NCM114 - Endocrine System

Lesson 1.4. Adrenal Glands

 Adrenal glands, also known as

suprarenal glands, are small,
triangular-shaped glands located
on top of both kidneys.
 Adrenal glands produce hormones
that help regulate your
metabolism, immune system,
blood pressure, response to stress
and other essential functions.
 An adrenal gland is made of two
main parts:
o The adrenal cortex is the
outer region and also the
largest part of an adrenal
gland.
o The adrenal medulla is
located inside the adrenal
cortex in the center of an
adrenal gland
o The adrenal cortex and
adrenal medulla are
enveloped in an adipose
capsule that forms a potassium).
protective layer around an
adrenal gland.
 Hormones of the Adrenal
Glands
o from the Adrenal Cortex
 Cortisol - is a
glucocorticoid hormone
that helps control the
body’s use of fats,
proteins and
carbohydrates;
suppresses
inflammation; regulates
blood pressure;
increases blood sugar;
and can also decrease
bone formation.
 This hormone
also controls the
sleep/wake cycle.
It is released
during times of
stress to help your
body get an
energy boost and
better handle an
emergency
situation.
 Aldosterone - This
mineralocorticoid
hormone plays a central
role in regulating blood
pressure and certain
electrolytes (sodium and
 Androgenic Steroids -
are weak male
hormones. They are
precursor hormones that
are converted in the
ovaries into female
hormones (estrogens)
and in the testes into
male hormones
(androgens). However,
estrogens and
androgens are produced
in much larger amounts Glands
by the ovaries and
testes.
o From the Adrenal Medulla
 controls hormones that
initiate the flight or fight
response, the epinephrine
(adrenaline) and
norepinephrine
(noradrenaline)
 these hormones are capable
of increasing the heart rate
and force of heart
contractions, increasing
blood flow to the muscles
and brain, relaxing airway
smooth muscles, and
assisting in glucose (sugar)
metabolism.
 They also control the
squeezing of the blood
vessels (vasoconstriction),
helping maintain blood
pressure and increasing it in
response to stress.
 Epinephrine and
norepinephrine are often
activated in physically and
emotionally stressful
situations when your body
needs additional resources
and energy to endure
unusual strain.
Hypofunction of the Adrenal
 ADRENAL
INSUFFICIENCY/ADDISON’
S DISEASE
o Addison’s disease is
a disorder in which the
adrenal do not produce
 enough of the hormones infections, and fungal
cortisol and aldosterone. infections
 Cancer cells from
o Cortisol helps the body another part of the body
respond to stress, including that have invaded the
the stress of illness, injury, adrenal glands
or surgery. It also helps  Bleeding into the
maintain blood pressure, adrenal glands
heart function, the immune  Surgical removal of the
system and blood glucose adrenal glands
(sugar) levels.  Genetic defects
o Symptoms:
o Aldosterone affects the  Abdominal pain
balance of sodium and  Abnormal menstrual
potassium in the blood. periods
This in turn controls the  Craving for salty food
amount of fluid the kidneys  Dehydration
remove as urine, which  Depression
affects blood volume and  Diarrhea
blood pressure.  Irritability
 Lightheadedness
o Affects 1 in 100,000 or dizziness when
people. It occurs in both standing up
men and women equally  Loss of appetite
and in all age groups, but is  Low blood glucose
most common in the 30-50  Low blood pressure
year-old age range.  Muscle weakness
o Causes:  Nausea
 Autoimmune Disorder  Patches of dark skin,
 Injury to the adrenal especially
glands around scars, skin
 Infection, folds, and joints
including tuberculosis,   Sensitivity to cold
HIV/AIDS-related  Unexplained weight
loss
 Vomiting
 Worsening fatigue
(extreme tiredness)
o Addisonian Crisis
 In some cases – such
as an injury, illness, or
time of intense stress –
symptoms can come on
quickly and cause a
serious event called an
Addisonian crisis, or
acute adrenal
insufficiency. An
Addisonian crisis is a
medical emergency. If it
is not treated, it can
lead to shock and
death.
 Symptoms:
 Feeling
restless, confused, or
afraid, or other mental
changes
 Dehydration
 Extreme weakness
 Having trouble
staying awake, or
a total loss of
consciousness
 High fever
 Lightheadedness or
feeling faint
 Paleness
 Severe vomiting and
diarrhea
  Sudden, deep pain in
the lower back, belly
or legs
o Diagnosis
 History and physical:
 Blood tests: These will
be done to measure the
levels of sodium,
potassium, cortisol and
ACTH in the blood.
 ACTH stimulation
test: This tests the
adrenal glands’
response after being
given a shot of artificial
ACTH. If the adrenal
glands produce low
levels of cortisol after
the shot, they may not
be functioning properly.
