Endocrine Disorder.pptx

ASSESSMENT AND MANAGEMENT OF
PATIENTS WITH ENDOCRINE
DISORDERS
ARBA MINCH UNIVERSITY, SCHOOL OF NURSING.
March, 2023

Learning Objectives
2
On completion of this session, you will be able
to:
Describe the functions of each of the endocrine
glands and their hormones.
Identify the diagnostic tests used to determine
alterations in function of each of the endocrine

3
+ Compare hypothyroidism and hyperthyroidism:
their causes, clinical manifestations, management,
and nursing interventions.
+ Compare hyperparathyroidism and
hypoparathyroidism: their causes, clinical
manifestations, management, and nursing
intervention

Endocrine system - together with the nervous system, acts as
the body´s communication network
- it is composed of various endocrine
glands and endocrine cells
- the glands are capable of synthetizing and
releasing special chemical mesengers -
hormones
Hormones - substances which are secreted by specialised cells in
very low concentrations and they are able to influence
secreted cell itself (autocrine influence), adjacent cells
(paracrine influence) or remote cells (hormonal influence)

Endocrine Organs
5
Scattered throughout the body
Pure endocrine organs
Pituitary, pineal, thyroid, parathyroid, and adrenal
glands
Organs containing endocrine cells
Pancreas, thymus, gonads, and the
hypothalamus

Comparison of Nervous and Endocrine Systems
(Differences)
 Both serve for internal communication
 Nervous - both electrical and chemical
 Endocrine - only chemical
 Speed and persistence of response
 Nervous - reacts quickly (1 - 10 msec), stops quickly
 Endocrine - reacts slowly (hormone release in
seconds or days), effect may continue for weeks

7
ê Adaptation to long-term stimuli
ê Nervous - response declines (adapts quickly)
ê Endocrine - response persists (adapts slowly)
ê Area of effect
ê Nervous - targeted and specific (one organ)
ê Endocrine - general, widespread effect

Nervous and Endocrine Systems
(Similarities)
 Both systems can have overlapping effects on
same target
 Norepinephrine and glucagon cause glycogen
hydrolysis in liver
 Systems regulate each other
 Neurons trigger hormone secretion
 Hormones stimulate or inhibit neurons

 Nervous System
 Nervous system performs short
term crisis management
 The nervous system sends
electrical messages to control and
coordinate the body
 Nerve impulse is delivered by the
axon of a nerve cell called neuron
Intercellular Communication
Endocrine versus Nervous system
• Endocrine System
• Endocrine system regulates long
term ongoing metabolic activity
• The endocrine system uses
chemicals messenger called
hormones to “communicate”.
• Hormones alter metabolic
activities of tissues
• A hormone is secreted by a group
of specialized cells called gland
• Hormones are transported by the
blood vessels
• Paracrine communication involves
chemical messengers between
cells within one tissue

Glands of the Endocrine System
10
 Hypothalamus
 Posterior Pituitary
 Anterior Pituitary
 Thyroid
 Parathyroids
 Adrenals
 Pancreatic islets
 Ovaries and testes

Assessment and
Management of Patients with Diabetes Mellitus
16

Learning Objectives
17
At the end of this session, you will be able to:
Differentiate between type 1 and type 2 diabetes.
Describe etiologic factors associated with
diabetes.
Relate the clinical manifestations of diabetes to
the associated pathophysiologic alterations.
Identify the diagnostic and clinical significance of
blood glucose test results.

18
Explain management modalities of diabetes
Differentiate between hyperglycemia with DKA
And HHNS
Describe the major macrovascular, microvascular,
and neuropathic complications of diabetes and
the self-care behaviors that are important in their
prevention.

Is healthy living with diabetes
possible?

Definition
21
æ Diabetes mellitus is a group of metabolic
disorders characterized by elevated levels of
glucose in the blood (hyperglycemia) resulting
from defects in insulin secretion, insulin action, or
both.

World Wide Burden of Diabetes
22
 About 422 million people worldwide have diabetes
 the majority living in low-and middle-income
countries,
 1.5 million deaths are directly attributed to
diabetes each year.
 Both the number of cases and the prevalence of
diabetes have been steadily increasing over the
past few decades.

Reasons for Increase
Increasing Age
Unhealthy Diet
Obesity (Diabesity)
Sedentary Life Style
Smoking

CLASSIFICATION OF DIABETES
MELLITUS
25
Type I Diabetes: autoimmune
Was previously called IDDM or juvenile-onset
diabetes.
B/c of pancreatic beta cell destruction results in
total insulin deficiency.

26
Usually strikes children and young adults,
although disease onset can occur at any age.
Risk factors include autoimmune, genetic, and
environmental factors (some viral infections,
chemical toxins),idiopathic.

Auto immune destruction of Beta
cells of pancreas
How the immune system destroys
beta cells is not known
Molecules such as Fas ligands may
induce apoptosis of beta cells
Cytokines and CD8 cytotoxic
lymphocytes also contribute for the
beta cell destruction

Natural History of Type 1 Diabetes
TIME
BETA
CELL
MASS
DIABETES
“PRE”-
DIABETES
GENETIC
PREDISPOSITION
INSULITIS
BETA CELL INJURY
ENVIRONMENTAL
TRIGGER
CELLULAR (T CELL) AUTOIMMUNITY
LOSS OF FIRST PHASE
INSULIN RESPONSE
(IVGTT)
GLUCOSE INTOLERANCE
(OGTT)
CLINICAL
ONSET

Type II Diabetes
29
 was previously called NIDDM or adult-onset
diabetes.
Due to:
 Decreased tissue sensitivity to insulin(insulin
resistance)
 Inadequate insulin production
 Decreased beta-cell function

Risk factors for type -2 DM
30
 Older age(>45) and obesity
 Family history of diabetes
 History of gestational diabetes
 Impaired glucose metabolism
 Physical inactivity
 Race/ethnicity(Afro-American,Hispanic, native
American, Asian-American)

 Usually under 30
 Rapid onset
 Normal or underweight
 Little or no insulin
 Ketosis common
 Make up 15% of cases
 Autoimmune plus
environmental factors
 Low familial factor
 Treated with insulin, diet
and exercise
 Usually over 40
 Gradual onset
 80% are overweight
 Most have insulin resistance
 Ketosis rare
 85% of diagnosed cases
 Metabolic insulin resistance
syndrome
 Strongly hereditary
 Diet & exercise, progressing
to tablets, then insulin
31
Type 1 Type 2

Gestational diabetes
32
Diabetes diagnosed during pregnancy
Placental hormones contributes to insulin
resistance(inhibit action of insulin)
Common between 24-28 weeks of gestation.
Goes away after birth, but increased risk of
developing Type 2 DM

DM associated with other conditions
33
 Previously classified as secondary diabetes
 Because of underlying conditions like
ö Surgery, drugs(corticosteroids, thiazides,
atypical antipsychotics
ö Malnutrition and illnesses (Cushing's,
hyperthyroidism, recurrent pancreatitis)
 Accounts 1-5% of cases

Pathophysiology of DM 1
34
Destruction of the pancreatic beta cells.
Decreased or absence of insulin production.
Unchecked glucose production by the liver.
Glucose derived from food cannot be stored in the liver but
instead remains in the bloodstream.
Glucose becomes above the renal threshold and it appears in
the urine (glucosuria)
Production of ketone bodies from metabolism of fatty acids.

