Management of Patient with

Metabolic and Endocrine Disorders

By: Negesse T.(M.Sc, N)

1
 Learning Objectives
 At the end of this session, the learner will able to:
 Define Disorders of Endocrine System
 Mention the clinical manifestation, and treatment of
Disorders of Endocrine System

2
 Diabetes mellitus
Definition
 Metabolic disorder characterized by hyperglycemia due
to an absolute or relative lack of insulin or to a cellular
resistance to insulin.
 Sixth leading cause of death due to cardiovascular
effects resulting in atherosclerosis, coronary artery
disease, and stroke
 Leading cause of end stage renal failure
 Major cause of blindness
 Most frequent cause of non-traumatic amputations

3
 Risk factors
 Family history/ Genetic predisposition
 Environmental triggers stimulate an autoimmune
response
 Cardiovascular disease
 Obesity(especially of upper body)
 Sedentary lifestyle
 History of impaired fasting glucose or impaired glucose
tolerance
 Hypertension
 Race /ethnicity
 Physical inactivity
 Gestational diabetes 4
 DIAGNOSTIC CRITERIA
Cardinal symptoms for DM( the 3 P’s)
Polydyspia
Polyphagia
Polyurea
Investigation
Sx of diabetes plus
1. Random plasma glucose > 200 mg/dl(11.1 mmol/l)
2. Fasting Plasma Glucose > 126 mg/dl (7.0 mmol/l)
3. OGTT: 2 hr postload glucose > 200 mg/dl (11.1
mmol/dl)
5
 IMPAIRED GLUCOSE TOLERANCE
(IGT):
 A state between normal glucose homeostasis and diabetes
High risk for progression to DM
Pathologic only in pregnancy
FASTING PLASM GLUCOSE > 110 but < 126 mg/dl

IMPAIRED FASTING GLUCOSE (IFG):

The state between normal glucose homeostasis and diabetes
FASTING PLASM GLUCOSE > 110 but < 140 mg/dl

6
 Types of DM
 Type I—beta cells destroyed by autoimmune
process
 Type 2—decreased insulin production and
decreased sensitivity to insulin
 Gestational DM: Any degree of glucose
intolerance first detected during pregnancy
 Diabetes mellitus associated with other
conditions or syndromes

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 Diabetes Mellitus(Type 1)
 Metabolic condition in which the beta cells of
pancreas no longer produce insulin;
characterized by hyperglycemia, breakdown of
body fats and protein and development of ketosis
 Accounts for 5 – 10 % of cases of diabetes; most
often occurs in childhood or adolescence
 Formerly called Juvenile-onset diabetes or
insulin-dependent diabetes (IDDM)

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 DM Type 1…
Pathophysiology
 Autoimmune reaction in which the beta cells
that produce insulin are destroyed
 Alpha cells produce excess glucagons causing
hyperglycemia
 Process of beta cell destruction occurs slowly;
hyperglycemia occurs when 80 – 90% is
destroyed; often trigger stressor event (e. g.
illness)
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 DM Type 1…
Hyperglycemia leads to manifest:
 Polyuria (hyperglycemia acts as osmotic diuretic)
 Glycosuria (renal threshold for glucose: 180 mg/dL)
 Polydipsia (thirst from dehydration from polyuria)
 Polyphagia (hunger and eats more since cell cannot
utilize glucose)
 Weight loss (body breaking down fat and protein to
restore energy source
 Malaise and fatigue (from decrease in energy)
 Blurred vision (swelling of lenses from osmotic effects)
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 DM Type 2
 It is a condition of fasting hyperglycemia
occurring despite availability of body’s
own insulin
 Was known as non-insulin dependent
diabetes or adult onset diabetes
 The two main problems related to insulin in
type 2 diabetes are insulin resistance and
impaired insulin secretion.
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 Type 2 DM…
Pathophysiology
 Sufficient insulin production to prevent
DKA; but insufficient to lower blood
glucose through uptake of glucose by
muscle and fat cells
 Cellular resistance to insulin increased by
obesity, inactivity, illness, age, some
medications
12
 Type 2 DM…
 Risk factors which increase insulin
resistance includes:
 Obesity
especially around the waist and
abdomen
 Low levels of physical activity
 High blood pressure
 Increasedblood cholesterol (high LDL, low
HDL, high triglycerides )
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 Type 2 DM…
Manifestations
1. Client usually unaware of diabetes
 Discovers diabetes when seeking health care for
another concern
 Most cases aren’t diagnosed for 5-6 years after
the development of the disease
 Usually does not experience weight loss

