Endocrine system

1. Let us Pray…

2. Endocrine
System
Prepared by:
Czarina Sales, RN

3. At the end of this lecture, the students will be able:
1. To identify and describe the major structures and functions of the endocrine
system and its hormone.
2. To compare and contrast the different mechanisms of action of hormones in the
body.
3. To determine the alterations in function of each of the endocrine glands: their
causes, clinical manifestations, management, and nursing interventions.
4. To apply nursing principles in the pathophysiological basis and consequences of
specific endocrine disorders.
Learning Objectives:

4. Structures and Functions of Endocrine System
 Hormones exert their effects on target tissue.
 The specificity of hormone–target cell interaction is determined by receptors
in a “lock-and-key” type of mechanism.
 The regulation of hormone levels in the blood depends on a highly specialized
mechanism called feedback.
 With negative feedback, the gland responds by increasing or decreasing the
secretion of a hormone based on feedback from various factors.
 The hypothalamus and pituitary gland integrate communication between
nervous and endocrine systems, forming a neuroendocrine system.

6. Pituitary Gland (Hypophysis)

7. Hormones Target Tissue Functions
Anterior Pituitary Gland (Adenohypophysis)
Growth Hormone (GH), or
somatotropin
All body cells
Promotes protein anabolism (growth,
tissue repair) and lipid mobilization
and catabolism.
Thyroid-stimulating hormone
(TSH), or thyrotropin
Thyroid Gland
Stimulates synthesis and release of
thyroid hormones, growth, and
function of thyroid gland.
Adrenocorticotropic hormone
(ACTH)
Adrenal cortex
Fosters growth of adrenal cortex.
Stimulates secretion of corticosteroids.
Gonadotropic hormones -
Follicle-stimulating hormone
(FSH); Luteinizing hormone
(LH)
Reproductive organs
Stimulate sex hormone secretion,
reproductive organ growth,
reproductive processes.
Melanocyte-stimulating
hormone (MSH)
Melanocytes in skin
Increases melanin production in
melanocytes to make skin darker.
Prolactin
Ovary and mammary
glands in women.
Testes in men
Stimulates milk production in lactating
women. Increases response of follicles
to LH and FSH. Stimulates testicular
function in men.

8. Hormones Target Tissue Functions
Posterior Pituitary Gland (Neurohypophysis)
Oxytocin Uterus,
mammary
glands
Stimulates milk secretion,
uterine contractility.
Antidiuretic hormone
(ADH), or vasopressin
Renal tubules,
vascular smooth
muscle
Promotes reabsorption of
water, vasoconstriction.
Posterior Pituitary Gland

9. Disorders of Anterior Pituitary Gland
Hyperactivity Hypoactivity
1. Hyperpituitarism 1. Hypopituitarism

10. HYPERPITUITARISM
(Pituitary Adenomas)
CARCINONA –rare
- Mostly non-functional
- Dx requires evidence of
metastasis: bone, liver, etc.
General Features:
- Usually single cell type (monomorphic)
- Non-functional larger at Dx
- Adults (30’s-50’s) esp. MALE
- APOPLEXY – acute hemorrhage -> rapid
enlarging mass
- Bitemporal hemianopsia
- Bony erosion -> cavernous sinus =
ophthalmoplegia (III, IV,VI); cranial nerve V
(neuralgia); esp. prolactinoma
- Inc. ICP: nausea & vomiting, headache
NULL CELL ADENOMA – 20%
- No hormonal products
- Signs & Symptoms: mass
effects, hypopituitarism
THYROTROPHIC ADENOMA – 1%
- Rare cause of hyperthyroidism
GONADOTROPH ADENOMA
- LH & FSH (10-15%)
- Subtle signs & symptoms
- Usual diagnose when big ->
vision and headaches
- Middle-aged
- Deficiencies: MEN =
decreased energy, libido,
WOMEN = amenorrhea
CORTICOTROPH CELL ADENOMA
(10-15%)
- PAS (periodic-acid-Schiff) positive d/t
ACTH -> hypercortisolism (Cushing’s
Disease)
- Nelson Syndrome – large adenoma after
adrenal removal -> no hypercortisolism
- Can be hyperpigmentation d/t ACTH on
melanocytes
PROLACTINOMA (20-30%)
- even small tumors -> lots of prolactin
- - inhibit LH surge
- >50% in men -> lose libido,
impotence, headache
Prolactinemia: found earlier in young
female -> amenorrhea, galactorrhea, loss
of libido, infertility
(physiological in pregnant, lactating)
- Also in lactotroph hyperplasia (low
dopamine)
- Dopamine antagonist, Reserpine
- Renal failure, hypothyroid, estrogens
- Tx: DA antagonist - > shrink adenoma
= Bromocriptine
GH Adenoma – 5%
(SOMATOTORH CELL)
- 40% with GSH oncogene
- mutant genes
- Subtle symptoms, so late, large Dx ->
clinical features d/t IGF-I
- GIGANTISM/ACROMEGALY
- Before or after epiphyses close
- “acro”: 20s-30s big soft tissues: heart,
thyroid, liver, adrenals – hyperostosis,
prognathism
- Can -> DM, gonadal dysfunction,
arthritis, CHF
Concept Map
Of
Hyperpituitarism

11. HYPOPITUITARISM
- With 75%
parenchyma gone
- may also have pallor
(MSH loss)
Causes:
- tumors, mass lesions
- Pituitary surgery/radiation
- Hemochromatosis-iron into pituitary
- Rathke Cleft Cyst – proteinaceous fluid
- Pituitary Apoplexy – sudden
hemorrhage, sudden headache,
pressure on nervous networks
- Ischemic Necrosis
- Sheehan Syndrome – most common
= postpartum necrosis
=sudden hypotension -> spasm -> necrosis
of anterior pituitary
= pituitary enlarged during pregnancy
= also in disseminated intravascular
coagulation, sudden cardiac arrest ->
replaced by fibrosis
- Genetic defects – (x-factors) – pit-1
defect (GH,PRL,TSH)
KALLMAN SYNDROME
- Gene mutation
- isolated LH/FSH deficiency
- No puberty
- Associated with ANOSMIA,
CLEFT PALATE
Panhypopituitarism
- Total failure
- Most common defects:
 THYROID FUNCTION
 ADRENAL FUNCTION
 GROWTH RETARDATION
W/ DELAYED PUBERTY
 FAILURE TO THRIVE (FTT)
EMPTY SELLA SYNDROME
- EMLARGED AND EMPTY
Primary – CSF into sella ->
compressed pituitary
- obese with multiple
pregnancies Secondary –
mass enlarges sella, then
removed
Hypothalamic Lesions:
- Tumors
(craniopharyngiomas, breast, lung
muscles)
- Radiation nearby
Infiltrative disorders, infection
(sarcoid, TB, meningitis)
Concept Map
Of
Hypopituitarism

12. Gigantism Acromegaly

13. TREATMENT
focuses on returning GH levels to normal through surgery,
radiation, and drug therapy
Prognosis is dependent on the age at onset, when treatment is
initiated, and tumor size.
Pituitary Surgery
Nursing care for the patient following transsphenoidal hypophysectomy
includes avoidance of vigorous coughing, sneezing, and straining at stool;
elevating the head of bed to a 30-degree angle at all times; and monitoring of
fluid, electrolyte, and neurologic status.
Mild analgesia is used for headaches.
Teeth brushing is avoided for at least 10 days.
If hypophysectomy is done or pituitary is damaged, antidiuretic hormone
(ADH), cortisol, and thyroid hormone replacement are needed for life. Patient
teaching is essential with hormone therapy.

