Endocrine Disorders
- ASTH: adrenocorticotropic hormone
Physiology
- Regulates functions in the body in response
to CNS detects internal and external stimuli
and send signals to endocrine system
- CNS responsible to regulation of function
- Hormones goes into the bloodstream
- Exocrine glands; secrete directly into
mucosal surface (epithelial surface) derecho
sa skin, oral mucosa, gastric mucosa, does
not agi sa blood stream
Goal of the (-) feedback loop is to maintain balance
(homeostasis)
Main regulating organ:
- pituitary gland (master gland)
- Assisted by the hypothalamus
Pineal gland:
- Secretes melatonin
Pituitary gland
- Has stimulating hormones
Posterior pituitary secretes vasopressin (ADH)
and oxytocin
Anterior pituitary secretes several hormones
- TSH: thyroid stimulating hormone AKA
thyrotrophin -> creates thyroid hormone
↓ in T4 and T3 will be felt or detected by
hypothalamic pituitary portal circulation
- Once detected, the message is to increase
the production of thyroid hormones
↑ in T4 and T3 the pituitary gland will message the
thyroid gland to decrease the function of TSH
(messenger) known as negative feedback loop
- LH and FSH: stimulates the gonads, follicle
stimulating hormone
- GH: growth hormone: somatotropin
Hypothalamus
- Link between the pituitary gland and the
other endocrine glands
- Can detect the increase and decrease of
hormone levels
- Is the one who releases releasing
hormones
- Hypothalamus is the one who messages
the pituitary gland into the end organs
- Hypothalamic pituitary axis
Diagnostic Modalities to diagnose patients with
endocrine disorders
Blood tests
- Hormone levels in the blood or the plasma
Urine tests
- Detects hormone levels
Stimulation tests
- Detects hypofunction of the gland
- Eg. stimulates the hypo function and the
response is to increase the production of
thyroid hormones; yet if naga hypofunction
nd mag respond ang thyroid hormone and
will just continue to decrease (amo na ma
detect if naga hypofunction gid man)
Suppression tests
- Assess the hyperfunction of the gland
- Eg. patient is hyperthyroid then if
suppression test is done, it is to decrease
the thyroid hormones; the normal response
to the suppression test would be to
decrease the production of thyroid
hormones; yet if the organ is abnormally
hyperfunctioning– it will not respond to the
suppression test, it will not respond to the
stimulus
Endocrine Disorders

Thyroid

Main function of the thyroid hormone is to control

Thyroid gland
- is highly vascular
- Produces T4, T3, calcitonin
- Anterior to trachea
- Anterior to esophagus
- Anterior most to the neck and its back is
trachea and likod sang trachea is the neck
- Highly vascular than liver
T3 and T4
- Iodine containing
- Amino acid hormones
- Bound to proteins for storage and transport
- TBG: thyroid binding globulin AKA as the
protein for storage and transport
- Eg. T3 and T4 will ride TBG (not yet
functioning util reached the target organ)
from thyroid gland and will go through the
bloodstream then if it is going to CVS the
TBG will become active kay na naog na si
T3 and T4
cellular metabolic activity
T4: thyroxine; weak
T3: thriiodonine is 5x potent as T4 (active)
Calcitonin/thyrocalcitonin
- Thyroid inhibits the excess calcium in the
blood into the bones to decrease the blood
calcium levels to maintain a normal level of
ca in the blood
- Normal value of calcium in the body: 8-10
mg/dL
- ↓ 8 mg/dL: hypocalcemia
- ↑ 10 mg/dL: hypercalcemia
- In mmol/L: normal value is 2-25

Pharmacology
Highly protein bound -> less bioavailability

TSH
- Thyroid stimulating hormone otherwise

This happens in the metabolism if there is an

increase and decrease in the thyroid hormone
levels

- known as thyrotropin
- EU means normal
Hyperthyroidism

Thyrotoxic crisis
Endogenous: means that thyroid hormone came
- Exaggerated state
from the production of the body
Hyperpyrexia: fever
- From the body’s own production of hormone
More than 38 degree celsius
Exogenous: patient might have taking levothyroxine
Extreme tachycardia: more than 120-130 bpm
or synthetic thyroid hormones causes excess of the
Altered sensorium: patient is lethargic
hormones
Complications
Grave’s disease
- Ig is similar with TSH
Myocardial hypertrophy
- Autoimmune disease
Heart Failure

