7endocrine System Disorders

Medical Surgical Nursing by Selamu Amanuel 1
DISORDERS OF THE
ENDOCRINE SYSTEM
02/28/2023
Anatomy and physiology
2
 The endocrine system has far-reaching effects in the

human body because of its links with the nervous system
and the immune system.
 The endocrine glands secrete their products directly in to

the blood stream, which differentiates them from
exocrine glands such as sweat glands, which secretes their
products through ducts in to epithelial surface or into the
GIT.
Medical Surgical Nursing by Selamu Amanuel 02/28/2023

Cont---
3
 The hypothalamus is the link between the nervous system

and the endocrine system.
 It plays an important role in the Endocrine System
because it regulates the pituitary secretion of hormones
that influence metabolism, reproduction, stress response
and urine production.
 It works with the pituitary to maintain fluid balance and
temperature regulation by promoting vasoconstriction or
vasodilatation.

Cont---
4
 Glands of the Endocrine system includes:

 Pancreatic islets
 Pituitary gland
 Thyroid gland
 Parathyroid gland
 Adrenals
 Ovaries and Testes

Fig. components of endocrine system
5

Pancreas
6
 is a fish shaped organ located in the upper abdomen

behind & inferior to the liver & stomach.
 It has both endocrine & exocrine function
 Islets of Langerhans's [the endocrine part of the
pancreases] composed of:
 Alpha cells which secret glucagon
 Beta cells which secret insulin
 Delta cells which secret somatostatin.
 Gamma cells which secret pancreatic polypeptide.
Fig. pancreas
7

Cont---
8
 Insulin
 is one of the polypeptide hormones.
 it is a powerful hypoglycemic agent i.e.it acts to lower
blood glucose level by promoting the passage of glucose
in to cells.
 it is the only hormone in the body that decreases blood
glucose level.
 Plays a key role in the metabolism of CHO, fat & protein
 It is an anabolic (storage) hormone.
Function of Insulin
9
 Stimulate the active transport of glucose in to muscle and

liver.
 Enhances storage of dietary fat in adipose tissue.
 Regulate the rate at which CHO are used by the cells for
energy.
 promotes conversion of glucose in to glycogen but inhibits the
conversion of glycogen to glucose
 promotes the conversion of fatty acids in to fat but inhibits
break down of adipose tissue, mobilization of fat (fat to
glucose) & conversion of fat in to ketone bodies.
Cont----
10
 Promote protein synthesis with in the tissues but inhibits

the conversion of protein in to glucose.
 Accelerates transport of amino acids (derived from
dietary protein) in to cells
 It also inhibits the breakdown of stored glucose, protein
and fats.

Cont---
11
 During fasting periods (between meals and overnight)

the pancreas continuously releases a small amount of
insulin another pancreatic hormone called glucagon is
release stored glucose.
 The insulin and the glucagon together maintain a
constant level of glucose in the blood by stimulating the
release and uptake of glucose from the liver.

Cont---
12
 Initially, the liver produces glucose through the

breakdown of glycogen (glycogenolysis)
 After 8 to 12 hours w/o food, the liver forms glucose
from the breakdown of non carbohydrate substances,
including amino acids (gluconeogenesis)

Cont---
13
 Antagonists of insulin.
 Epinephrine
 Corticosteroid
 Growth hormone
 Glucagon
 Glucagon
 Is a potent hyperglycemic agent which rises blood sugar by
promoting the conversion of glycogen [the principal form
in which CHO are stored] to glucose with in the liver.
Pituitary gland
14
 Anatomy and physiology of pituitary gland

 It is commonly referred as a master gland.
 It secretes hormones that control the secretion of
hormones by other endocrine glands.
 It is divided in to the anterior and posterior lobes.

Posterior pituitary
15
 ADH (anti diuretic hormone) or vasopressin and

Oxytocin are the important hormone that is secreted
by the posterior lobe.
 Vasopressin controls the excretion of water by the
kidney; its secretion is stimulated by an increase in
the osmolarity of the blood or by decreased in BP.
 Oxytocin facilitates milk ejection during lactation and
increase the force of uterine contraction during labor
and delivery. Its secretion is stimulated during
pregnancy and at child birth.
Anterior pituitary
16
 The major hormones of Anterior pituitary gland

are :
 TSH (Thyroid-stimulating hormone), which
stimulates synthesis and secretion of thyroid
hormone.
 ACTH (Adrenocorticotropic hormone) stimulates
synthesis and secretion of adrenal cortical hormone.
 FSH (Follicle-Stimulating hormone), Female:
stimulates growth of ovarian follicle, ovulation; for
male: stimulate sperm production.
Cont----
17
 LH (Luteinizing hormone), Female- stimulates

development of corpus luteum, release of oocyte,
production of estrogen and progesterone. For
Male stimulates secretion of testosterone,
development of interstitial tissue & testes.
 GH (Growth hormone or somatotropin),
stimulates growth of bone and muscle.

 THYROID GLAND
18
 It is a butterfly-shaped organ located in the lower neck anterior

to the trachea. (It weights about 30 g.).
 It consists of two lateral lobes connected by an isthmus
 The blood flow to the thyroid is very high (about 5ml/min/gram
of thyroid tissue); it is above five times the blood flow to the
liver. This reflects the high metabolic activity of the TG.
 The thyroid gland produces three hormones :- Thyroxine (T4),
Triiodothyronine (T3) and calcitoin
 Various hormone and chemicals are responsible for normal
thyroid function. Key among them are thyroid hormone (T4 &
T3), calcitonin and iodine.

Fig. thyroid gland
19

Cont---
20
 T4 contains four and T3 contains three iodine

atoms in each molecule
 Iodine is essential to the thyroid gland for synthesis
of its hormones.
 the major derangement in iodine deficiency is
alteration of thyroid function.
 It is ingested in the diet and absorbed in to the
blood in the GIT.

Cont---
21
 Regulation of TH
 The secretion of T3 and T4 by the thyroid gland is
controlled by TSH or thyrotropin. It controls the
release of thyroid hormone. In turn the level of TH
in the blood determines the release of TSH.
 If thyroid hormone concentration in the blood
decreases, the release of TSH increases which
causes increased out put of T3 and T4. This is an
example of negative feed back.

Cont---
22
 Function of T3 and T4
 The primary function of the thyroid hormone is to
control the cellular metabolic activity.
 T4, a relatively weak hormone, maintains body
metabolism in a steady state.
 T3 is about 5 times as potent as T4 and has a more rapid
metabolic action.
 The THs, influences cell replication and are important in
brain development.
 TH is also necessary for normal growth
Cont---
23
 The TH, though their widespread effects on cellular

metabolism, influences every major organ system.
 Normal range for T4 is 4.5 to 11.5g/dl;
 although serum T3 and T4 levels generally increase
or decrease together; the T3 level appears to be a
more accurate indictors of hyperthyroidism
 Normal range for serum T3 is 70 to 220 g/dl
(1.15 to 3.10mol/l).

Cont---
24
 CALCITONIN (THYROCALCITONIN)
 It is secreted in response to high plasma levels of
calcium, and it reduces the plasma level of Ca++
by increasing its deposition in bone.

PARATHYROID GLAND
25
 Are four in number

 They are situated in the neck and embedded in the
posterior aspect of the thyroid gland.
 These small glands are easily overlooked and can
be removed inadvertently during thyroid surgery

Cont----
26
 PARATHORMONE
 It is the protein hormone from the parathyroid glands
regulates calcium and Phosphorus metabolism.
 Increased secretion of parathormone results in
increased ca absorption from the kidney, intestine, &
bones there by raising the blood ca++ level.
 Excess Parathormone can result in markedly elevated
levels of serum ca++ a potentially life threatening
situations

Cont---
27
 When the product of serum ca++ and serum

phosphorus rises calcium phosphate may
precipitate in various organs of the body and cause
tissue calcification
 The serum level of ionized ca ++ regulates the
output of Parathormone. Increased serum ca ++
results in decreased parathormone secretion,

creating a - ve feedback system.

ADRENAL GLAND
28
 There are two adrenal glands in the human, each

attached to the upper portion of a kidney.
 Each adrenal glands has independent functions.
 The adrenal medulla at the center of the gland
secretes catecholamine and the outer portion of the
gland, the adrenal cortex secretes steroid hormones.
 The secretion of hormones from the adrenal cortex is
regulated by the hypothalamic pituitary-adrenal
axis.

Fig. adrenal gland
29

Cont----
30
 The hypothalamus secretes corticotrophin releasing

hormone (CRH), which in turn stimulates the
pituitary gland to secrete ACTH.
 ACTH then stimulates the adrenal cortex to secrete
glucocorticoid hormone (cortisol).
 Increased level of the adrenal hormone then inhibit
the production or secretion of CRH and ACTH.

