ENDOCRINE SYSTEM DISORDERS:

Grave's Disease, Diabetes Mellitus, Cushing's

Syndrome & Acromegaly.
Presented by: Group Banana

ENDOCRINE SYSTEM DISORDERS:

What is Acromegaly
The name acromegaly comes from the
Greek words for extremities and
enlargement,.
It is a hormonal disorder that results from
the production of excessive amount of
growth hormone (GH) in the body by
pituitary gland.
3

The Etiology of Acromegaly

Acromegaly is caused by prolonged
overproduction of growth hormones by the
pituitary gland.
Secretion of growth hormone by the pituitary
into the bloodstream stimulates the liver to
produce another hormone called insulin-like
growth factor I (IGF-I).
High levels of insulin-like growth factor
signals the pituitary to reduce growth
4
hormone production.

The Clinical Manifestation of

Acromegaly
Early signs and symptoms includes :
Swelling hands and feet and bones altering the
face

 When the tissue thickens, nerves are

trap causing carpal tunnel syndrome,
which results in numbness and
weakness of the hands.
Body organs may also enlarge e.g. Heart

Prognosis of
Acromegaly
The prognosis of an individual with
Acromegaly depends on how far the disease
has progressed before successful treatment.
An individual with advanced Acromegaly
may suffer serious complications such as
congestive heart failure, diabetes mellitus,
respiratory diseases, or cerebrovascular
diseases.
9

Medical Management of
Acromegaly
The medical management of Acromegaly
includes reducing GH and IGF-1 levels to
normal, correcting metabolic abnormalities
and reducing the tumor mass and its central
pressure effects.
The medical management of Acromegaly
involves three potential methods: Surgery,
irradiation and medical (pharmacologic).
10

Medical Management of
Acromegaly Contd
Surgery is used to remove the pituitary tumors
surgically by making an incision in the nose by
using special tools to remove the tumor tissue
in a procedure called transsphenoidal surgery.
Medication (pharmacological) can be use to
treat Acromegaly by reducing the size of the
tumor or by reducing the amount of growth
hormone produced.
11

Medical Management of
Acromegaly Contd
Bromocriptine, a dopamine receptor agonist,
lowers the growth hormone levels to normal .
Octreotide, a somatostatin analogue, is
effective in reducing GH levels to normal and
also decreases the tumor size. The drug must
be injected three to four times daily or given
by constant subcutaneous infusion.
12

Prevention of Acromegaly
There is no specific prevention for
Acromegaly. Early detection is the best way
to prevent severe symptoms and
complications of the disease from getting
worse

13

Graves Disease
This is an autoimmune
disorders where there is
over activity of the thyroid
gland.

14

Aetiology

Graves disease causes a disorder known as hyperthyroidism

which is a disorder that occurs when the thyroid gland produces
thyroid hormone which is greater than the bodys requirement.

This phenomenon occurs as a result of a production of

antibodies by the immune system of a person suffering from
Graves disease known as thyroid-stimulating immunoglobin
(TSI).

These antibodies copy the action of thyroid stimulating

hormone and stimulate the thyroid gland which results in it
producing too much thyroid hormone.
15

Pathophysical Changes of
Graves Disease

Increase in oxygen consumption.

Increase in sympathetic nervous system activity.

Thyroid hormone may heighten the sensitivity of the

body to the catecholamines.

Hypermetabolic state causes frequent complaints of

nervousness, irritability and frequent fatigability.

16

Pathophysical Changes
This condition is mediated by T and B lymphocytes and the
presence of thyroid stimulating immunoglobulin .
These immunoglobulins targets the different thyroid antigens
namely: Thyroglobulin,
sodium-iodide symporter
The receptor thyroid stimulating hormone (TSH) called
Thyrotropin
17

Pathophysical Changes
Over activity of thyroid
gland is due to the binding
of the thyroid stimulating
immunoglobulins to the
Thyrotropin receptor of the
thyroid cells.
The gland is stimulated to
grow and produce more
thyroid hormone, thus
causing hyperthyroidism.
18

Pathophysical Changes
Hyperstimulation of thyroid cause increased production of
thyroid hormones .
This then affects other systems of the body.
E.g. Cardiovascular stimulation cause as rapid pulse rate,
palpitations and other cardiovascular problems.

