Medical-Surgical Nursing: Endocrine Disorders.

1. ENDOCRINE DISORDERS
1. Diabetes Mellitus

2. 1. Diabetes Mellitus
• DM is not single disease, rather, it is a group of
genetically and clinically heterogeneous disorders
X’zed by abnormalities in glucose homeostasis
resulting in hyperglycemia.
• The hyperglycemia of diabetes is caused by a
decrease in the secretion or activity of insulin.
• These insulin alterations result in disordered
metabolism of CHO, fat & protein.
• In time structural abnormalities in the heart,
kidneys and eyes develop.

3. Etiology
• Genetic
• Auto immune
• Viral long rubella, mumps coxsackievirus
• Environmental - obesity
• Drug induced:
– Corticosteroids
– Thiazide diuretics
– Phenytoin

4. Classification
• There are primarily two types of DM
• Type I/IDDM
– In which insulin production by the β-cells is reduced or
completely absent and for which the mg’t requires
insulin replacement.
• Type II/NIDDM
– Which is the more prevalent type of DM 90% of pts are
in this classification.
– Commonly occurs in obese and insulin resistant subjects
– These two factors alone are insufficient to cause DM
unless accompanied by impaired β-cell function.

5. Characteristics of type I & type II DM
Factor Type I Type II
1 Age of onset Usually in youths
/juvenile onset but
possible at any age
Usually at the age of
>35 yrs but can
occurs at any age
2 Type of onset Abrupt Insidious
3 Genetic
susceptibility
HLA-DR3, DR4 & others Gentetic
predisposition is high
4 Env’tal factors Virus, toxins Obesity, nutrition
5 Endogenous
insulin
Minimal or absent Minimal or resistant
6 Control Difficult with wide
glucose fluctuation
Variable, can be
controlled with diet and
exercise
7 Insulin Required for all Required for 30-40%
8 Sulfonylurea Not efficacious Efficacious
9 Vascular and
neurological
In majority of pts
post yrs of DM onset
Frequent

6. Pathophysiology
• A glucose balance is preserved b/n the entry
of glucose into the circulation from the liver,
– Supplemented by intestinal absorptive after meals
– Glucose up take by peripheral tissues particularly &
skeletal muscles
• A continuous supply of glucose is, essential for
the brain; w/c uses glucose as its principal
metabolic fuel.
• When intestinal glucose absorption declines b/n
meals, hepatic glucose out put is increased in
response to the counter–regulatory hormones:
Glucagon & Adrenalin falls during prolonged
starvation.

7. Pathophysiology ……
• The liver produces glucose by
gluconeogenesis and glycogen break down.
• Insulin is the only anabolic hormone & it
has profound effects on the metabolism of
CHO, fat & protein.
• Insulin is secreted from pancreatic beta cells
into the portal circulation. It increases in
response to a rise in blood glucose (e.g. Post
meals).
• A glucose sensor has been identified in the
portal vein w/c, mediates insulin secretion via
neural mechanism.
• Insulin lowers BGL by suppressing hepatic
glucose production stimulating peripheral
glucose up take in skeletal muscle.

8. Pathophysiology ……
• Normally, insulin & its counter
regulatory hormones maintain BGL
within a range of 70-120mg/dl (3.9-6.7
mmol/l).
• Elevated BGL produce symptoms
related to the degree of actual or
relative insulin deficiency.
• When an absolute insulin deficiency or
decreased insulin activity remains in
the b/d stream & produces an osmotic
effect on intra cellular & interstitial fuid.
• This shifts, in fluid balance result in
clinical symptoms.

9. Clinical Presentations
are the cardinal features
– Wt loss
– Skin infections boils, candidiasis gtt – 30’ – 30 – 60 > fbs
– Dry mouth & tongue - 60’ – 20 – 50 > fbs
– Nocturia - 120’ – 5 – 15 > fbs
– Blurring vision - 180’–fasting level or
lower
– Extreme fatigue
– Delayed wound healing
- Polyuria
- Polydipsia
- Polyphagia

10. Diagnostic studies
• Hx & P/E
• Blood tests
–Fasting blood glucose/FBG/ -[70 – 100 mg/dl]
– Post parandial low glucose test (glucose tolerance
test) (GTT)
• Urine
– for urine glucose
– complete urinalysis
• Fundoscopic exam
• Neurologic exam

11. P/E of pt with DM & Clinical findings
a. Examination of hands reveals
– Pain less stiffness, limited joint mobility
– Dupultrens contracture
– Carpal tunnel syndrome
– Trigger finger (flexor tenosynovitis)
– Muscle wasting
b. The eyes
– Distance vision using snellen chart at 6 meters
– Near vision using standard reading chart
– Impaired visual acuity may indicate the presence of diabetic
eye disease
– Lens opacification
– Fundal examination for retinopathy

12. P/E …..
c. Examination of the feet
– Look for evidence of calls
on
– Feature of neuropathy
– Clawing of toes
– Discoloration of the skin
or infection, any lesion
– for deformity
d. Circulation
– peripheral pulses
– skin temperature
– capillary refill should be
tested
e. Sensation
– Light touch
– Vibration sense/use 12 &
hz
– Pin prick
– Pain pressure on Achilles
tendon
– Test for distal anesthesia
f. Reflexes
– Test plantar & ankle
reflexes

13. • The five aspects of diabetes mg’t make up the
complete program for good control.
• These are:
1. Diet
2. Activity
3. Monitoring
4. Medication
5. Education