Pathophysiology
Assessment and Dx
IPPA

Thyroid storm/ thyrotoxic crisis

Decreased serum TSH in the blood

FNAB: fine needle aspiration biopsy

Caloric consumption
Exophthalmos: caused by a deposition of
polysaccharides retro orbitally; Pushing the eyeball
outward
Sinus: normal rhythm
Arrhythmias: abnormal, disturbance in rhythm
Antithyroid agents:
- PTU: 1st trimester during pregnancy is the
organogenesis; hepatotoxic
- methimazole (teratogenic) after few months

Beta Blockers:
- Propranolol
- ‘--lol’
- Given because the patients presents
tachycardia, for symptomatic palpipations
 - Radioactive iodine (recommended Pathophysiology
treatment): slowly tries to kill the thyroid
cells since thyroid loves iodine; decrease
the synthetic activity of the thyroid
- Surgery- thyroidectomy

Nursing Interventions

Advice to have protective eyewear

Cool environment
Advice to wear light clothing
Increase fluid intake due to perspiration
Nutrient-dense food Decrease in the production of the thyroid
Regulate daily activities hormones
Monitor cardiac function, rhythm (ECG)
Monitor weight Clinical Manifestations
NCRRR: normal cardiac rate with regular rhythm
Thyroidectomy POST-OP
- Soaked dressing
- Avoid hyperextension of the neck
- Calcium gluconate (for hypocalcemia), also
prepare tracheostomy set
- Check hoarseness of voice; there might
have been iatrogenic damage, the recurrent
laryngeal nerve (RLN)
Radioactive Iodine
- Double flush toilet
- Patient is still radioactive

Hypothyroidism (hashimoto disease)

Sobrahan ka anti-thyroid medication;

nasobrahan ka decrease in thyroid hormone

Damages the thyroid cells - hashimoto

Primary
- Thyroid gland itself problem
Secondary
- Problem in the pituitary gland
Tertiary
- Hypothalamus regulation in the
hypothyroidism

Myxedema
- Untreated; extreme symptoms

Atherosclerosis
- Athero (ma tambok nga na deposit sa ugat)
- Sclerosis lost elasticity and ugat
Assessment and Dx
- 60-70 years
Serum TSH - Half of the diagnosed cases do not have
Primary hypothyroidism cannot produce thyroid symptoms
hormones well - Secondary hyperparathyroidism: occurs
- ↑ TSH level in patient of have CKD as a result of
phosphorus retention
T3 and T4 levels ↓ CKD has decreased urinary output that is why
phosphorus is not excreted in the body causing
UTZ increase blood levels of serum phosphorus, also
FNAB Ca increases that comes along with the
Thyroid scan phosphorus in the kidney

Medication Pathophysiology

levothyroxine (synthetic agent)

- Increases thyroid hormone levels

Nursing Interventions

Skin moisturizer
Caution when giving sedatives
Semi-fowlers position to improve efficiency of
ventilation
Provide a warm environment (woolen blanket)
Attach to cardiac monitor due to bradycardia
Monitor for myxedema and sensorium
Provide bedrest but encourage self care activities
with rest periods
Include mobility with the activities (weight bearing Clinical Manifestations similar to hypercalcemia
activities stimulates the bone not to decrease
calcium) May be asymptomatic
High fiber diet Apathy
Emphasize the need for iodized salt Fatigue
Muscle weakness
Parathyroid Nausea
Vomiting
Constipation
Hypertension
Cardiac arrhythmias
Psychological changes
Nephrolithiasis
Benign bone tumors: osteoclast origin
Bone pain
Pathologic fractures: nabali tungod kay may
masakit
Parathyroid gland creates -> PTH or parathormone Deformities
(pagwaon sa bone ang Ca) ↑ Ca in the blood but
opposite in phosphorus (secretin it in the urine) Assessment and Diagnostics

Hyperparathyroidism S. Ca
- Caused by overproduction of parathormone Radioimmunoassays for parathormone
by the parathyroid glands X-rays: can see that bone is less calcified, results
- Characterized by bone decalcification (Ca would be that the bone has less opacity (lasaw)
gina pa gwa sa bone) and development of Bone scan
calcium-containing kidney stones (super Double-antibody PTH test
saturation of Ca in the kidney creates Ca UTZ
containing bones) MRI
- 2F:M FNAB
Medical/ Surgical Treatment Assessment and Diagnostics