19

Clinical Manifestation of
Graves Disease

Nervousness or irritability

Fatigue or muscle weakness

Heat intolerance

Trouble sleeping

Hand tremors

Rapid and irregular heartbeat

Frequent bowel movement

Weight loss

Goiter

Enlarged eyes called Graves

Ophthalmopathy.
Thickening and reddening of the
skin on their shins called Graves
Dermopathy.

20

Clinical Manifestation of
Graves Disease
Dermopathy of Graves
disease

Varying degree of graves

Ophthalmopathy.

21

Medical Management
Antithyroid medications:
e.g.Propylithiouracil (PTU) and
Methimazole
reduces the production of T4
and T3 hormones by the
thyroid gland.
Beta blockers :
inhibits the effect of the
thyroid hormones release in
the body; symptoms are
reduced.

22

Medical Management
Radioactive iodine therapy:
destroys the overactive thyroid
gland and other cells that
takes up iodine.
Involves the administration of
oral radioactive iodine-131
medications.
Long term replacement
thyroid hormone is give to
those who use this medical
management.

23

Medical Management
Surgery or
Thyroidectomy : Is
complete or partial
excision of the thyroid
gland.

Those who refuse

radioactive iodine therapy

Pregnant women with

advance hyperthyroidism

Recommended for :
Individuals with Graves
disease eye changes
large nodular thyroid
goiters

24

Prevention and Control

Life style changes such as:
reducing or limiting iodine intake
cessation of smoking
stress management can help to manage symptoms of graves
disease.

25

Prevention and Control

To prevent the advancement of graves disease :
Find out if any family member had the disease or any
thyroid condition
Do yearly physical examination to identifying sings and
symptoms associated with graves disease.
Proper stress management ; since stress tends to alter the
immune system
Take medications that are prescribed to treat the condition. 26

Prognosis
Patients usually recover after
treatment.
Hypothyroidism normally
occur after radioactive iodine
therapy and surgery.
After thyroidectomy:
Infection, bleeding, airway
obstruction, voice hoarseness
and
low blood calcium levels may
result

Replacement hormone
therapy is required after
surgery or radioactive
iodine therapy use
Gravess disease eye signs
improve with antithyroid
drug treatment.

27

Prognosis
The relapse rate after
antithyroid drug therapy is
very high;
Hyperthyroidism may
reoccur and another dosage
of antithyroid medication or
radioiodine therapy is need to
treat the condition.

Agranulocytosis: which is
the presence of very low
levels of white blood cells
to fight infection can result
with the use of antithyroid
medication.

28

Prognosis
If untreated complications are:
Thyroid storm

Keratitis (inflammation of the

eyes)

heart problems
Anxiety, depression, bone loss
fractures,
Birth defects in pregnancy and
elevated risk of miscarriage.

29

Reference

The National endocrine & Metabolic Diseases Information services, 6

Information Way Bethesda M D, 20892-3569, published by National Institute of
Diabetics & Digestive & Kidney Diseases, May 2008. [Retrieved 26, September
2010].http://www.endocrine.niddk.nih.gov/pubs/graves/

Porth , C., Matfin, G.(2009). Pathophysiology Concepts of altered Health States,

8th edition. Lippcott Williams & Wilkins. Philadelphia. Pg1034-1037.