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 Type 2 DM…
2. Possible symptoms or concerns
 Hyperglycemia (not as severe as with Type 1)
 Polyuria
 Polydipsia
 Blurred vision
 Fatigue , Skin Infections
 Paresthesias (numbness in extremities)
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 Management
 Nutritional
 Exercise

 Monitoring
 Pharmacologic
 Education

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 Dietary Management
 Carbohydrate 45-65% total daily calories
 Protein-15-20% total daily calories
 Fats—less than 30% total calories, saturated fats only
10% of total calories
 Fiber—lowers cholesterol; soluble—legumes, oats,
fruits Insoluble—whole grain breads, cereals and some
vegetables. Both increase satiety.
 Slowing absorption time seems to lower glycemic index.
 Consistent, well-balanced small meals several times per
day
 Exchange system or counting carbohydrates
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 Exercise and Diabetes
 Exercise increases uptake of glucose by
muscles and improves utilization, alters lipid
levels, increases HDL and decreases TG
 If on insulin, eat 15g snack before beginning
 Check BS before, during and after exercising
if the exercise is prolonged

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 Glucose monitoring
 Patients on insulin should check sugars 2-4 times
per day
 Not on insulin, two or three times per week
 Should check before meals and 2 hours after
meals
 Parameters from physician very important
 Evaluates trends and efficacy of treatment over
24h period
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 Insulin therapy
 Rapid acting—lispro (Humalog) and insulin
aspart (Novolog) onset 15’, peak 60-90’ and last
from 2-4 hours
 Short acting—regular. Onset is 30-60’, peak in
2-3h and last for 4-6 hours.
 Regular insulin is only kind for IV use.

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 Insulin Therapy
 Intermediate insulins—NPH or Lente.
 Onset 3-4h, peak 4-12 hours and lst 16-20
hours.
 Names include Humulin N, Novolin N, Long
acting—Humulin Ultralente. Onset 6-8h, peak
12-16 h and lasts 20-30h.
 Peakless insulins: determir and glargine

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 Complications of Insulin Therapy
 Local & systemic allergic reactions
 Insulin lipodystrophy (lipoatrophy or lipohypertrophy)
 Insulin resistance
 Morning hyperglycemia—Dawn phenomenon
(nocturnal surges of growth hormone) so give dose at
hr not before dinner
 Somogyi effect—nocturnal hypoglycemia followed by
rebound hyperglycemia-decrease evening dose of
insulin
 To determine cause, test at HS, 3am and upon
awakening
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 Methods of Insulin Delivery

 Insulin pumps—insulin is delivered at .5-2

units/hour.
 Most common risk of insulin pump therapy is
ketoacidosis.
 Transplantation of pancreatic cells

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 Oral antidiabetic agents
 Sulfonylureas—glipizide, glyburide and
glimepiride. Hypoglycemia
 Biguanides—metformin.
 Lactic acidosis.
 Alpha-glucosidase inhibitors—acarbose.
 Delay absorption of CHO
 Non-sulfonylurea secretagogues—repaglinide.
Cause secretion of insulin.
 Thiazolidinediones—pioglitazone and
rosiglitazone. Sensitize. Weight gain. Fertility.
Liver. 24
 Teaching Plan
 Education is critical
 Simple pathophysiology
 Treatment modalities
 Recognition, treatment and prevention of acute
complications
 When to call the doctor
 Foot care, eye care, general hygiene, risk
factor management