Cont---
31
 Adrenal medulla
 Function as part of the ANS
 Stimulation of preganglionic sympathetic nerve
fibers, which travel directly to the cells of the
adrenal medulla, causes release of the
catecholamine hormones i.e. Epinephrine and
Nor epinephrine
 About 90% the secretion of the human adrenal
medulla is epinephrine (also called adrenaline).
Cont----
32
 The major effect of epinephrine release are to prepare

& to meet a challenge [fight-or-flight response]
 Secretion of epinephrine causes decreased blood flow
to tissues that are not needed in emergency situation,
such as GIT, & causes increased blood flow to tissues
that are important for effective fight or flight such as
cardiac and skeletal muscle.
 It also induces the release of free fatty acids, increase
the basal metabolic rate, and elevate the blood glucose
level.
Cont---
33
 Adrenal cortex
 The three types of steroid hormones produced by
the adrenal cortex are:-
 Glucocorticoids, the prototype of which is
hydrocortisone
 Mineralocorticoids, mainly aldosterone and
 Androgens, sex hormone (male)

Cont---
34
 Glucocorticoids
 Are so named because they have an important influence on
glucose metabolism.
 Increased hydrocortisone secretion results in elevated blood
glucose levels. How ever, the Glucocorticoids has major
effects on the metabolism of almost all organs of the body.
 The presence of Glucocorticoids in the blood inhibits the
release of corticotropin-releasing factor from the
hypothamlus and also inhibits ACTH secretion from the
pituitary.

Cont----
35
 Mineralocorticoids
 Exert their major effects on electrolyte metabolism.
 They act principally on the renal tubular and GI
epithelium to cause increased Na+ ion absorption
in exchange for excretion of K+ and OH-.
 ACTH only minimally influences aldosterone
secretion.
 It is primarily secreted in response to the presence
of Angiotensin II in the blood stream.
Cont---
36
 Angiotensin II is a substance that elevates the BP by

constricting arterioles. Its concentration is increase
when rennin is released from the kidney in response
to decreased perfusion pressure.
 The resultant increased aldosterone levels promote
sodium reabsorption by the kidney and the GI tract,
which tends to restore BP to normal.
 Aldosterone is the primary hormone for the long-
term regulation of sodium balance.

Diabetes Mellitus (DM)
37
 Definition: is an endocrine disease characterized by

metabolic abnormalities (Carbohydrate, fat, protein) in
which the central feature is hyperglycemia due to
absolute or relative insulin deficiency.
 It results from defects in insulin secretion, insulin action
or both.

Epidemiology
38
 Is a diseases of world wide distribution

 50 million people in the world suffer from DM.
 Varies in different areas
 The prevalence of DM in USA is 3% In Africa 1-2% and In Ethiopia
is around 1%
 The 3rd leading cause of death in developed countries.
 The 2nd leading cause of renal failure in developed countries.
 The 1st cause of blindness among adults in USA.
 The most common cause of amputation

Types of DM
39
 There are several type of DM , but the major

classifications are:
1) Type I, Insulin dependent DM (IDDM).
2) Type II, non-insulin dependent DM (NIDDM).
3) Gestational DM
4) DM associated with other factors

Etiology
40
 Genetic – especially there is a genetic correlation with NIDDM of

identical twins.
 Linked to HLA(human Leukocyte antigen) in IDDM (20x risk).
 Environmental factors
 Obesity
 Age
 Protein energy malnutrition/ PEM
 Infection (viral)- β- cell destruction.
 Chemical burns
 Auto immunity - Type I
1) TYPE 1 DIABETES
41
 It is characterized by destruction of the pancreatic beta

cells.
 It is thought that combined genetic, immunologic, and
possibly environmental (ex. Viral) factors contribute to
beta cell destruction.
 Although the events that lead to beta cell destruction are
not fully understood, it is generally accepted that a genetic
susceptibility is a common underlying factor in the
development of type 1 diabetes.

Cont---
42
 People do not inherit type 1 diabetes itself; rather, they

inherit a genetic predisposition, or tendency toward
developing type 1 diabetes.
 This genetic tendency has been found in people with
certain HLA (human Leukocyte antigen) types.
 HLA refers a cluster of genes responsible of
transplantation antigens and other immune processes.
 Immune –mediated diabetes commonly develops during
childhood and adolescence.

Cont---
43
 There is also evidence of an autoimmune response in type

I diabetes.
 This is an abnormal tissue of the body, responding to
these tissues as if they are foreign.
 In addition to genetic and immunologic components
environmental factors, such as viruses or toxins that may
initiate destruction of the beta cell are being investigated.

Pathophysiology
44
 Pancreatic β-cells destroyed by auto immune process ⇨ ↓

(no) insulin production ⇨ unchecked glucose production by
the liver ⇨ hyperglycemia
 Glucose delivered from food cannot be stored in the liver,

instead remain in the blood stream & contributes in post
prandal hyperglycemia.
 Fasting hyperglycemia occurs as a result of unchecked

glucose production by the liver.
Cont---
45
 Deficiency of insulin → glucose will not be conveyed

from extra cellular to intracellular compartment → the
cells become energy depleted → fat & protein will be
drawn from adipose tissue & muscle & negative nitrogen
balance and ketosis → increased appetite →polyphagia.
 increased blood glucose level pulls cellular water in the
blood → cellular dehydration → polydepsia

Cont---
46
 increased blood glucose level→ the kidneys may not

reabsorb all the filtered glucose [blood exceeds the renal
threshold for glucose usually 180 to 200 mg/dl]→
glucosuria→ decrease re-absorption of water by the renal
tubules polyuria.
 When excess glucose is excreted in the urine, it is
accompanied by excessive loss of fluids and electrolytes.
This is called Osmosis diuresis.

Cont---
47
 Because insulin normally inhibits glycogenolysis

(breakdown of stored glucose) and gluconeogenesis
(production of new glucose from amino acids and other
substrates) in people with insulin deficiency, these process
occur in an unrestrained fashion and contribute further to
hyperglycemia.
 In addition, fat breakdown occurs, resulting in an
increased production of Ketone bodies which are the by
products of fat breakdown

2- Type-II DM ( NIDDM)
48
 The two main problems related to insulin in type-II

diabetes are:-
 Insulin resistance (IR) and
 Impaired insulin secretion
 IR refers to a decreased tissue sensitivity to insulin
 Normally, insulin binds to special receptors on cell
surfaces and initiates a series of reactions involved in
glucose metabolism.

Cont---
49
 In type 2, these intracellular reactions are diminished, thus

rendering insulin less effective at stimulating glucose
uptake by the tissues and at regulating glucose release by
the liver
 Insulin resistance impairs glucose utilization by insulin
sensitive tissues & increases hepatic glucose out put
→hyperglycemia
 The exact mechanisms that lead to this problem in type 2
diabetes are unknown, although genetic factors are
thought to play a role
Cont---
50
 To overcome insulin resistance and to prevent the builds up

of glucose in the blood, increased amounts of insulin must
be secreted to maintain the glucose level at a normal or
slightly elevated level. However, if the level rises, and type
2 diabetes develops
 It occur most commonly in people older than, 30years who
are obese.
 Because it is associated with a slow (over years),
progressive glucose intolerance, the onset of type 2 DM
may go undetected for many years.
Cont---
51
 Despite the impaired insulin secretion that is characteristic

of type 2 diabetes, there is enough insulin present to
prevent the breakdown of fat and the accompanying
production of ketone bodies.
 Therefore, DKA doesn’t typically occur in type II DM .
Uncontrolled type II DM may, lead to other acute
problem, HHNS (Hyperglycemic Hyperosmolar non
Ketotic Syndrome).

clinical comparison of Type I & type II DM
52
Factors Type I Type II
 Synonymous formerly known as juvenile onset Maturity onset DM

DM /growth onset DM
 Age of set usually before the age Usually above 40 but may occur at
of 15 but may occur at any age any age
 Body habits too wasted Obese
 Acute complications Diabetic Ketoacidosis (DKA) Hyper osmolar non ketotic coma
(HHNK)
 HLA association Yes No
 Therapeutic control with Yes Yes /NO
insulin
 Concordance in identical <50% 100%
twins
 Possible etiology absolute insulin deficiency Relative insulin deficiency
3. Gestational DM
53
 Occurs in women who did not have diabetes before

pregnancy.
 Is any degree of glucose intolerance with its onset during
pregnancy.
 Hyperglycemia develops during pregnancy because of the
secretion of placental hormones, which causes insulin
resistance
 Insulin resistance related to the metabolic changes of late
pregnancy increase insulin requirements.
Cont---
54
 after delivery blood glucose levels return to normal ,

However, many women (30- 40%) who have had
gestational DM may develop type 2 diabetes later in life.
 Therefore all must be counseled to maintain their ideal
body weight and to exercise regularly to reduce their risk
for type 2 diabetes

4. DM associated with other medical conditions
55
 Accompanied by conditions known or suspected to

cause the disease.
 Pancreatic disease.
 hormonal abnormalities.
 drugs such as glucocorticosteroids, thiazide
diuretics , estrogen containing preparations.