Pathophysiology of DM 2
35
Cellular insulin resistance and impaired insulin
secretion
To overcome insulin resistance increased
production of insulin.
The pancreas gradually begins to lose its ability to
produce the extra insulin .
As body insulin levels fall, blood sugars begin to

36
But, enough insulin to prevent the breakdown of
fat and production of ketone bodies
DKA does not typically occur in type 2DM.
Uncontrolled type 2 diabetes may, however, lead
to another acute problem, HHNS

Clinical Manifestations
39
 “Three Ps”(classic symptoms of diabetes)
 Polyuria (increased urination)
 Polydipsia (increased thirst)
 Polyphagia (increased appetite)
 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.
 Sudden weight loss, nausea, vomiting (In type 1

Diagnostic Criteria
40
* Symptoms of diabetes plus casual(random)
plasma glucose concentration > 200 mg/dl. Or
* Fasting plasma glucose > 126 mg/dl on two
separate occasions. I.E. No caloric intake for at
least 8 hours. Or
* OGTT level > 200mg/dl after 2 hrs (not
recommended for routine clinical use)

Pre diabetes
41
Is when blood glucose levels are higher than normal but
not high enough for a diagnosis of diabetes.
OGTT b/n 140 and 199 mg/dl after 2 hours shows
impaired glucose tolerance (IGT)
A diagnosis of impaired fasting glucose (IFG) is made
when the fasting glucose level is between 110 and 125
mg/dl.
A person is at increased risk for developing type 2
diabetes (many people within 10 years)

Cornerstones of Diabetes
Management
42
Nutritional management
Exercise
Monitoring
Pharmacologic therapy
Education

Mangt cont’d….
43
Type one: insulin + healthy eating + exercise
Type two:
Healthy eating + exercise
Then healthy eating + exercise + OHA
Then healthy eating + exercise + OHA +
insulin

Health eating cont’d….
44
 50% - 60% of calories from carbohydrates
(complex and high in fibre)
 20-30% or less of calories from fat(but saturated
fat intake should not exceed 10% of total energy)
 10-20% of calories from protein –the use of some
non animal sources of protein help to reduce
saturated fat and cholesterol intake.

Health eating cont’d…
46
 Avoided excessive salt intake particularly
restricted in people with hypertension and those
with nephropathy.
 Moderate alcohol
 Spreading meals evenly with the addition of
snacks if necessary, helps to prevent
hypoglycemic reactions and maintain overall
blood glucose control.

Include Limit
Fiber-rich Whole Grains
(for example: oatmeal, barley,
brown rice, whole grain pasta,
whole wheat, and corn)
Sweets and added sugars
(for example: table sugars sucrose, glucose, fructose, maltose, dextrose,
corn syrups, high- fructose corn syrup, concentrated fruit juice, honey, soda,
fruit drinks, candy, cake, and jellies)
Non-fried fish at least twice per
week, especially those high in
omega-3 fatty acids
(such as: salmon, lake trout,
mackerel, and herring)
Fatty and processed meats
(such as: fatty beef and pork, salami and hot dogs)
Chicken or turkey
(without the skin)
Sodium
(consume less than 2,300 milligrams (mg) a day and an ideal limit of less
than 1,500 mg per day for most adults.)
Lean meats
(round, sirloin, chuck, and loin)
Cholesterol
(consume less than 300 mg per day)
Fruits and Vegetables
(deeply colored such as spinach,
carrots, peaches and berries)
Partially hydrogenated or trans fats
(contained in hard margarine, shortening, cakes, cookies, crackers, pastries, pies,
muffins, doughnuts, and French fries)
Vegetable oils and margarines
(soft/tub or liquid)
Saturated fats
(contained in dairy products such as butter, whole milk, 2% milk and cheese, fatty meats
and poultry, coconut oil and palm oil, hydrogenated oils, and foods made with these
ingredients).

Exercise
 improving circulation
and muscle tone
 decreasing total
cholesterol and
triglyceride levels
48
 lowers blood glucose by:
 Increasing uptake of
glucose by muscles
and improves insulin
utilization

Precautions during
exercise
Need to monitor BS before,
during and after exercise
Not exercise until urine test
negative for ketones and
blood glucose levels are near
to normal
If on insulin, eat 15g snack
52

…precaution cont’d
 Carry a quick source of
sugar when exercising
 It should be moderate
and regular
 Avoid trauma to the feet
It should be under
physician supervision.
 Regular exercise 20-
30 minutes, aerobic
exercise such as
jogging, walking,
swimming etc. 3 – 4
days is
recommended.
53

Monitoring
54
 Self-monitoring of blood glucose
 Patients on insulin should check sugars 2-4 times per
day(usually before meals and at bedtime).
 Not on insulin, at least 2 -3 times per week
 For all patients, testing is recommended whenever
hypoglycemia or hyperglycemia is suspected, with
changes in medications, activity, or diet, and with
stress or illness.

…monitoring cont’d
55
Urine Glucose and Ketone Monitoring
 Most people have glucose in their urine when their
blood glucose is more than 180 mg/dl.
 Urine should be tested for ketones during acute
illness or stress, during pregnancy when BGL are
consistently >240mg/dl, or when symptoms of
Ketoacidosis are present.

Anti-Diabetic medications
56
 Oral hypoglycemic agents
Includes
 First and second generation sulfonylureas
 Thiazolidinediones
 Biguanides
 Meglitinides
 Alpha-glucosidase inhibitors

General guide lines to use OHGA
58
 Not recommended for diabetes in pregnancy
 Are not the first line therapy in diabetes diagnosed
during stress, such as infections.
 When indicated, start with a minimal dose, while
reemphasizing diet and physical activity.
 An appropriate duration of time (2-16 weeks
depending on agents used).