Yeung, J, S, (2010) .Graves Disease: Treatment & Medication. Retrieved on

October 7, 2010,from http://emedicine.medscape.com/article/120619-treatment

30

CUSHINGS
SYNDROME
Pathophysiology
Group Banana

31

Cushing's syndrome
also called hypercortisolism or
hyperadrenocorticism.
a condition resulting from an excess of cortisol,
a hormone produced by the adrenal glands.
Cortisol has many important functions and is
necessary for life.
32

Cushing's syndrome
An excess of this hormone has wellknown negative effects on the body.
Cortisol - is also classified as
glucocorticoid and Hydrocortisone

33

Cushing's syndrome
Contd
Adrenal glands'
production of
cortisol is carefully
controlled by the
hypothalamus and
pituitary gland.

34

Cushing's syndrome
Contd
Cushing's syndrome affects about three
times more women than men.
People with Cushing's syndrome can be
treated effectively, and most times can be
cured.

35

Cushing's syndrome
Contd
Cushing's syndrome is potentially fatal if
untreated, people with this condition
should have regular medical care and
follow their treatment plan closely.

36

Cause of Cushing's
syndrome
Cause of Cushing's syndrome is usually divided
into two broad categories:
1. Whether the problem lies in the pituitary gland.
2. Or in the adrenal glands.
NB: Cushing's syndrome can also occur in
individuals who take large doses of glucocorticoids
(eg, prednisone) for diseases such as asthma and
rheumatoid arthritis.
37

Cause of Cushing's
syndrome Contd
High blood corticotropin
(ACTH) levels

Normal or low blood

ACTH levels

This is caused by high blood ACTH

levels which includes non-pituitary
tumors that produce ACTH.

Occur when benign or malignant

(cancerous) tumors of the adrenal
gland, which produce excess cortisol
are present.

38

Types of Cushings
syndrome
Endogenous is caused by excess
cortisol production within the body
Exogenous the causal factor is typically
steroid medication mimicking cortisol
activity.

39

Pathogenesis
Pituitary Cushings syndrome
Adrenal Cushings syndrome
Ectopic Cushings syndrome
40

Pathophysiology
The paraventricular nucleus (PVN) of the
hypothalamus releases corticotropinreleasing
hormone (CRH), which stimulates the
pituitary
gland to release adrenocorticotropin
(ACTH).

41

Pathophysiology Contd
ACTH travels via the blood to the adrenal
gland, where it stimulates the release of
cortisol.
Cortisol is secreted by the cortex of the
adrenal gland from a region called the zona
fasciculata in response to ACTH.

42

Pathophysiology Contd
Elevated levels of cortisol exert negative
feedback on the pituitary, which decreases the
amount of ACTH released from the pituitary
gland. BUT remember the definition of CS.
The adenoma causes cortisol levels in the
other structures to produce large
amounts of hormones.
43

SUMMARY OF
PATHOPHYSIOLOGY

44

Clinical Manifestation
Glucose intolerance Excess cortisol can cause
an elevation of blood glucose levels. Therefore
these persons will experience glucose
intolerance, a prediabetic condition that can
progress to diabetes mellitus.
androgen excess Women may have signs of
male hormone (androgen) excess, such as
hirsutism, oily skin, and acne.
45

Weight gain usually affects the face, neck, trunk, and

abdomen more than the limbs, they often develop a rounded
face.
In children, Cushing's syndrome involves the
limbs and is usually associated with poor growth.
Skin changes the skin tends to become thin, fragile, and
more susceptible to bruises and infections.

46

Psychologic Over half of all patients with

Cushing's syndrome have Psychologic
symptoms
that range from loss of emotional control,
irritability, and depression to panic attacks
and
paranoia.
Others: Infections, Blood clots, Bone loss,
Menstrual irregularities, Muscle loss and
Weakness and Hypertension and
cardiovascular disease.
47

Moon Face in Cushings

Syndrome

48

Centripetal Obesity in
Cushings Syndrome

49

Physiology of treatment & its

relationship to cause & effect of
the Endocrine Disorders
The function of the treatment is to remove
or
correct the source of hypercortisolism
without
causing permanent pituitary or adrenal
damage.
Treatment depends on the causes of
Cushings Syndrome

