Pathophysiology of

Endocrine System
Principles of hormone’s action
 Types of effects:
 Endocrine effect (target cells are far from
endocrine gland)
 Paracrine effect (target cells in the same
organ)
 Autocrine effect (affection on the same cell
type)
 Interaction with receptors:
 Receptors inside cells (influence on gene
expression).
 Receptors on the cell surface (influence on
enzyme activity or ion channels).
Symptoms of endocrine disorders
 Common symptoms:
 fatigue/weakness
 metabolism disorders
 alterations in height, weight, BMI
 mental disturbances
 Principles of diagnostics:
 physical examination
 blood plasma level
 CT, MRI
Endocrine Gland Hypofunction
 Congenital defects
 absence or impaired development of the gland
 absence of an enzyme needed for hormone
synthesis
 Destruction of gland
 acute ischemia, trauma, hemorrhage
 infection/inflammation,
 autoimmune destruction
 neoplastic growth (non-endocrine tumor or
metastases)
Endocrine Gland Hypofunction
Problems outside the endocrine gland:
 understimulation by the pituitary
 lack of substances needed for hormone synthesis
 depression of hormones secretion by drugs or food
 circulating antibodies against hormone
Receptor defects:
 absence of receptor
 defective receptor
 antibodies to receptor
 impaired cellular responsiveness to the hormone.
Endocrine Gland Hypofunction
A decrease in
hormone can Pituitary

lead to
peripheral Stimulating
endocrine hormone Negative
gland feedback
Gland Hyperplasia
hyperplasia

Lack of hormone
Endocrine Gland Hyperfunction
 Causes of increased hormone level:
 overstimulation by the pituitary
 hyperplasia or neoplasia of the gland
 stimulation of gland by antibodies
 rapid destruction of a gland
 ectopic tumor
 excess exogenous hormone administration.
General principles of therapy
Hypofunction:
 replacement of the hormone
  hormone resistance.
Hyperfunction:
 radiation therapy
 surgery
  hormone production
 receptor antagonist
The levels of disorders
Hypothalamus

Pituitary
Endocrine gland

Releasing Stimulating
hormone hormone

Tertiary Secondary Primary

Pituitary disorders
Causes :
 tumor
 hemorrhage
 trauma
 irradiation
 Pituitary disorders
Growth hormone
deficiency
 children - short stature
(pituitary dwarfism),
normal intelligence,
obesity
 adults - central obesity,
reduced muscle mass
and exercise capacity.
Growth Hormone Functions
Pituitary disorders
Excess of GH in childhood
Pituitary gigantism
  growth velocity
 proportional enlargement of
skeleton and inner organs
 enlargement of the
peripheral nerves
 delayed puberty and
hypogonadism
 Pituitary disorders
Excess of GH in adults
Acromegaly
 reason –somatotrope adenoma
 hyperplasia and hypertrophy of soft
tissues
  size of hands, feet, nose, ears
 cartilaginous proliferation of the
larynx
 coarsening of the facial features.
 enlarged tongue and increase of
inner organs
 thick and dark skin.
 degenerative arthritis.
Pituitary disorders
 GH excess – Metabolic disturbances
  GH and IGF-1.
 synthesis of lipids in adipocytes,  lipolysis and
free fatty acids level in blood plasma,  of
glycogen in hepatocytes
  tolerance to carbohydrates and diabetes
mellitus
 hyperthyroidism
 CVS - hypertension, cardiomegaly, heart failure
 hyperphosphatemia ( tubular reabsorption of
phosphate)
Pituitary disorders
Excess of ACTH - Cushing’s
disease.

High ACTH levels  bilateral

adrenal hyperplasia.
Melanocyte stimulation by ACTH
 hyperpigmentation of skin

 Cushing’s syndrome (different)