14. 1- Nutritional mg’t
– To plan a diet for a diabetic individual, the daily
requirement of calories is calculated according to:
• Occupation
• Build &
• Age
– The need for additional nutrients including; Iron, Ca,
vitamin supplements depends on nutritional status of the
pt.
– The best method is to give 5 or 6 meals per day instead of 2
0r 3 large meals as usual.
– Generally 50% of total calories should come from CHO
while fat & protein should consist of 25% each.
– Avoid refined CHO in take

15. 2. Insulin and oral hypoglycemic therapy
• Insulin can not be given orally as it is destroyed by
digestive enzymes
• It is administered, sc, im or iv
• For continuous replacement in IDDM
• There are dft preparations of insulin depending on
duration of action
a) Short acting
E.g. – crystalline or regular insulin (soluble insulin)
–isopane insulin
b) Long acting
E.g – Protamine zinc insulin (PZI)
• Extended zinc insulin

16. • Insulin is administered for diabetic cases
– When not controlled by diet or exercise
– Failure of oral hypoglycemic
– Temporarily to tide over in factions, trauma sugary &
pregnancy
– In any cxn of DM
• Optimal controls generally best active by 2 doses of
soluble insulin 30 minutes before break fast & dinner
– Normally most IDDM needs 30 – 50 units daily as normal
pancreas secretes 30 – 40 units per day
• Roughly the following schedule may be followed:
– Blood sugar > 300 mg/dl - 20 units
– Blood sugar 200 – 300 mg/dl - 2 – 10 units

17. • The dose is adjusted according to usual routine BGL
amount/or urine sugar
– Urine sugar 3 + 30 units
– Urine sugar 2+  20 units
– Urine sugar > 1  10 units
• Daily increments of doses should be 4 units
• When the pt is stabilized 2/3 of the total daily dose is
given 30 minutes before break fast and 1/3 before dinner.
• Insulin in sites
– Anterior abdominal wall
– Upper thighs/buttocks
– Upper outer arms

18. Oral Anti Diabetic Drugs
• Are effective in non complicated NIDDM
• Sulfonylurea
– Tolbutamide – rastinion – orinase. Dose 0.5 – 1 gm BID
– Chlorpropamide – diabenese. Dose – 100 – 250 mg daily
– Glibenclamide – daonil. Dose – 5 mg 1 – 3 times/day
• Drug failure may be encountered for:
– Irregular drug administration
– Presence of infection or metabolic disorder
– Simultaneous use of antagonistic drugs e.g.- steroids,
OCP, diuretics

19. 3- Psychological preparations and adjustment
of life style
• Basic health education on the disease character.
• Adjustment of feeding habits as
– Frequent feeding
– Use artifleal
– Balanced diet intake
• Avoid injuries/trauma
• General awareness & enough knowledge of the disease character
• Specific teaching on follow up program
– How to inject insulin
– Results of blood and urine glucose tests
– Recording of the test results
– Symptoms of hypo & hyperglycemia
• Avoidance of excessive exhaustion
• Mild physical exercise

20. Cxns of DM
A. Acute complications
1. Hypoglycemia
– Blood glucose < 3.5 mmol/l or < 50 mg/dl
– Occurs often in pts treated with insulin, but relatively in
frequently in those taking oral anti diabetic drugs
Etiology–
– Missed, delayed or inadequate meal
– Unexpected or unusual exercise
– Alcohol
– Too much diabetic medications
– Use of beta blockers interfering with recognition of
symptoms

21. Clinical Presentations
• Blood glucose < 50mg/dl
• Cold clammy skin
• Numbness of fingers, toes, mouth
• Tachycardia
• Emotional changes
• Headache
• Nervousness, trainers
• Unsteady glut
• Slurred speech
• Hunger
• Change invasion
• Seizures, coma

22. Management
• Immediate ingestion 5 – 20 gm. Simple CHO
• Add another 5 – 20 gm with in 15 minutes
• If unable to swallow iv glucose 50% 30 – 50 ml
or glucagon 1 mg im
• Try to identify the cause& make appropriate
adjustment to the pt’s therapy

23. Prevention
• Taking of prescribed dose of medication at proper
time
• Accurate administration of insulin
• Ingestion of all ordered diet at regular time
• Provision of compensation for exercises
• Ability to recognize & know symptoms & Rx them
immediately
• Carrying of simple CHO
• Health education – on symptoms
• Checking blood glucose as ordered

24. 2. Diabetic Ketoacidosis/ DKA
• A true medical emergency 2° to absolute or relative insulin
deficiency x’zed by hyperglycemia, ketonemia, metabolic
acidosis & electrolyte depletion.
Etiologies
– IDDM (20–30%) in newly diagnosed diabetics
– Myocardial infarction (5–7%)
– Infection usually respiratory or urinary
– Medication non compliance
– CVA
– Trauma
– Surgery
– Emotional stress
– Idiopathic (20–30%)

25. • The cardinal biochemical
features of DKA are:
 Hyperglycemia
 Hyperketonemia
 Metabolic acidosis

26. C/M
• Kussmaul breathing / labored breathing
• Polyuria
• Polydipsia
• Generalized weakness/lethargy
• Nocturia
• Nausea & vomiting
• Abdominal Pain & tenderness
• Decreased bowel sounds

27. C/M ……
• Decreased perspiration
• Hypotension
• Hypothermia
• Reflexes
• Confusion, coma
• Tachycardia, tachypnea
• Breath fruity with acetone smell
• Dry mucous membranes
• Anorexia or increased appetite

28. Diagnostic approaches/findings
–Elevated blood sugar to 250 – 800 mg/dl
–Serum ketosis
–Urine ketosis
–Glycosuria
–Increased BUN