5. Impaired glucose tolerance (borderline diabetes)
56
 blood glucose level is b/n normal & that of DM

(110-140 mg/dl)
 may be obese or non obese.
 Renal & retinal complications usually not
significant.
 Should be screened for DM periodically.

CLINICAL MANIFESTATIONS
57
 “three Ps” (3P’s) + weight loss

 Polyuria
 Polydipsia and
 Polyphagia
 Increased urination and thirst occur as a result of the
excess loss fluid associated with osmotic diuretics.
 The patients also experience increased appetite resulting
from the catabolic state induced by insulin deficiency and
the breakdown of proteins and fats.

Cont---
58
 Other symptoms include

 Fatigue and weakness
 Sudden vision changes
 Tingling or numbness in hands or feet
 Dry skin
 Skin lesions or wounds that are slow to heal and
 Recurrent infections

Previous session
59
 Anatomy and physiology /Functions of insulin

 DM - definition
- incidence
- etiology
- types
- patho physiology
- clinical manifestation

Diagnostic evaluation
60
 IDDM is diagnosed on the presence of the 4 cardinal

symptoms i.e. 3 P's + weight loss and lab findings
[glucosuria, hyperglycemia, ketoneuria, and acidosis]
 The two major diagnostic tests for diabetes are blood &
urine
A) Blood Tests
1. Fasting blood sugar (FBS)
2. Random Blood sugar(RBS)
3. Oral Glucose tolerance test (OGTT)
Cont---
61
 Fasting Blood sugar (FBS)

 Determines the amount of glucose in the blood when the
patient is fasting.
 patient stays NPO for 8-12 hrs prior to test
 Blood is drawn &sent to lab.
 Normal 80-120 mg/dl
 Abnormal ≥ 140 /dl
 Random blood sugar (RBS)
 Normal <200mg/dl
 abnormal >200mg/dl
Cont---
62
 Oral glucose tolerance test (OGTS)

 Patient preparation
 put the patient on high carbohydrate diet (150-300 mg) meal for three
days preceding the test.
 After an overnight fasting a blood sample is drawn.
 Then a 75 gm carbohydrate load (sugar) diluted in100 ml of water
(lemon juice) or carbonated sugar beverage is given to the patient.
 Instruct the patient to sit quietly during the test & to avoid exercise
smoking & other oral intake except H 20.
 Then draw blood at intervals 30', 60', 90' & 120'.
 If > 200 mg /dl = DM
Cont---
63
 WHO Diagnostic criteria for DM in non- pregnant

Adults
 RBS ≥200mg/dl [11.1mmol/L ] 1mmol/L = 18 mg/dl

 FBS ≥140mg/dl
 OGTT ≥200 mg/dl on two occasions

Cont---
64
B ) Urine tests
 Applying urine to a reagent strip or tablet matching colors
on strip with a color chart at the end of specified time.

 It is cheap and easily diagnostic method.
 Not specific for glucose (lactose in pregnancy gives false
+ve result)
 Does not indicate hypoglycemia

DIABETES MANAGEMENT
65
 The aim of Rx of DM
 to control the patients symptoms & maintain a sense of well
being
 to normalize insulin activity and achieve normal blood glucose
level (euglycemia) with out hypoglycemia
 To maintain normal weight in adult & normal growth &
development in children
 To prevent acute metabolic complications such as ketoacidosis,
hypoglycemia.
 To prevent or deter the long-term complications of DM.
Cont--
66
 There are 5 components of diabetic management

 Dietary [ nutritional Management]
 Exercise
 Medication [Pharmacologic therapy]
 Education and
 Monitoring [follow up]

A) Dietary Management
67
 Aim
 to control total calorie intake
 to attain /maintain a reasonable body weight
 to control blood glucose levels

Cont---
68
 Nutritional, diet and weight control are the foundation of

diabetes management
 The most important objective in the dietary and nutritional
management of diabetes is control of total caloric intake
to attain or maintain a reasonable body weight and control
of blood glucose levels.
 For obese diabetic patients (especially those with type 2
diabetes), wt loss is the key to Rx

Cont---
69
 Long term adherence to the meal plan is one of the most

challenging aspects of diabetes management
 For all pts with diabetes, the meal plan must consider the
pt’s food preference, lifestyle, usual eating times & ethnic
& cultural backgrounds.

Principles of Diabetic Dietary therapy
70
1) Food intake must be spread evenly through out the walking

hours and taken at regular times in relation to insulin dose.
2) The diet must be balanced in relation to fat protein & CHO
3) Approximately the same amount of food should be eaten every
day.
4) Diet should be based on the ordinary foods used by the family.
5) The obese diabetic must restrict food intake & lose weight if
diabetic control is to be achieved

Cont---
71
 N.B. Several decades ago, it was recommended that

diabetic diets contain more calories from proteins & fats
foods than from carbohydrates to reduce postprandial
increases in blood glucose levels. However, this resulted
in a dietary intake inconsistent with the goal of reducing
the cardiovascular disease commonly associated with
diabetes.

Cont----
72
 The caloric distribution currently recommended is

higher in carbohydrates than in fat & protein.
 Currently the American Diabetic Association
(ADA), recommend that for all levels of caloric
intake, 50% to 60% of calories should be derived
from carbohydrates, 20% to 30% from fat, & the
remaining 10% to 20% from protein.

General dietary Instructions
73
 Foods which the diabetic should avoid (i.e rapidly

absorbed CHO)
 Sugar , honey, candy
 cakes, sweet biscuits
 soft drinks, and alcohol [tej, whisky, areki--]

Cont---
74
 Food allowed in moderation (shouldn't be eaten in excess

amount)
 foods from grain e.g enjera, bread, kinche, kita, porridge,
atmite
 foods from peas, beans & chick peas
 potato , sweat potatoes, kocho, bulla
 all fruit except lemon & grape fruit
 macaroni, pasta etc.

Cont---
75
 foods freely allowed or with minimal restriction

 lean meat &fish
 eggs , cheese, milk
 green or leafy vegetables
 lemon & grape fruit
 tea, coffee, with out sugar
 mineral water
 Spices, pepper, berbere , garlic etc.

Exercise
76
 Aim:
 to reduce the blood glucose level
 to improve insulin utilization
 to improve circulation & muscle tone as well as to
decrease weight

Exercise cont---
77
 exercise is extremely important in the of DM because of

its effect on lowering blood glucose & reducing
cardiovascular risk factors
 It lowers the blood glucose level by increasing the uptake
of glucose by body muscles & by improving insulin
utilization
 It also improves circulation and muscle tone.
 Regular daily exercise rather than sporadic exercise
should be encouraged

Exercise cont---
78
 Unplanned exercise can course a dangerous

hypoglycemic reaction unless the patient in tests
additional food.
 N.B. gradual increase in length of the exercise
period is encourage with patients with DM.

Exercise precautions
79
 Patients who have blood glucose levels exceeding

250mg/dl and who have ketones in their urine should not
begin exercising until the urine test becomes –ve for
ketone; otherwise, the blood glucose level increases the
secretion of glucagon, GH and catecholamine. The liver
then releases more glucose, & the result will elevate blood
glucose level rather than lowering.

Exercise precautions cont---
80
 Another potential problem for patients who take insulin is

hypoglycemia that occurs many hours after exercise.
 To avoid post exercise hypoglycemia, especially after
strenuous or prolonged exercise, the patient may need to
eat a snack at the end of the exercise session and at bed
time and monitor the blood glucose level more frequently.

Cont---
81
 General precautions for exercise

 Use proper footwear and, if appropriate, other protective
equipment
 Avoid exercise in extreme heat or cold env’t
 Inspect feet after exercise
 Avoid exercise during periods of poor metabolic control

Cont----
82
 Exercise recommendations
 People with diabetes should exercise at the same time
(preferably when blood glucose levels are at their peak) and in
the same amount each day
 Regular daily exercise, rather than sporadic exercise should be
encouraged
 In general, a slow, gradual increase in the exercise periods is
encouraged

Monitoring Glucose levels
83
 Blood glucose monitoring is cornerstone of diabetes

management, and Self Monitoring of blood glucose
(SMBG) levels by patients has dramatically altered diabetes
care.
 Frequent SMBG enables people with diabetes to adjust the
Rx regimen to obtain optimal blood glucose control.
 This allows for detection and prevention of hypoglycemia
and hyperglycemia and plays a crucial role in normalizing
blood glucose levels, which in turn may reduce the risk of
long-term diabetes complication.
Cont----
84
 Various SMBG methods are available.

 Most involve obtaining a drop of blood from
fingertip, applying the blood to a special reagent
strip, and allowing the blood to stay on the strip for
seconds and finally the meter gives a digital
readout of the blood glucose value.