14. Disorder
of
Posterior Pituitary
Gland
Hyperactivity Hypoactivity
1. Syndrome of
Inappropriate
Antidiuretic
Hormone
(SIADH)
1. Diabetes
Insipidus (DI)

15. SYNDROME OF INAPPROPRIATE
ANTI-DIURETIC HORMONE
(SIADH)
Etiology & Pathophysiology:
- Acquired SIADH: continuous
production of ADH without
proper feedback mechanism
control
- Hereditary: gene mutation
affects renal V2 receptor
(nephrogenic)
- Both: causes free-water
absorption -> dilutional
hyponatremia -> cerebral
edema & neurologic symptoms
Clinical Manifestations:
- Cerebral edema (main
problem)
- Mostly neurologic: N/V,
seizures, brain
herniation, coma, death
- Major complication:
hypoxemic respiratory
failure
Diagnostic Test:
- Laboratory results:
- Serum Na < 135 mEq/L
- Serum osmolality < 280 mOsm/kg
- Urine sodium > 20-40 mEq/L (unless in low NA diet)
- Urine osmolality > 100 mOsm/kg
- Chest X-ray, CT scan
- Creatinine level to assess renal function
Management:
- Goal: restore normal fluid volume & osmolality
- Correction should be done gradually (<8 mEq/L
in first 24 hours) – to prevent osmotic
demyelination syndrome (dysphagia, dysarthria,
diplopia, ataxia, mutism, locked-in syndrome)
- Acute & severe symptoms (e.g seizure) –
hypertonic saline
- Mild symptoms: fluid restriction, salt tablets
- Adjunctive medications: Furosemide,
Vasopressin antagonist (conivaptan, tolvaptan),
Demeclocycline
Concept Map
of
SIADH

16. Clinical Features:

17. DIABETES INSIPIDUS
Nephrogenic
- Normal synthesis of ADH but
a defective renal tubular
response to ADH
Central/Neurogenic
- When synthesis & release of
ADH is reduced
Causes:
- Genetic errors in kidney
function
- Kidney cyst, infection
- Cancer
- Medications, esp.
Lithium
Treatment:
- low salt diet
- Microzide
Causes:
- Genetic errors in brain
- Brain injury
Treatment:
- Mild: increase water
intake
- Severe:
Desmopressin,
hormone that
replaces ADH
Laboratory Findings:
- Diluted urine
- Specific gravity: < 1.005
- Urine output: > 200 mL/hr
Confirmatory Test:
- Water
Deprivation Test
- ADH blood level
- MRI
Primary/Dipsogenic
Nursing Care:
- Early detection
- Maintain adequate
hydration
- Patient teaching of
long-term
management
- Cornerstone of Tx:
Fluid and hormone
therapy
Concept Map
of
Diabetes Insipidus
Clinical Manifestations:
- Polydipsia
- Polyuria
Complications:
- Severe fluid volume deficit ->
hypotension -> hypovolemic shock
- Increased urinary output & plasma
osmolality -> severe fluid and
electrolyte imbalances

18. Thyroid Gland & Parathyroid Glands

19. Hormones Target Tissue Functions
Thyroid Gland
Thyroxine (T4) All body tissues Precursor to T3.
Triiodothyronine (T3) All body tissues Regulates metabolic rate of all cells
and processes of cell growth and
tissue differentiation.
Calcitonin Bone tissue Regulates calcium and phosphorus
blood levels. Decreases serum
Ca levels.
Hormones Target Tissue Functions
Parathyroid Gland
Parathyroid hormone (PTH), or
parathormone
Bone, intestine,
kidneys
Regulates calcium and phosphorus
blood levels. Promotes bone
demineralization and increases
intestinal absorption of Ca. Increases
serum Ca levels.

20. Goiter
Thyroiditis
Acute Thyrotoxicosis
Thyroid Nodules and
Cancer
Hyperthyroidism
Hypothyroidism
Disorders of Thyroid Gland

21. DIFFUSE NONTOXIC (Simple) GIOTER
- aka colloid goiter
Endemic - low iodine – mountain ranges
- Goiters in >10%
- Alps, Himalayas
- Low 12 -> high TSH -> more cells
- Goitrogens – high Ca, veggies
(cabbage, cauliflower, brussels, turnips)
- Cassava (inhibits Iodine transport)
- Females at puberty
GOITER
MULTINODULAR GIOTER
- Recurrent hyperplasia & involution
- Almost all long-standing simple goiter
- Can be nontoxic or -> toxicosis
- May have oncogene activation
-> disorganized -> rupture, hemorrhage
-> fibrosis, calcifications
- intrathoracic/plunging (retrosternal)
Clinical-mass Effect
- Mostly euthyroid (simple toxic goiter with or
without nodule)
- Some with hyperfunction nodules ->
HYPERTHYROIDISM – toxic – PLUMMER
SYNDROME
- Test: uneven radioactive iodine update

22. Goiter
an enlarged thyroid gland.
thyroid cells are stimulated to grow (process of hyperplasia),
which may result in an overactive thyroid (hyperthyroidism) or
an underactive gland (hypothyroidism).
Thyroid-stimulating hormone (TSH) and T4 levels are measured
to determine the level of thyroid function associated with the
goiter.
Treatment may involve therapy with thyroid hormone to
prevent further thyroid enlargement or surgery to remove large
goiters.
Patients with cardiovascular disease are at risk for adverse drug
events from thyroid replacement. Careful nursing assessment
and patient teaching regarding signs and symptoms of
overdose is essential.