29. Mg’t
• IV fluids adults 100ml N/S over 1st hr then 500ml/hr
i.e. 7 ml/kg/hr for 4 hrs or until DHN subsides, then
250 ml/hr insulin 10u iv 10 u.im stat
• 5 with DW50 when the BGL reaches < 300 mg/dl.
• Keep NPO
• For preventive careful control of BGL
• Monitor glucose carefully during periods of stress,
infection, trauma, etc. carefully
• Insulin initiates infusion at 0.1 u/kg/hr

30. Mgt ……
• Administer O2
• V/S regularly
• Assessment of mental status & renal status
• Assessment of BGL
• Assessment of blood & urine for ketones
• Cardiopulmonary monitoring
• Insulin administration regular IV
• Electrolyte balance

31. 3. Hyperglycemic Hyperosmolar
Nonketosis/HHNK
• Occurs in the pt with diabetes who is able to
produce enough insulin to prevent DKA, but not
enough to prevent:
– severe hyperglycemia,
– osmotic diuresis and
– extra cellular fluid depletion.
• The increasing hyperglycemia causes intracellular
DHN b/c of a shift of fluid from intracellular to
extracellular space.

32. • This causes are neurologic abnormalities such as:
– Somnolence
– Coma
– Seizures
– Hemiparesis &
– Aphasia
• There is usually a hx of:
– Inadequate fluid intake
– Increasing mental depression &
– Polyuria
• HHNK often occurs in older adults with type II DM
• Mgt similar to DKA

33. B. Chronic Cxns of DM
1. Angiopathy
–Angiopathy or blood vessel ds is estimated
to account for the majority of deaths
among DM pts.
–This chronic blood vessel dysfunction are
divide in to two categories
• Macroangiopathy
• Microangiopathy

34. I. Macro-Angiopathy
– A disease of large & medium blood vessels
– The atherosclerotic plaque formation has a genetic
predisposition.
– The degree of vascular damage related to the
duration of the disease cases not its severity.
– It is due to altered lipid metabolism
–The cxns are –
• Cerebrovascular disease
• Cardiovascular disease
• Peripheral vascular disease

35. II. Micro-Angiopathy
• It is a disease of small blood vessel
• Result from thickening of the basement
membranes in the capillaries and arterioles
• A highly xic concomitant of long term DM
• The areas most noticeably affected are ;
• The eyes/retinopathy
• The kidneys/nephropathy
• The skin/dermatopathy
• The C/M usually do not appear 15 – 20 yrs after the
onset of DM.

36. 2. Peripheral Vascular Disease/PVD
• It is a combination of micro-angiopathy & macro- angiopathy
as well as clotting abnormalities
• The legs & feet are most often affected
• The sequelae can lead to -
– Infection
– Gangrene
– Amputation
• S/s of PVD include –
– Intermittent claudication
– Pain at rest
– Cold feet
– Loss of hair
– Delayed capillary filling
– Dependent rubour

37. 3. Diabetic Retinopathy
• Microangiopathy of the retina
• The after problem is microvascular damage &
occlusion of retinal capillaries.
• It is observed after 10 yrs on 50% of pts &
after 15 yrs on 80% of the pts.

38. 4. Diabetic Nephropathy
• It is the leading cause of end stage of renal disease
• Occurs as a result of micro vascular abnormalities
• Microangiopathy in the kidneys causes diffuse &
nodular glomerulosclerosis.
• Basement membranes of all glumerular capillaries
are affected & become thick & leaky
• Sclerosis of glomerular vascular tufts leads to
progressive renal failure.

39. 5. Diabetic Neuropathy
• Result in reduced nerve conduction and demyelination
• Neuropathy can precedes, accompany or follow the dx
of DM.
• The paresthesias are associated with tingling, burning
& itching sensations.
• Complete or partial loss of sensitivity to touch &
temperature is common.
• Foot injury and ulcerations can occur without the pt
ever having pain
• Hyperesthesia that even light pressure from bed sheets
can not be tolerated
• Neuropathy in hands causes atrophy of the small
muscles, limiting fine mov’t.

40. 2. Thyroid Gland Disorders
• Thyroid gland produces
1. Thyroxine (T4)
2. Triiodo thyronine (T3) more active
• Thyroid hormones regulate energy metabolism,
growth and dev’t
• Thyroid gland disorders are manifested as –
– Hypofunction
– Hyperfunction
– Inflammation or
– Enlargement (goiter)
• A goiter may interfere with surrounding structures
and can be associated with increased, normal or
decreased hormone production.

41. C/Ms of Thyroid Dysfunction
Hypofunction Hyperfunction
CVS
• Bradycardia - tachycardia, bounding
• Varied changes in B/P - systolic HTN
• Distant heart sounds - dysrhythmias
• Anemia - palpitations
• Tendencies to develop - atrial fibrillation
– CHF - common in older adult
– Angina - Angina
– MI

42. C/Ms …..
Respiratory System
• Dyspnea - increased respiratory rate
• ed breathing capacity - dyspnea on mild exertion
GIS
• ed appetite - ed appetite, thirst
• Nausea & vomiting - wt loss
• Wt gain - increased peristalsis
• Constipation - diarrhea, frequent defecation
• Distended abdomen - ed bowel sounds
• Enlarged, scaly tongue - splenomegaly, hepatomegaly

43. C/Ms …..
Integumentary system
• dry, thick, inelastic cold skin - warm, smooth, moist skin
• thick, brittle nails - thin brittle nails
• dry, sparse, coarse hair - hair loss, fine sticky hair
• poor turgor of mucosa - palmar erythema
• generalized interstitial edema - premature graying (in
men)
• puffy face
• ed sweating - diaphoresis
• pallor - vitiligo

