Anterior Pituitary
 Thyroid Gland
 Parathyroid Gland
 Adrenals
 Pancreatic islets
 Ovaries and testes
3

4. 4

5. 5

6. 6

7. Hypothalamus
Releasing and inhibiting hormones
Corticotropin-releasing hormone
Thyrotropin-releasing hormone
Growth hormone-releasing hormone
Gonadotropin-releasing hormone
Somatostatin-inhibiting hormone that
inhibits GH and TSH
7

8. Anterior Pituitary
 Growth Hormone
 Stimulates growth
 Adrenocorticotropic hormone
 Stimulates glucocorticoid and Mineralocorticoid
 Thyroid stimulating hormone
 Stimulate releasing of T3 & T4
 Follicle stimulating hormone
 Stimulates ovary in female, sperm in males
8

9. Cont…
 Luteinizing hormone:
 Stimulates corpus luteum in females, secretion of
testosterone in males
 Prolactin:
 prepares female breasts for lactation
9

10. Posterior Pituitary
 Antidiuretic Hormone
 Causes reabsorption of water and sodium from
the collecting tubule of kidney thus decrease urine
output.
 Oxytocin
 Causes contraction of uterus, and milk ejection
from breasts
10

11. Adrenal Cortex
 Mineralocorticoid—aldosterone. Affects sodium
absorption, loss of potassium by kidney
 Glucocorticoids (Cortisol). Affects metabolism,
regulates blood sugar levels, affects growth,
anti-inflammatory action, decreases effects of
stress
 Adrenal androgens—dehydroepiandrosterone
and androstenedione. Converted to
testosterone in the periphery.
11

12. Adrenal Medulla
 Epinephrine and norepinephrine-serve as
neurotransmitters for sympathetic Nervous
system
12

13. Thyroid
 Follicular cells—excretion of triiodothyronine
(T3) and thyroxine (T4) that Increase BMR,
increase bone and calcium turnover, increase
response to catecholamines, need for fetal
growth & development
 Thyroid C cells—calcitonin. Lowers blood
calcium and phosphate levels
13

14. Parathyroid
 Parathyroid hormone—regulates serum
calcium
14

15. Pancreatic Islet cells (Islets of
Langerhans)
 B- Cells
 Secrete Insulin: Insulin stores glucose in liver and
muscle as glycogen. Metabolize glucose in the cells
 A-Cells
 Secrete Glucagon: Glucagon Stimulates
glycogenolysis and glyconeogenesis
 D-Cells
 Secrete Somatostatin: Somatosatin
decreases intestinal absorption of
glucose
15

16. Physiology of Glucose Metabolism
Blood Glucose
 Normal serum level glucose 65 – 105 mg/dl
 Inside CNS
 Brain uses glucose as primary fuel
 Brain cannot store/produce glucose
 Outside CNS
 Fatty acids converted to glucose and stored as
 Glycogen (liver/muscles)
 Triglycerides (fat cells)
16

17. Regulation of Glucose
Blood Glucose level is regulated by two Hormones:
Insulin and Glucagon
 Endocrine portion of pancreas has group of cells
called ‘Islets of Langerhans’ which contains Beta
Cell & Alpha Cells
Beta cells make insulin
 Allows body cells to store and use
carbohydrate, fats, and protein
 Alpha cells make glucagon
 “counterregulatory”, acts opposite of insulin
17

18. Function of Insulin
When blood glucose becomes high ,insulin
lowers glucose level in the following methods:
 Liver
 Helps in production and storage of glucose in the
form of glycogen
 Inhibits glycogen breakdown
 Increased protein & fat synthesis (VLDL
formation)
 Muscles
 Promotes protein and glycogen synthesis
 Fat cells
 Promotes storage of triglycerides
18

19. Function of Glucagon
 Glucagon causes release of glucose from
liver
 “Glycogenolysis (breakdown of glycogen
to glucose)
 “Glyconeogenesis (formation of glucose) if
glucose not available
 Lipolysis (breakdown of fat)
 Proteolysis (breakdown of amino acids)
19

20. Diabetes Mellitus
A group of diseases characterized by high levels of blood
glucose resulting from defects in insulin production,
insulin action, or both which result in impaired
metabolism of carbohydrates, fats and protein
20

21. Prevalence of DM
 Estimated 7% of US population is diabetic
 Twice that many have prediabetes
 21% of those over 60 have diabetes
 45% of new diagnoses are being made in
children and adolescents
21