Parathyroidectomy Trousseau sign (troso)

- Kakson ang ga sobra nga PTH - Take patient BP first, kung pila ang systolic
- Outpatient basis BP and then add 20-30 mmHg, wait for 2-3
Observation may be done for asymptomatic minutes, the fingers will flex to knuckles if
patients (+)
Daily fluid intake of 2000mL or more (to dilute the Chvostek sign
excess calcium) - Tap the facial nerve ipsilateral itching
Mobilization (patient will half smile)
Restrict calcium in diet S. Ca
S. Phosphate
Nursing Intervention X-rays
- Hypermineralized (super white)
Daily fluid intake of 2000mL or more (to dilute the
excess calcium) Medical/ Surgical Treatment
Mobilization (weight bearing activities) with caution Goal: Increase S. Ca to 9-10mg/dL (2.2 to 2.5
Restrict calcium in diet mmol/L) and eliminate s/sx
MIO because of OFI
Pain management or medication as ordered Combination treatment: calcium, magnesium,
Safe environment bcos prone of pathologic fracture ergocalciferol (Vit D2) or calcitriol (Vit D3)
Thiazide diuretic
HYPOPARATHYROIDISM - urinates but will hold the Ca
Calcium gluconate
OVERVIEW Calm environment
- Patient will have spasm
- Opposite of hyperparathyroidism Possible tracheostomy/ mechanical ventilation
- Caused by abnormal parathyroid Bronchodilators
development, destruction of the parathyroid Calcium supplements
glands, and vitamin D deficiency Aluminum hydroxide/ aluminum carbonate
- Most common cause: near-total removal - Binds the phosphate to be released in the
of the thyroid gland GI tract
- Results in hyperphosphatemia and
hypocalcemia Nursing Intervention
- Hyperphosphatemia ↑ phosphate ↓ calcium
- Hypocalcemia ↓ phosphate ↑ calcium - ↑ Ca ↓ phosphate in the diet
- Cardiac monitoring
Pathophysiology - Vit D supplementation
- Provide calm environment
- Inverse of hyperparathyroidism - Adequate rest
- ↓ in the production of PTH
- ↓ circulating of PTH there is no one to Posterior Pituitary
withdraw sang calcium kay bone, wala may Vasopressin (ADH)
ma pugong sa ihi, kag sa kinakon Oxytocin
- ↓ calcium levels
DIABETES INSIPIDUS
Clinical Manifestations
- A rare disorder that occurs due to injury to
Hypocalcemia—tetany the hypothalamus or pituitary gland with a
Numbness, tingling, cramps in the extremities deficiency of ADH that results in excretion of
Bronchospasm large volumes of dilute urine, and extreme
Laryngeal spasm thirst
Carpopedal spasm - May be characterized as central (problem
Dysphagia with the pituitary gland), nephrogenic (good
Photophobia production of ADH yet kidney is the
Cardiac arrhythmias problem), or dipsogenic (hypothalamus is
Seizures the problem causes extreme causes), as
Psychological changes well as gestational (caused by placental
secretion of vasopressin)