44. • MSS
• - fatigue - fatigue
• - muscular aches & pain - muscle weakness
• - Proximal muscle wasting
• - Slow mov’t - dependent oedema
• - Arthralgia - osteroporosis
•
• Nervous System
• - Apathy - difficulty in focusing eyes
• - Lethargy - nervousness
• - Forgetfullness - fine tremor of fingers & to nerve
• - Slowed mental processes - insomnia
• - Paresthesias - lability of mood, delirium
• - Anxiety, depression - restless ness
• - Polyneuropathy - personality changes of irritability,
Agitation
• - Stupor, cuma - Exhaustion
• - Lack of ability to constant rate
• - Stupor, coma

45. • Reproductive system
• Prolonged menses real periods - menstrual
irregularities
• or amenorrhea - amenorrhea
• - ed libido - ed libido
• - infertility - impotence in men
• - Gynocomastia
• - ed fertility

46. Others
• ed susceptibility to infection - intolerance to heat
• ed sensitivity to narcotic barbiturates, -ed
sensitivity to stimulant drugs
• Anesthetic - elevated basal temp
• - intolerance to cold - lid lag, stare
• - decreased hearing - yet hd retraction
• - sleepiness - exophthalmos
• - goiter - rapid speech

47. Hyperthyroidism
• Results from excess circulating levels of T4, T3 or
both
• Incidence in sex ratio m:f 6:1
• Highest frequency in 30-50 yrs age groups
• Iodine deficiency is believed to predispose the pt.
• Common in iodine-poor geographic locations
/goiter belt/
• The most common forms are:
–Graves’ disease
–Multinodular goiter

48. 1. Graves’ Disease
• is an autoimmune ds of unknown etiology marked
by increased production of thyroid hormone
• has genetic predisposition
• Abs are developed against various Ag with in the
thyroid gland & to other tissues.
• These abs known collectively at thyroid-
stimulating antibodies (TS Abs) stimulate the TSH
receptors activate the production of thyroid
hormones.

49. Graves’ …..
• The ds is X’zed by remissions & exacerbations with
or with out Rx.
• It may progress to destruction of the gland resulting
in hypothyroidism
• Precipitating factors include:
– Insufficient iodine supply
– Infections
– Emotions may interact genetic factors that control
immunologic & metabolic abnormalities to cause graves’
disease

50. 2. Multi-Nodular Goiter (MNG)
• MNG is xized by small discrete, autonomously
functioning nodules that secrete thyroid hormone
• Associated with hyperthyroidism
• The nodule is termed as toxic adenoma
• Pt has hx of simple goiter for year.
• The C/Ms of hyperthyroidism are related to the
effects of excess thyroid hormones in two ways:
– Their direct effect of increasing metabolism
– An increased tissue sensitivity to stimulation by the
sympathetic division of the autonomic nervous system

51. 3. Exophthalmos (Proptosis)
• is the condition in which the eye balls protrude from
the orbits,
• is due to impaired venous drainage from the orbit
leading to increased deposits of fat & fluid (edema) in
the retro orbital tissues
• upper lids are usually retracted & elevated
• eyeball forced out ward with the sclera above the iris
visible
• this produces the x’cs stare & protrusion of the eye ball
• is usually bilateral but can be unilateral or asymmetric.
• the exposed corneal surfaces become dry and irritated
• serious consequences, such as corneal ulcers &
eventual loss of vision can occur.

52. 4. Hyperthyroid Crisis/Thyrotoxicosis
• is a complication of hyperthyroidism
• an acute but rare condition where all hyperthyroid
manifestations are heightened.
• is potentially fatal, but death is rare when Rx is
vigorous & initiated early.
• causes are presumed to be stressors such as;
–Infection
–Trauma
–Surgery in a pt with pre-existing hyperthyroidism
either diagnosed or undiagnosed

53. 4. Thyrotoxicosis ….
• Manifestations include
– severe tachycardia
– heart failure
– abdominal pain
– shock
– nausea, vomiting
– hyperthermia (up to 40.7 oc)
– diarrhea
– Restlessness
– delirium, coma
– agitation

54. 5. Thyroid Enlargement/Goiter
• Goiter may result from hypertrophy caused by
excess TSH stimulation; w/c in turn can be
caused by:
– Inadequate circulating thyroid hormones
– Also by growth stimulating immunoglobulin's &
– Other growth factors
– Goiterogens w/c inhibit synthesis of thyroid
hormone in an iodine deficient area/endemic
goiter/

55. 5. Thyroid
Enlargement/Goiter …..
• TSH & T4 are measured to determine whether a
goiter is associated with
– Hyperthyroidism
– hypothyroidism or
– normal thyroid function
• Thyroid antibodies are measured to assess for
thyroiditis
• Rx of thyroid hormone may prevent further
enlargement
• Surgery is the rx of choice in very large goiters

56. 5. Thyroid
Enlargement/Goiter …..
Common goitrogens
• Soybeans
• Skins of pea nuts
• Milk from kare fed
cattle
• Sea food
• Green leafy vegetables
• Peanuts
• Peas
• Straw berries
• Carrots
• Cabbages
• Thyroid inhibitor drugs
• Sulfonamides
• Salicylates

57. 5. Thyroid Enlargement/Goiter …..
• Thyroiditis is an inflammatory process in the thyroid
gland.
• Sub acute granulomatous thyroiditis (de quervan’s
thyroiditis)
– Present with hyperthyroidism
– Caused by viral infection
• Acute thyroiditis is 20 to bacterial or fungal infection
• Sub acute & acute forms have abrupt onset
• Silent thyroiditis a form of lymphatic thyroiditis has a
variable onset.
• T4 & T3 are initially elevated in all types & may be come
depressed later
• TSH levels are low & then elevated