 X-rays
 Computed
tomography (CT scan)
o Treatment: Hormonal
Replacement Therapy
 hydrocortisone pills for
cortisol replacement  CUSHING’S SYNDROME
 fludrocortisone acetate
pills for aldosterone
replacement
 CONGENITAL ADRENAL
HYPERPLASIA
o A genetic disorder.
o Children who are born with
this disorder are missing an
essential enzyme
necessary to produce
cortisol, aldosterone or
both. At the same time,
they often experience
excess of androgen, which
may lead to male
characteristics in girls
and precocious puberty in
boys.
o Congenital adrenal
hyperplasia can remain
undiagnosed for years
depending on the severity
of the enzyme deficiency.
In more severe cases,
infants may suffer from
ambiguous genitalia,
dehydration, vomiting and
failure to thrive.
Hyperfunction of the Adrenal
Glands
o Cushing’s Disease results
when too much ACTH
(adrenocorticotropic
hormone) is produced by a
tumor of the pituitary gland.
o Cushing’s syndrome which
refers to the clinical
manifestations of cortisol
excess, has two causes:
 Adrenal tumor that causes
the adrenal gland to
produce excessive
glucocorticoid (cortisol)
 Prolonged administration
of corticosteroid therapy
o Risk factors
 Female
 Altered pituitary function
 Prolonged corticosteroid
therapy
 Tumor of the adrenal
cortex
o Signs and symptoms

Weight gain specially in the
trunk, face and neck
(“buffalo hump”)
  Muscle wasting of c. Signs of infection  HYPERALDOSTERONISM
extremities d. Urinary and serum o Hyperaldosteronism results
 Weakness glucose levels from overproduction of
 Ruddy complexion 2. Nursing Activities aldosterone from one or
 “moon face” a. Provide emotional both adrenal glands. This is
 Abdominal striae support related to characterized by increase in
 Hyperglycemia body image changes blood pressure that often
 Electrolyte imbalances and mood swings requires many medications
 Emotional b. Promote skin integrity to control. Some people can
changes/depression c. Prevent injury develop low potassium
 Excessive hair growth in d. Encourage intake in levels in the blood, which
women high protein, low can cause muscle aches,
 Thin, easily bruised skin calorie diet weakness and spasms.
 Risk for infection, immune e. Assist with o When the cause is adrenal
suppression preparation for oversecretion, the disease is
 Bone demineralization surgery if indicated called Conn syndrome.
 Cataracts f. Prepare for radiation  PHEOCHROMOCYTOMA
 Glaucoma therapy if indicated  is a tumor that results in
 Hypertension g. Teach the client the excess production of
o Diagnostic and Laboratory importance of not adrenaline or
Tests discontinuing noradrenaline by the
 History and physical corticosteroid adrenal medulla that often
examination medications abruptly happens in bursts. 
 Urine cortisol o Pharmacology o Pheochromocytoma may
 Plasma cortisol  Adrenal enzyme inhibitors cause persistent or sporadic
 Dexamethasone for Cushing’s disease high blood pressure that
suppression test caused by tumor may be difficult to control
 MRI o Complications with regular medications.
 CT Scan  Secondary diabetes Other symptoms include
 Ultrasound mellitus headaches, sweating,
o Therapeutic Nursing  Osteoporosis and tremors, anxiety and rapid
Management spontaneous fractures heartbeat. Some people are
1. Assess/Monitor  Alteration in mental status genetically predisposed to
a. Intake and Output  Shock developing this type of
b. Weight  Death tumor.
  Insulin are secreted by the beta
cells
 Glucagon are secreted by the
alpha cells
 Somatostatin and gastrin are
synthesized by the delta cells.
 Gastrin is used in the metabolism
of foods
 Somatostatin decreases the
secretion of insulin, glucagon,
growth hormone, gastrin
 Insulin and Glucagon are the
primary pancreatic hormones
secreted by these cells and plays
a vital role in the control of
carbohydrate metabolism
 Insulin:
o Stimulates the active
transport of glucose into
muscle and adipose tissue
cells
o Regulates the rate at which
carbohydrates are used by
Lesson 1.5. Pancreas cells for energy
 o Promotes the conversion of
 Pancreas is a large fish-shaped glucose to glycogen for
organ that lies Sbehind the storage and inhibits the
stomach conversion of glycogen into
 It has both exocrine and glucose
endocrine functions o Promotes the conversion of
 The endocrine functions of the fatty acids into fat, to be
pancreas are carried out by the stored as adipose tissue,
islets of Langerhans which inhibits the breakdown of
contains alpha, beta and delta adipose tissue, mobilization
cells
of fats and conversion of fat
into ketone bodies
o Stimulates protein synthesis
within the tissues and inhibits
the breakdown of protein into
amino acids
 Glucagon:
o Promotes a rise in blood
glucose level when glucose
levels drop too low by
promoting the conversion of
liver glycogen into glucose.