 This may be seen in a client
who is receiving steroids as a
medication (exogenous form of
steroid) for problems such as
asthma
Cushing disease/syndrome
Clinical manifestation:
 "moon" face and "buffalo hump“.
 muscle wasting and weakness - due to
hypokalemia and  glucose level in the
muscles.
 atrophic skin, with poor wound healing and
purple striae
 activation of protein catabolism and  of
proteins synthesis in the skin.
Cushing’s Syndrome
Pituitary disorders ( already
learned!)
Lack of ADH - Diabetes insipidus - polyuria,
polydipsia, dehydration.
 Central Diabetes insipidus – lack of ADH (trauma,
stroke, infection)
 Nephrogenic Diabetes insipidus DI - inability of the
kidney to respond normally to ADH.
Excess of ADH - Syndrome of Inappropriate ADH
(decreased excretion of free water).
 production of ectopic ADH or ADH-like substance by
neoplasms.
Thyroid Control and Feedback
When thyroid hormone levels get low, the
hypothalamus is triggered to release
thyroid-releasing hormone
(TRH):
→ TRH triggers the anterior pituitary to
release thyroid-stimulating
hormone (TSH).
→ TSH stimulates the thyroid gland to
produce thyroid hormone that
is released into the blood.
→ Metabolism increases and energy levels
increase
Thyroid disorders
Thyroid Hormone Action:
 adequate fetal growth
 development of neural and skeletal systems.
 regulation of BMR and O2 consumption.
  heat production
 sympathetic effect on myocardium
  erythropoiesis.
 Thyroid disorders
Goiter -  size of the thyroid gland.
(not related of TH level)
 Complications of goiter:
 difficulty in swallowing,
 distention of the veins of the
neck and upper extremities,
 edema of the eyelids and
conjunctiva,
 syncope with coughing.
 HYPO THYROIDISM
 Secondary and Tertiary
 low circulating thyroid hormones. Hypothyroidism Pituitary-based
 Cause? deficiencies of TRH or TSH
 Primary Hypothyroidism  Rare disorders related to impaired
 Hashimoto disease (autoimmune stimulation of the thyroid gland at the
thyroiditis) pituitary level
 Iodine deficiency  Pituitary adenoma
 Surgical removal of the thyroid gland
 Thyroid ablation with radioactive iodine
 External radiation
 Temporary inflammation of thyroid gland
 Too little thyroid medication
 Exposure to some pharmacologic
agents (i.e., amiodarone, lithium,
thalidomide)
Example: Hashimoto
 Hashimoto’s thyroiditis is a more common
cause of goiter formation in the US.
 autoimmune condition in which there is
destruction of the thyroid gland by one’s own
immune system.
 As the gland becomes more damaged, it is
less able to make adequate supplies of thyroid
hormone.
 The pituitary gland senses a low thyroid
hormone level and secretes more TSH to
stimulate the thyroid. This stimulation causes
the thyroid to grow, which may produce a
goiter.
SO….what do you think
symptoms consist of?
Clinical Considerations
 Tell patient that thyroid replacement treatment
will likely continue for life.
 If the brand of medication changes, recheck
the patient’s TSH level.
 Advise patient that medication should be
taken at the same time each day on an empty
stomach (at least one hour before other
medications).
 Teach patient that significant interference with
absorption can occur when taken with
calcium, iron, vitamins, antacids, colestipol or
other medications that bind bile acids or fiber
supplements.
HYPERTHROIDISM
 high circulating thyroid hormones.
 Cause?

• Graves’ Disease
• Thyroid tumor/nodule
• Excessive intake of thyroid hormones
• Abnormal secretion of TSH
• Thyroiditis
• Excessive iodine intake
SO….what do you think
symptoms consist of?
Special Populations
Pregnancy
Thyroid dysfunction in pregnancy is associated with
preeclampsia, spontaneous abortion, abnormal fetal brain
development, and fetal mortality. In general, increased dosage
requirements of thyroid replacement medications should be
anticipated, especially during first and second trimesters.

Children
Thyroid hormones play a critical role in neurologic development
in children. Low or absent levels of thyroid hormone may result
in cretinism, and neonatal hypothyroidism accounts for the most
preventable cause of intellectual disability.

Elderly
Signs and symptoms of hypothyroidism may be very subtle and
mistakenly attributed to normal aging changes. Taking a careful
history is important to make the correct diagnosis and helps to
avoid erroneous diagnoses of heart failure, dementia or
 Thyroid Function Tests (TFTs)

 Thyroid function tests (TFTs) are used to screen thyroid activity.

Thyroid stimulating hormone (TSH) is the gold standard for
evaluating thyroid function.

When screening for thyroid dysfunction:

• If the TSH is normal, no further testing is required.
• If the TSH is high, check free T4 to determine the degree of
hypothyroidism.
• If the TSH is low, check free T4 and T3 to determine the
degree of hyperthyroidism.
• If pituitary or hypothalamic disease is suspected, check
both serum TSH and free T4.
• If TSH is normal, but patient has convincing symptoms of
thyroid dysfunction, check free T4.
Q
Grave’s disease is:
 The most common cause of hypothyroidism
 The most common cause of
hyperparathyroidism
 The most common cause of hyperthyroidism
 The most common cause of adrenal
insufficiency
Adrenal Cortex Control and
Feedback