58. 5. Thyroid Enlargement/Goiter …..
• Thyroid hormone levels are usually low in chronic
hashimotos thyroiditis & TSH is high.
• Recovery from thyroiditis may be complete in
weeks or months with out Rx.
• Specific abts & surgical drainage may be needed
– NSAIDs are used
– Abdominal pain
– Nausea vomiting
– Diarrhea
– Delirium coma

59. • Rx of thyrotoxicosis is aimed at
– Reducing circulating thyroid hormone levels
– Fever reduction
– Fluid replacement
– Elimination or mg’t of the initiating stressors
• Diagnostic procedures of hyperthyroidism
– Hx & P/E
– Ophthalmologic examination
– ECG
– Lab tests – serum T3, T4 & TSH levels
– Pt mg’t in hyperthyroidism

60. Hyperthyroid Management
a) Medcal mg’t
a. Antithyroid drugs-
• Propylthiouracil (PTU)
• Methimazole
b. Adrenergic blockers such as propranolol/inderal/
c. Ablation of thyroid tissue –
• Lobular
• Subtotal or
• Total thyroidectomy
d. Radioactive iodine
e. High caloric diet

61. b) Nursing Mg’t
• Nutritional Mg’t
– To satisfy hunger & prevent tissue breakdown
– High in protein, CHO, minerals to vitamins
– Six full meals & snacks are recommended
• Weigh the pt daily to monitor adequacy of diet
• Frequent fluid offering to prevent volume deficit.
• Avoid high seasoned & high fiber foods to avoid
hypermotility of GIT.
• Restful, calm & quiet env’t – b/c sed
metabolism result in steep disturbance.

62. b) Nursing Mg’t …..
• Changing bed sheet frequently
• Encourage & assist with dress
• Restrict visitors who upset the pt.
• Applying artificial tears to sooth & moisten
conjunctival membranes.
• Salt restriction to reduce periorbital edema
• Elevation of the pts head .
• Dark eye glasses reduce glare & eye irritation.

63. b) Nursing Mg’t …..
• Tape the eye to shut when sleep
• Appropriate administration of iodine (laugol’s
solution, potassium iodide)
• Usually one drop of saturated potassium iodide
TID before surgery.
• Iodine decreases the size & vascularity of the
thyroid making resection safer & easier.
• Administration of PTU with iodine therapy
should be for 10 days to prepare for surgery.

64. Pre operative care in thyroid surgery
• Subtotal thyroidectomy is the TOC.
• The s/s of hyperthyroidism must be alleviated
• Cardiac problems must be controlled
• The iodine should be mixed with water source
• Assess for iodine toxicity
• Pre operative teaching should include comfort & safety
measures like
– Coughing
– Deep breathing
– How to support head manually to avoid stress on suture while
turning aside
– About talking difficulty

65. Post operative
• O2 & suctioning equipment preparation
• Ready tracheostomy set.
• Assess the pt Q2hrs for 24 hrs for signs of
– Haemorrhage
– Tracheal compression as –
– Irregular breathing
– Neck swelling
– Frequent swallowing
– chocking
– Blood on the dressing
• Place the pt in semifowlers position & support the head with
pillows
• Avoid flexion of the neck & any tension on the suture lines
• Monitor V/S
• Control postoperative pain with analgesics

66. Hypothyroidism
• Result from insufficiency of circulating thyroid
hormone
• All hypothyroid cases have certain features in
common
• Some differences depend on the pts age at onset of
the deficiency.
• May be occurred in –
– Infancy (cretinism)
– Childhood or
– Adulthood

67. A) cretinism
–is caused by thyroid hormone
deficiencies during fetal or early
neonatal life.
–it can be caused by maternal iodine
deprivation or congenital thyroid
abnormalities

68. Hypothyroidism….
Clinical Manifestations
• Defective physical dev’t
• Mental retardation
• Should be suspected with long gestational
period, large infant, flats to thrive
• Large posterior fontanel
• Squinting
• Excessive sleeping
• Thickened skin & lips
• Enlarged tongue

69. Hypothyroidism….
Clinical Manifestations ……
– Abdominal distension with vomiting
– Hoarse cry
– Dull facial expression
– Feeding & respiratory difficulty
– Peripheral bruisis
– Supraclavicular & periorbital edema
– Umbilical hernia
– Hypothermia

70. B) Myxedema
• is often synonymously used with hypothyroidism
• but actually connotes severe, long standing hypothyroidism
• with myxedema thery is accumulation of
mucopolysaccharides in the ground substance of the dermis
& other tissues
• this mucous edema causes the characteristic faces of
hypothyroidism & puffiness, periorbital edema & mask like
affect.
• mental sluggishness, drowsiness & lethargy of
hypothyroidism may progress to impairment of consciousness
or Coma.
• this situation is termed as myxedema coma needs medical
emergency.