Pathophysiology
- Diabetes Indi ka produce ADH
- Less production of ADH (antidiuretic
hormone); prohibits urination
- Physiologically the ADH will produce water
in the body
- ↑ in plasma osmolality due to increase
urination
- Urine: decrease in specific gravity (lapoyot)
and osmolarity
- Normal plasma osmolality 275-295
mosm/kg
- Sp. g for urine is ↓ 1.005 (lasaw ang dugo) ↑
1.020 (lapoyot and dugo)
Clinical Manifestations
Large urine output (>250mL/hr); normal for 60 kg
person– 30 ml/hr
Very dilute urine (Specific gravity 1.001 to 1.005)
Intense thirst
Assessment and Diagnostics
Fluid deprivation test
Measurements of plasma levels of ADH
Urine and plasma osmolality
Desmopressin trial: whether DI is central or
nephrogenic
IV infusion of hypertonic saline
Medical/ Surgical Treatment
Objectives: replace ADH, ensure adequate fluid
replacement, and identify and correct the
underlying pathology
Desmopressin for central DI; give what is
lacking
Chlorpropamide; antidiabetic drug, increase
production of beta islet cells, increase the receptor
of desmopressin (given with caution)
Thiazide diuretics; same supportive role with
chlorpropamide
Mild salt depletion
Prostaglandin inhibitors; attack the receptor of ADH
in the kidneys
Nursing Intervention
Strict MIO
Increase OFI/hydration
Patient education of medication compliance
SYNDROME OF INAPPROPRIATE ADH
SECRETION (SIADH)
- Results from a failure of the negative
feedback system that regulates the release
and inhibition of ADH
- Patients cannot excrete a dilute urine—
dilution hyponatremia (more water than salt)
- Often of non-endocrine origin
- Malignancy is in the lungs
Clinical Manifestations
Subnormal urine output
Concentrated urine
Gamay ihi and lapoyot pa
↓ 30 cc/h
↓ 0.5 - 1 cc/kg/h
Assessment and Diagnostics
Measurements of plasma levels of ADH
Urine and plasma osmolality
Medical/ Surgical Treatment
Generally self-limiting; treatment is focused on
eliminating the
underlying cause
Fluid restriction
Diuretics (kay indi ka ihi)
3% NaCl (severe hyponatremia)- high salt diet
Serum Sodium Level: 135-145 mEq/L
Gradual correction of sodium
Nursing Intervention
Strict MIO
Fluid restriction
Daily weight monitoring (same time/clothing each
day)
Neuro vital signs (patient’s neurologic)
ADRENAL DISORDERS
Each person has 2 adrenal glands, superior to
each kidney
Adrenal medulla: center of the gland; secretes
catecholamines
Adrenal cortex: outer portion; secretes steroid
hormones
Regulated by the HPA axis
Adrenal Medulla
- Functions as a part of the ANS - autonomic
nervous system
- Located at the center; secretes
catecholamines
- Catecholamines regulate metabolic
pathways to promote catabolism of stored
fuel to meet caloric needs from endogenous
sources
- 90% of its secretion is epinephrine
- “Fight-or-flight response” (SNS)
- Promote catabolism of sympathetic
response
Effect - stimulation of sympathetic response
SNS - sympathetic nervous system
- Amputate bodily systems that are needed in
emergency situation
- Stimulate responses such as HR, RR,
increases blood flow in skeletal muscle,
dilated pupil, shutdown/decrease GUT
response
PHEOCHROMOCYTOMA
● A rare tumor that is usually benign and
originates from the chromaffin cells of the
adrenal medulla
● Cause of high BP in 0.1% of patients with
hypertension
● Usually fatal if undetected and untreated
● Arises in the adrenal medulla in 90%; may
occur in extra-adrenal chromaffin tissue
● 10% occurs bilaterally; 10% are malignant
● Familial occurrence; may occur as part of
MEN type 2
● May occur at any age; peaks between 40
and 50
● F=M
Pathophysiology
Normal adrenal gland
- Secretes catecholamine
With pheochromocytoma
- If it has a catecholamine producing tumor it
does not correspond with the SNS
- ↑ circulating levels of catecholamine
- ↑ in basal metabolic rate
- ↑ oxygen consumption
Clinical Manifestations Pre-op: low dose alpha blocker (terazosin)
May use beta blockers or CCB
Triad: headache, diaphoresis, palpitations Adrenalectomy - tumor removal
Hypertension, and other cardiovascular IV or oral corticosteroids post adrenalectomy to
disturbances avoid addisonian crisis
Tremors
Flushing Nursing Intervention
Anxiety
Hyperglycemia Monitor VS esp BP
Orthostatic hypotension MIO
Provide a calm/environment to avoid stimulation of
Clinical Manifestations 5 H’s SNS
CBG monitoring for hypoglycemia
Hypertension POST-OP
Headache - Fluid & electrolyte balance monitoring
Hyperhidrosis - Monitor for addisonian crisis
Hypermetabolism - Ensure a patent IV access for emergency
Hyperglycemia (IV reserve drugs)