Pharmacologic therapy
85
 Insulin therapy
 Because the body loses the ability to produce insulin in type
1 diabetes, exogenous insulin must be administered for life.
 In type 2 diabetes, insulin may be necessary on a long term
basis to control glucose level if diet and oral agents fail.
 In addition, some patients in whom type 2 diabetes is usually
controlled by diet alone or by diet and an oral hypoglycemic
agent may require insulin temporarily during illness,
infection, pregnancy, surgery, or some other stressful event.

Cont---
86
 So, Indications of insulin therapy includes

 All type I DM
 DM with complication (DKA and HHNK)
 During or after serious illness or infection
 During surgery & pregnancy
 NIDDM- resistant to diet & oral hypoglycemic agents
 N.B. Insulin injections are taken two times /day or even
more often to control post prandal & overnight increase in
blood glucose.
Cont---
87
 Insulin preparation varies according to four main

characteristics
 time course of action
 Concentration
 Source and Manufacture
 Time course
 short - acting
 intermediate acting
 Long acting insulin
Cont---
88
 Short acting e.g. regular crystalline and semilente

 usually administered 20-30 before meal wither alone or in combination
 Route - sc/IM/IV
 Intermediate acting e.g. lente insulin, isophane (NPH) and globin zinc
insulin
 usually taken after food
 Route - Sc only
 long acting eg. ultra lente, protamin zinc insulin (PZI)
 route - SC only
 some times referred to as " peak less " insulin because it tends to have long
slow sustained action

Comparison of insulin preparations
89
Preparation Appearance Action hrs compatibly mixed

with
onset peak duration
short acing / semilente clear cloudy 1/2 -1 2-4hr 6-8 hr All insulin
preparations
Intermediate acting Cloudy 3-4 4-12hr 6-20hr Regular
Long acting Cloudy 6-8hr 12-16 hr 20-30 hr Regular

Cont---
90
 concentration
 Insulin dosage is always prescribed in units
 All type of insulin are prepared in 10 ml vials w/h contain either 40,
80 or 100U/ml
 e.g. U-100 means there is 100 units of insulin per 1 ml and U-80
insulin is 2x as concentrated as U-40 insulin
 species /sources
 Insulin is obtained from beef/cow pig/pork's pancreas & from human.
 Human insulin is now widely available
 Human insulin preparations have a shorter duration of action than
insulin from animal sources
Cont---
91
 Insulin syringes
 Insulin syringes must match with insulin
concentration in the vial.
 Most insulin syringes have 27 to 29 gauge needle
that is approximately 1/2 inch in the length.
 Currently, three size of insulin needle are available -
1 ml/cc syringe- hold 100U.
 1/2 ml/cc syringe hold 50 U
 3/10 ml/cc syringe hold 30 U
Fig. insulin syringes
92

Cont---
93
 Dosage- varies with response to the patient and other factor

like illness, stress , surgery, pregnancy etc. 0.5-1.0 U/Kg
per day of Insulin.
 Adult - 15-20 u/d - initial therapy
 obese - 25-30 u/day
 For BID Spilt insulin therapy 2/3 before break fast &1/3 in
the evening before dinner
 Routes of Insulin Administration
 Insulin can be given in Sc [the most common route], IM or
IV.
Cont---
94
 Insulin Administration Sites

 The common insulin injection sites are the thighs,
abdomen ,the upper arms & the buttock.
 Abdomen - is the best site
 Speed of absorption = Abdomen > arm > thigh > buttock
 use available sites in one area and then rotate,
 patient should not use the same site more than once with
in 2-3 weeks.
 There should be ½ -1 inch gap b/n each injection site.

Fig. insulin administration sites
95

Cont---
96
 systemic rotation of injection sites is important to:

 prevent localized changes in fatty tissues /
lipodystrophy.
 promote consistency insulin absorption.
 NB: If the patient is planning to exercise, insulin should
not be injected into the limb that will be involved in the
exercise because it will be absorbed faster & may result
hypoglycemia.
 Methods of needle insertion:- bunching the tissue
(pinching) - 450 or spreading - 900
Methods of needle insertion
97

Cont---
98

Precautions
99
 N.B:
 Don't shake insulin but roll b/n hands.
 Don't administer cold (extremely freezed) insulin
 In mixing regular insulin with long acting insulin, first draw the
regular insulin in order not to contaminate the regular insulin
(1st from the cloudy vial & then from the clear vial)
 Don't give insulin to NPO patient
 Always check the label on the insulin bottle the appearance of
insulin (color)
 Prepare insulin at room temperature don't allow insulin to
freeze extreme To
Complications of Insulin Therapy
100
A) Insulin allergy – Local Vs Systemic

 Local Allergic reaction.
 Usually allergic to the protein component of the insulin.
 The patient may have redness, swelling, tenderness &
indurations of the site 1 or 2 hrs after injection.

 usually occur during the beginning stage of therapy &
disappear with continued use of insulin

 Rx- antihistamine may be prescribed 1 hr before injection.
 Systemic allergic reaction- rare
 Rx- desensitization with small dose of insulin & gradually
increase the dose.

Cont---
101
B) Insulin Lipodystrophy
 Lipodystrophy refers to a localized disturbances of
fat metabolism.
 It may be lipoatrophy or lipohypertrophy.
 Lipo atrophy - is loss of subcutaneous fact or
depression at the site of injection.

 Lipo hypertraphy (some times called insulin
tumor) is a thickening of the subcutaneous tissue at

injection site.
Cont---
102
 Lipodystrophy may be associated with:

 the use of cold insulin
 failure to rotate the sites & injection of insulin
directly in to fat
 Rx- avoid the affected areas with good rotation plan
 use warm insulin to room temperature.
 rotate the injection site systematically
 injection insulin in to the pocket b/n the fat & muscle

Cont---
103
C) Insulin Resistance
 ~ is need of more insulin for the control of diabetes
(a daily requirement of 100 units or more).

 Cause - the exact cause is unknown but may be
caused by
 Specific insulin antagonists with in blood
 Circulating antibodies which are destructive of
insulin
 Obesity

Cont---
104
 It can be classified as:-

 Mild resistance 80-125U required /day
 Moderate resistance 126-200 U /day
 Sever resistance more than 200U /day
 Mgt-
 exercise
 prednisone - to block the production of antibodies
 use pure insulin preparation

Cont---
105
D) Hypoglycemia (insulin shock )- occurs when the

blood glucose level drops to 60 mg/dl or less.
 Cause - insulin over does -usually
- over exercise
E) Hyperglycemia - occurs when the blood glucose
concentration is too high (> 180 mg/dl).

Oral ant diabetic Agents
106
 Oral ant diabetic agents may be effective for type II

diabetic patient who cannot be treated by diet &
exercise alone, however they cannot be used during
pregnancy.
 It includes
 sulfonylureas
 Biguanides

Cont---
107
A) Sulfonylureas
 Stimulate the release of insulin from the β- cells of the
pancreas, also reduce the glucose output from the liver &
improve insulin sensitivity.
 Examples
 Tolbutamide (Restinon) 0.5 - 3.0 gm BID /TID
 Chlorpromide (Diabinase)- for IDDM only - 100- 500 mg/d
 Glipizide - 5-40 ml/d
 Glibenclamide (Donil) 25 -20 mg/d (1-2X/d)- maximum
dose 20 mg/day -most commonly used

Cont---
108
B) Biguanides
 Inhibit gluconeogenesis there by leading to lowered
blood glucose level.

 facilitate insulin's action on peripheral receptor sites
 It is used only in the presence of insulin because they
don't have any effect on pancreatic β-cells.

 e.g.
 Phenformin - not commonly used, safer but unavailable
 Metiformin 500 mg/day

Cont---
109
 Approximately half of all patients who initially use

oral anti diabetic agent eventually require insulin.
This is referred to as a secondary failure.
 primary failure occurs when the blood glucose level
remains high amount after the initial medication use
 If the patient's blood glucose values that were once
responsive to oral anti diabetic agents are no longer
responsive to these agents the patient is then treated
with insulin

Previous session
110
 Components of diabetic mgt

 Medication
 Insulin therapy indication of insulin
 Preparation/types, concentration , dose, routes and
sites of administration
 Insulin complication
 Oral ant diabetic/ hypoglycemic agents

Education
111
 The overall overview of education in DM patient’s has a
broad ,generally it includes
 Teaching patients to self-administer insulin
 Routes of insulin administration
 Systematic rotation of injection sites
 Avoid use of alcohol to cleanse the skin
 How to keep the foot clean, wear shoe
 To have diabetic ID card or bracelet
 Signs of hypoglycemia
 About diet , medication and exercises
 The natures of the diseases etc
Complications of Diabetes
112
A) Acute complication
 There are three major acute complication of
diabetes related to short-term imbalance in blood
glucose levels.
 Includes
 Hypoglycemia [insulin reaction/ insulin shock]
 Diabetic ketoacidosis [DKA]
 Hyperglycemia hyperosmolar non ketotic coma
[HHNK]
Cont----
113
1) Hypoglycemia
 When blood glucose level falls below 50-60 mg/dl
(2.7 to 3.3 mmol /L)

 Cause
 to much insulin or oral hypoglycemic agents
 too little food or late lack of meal after insulin
 Excessive physical activity
N.B. It may occur at any time of the day or night.