71. B) Myxedema …..
• Myxedema coma can be precipitated by
– Infection
– Drugs – (narcotics, tranquilizers, barbiturates
– Exposure to cold
– Trauma
• X’zed by –
– abnormal temperature
– hypotension
– hypoventilation
• for pt survival
– Vital functions must be supported
– IV thyroid hormones must be administered

72. Myxedema ….
• Diagnostic studies
– Serum thyroid hormones determination
–T3 & T4 - low
–TSH - high
– ECG - Bradycardia

73. Myxedema …
Therapeatic mg’t
• The objective is restoration of euthyroid state as safely &
rapidly as possible with hormone replacement therapy
• Low calorie diet /in adult/
• Promote wt loss
• Life long thyroid replacement therapy
• Synthetic oral thyroxine/synthroid, levothyroid noroxine/
• Report any chest pain during rx initiation
• Provide comfortable, warm env’t
• Prevent skin break
• Avoid using sedatives
• Prevent constipation
• Health education on –
– Diseas character
– Self care practices
– Sign & symptoms to be monitored

74. Parathyroid Glands Disorders
• Parathyroid glands secret Parathyroid
hormones (PTH)
• This hormones helps to regulate Ca &
phosphate levels by stimulating
– Bone resorption
– Renal tubular reabsorption of calcium
– Activation of Vit. D

75. Hyperparathyroidism
• is a condition involving increased
secretion of PTH
• Hyperparathyroidism is classified as –
–Primary
–Secondary &
–Tertiary

76. A) Primary Hyperparathyroidism
• is due to an ed secretion of PTH
• leads to d/os of Ca, P & bone metabolism
• The excess circulating PTH usually results in
hypercalcemia & hypophosphatemia.
• The commonest causes is benign neoplasm or
simple adenoma.

77. B) Secondary Hyperparathyroidism
• Hyperparathyroidism is more common in women
than men.
• usually occurs b/n 30 & 70 yrs of age
• the peak incidence is 5th & 6th decades
• appears to be a compensatory response to states
that induce or lower hypocalcaemia.
• Disease conditions include –
• Vit D deficiencies
• Malabsorption
• Chronic renal failure &
• Hyperphosphotemia

78. C) Tertiary Hyperparathyroidism
• occurs when there is hyperplasia of
parathyroid gland
• loss of circulating Ca levels that cause
abnormal secretion of PTH
• observed in pts with kidney transplant
• after a long period of dialysis rx for
chronic renal failure

79. Hypoparathyroidism
• inadquate circulating PTH X’zed by hypocalcemia
• PTH resistance at cellular level may also occur
(pseudo hypoparathyroidism)
• Caused by genetic defect inspite of high PTH
level
• Often associated with hypothyroidism or
hypogonadism
• The most common cause is accidental removal
of the parathyroids or damage to the vascular
supply of the glands during neck surgery.

80. Hypoparathyroidism ….
• Idiopathic hypoparathyroidism result from
– Absence
– Fatty replacement or
– Atrophy of the glands
– Can be associated with other endocrine d/os
• Affected pts may have antiparathyroid antibodies
• Hypomagnesemia is recognized as cause of
hypoparathyroidism & is seen in
– Alcoholisms’
– Malabsorption
– Impaired PTH secretion & its action on bone & kidneys

81. Parathyroid Dysfunction …
Clinical manifestations
Hypo function
• ed CO
• Dysrhythmia
• Urinary fecal incontinency
• Dry scaly skin
• Hair loss
• Painful muscle cramps
• Personality changes
• Memory impairment
• Convulsion, tremor
• Urinary frequency
Hyper function
• Hypertension
• Dysrhythmias
• Constipation
• Nausea & Vomiting
• Wt loss
• Moist skin
• ed muscle tone
• Osteoporosis
• Personality disturbance
• Abnormality of gait
• Memory impairment
• UTI, Kidney stones, cholelithiasis

82. Parathyroid Dysfunction …
Diagnostic studies
• Serum Ca level  ed
• Serum P level  ed
• Urine Ca  ed
• Serum chloride  ed
• Serum creatinine  ed
• Serum amylase  ed

83. Hyperparathyroidism
Therapeutic mg’t
• The choice of therapy depends on
– The urgency of the clinical situation
– The degree of hyper calcemia
– The underlying disorder
– The status of renal & hepatic function
– The clinical presentation of the pt &
– The particular advantages & disadvantages of the
different therapeutic modalities

84. Hyperparathyroidism Mg’t ….
• parathyroid tumors should be removed surgically
• regular annual assessment of the PTH
• maintenance of high fluid in take
• moderate Ca intake
• sodium intake to replace the loss in urine
• continued ambulation & exercise
• N/S IV administration To replace fluid & electrolyte loss
• estrogen therapy to reduce serum Ca levels in post menopausal
women.
• close monitoring of V/S
• Mithramycin is an antihypercalcemic agent to se cerum Ca
• the majaor post operative cxns in parathyroid surgery are:
– Tetany
– Fluid & electrolyte disturbances

85. Hypoparathyroidism Mg’t
• The main objectives of rx one to Rx tetany if
present.
• Prevent long-term cxns by maintaining
eucalcemia.
• Tetany is treated with IV or slow push of calcium
salts as:
– Calcium gluconate
– Calcium lactate
• Vit D administration
• supplemental Ca & oral phosphate
• Ca salts can cause hypotension & cardiac arrest,
thus a slow IV push is required

86. Hypoparathyroidism Mg’t ….
• also cause venous irritation & inflammation if
leakage occurs into extra vascular tissue
• specific hormone replacement of PTH is not used
to treat hypoparathyroidism b/c of:
– antibodies formation to the PTH
– expense
– need of parenteral administration
• Vit D is used in chronic & resistant
hypocalcaemia to enhance intestinal Ca
absorption & bone resorption.

87. Nursing assessment & interventions
• Assessment for signs of tetany
• The pt should be observed closely for carpopedal spasm
trousseaus phenomenon) while B/P is taken w/c
indicate the initial onset.
• period assessment for chuvostek is sign.
• Tingling in the finger tips & around the mouth,
irritability, apprehension, muscular hyper tonicity &
cramps may precede acute tetany.
• Re breathing in the paper bag to alleviate the
symptoms lowers body Ph.
• B/c an acid env’t enhances both solubility & degree of
ionization of Ca.
• Bed side rails should be padded a seizure precaution
• Keep the pt in non stimulating env’t
• Assist with hygienic needs.