23. THYROIDITIS
Infections:
- Acute or chronic
- Direct seeding or hematogenous
- Mycobacterium, fungi, Pneumocystis
(immunocompromised)
- Acute sudden neck pain (fever, chills, etc.)
- Usually no sequalae, +/- scarring
REIDEL THYROIDITIS
- Rare, chronic, idiopathic
- Middle age women
- Dense fibrosis that
replaces normal thyroid
parenchyma
- Fibrotic process invades
that adjacent structure of
neck & extends beyond
the thyroid capsule
- Wood-like hardness
“Ligneous Thyroiditis)
HASHIMOTO THYROIDITIS
- 45-65 Y.O.; F:M=20:1
- autoimmune
- Even kids
- Usually gradual
- Formation of Hurthle cells line
follicles
- Clinical: some hypothyroidism
- PAINLESS ENLARGEMENT
- can be preceded by
thyrotoxicosis -> d/t ruptured
follicles
- High T3,T4, low TSH ->
hypothyroidism
SUBACUTE (GRANULOMATOUS THYROIDITIS)
- 30-50 Y.O; F:M=5:1, summer
- 2nd most common thyroiditis
- Viral infection or post inflammation (mumps,
measles, etc.)
- Bi- or unilaterally enlarged, firm
- Micro abscesses early with neutrophils then
lymphocytes
- Collapsed, damaged follicles
- Giant cells around colloid -> fibrosis
- Clinical: sudden or gradual neck pain -> jaw,
throat, ears
- Fever, fatigue, malaise, anorexia, myalgia
- Inflammation & hyperthyroidism (2-6 weeks) ->
hypothyroidism -> for 2-8 weeks -> complete
recovery
- Lab: high T3, T4, low TSH, low Iodine uptake
SUBACUTE LYMPHOTIC (Painless)
THYROIDITIS
- 1-10% of hyperthyroidism
- Middle-age women
- Mild hyperthyroidism or/and goiter
- Hyperthyroidism for 2-8 weeks
- Non-tender, enlarged thyroid
- Lab: high T3 & T4, Low TSH & Iodine
uptake
Concept Map
of
Thyroiditis

24. NEOPLASMS
More likely neoplastic:
- Solitary nodule
- Nodules in younger
patients; male
- History of radiation
- Cold – don’t take
radioactive I
Risk factors:
- Ionizing radiation
- Nodular goiter
- Hashimoto
- More unlikely to
have family history
ANAPLASTIC CARNIMONA
- < 5%
- Aggressive
- No treatment, always
fatal
- Rapidly enlarging
- Metastasis to lungs
PAPILLARY CARCINOMA
- 75-85%; women (20-40’s)
- Fibrovascular stalk, can be cystic
- Poorest prognosis
- Diffuse sclerosing variant-fibrosis
-> lymphocytes infiltrate ->
Hashimoto
- Asymptomatic, singular
- Mostly COLD nodule on
scintigraphy
FOLLICULAR CARCINOMA
- 10-20%; women (40-50’s)
- More malignant than papillary
- Calcification, hemorrhage,
fibrosis
- Slowly enlarging, painless
- COLD nodule
- Lymphocytes uncommon,
blood common
- To bone, lungs, liver, etc.
MEDULLARY CARCINOMA
- 5%; (40-50s)
- Amyloid deposits – altered
calcitonin molecules
- Mass in neck, hoarse voice
- Diarrhea
- Unilateral (sporadic)
- Bilateral (familial)
Concept Map
of
Thyroid Cancer

25. Thyroid Nodules and Cancer
 A palpable deformity of the thyroid gland may be benign or malignant.
 Benign nodules are usually not dangerous but can cause tracheal
compression if they become too large.
 Thyroid cancer is the most common endocrine-related cancer. Papillary
thyroid cancer is the most common form.
 A major sign of thyroid cancer is the presence of a hard, painless
nodule or nodules on enlarged thyroid gland.
 A thyroidectomy is usually recommended for thyroid cancer. Surgical
procedures may range from unilateral total lobectomy to near-total
thyroidectomy with bilateral lobectomy. Radioactive iodine therapy and
external beam radiation may be given after surgery.
 Nursing care for thyroid cancer is similar to care for patients who
undergo thyroidectomy. Safe patient care requires a tracheostomy tray
at bedside to provide immediate intervention for swelling or hemorrhage
that compromises the airway.

26. HYPERTHYROIDISM
Epidemiology:
- Women > men
- > 40 yrs. old
Pathophysiology
a. Primary: Grave’s Disease,
Goiter, toxic adenoma
(Autoimmune Type 2
hypersensitivity: antibodies
against TSH receptor
b. Secondary: TSH pituitary
adenoma
c. Thyrotoxicosis: excess TH
d. High TH, low TSH
Risk factor:
- Family history
- Monozygotic twin
- Other autoimmune
disease
Diagnostics:
- Thyroid function tests:
suppressed TSH, raised T3 & T4
- FBC: mild normocytic anemia &
mild leucopenia, raised ESR,
raised Ca, raised LFTs.
- Radioactive Iodine Uptake and
scan
- TBII (Thyrotropin-binding
inhibitory immunoglobulin)
Clinical Features:
- Symptoms: weight loss, inc. appetite, heat intolerance,
sweating, diarrhea, tremor, irritability, frenetic activity,
emotional lability, psychosis, itch, oligomenorrhea-may
cause infertility.
- Signs: raised HR, AF, warm peripheries, fine tremor,
palmar erythema, hair thinning, lid lag, lid retraction,
thyroid nodules or bruit depending on cause.
- Features for Grave’s: exophthalmos, ophthalmoplegia.
Pretibial myxedema: edematous swelling above lateral
malleoli, thyroid acropatchy: clubbing, painful finger &
toe swelling, periosteal reaction in limb bones.
- Features of thyrotoxicosis: fever, agitation, confusion,
coma, tachycardia, AF, diarrhea, vomiting, thyroid
bruit, “acute abdomen”.
- Complications: heart failure (elderly), angina, AF,
osteoporosis, ophthalmopathy, gynecomastia, thyroid
storm.
Treatment:
- Pharma: Beta-blockers (propranolol) for symptoms
control; anti-thyroid meds: either titration with
Carbimazole, gradually reducing dose or block and
replace with simultaneous Carbimazole & thyroxine
(less risk of hypothyroidism). In Grave’s, maintain on
therapy for 12-18 months then withdraw, 50% will
relapse = radioidine or surgery.
- Radioactive Thyroid Therapy : most become
hypothyroid. No evidence of increased cancer, birth
defects or infertility. CI: pregnancy & lactation. Caution
in active hyperthyroidism as risk for thyroid storm.
- Thyroidectomy -> risk of damaging recurrent laryngeal
nerve: hoarseness & hypothyroidism. Patient may
become hypo or hyperthyroid.
Carbimazole:
agranulocytosis =
sepsis – rare but can
be life-threatening.
Warn to stop and
get urgent FBC If
signs of infection.
Alternative drug:
Propylthiouracil
Thyrotoxicosis:
- Get expert help.
- Give IV saline, Ng tube if vomiting, take
blood for T3 &T4, culture (if suspect
infection), sedate if necessary with
chlorpromazine, if no CI give propranolol,
high dose digoxin.
- Anti-thyroid drugs: Carbimazole and after 4
hrs Lugol’s solution IV hydrocortisone or PO
dexamethasone
- Treat suspected infection: cefuroxime
- Cool with tepid sponging/paracetamol.
- After 5 days reduce carbimazole, after 7
days stop Lugol’s solution, after 10 days
stop propranolol & iodine.
Concept Map
of
Hyperthyroidism