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Acute Complications of Diabetes
 Hypoglycemia—50-60 or less

 DKA

 HHNS

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 Hypoglycemia
 Caused by too much insulin or oral agents, too
little food or excessive physical activity
 Surge in epinephrine and norepinephrine results
in sweating, tremors, tachycardia, palpitations,
nervousness and hunger
 CNS effects—inability to concentrate, headache,
lightheadedness, confusion, memory problems,
slurred speech, incoordination, double vision,
seizures and even loss of consciousness.
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 Treatment for hypoglycemia
 2-3 tsp. of sugar or honey
 6-10 hard candies
 Fruit juice or soda
 3-4 commercially prepared glucose tablets
 Recheck BS 15 minutes, same s/s, repeat treatment.
 After improvement, then cheese and crackers or milk.
 Extreme situations, give glucagon. (can cause n/v).
D50W.

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 Diabetic Ketoacidosis

Clinical features are:

1. Hyperglycemia
2. Dehydration and electrolyte loss
3. Acidosis
Three main causes: illness, undiagnosed and
untreated and decreased insulin
Other causes: patient error, intentional skipping
of insulin
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 Presentation of DKA
 3 P’s
 Orthostatic hypotension
 Ketosis
 GI s/s
 Acetone breath
 Hyperventilation

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 Diagnostic Findings of DKA
 BS between 300-800mg/dl
 Acidosis
 Electrolyte abnormalities
 Elevated BUN, creatinine and hct r/t
dehydration

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 Medical Management of DKA
 Rehydrate with normal saline, then follow
with .45% NaCl then D5.45NS (or other)
 Restore electrolytes
 ECGs
 Hourly blood sugars
 IV insulin

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 Nursing Management
 Administer fluids
 Insulin
 Prevent fluid overload
 Strict I&O
 ECG monitoring
 Vital signs
 Monitor patient responses to treatments

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 Hyperglycemic Hyperosmolar
Nonketotic Syndrome
 Predominated by hyperosmolarity and
hyperglycemia
 Minimal or no ketosis
 Osmotic diuresis
 Glycosuria and increased osmolarity
 Occurs over time
 Blood sugar is usually over 600mg/dl
 Hyperglycemia, dehydration and hyperosmolarity
may be more severe than in DKA
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 Medical Management
 Similar treatment as seen in DKA
 Watch fluid resuscitation if history of heart
failure
 ECG
 Lytes monitoring
 Fluids with potassium replacement

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

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 Long term complications of
Diabetes
 Increasing numbers of deaths from
cardiovascular and renal complications
 Renal (microvascular) disease is more
common in type 1 diabetics
 Cardiovascular disease (macrovascular)
complications are more common in type 2
older diabetics

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 Diabetic Vascular Diseases
 Chronic hyperglycemia causes irreversible
structural changes in the basement membranes
of vessels. Result is thickening and organ
damage.
 Glucose toxicity affects cellular integrity
 Chronic ischemia in microcirculatory
brances>>cause connective tissue hypoxia and
microischemia
 Up to 21% of diabetics have retinopathy at time
of diagnosis 38
 Macrovascular Complications
 Medium to large blood vessel walls thicken,
sclerose, and become occluded by
plaque./atherosclerosis
 The three main types of macrovascular
complications
 Coronary artery disease(50% - 60% of all
deaths)
 Cerebrovascular disease
 Peripheral arterial disease

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 Management of Macrovascular
Diseases
 Modify/reduce risk factors
 Meds for hypertension and
hyperlipidemia
 Smoking cessation
 Control of blood sugars which will help
reduce TG

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 Micro vascular Complications