Adrenal cortex: outer layer that produces

steroid hormones
Adrenal medulla: inner part of the gland
that produces catecholamines
Cortisol
• Increases
– Plasma proteins
– Catabolism
– Muscle breakdown
– Free fatty acids
– Blood glucose
– SNS response
• Suppresses
– The immune and inflammatory systems
Pathology of adrenal gland
Hypofunction of adrenal cortex (cortisol,
aldosterone, androgen).
Primary adrenal hypofunction - ADDISON'S
DISEASE
 Cause: atrophy of the adrenal cortex as a
result of
 autoimmune processes
 tuberculosis
 tumor or metastatic disease
 surgical ablation
 inflammatory necrosis
 Hypofunction of adrenal
cortex
Aldosterone deficiency
  excretion of Na and  excretion of K,
 low blood concentrations of Na and Cl and a high
concentration of serum K.
 severe dehydration, plasma hypertonicity,
 decreased circulatory volume, hypotension.
Cortisol deficiency
 disturbances in carbohydrate, fat, and protein
metabolism
 low resistance to infection, trauma, and other stress
 hyperpigmentation of skin and mucous membranes
Steroids?
 Imagine you have a client who is taking
steroid ( prednisone) for rheumatoid arthritis
 Adrenals stop working
 If abrupt stop of prednisone, crisis
 tapering the drug gives the adrenal glands
time to return to their normal patterns of
secretion
Addison's disease clinical manifestations
= GRADUAL
 Weakness, fatigue
 Increased pigmentation
 GIT: anorexia, nausea, vomiting, diarrhea
 Hypometabolism
 Heart activity disturbances
 Weight loss, dehydration, hypotension
SOOOOOO
 the body cannot hold on to sodium and water
anymore so, the body begins to lose (excrete)
sodium and water. As a result, the vascular
volume drops.
 So, now you have to go back and review all
the signs and symptoms of hypovolemia!
 If sodium and water are excreted, then
potassium is saved in the vascular space.
The client becomes hyperkalemic.
 Now you have to review the signs and
symptoms of hyperkalemia!
Considerations
 A high-sodium and low-potassium diet is
needed.
 Dietary sodium replaces the sodium that is
excreted, and dietary potassium is limited due
to the existing potassium excess.
 HOWEVER, if the client is undergoing steroid
replacement therapy, remember that steroids
generally cause sodium and water retention
and potassium excretion. In this case, the
client would need a low-sodium diet with
increased potassium.
Acute adrenal failure –
Adrenal crisis
 Causes:
 trauma,
 hemorrhage
(overdose of heparin,
acute or fulminant
sepsis)
 Clinical manifestation:
 acute hypotension;
 dehydration of the
organism;
 insufficiency of
bloodflow on all the
levels (results in
patient’s death).
Diabetes Mellitus

Glucose, Pancreas…
Who is involved?
Types
Type 1
 chronic autoimmune disorder
 How?
 T cell–mediated autoimmune disease
involving the specific destruction of insulin-
producing pancreatic β-cells.
 “trigger”
 Symptoms

(Mapes & Faulds, 2014).

But why?
 Polyuria or increased urination.
 Polyuria occurs because the kidneys remove excess sugar from
the blood, resulting in a higher urine production.
 Polydipsia or increased thirst.
 Polydipsia is present because the body loses more water as
polyuria happens, triggering an increase in the patient’s thirst.
 Polyphagia or increased appetite
 Although the patient may consume a lot of food but glucose could
not enter the cells because of insulin resistance or lack of insulin
production.
 Fatigue and weakness.
 The body does not receive enough energy from the food that the
patient is ingesting.
 Sudden vision changes.
 The body pulls away fluid from the eye in an attempt to compensate
the loss of fluid in the blood, resulting in trouble in focusing the
vision.
 Diagnostics?
 Tests (types I and II combined):  HbAIC (glycosylated hemoglobin):
 Urinalysis: glucosuria (sugar in is produced by a reaction between
the urine) and ketonuria protein and glucose. The level is
(ketones) may be present. obtained at the time of diagnosis
 A fasting blood sugar of 126
and obtained every 3 months.
mg/dL on more than one  American Diabetes Association
recommends HbAIC to be less than
occasion is diagnostic.
7%. If consistently 8%, then therapy
Therefore, further evaluation should be re-evaluated.
with a glucose challenge is
 Blood and urine for renal function
unnecessary.
tests to detect presence of kidney
 If diabetes is suspected but
damage.
fasting blood sugar is less than
 Monitor arterial blood gases
126 mg/dL, a standardized oral
(ketoacidosis) and vital signs
glucose tolerance test may be
initiated (generally done in clinic
setting).
Testing for Glycated Hemoglobin