28. Concept Map
of
Hyperthyroidism

29. Myxedema

31. Myxedema Coma

32. Disorders of Parathyroid Gland
Hyperactivity Hypoactivity
1. Hyperparathyroidism 1. Hypoparathyroidism

33. HYPERPARATHYROIDISM
-caused by inc. level of PTH
-cases: inc. kidney reabsorption of
calcium (hypercalcemia), inc.
phosphorus excretion
(hypophosphatemia), dec. bone
density
Laboratory Test:
Inc. serum Ca ( primary
hyperparathyroidism)
Dec. serum phosphorus
Inc. serum magnesium
Inc. serum PTH
Inc. urine cAMP
Dx. Procedures:
- Blood and urine test
- X-ray, MRI, & CT scans
- Arteriography
- Venous sampling of
thyroid blood PTH
levels
- ultrasonography
Medications:
- Furosemide with IV saline (mild)
- Calcimimetic or oral phosphate (severe)
- IV phosphates (if needed to dec. Ca rapidly)
- Calcitonin (dec. skeletal Ca & dec. Ca excretion);
must be given with glucocorticoids
Causes:
- parathyroid tumor
- Congenital hyperplasia
- Neck trauma or radiation
- Vit. D deficiency
- CKD with hypocalcemia
- PTH secreting carcinomas of
lung, kidney, or GI tract
Surgical Management:
Parathyroidectomy
- Before surgery, pt. is stabilized, and Ca levels need to
be dec. to normal
- A hypocalcemic crisis can occur post-surgery. Ca level
needs to be assessed frequently. Check for S/S of
hypocalcemia (tingling and twitching of face)
- Assess laryngeal nerve damage by assessing pt’s
changes in voice patterns and hoarseness.
Assessment:
- Weight loss
- Possible bone fractures, bone deformities (extremities or
back), bone cysts, osteoporosis, or arthritis
- Waxy, pallor of skin (chronic)
- Kidney stones and Ca deposits in kidney soft tissues
- Anorexia
- N/V
- Epigastric pain/ constipation
- Elevated gastrin levels cause peptic ulcer disease
- Fatigue & lethargy
- If Ca level is > 12mg/dL, psychosis with confusion,
followed by coma or death.
Nursing Care:
- Monitor cardiac function and I/O q 2 hrs during hydration
therapy.
- Check ECG; look for T waves or QT interval
- Assess HR & rhythm
- Monitor serum Ca levels. Report sudden drops to MD.
- Prevent injury d/t high risk of fracture.
- Encourage pt. to take Vit. D supplements or food.
Concept Map
of
Hyperparathyroidism

34. HYPOPARATHYROIDISM
- Parathyroid function dec. d/t deficient
PTH or dec. effectiveness of PTH to
target tissue that results to
hypocalcemia
- Serum Ca normal range: 8-10 mg/dL (< 6
= risk for tetany)
Etiology:
Iatrogenic: accidental removal of
parathyroid gland
Idiopathic: autoimmune r/t adrenal
insufficiency, hypothyroidism, DM,
pernicious anemia, vitiligo
Hypomagnesemia: seen in alcoholic,
malabsorption syndrome, CKD,
malnutrition (impairs effects of PTH)
Pathophysiology:
- Iatrogenic, Idiopathic,
Hypomagnesemia
- Impaired effectiveness of PTH
or deficit PTH
- Interfere with effects of PTH on
bones, kidney, Ca regulation
- HYPOCALCEMIA
Dx. Test:
- ECG
- Blood test (serum Ca,
phosphate,
magnesium, vit. D,
urine cyclic adenosine
monophosphate
(cAMP)
- CT scans of neck
Drug Therapy:
- IV Ca – for acute & severe
hypocalcemia
- 10% Calcium chloride IV or
calcium gluconate over 10-15 min.
- Calcitriol (Rocaltrol) – for Vit. D
deficiency which inc. Ca
absorption in small intestine
- 50% Magnesium sulfate (up to 4
g/day) IM or IV
- Calcium – o.5 to 2 g/day PO
- Ergocalciferol 50,000 to 400,000
units – improves Ca level
Nursing Assessment:
- History – ask for any
head/neck surgery or
radiation treatment
- Tingling and
numbness around
mouth, hands, feet
- Severe muscle
cramps, spasms of
hands and feet
- Irritability, psychosis
- Tetany – Chvostek’s
sign or Trousseau’s
sign
Management of Care:
- Drug therapy
- Teaching on drug regimen and
interventions
- Educate on food high in Ca but
low in phosphorus – milk,
yogurt, salmon, sardines
(processed cheese to be avoided
d/t rich in phosphorus)
- Emphasize that therapy is
lifelong.
Concept Map
of
Hypoparathyroidism

35. Chvostek’s Sign & Trousseau’s Sign

36. Adrenal Gland (Suprarenals)

37. Hormones Target Tissue Functions
Adrenal Gland (Suprarenals)
Adrenal Medulla
Epinephrine (adrenaline) Sympathetic effectors
Increases in response to stress.
Enhances and prolongs effects of
sympathetic nervous system.
Norepinephrine
(noradrenaline)
Sympathetic effectors
Increases in response to stress.
Enhances and prolongs effects of
sympathetic nervous system.
Adrenal Cortex
Corticosteroids (e.g., cortisol,
hydrocortisone)
All body tissues
Promote metabolism. Increased in
response to stress. Anti-inflammatory.
Androgens (e.g., DHEA,
androsterone) and estradiol
Reproductive organs
Promote growth spurt in adolescence,
secondary sex characteristics, and
libido in both sexes.
Mineralocorticoids (e.g.,
aldosterone)
Kidney
Regulate sodium and potassium
balance and thus water balance.