Insulin Therapy
59
 Functions of insulin
 Enables glucose to be transported into cells for
energy for the body
 Converts glucose to glycogen to be stored in
muscles & the liver
 Facilitates conversion of excess glucose to fat
 Prevents breakdown of body protein for energy

Who should have insulin
therapy?
60
Newly diagnosed type 1
In type 2 diabetic on maximum tablets,
contraindications to OHA (renal failure, poor
tolerance)
Stress or situations such as surgery,
corticosteroid therapy, infections, treatment for
DKA, HHNS
Pregnancy; gestational diabetes who are not

Insulin
preparations
61
 Rapid acting (lispro, asparte)
 Short acting (regular)
 Intermediate acting (Lente)
 Long acting
-Ultralente
-Glargine/lantus

Adverse effects of insulin therapy
63
 Hypoglycaemia
 Local allergic reaction( itching, erythema, and
burning around injection site)
 Usually occur during the beginning stages of
therapy
 Antihistamine may be taken 1 hour before the
injection
 Systemic allergic reactions (urticaria and
anaphylactic shock)-rare
 Treatment is desensitization, small doses of

…adverse rxn cont’d
64
 Insulin lipodystrophy
 Atrophy or hypertrophy of subcutaneous fat at
injection sites
 Rotate within site to prevent the problem
 Insulin insensitivity or resistance
 Being obese (common cause)
 Interrupting insulin therapy for several months
 Require high dose of insulin/more concentrated
insulin preparation

65
Morning hyperglycemia -can be due to
 Insulin waning; progressive rise in blood
glucose from bedtime to morning
Managed by increasing evening dose
 Dawn phenomenon; relatively normal blood
glucose until about 3 am, when the level begins
to rise
 Result from nocturnal surges in GH secretion
Change time of injection of evening insulin from
dinnertime to bedtime.

66
Somogyi Effect
 Normal or elevated blood glucose at bedtime, a
decrease at 2–3AM to hypoglycemic levels, and
a subsequent increase caused by the production
of counter regulatory hormones
 Managed by decreasing the evening dose, or
increase bedtime snack.

Insulin administration sites
 Abdomen- more stable and
rapid absorption
 Posterior arms
 Anterior thighs
 Hips
 Inject at appropriate angle
(45-90) depending on depth of
subcutaneous tissue
 Do not inject insulin to limb
which will be used to exercise.
67

Rotation
Use same anatomic area at the
same time of day
Rotation within site must occur
to prevent lipodystrophy and to
promote consistency in
absorption (0.5 to 1 inch
away)from the previous injection.
Not to use the same site more
than once in 2 to 3 weeks
68

Teaching Patients to Self-Administer
Insulin
69
 Basic information includes explanations of :
Insulin Storage-insulin vial in use should be kept at
room temperature
Selecting Syringes- Syringes must be matched with
the insulin concentration
Mixing Insulins- regular insulin can be drawn up first
 longer-acting insulins must be mixed thoroughly
before drawing into the syringe

….education cont’d
70
 Withdrawing Insulin- instruct patients to inject air
into the bottle of insulin equivalent to the number
of units of insulin to be withdrawn
 Selecting and Rotating the Injection Site
 Preparing the Skin-use of alcohol to cleanse the
skin is not recommended

….edc cont’d
71
Inserting the Needle -for a normal or
overweight per-son, a 90-degree angle is
the best insertion angle
aspiration is not recommended
Removing the needle and holding cotton
ball over site
Disposing of Syringes and Needles

Acute complications of Diabetes
Mellitus
73
Hypoglycemia
 abnormally low blood glucose level occurs
when the blood glucose falls to less than
50 to 60 mg/dL.
is caused by
Overdose of insulin or hypoglycemic
agents
Missing of meal
Strenuous exercise

Clinical manifestations
74
 Early: cold sweat, tremor, hunger,
tachycardia, palpitations.
 Late: dizziness, inability to concentrate,
blurring, headache, numbness of the lips
and tongue, difficulty arousing from sleep,
nightmares, seizure and coma

Management
75
Treatment must be immediate
Quickly check BGL if able. if in doubt, treat as a
hypoglycemia.
If conscious and safely able to swallow; 15 g of
fast-acting carbohydrate given orally
3 or 4 commercially prepared glucose tablets
or
4 to 6 oz of fruit juice or
6 to 10 hard candies or
2 to 3 teaspoons of sugar or honey

….Magt cont’d
76
Recheck BS after 15 minutes, if it is less than 70 to
75 mg/dl , repeat treatment.
If the symptoms persist more than 10 to 15 minutes
after initial treatment, the treatment is repeated
even if blood glucose testing is not possible.

77
After improvement, a snack containing protein
and starch (e.g., milk or cheese) is
recommended.
Prolonged unconsciousness requires
administration of glucagon (1mg)Sc or IM
injection or 25 to 50 mL of 50% dextrose in water
(D50W) IV.

Teaching prevention techniques
78
Consistent pattern of eating, administering
appropriate dose of insulin, and exercising
Snacks may be needed to counteract the
maximum insulin effect
Need for routine blood glucose tests
Advice to wear an identification bracelet or tag
stating that they have diabetes

….teaching cont’d
79
 Patients and family members must be instructed
to recognize the symptoms of hypoglycemia.
 Patients with DM especially those receiving
insulin, learn to carry some form of simple sugar
with them at all times.

Diabetic Ketoacidosis
80
 DKA is caused by an absence or markedly
inadequate amount of insulin.
 It is often the reason a person with undiagnosed
type 1 diabetes first seeks help
 The three main causes of DKA
 Decreased or missed dose of insulin
 Illness or infection
 Undiagnosed or untreated diabetes

Pathophysiology
81
ö Absence or markedly inadequate amount of
insulin to allow glucose into cells
ö The body then breaks down fat to be used for
energy.
ö The fat breakdown releases an acid substance
called ketones.
ö Increases blood levels of ketone bodies
_metabolic acidosis
ö Osmotic diuresis, which is characterized by
excessive urination (polyuria), leads to
dehydration and marked electrolyte loss.

Clinical Features
82
Three main clinical features:
Hyperglycemia
Dehydration and electrolyte loss
Acidosis(ketosis)

….s/s cont’d
83
 Polyuria and polydipsia
Extreme fatigue and weakness
 Dry tongue and bucal mucosa , poor skin
turgor and hypotension
 Nausea and vomiting, abdominal pain
 Kussmaul respiration : deep and fast
breathing (hyperventilation)
 Acetone ("fruity") odour of breath
 The patient may be alert, lethargic, or

Diagnostic tests
84
 RBS (BGL b/n 300-800mg/dl)
 Ketonaemia > 3.0mmol/L or significant ketonuria
(more than 2+ on standard urine sticks)
 Electrolyte abnormalities
 Low Sodium and potassium

Management
85
Requires immediate medical attention and usually
admission to hospital
In addition to treating hyperglycemia,
management is aimed at correcting dehydration,
electrolyte loss, and acidosis.

Restore fluid balance
86
Initially 1 L of normal saline (0.9 % NaCl) is given
over ½ an hour.
Continue with 1 L of normal saline/hr for the first
2-3 hours
Then ½ normal saline (0.45 % NaCl) at slower
rate till the patient is well hydrated.
When the serum glucose level falls to 200-300
mg/dl, change the IV fluid to 5 % - 10 % DW to
prevent hypoglycaemia.

Dosage and administration of
Insulin
87
ö 20 Units of regular insulin, 10 U IV and 10 U IM is
given with the initial fluid resuscitation.
ö Then 5-10 units of regular insulin is given per hour
till the blood glucose level drops to 250-300mg/dl
ö Blood glucose determination is done every hour.
The expected rate of fall in serum glucose is 75-100
mg/dl/hr.