Cont---
114
 S/Sx - occur suddenly  Advanced sx- signs of impaired

from of the CNS
& unexpectedly  Headache
 Early Sx  light headedness
 sweating  confusion
 in coordination
 tremor  memory lapse
 Hunger  numbness of lips & tongue
 Tachycardia  slurred speech
 double vision
 palpitation&  drowsiness
 Nervousness
Cont---
115
 Severe Sx- disoriented behavior

 seizures
 difficulty in arousing from sleep
 loss of consciousness
 Management
 For conscious patient : oral glucose 20-30gm/2-3 TSP/ in water
or tea and regular meal
 For unconscious patient /severe hypoglycemia: 25-50 ml of 50 %
dextrose in water IV
 If available, glycogen 1 mg Sc or IM/stimulates the liver to
release glucose through the break down of glycogen
Cont---
116
2) Diabetic ketoacidosis /DKA

 when glucose level is > 300 mg/dl
 DKA result from relative or absolute insulin deficiency
combined with counter regulatory hormone excess

(glycogen catecholamine’s, cortisol & growth hormone)
 Both insulin deficiency & glycogen excess are
necessary for DKA to develop.

 This results in disorder of CHO , fat & protein
metabolism.

Cont---
117
 Cause
 Three main causes of DKA are
 A decrease or missed dose of insulin /insulin
withdrawal
 An illness or infection such as skin , UTI, lung etc
 The initial manifestation of undiagnosed &
untreated diabetes

Cont---
118
 other causes - stress , surgery.

 In response to physical and emotional stressors, there is
an increase in the level of “stress” hormones-
glucagon, epinephrine, norepinephrine, and cortisol.
 These hormones promote glucose production by the
liver and interfere with glucose utilization by muscle
and fat tissue, counteracting the effect of insulin
 If insulin levels are not increased during times of illness
and infection, hyperglycemia may progress to DKA.

C/M
119
 C/M
 The three main problems /clinical features of DKA
are
 Dehydration
 Electrolyte loss
 Acidosis

Cont---
120
 In an attempt to rid of the excess glucose from the body the

kidneys excrete the glucose along with water & electrolyte
(such as Na+ & K+)
 This osmotic diuresis which is x-zed by excessive urination
/polyuria/ leads to DHN & marked electrolyte loss.
 Patients with severe DKA may lose an average of 6.5 lt of
water & up to 400-500 mEq each of Na+, k+&Cl- over 24
hrs.
 deficiency of insulin→ breakdown of fats/lypolysis/ in to
free FAS & glycerol →converted to ketone bodies by the
liver→ accumulate
Medical Surgical Nursing in the circulation
by Selamu Amanuel =02/28/2023
metabolic acidosis.
Other C/Fs
121
 Hyperglycemia of DKA leads to polyuria and polydispia

 Hypotension- due to volume depletion
 Kussmaul respirations (hyperventilation with very deep
respiration): it represent the body’s attempt to decrease the
acidosis,
 GI symptoms such as anorexia, nausea ,vomiting and
abdominal; pain
 Acetone breath /fruit odor/ 20 metabolic acidosis
 Blurred vision, weakness, headache
 Lethargy & CNS depression- in severe cases
Cont---
122
 LAB-VALUES
 Blood glucose level from 300mg -800 mg/dl (may be
lower or higher)
 Low serum bicarbonate 0-15 meg/L
 Low pH (6.8-7.3) low Pco2 (10-30 mm Hg)
 Na & K levels may be low, normal or high depending on
the amount of water loss (dehydration).
 Elevated creatinine.

Cont---
123
 MANAGEMENT OF DHN
 a patient may need up to 6-10 liters of IV fluid to replace the
fluid loss.
 Initially 0.9% Ns is administered at a high rate of 0.5 -1 lit/hr
for 2-3hrs (0.45% Ns may be used for HTN, CH for
hypernatremia)
 0.45 % Ns is fluid of choice after the 1st few hours provided
that BP is stable & sodium level is not low
 Monitor fluid volume status intake & out put . Initial urine out
put will lag behind IV fluid intake due to DHN.
Cont---
124
 MANAGEMENT OF ELECTROLYTE LOSS

 Potassium the main electrolyte of concern in the Rx of
DKA
 Cautious replacement of potassium is vital for avoidance
of serve cardiac dysarrhythmias that occur with
hypokalemia.
 observe for signs of hyperkalemia.

Cont---
125
 MANAGEMENT OF ACIDOSIS
 Infuse insulin at slow continuous rate e.g. 5u/hr.
 Monitor blood glucose values hourly
 Add dextrose to IV when blood glucose reaches 250-300
mg/dl to avoid too rapid drop in blood glucose
 insulin must be infused continuously until SC
administration of insulin is resumed.
 Iv insulin must be continued until the serum bicarbonate
improves & patient can eat.
Cont---
126
 Prevention & Education

 Teach patient not to eliminate insulin doses when sick &
when nausea & vomiting occur
 Teach patients to take their usual insulin doses
 check blood glucose Q 3-5 hrs
 Teach insulin self injection, blood glucose testing &assess
skills.

Cont---
127
3) Hyperglycemic Hyperosmolar non ketotic syndrome

[HHNS]
 is a situation in which hyperglycemia & hyperosmolarity
predominate with alterations of senserium (sense of

awareness)
 Cause
 relative insulin deficiency and/or
 lack of effective insulin

Cont---
128
 Ketosis is minimal or absent

 Insulin deficiency increases hepatic glucose production
(through glucogenolysis & gluconeogenesis) and impairs
glucose utilization in skeletal muscle⇨ hyperglycemia
⇨osmotic diuresis ⇨ intravascular volume depletion
which is exacerbated by inadequate fluid replacement
 Even through is no adequate insulin to prevent

hyperglycemia, it is enough to prevent fat breakdown

Cont---
129
 Occurs most frequently in older people (50-70yrs) who

have had no previous history of diabetes or only mild
type II diabetes
 Precipitated by acute illness (MI, stroke, pneumonia)

ingestion of medications known to provoke insulin
insufficiency (thiazide diuretics, propranolol) or
therapeutic procedures like peritoneal hemodialysis

Cont---
130
 Clinical Manifestation
 polyuria & polydipsia for days to weeks
 weight loss
 hypotension, tachycardia
 profound DHN ( dry mucus membranes, poor skin turgor)
 altered mental status (confusion lethargy or coma)

Cont---
131
 Management
 similar to DKA
 fluid replacement
 Correction of electrolyte imbalances
 Insulin administration to prevent hyperglycemia

Comparison of DKA &HHNK
132
DKA HHNK
Age All ages Usually over 50 years
Duration of DM Variable Recent onset
Precipitating factors Infection. Stress Infection, steroids. Diuretics
Mortality 5% 50%
Blood sugar 300 -800mg/dl [ usually >900mg/dl [ usually

>250mg/dl] >600mg/dl]
Dehydration Variable [total body weight loss Sever [total body weight loss 5-
5 -15% 25%]
PH Low Normal
Breathing Kussmaul Normal
Serum acetone Present Absent

Diabetic complication
133
 Acute complication
 Hypoglycemia
 DKA
 HHNS

Chronic complications of Diabetes
134
 As more people live longer with diabetes long-term

complications become more common
 The long term complication of diabetes can affect almost
every organ system of the body
 The general categories of chronic diabetic complications
are :-
 MACROVASCULAR DISEASE
 MICROVASCULAR DISEASE and
 NEUROPATHY

Macrovascular Disease
135
 Diabetic macrovascular complications result from changes

in the medium to large blood vessels
 Blood vessels walls thicken, scleroses, and become

occluded by plaque that adheres to the vessel walls.
Eventually, blood flow is blocked
 These atherosclerotic changes are indistinguishable from

atherosclerotic changes in people w/o diabetes, but they
tend to occur more often and at an earlier age in diabetes
Cont---
136
 The three main types of macrovascular complications

that occur more frequently in the diabetic includes
 Coronary artery disease (CAD),
 Cerebrovascular disease (CVD), and
 Peripheral vascular disease (PVD).