38. Disorders of Adrenal Cortex
Hyperactivity Hypoactivity
1. Cushing’s Disease
2. Hyperaldosteronism
1. Addison’s Disease

39. CUSHING’S DISEASE
Etiology:
Hypercortisolism
- Adrenal cortex disorder (primary)
- Anterior pituitary gland disorder
(secondary)
- Hypothalamic etiology (tertiary)
Cushing’s Disease
- Excessive hormone production from anterior
pituitary tumor producing ACTH (70%) or
- Excess hormone secretion from the pituitary
tumor of adrenal cortex (15%)
- 15% of cases cased by ectopic tumor, usually
in lungs that secretes ACTH
- Females are 5 times more likely to develop
Systems affected:
- Cardiovascular
- Reproductive
- Integumentary
- Renal
- Mental
- Respiratory
- Musculoskeletal
- Immune
- Eyes
Clinical Manifestations:
- Hyperglycemia
- Fluid retention
- Cardiac hypertrophy
- Hypokalemia
- Abnormal fat distribution/obesity
- Dec. Muscle mass
- Virilization
- Breast atrophy
- Vocal changes
- Amenorrhea
- Dec. inflammatory & immune responses
- Inc. risk of infection
- Poor wound healing/skin ulcers
- Purpura
- Abdominal striae
- Thin, wrinkled skin
- Buffalo hump
- Emotional disturbances
- Osteoporosis
- Enlarged sella turnica
Nursing Management:
Assessment
- VS: inc. risk of infection; small inc.
in body temp. may be sign of
infection; BP & HR may inc.
secondary to fluid retention
- Daily weight, I/O
- Serum glucose, potassium
Actions
- Administer mediations that
interfere with production/release
of cortisol
- Head of bed elevated 45 degrees
- Turn patient frequently & protect
skin for integrity
Patient Teaching
- Overview of disease process
- Modify salt in diet as directed by
MD
Treatment:
- Prevention of complications associated
with fluid overload, changes in immune
status, skin integrity, & body structure
- Aminoglutethimide (interferes with
cortisol production in adrenal cortex)
- Cyproheptadine (impacts ACTH
production)
- With these meds, nurse must monitor
for signs of adrenal suppression
(hypoglycemia & hypernatremia)
- Pasireotide (Signifor) – inhibits release
of corticotropin in pats with Cushing’s
secondary to pituitary adenoma
- Transsphenoidal hypophysectomy or
radiation may be needed
Concept Map
of
Cushing’s
Disease

40. Clinical
Manifestations:

42. ADDISON’S DISEASE
Pathophysiology:
- Damage or dysfunction of
adrenal cortex
- Mineralocorticoids &
glucocorticoids are diminished
- Dec. aldosterone & cortisol
Etiology:
- Autoimmune dysfunction
(most common)
- TB
- Histoplasmosis
- Adrenalectomy
- Cancer
Laboratory Test:
- Serum electrolytes
- BUN creatinine
- Serum glucose
- Serum cortisol
- ACTH stimulation test
Nursing Care:
- Monitor fluid deficits and electrolyte
imbalances
- Administer medications as ordered
(glucocorticoids & mineralocorticoids)
- Monitor and treat hyperkalemia
- Monitor and trat hypocalcemia
- Maintain safe environment (assist with
ambulation, prevent falls)
- Frequent neuro checks
- Advised meds compliance
- Avoid alcohol & caffeine
- Monitor GI bleeding
- Monitor hypoglycemia
- Report manifestation of adrenal
insufficiency
Diagnostic Test:
- ECG
- X-ray, CT, MRI scans
Clinical manifestations:
- Hyperpigmentation
- Weight loss
- Craving for salt
- Weakness
- Fatigue
- N/V
- Orthostatic dizziness
Complications:
Addisonian Crisis
- Acute adrenal insufficiency occurs
when there is acute drop in
adrenocorticoids d/t sudden
discontinuity of glucocorticoid meds
or hen induces by severe trauma,
infection, or stress.
Concept Map
of
Addison’s
Disease

43. Clinical
Manifestations:

45. PRIMARY HYPERALDOSTERONISM
(CONN’S SYNDROME)
- Excess aldosterone d/t autonomous
overproduction, usually at adrenal cortex
Epidemiology:
- underdiagnosed, common cause of
secondary HTN
- Higher prevalence in African-American
Etiology:
- Bilateral idiopathic hyperplasia of
adrenal glands (most common)
- Aldosterone-producing adenoma/
aldosteronoma
- Less common: unilateral hyperplasia
of adrenal gland; familial
hyperaldosteronism; ectopic
aldosterone-producing tumor (e.g.
kidney, ovaries)
Pathophysiology:
- Autonomous overproduction
- Inc. Na & water retention, and
volume expansion
- HTN, edema, frank
hypernatremia, hypokalemia
Clinical Manifestations:
- Hypertension
- Hypokalemia = fatigue, muscle
weakness, cramping, headaches,
polyuria & polydipsia, palpitations,
constipation
- Classic Triad: (1)severe pounding
headache, (2) tachycardia with
palpitations and profuse sweating, (3)
unexplained abdominal or chest pain
- Lack of significant edema
- Paresthesia d/t metabolic alkalosis
(severe)
Diagnostic Tests:
- PAC:PRA ratio
- Captopril Suppression test
- 24-hr Urinary Excretion of Aldosterone Test
- Saline Suppression Test
- CT scan or MRI (adenoma or hyperplasia)
Treatment:
- Bilateral adrenal hyperplasia =
aldosterone receptor antagonist
(Eplerenone, Spironolactone)
- Unilateral autonomous aldosterone
secretion (adenoma, unilateral
hyperplasia, carcinoma) =
Adrenalectomy
• Prior surgery: correct hypokalemia with
spironolactone & K supplements
• Post-surgery: monitor hyperkalemia
Concept Map
Of
Hyperaldosteronism

46. Disorder of Adrenal Medulla
Hyperactivity
1. Pheochromocytoma

47. Pheochromocytoma
- Catecholamines – secreting
tumor, typically develops in
adrenal medulla
Epidemiology:
- Age range 30-50 years old
- Present in up to 1% of all
hypertensive patients
Etiology:
- Tumor arise from chromaffin
cells, derived from neural
crest
- Localization: 90% adrenal
medulla; 10% extra-adrenal
in sympathetic ganglia
- 25% hereditary, men
Diagnostics:
Lab: all meds should be put on hold 1 week before
testing
- Best initial test: metanephrines (metabolites of
catecholamines) in plasma – high sensitivity
- Confirmatory test: Metanophrines &
catecholamines in 24-hr urine – high specificity
- Genetic testing
- Other: 24 hr ambulatory BP monitoring
- Adrenal/abdominal CT/MRI, Scintigraphy (MIBG)
Clinical Features:
- Fluctuating levels of excess epi, nor epi, dopamine
- Episodic HTN (or persistent in some)
- Paroxysmal: throbbing headache, diaphoresis, pallor,
heart palpitation & tachycardia, abdominal pain &
nausea, anxiety
- Weight loss (d/t inc. basal metabolism)
- Hyperglycemia
Treatment:
Operable
- Pre-op BP management., then surgery
- Beta-blocker – for additional BP control &
control of tachyarrhythmias
- Non selective alpha-blocker:
phenoxybenzamine
• Start beta-blockers BEFORE alpha-blockers
(contraindicated) – beta-blockers cancel out
vasodilatory effect of peripheral B2
adrenoceptors – unstopped alpha-
adrenoceptor stimulation = VASONSTRICTION
& HYPERTENSIVE CRISIS
Non-operable (extensive metastasis or
unresectable 1 degree)
- Benign: 1 degree therapy with
phenoxybenzamine
- Malignant: MIBG therapy (similar structure to
norepinephrine; when MIBG + RAI = radiation
directly to cells, or palliative (chemo, tumor
embolization)
Concept Map
of
Pheochromocytoma

48. Pancreas

49. Hormones Target Tissue Functions
Pancreas (Islets of Langerhans)
Insulin (from β cells) General Promotes movement of glucose out of
blood and into cells.
Amylin (from β cells) Liver, stomach Decreases gastric motility, glucagon
secretion, and endogenous glucose
release from liver. Increases satiety.
Glucagon (from α-cells) General Stimulates glycogenolysis and
gluconeogenesis.
Somatostatin Pancreas Inhibits insulin and glucagon secretion.
Pancreatic polypeptide General Influences regulation of pancreatic
exocrine function and metabolism of
absorbed nutrients.