Insulin cont…
88
 When blood glucose reaches a range of 250 to 300
mg/dl, 5 -10 % glucose solution should be infused to
prevent hypoglycemia.
Insulin infusion should not be stopped until the
Ketonemia clears.
 It is preferable to give 5% or 10% DW with insulin
injection, rather than stop the insulin, because insulin
is still required to clear the acidosis and ketotic state.

89
 In general, bicarbonate infusion to correct severe
acidosis is avoided because it precipitates
further, sudden (and potentially fatal) decreases
in serum potassium levels

Electrolyte replacement:
90
 Major electrolyte of concern during treatment of
DKA is potassium.
 Insulin enhances the movement of potassium from
the extracellular fluid into the cells
 Patient’s serum potassium level may drop quickly
as a result of rehydration and insulin treatment thus
potassium replacement must begin once potassium
levels drop to normal.

Hyperglycemic Hyperosmolar Non-
Ketotic Syndrome (HHNS)
91
 Is a serious condition in which hyperosmolarity and
hyperglycemia predominate.
 Enough insulin is secreted to prevent ketosis, but not
enough to prevent hyperglycemia
 Hyperglycemia causes osmotic diuresis, resulting in
losses of fluid and electrolytes.
 Since ketosis is not present, the patient may not feel as
physically ill as the patient with DKA and may delay
seeking treatment

Clinical features
92
Several weeks history of polyuria
Dehydration(more sever), hypotension,
tachycardia
Mental status changes, focal neurologic deficits,
and hallucinations are common secondary to the
cerebral dehydration that results from extreme
hyperosmolality

Management
93
Similar treatment as seen in DKA
Fluid replacement, correction of electrolyte
imbalances, and insulin administration
Potassium is added to IV fluids
Watch fluid restriction carefully(old age)
Identifying and treating the precipitating factor.

Comparison of DKA and HHNS
Can occur in both DM
types, usually in Type
1
Precipitated by:
omission of insulin,
physiologic stress
(infection, surgery,
etc.)
Rapid Onset
(<24 hours)
usually in Type 2
(esp. elderly)
Precipitated by:
Physiologic stress
(infection, surgery,
etc.)
Slower Onset (over
several days)
Usually > 600mg/dl
94
DKA HHNS

Arterial pH levels <
7.3
Serum and urine
ketones Present
Serum Osmolality
300-350
Mortality Rate < 5%
Normal PH
Ketone Absent
Increases >350
High mortality
Rate(10-40%)
95
DKA HHNS

Long term Complications of DM
96
Macrovascular Complications
 Diseases of large and medium-size vessels
 Are due to atherosclerotic changes
 Coronary artery disease(MI,CHF,HTN)
 Cerebrovascular disease(stroke,)
 Peripheral arterial disease(gangrene)

Management
97
Prevention and treatment of the commonly accepted
risk factors for atherosclerosis.
Diet and exercise
Use of medications to control hypertension and
hyperlipidemia
Smoking cessation

….magt cont’d
98
 Control of blood glucose may reduce triglyceride
levels
 Treat complications the same as with nondiabetic
patients.
 Patients may need increased amounts of insulin
or may switch from oral antidiabetic agents to
insulin during illnesses.

Micro vascular complications
99
 Are unique to diabetes
 Increased blood glucose levels thicken the basement
membrane of small blood vessels and capillaries
 Includes
 Retinopathy
 Nephropathy
 Renal disease is more prevalent in patients with type 1
diabetes

Retinopathy
100
ö Deterioration of the small blood vessels
that nourish the retina
ö Leads to retinal ischemia and breakdown
of blood-retinal barrier
ö Leading cause of blindness in ages 25 –
74

101
Affects almost all Type 1 diabetics after 20 years
& 60 % of Type 2
Difficulty of reading , blurring of vision,
shadowing which may later on progress to total
blindness, swelling, decreased vision.

Management
102
Prevention is key
Need regular eye exams
Control of blood glucose-intensive control of blood
glucose reduced risk by 76% compared to that of
conventional therapy.
Control of hypertension

103
Cessation of smoking
ASA 100 mg /day may prevents further occlusion
of small capillaries
Surgery(vitrectomy) removes blood clots and
fibrosis that obstruct vitreous humor.

Nephropathy
104
 Diabetes causes hypertension in renal vessels
which cause leaking glomeruli, deposits in narrow
vessels, scarring and vascular damage.
 Is leading cause of end-stage renal disease
 Earliest clinical sign is microalbuminuria
(>30mg/24hrs)

105
 Periorbital edema, pedal edema, anasarca
 Laboratory: progression from micro
albuminuria to macroalbuminuria

Management
106
Tight blood pressure control decrease or delay
the onset of early proteinuria
Glycemic Control
Yearly screening for microalbuminuria in the
urine.
ACE- inhibitors: decreases progression of renal
diseases

107
 Tx of UTIs
 Low-sodium diet
 Low-protein diet
 Renal transplantation or Dialysis may be needed

Diabetic Neuropathy
 A group of diseases that affect all
types of nerves.
Peripheral (sensory motor)
Autonomic and
Spinal nerves.
 Elevated blood glucose levels over
a period of years causes capillary
basement membrane thickening and
capillary closure. In addition, there
may be demyelinization of the
nerves
108

Symptoms
109
Initial symptoms include paresthesias (prickling,
tingling, or heightened sensation) and burning
sensations, numbness
Decreased sensations of pain and temperature
Cardiac, gastrointestinal and renal symptoms
Hypoglycemic unawareness -inability to detect warning
signs of hypoglycemia like shakiness, sweating,
nervousness and palpitations
Sexual Dysfunction and Foot ulcer

Management
110
 Symptomatic treatment
 pain control
 Diarrhea control
 Treatment of impotence

Diabetic foot ulcer
Mechanisms:
 Neuropathy: Sensory neuropathy leads to loss of
pain and pressure sensation, and autonomic
neuropathy leads to increased dryness and
fissuring of the skin. Motor neuropathy results in
muscular atrophy,
111

112
Peripheral VD: Poor circulation of the lower
extremities contributes to poor wound healing and
the development of gangrene.
Immunocompromise: Hyperglycemia impairs
the ability of specialized leukocytes to destroy
bacteria.