50

 Slowly decrease
Cushings
Syndrome
the drug dose (if
possible) under
medical supervision.
caused
by corticosteroid

51

CS caused by a pituitary
tumor
tumor
that
Surgeryor
to remove the tumor
releases
ACTH
Radiation after
removal of a pituitary
tumor
Hydrocortisone replacement therapy
Surgery to remove the tumor
Radiation after removal of a pituitary
tumor
52

CS due to an adrenal
tumour
Surgery to remove the tumour

If the tumour cannot be removed,

medications to help block the release of
cortisol

53

Complications

Diabetes
Enlargement of the Pituitary Tumour
Fractures due to Osteoporosis
Hypertension
Kidney Stones
Serious Infectious
54

References
National Endocrine and Metabolic Diseases
Information Service, a Service of the National
Institute of Diabetes and Digestive and Kidney
Diseases (NIDDK) NIH Publication No. 08
3007 July 2008 Retrieved on October 10,
2010 from
http://endocrine.niddk.nih.gov/pubs/cushings/
cushings.htm
55

References Cont
Bullock, L, B, (1996), Pathophysiology
Adaptations and Alterations in Function,
Lippincott, (4th Ed) (pg-723-724)
Porth, Mattson, P, (2004), Essentials of
Pathophysiology: Concepts of Altered
Health States, (6th Ed), Lippincott Williams
& Wilkins, (Pg 557-558).
56

57

DIABETES
MELLITUS
PRESENTERS:
CHRISTAN BLACK
NASTASSIA GENUS
58

OBJECTIIVES

To define Diabetes Mellitus.

To state the Aetiology of the disease.
To give the Clinical Manifestations.
To explain the Pathophysiological changes.
Discuss the prognosis of the disease.
Discuss the complications of the disease.
To outline measures of prevention
To describe the Medical management
59

Diabetes Mellitus
Definition

A metabolic disorder of multiple aetiology

characterized by chronic hyperglycaemia with

disturbances of carbohydrate, fat and protein
metabolism resulting from a deficiency of insulin
secretion, insulin resistance and insulin action or
both.

60

Types Of Diabetes
Type 1 Diabetes (juvenile onset) auto immune
mediated beta cell dysfunction which leads to
absolute insulin deficiency, in which there is an
elevation in blood glucose, and a breakdown of
body fats and proteins.
Type 2 Diabetes (adult onset) which is due to
insulin resistance, relative insulin deficiency or a
reduction in insulin secretion.
61

Types of Diabetes
contd
Type 3 Maturity onset diabetes of the young (MODY)
refers to any of several hereditary forms of diabetes caused
by mutations in an autosomal dominant gene (sex
independent, inherited from any of the parents).
Type 4 Diabetes/Gestational diabetes occurs in pregnant
women, who have never had diabetes before, have a high
blood glucose level during pregnancy. It may precede
development of type 2 DM.
Type 5 Diabetes Insipidus (DI): Is a condition
characterized by excessive thirst and excretion of large
amounts of severely diluted urine.
62

Aetiology of Type 1
Diabetes Mellitus
Changes in lifestyle and obesity are predisposing to
diabetes.
Genetic predisposition: transmission of traits from parents
to their offspring and resulting from inherited factors (genes)
and also related to Human leukocyte antigens (HLA) on the
sixth chromosome linked to immune response genes that
promote a genetic susceptibility
Immunologic and Environmental factors: bodys response
to foreign exposure/invasion to viruses. E.g.: a viral
infection like the Coxsackie B virus.
63

Aetiology of Type II
diabetes
It appears that a combination of strong genetic and
environmental factors such as: Obesity and lack of
exercise.
The hereditary pattern appears to be complex,
involving multiple genetic factors rather than one
specific type of hereditary pattern.