Clinical Manifestations (Paroxysmal form) Adrenal Cortex

Acute, unpredictable attacks lasting seconds to Secretions make it possible for the body to adapt to
several hours; symptoms usually begin abruptly stress of all kinds
and subside slowly
Extreme anxiety 3 layers
Tremors Mineralocorticoids (SALT): mainly aldosterone
Weakness - Zona glomerulosa (1st layer)
Headache
Vertigo Glucocorticoids (SUGAR): mainly cortisol
Blurring of vision - Zona fasciculata (middle layer)
Tinnitus
Air hunger Sex hormones (SEX): mainly androgens
Dyspnea - Andro - male
Polyuria - Zona reticularis (innermost layer)
Nausea
Vomiting Without the adrenal cortex, severe stress would
Diarrhea cause peripheral circulatory failure, circulatory
Abdominal pain shock, and prostration
A feeling of impending doom
BP may exceed 250/150mmHg Zona glomerulosa

Assessment and Diagnostics Mineralocorticoids: mainly aldosterone

Suspected if s/sx of SNS overactivity occur in
association with marked elevation of BP
Urine and plasma levels of catecholamines and
metanephrine could be measured
24H urine collection for MN and VMA (vanellel
mandelic acid)
Clonidine suppression test (does not improve the
BP of the patient and will come out positive) plasma
and urine tests are inconclusive
Imaging: CT, MRI, UTZ, scintigraphy
Medical/ Surgical Treatment
Goal: control HTN before and during surgery
Bed rest with head of the bed elevated
Volume expansion to prevent a catecholamine
storm
Major effects on electrolyte metabolism; increased
Na absorption in exchange for excretion of K or H
Ions
- Increase in serum sodium levels kay gina
hawiran ang sodium and a decrease in
serum potassium levels kay gina baylo ang
potassium and the hydrogen is acidic in
nature (excess H ion will lead to metabolic
alkalosis)
Main hormone for the long-term regulation of Na
balance
Triggers: RAAS, hyperkalemia
Renin angiotensin aldosterone system (RAAS)
Starts with kidney that has a low perfusion pressure
- BP of kidney is nubo
Kidney will produce renin
 - Liver produced angiotensinogen (precursor
hormone, inactive)
- If activated it will be angiotensin I (if this will
be activated it will make a way to lung
epithelium (there is ACE)
- ACE will be converted to angiotensin II
(more potent angiotensin, vasoconstrictor,
stimulate the production of aldosterone)
- Stimulate the effect of angiotensin II
- ↑ of aldosterone functions to retain fluid,
retain salt, excrete potassium, and has a
mild vasoconstrictive effect

RAAS NET EFFECT IS TO BASICALLY ↑ BP -

The one that triggers aldosterone production

Hyperkalemia can be a trigger of aldosterone

production In patients with Conn’s syndrome, it does not need
the stimulation of RAAS because it voluntarily
Adrenal Cortex produces aldosterone leading to increase Na
Zona fasciculata retention, increase K secretion, water retention,
hypertension
Glucocorticoids: mainly cortisol
Clinical Manifestations
Important influence on glucose metabolism
↑ cortisol = ↑ blood glucose levels Hypertension- most prominent, almost universal
Secreted in response to ACTH from APG sign of Conn’s
Negative feedback with CRH and ACTH Hypertension with/ without hypokalemia (excess
urination of potassium)
Adrenal Cortex s/sx of hypokalemia
Zona reticularis - Variable muscle weakness
Sex hormones: mainly androgens/testosterone - Paralysis
Exert effects similar to those of male sex hormones - Cramping
May secrete small amounts of estrogens - Fatigue
Controlled by ACTH Polydipsia
Hypocalcemia
One disease entity concerning the adrenal cortex is Glucose intolerance may occur
Primary Aldosteronism AKA Conn Syndrome
- The principal action of aldosterone is to Assessment and Diagnostics
conserve Serum Na (sodium)
- More K and H excretion Measure circulating hormone levels
- Etiologic factors: tumors of the adrenal Plasma aldosterone concentration
gland, ovarian tumors, family history Plasma renin activity bcos renin begins the
cascade
Aldosterone-renin ratio