22. Types of Diabetes Mellitus
Type 1 Diabetes
 Cells that produce insulin
are destroyed
 Results in insulin
dependence
 Commonly detected
before 30
 10% diabetes is type I
Type 2 Diabetes
Blood glucose levels rise due to
 Lack of insulin production
 Insufficient insulin action (resistant
cells)
 Commonly detected after 40
 > 90% diabetes is type II
 This type eventually leads to β-
cell failure (resulting in insulin
dependence)
Gestational Diabetes
3-5% of pregnant women in the world develop gestational diabetes
22

23. Pathophysiology of Type I
23

24. Pathophysiology of Diabetes II
Decresed level of circulatory insulin
Impaired metabolism of glucose
Decreased production of insulin by beta cells or increased
Insulin demand
Destruction or resistance of insulin receptors
24

25. Risk factor/Causes of Type I
 Autoimmune: Destruction of beta cell by
antibodies
 Destruction of beta cells by virus
 Genetic factors
25

26. Risk Factors/Causes of Type II
Predisposing Factors:
 Obesity (80%)
 Heredity
 Hypertension
 Sedentary life style: lack of excersice
 Consistent High caloric diet intake
 Stress
 High cholestrol level
26

27. Clinical Manifestation
 3 P’s
 Polyuria
 Polydipsia
 Polyphagia
 Fatigue, tingling or numbness in hands, slow
healing wounds and recurrent infections
27

28. Diagnosi
s
Fasting Plasma Glucose Test
(FPG) –cheap & fast
 Fasting B.G.L. 100-125 mg/dl
signals pre-diabetes
 >126 mg/dl signals diabetes
Oral Glucose Tolerance Test
(OGTT)
 Tested for 2 hrs after glucose-
rich drink
 140-199 mg/dl signals pre-
diabetes
 >200 mg/dl signals diabetes
Glycated Hemoglobin (A1C) tests
For people without diabetes, the normal range for the hemoglobin
A1c level is between 4% and 5.6%. Hemoglobin A1c levels
between 5.7% and 6.4% indicates prediabetes and a higher chance
of getting diabetes. Levels of 6.5% or higher signals diabetes.
28

29. 29

30. 30

31. Cont…
 Fasting plasma glucose—125 mg/dL
 Random sugar >200mg/dL
 According to text, OGTT and IV glucose tolerance
test no longer used routinely—see latest
guidelines
31

32. Complications
 Acute Complications
 Hyperglycemia
 Diabetic Keto Acidosis (DKA) occurs in Type 1 DM
 Hyperglycemic Hyperosmolar Non-ketotic Syndrome
(HHNK): Occurs in Type II DM
 Hypoglycemia
 Ussoally occurs in Type I due to insulin reaction, and rarely
in Type II due to increased intake of hypoglycemic drug
 Chronic Complications
32

33. Hyperglycemia
 A condition in which fasting blood glucose (FBS)
is greater than 125mg/dl, and Random Blood
Sugar (RBS) is greater than 200mg/dl
33

34. Clinical manifestation of
Hyperglycemia
 Drowsiness, flushed face, increased thirst, blurred
vision
 Polyuria
 Sodium, chloride, potassium excreted
 Electrolyte and fluid imbalance
 Polydipsia from dehydration
 Polyphagia: cells are starving, so person feels
hungry despite eating huge amounts of food.
Starvation state remains until insulin is available.
34

35. Diabetic Ketoacidosis (DKA)
 Causes:
 Three main causes are:
 Illness,
 Undiagnosed DM
 Untreated DM, and decreased insulin
 Other causes: patient error, intentional skipping of
insulin.
35

36. Manifestation of DKA
 3 P’s
 Orthostatic hypotension
 Ketosis
 GI s/s: N/V, diarrhea, abdomen pain
 Acetone breath
 Hyperventilation (Kuassmal breathing)
 Dehydration and electrolyte loss
36

37. Diagnosis of DKA
 BS between 300-800
 Acidosis
 Electrolyte abnormalities
 Elevated BUN, creatinine and hematocrit related
to dehydration
37

38. Management
 Rehydrate with normal saline, then follow with
.45% NaCl then D5.45NS (or other)
 Restore electrolytes
 ECGs
 Hourly blood sugars
 IV insulin
 Avoid bicarbonate as can affect serum K+
38

39. Nursing management
 Nursing Diagnosis
 Body fluid and electrolytes imbalance R/L excessive
loss through GI (diarrhea, N/V)
 Ineffective breathing pattern i.e hypoventilation R/L
increased acidity of blood
 Altered thought process R/L increased blood sugar
level
39

40. Nursing management
 Administer fluids
 Insulin
 Prevent fluid overload
 Strict I&O
 Follow lytes
 ECG monitoring
 Vital signs
 Monitor patient responses to treatments
40

41. Hyperosmolar Hyperglycemic Non
Ketosis Syndrome (HHNS)
 Predominated by hyperosmolarity and
hyperglycemia
 Minimal ketosis
 Osmotic diuresis
 Glycosuria and increased osmolarity
 Occurs over time
 Blood sugar is usually over 600
41