50. Disorders of Pancreas
Disorders:
1. Prediabetes
2. Gestational Diabetes
3. DM Type 1
4. DM Type 2

52. Genetic Predisposition (Susceptibility)
Environmental insult
-Viral infection
-Toxic chemical
Autoimmunity
-Lymphocyte infiltration
-Insulitis
Immunologic Response
- Islet cell antibodies
- Cell- mediated immunity
β cell destruction
Lack of insulin release
Insulin Dependent Diabetes Mellitus (IDDM)
Hereditary
Factors Obesity
Delayed or insufficient
insulin secretion
Insulin resistance (Receptor
defect or other events)
Increased insulin demand
Β cell exhaustion and
dysfunction
Impaired
secretion of
insulin
Hyperglycemia
Non- Insulin Dependent DM
(NIDDM)
Diabetes Mellitus Type 1 Diabetes Mellitus Type 2

53. Acute Complications of Diabetes Mellitus:
1. Diabetic Ketoacidosis (DKA)
- Life-threatening condition caused by profound
deficiency of insulin.
- Characterized by: hyperglycemia, ketosis,
acidosis, and dehydration
2. Hyperosmolar Hyperglycemic Syndrome (HHS)
- Life-threatening syndrome that can occur in
patient with diabetes who is able to produce
enough insulin to prevent DKA but not enough
to prevent severe hyperglycemia, osmotic
diuresis, and extracellular fluid depletion.
3. Hypoglycemia or low blood glucose
- Occurs when there is too much insulin in
proportion to available glucose in the blood.
- Often r/t a mismatch in the timing of food
intake and the peak action of insulin oral
hypoglycemic agents
- Nurse critical role: Prompt recognition of
hypoglycemia & the appropriate initiation of
appropriate treatment dependent on the pt.’s
status

54. Chronic Complications of Diabetes Mellitus
Macrovascular Microvascular
Organ involve: heart, peripheral
system, brain
Organ involve: eyes, kidney,
nerve
Heart: hypertension, coronary
heart disease
Extremities: peripheral vascular
disease ->narrowing blood vessels
-> reduced or lack of blood flow in
legs -> feet wounds (heal slowly) ->
gangrene -> amputation
Brain: stroke, cerebrovascular
disease, TIA, cognitive impairment,
etc.
Eyes: Diabetic retinopathy Kidney: Diabetic nephropathy Nerves: Diabetic neuropathy
2 Types:
Proliferative &
Nonproliferative
Teach: to have annual
dilated eye examination
Teach: to get screened
annually for albuminuria
(albumin-creatine ratio
from urine)
Sensory
Neuropathy
Autonomic
Neuropathy
Affects hands
and/or feet
bilaterally: pain
and numbness
Hypoglycemic
unawareness, delayed
gastric emptying
(gastroparesis),
constipation, diarrhea,
urinary retention, &
sexual dysfunction

55. ASSESSMENT SCREENING
LABORATORY TESTS
DIABETES
MELLITUS
A1C TEST
FASTING BLOOD SUGAR TEST
GLUCOSE TOLERANCE TEST
RANDOM BLOOD SUGAR TEST
KETONURIA
GLUCOSE SCREENING TEST
SELF-MONITORING OF
BLOOD GLUCOSE
(SMBG)
 Increased frequency of
intak
e
fatigue
,
urination (polyuria)
 Increased thirst or fluid
intake (polydipsia)
 Weight loss despite hunger
 Increased food
(polyphagia)
 Family history
 Weakness
and dizziness
 Recurrent blurred
vision
 Pruritis,skin
infections,vaginiti
s
Type 1 Diabetes Mellitus
 Ketonuria
Type 2 Diabetes Mellitus
 Obese
 GUIDELINES FOR
TESTING FOR DM
 GUIDELINES
FOR
DIAGNOSIS OF
DM
Result* A1C Test
Fasting
Blood
Sugar Test
Glucose
Tolerance
Test
Random
Blood
Sugar Test
Diabetes
6.5% or
above
126 mg/dL
or above
200 mg/dL
or above
200 mg/dL
or above
Prediabetes
5.7 –
6.4%
100 – 125
mg/dL
140 – 199
mg/dL
N/A
Normal
Below
5.7%
99 mg/dL
or below
140 mg/dL
or below
N/A
SITUATION Recommended self-monitoring times and frequency
Person being treated with four or more insulin injections per
day, or with an insulin pump
At least 4 blood glucose readings per day (before meals, at
bedtime and, in certain circumstances, 2 hours after a meal
and when any other situation presents a risk of hypoglycemia)
Person with type 2 diabetes being treated with a single insulin
injection per day and antidiabetic medication
At least 1 blood glucose reading per day at different times of
the day (fasting, before meals, 2 hours after a meal or at
bedtime)
Person with type 2 diabetes being treated with insulin
secretagogues (gliclazide (Diamicron and Diamicron MR),
glimepiride (Amaryl), glyburide (Diabeta), repaglinide
(GlucoNorm)
At the first sign of hypoglycemia
Person with type 2 diabetes being treated with antidiabetic
medication with no hypoglycemia or lifestyle risks
Generally not required, except in specific situations
Type 2 diabetes screening
Type 2 diabetes testing should be
done in all asymptomatic adults
who are overweight or obese (BMI
≥ 25 or ≥ 23 in Asian Americans)
and who have one or more
diabetes risk factors.
For all other patients, testing
should begin at age 45 years. If
results are normal, testing should
be repeated at minimum of three-
year intervals with more frequent
testing depending on initial results
and risk status.
Prediabetes screening
The ADA recommends that testing should begin at age 45 for all people. Testing
for prediabetes and risk for future diabetes in asymptomatic people should be
considered in adults of any age who are overweight and who have one or more
additional risk factors for diabetes. Prediabetes testing can be done using Hgb
A1C, FPG, or 2-h PG after 75-g OGTT.
In addition, the ADA recommends that prediabetes testing should be
considered in children and adolescents who are overweight/obese and have
two or more diabetes risk factors. .