Treatment of Foot Ulcers
114
 Bed rest
 Antibiotics
 Debridement
 Good control of blood glucose (usually increases
with infection).
 Amputation may be necessary to prevent spread
of infection

Essentials of Foot Care
115
Examination
 Annually for all patients
 Patients with neuropathy-visual inspection of feet at
every visit with a health care professional
Advise patients to:
 Use lotion to prevent dryness and cracking
 Cut toenails weekly or as needed
 Reducing risk factors, such as smoking and elevated
blood lipids, that contribute to peripheral vascular
disease
 Always wear socks and well-fitting shoes
 Good foot hygiene
 Notify their health care provider immediately if any
foot problems occur(daily assessment)

Diabetic
retinopathy
Leading cause
of blindness
in working-age
adults1
Diabetic
nephropathy
Leading cause of
end-stage renal disease2
Cardiovascular
disease
Stroke
1.2- to 1.8-fold
increase in stroke3
Diabetic
neuropathy
Leading cause of
non-traumatic lower
extremity amputations5
75% diabetic patients
die from CV events4
Type 2 diabetes is NOT a mild disease
4/4/2023
Tedla K, DM burden
116
1Fong DS, et al. Diabetes Care 2003; 26 (Suppl. 1):S99–S102. 2Molitch ME, et al. Diabetes Care 2003; 26 (Suppl. 1):S94–S98.
3Kannel WB, et al. Am Heart J 1990; 120:672–676. 4Gray RP & Yudkin JS. In Textbook of Diabetes 1997.
5Mayfield JA, et al. Diabetes Care 2003; 26 (Suppl. 1):S78–S79.

Hypothalamus Hormones
121
 Produces inhibiting and Releasing hormones
which controls the release of pituitary
hormone
Corticotropin-releasing hormone
Thyrotropin-releasing hormone
Growth hormone-releasing hormone
Gonadotropin-releasing hormone

Pituitary gland (hypophysis)
122
 Is a round structure located on the inferior aspect of
the brain.
 It control the activity of many other endocrine glands.
“ Master gland”
Controlled by the hypothalamus
 Has two lobes:
 Anterior Pituitary gland
 Posterior Pituitary gland

Posterior Pituitary-
neurohypophysis
123
 Does not produce hormones
 Stimulates the secretion of two hormones
 Antidiuretic Hormone-Promotes water retention
 Oxytocin-contraction of uterus, milk ejection from
breasts

Anterior Pituitary (Adenohypophysis)
124
 Stimulates the secretion of six hormones
1. Growth Hormone(GH)-Stimulates growth
2. Adrenocorticotropic hormone(ACTH)- adrenal
Cortical synthesis & release
3. Thyroid stimulating hormone(TSH)-TH
synthesis & release

125
4. Follicle stimulating hormone(FSH)-
Egg/sperm production.
5. Luteinizing hormone(LH)-sex hormones
6. Prolactin- milk production

Disorders of the Pituitary
127
 Abnormalities of the pituitary gland result from
either oversecretion or under secretion
 Abnormalities of the anterior and posterior portions
of the gland may occur independently
 Over secretion most commonly involves ACTH
leading to Cushing's syndrome, or GH leading to
acromegaly.

… Disorders cont’d
128
 Acromegaly- an excess of growth hormone in
adults, results in bone and soft tissue deformities
and enlargement of the viscera without an increase
in height.
 Gigantism: GH hyper secretion beginning in
childhood before closure of epiphyses may cause
increase linear growth of long bones resulting

129
 There is little bony deformity, soft tissue swelling
or enlargement of peripheral nerves
 Delayed puberty or hypogonadotropic
hypogonadism may be present.
 Insufficient secretion of growth hormone during
childhood results in generalized limited growth
and dwarﬁsm.

… Disorders cont’d
130
 Pan hypopituitarism (Simmonds’ disease) is
total absence of all pituitary secretions and is rare.
 In this condition, the thyroid gland, the adrenal
cortex, and the gonads atrophy (shrink) because
of loss of the trophic-stimulating hormones.
 The most common disorder related to posterior
lobe dysfunction is diabetes insipidus.

Clinical manifestation of
acromegaly
131
æ Enlargement of hands(especially fingertips) and
feet: increased ring, gloves and shoe size.
æ Coarsening of facial features
æ Thick skin folds: brows and nasolabial folds
æ Enlargement of the nose
æ Enlargement of mandible: Prognathism, spreading
of teeth

Clinical manifestation cont’d
132
+ Body hair increases and the skin thickens and
becomes darker.
+ Excessive perspiration, offensive body odor may
be noted.
+ Voice becomes husky, tongue enlarged and
furrowed.
+ Barrel chest deformity may be noted.

Diagnosis
133
Clinical manifestations.
GHz level:
Skull x-ray
CT or MRI (if available):will help to visualize the
tumor.
Other X-ray changes: Enlargement of sinuses
,tufting of distal phalanges, cortical thickening

Treatment
134
1. Ablative therapy
 Transpheniodal pituitary adenomectomey :
 Radiation therapy: radiation is generally indicated,
but be aware of danger of hypopituitarism.
2. Medical therapy is indicated if surgery and
radiotherapy are contraindicated or have failed.
 Give Bromocriptine up to 15 mg/d PO in divided
doses

GH as
Juvenile
135
GH = pituitary
dwarfism

Diabetes insipidus
137
Diabetes insipidus is a disorder of the posterior lobe of the
pituitary gland characterized by a deficiency of ADH, or
vasopressin
Three forms of DI do exist:
Neurogenic or central form -  amount of ADH production
Nephrogenic form - inadequate response to ADH
Psychogenic form - extremely large volumes of fluid intake
  inhibition of ADH production

Can occur
138
ê Secondary to head trauma, brain tumor, or
irradiation of the pituitary gland.
ê Infections of the central nervous system
(meningitis, encephalitis,TB)
ê Nephrogenic - failure of the renal tubules to
respond to ADH; related to hypokalemia,
hypercalcemia, medications
ê Primary/Idiopathic: account for approximately 50 %
of the cases of diabetes insipidus.

Manifestations
139
ê Excessive thirst (Polydipsia)- 2 to 20 Ls of fluid
daily
ê Large volumes of dilute urine (water-like urine) 2
to 20 L per day
ê chronic ingestion of large volumes of fluid causes
the renal medullary electrolyte concentration to
become diluted; thereby inhibiting the kidney's
ability to produce concentrated urine.

Assessment and Diagnostic
Findings
140
 Plasma ADH levels
 Plasma and urine osmolality
 Fluid deprivation test: started in the morning by
weighing the patient, obtaining venous blood to
determine electrolyte concentrations and osmolality,
and measuring urinary osmolality.
 Fluid intake is withheld 8-12 hrs, and voided urine is
collected hourly and its osmolality is measured

Water deprivation test cont..
141
Dehydration is continued until
 Orthostatic hypotension and postural tachycardia
appear,
 5% or more of the initial body weight has been lost,
or

142
 The urinary concentration does not increase by more
than 30 mOsm/L in sequentially voided specimens for
3 hrs.
 At this point, serum electrolytes and osmolality are
again determined, and Five (5 U) of aqueous
vasopressin or 2 µg of desmopression is then injected
SC. Urine osmolality is measured 1 hr later.