 Unique to diabetes.
 Capillary basement membrane thickening.
 Microvascular complications may involve:
 Retinopathy
 Nephropathy
 Neuropathies (i.e. peripheral & Automatic)
 Foot and Leg Problems 41
 Retinopathy
 Deterioration of the small blood vessels that
nourish the retina
 Leading cause of blindness in those 20-74
yrs.
 Three stages of retinopathy
 Non proliferative(background) retinopathy
 Preproliferative

 Proliferative 42
 Background: Early stage, asymptomatic retinopathy.
Blood vessels within the retina develop micro aneurysms
that leak fluid, causing swelling and forming deposits
(exudates). In some cases, macular edema causes
distorted vision.
 Pre-proliferative: Represents increased destruction of
retinal blood vessels
 Proliferative: Abnormal growth of new blood vessels on
the retina.
 New vessels rupture, bleeding into the vitreous and
blocking light.
 Ruptured blood vessels in the vitreous form scar tissue,
which can pull on and detach the retina. 43
 Also an increased incidence of cataracts
and glaucoma in diabetics.
 Need regular eye exams
 Control BP, control BS and cessation of
smoking can help

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 Nephropathy
 Secondary to diabetic microvascular changes in
the kidney
 May progress to ESRD
 Earliest clinical sign of nephropathy is
microalbuminuria.
 Diabetes causes hypertension in renal vessels
which cause leaking glomeruli, deposits in
narrow vessels, scarring and vascular damage
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 Cont….
 Medical management: control BP, Tx of UTIs
 Avoid nephrotoxic agents, contrast dyes
 Low sodium & Low protein diet
 Tight glycemic control
 May require dialysis
 May have co-existent retinopathy
 Kidney transplantation—success now 75-80%
for 5 years

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 Neuropathies
 Group of diseases that affect all types of nerves.
 Includes peripheral, autonomic and spinal
nerves.
 Prevalence increases with duration of the disease
and degree of glycemic control
 Capillary basement membrane thickening and
capillary closure may be present.
 May be demyelination of the nerves, nerve
conduction is disrupted.
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 Peripheral neuropathy
 Manifestations: paresthesia, burning
sensations, numbness, decrease in
proprioception.
 Decreased sensation of temperature and touch
Rx. Pain management and control BS level

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 Autonomic Neuropathies

 Cardiac, gastrointestinal and renal systems

 Cardiac—myocardial ischemia may be
painless
 GI—delayed gastric emptying with early
satiety, nausea, bloating, diarrhea or
constipation
 Urinary retention—decreased sensation of
bladder, neurogenic bladder
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1. Hypoglycemia unawareness
No longer feel shakiness, sweating, nervousness and
palpitations associated with hypoglycemia
2. Sudomotor neuropathy
 neuropathic condition refers to a decrease or absence
of sweating of the extremities with compensatory
increase in upper body sweating.
2. Sexual dysfunction
 Especially impotence in men, reduced vaginal
lubrication, decreased libido and lack of orgasm.

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 Management of neuropathies
 Early detection, periodic follow up on patient’s
with cardiac disease
 Monitor BP frequently for s/s orthostatic
hypotension
 Low fat diet, frequent small meals, close BS
monitoring and use of prokinetic medications
 Meticulous skin care

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 Foot and Leg Problems
 Sensory loss
 Sudomotor neuropathy leads to dry, cracking
feet
 Poor wound healing/gangrene
 Lowered resistance to infection

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 Management of Foot and Leg
Problems
 Teaching patient foot care-inspect feet and shoes
daily
 Examine feet every time goes to doctor
 See physicians at least annually
 Closed toe shoes
 Good foot hygiene
 Glycemic control is the key to preventing
complications

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 Special issues
 Hyperglycemia in the hospital—increased food, decreased
insulin, steroids, IV dextrose,overly vigorous treatment of
hypoglycemia, inappropriate holding of insulin
 Hypoglycemia in the hospital—overuse of sliding scale,
lack of insulin change when dietary intake withheld,
overzealous treatment of hyperglycemia, delayed meals
after insulin given
 Alterations in diet.
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 Recommended Screening
 Fasting glucose levels
 Oral glucose tolerance testing using 75g of
Glucola
 Fasting glucose of
100-125mg/dL=prediabetes
 Fasting level >126 is diagnostic
 OGTT>200 is diagnostic