56. DM TYPE 1
&2
MICROVASCU
LAR
COMPLICATIO
NS
MACROVASCULAR
COMPLICATIONS
MANAGEMEN
TS
 Plan a Physical
Activity Program
 Prevent Complications from
Physical Activity
 Provide Instructions on
Blood Glucose Monitoring
 Provide Instruction on
Insulin Administration
 Surgical Client
 DIET
 EXERCISE
S
 MEDICATI
ON
 DIABETIC
RETINOPATHY
 DIABETIC
NEPHROPATHY
 DIABETIC
NEUROPATHY
 CAD
 CEREBROVASCULAR
DISEASE
 HYPERTENSION
 PERIPHERAL VASCULAR
DISEASE
 INFECTIONS
MEDICAL
MANAGEMENT
NURSING
INTERVENTI
ON
COMPLEMENTARY &
ALTERNATIVE
THERAPY FOR DM
Bariatric Surgery: Type 2 DM
with BMI > 35 kg/km²
Pancreas Transplantation: Type
2 DM; with end-stage kidney
disease & having kidney
transplant

57. Understanding
Insulin Therapy:
Onset Peak Duration

58. Problems associated
with
Insulin Therapy:
1. Lipodystrophy May occur if same injection sites are used frequently.
2. Somogyi Effect
Elevated morning glucose level – rebound cause by
hypoglycemia during night that stimulates
counterregulatory response.
3. Dawn Phenomenon
Hyperglycemia that is present on awakening in the morning,
resulting from the release of counterregulatory hormones in
the predawn hours.
4. Hypoglycemia
Poorly times insulin administration; inappropriate use of
insulin; increased glucose utilization following exercise
5. Allergic reactions
Rare; symptoms occur immediate after injection (urticaria,
angioedema, pruritus, bronchospasm)

59. Drug Therapy: Oral & Noninsulin Injectable Agents
Oral Agents Drug Name Action
1. Metformin
Glucophage, Glumetza,
Fortamet, Riomet
- Biguanide glucose lowering-agent
- Primary action: reduce glucose production in
liver
- 1st Line of Therapy: metformin + lifestyle
interventions
2. Sulfonylureas
Amaryl (glimepiride),
Diabinese
(chlorpropamide), Glucotrol
(glipizide)
- Increase insulin production from the pancreas
- Can cause hypoglycemia: teach pt. how to
recognize & manage low blood glucose
- Added with Metformin; lifestyle interventions
are not effective
3. Meglitinides Repaglinade
- Increase insulin production from the pancreas
- Reduced potential for hypoglycemia: more
rapidly absorbed & eliminated
- Taken before meals; dosing TID
4. α-Glucosidase Inhibitors Acarbose
- aka “starch blockers”
- slowing down absorption of carbohydrates in
the small intestines
5. Thiazolidinediones
Pioglitazone (Actos),
Rosiglitazone (Avandia)
- Most effective: insulin resistance
- Severe adverse effects, rarely used (edema,
weight gain, chest pain, hypoglycemia)
6. Dipeptidyl peptidase IV
(DPP – 4) Inhibitors
Sitagliptin, Saxagliptin,
Vildagliptin, Linagliptin
- Slow degradation of incretin hormone GLP-1 ->
inhibited secretion of glucagon, increased
insulin secretion, slow gastric emptying, &
decreased appetite
7. Sodium-glucose co-
transporter 2 (SGLT2)
Inhibitors
Dapagliflozin, Empagliflozin
- Decrease renal glucose reabsorption & increase
urinary glucose excretion
Noninsulin
Injectable Agents
Drug Name Action
1. Glucagon-like
peptide (GLP)-1
receptor Antagonist
Dulaglutide
(Trulicity),
Exenatide
(Byetta)
- Target incretin hormones
- Improve blood glucose levels &
have additional effect of reducing
body weight
2. Pramlintide Symlin
- Synthetic analog of human
amylin, hormone secreted by β
cells of pancreas
- Only taken concurrently with
insulin & its use can improve
blood glucose levels
- -given before each major meal

60. Gonads

61. Hormones Target Tissue Functions
Gonads
Women: Ovaries
Estrogen Reproductive system,
breasts
Stimulates development of secondary
sex characteristics, preparation of
uterus for fertilization and fetal
development. Stimulates bone growth.
Progesterone Reproductive system Maintains lining of uterus necessary for
successful pregnancy.
Men: Testes
Testosterone Reproductive system Stimulates development of secondary
sex characteristics, spermatogenesis.

62. Pineal Gland

63. Hormones Target Tissue Functions
Pineal Gland
Melatonin (anti-oxidant) Various tissues Regulates sleep-wake cycles
(circadian rhythm); may play a
role in influencing reproductive
processes

64. ● https://www.ck12.org/c/biology/endocrine-glands/lecture/The-
Endocrine-System-Explained-in-Under-Four-Minutes/
● https://www.ck12.org/c/biology/endocrine-glands/lesson/Glands-BIO/
● http://inside.mines.edu/~nstambac/Body%20Systems%20Lesson%20Pla
n.pdf
● http://inside.mines.edu/~nstambac/Body%20Systems%20Lesson%20Pla
n.pdf
● https://link.springer.com/chapter/10.1007/978-4-431-54490-6_3
● https://nursekey.com/nursing-assessment-endocrine-system/
● https://columbiasurgery.org/conditions-and-treatments/primary-
hyperaldosteronism-conns-
syndrome#:~:text=Primary%20hyperaldosteronism%20is%20diagnosed%
20by,will%20be%20low%20or%20undetectable.
● https://www.cdc.gov/diabetes/basics/getting-
tested.html#:~:text=Fasting%20Blood%20Sugar%20Test,higher%20indica
tes%20you%20have%20diabetes.
REFERENCES

65. Evaluation Test

66. 1) The nurse is caring for a patient recently started on levothyroxine
for hypothyroidism. What information reported by the patient
requires immediate action?
A. Weight gain or weight loss
B. Chest pain and palpitations Correct
C. Muscle weakness and fatigue
D. Decreased appetite and constipation

67. Correct answer: B. Chest pain and palpitations Correct
Levothyroxine is used to treat hypothyroidism. With
replacement, the patient can be overmedicated, causing
hyperthyroidism. Any chest pain, heart palpitations, or heart rate
greater than 100 beats/min experienced by a patient starting
thyroid replacement should be reported immediately, and
electrocardiography and serum cardiac enzyme tests should be
performed.

68. 2) The nurse is caring for a patient after a parathyroidectomy. The nurse
would prepare to administer IV calcium gluconate if the patient exhibits
which clinical manifestations?
A. Facial muscle spasms and laryngospasms Correct
B. Tingling in the hands and around the mouth
C. Decreased muscle tone and muscle weakness Incorrect
D. Shortened QT interval on the electrocardiogram

69. Correct answer: A. Facial muscle spasms and laryngospasms
Nursing care for a patient after a parathyroidectomy includes
monitoring for a sudden decrease in serum calcium levels
causing tetany, a condition of neuromuscular hyperexcitability.
If tetany is severe (e.g., muscular spasms or laryngospasms
develop), IV calcium gluconate should be administered. Mild
tetany, characterized by unpleasant tingling of the hands and
around the mouth, may be present but should decrease over
time without treatment. Decreased muscle tone, muscle
weakness, and shortened QT interval are clinical
manifestations of hyperparathyroidism.