88. 4. Adrenal Gland D/Os
• The adrenal glands lie at the superior pole of each kidney
& are composed of two distinct regions:
• The corterx
• The medulla
• The adrenal corter consists of 3 antamic zones & secretes.
– Mineralo corticoid aldestrone-regulate metabolism & are
critical in the physiologic stress response
– Cortisol hormone – regulated Na & K balance
– Adrenal androgens- contribute to the growth & dev’t in both
glades & to sexonal activity in adult women
• The adrenal medulla, lying in the center of the adrenal
gland, is functionally related to the sympathetic nervous
system & secretes the catecholamines
• - epinephrine &
• - norepinephrine – in response to stress

89. 4.1. Adrenal hormones
excess/hyperfunction/
1. Cushing’s syndrome
• Is a spectrum of clinical abnormalities caused by
excess corticosteroids, particularly glucocorticoids
Etiology –
• prolonged adm of high dose of corticosteroids
• ACTH – secreting pituitary tumor
• cortisol secreting neoplasm with in the adrenal cortex
• excesss secretion of ACTH from carcinoma of lung or
other malignant growths outside pituitary or adrenals

90. Cushing’s syndrome….
clinical Manifestations
• thinning of scalp hiar & ted body & facial hair
• red cheeks
• moon face
• buffalo hump
• supra clavicular fatpad
• wt gain
• purple striae
• thin extremities with muscle atrophy
• slow wound healing

91. Diagnostic procedures
• Hx & P/E
• Mental status exam
• CBC
• Plasma – cortisol levels
• - ACTH levels
• Blood chemistries for – Na, K & glucose
• CT scan, MRI

92. Management
• V/S every 4 hrs respiration, BP
• Daily weight measure
• Assess s/s of infection pain, loss of function
• Surgical removal of the gland or the growth/tumor/
• HTN & hyperglycemia need to be controlled
• Hypokalemia is corrected & ditt & k supplement
• High protein
• Pre- operative & post operative care
• IV infusion
• NGT suctioning p surgery
• Coughing, deep breathing & exercises
• B/c of hormone fluctuations: BP, fluid balance & electrolyte levels tend to be
unstable after surgery.
• High doses of cortisone are administered iv during surgery & for several days
afterward to ensure adequate responses to the stress of the procedure.
• Any rapid or significant changes in b/p, resp, or heart rate should be reported.
• Monitor fluid in take & out put
• Tahe coitical period for grlvlatury insability ranges from 24-48 hrs after surgery.

93. 2. Adrenocortical
insufficiency
• Hypofunction of the adrenal rootere may be
A) primary- (addison’s ds) or
B) secondary- from lack of pituitary acyst
• In addison’s ds. All the three adrenal steroids
are reduced
• In 2o adrenocortical in sufficiency
• Corticosteroids &
• Androgens are deficient.

94. 4.2. Addison’s disease
• Addision’s os is an auto immune in w/c the adrenal tissue is destroyed by
antibodies agionst the pt’s own adrenal cortex
• Often other endocrine conditions are present & addison’s disease is
considered a component of poly endocrine deficiency syndrome.
• Etiology
• – Autoimmune disorder
• - TB
• - haemorrhage
• - infarction
• - fungal infections(e.g. histoplasmosis)
• - AIDS
• - metastatic Ca
• - anticoagulant therapy/iatrogenic/
• - antincoplastic therapy

95. • C/m – progressive weakness, fatigue
• Wt loss & anurexih
• Hyperpig mentation of skin (on sun expused arcas, pressure
points, over joint, & in creases espebblly palmar creases.
• -hypotension (usual & serious)
• - serum Na & ed k
• - nausea & vomiting & diarrheas
• - circulatory collapse can progress to shock w/c is non
responsive to usual mg’t (needs glucocorticoid
administration to revers the hypotension)
• - tachycarda, DHN
• - vague abdominal pain

96. • Diagnostic studies
• Pt ht & p/c
• Blood serum results – hyperkalemia
• - hypochloremia
• - hyponatremia
• - hypoglycemia
• - anemia
• -  ed bun
• - ACTH stimulation test
• - Tuberclin aest
• - CT scan, MRI

97. • Mg’t
• Cortisure replacement
• Salt additive diet
• V/S & signs of fluid deficiet monitoring & electrolyte in
balance
• Daly wt
• Diligent steroid administration
• Prevent infection
• Avoid noise, light & enviromental temperature extremes
• The pt can not cope with these stressors b/c s/he can not
produce cortico steroids
• Hospitalization is done in adrenal

98. 5. Pituitary Gland Disorders
• The pituthry gland werghing 500-900 lies at the base of the skull in
the sella turcica, within the sphcnoid bone.
• the pituitary gland is composed of two lobes
• 1. The anterior lobe w/c consists of 2/3 of the gland & secretes
• A) Adrenocortico Tropic Hormone /ACTH/
• B) Growth hormone (GH)
• C) Prolaction /Prl)
• D) Thyroid stimulating hormone /TSH)
• E) Follicle stimulating hormone /FSH)
• F) Leuteinizing Hormone /LH)
• 2. The posterior lobe which consists of neural tissue & is an extension
of hypothalamus
• It seeretes – antidiretic hormone /ADH/
• - Oxytocin
• Disorders of the anterior pituitary gland