Microvascular Complications
137
 Although macrovascular changes are seen in both diabetic

and non diabetic patients the microvascular changes are
unique to diabetes
 Diabetic microvascular disease is characterized by capillary

basement membrane thickening
 Increased blood glucose levels react through a series of

biochemical responses to thicken the basement membrane
to several times its normal thickness
Cont---
138
 The two areas affected by these changes are the retinal

[retinopathy] and the kidneys [nephropathy]
 Diabetic retinopathy is the leading cause of blindness in

people with diabetes
 Similarly, about one in every four individuals starting

dialysis has diabetes nephropathy ( it is the leading
cause for ESRF)
Diabetic Neuropathies
139
 It refers to a group of diseases that affect all types of

nerves including peripheral, autonomic and spinal nerves.
 The disorders appear to be clinically diverse and depend

on the location of the affected nerve cells
 It can be :-
 Peripheral neuropathy
 Autonomic neuropathy
Cont---
140
 Others
 Sexual dysfunction
 Sexual dysfunction, especially impotence in men, is a
complication of diabetes
 It occurs with greater frequency in diabetic men than in non
diabetic men of the same age
 The effect on female sexual functioning are no well documented.
 Foot and Leg Problems
 From 5% to 75% of lower extremity amputations are performed
on people with diabetes
Cont---
141
 Complications of diabetes that contribute to the increased risk of

foot infections include:
 Neuropathy:- Sensory neuropathy leads to loss of pain and pressure

sensation and autonomic neuropathy leads to increased dryness and
fissuring of the skin ( secondary to decreased sweating)
 Immunocompromisation:- Hyperglycemia impairs the inability of

specialized leukocytes to destroy bacteria. thus, in poorly controlled
diabetes, there is a lowered resistance to certain infections

Cont---
142
 Peripheral vascular disease:- Poor circulation of the

lower extremities contributes to poor wound healing and
the development of gangrene
 Hyperglycemia: the presence of high glucose level in the
blood is a very conducive environment for bacterial
growth.
 If the patient is not in the habit of thoroughly inspecting
both feet on a daily basis, the injury or fissure may go
unnoticed until a serious infection has developed i.e.
leading to gangrene!
Disorders of the Thyroid gland
143
 HYPOTHYROIDISM
 It results from suboptimal levels of thyroid hormone.
 Thyroid deficiency can affect all body functions and can range
mild, sub clinical forms to myxedema, an advanced form.
 Hashimoto’s disease, autoimmune thyroiditis is the most
common cause of hypothyroidism in adults, in which the
immune system attacks the thyroid gland.
 Hypothyroidism also commonly occurs in patients with
previous hyperthyroidism who have been treated with
radioiodine or antithyroid medications or who have had a
surgery
Cont----
144
 Primary or thyroidal hypothyroidism, which refers to

dysfunction of the thyroid gland it self, covers 95% of
hypothyroidism patients
 Central hypothyroidism, when thyroid dysfunction is
caused by failure of the pituitary gland, the hypothamlus or
both
 In adequate secretion of thyroid hormone during fetal and
neonatal development results in stunted physical and mental
growth (cretinism) because of the general depression of
metabolic activity
Cont----
145
 When thyroid deficiency is present at birth, the condition

is known as cretinism.
 Myxedema refers to the accumulation of
mucopolysaccharides in subcutaneous and other
interstitial tissues
 Although it occurs in long –standing hypothyroidism, the
term is used appropriately only to describe the extreme
symptoms of severe hypothyroidism

Clinical features
146
 extreme fatigue
 Hair loss, brittle nails, and dry skin are common
 numbness and tingling of the finger may occur.
 On occasion, patient may complain of hoarseness of
sound
 Menstrual disturbance such as menorrhagia or amenorrhea
occur
 Severe hypothyroidism results in a subnormal temperature
(being cold even in warm env’t) & pulse rate
Cont----
147
 The pt starts to develop wt gain without an increase in food

intake. Their skin becomes thickened b/c of accumulation of
mucopolysaccharides in the SC tissue.
 Their face also seems expressionless & masklike.
 Their speech become slow, develop enlarged tongue, & their
hands & feet increase in size.
 Pt frequently complains constipation.
 Severe hypothyroidism is associated with an elevated serum
cholesterol level, atherosclerosis, CAD and poor left
ventricular function
Medical management
148
 Primary objective : to restore a normal metabolic state by

replacing the missing hormone
 Pharmacologic therapy: synthetic levothyroxine is the

preferred preparation for treating hypothyroidism and
suppressing nontoxic goiters.
 Prevention of cardiac dysfunction, prevention of medication

interactions and supportive therapy include maintaining vital
functions
Cont----
149
 Nursing interventions
 Modifying activity
 promoting physical comfort
 Monitoring physical status
 providing emotional support etc

HYPERTHROIDISM
150
 Is the second most prevalent endocrine disorder, after DM
 Graves’ disease, the most common type of hyperthyroidism

results from an excessive out put of thyroid hormone caused by
abnormal stimulation of the thyroid gland.
 It affects women eight times more frequently than men.
 Some of the causes include thyroiditis and excessive ingestion

of thyroid hormone
Cont----
151
 C/M
 Nervousness, patients are often emotionally hyper
excitable, irritable, and apprehensive; they can not sit
quietly;
 they suffer from palpitation; and their pulse is abnormally
rapid at rest as well as on exertion.
 They tolerate heat poorly
 The skin is flushed continuously, and is likely to be warm,
soft and moist
Cont----
152
 Patient may exhibit exophthalmos (bulging eyes)
 Other manifestations include an increased appetite and dietary

intake, progressive wt loss, abnormal muscular fatigability
and weakness, amenorrhea and changes in bowel function.
 The pulse rate ranges in b/n 90-160beats/min.
 Osteoporosis & fracture are also associated with

hyperthyroidism
Cont----
153
 Dxtic findings
 The thyroid gland invariably is enlarged to some extent
 It is soft and may pulsate; a thrill often can be palpated,

and a bruit is heard over the thyroid arteries. These are
signs of greatly increased blood flow through the thyroid
gland
 Increase in serum T4 and T3 in excess of 50%

Cont---
154
 Medical management
 Rx is directed toward reducing thyroid hyperactivity to relieve
symptoms and remove the cause of important complications
 Pharmacologic therapy: two forms are available for treating
hyperthyroidism and controlling excessive thyroid activity:
 use if irradiation by administration of the radioisotopes 123I
or 131I for destructive effects on the thyroid gland
 anti thyroid medications that interfere with the synthesis of
thyroid hormone and other agents that control manifestation of
hyperthyroidism

Cont----
155
 Antithyroid medications
 It block the utilization of iodine by interfering with the
iodination of thyrosine and the coupling of iodothyrosines in
the synthesis of thyroid hormone; this prevent the synthesis
of thyroid hormone
 The most commonly used medications are propylthiouracil
(propacil, PTU) or methimazole (Tapazole) until the
patient is euthyroid
 They are contraindicated in late pregnancy because they may
produce goiter and cretinism in the fetus
Cont---
156
 Surgical management: today surgery is reserved for

special circumstances- for example patients with large
goiters, patients unable to take antithyroid agents
 Surgery for Rx of hyperthyroidism is performed as soon

after the thyroid function has returned to normal (4 to 6
weeks)

THYROID STORM (THROTOXIC CRISIS,
TYROTOXICOSIS)
157
 It is a form of severe hyperthyroidism, usually of abrupt

onset
 The patient with thyroid storm is critically ill and requires

good observation and aggressive and supportive nursing
care during and after the acute stage of illness

Cont---
158
 C/M
 High fever above 38.5oC
 Extreme tachycardia (more than 130 beats/min)
 Exaggerated symptoms of hyperthyroidism,
 GI (wt loss, diarrhea, abdominal pain) or
 CVS (edema, chest pain, dyspnea, palpitations)
 CNS (Altered neurologic or mental state)

Cont---
159
 Life threatening thyroid storm is usually precipitated by:

 Stress, such as injury, infection,
 Thyroid and non thyroid surgery,
 Insulin reaction,
 Diabetic acidosis,
 Pregnancy,
 Digitalis intoxication,
 Abrupt withdrawal of antithyroid medications, & extreme
emotional stress.
Management
160
 Immediate objectives are reduction of body temperature and heart

rate and prevention of vascular collapse
 A hypothermia mattress or blanket, ice packs, a cool environment,
hydrocortisone and acetaminophen
 Humidified O2 is administrated to improve tissue oxygenation and
meet the high metabolic demands.
 IV fluids containing dextrose are administered to replace liver
glycogen stores that have been decreased in the hyperthyroid
patients.
 Hydrocortisone is prescribed to treat shock or adrenal insufficiency

THYROIDITIS
161
 Is an inflammation of the thyroid gland, can be acute, sub

acute or chronic
 Each type of thyroiditis is a characterized by

inflammation, fibrosis or lymphocytic infiltration of the
thyroid gland

Cont---
162
 THYROID TUMORS
 They are classified on the basis of benign or malignant, the
presence or absence of associated thyrotoxicosis and the diffuse or
irregular quality of the glandular enlargement
 If the enlargement is sufficient to cause a visible swelling in the

neck, the tumor is referred to as a Goiter
 Some are accompanied by hyperthyroidism, in which case they are

described as toxic; others are associated with a euthyroid state and
are called nontoxic goiter
Fig. THYROID TUMORS
163