42. Cont…
 Occurs more often in older people
 Type 2 diabetes mellitus
 No ketosis
 Do not usually have the concomitant n/v
 Hyperglycemia, dehydration and hyperosmolarity
may be more severe than in DKA
42

43. Medical Management
 Similar treatment as seen in DKA
 Watch fluid resuscitation if history of heart failure
 ECG
 Electrolytes monitoring
 Fluids with potassium replacement
43

44. Nursing Management
 Monitor neurologically
 Monitor ECG
 Monitor vital signs
 Labs
 Hourly blood glucose monitoring
 Insulin IV
 Cautious correction of hyperglycemia to avoid
cerebral edema
44

45. 45

46. Chronic complications of DM are grouped in to the
following categories.
• Vascular disease
1. Macrovascularopathy
– Coronary artery diseases (CAD)
– Hypertension
– Stroke
2. Microvascularopathy
– Retinopathy
– Nephropathy
• Neuropathy
• Diabetic Foot problems (Due to both Vascular and
neuropathy)
46

47. Vascular Disease
• Macro vascular Disease: Thickening of the arteries-
Arthrosclerosis which leads to coronary artery disease
(CAD), Hypertension and heart failure.
• Micro vascular disease: Thickening of the capillary
basement membrane that surrounds
the endothelial cells of the capillary, increased capillary
permeability and capillary occlusion
• Affects the areterioles, venules, & capillaries of eye,
kidney and other organs. Examples are Retinopathy &
Nephropathy
47

48. Diabetic Retinopathy
• Leading cause of blindness in the United
States
• Characterized by deterioration of the small
blood vessels in the retina
• After 10 years of having diabetes 50% of all
diabetics have it and 90% of those who have
poor control of blood glucose levels 48

49. Diabetic Nephropathy
• Occurs in patients with Type 1 diabetes after
15 -20 years (30% to 40% progress to end -
stage renal disease)
• Occurs after 5 to 10 years with Type 2
diabetics
• Deterioration of kidney function takes place
over many years - first sign is protein in the
urine
49

50. Manifestations of Nephropathy
• Frequent urinary tract infections and
incontinence
• Sexual - Impotence in men and inability to
have an orgasm
• Characterized by proteinuria,
hypertension,edema and renal insufficiency
50

51. Nephrotic Syndrome
• Nephrotic syndrome is diagnosed when
protein excreted exceeds 3.5 g/d.
• When protein is lost in the urine, the serum
protein also decreases.
• Low serum protein causes decreased oncotic
pressure and retention of fluid that leads to:
– Weight gain
– Edema
– Protein tissue wasting
51

52. Diabetic Neuropathy
• Occurs in 70% of diabetic patients
• Prevalence increases with age and severity of
hyperglycemia
• Results in loss of large and small myelin nerve
fibers, connective tissue proliferation and
thickening of the capillary basement
membrane
52

53. Cont..
• Can have mononeuropathy such as carpal
tunnel syndrome, extraocular motor paralysis
& foot-drop
• Most patients have numbness, tingling,
burning, dull ache & cramping that begins in
the digits & progresses to the foot and hand
(worse at night)
53

54. Cont…
• progresses to muscle weakness & sensory
loss, an unbalanced gait, foot ulcers and loss
of fine motor skills.
• Sensory neuropathy leads to loss of pain &
pressure sensation & increases the risk of
undetected injury, tissue ischemia or
infection
54

55. • Insulin ( Type 1 DM)
• Excersice
• Nutrition
• Medicine
• Insulin (in some cases in Type 2 DM)
55

56. 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
56

57. Cont…
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, HHNS
d. Women with gestational diabetes who are not
adequately controlled with diet
e. Some clients receiving high caloric feedings including
tube feedings or parenteral nutrition
57

58. Types of Insulin
58

59. 59
Start 3-4
hrs.
Peakless
Humulin® U vial only
Lantus (Glargine) vial only
Levemir (Detemir) cartridge
Prolonged
action
Start 1.5
hrs
Peak 7 hr
Novolin®ge NPH
Humulin® N
Intermediate
Vial and cartridge
Start 30-60
min.
Peak 4 hr
Novolin®ge Toronto
Humulin® R
Short-acting
(regular)
Vial and cartridge
Start < 15
min.
Aspart (NovoRapid®)
Lispro (Humalog®)
Rapid-acting
Vial and cartridge

60. Cont…
• Regular + intermediate
• Novolin® 10/90, 20/80, 30/70, 40/60, 50/50
• Humulin® 30/70, 20/80
• Analogue Pre-Mix
• Humalog® 25/75 (insulin lispro protamine
suspension)
• NovoMix 30* (protaminated insulin aspart)
60