 Factors needed for insulin and
glucagon release:
o A healthy pancreas with
functioning alpha and beta
cells
o A diet adequate in protein.
Both insulin and glucagon
are protein substances
o Normal potassium levels
Diabetes Mellitus
 DEFINITION
o Diabetes Mellitus is a group
of metabolic diseases
characterized by increased
levels of glucose in the blood
resulting from defects in
insulin secretion, insulin
action or both (American
Diabetes Association, 2004).
o Hyperglycemia refers to
elevated in blood glucose
level, fasting level greater
than 110mg/dL (6.1 mmol/L)
 o Hypoglycemia refers to low Diabetes environmental Non-ketotic
blood glucose level (less than Mellitus factors coma
60 mg/dL [less than 2.7 (IDDM) Little or no
mmol/L]) endogenous Gestati Gestational Onset during
 RISK FACTORS insulin onal Diabetes pregnancy,
o Family History Need insulin Diabete usually in the
o Obesity to preserve s 2nd or 3rd
o Race/ethnicity (African- life trimester of
American, Hispanic- High risk to pregnancy
American, Native Americans, diabetic Due to
Asian Americans) ketoacidosis hormones
o Age >45 yo (DKA) secreted by
o Previously identified impaired the placenta,
Type 2 Adult-onset Onset at any which inhibit
fasting glucose or impaired
DM (90- diabetes age, usually the action of
glucose tolerance
95% of Non-Insulin over 30 yo insulin
o Hypertension
all Dependent Usually obese Occurs about
o Elevated HDL and/or
diabete Diabetes at diagnosis 2-3% of all
triglyceride level s) Mellitus Causes pregnancies
o History of gestational Obese (NIDDM) includes
diabetes or delivery of babies (80% of obesity,
over 9lb type 2) heredity and  PHYSIOLOGY
 TYPES/CLASSIFICATIONS Non- environmental o Insulin is secreted by beta cells
obese factors of the Islets of Langerhans in
TYPE PREVIOUS CLINICAL
(20% of Decrease in the pancreas.
CLASSIFICA CHARACTERI
TIONS STICS AND
type 2) endogenous o When a person eats, insulin
IMPLICATION insulin, or secretion increases and moves
S increased glucose from the blood to the
Type 1 Juvenile Onset at early with insulin muscle, liver and fat cells. In
DM (5- Diabetes age resistance those cells, insulin
10% of Juvenile- Etiology Acute  Transports and
all onset includes complication: metabolizes glucose for
diabete Diabetes genetic, Hyperglycemi energy
s) Insulin immunologic c  Stimulates storage of
Dependent and Hyperosmolar glucose in the liver and
 muscle (in the form of
glycogen)
 Signals the liver to stop
the release of glucose
 Enhances storage of
dietary fat in the adipose
tissue
 Accelerates the transport
of amino acids (derived
from dietary protein) into
cells
o Insulin also inhibits the
breakdown of stored glucose,
protein and fat
o Glucagon is another pancreatic
hormone secreted by the alpha
cells of the islets of
Langerhans which is released
when blood glucose levels
decrease and stimulates the
liver to release stored glucose.
o Both insulin and glucagon
maintain a constant level of
glucose in the blood by
stimulating the release of
glucose from the liver.
 PATHOPHYSIOLOGY
o IDDM
 Associated with
inflammation of the islets
of Largerhans (Insulitis)
which appears to be an
autoimmune response
o NIDDM
 Refractoriness to insulin
in the cell membrane
receptor
 Seen in persons with
long-term obesity
 METABOLIC EFFECTS OF
DIABETES
o Decreased utilization of
glucose
 Glucose remains in the
blood causing blood
glucose level to rise –
HYPERGLYCEMIA
 The kidney will excrete
excess glucose –
GLUCOSURIA
 Glucose excreted in the
urine acts as osmotic
diuretic that causes
increase fluid excretion
(POLYURIA) and  CARDINAL SIGNS OF
results to fluid volume
deficit, increased thirst
and increase fluid
intake (POLYDIPSIA)
o Increased fat metabolism
 The body rely on fat
stores as source of
energy
 The process of fat
metabolism leads to the
formation of breakdown
products called
KETONES
 This can lead to
acidosis (diabetic
ketoacidosis) and
increased osmotic
diuresis
 When fats are used for
a primary source of
energy, the body fluid
level increases and can
lead to atherosclerosis
o Increased protein utilization
 Without insulin to
stimulate protein
synthesis, protein
wasting happens
 Results to being thin
and emaciated of the
affected individual, this
leads to increase desire
to eat (POLYPHAGIA)
DIABETES
Clinical Pathophysiologic
Manifestations Bases
Polyuria Water not
(frequent reabsorbed from
urination) renal tubules
because of the
osmotic activity
of glucose in the
tubules
Polydipsia Polyuria causes
(excessive severe
thirst) dehydration
which causes
 thirst syndrome (HHS) is a resulting to
Polyphagia Tissue serious complication hyperglycemia
(excessive breakdown and of NIDDM. HHS and metabolic
hunger) wasting cause a occurs when a acidosis.