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 Controlling blood sugar
 Hemoglobin A1C less than or equal to 6.5%
 Fasting plasma glucose <110
 Two hour postprandial sugar <140
 Comprehensive education

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 Treating Type I Diabetes
 Basal bolus insulin and mealtime rapid-acting
insulin analog (lispro, aspart, or glulisine)
 Basal insulin should include determir or
glargine
 Continuous subcu insulin infusion or pump very
effective
 If poor control—check 2h postprandial and at
2AM
 Check urine ketones if BS>250
57
 Type 2 diabetes
 Diagnosed 9-12 years after they develop the
condition
 HgbA1C 6-7% needs monotherapy
 Oral antidiabetic agent
 Evaluate treatment response within 3 months
 HgbA1C >8% in patient who has been educated
about DM should begin insulin therapy

58
 Using insulin in Type 2 DM
 Usually will meet patient resistance
 May benefit from a 70/30 combination
 Requires frequent blood glucose monitoring

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 Question ?
 Comments?
 Suggestions?

60
 y ou
a n k
Th
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 Disorders of pituitary gland
 Abnormalities of pituitary function are caused
by oversecretion or undersecretion.

63
 Hypopituitarism
 A complex syndrome marked by metabolic
dysfunction, sexual immaturity, and growth
retardation.
 Commonly involves all of the anterior
pituitary hormones.
 Pan-hypopituitarism (Simmonds’ disease):
is total absence of all pituitary secretions and is
rare.
 Diabetes insipidus: a deficiency of anti diuretic
64
 Hyper-pituitarism
 Oversecretion most commonly involves ACTH
or growth hormone and results in Cushing’s
syndrome oracromegaly, respectively.
 Gigantism: proportional overgrowth of all
body tissues.
 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.
65
 Disorder of thyroid disorder
hypothyroidism
 Inadequate secretion of thyroid hormone during
child hood results in stunted physical and
mental growth (cretinism).
 In adults, hypothyroidism manifests as lethargy,
slow mentation, and generalized slowing of
body functions.
 Can range from mild, subclinical forms to
myxedema.

66
 The most common cause of hypothyroidism in
adults is autoimmune thyroiditis (Hashimoto’s
disease).
 May be primary(95%), secondary or tericiary
hypothyroidism.
 Myxedema refers to the accumulation of
mucopolysaccharides in subcutaneous and other
interstitial tissues. describe the extreme symptoms
of severe hypothyroidism.

67
 Manfestation
 Extreme fatigue, being cold even in a warm
environment, hypothermic.
 Speech is slow, the tongue enlarges, and hands
and feet increase in size.
Management :
 The primary objective is to restore a normal
metabolic state by replacing the missing
hormone.
 Synthetic levothyroxine (Synthroid or
Levothroid) 68
 Hyper-thyroidism
 Second most prevalent endocrine disorder,
after diabetes mellitus
 Graves’ disease, the most common type of,
caused by abnormal stimulation of the thyroid
gland by circulating immunoglobulins.

69
 Manifestation:
 Exhibit signs and symptoms of thyrotoxicosis.
 Emotionally hyper-excitable, irritable, and
apprehensive
 They cannot sit quietly; they suffer from
palpitations; and their pulse is abnormally rapid
at rest or on exertion.
 Poorly tolerate heat and perspire unusually.

 The skin is likely to be warm, soft, and moist.