Cont---
164
 ENDEMIC (IODINE-DEFICIENT) GOITER

 The most encountered type of goiter, chiefly in geographic
regions where the natural supply of iodine is deficient, is
the so-called simple goiter
 Simple goiter represents a compensatory hypertrophy of the
thyroid gland, caused by stimulation by the pituitary gland
 The pituitary gland produces thyrotropin or TSH, a
hormone that controls the release of thyroid hormone from
the thyroid gland

Cont---
165
 Its production increase if there is abnormal thyroid

activity, as when insufficient iodine is available for
production of the thyroid hormone
 Such goiters usually cause no symptoms, except for the

swelling in the neck, which may result in tracheal
compression when excessive

Cont---
166
 Many goiters of this type recede after iodine imbalance is

corrected
 When surgery is recommended, the risk for postoperative

complications is minimized by ensuring a preoperative
euthyroid state by Rx with antithyroid medications and
iodide to reduce the size and vascularity of the goiter

Disorder of the Parathyroid Gland
167
 The parathyroid gland is situated in the posterior aspect of

the thyroid gland
 These small glands are easily over looked and can be

removed in- adverently during thyroid surgery
 Inadvertent surgical removal is the most common cause of

hypoparathyroidism

Cont----
168
 HYPOPARATHYROIDISM
 The most common cause is
 surgical removal of parathyroid gland tissue or
 during thyroidectomy or
 inadequate secretion of parathyroid hormone after interruption
of the blood supply
 The symptoms are caused by a deficiency of
parathormone that results in: elevated blood phosphate
(Hyperphosphatemia) and decreased blood calcium
(Hypocalcaemia)
Cont----
169
 In the absence of parathormone, there is decreased

intestinal absorption of dietary calcium and decreased
resorption of calcium from bone and through the renal
tubules
 Decreased renal excretion of phosphate causes

hypophospahturia and low serum calcium level result in
hypocalcuria

Cont---
170
 C/M
 hypocalcaemia causes irritability of the neuromuscular system &
contributes to the chief symptom of hypothyroidism  Tetany
 Tetany is a general muscle hypertonia, with tremor and spasmodic or
uncoordinated contractions occurring with or without efforts to make
voluntary movements
 Symptoms of latent tetany are:
 Numbness
 Tingling
 Cramps in the extremities
 The patient complains of stiffness in the hand and feet
Cont---
171
 In overt tetany, the signs include:

 Bronchospasm
 Laryngeal spasm
 Carpopedal spasm
 Dysphagia
 Photophobia
 Cardiac dysrhythimas and
 Seizures
Cont---
172
 Dxtic findings
 A positive Trousseau’s sign or a positive Chvostek’s sign
suggests latent tetany
 Trousseau’s sign is positive when carpopedal spasm is induced

by occluding the blood flow to the arm for 3 min with a BP cuff
 Chvostek’s sign is positive when a sharp tapping over the facial

nerve just in front of the parotid gland and anterior to the ear
cause spasm or twitching of the mouse, nose and eye

Cont---
173
 Lab studies are especially helpful because of the Dx of

hypoparathyroidism is difficult as a reason of vague
symptoms, such as aches and pains
 Tetany develops at serum Ca++ levels of 5 to 6mg/dl (1.2

to 1.5 mmol/L) or lower serum phosphate levels are
increased, and X-rays of bone show increased density

Cont---
174
 Management
 The goals of therapy are to raise the serum calcium level to 9 to 10
mg/dl (2.2 to 2.5mmol/l) and to eliminate the symptoms of
hypoparathyroidism and hypocalcaemia
 When hypocalemia and tetany occur after a thyroidectomy, the

immediate treatment is to administer calcium gluconate intravenously
 Parenteral parathormone can be administered to treat acute hypo. With

tetany (high incidence of allergic reaction limits its use to acute episode
of hypocalemia)

Cont---
175
 Tracheostomy or mechanical ventilation may become

necessary, along with bronchodilating medications, if the
patient develops respiratory distress
 Variables dosages of a vitamin D preparation-

ergocalciferol (VitD) cholecalciferol (VitD) are usually
required and enhance ca++ absorption for the GIT.

Cont----
176
 Hyper parathyroidism
 is a condition of excessive secretion of parathyroid hormone by
parathyroid gland
 Hyperparathyroidism can be classified as either: Primary or

secondary disease
 Primary hyper parathyroidism may be due to secreting tumors

or hyperplasia of the parathyroid glands (most cases are a single
adenoma)
Cont----
177
 Incidence:- primary hyperfunction occurs most frequently

in women between the ages of 35 &65 than men,
 It is most common after menopause
 Secondary type of hyperparathyroidism: hyper
function/over production of parathyroid hormone: It is
appears to be a compensatory response to abnormal states
which induce or cause hypocalcaemia.
 This hypocalcaemia is the main stimulus to parathyroid
gland activity

Cont---
178
 Other predisposing factors

 Disease conditions associated with secondary
parathyroidism include:
 Vitamin D deficiencies
 Malabsorption
 Chronic renal failure (or renal rickets)
 Hyperphosphatemia

Cont---
179
 Clinical manifestations
 It has different characteristics and is not always associated
with bone disease
 Some patients are asymptomatic and show only an increased
serum calcium,
 Psychological irritability and neurosis to psychoses
[Delirium, confusion, incoordination]
 Hyperactive deep tendon reflexes
 Renal colic, renal stones, urinary tract infections & polyuria
Cont----
180
 Diagnostic study abnormalities

Blood tests
 Elevated serum calcium levels
 Low serum phosphate levels and parathormone
 Serum chloride and serum alkaline phosphates
Urine tests
 calcium and phosphate [increased]
Radiologic studies
 Demineralization of bones

Cont---
181
 Complications:-
 Hypercalcemic crisis
 Calcification of kidney parenchyma, renal failure &
uremia
 Collapse of vertebral bodies and rib fractures

Cont---
182
 Medical and surgical management

 The objective of treatment
 To relieve symptoms and prevent complications
due to excessive secretion of parathyroid hormone

Cont---
183
 The choice of therapy depends upon

 The urgency of the clinical situation
 The degree of hypercalcemia
 The underlying disorder
 The status of renal and hepatic function
 The presentation of the patient
 The particular advantages and disadvantages of the
different therapeutic modalities

Cont---
184
Medical management
 To minimize the formation of calcium renal stones can be
managed by
 Forcing fluid intake to dilute the excess calcium
 Avoiding immobilization
 Administering certain drugs

Cont---
185
 E.g. IV normal saline solution to expand the body’s fluid

volume and the excess sodium promotes excretion of
calcium
 In severe hypercalcemic states, phosphate may be given
to reduce the serum calcium in order to facilitate a positive
response to surgery,
 Diuretics– furosemide or Lasix or Ethacrynic acid: to
decrease renal tubular reabsorption of calcium If the client’
is past menopause estrogenic hormones may be used

Cont----
186
 Surgical management
 Surgical removal of parathyroid tumors
 Nursing intervention (management)
 If surgery is performed close monitoring of the client’s
vital sign is required
 Prevent the major postoperative complications: Tetany and
fluid and electrolyte imbalances/disturbances
 Limit ambulation to short walks because the client
problem is fatigue and weakness
cont---
187
 Prevention of accidental injury

 Provide a low calcium diet or reduce milk and milk
products,
 Encourage fluid intake to the point of moderate over
hydration
 Closely monitor the patient to detect symptoms of tetany
(an early postoperative complication)

Cont---
188
 Give mouth care frequently, using flavored mouth wash or

tooth paste
 Monitor patient for epigastric pain and heart burn or signs

and symptoms of peptic ulcer (wt loss, vomiting, blooding/
 Encourage consumption of potassium rich foods (orange

juice, bananas, meats and coffee) in case of cardiac
arrhythmias patients

Disorder of the Pituitary Gland
189
 Abnormalities of pituitary functions are caused by over-

secretion or under-secretion of any of the hormones
produced or released by the gland
 HYPOPITUITARISM
 Hypofunction of the pituitary gland (hypopituitarism) can
result from the disease of the pituitary gland itself or of
the hypothalamus
 It may result from destruction of the anterior lobe of the
pituitary gland

Cont---
190
 Panhypopituitarism (Simmonds disease ) is total

absence of all pituitary secretions
 Postpartum pituitary necrosis (Sheehan’s syndrome) is

another uncommon cause of failure of the anterior
pituitary
 It is more likely to occur in women with severe blood
loss, hypovolemia and hypotension at the time of delivery

Total destruction of PG can result in:
191
 Extremely wt loss  Amenorrhea

 Emaciation  Hypometabolism and
 Hair loss  Hypoglycemia
 Atrophy of all endocrine  Coma and death occur if
glands and organs the missing hormones are
 Impotence not replaced..