 Glycated hemoglobin or glycosylated

hemoglobin, HgbA1C, or A1C reflects the
average blood glucose levels over a period of
approximately 2 to 3 months.
 The longer the amount of glucose in the
blood remains above normal, the more
glucose binds to hemoglobin and the higher
the glycated hemoglobin becomes.
 Normal values typically range from 4% to 6%
and indicate consistently near-normal blood
glucose concentrations.
Scenario
 X.Y.: a 32-year- old, always complains of his
increasing need for water.
 He also feels an increasing need to urinate & almost
always feels hungry.
 There is tingling on his extremities and numbness.
 His once clear vision is now experiencing cloudiness.
 He already feels tired just a few hours after waking
up even though he does not have any job and only
stays at home.
 The wound on his right knee has been there weeks
but no improvement is seen.
Type 2
major problems of insulin
resistance and impaired
insulin secretion.
Insulin could not bind with the
special receptors so insulin
becomes less effective at
stimulating glucose uptake
and at regulating the glucose
release.
There must be increased
amounts of insulin to maintain
glucose level at a normal or
slightly elevated level.
However, there is enough
insulin to prevent the
breakdown of fats and
production of ketones.
Cause?
 Weight. Excessive weight or obesity is one of
the factors that contribute to type 2 DM
because it causes insulin resistance.
 Inactivity. Lack of exercise and a sedentary
lifestyle can also cause insulin resistance and
impaired insulin secretion.
Insulins
 Exogenous insulin. In type 1 diabetes, exogenous insulin must be
administered for life because the body loses the ability to produce insulin.
 Insulin in type 2 diabetes. In type 2 diabetes, insulin may be necessary on a
long-term basis to control glucose levels if meal planning and oral agents are
ineffective.
 Self-Monitoring Blood Glucose (SMBG). This is the cornerstone of insulin
therapy because accurate monitoring is essential.
 Human insulin. Human insulin preparations have a shorter duration of action
because the presence of animal proteins triggers an immune response that
results in the binding of animal insulin.
 Rapid-acting insulin. Rapid-acting insulins produce a more rapid effect that is
of shorter duration than regular insulin.
 Short-acting insulin. Short-acting insulins or regular insulin should be
administered 20-30 minutes before a meal, either alone or in combination
with a longer-acting insulin.
 Intermediate-acting insulin. Intermediate-acting insulins or NPH or Lente
insulin appear white and cloudy and should be administered with food around
the time of the onset and peak of these insulins.
Nursing Management
 Nurses should provide accurate and up-to-
date information about the patient’s condition
so that the healthcare team can come up with
appropriate interventions and management.

 Nursing Assessment
 The nurse should assess the following for
patients with Diabetes Mellitus:
Assessment
 Assess the patient’s history. To determine if there is presence of
diabetes, assessment of history of symptoms related to the
diagnosis of diabetes, results of blood glucose monitoring,
adherence to prescribed dietary, pharmacologic, and exercise
regimen, the patient’s lifestyle, cultural, psychosocial, and
economic factors, and effects of diabetes on functional status
should be performed.
 Assess physical condition. Assess the patient’s blood pressure
while sitting and standing to detect orthostatic changes.
 Assess the body mass index and visual acuity of the patient.
 Perform examination of foot, skin, nervous system and mouth.
 Laboratory examinations. HgbA1C, fasting blood glucose, lipid
profile, microalbuminuria test, serum creatinine level, urinalysis,
and ECG must be requested and performed.
Priorities?
 Restore fluid/electrolyte and acid-base
balance.
 Correct/reverse metabolic abnormalities.
 Identify/assist with management of underlying
cause/disease process.
 Prevent complications.
 Provide information about disease
process/prognosis, self-care, and treatment
needs.
Q
 Nurse Andy has finished teaching a client with
diabetes mellitus how to administer insulin. He
evaluates the learning has occurred when the
client makes which statement?
 A“I should check my blood sugar immediately
prior to the administration.”
 B “I should provide direct pressure over the site
following the injection.”
 C “I should use the abdominal area only for
insulin injections.”
 D“I should only use calibrated insulin syringe for
the injections.”
A
 Option D: To ensure the correct insulin dose,
a calibrated insulin syringe must be used.
Option C: Insulin injections should be rotated
to the arm and thigh, not just the abdominal
area. Option B: There is no need to apply
direct pressure over the site following an
insulin injection. Option A: There is no need to
check blood glucose immediately prior to the
injection.