Management
143
 Replacement of ADH
 Adequate fluid replacement
 Identify and correct the underlying intracranial
pathology
 Rx of Nephrogenic DI is different

Thyroid disorders
144
 The thyroid gland is a butterfly-shaped organ
located in the lower neck anterior to the trachea.
 The gland produces 3 hormones:
 Thyroxine (T4)
 Triiodothyronine (T3)
 Calcitonin or thyro calcitonin

Regulation of hormone
production
145
 Hypothalamic TRH stimulates pituitary production of
TSH, which in turn stimulates thyroid hormone
synthesis and secretion.
 The presence of adequate thyroid hormone sends a
negative feedback signal that inhibits TRH and TSH
production.
 When the level of thyroid hormone in the serum
decreases the production and release of TRH and TSH

….thyroid d/o cont’d
146
 TSH regulates the secretion of T3 and t4;which in turn
modulated by Thyrotropin-releasing hormone (TRH).
 If the thyroid hormone concentration in the blood
decreases, the release of TSH increases, which causes
increased
output of T3 and T4.
 Iodine is essential to the thyroid gland for synthesis of
its hormones.

Calcitonin
147
Calcitonin, or thyrocalcitonin, is another important
hormone secreted by the thyroid gland.
 It is secreted in response to high plasma levels of
calcium, and
 It reduces the plasma level of calcium by
increasing its deposition in bone.

Thyroid function tests:
148
1. Serum T3 and T4 level: measures the total bound (99 %)
and free (1 %) hormone level in the circulation.
 This gives some clue about serum level of thyroid
hormone, but has limitation since serum level of the
hormone is influenced by conditions affecting the level of
carrier proteins.
 T3 and T4 levels are elevated in hyperthyroidism and
decreased in hypothyroidism.

149
2. Serum TSH level: is the most important test to asses
thyroid hormone function.
 In hypothyroidism, TSH level is elevated, as a
result of feedback effects of low thyroid hormone
level.
 In hyperthyroidism, TSH level is decreased,
because the elevated thyroid hormone concentration,
leads to suppression of TSH release, through a

Thyroid function tests cont..
150
3. Radioactive iodine uptake (RAIU):by the thyroid
gland 24 hrs after administration of the Iodine
(I131)isotope, assesses the rate of iodine uptake
by the thyroid gland which demonstrates the
degree of glandular activity.
 Increased uptake in hyperthyroidism, and
decreased uptake in hypothyroidism.

151
 This test is especially useful in diagnosing ectopic
hormone production
4. Thyroid stimulating antibodies, circulating
antibody against T3 and T4 is an evidence for
autoimmune disease of thyroid glands.

Hypothyroidism
153
 Is the disease state caused by insufficient
production of thyroid hormone by the thyroid
gland.
 The most common cause in adults is
autoimmune thyroiditis (hashimoto’s disease).

154
Primary(thyroidal) hypothyroidism: refers to a
thyroid hormone deficiency as a result of thyroid
gland disease(>90% of cases).
Hypothyroidism also commonly occurs in patient
who have been treated with radioiodine or anti
thyroid medications or who have had thyroid
surgery.

….cont’d
155
ê Secondary hypothyroidism: it is caused entirely
by a pituitary disorder, and hypothalamic ,results
from TSH deficiency.
ê Tertiary hypothyroidism: if it is attributable to a
disorder of the hypothalamus resulting in
inadequate secretion of TSH because of
decreased stimulation by TRH

156
 Central hypothyroidism is thyroid
dysfunction caused by failure of the
pituitary gland (TSH), the hypothalamus
(TRH), or both

…cont’d
When thyroid deficiency
is present at birth, the
condition is known as
cretinism which results
in stunted physical and
mental growth.
157

158
ö Extreme fatigue, weakness, lethargy, slow movement,
cold intolerance, weight gain with diminished appetite
ö Edema of the face and extremities, hearing loss,
hoarseness of the voice, dry skin , hair loss ,sparse
eyebrows
ö Pericardial effusion and ascites, constipation,
menorrhagia, memory impairment, psychosis
ö Atherosclerosis ,coronary artery disease

…cont’d
159
 Myxedema- refers to the accumulation of
mucopolysaccharides in subcutaneous and other
interstitial tissues.
 Myxedema coma describes the most extreme,
severe stage of hypothyroidism, in which the
patient is hypothermic and unconscious.

Assessment and Diagnosis
160
 History and Physical examination
 Serum TSH level
 Serum T3 and T4 level

Management
161
The primary objective in the management of
hypothyroidism is to restore a normal metabolic state
by replacing the missing hormone.
 Thyroid hormone replacement: levothyroxin sodium
 Prevention of cardiac dysfunction
 Prevention of medication interactions
 Prevention of myxedema coma
 Supportive management to maintain vital functions

Hyperthyroidism
162
ê Is a hypermetabloic state, resulting from excessive thyroid
hormone function and it is the second most prevalent
endocrine disorder.
ê Graves’ disease: the most common type of
hyperthyroidism, results from an excessive output of
thyroid hormones caused by abnormal stimulation of the
thyroid gland by circulating immunoglobulin's.
ê Other causes- thyroiditis ,excessive ingestion of thyroid
hormone

Clinical features
163
ö Nervousness , hyperactivity, irritability
ö Palpitations, dysrhythmias, systolic hypertension
ö Heat intolerance and sweating ,fine silky hair
ö Fine tremor, muscle weakness and fatigue
ö Exophthalmos (bulging eyes)
ö Weight loss with increased appetite
ö Amenorrhea , diarrhea, polyuria,

164
 History and physical examination
 Thyroid thrill and or bruit may be present
 Thyroid may be enlarged
 Blood tests.
 Serum T3 and T4 level may be raised
 Low or nonexistent amounts of TSH indicate an overactive
thyroid.
 An increased radioactive iodine uptake that indicates
thyroid gland is producing too much thyroxine

Management
165
Radioactive therapy
 To destroy the overactive thyroid cells.
 Not used in pregnancy and in nursing mothers
because radioiodine crosses the placenta and is
secreted in breast milk.

166
Antithyriod Medication:
 PTU/Propylthiouracil & methimazole-blocks
extra thyroidal conversion of T4 to T3.
 Solutions of iodine and iodide -prepare patient
for surgery by reducing the vascularity of the
thyroid gland.

….magt cont’d
167
Surgery -Subtotal thyriodectom
 Reserved for special circumstances, e.g. large
goiters, those who cannot take antithyroid meds,
or who need rapid normalization
 Needs pretreatment with PTU

168
Symptomatic treatments
 Beta-adrenergic blockers like propranolol-
control the sympathetic nervous system
effects of hyperthyroidism

Thyroiditis
169
 Inflammation of the thyroid gland.
 Can be acute, subacute, or chronic (Hashimoto's
Disease)
 Each type of Thyroiditis is characterized by
inflammation, fibrosis, or lymphocytic infiltration of
the thyroid gland.
 Several forms are characterized by autoimmune

Thyroid tumors
170
 Can be benign or malignant.
 If the enlargement is sufficient to cause a visible
swelling in the neck, the tumor is referred to as a
goiter
 Some are symmetric and diffuse; others are
nodular.