state of person’s blood  Blood glucose
starvation that glucose (sugar) levels levels higher than
compels the are too high for a long 300mg/dL
client to eat period, leading to  Kussmaul’s
excessive severe dehydration respirations
amounts of food (extreme thirst) and (deep, gasping,
Weight loss Glucose not confusion rapid breathing
(primarily available on the  High blood sugar associated with
IDDM) cells, thus the level (over 600 severe diabetic or
body breaks mg/dL) renal acidosis or
down fat and  If not treated, can coma)
protein stores for lead to  Blood pH less
energy  Seizures than 7.3
 Coma.  Presence of
 Other manifestations  Swelling of the serum ketones,
o Fatigue and weakness brain. urine ketones
o Vision disturbances  Organ failure. (KETONURIA)
o Confusion and changes in  Death. and glucose
mentation  Abnormal levels
o Delayed wound healing o Diabetic Ketoacidosis of serum sodium,
o Behavioural changes, (DKA) is a life- potassium and
including irritability threatening chloride
 Complications complication of IDDM,  Fruity (acetone)
o Hyperglycemic resulting from severe odor to breath
Hyperosmolar Nonketotic insulin deficiency.  Hypotension
Coma  In response to  CNS depression
(HHNK)/Hyperosmolar insulin deficiency, progressing to
Hyperglycemic Syndrome the body uses fats coma, cerebral
(HHS) and proteins to anoxia and death
 Hyperosmolar meet cellular
hyperglycemic metabolic needs,  CHRONIC COMPLICATIONS
o Macroangiopathy numbness and  Therapeutic Nursing
(Atherosclerosis) pain, usually in Management
 A disease of the large the hands and o Assess/monitor
blood vessels in feet.  Dietary intake
which fat and blood o Autonomic  For factors that may
clots build up and Neuropathy impede the client’s
stick to the vessel  Occurs when ability to learn or
walls, blocking the there is damage perform self-care
flow of blood to the nerves  For signs of
 Coronary artery that control hypoglycaemia or
disease (CAD) automatic body insulin shock
 Cerebrovascula functions. It can  Skin for alterations
r disease affect blood  For signs of infection
 Peripheral pressure,  For risk of injury/falls
vascular temperature related to
disease control, neuropathies
o Microangiopathy digestion,  For signs of DKA
 Is a disease of the bladder function  Acid-base status
microvessels, small and sexual  Electrolyte status
blood vessels in the function. o Nursing Activities
microcirculation o Infections  Encourage self-care
 Retinopathy  Diagnostic and laboratory test  Teach regarding self-
 Nephropathy o History and physical administration of
o Neuropathy examination insulin or oral
o Peripheral o GTT (glucose tolerance hypoglycemic agents
Neuropathy test)  Teach regarding
 A result of o FBG/FBS (fasting blood specific dietary
damage to the glucose/fasting blood requirements
nerves located sugar)  Teach client signs
outside of the o GHb (glycosylated and symptoms of
brain and spinal haemoglobin) hypoglycaemia and
cord (peripheral o Urine glucose and ketone insulin shock
nerves) that levels  Encourage increased
often cause o Serum electrolytes intake of dietary fiber
weakness,
  Encourage daily
exercise. Exercise
promotes utilization
of carbohydrates
 Teach regarding
alterations in insulin
administration if sick,
NPO or physically
active. Infection is
associated with
insulin resistance  Insulin resistance Foot and Skin
 Encourage
avoidance of
smoking to reduce
cardiovascular risks
 Provide emotional
support for family
and client
 Teach regarding
blood glucose
monitoring
 Encourage regular
blood glucose
monitoring
 Encourage use of a
medical alert bracelet
or card
 Teach client and
family the signs of
hyperglycemia,
hypoglycaemia or
DKA
 Pharmacology and Treatment
o Oral Hypoglycemic agents o Avoid tight socks and
(acarbone, metformin) shoes
o Insulin therapy o
o Complications of Insulin
therapy
 Hypoglycemia
 Tissue
hyperthrophy or
Atrophy
 Insulin allergy
Care 1
o Do not soak feet unless
directed to do so
o Use mild soap and
washcloth to clean
between toes
o Check water temperature
o Use lotion with lanolin
o Do not use harsh
chemicals (betadine,
peroxide) on the feet 2
o Cut nails straight across
and not an angle
o See a podiatrist if possible
o Do not go barefoot
o Do not use hot water
bottles, heating pads
o Wear good-fitting shoes,
leather shoes are
encouraged
3