64

Aetiology of Type II
diabetes
The metabolic abnormalities that lead to type 2
diabetes include:
Insulin resistances main cause
Unbalanced secretion of insulin by the pancreatic
beta cells.
Increased glucose production by the liver

65

Clinical Manifestation
Polyuria

Polydipsia

Fatigue

Mood Changes

Polyphagia

Weight Loss

Edginess

Nausea

Vomiting

Weakness
66

67

Clinical Manifestation
contd

Severe cases may lead to:

More commonly visual blurring.
Neuropathic complications (such as pain in the feet) .
Skin infections.
Paresthesias (dysfunction of the peripheral sensory
nerves).
Vulvovaginitis (due to Candida infections in women).
Inflammation of the vulva.
Balanitis secondary to Candida infections can occur in
men. Inflammation of the head/glans of the penis
68

Pathophysiological
Changes
Dryness of the skin.
Poor skin turgor .
Cellulites.
Growth of Candida
Albicans.
Orgasmic
dysfunctions in
Female.

Liver Size increases.

Degenerative
muscle.
Erectile Dysfunction
in male.
Diabetic amyotrophy.

69

Prognosis
Diabetes can lead to blindness; other Eye problems
including cataracts, glaucoma, and diabetic
retinopathy.
It doubles the risks of heart disease and increases
the risk of stroke, heart attack and other cardiac
problems.

70

Prognosis contd

Contributing to diabetic foot ulcers.

Poor blood circulation and delayed wound healing.
Amputation of toes, feet, or legs due to severe
infection; therefore diabetes may lead to
amputations of limb.

71

Prognosis cont'd
Heart disease and kidney disease are common
complications of diabetes.
Long-term complications may include the need for
kidney dialysis or a kidney transplant due to kidney.

72

73

Diabetic Foot Ulcer

74

Complications of Diabetes
Mellitus
There are two acute Complications:
Hypoglycemia-also called low blood glucose or low
blood sugar.
Hyperglycemia- develops when there is too much
sugar in the blood.

75

Manifestation of
Complications of DM
Hypoglycemia
Hunger
Shakiness.
Nervousness
Sweating.
Dizziness and sleepiness
May lead to: confusion
fainting and coma.

Hyperglycemia

Difficulty concentrating
Blurred vision
Frequent urination.
Fatigue.
Increased weight loss.

May lead to: vaginal and

skin infections, slowhealing, decreased vision.
76

Prevention of
Diabetes
Mellitus
Diet management

Exercise

Prevention Of DM

77

Diabetes
Management
Diet management.
Exercising
Maintaining proper circulation in extremities.
Reducing other external factors such as stress, illness,
menses, injection site scarring, and other physiological
factors.
GMR (testing).
78

79

Management
Oral medications :
Anti-diabetic drug, sulfonylurea drugs have been used
in the management of type 2 diabetes for more than 40
years.
Sulfonylurea exert their hypoglycemic effects by
including insulin release by B cells.
The so-called first generation agents are tolbutamide
chlorpropamide, acetohexamide, and tolazamide.
80

Management Cont'd
Education .
Diabetic Support systems.
Peer Support.

81

82

References
John Hopkins Autoimmune Disease Research Center (2007).
Autoimmune Diseases. Retrieved on October 11, 2010 from
http://autoimmune.pathology.jhmi.edu/diseases.cfm?
systemID=3&DiseaseID=23.
Porth, C., & Matfin, G, (2009). Pathophysiology: Concepts of
altered Health States, 8th edition. Pgs1034-1037& 1054-1057.
Lippincott Williams & Wilkins, Philadelphia.
Bullock., A.B. (2000). Focus on Pathophysiology. Pgs.642-646. Reet
L Henze/ Lippincott, Williams & Wilkins.
Bullock., L.B. (1996). Pathophysiology: Adaptations and Alterations
in Function. - 4th Ed .Pgs.696-699&723-724. Lippincott Company.
83