171
 Some goiters are accompanied by
hyperthyroidism, in which case they are
described as toxic; others are associated with a
euthyroid state and are called nontoxic goiters.

Endemic (iodine-deficient) goiter
172
 Most common type of goiter
 Also called simple or colloid goiter
 Caused by iodine deficiency or an intake of large
quantities of goitrogenic substances i.e. excessive
amounts of iodine or lithium, which is used
in treating bipolar disorders.

173
 Is a compensatory diffuse hypertrophy of the
thyroid gland
 Appearance: Large
Smooth firm
Non-tender goiter

174
 Such goiters usually cause no symptoms, except for the
swelling in the neck, which may result in tracheal
compression when excessive.
 Supplementary iodine, such as SSKI, is prescribed to
suppress the pituitary’s activity.
 Surgery may be recommended
 The introduction of iodized salt has been the single most
effective means of preventing goiter in at risk
populations.

Multi nodular Goiter
175
Most often caused by iodine deficiency
Thyromegaly, occasionally with rapid enlargement
and tenderness secondary to haemorrhage into a
cyst.
Rarely, tracheal compression may occur, causing
coughing or choking.
Some patients may complain of a feeling of lump in
the throat.

176
 Appearance: Large
irregular
Nodular goiter

177
 Many nodules of varying sizes are usually
palpable.
 Thyroid function tests: Performed to rule
out hypo or hyperthyroidism

Management
178
Surgery, needle biopsy or subtotal
thyriodectomy should be considered if thyroid
enlargement persists despite adequate TSH
suppression.
Radioiodine therapy ,
Percutaneous injection of ethanol in to the
toxic nodule.

179
Complication of operation
 Hemorrhage
 Hematoma formation
 Laryngeal nerve damage
 Hypoparathyrodism
 Hypothyroidism
 Postoperative infection

180
Parathyroid and Adrenal gland
Disorders

Parathyroid gland
181
+ The parathyroid glands (normally four) are situated in the
neck and embedded in the posterior aspect of the thyroid
gland.
+ Parathormone (parathyroid hormone), the protein hormone
produced by the parathyroid glands, regulates calcium and
phosphorus metabolism.
+ Increased secretion of parathormone results in increased
calcium absorption from the kidney, intestine, and bones,
which raises the blood calcium level.

182
 Some actions of this hormone are increased by
the presence of vitamin D.
 Parathormone also tends to lower the blood
phosphorus level.

Hyperparathyroidism
184
Is caused by overproduction of parathormone by
the parathyroid glands
Is characterized by bone decalciﬁcation and the
development of renal calculi (kidney stones)
containing calcium.

Primary hyperparathyroidism
185
Is due to excessive production of PTH by one or
more of hyperfunctioning parathyroid glands.
The cause is unknown; genetic factor may be
involved.
The incidence of the disease increases dramatically
after the age of 50 and it is 2-4 folds more common
in women

Secondary hyperparathyroidism
186
An increase in PTH secretion which is adaptive
and unrelated to intrinsic disease of the
parathyroid glands.
This is due to chronic stimulation of the
parathyroid glands by a chronic decrease in the
ionic calcium level in the blood.
Occurs in patients with chronic renal failure as a
result of phosphorus retention.

187
Apathy, fatigue, muscle weakness, nausea,
vomiting, constipation, hypertension and cardiac
dysrhythmias
Excess calcium in the brain can lead to psychoses
Renal lithiasis can lead to renal damage and even
failure
Demineralization of bones with back and joint pain,

Findings
188
Persistent elevated serum calcium and parathormone
levels
Serum phosphate is usually low but may be normal
Double antibody PTH test- used to distinguish between
primary hyperparathyroidism and malignancy as a cause
of hypercalcemia
Imaging and fine needle biopsy -to evaluate the function
of the parathyroids & to localize cysts, adenomas, or

Management
189
Parathyroidectomy ( for primary)
Hydration therapy to prevent renal calculi
Avoid thiazide diuretics as they decrease renal excretion of
calcium
Increase mobility to promote bone retention of calcium
Avoid excess calcium in the diet
Watch for s/s of tetany postsurgically (numbness, tingling,
carpopedal spasms) as well as cardiac dysrhythmias and
hypotension

Complication: hypercalcemic
crisis
190
 Seen with extreme elevation of serum calcium
levels(>15mg/dl)
 Can result in life-threatening neurologic,
cardiovascular and renal symptoms
 Treatments
 Rehydration(iv)
 Loop diuretics to promote renal excretion of

191
Phosphate therapy to promote calcium deposition in bone
and reducing GI absorption of calcium
Cytotoxic agents (eg,mithramycin), calcitonin, may be
used in emergency situations to decrease serum calcium
levels quickly.
A combination of calcitonin and corticosteroids has been
administered in emergencies to reduce the serum calcium
level by increasing calcium deposition in bone.

Hypo parathyroidism
192
 Is deficiency of parathormone usually due to
surgery(the removal of the parathyroid glands or
interruption of blood supply to the glands)
 Atrophy of the parathyroid glands of unknown
cause is a less common cause
 Results in hypocalcaemia and hyper phosphatemia

Clinical Features
193
 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:
 Numbness and tingling in extremities, Stiffness of hands
and feet, Bronchospasm, laryngeal spasm, carpopedal
spasm, Photophobia, cardiac dysrhythmias and seizures,
Anxiety, irritability, depression, delirium and Hypotension
also may occur.

Diagnostic Findings
194
 Positive Trousseau’s sign- carpopedal spasm is
induced by occluding the blood flow to the arm for 3
minutes with a blood pressure cuff.
 Positive Chvostek’s sign-when a sharp tapping over
the facial nerve just in front of the parotid gland and
anterior to the ear causes spasm or twitching of the
mouth, nose, and eye.

….dx cont’d
195
 Lab:
Hypocalcaemia and
hyperphosphataemia in the absence of renal
failure
 x-rays of bone shows
increased bone density.
 ECG changes

Management
199
 The goal of therapy is to increase the serum
calcium level to 9-10 mg/dl and to eliminate the
symptoms
 May need to give IV calcium gluconate for
immediate treatment
 Sedatives such as pentobarbital may be needed
 Use of parathormone IV reserved for extreme

….mangt cont’d
200
 Bronchodilators and even ventilator assistance ,if
the patient develops respiratory distress.
 Vitamin D
 Diet high in calcium and low in phosphorus
 Restrict milk and milk products
 Environment free of noise, drafts, bright lights, or
sudden movement

Adrenal Disorder
201
Adrenal gland
 Is pyramid-shaped organs attached to the upper
portion of a kidney
 Each adrenal gland is, in reality, two endocrine
glands with separate, independent functions
 Each has two parts:
 Outer cortex
 Inner medulla

Cont…
202
 The secretion of hormones from the adrenal cortex is
regulated by the hypothalamic pituitary-adrenal axis.
 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 gluco
corticoid hormone (cortisol).
 Increased levels of the adrenal hormone then inhibit the
production or secretion of CRH and ACTH. .