 Exophthalmos(bulging eyes)

 Increased appetite
70
 Treatment:
 Radioisotope 123I
or 131I(Radioactive Iodine
Therapy: for destructive effects on the thyroid
gland and
 Anti-thyroid medications: that interfere with
the synthesis of thyroid hormones
e.g. propylthiouracil (PTU)
methimazole (Tapazole)
 Surgical removal(thyroidectomy): of most of
the thyroid gland. 71
 Disorders Parathyroid
1. Hyperparathyroidism
 Caused by over production of parathormone.
 Characterized by bone decalcification and
renal calculi (kidney stones) containing
calcium.
Manifestation:
 Apathy, fatigue, muscle weakness, nausea,
vomiting, constipation, hypertension, and
cardiac dysrhythmias.
 Irritability and neurosis to psychoses

 Renal and musculoskeletal manifestations 72

Complication:
 Acute hypercalcemic crisis:- can occur
resulting neurologic, cardiovascular, and
renal symptoms that can be life-threatening.
Treatment:
 Hydration therapy and mobility
 Calcitonin and corticosteroids
 Bisphosphonates

 Diet
 Surgical removal

73
 Hypo parathyroidism
 Causes may be interruption of the blood supply,
surgical removal or atrophy of the parathyroid
glands.
 Results hyper-phosphatemia and hypocalcemia
 Decreased intestinal absorption of dietary calcium
and decreased resorption of calcium from bone
and through the renal tubules.
 Decreased renal excretion of phosphate
(hypophosphaturia)
74
Clinical manifestation:
 Tetany, with tremor and uncoordinated
contractions
 Numbness, tingling, stiffness and cramps in
the extremities
 Air way spasm,
 Photophobia, anxiety, dysphagia, irritability,
dysrythmia,dipppression

75
Treatment
 Oral tablets of calcium salts(oral calcium
gluconate)
 calcium gluconate intravenously
 Sedative agents
 Parenteral parathormone
 Tracheostomy or mechanical ventilation
 Bronchodilating medications
 Dietary management 76
 ADRENOCORTICAL
INSUFFICIENCY
 Addison’s disease, results when adrenal cortex
function is inadequate.
 Autoimmune or idiopathic atrophy of the adrenal
glands is responsible for 80% of cases.
 Therapeutic use of corticosteroids is the most
common cause.

77
Clinical manifestation:
 Muscle weakness, anorexia, emaciation,
hypotension, and low blood glucose levels,
 Low serum sodium levels(results dehydration)
and high serum potassium levels
 Mental status changes such as depression,
emotional unstability, apathy, and confusion are
present in 60% to 80% of patients.
 Adison’s crisis(circulatory shock, cyanosis,
restless, confussion, GI symptoms…)

78
Management:
 Administering fluids and placing the patient in a
recumbent position with the legs elevated.
 Hydrocortisone is administered intravenously,
followed with 5% dextrose in normal saline.
 Vasopressor amines may be required if
hypotension persists
 Antibiotics if infection has precipitated adrenal
crisis
 Lifelong replacement of corticosteroids and
mineralocorticoids
79
 Cushing’s syndrome
 Results from excessive adrenocortical activity.
 Cushing’s syndrome are primarily a result of
over-secretion of glucocorticoids and
androgens (sex hormones), although
mineralocorticoid secretion also may be
affected
 Commonly caused by use of corticosteroid
medications and infrequently due to excessive
corticosteroid production by the adrenal cortex
80
Clinical manifestation:
 Arrest of growth(excessive protein catabolism
and muscle wasting)
 Obesity(central-type obesity, fatty“buffalo
hump”)
 Moon-faced appearance and increased oiliness of
the skin and acne.
 Musculoskeletal changes(osteoporosis; kyphosis,
backache, and compression fractures)
 The skin is thin, fragile, and easily traumatized
 Hyperglycemia or overt diabetes
81
Management:
 Trans-sphenoidal hypo-physectomy (if
pituitary tumors rather than adrenal cortex
tumors).
 Radiation of the pituitary gland
 Adrenalectomy
 Reduce or taper the medication to the
minimum dosage( if it is caused by
administration of cor-ticosteroids
82