70. 3) The nurse is caring for a patient receiving high-dose oral
corticosteroid therapy after a kidney transplant. Which
potential side effect presents the greatest risk?
A. Infection Correct
B. Low blood pressure Incorrect
C. Increased urine output
D. Decreased blood glucose

71. Correct answer: A. Infection
Side effects of corticosteroid therapy include increased
susceptibility to infection, edema related to sodium and water
retention (decreasing urine output), hypertension, and
hyperglycemia.

72. 4) What should be included in the interprofessional plan of
care for a patient with Cushing disease?
A. Lab monitoring for hyperkalemia
B. Vital sign monitoring for hypotension
C. Counseling related to body image changes Correct
D. Diet consultation to determine low protein choices

73. Correct answer: C. Counseling related to body image changes
Elevated corticosteroid levels can cause body changes,
including truncal obesity, moon face, and hirsutism in women
and gynecomastia in men. Counseling and support should be
offered because of the changes in body image. Hypokalemia
and hypertension are consistent with Cushing disease.
Sodium restriction and potassium supplementation are
indicated. High protein choices are necessary to counteract
catabolic processes and assist with wound healing

74. 5) The patient in the emergency department after a car accident is
wearing medical identification listing Addison’s disease. What
should the nurse expect to be included in the care of this patient?
A. Low-sodium diet
B. Increased glucocorticoid replacement Correct
C. Limiting IV fluid replacement therapy
D. Withholding mineralocorticoid replacement

75. Correct answer: B. Increased glucocorticoid replacement
The patient with Addison’s disease needs lifelong glucocorticoid
and mineralocorticoid replacement and has an increased need with
illness, injury, or stress, as this patient is experiencing. The patient
with Addison’s may need large volumes of IV fluid replacement and
a high-sodium diet. Withholding mineralocorticoid replacement
cannot be done for patients with Addison’s disease.

76. 6) The patient with systemic lupus erythematosus is diagnosed with
syndrome of inappropriate antidiuretic hormone (SIADH). What should
be included in the plan of care (select all that apply.)?
A. Obtain weekly weights.
B. Limit fluids to 1000 mL/day. Correct
C. Monitor for signs of hypernatremia. Incorrect
D. Administration of diuretics as ordered. Correct
E. Minimize turning and range of motion.
F. Keep the head of the bed at 10 degrees or less
elevation. Correct

77. Correct answer: B. Limit fluids to 1000 mL/day. ; D. Administration of
diuretics as ordered. ; F. Keep the head of the bed at 10 degrees or less
elevation.
The care for the patient with SIADH will include limiting fluids to
1000 mL/day or less to decrease weight, increase osmolality, and
improve symptoms and keeping the head of the bed elevated at 10
degrees or less to enhance venous return to the heart and increase
left atrial filling pressure, thereby reducing the release of ADH.
Measure weights daily and maintain accurate intake and output.
Monitor for signs of hyponatremia. Frequent turning, positioning,
and range-of-motion exercises are important to maintain skin
integrity and joint mobility.

78. 7) The nurse is teaching a patient who has diabetes about
vascular complications of diabetes. What information is
appropriate for the nurse to include?
A. Macroangiopathy does not occur in type 1 diabetes but
rather in type 2 diabetics who have severe disease.
B. Microangiopathy is specific to diabetes and most commonly
affects the capillary membranes of the eyes, kidneys, and
skin. Correct
C. Renal damage resulting from changes in large- and medium-
sized blood vessels can be prevented by careful glucose
control.
D. Macroangiopathy causes slowed gastric emptying and the
sexual impotency experienced by a majority of patients with
diabetes.

79. Correct answer: B. Microangiopathy is specific to diabetes and most
commonly affects the capillary membranes of the eyes, kidneys, and
skin.
Microangiopathy occurs in diabetes mellitus. When it affects the
eyes, it is called diabetic retinopathy. When the kidneys are
affected, the patient has nephropathy. When the skin is affected,
it can lead to diabetic foot ulcers. Macroangiopathy can occur in
either type 1 or type 2 diabetes and contributes to
cerebrovascular, cardiovascular, and peripheral vascular disease.
Sexual impotency and slowed gastric emptying result from
microangiopathy and neuropathy.

80. 8) The nurse is evaluating a patient diagnosed with type 2
diabetes mellitus. Which symptom reported by the patient
correlates with the diagnosis?
A. Excessive thirst Correct
B. Gradual weight gain Incorrect
C. Overwhelming fatigue
D. Recurrent blurred vision

81. Correct answer: A. Excessive thirst Correct
The classic symptoms of diabetes are polydipsia (excessive
thirst), polyuria, (excessive urine output), and polyphagia
(increased hunger). Weight gain, fatigue, and blurred vision may
all occur with type 2 diabetes, but are not classic manifestations.

82. 9) The newly diagnosed patient with type 2 diabetes has been
prescribed metformin. What should the nurse teach the patient
to best explain how this medication works?
A. Increases insulin production from the pancreas
B. Slows the absorption of carbohydrate in the small
intestine
C. Reduces glucose production by the liver and enhances
insulin sensitivity
D. Increases insulin release from the pancreas, inhibits
glucagon secretion, and decreases gastric emptying

83. Correct answer: C. Reduces glucose production by the liver and
enhances insulin sensitivity
Metformin is a biguanide that reduces glucose production by the
liver and enhances the tissue’s insulin sensitivity. Sulfonylureas
and meglitinides increase insulin production from the pancreas.
α-Glucosidase inhibitors slow the absorption of carbohydrate in
the intestine. Glucagon-like peptide receptor agonists increase
insulin synthesis and release from the pancreas, inhibit glucagon
secretion, and decrease gastric emptying.

84. 10) The nurse teaches a patient recently diagnosed with
type 1 diabetes mellitus about insulin administration. Which
statement by the patient requires an intervention by the
nurse?
A. “I will discard any insulin bottle that is cloudy in
appearance.” Correct
B. “The best injection site for insulin administration is
in my abdomen.”
C. “I can wash the site with soap and water before
insulin administration.”
D. “I may keep my insulin at room temperature (75oF)
for up to 1 month.”

85. Correct answer: A. “I will discard any insulin bottle that is cloudy in
appearance.”
Intermediate-acting insulin and combination-premixed insulin will
be cloudy in appearance. Routine hygiene such as washing with
soap and rinsing with water is adequate for skin preparation for
the patient during self-injections. Insulin vials that the patient is
currently using may be left at room temperature for up to 4 weeks
unless the room temperature is higher than 86°F (30°C) or below
freezing

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