Adrenal Cortex
203
 The three types of steroid hormones produced by the adrenal cortex
are
 Mineralocorticoid: mainly aldosterone; w/c affects sodium
absorption, loss of potassium by kidney
 Glucocorticoids:(cortisol);affects metabolism, regulates blood sugar
levels, affects growth, anti-inflammatory action, decreases effects of
stress
 Adrenal androgens: effects similar to those of male sex hormones
 Adrenocortical secretions make it possible for the body to adapt to
stress of all kinds

Adrenal Medulla
204
 The adrenal medulla functions as part of the autonomic
nervous system.
 Secretion of catecholamine's hormones (Epinephrine
and Nor epinephrine)
 Serve as neurotransmitters for sympathetic nervous
system
 Involved with the stress response
 induce release of free fatty acids, increase the basal
metabolic rate, and elevate the blood glucose level

Pheochromocytoma
206
A tumor of chromaffin cells that secrete
catecholamines
Typically benign and unilateral
10% of the tumors are bilateral, and 10% are
malignant.
Major location is in the adrenal medulla (80%)

207
They may also be found in the extra-adrenal
chromaffin tissue located in or near the aorta,
ovaries, spleen, or other organs.
 May occur at any age, but its peak incidence is
between ages 40-50 years
Male=female
Can be familial

Clinical manifestations
208
 Typical triad of symptoms
 Headache
 Diaphoresis
 Palpitation (tachycardia)

209
 Hypertension
 Tremor, flushing, and anxiety
 Hyperglycemia
 Pallor
 Orthostatic hypotension
 Visual blurring, Papilledema
 Weight loss, Polyuria, polydipsia

Assessment and diagnostic
findings
210
 Pheo chromo cytoma is suspected if signs of
sympathetic nervous system over activity occur.
These includes 5 H’s)-.
1. Hypertension
2. Headache
3. Hyper hidrosis/excessive sweating
4. hyper metabolism
5. hyperglycemia

…dx cont’d
211
 Urine and plasma levels of catecholamine's
(standard) are direct and conclusive tests
 Clonidine suppression test if plasma and urine
tests are inconclusive
 CT and MRI- to detect pheochromocytomas

Management
212
Bed rest with the head of the bed elevated-to
promote an orthostatic decrease in BP during
acute attack.
ICU is needed
Alpha and beta adrenergic-blockers
Catecholamine synthesis inhibitors

213
Surgery (adrenalectomy) is definitive Rx
Corticosteroids may be necessary if bilateral
adrenalectomy has been necessary.
Monitor and treat Hypotension and hypoglycemia
after surgery
Monitor urine catecholamine levels.

Addison’s Disease
214
 Addison's disease occurs when the adrenal cortex
function is inadequate to meet the patient’s need for
cortical hormones
 Also known as Adrenocortical Insufficiency.
 There is a decrease Glucocorticoids, mineralocorticoids,
and androgen hormones.
 Occurs when 90% of the adrenal cortex has been
destroyed

Causes
215
 Autoimmune or idiopathic atrophy of the adrenal glands
(80% to 90% of cases)
 Surgical removal of both adrenal glands
 Infection of the adrenal glands (Tuberculosis and
histoplasmosis )
 Inadequate secretion of ACTH
 Therapeutic use of corticosteroids.
 Sudden cessation of exogenous adrenocortical hormonal
therapy

Signs and Symptoms
 Hyperkalemia
 Hypotension
 Hypoglycemia
 result in Addisonian
crisis with disease
progression and
acute Hypotension
 Fatigue & muscle
weakness,
 GI symptoms
 Dark pigmentation
 Mental status
changes
 Hyponatremia
216

S/S of Addisonian crisis
217
 characterized by cyanosis and the classic signs of
circulatory shock: pallority, apprehension, rapid and
weak pulse, rapid respirations, and low blood
pressure.
 In addition, the patient may complain of headache,
Severe vomiting and diarrhoea

Findings
219
 The diagnosis is confirmed by low levels of
adrenocortical hormones in the blood or urine and
decreased serum cortisol levels
 Decreased blood glucose (hypoglycemia) and sodium
(hyponatremia) levels, an increased serum potassium
(hyperkalemia) level, and an increased white blood
cell count (leukocytosis).
 ACTH stimulation test

Management
220
 Immediate: Reverse shock
 Restore blood circulation; fluids and IV
corticosteroid
 Monitoring vital signs
 Placing the patient in a recumbent position with
the legs elevated.

221
 Identify and treat the cause. e.g. Antibiotics if
infection
 Hormone replacement therapy
 Limit activity
 Maintain, quiet, non-stressful environment

Cushing’s Syndrome
222
 Occurs due to prolonged exposure to elevated levels
of either endogenous or exogenous Glucocorticoids or
from hyperplasia of the adrenal cortex rare.
 Primarily oversecretion of Glucocorticoids and
androgens seen
 Women ages 20 to 40 years are five times more likely
than men to develop the disease
 Are primarily a result of oversecretion of
Glucocorticoids and androgens

Causes include:
223
 ACTH-secreting tumor of the pituitary (Cushing’s
disease)
 Excess secretion of cortisol by a neoplasm within the
adrenal cortex
 Ectopic secretion of ACTH by a malignant growth
outside the adrenal gland
 Excessive or prolonged administration of
steroids(common)

ö Central obesity
ö Moon face, buffalo
hump in the neck and
supra clavicular areas ,a
heavy trunk, and
relatively thin
extremities.
ö Weakness, malaise,
muscle wasting and
osteoporosis. Kyphosis,
backache, and
compression fractures
ö Depression and
psychosis
ö Striae, acne, skin-
thinning, bruising
ö Hypertension
ö Diabetes or impaired
glucose tolerance
224

….c/f cont’d
225
 Virilization in females -characterized by the
appearance of masculine traits and the recession of
feminine traits as a result of excess androgens.
 Oligomenoorrhoea or amenorrhoea
 Hirsutism (excessive growth of hair on the
face), breasts atrophy, clitoris enlarges, and
voice deepens
 Decreased libido and impotence in males

Findings
228
ê ↑ Na+ ↑ glucose
ê ↓ K+
ê Reduction in the number of blood eosinophils,
and disappearance of lymphoid tissue
ê Serum or urine cortisol level
ê Imaging studies

Management
229
 Treatment of underlining cause
 Surgery for neoplasia
 Adrenalectomy
 Adrenal enzyme inhibitors (eg, metyrapone,
aminoglutethimide, mitotane, ketoconazole)
 Attempt to reduce or taper corticosteroid dose(if it
result from the administration of corticosteroids)

Endocrine Disorder.pptx

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Endocrine Disorder.pptx