99. A) Growth Hormone Excess
• GH is an anabolic hormone, promotes protein
synthesis and mobilizes glucose & free fatty acids.
• over production of growth hormone w/c is
usually caused by a benign pituitary adenoma
/tumor).
• causes gigantism or acromegaly X’zed by soft
tissue & boney over growth.
• gigantism results when the onset occurs before
closure of the epiphyses, while the long bones
are still capable of longitudinal growth.
• the excessive growth is usually proportional. The
chtd may 240 cm & weigh 136 kg have of

100. • C/M –
• Insidious onset in the 3rd & 4th decades
• Both genders affected equally
• Bones  in thickness & width
• Enlargement of the hands & feet
• Deformities of the spine and mandidble.
• Enlargment of soft tissues - tongue
• - skin
• - speech difficulty & hoarseness abdorgans
• - sleep apnea
• - coardening of facial features
• - GH anthgnizes the action of insulin & can cause
hyperglllycemia

101. • Diagnostic studies
• Hx & P/E
• Determination of plasma gh
• Skull x-ray- may show a large sella turcica &
ed bone density
• Ct scan
• MRI

102. • Mg’t
• The therapeutic goal in gigantism & acromegaly is to return GH levels to normal
• It may be accomplished by
– Surgery
– Radiation
– pharmacologic or
– combination of the three
• - bromocriptine
• - dopamine agonist -
• - octreotide
• - somatostation analog
• - assess the tissue growth & evaluate the physical size
• - pre & post operative care
• - the pt should be instructed to avoid:
• Vigorous coughing
• Sneezing
• Straining at stool /valsalua maneuver) to prevent csf leakage
• P surgery the hcad of the pt should raised to 30 all times
• The elevation headache
• Anyclear nasal drainage shoul be sent to lab for glucose test a level > 30 mg/de indicate csf leakage w/c
es risk of meningitis
• Complaints of persisitent & severe generalized or suprh orbital headache may indicate csf leakage in
the cpinuses
• Cbr & elevation of head relieves the pain.

103. Hypo function of the pituitary gland
• Hypopitutarism is a rore d/o & involves a in are or more to the
anterior pifutary hormones
• Etiology – infections
• - auto immune d/os
• - tumors
• - vas cular diseases or
• - destruction of the gland
• - failure to secrete gh is the most common abnormality,
• - followed deficiencies of the gonadotropin
• - destruction of the pituitary can result from
• Trauma
• Radiation &
• Surgical proccdures
• In women, hypofunction can follow a postpartum hemorrhage this is
called PPH pitutary necrosis or sheehans sybdrome. It is suspected
when the mother be came amenorrhic or failure to lactate with
previous hx of PPH

104. • C/M – the symptoms are mostly nonspecific
• - Weakness - ftt
• - Fatigue - infertility
• - Headache - amenorrhea
• - Sexual dysfunction – dwarfism
• - Fasting hypoglycemia
• - Diminished tolerance for stress
• Mg’t
• Surgery
• Radiation for tumor removal
• Hormone replacement
• Assess any possibilities of sheehan’s syndroml
• Marital, vocational or prychological coonselling

105. • C) Disorders of the posterior pituitary
• - the hormones secreted by the post pituitary are antidiuretic
hormone /ADH/ also called arginic vasopressin /AVP) & oxytocin
•  Oxytocin controls lactation & uterine contraction
• Syndrome of inappropriate ADH(SIADH)
• Occurs in ADH excess secretion
• Etiology – bronchogenic carcinoma
• - Other pulmonary –conditons- pneumonia
• - PTB
• - Lung abscess
• - Trauma
• - Meningitis
• - sub arachnoid haemorrhage

106. • C/M - low urine out put
• - the excess adh es renal tubular permability
& reabsorptions of water in to the circulation
• - wt gain with edema
• - cerebral edema may occur
• - hyponatremia
• - lethargy anorexia
• - confusion, headache
• - convulsion & coma
• - muscle cramps & weakness

107. • Mg’t
• Fluid restriction from 800-1000 ml/day
• Diuretics administration/furosemide
• Remove the cause
• Discontinuing the causal medication
• Drugs that block the action of ADH os-
declomycin, TTC) causing nephrogenic DM
• Sucking or hard candy or ice chips to thirst.

108. II) Diabetes Insipidus
• It occurs when any organic lesion of the hypothalamus, infundibular
stem or posterior pituitary interfers with ADH synthesis, transport
or release
Etiology
• Malignant neoplasms
• Non malignant pulmonary disease
– TB
– Lung abscess
– Pneumonia
– empyema
– COPD
• Idiopathic factors
• Pituitary or other carotids
• Surgically closed head trauma
• CNS disorders
• Drugs
• Hypothyroidism
• Positive pressure, mechanical ventilation

109. • Mg’t
• Nursing Assessment:
– accurate intake & out put measurement
– hourly measurement of urine specific gravity
– level of consciousness
– for signs of hyponatremia every 2 hrs
– monitoring heart & lung sounds & BP

110. • Nursing Interventions
– restriction of fluid intake not more than 100
ml/day till urine out put < 700 ml
– position the pt in flat to facilitate venous return
– use side rails due to alteration in mental states
– frequent positioning of the pt.
– use seizure precaution
– assist with ambulation
– Provision of frequent oral hygiene
– Not written on the note Urine specific gravity 1-
005

111. Clinical Manifestations
• Polydipsia defined as urine out put > 250 ml/hr
• Polyuria 2- 20 L/day with a very low specific gravity
• The pt favours cold or iced drinks
• The pt is usually fatigued 29 nocturg
• S/s of fluid volume deficet as
• Wt loss
• Poor tissue turgor
• Hypotension
• Tachycardia
• Constipation &
• Shock
• CNS manifestations from irritability & mental dullness to
coma.

112. THANKS!!!