61. Cont…
• Injection sites
– Abdominal areas is the most preferred because of
rapid absorption
– Do not aspirate insulin injections
61

62. Insulin site
62

63. Cont…
• Alternative insulin administration
– Insulin pump
• Continuous subcutaneous infusion of a basal dose with
increases at meal times
– Implanted pumps
• Implanted into the peritoneal cavity
– Inhaled insulin
• Under developme
63

64. 64

65. 65

66. 1. Used to treat Diabetes Type 2
2. Client must also maintain prescribed diet and
exercise program; monitor blood glucose
levels
Not used with pregnant or lactating women
66

67. Cont…
4. Several different oral hypoglycemic agents
and insulin may be prescribed for the client
5. Specific drug interactions may affect the
blood glucose levels
6. Must have some functioning beta cells
67

68. Classifications and Action of
Hypoglycemic drugs
a.Sulfonylureas
Action: Stimulates pancreatic cells to secrete
more insulin and increases sensitivity of
peripheral tissues to insulin
Indication: to treat non-obese Type 2 diabetics
Example: Glipizide (Glucotrol),
Chlorpropamide (Diabinese), Tolazamide
(Tolinase)
68

69. b. Meglitinides
Action: stimulates pancreatic cells to secret
more insulin
Indication: Used in non-obese diabetics
Side effects: Taken just before meals, rapid
onset, limited duration of action. Major
adverse effects is hypoglycemia
Example: Repaglinide (Prandin), Nateglinide
(Starlix)
69

70. c. Biguanides
Action: decreases overproduction of glucose by
liver and makes insulin more effective in
peripheral tissues
Indication: Used in obese diabetics. Does not
stimulate insulin release
Contraindication: Metabolized by the kidney, do
not use with renal patients
Example: Metformin (Glucophage)
70

71. d. Alpha-glucoside Inhibitors
Action: Slow carbohydrate digestion and delay
rate of glucose absorption
• Take with first bite of the meal or 15 min.
after
• Adjunct to diet to decrease blood glucose
levels
Example: Acarbose (Precose), Miglitol (Glyset)
71

72. e. Thizaolidinediones (Glitazones)
Action: Sensitizes peripheral tissues to insulin
Indication: Used in obese diabetics
• Inhibits glucose production
• Improves sensitivity to insulin in muscle, and
fat tissue
Example: Rosiglitazone (Avandia), Pioglitazone
(Actos)
72

73. • Patients with Type 2 DM who are obese have
insulin resistance, they produce enough
insulin
– Should use Glucophage, Actos or Avandia
– Enhances insulin secretion in tissue, but does not
increase amount of insulin secreted
73

74. A.Goals for diabetic therapy include
1.Maintain as near-normal blood glucose levels
as possible with balance of food with
medications
2.Obtain optimal serum lipid levels
3.Provide adequate calories to attain or
maintain reasonable weight
74

75. Diet Composition
1. Carbohydrates: 60 – 70% of daily diet
– Carbohydrates convert quickly to sugars
• Advice patient to consume a similar amount of carbs at
each meal
• Medications can work on a consistent glucose response
from foods
2. Protein: 15 – 20% of daily diet
3. Fats: 10% of daily diet
– No more than 10% of total calories from saturated fats
75

76. • Fiber: 20 to 35 grams/day; promotes
intestinal motility and gives feeling of fullness
• 5. Sodium: recommended intake 1000 mg
per 1000 kcal
• 6. Sweeteners approved by FDA instead of
refined sugars
• 7. Limited use of alcohol: potential
hypoglycemic effect of insulin and oral
hypoglycemics
76

77. 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
77

78. Cont…
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
78

79. Common Nursing Diagnoses and
Specific Teaching Interventions
A. Risk for impaired skin integrity: Proper
foot care
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
79

80. Cont…
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
80

81. Cont…
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
81

82. Cont…
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
82

83. References
 Brunner & Suddarth (2008). Text book of Medical-Surgical
Nursing (10th Ed). Lippincott
 Renuka C. P. et.al (2002) J. Biol. Chem. 277, 22590–4
 Zoltan V. AND William C. D. (2001) Pharm. Rev. 52, 1-9
 Lauge S. et. Al (2003) PNAS 100, 4435-9
 Mark R. B. (1997) J. of Clin. Endoc.& Met. 82, 3-7
 Gianni C. (1992) FEBS 307, 66-70
 Irl B. H., (2001) Clin. Diabetes 19, 146-7
 BRUCE W. B. and POUL S. (2001) Diabetes care 24,69-72
http://www.indstate.edu/thcme/mwking/diabetes.html
83