Cont---
192
 DIABETES INSPIDUS
 It is a disorder of the posterior lobe of the pituitary gland
characterized by a deficiency of ADH, or vasopressin
 Great thirst (Polydipsia) and large volumes of dilute urine

characterize the disorder
 It may caused secondary to head trauma, brain tumor,

infections of the CNS, failure of the renal tubules to response
to ADH
Cont---
193
 C/M
 Polyuria: an enormous daily out put of very dilute, water-like
urine with a specific gravity of 1.00 to 1.0005 occurs
 Because of the intense thirst, the patient tends to drink 2 to 20
liters of fluid/day
 The disease can not be controlled by limiting fluid intake; because
the high volume loss of urine continuous even with out fluid
replacement
 Restriction of fluids causes the patient to experience an insatiable
craving for fluid and to develop hypernatremia and severe
dehydration
Cont---
194
 The objective of therapy are:

 To replace ADH ( which is usually a long-term
therapeutic program)
 To ensure adequate fluid replacement and
 To identify and correct the underlying intracranial
pathology

Pharmacologic therapy
195
 Desmopressin, a synthetic vasopressin with out the vascular

effects of natural ADH, is particularly valuable because it has
longer duration of action and fewer adverse effects
 Chloropropamide and thiazide diuretics are also used in
mild forms of the disease because they potentiate the action
of vasopressin
 If the diabetes inspidus is renal in origin, the previously
described Rxs: thiazide diuretics, mild salt depletion and
prostaglandin inhibitors (ASA, ibuprofen, and indomethacin)
are used to treat nephrogenic form of DI
Disorders of the Adrenal Glands
196
ADRENOCORTICAL INSUFFICIENCY (ADDISON’S

DISEASE)
 Addison’s disease, result when adrenal cortex function is
inadequate to meet the patients need for cortical hormones

 Autoimmune or idiopathic atrophy of the adrenal gland is
responsible for 80% of cases

 Tuberculosis and histoplasmosis are the most common infections
that destroy adrenal gland tissue

 Inadequate secretion of ACTH from the pituitary gland also results
in adrenal insufficiency because of decreased stimulation of the

adrenal cortex
Cont---
197
 Therapeutic use of corticosteroids is the most common

cause of adrenocortical insufficiency
 The symptoms may result from the sudden cessation of

exogenous adrenocortical hormonal therapy, which
supplies the body’s normal response to stress and
interferes with normal feed back mechanisms

Cont---
198
 C/M
 Muscle weakness
 Anorexia
 GI symptoms
 Fatigue
 Emaciation
 Dark pigmentation of the skin, knuckles, elbow’
 Hypotension
 Low blood glucose, Na+ level
 High K+ levels
Cont---
199
 with disease progression and acute hypotension, the

patients develops addisonian crisis which is characterized
by cyanosis and the classical signs of circulatory shock
 pallor
 apprehension
 rapid and weak pulse
 rapid respirations and
 low BP

Cont---
200
 Dxtic findings
 The diagnosis is confirmed by lab test result:-
 Decreased blood glucose, hyponatremia, increase K+
(hyperkalemia)
 level, and increased WBC count (Leukocytosis)

Cont---
201
 Management
 Immediate Rx is directed towards combating circulatory
shock: Restoring blood circulation, administering fluids
and corticosteroids, monitoring V/S and placing the patients
with legs elevated
 Hydrocortisone is administered intravenously followed
with 5% dextrose in normal saline; oral intake may be
initiated as soon as tolerated
 Additionally, the patient is assessed closely to identify other
factors, stressors or illness that led to the acute episode
Cont---
202
 CUSHING’S SYNDROME
 It results from excessive, rather than deficient, adrenocortical
activity.
 It may results from excessive administration of
corticosteroids or ACTH or from hyperplasia of the adrenal
cortex
 Over production of endogenous corticosteroids may be caused
by several mechanisms including a tumor of the pituitary gland
that produces ACTH and stimulates the adrenal cortex to
increase its hormone secretion despite adequate amounts being
produced
Cont---
203
 C/M
 The S/S of Cushing syndrome are primarily a result of
over secretion of glucocorticoids and androgens, although
mineralocorticoid secretion also may be affected
 Arrest of growth, obesity and musculoskeletal changes
occur along with glucose intolerance
 The classic picture of Cushing’s syndrome in the adult is
that of central- type obesity, with a fatty “buffalo hump”
in the neck and supraclavicular areas, a heavy trunk, and
relatively thin extremities
Cont---
204
 The patients complain of weakness and lassitude

 Sleep is disturbed because of altered diurnal secretion of
cortisol
 Excessive protein catabolism occurs, producing muscle
wasting and osteoporosis
 Patients develops a “moon-faced” appearance and may
experience increased oiliness of the skin and acne.
 There is an excessive growth of hair on the face
hirsutism, the breast atrophy, menses cease, the clitoris
enlarges and the voice deepens
Cont---
205
 Management
 If it is caused by pituitary tumors rather than tumors of the
adrenal cortex, Rx is directed at the pituitary gland.
 Hypophysectomy is the Rx of choice
 Postoperative temporary replacement therapy with

hydrocortisone may be necessary for several months.

Cont---
206
 Corticosteroids therapy
 Cortisterioids are used extensively for:-
 Adrenal insufficiency
 Suppressing inflammation and autoimmune reactions
 Controlling allergic reactions
 Reducing the rejection process in transplantation
 Their anti-inflammatory and antiallergy actions make them
effective in treating rheumatic or connective tissue disease,
such as rheumatoid arthritis and SLE (Systemic Lupus
Erymatosis)
-
207
---End---

7endocrine System Disorders

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Medical Surgical Nursing by Selamu Amanuel 1

 The endocrine system has far-reaching effects in the

 The endocrine glands secrete their products directly in to

Medical Surgical Nursing by Selamu Amanuel 02/28/2023

 The hypothalamus is the link between the nervous system

Medical Surgical Nursing by Selamu Amanuel 02/28/2023

 Glands of the Endocrine system includes:

Medical Surgical Nursing by Selamu Amanuel 02/28/2023

Medical Surgical Nursing by Selamu Amanuel 02/28/2023

 is a fish shaped organ located in the upper abdomen

Medical Surgical Nursing by Selamu Amanuel 02/28/2023

 Stimulate the active transport of glucose in to muscle and

 Promote protein synthesis with in the tissues but inhibits

Medical Surgical Nursing by Selamu Amanuel 02/28/2023

 During fasting periods (between meals and overnight)

Medical Surgical Nursing by Selamu Amanuel 02/28/2023

 Initially, the liver produces glucose through the

Medical Surgical Nursing by Selamu Amanuel 02/28/2023

 Anatomy and physiology of pituitary gland

Medical Surgical Nursing by Selamu Amanuel 02/28/2023

 ADH (anti diuretic hormone) or vasopressin and

 The major hormones of Anterior pituitary gland

 LH (Luteinizing hormone), Female- stimulates

Medical Surgical Nursing by Selamu Amanuel 02/28/2023

 It is a butterfly-shaped organ located in the lower neck anterior

Medical Surgical Nursing by Selamu Amanuel 02/28/2023

Medical Surgical Nursing by Selamu Amanuel 02/28/2023

 T4 contains four and T3 contains three iodine

Medical Surgical Nursing by Selamu Amanuel 02/28/2023

Medical Surgical Nursing by Selamu Amanuel 02/28/2023

 The TH, though their widespread effects on cellular

Medical Surgical Nursing by Selamu Amanuel 02/28/2023

Medical Surgical Nursing by Selamu Amanuel 02/28/2023

 Are four in number

Medical Surgical Nursing by Selamu Amanuel 02/28/2023

Medical Surgical Nursing by Selamu Amanuel 02/28/2023

 When the product of serum ca++ and serum

results in decreased parathormone secretion,

Medical Surgical Nursing by Selamu Amanuel 02/28/2023

 There are two adrenal glands in the human, each

Medical Surgical Nursing by Selamu Amanuel 02/28/2023

Medical Surgical Nursing by Selamu Amanuel 02/28/2023

 The hypothalamus secretes corticotrophin releasing

Medical Surgical Nursing by Selamu Amanuel 02/28/2023

 The major effect of epinephrine release are to prepare

Medical Surgical Nursing by Selamu Amanuel 02/28/2023

Medical Surgical Nursing by Selamu Amanuel 02/28/2023

 Angiotensin II is a substance that elevates the BP by

Medical Surgical Nursing by Selamu Amanuel 02/28/2023

 Definition: is an endocrine disease characterized by

Medical Surgical Nursing by Selamu Amanuel 02/28/2023

 Is a diseases of world wide distribution

Medical Surgical Nursing by Selamu Amanuel 02/28/2023

 There are several type of DM , but the major

Medical Surgical Nursing by Selamu Amanuel 02/28/2023

 Genetic – especially there is a genetic correlation with NIDDM of

 It is characterized by destruction of the pancreatic beta

Medical Surgical Nursing by Selamu Amanuel 02/28/2023

 People do not inherit type 1 diabetes itself; rather, they

Medical Surgical Nursing by Selamu Amanuel 02/28/2023

 There is also evidence of an autoimmune response in type

Medical Surgical Nursing by Selamu Amanuel 02/28/2023