Medical/ Surgical Treatment

Total removal of the tumor through

laparoscopic adrenalectomy
IV Corticosteroids
Weekly postop monitoring of Serum K levels
Spironolactone (drug of choice)
- K sparing diuretics
- Aldosterone antagonist
- Inhibits aldosterone function
Eplerenone
Nursing Intervention Muscle wasting
Osteoporosis
Provide rest periods Na and H2O retention
Serum electrolytes monitoring -> cardiac monitoring HTN, HF - hypertension and heart failure
if results is decreased Moon facies
Limit fluid intake - bcos function of aldosterone is Hyperglycemia/ overt diabetes
water retention Weight gain
Increase K in diet Slow healing of cuts or bruises
Reduce sodium Virilization
Decreased libido
CUSHING’S SYNDROME Distress and depression
Visual disturbances (if from pituitary tumor)
Use of corticosteroid medications (↑ intake of
asthma and hypersensitivity medication): the
most common cause of Cushing’s syndrome
AKA Cushing’s Disease
May be due to hyperplasia of the adrenal cortex,
pituitary tumor
May be from ectopic production of ACTH from
bronchial neoplasm

The Cushing’s syndrome might be a defect from

function in hypothalamus
↑ cortisol, salt, sugar, sex or all of the hormones
secreted by adrenal cortex
Normally hypothalamus detects the ↓ CRH, pituitary
↓ ACTH

Exogenous cause:
- Steroid hormones

Clinical Manifestations

Growth arrest
Obesity
Glucose intolerance
MSK changes
Central obesity
“Buffalo hump”
Thin, fragile skin
Ecchymoses and striae
Weakness
Assessment and Diagnostics

Serum cortisol
Urinary cortisol (24H urine collection)
Dexamethasone suppression test - takes
glucocorticosteroid will increase the circulating
hormones therefore should decrease the
production of CRH and ACTH; if the response is
correct then the adrenal glands overproduce
hormones
S. Na, S. K monitoring
Blood glucose levels (increase in cortisol could
increase in blood glucose level)

Medical/ Surgical Treatment

Surgical removal of the tumor (pituitary tumor)

Radiation of the pituitary gland - not too invasive
Adrenalectomy (unilateral primary adrenal
hypertrophy) - surgical tx, if the problem is within
the adrenal glands
Hydrocortisone post-op
Adrenal enzyme inhibitors (ectopic sources that
cannot be eradicated)
Reduction/tapering of corticosteroids (if caused by
steroid administration)
Insulin therapy and medication for PUD (peptic
ulcer disease bcos pt is high risk on developing
PUD when they have cushing’s)

Nursing Intervention

Reverse isolation - decrease unnecessary

exposure with people Clinical manifestations
Skin care due to fragile skin
Weight monitoring Excretion of Na, Cl, and H2O
CBG monitoring Retain K= Retention of K
Decrease salt and sugar Decreased CP
Increase K, Ca + Vit D in diet Hypoglycemia
Fall precautions Muscle weakness
Lethargy
Post op Anorexia
- Monitor for addisonian crisis Nausea and vomiting
- Psych support Weight loss
Hyperpigmentation of skin and mucous membranes
ADDISON’S DISEASE
Clinical Manifestations of Addisonian Crisis: A
Primary adrenal insufficiency life-threatening complication
- The result of dysfunction of the HPA Severe hypotension
feedback loop Cyanosis
- Autoimmune cause in 70-90% of cases Fever
- May be associated with tuberculosis or Nausea
histoplasmosis Vomiting
Secondary adrenal insufficiency Signs of shock
- May be the result of sudden cessation of Pallor
exogenous adrenocortical Headache
- hormonal therapy Abdominal pain
Diarrhea
Confusion
Restlessness Gluconeogenesis
- Will get fuel from noncarbohydrate stores
Assessment and Diagnostics (fats will be converted into glucose, and
Early-morning serum cortisol and plasma ACTH protein during prolonged fasting stage)
S. Na
S. K
Blood glucose FUNCTIONS OF INSULIN

Medical/ Surgical Treatment - Transports and metabolizes glucose for

energy
Restore circulation via administer fluids and - Stimulates storage of glucose in the liver
corticosteroids and muscle
Elevate legs - Signals the liver to stop the release of
IV hydrocortisone glucose
3-4L of PNSS or D5 (if hypoglycemic) containing - Enhances storage of dietary fat in adipose
solutions tissue
Vasopressors if hypotension persists - Accelerates transport of amino acids into
Antibiotics if with infection cells
Corticosteroid replacement - Inhibits breakdown of stored glucose,
protein and fat
Nursing Intervention
DM type 1
Monitor VS esp BP DM type 2 (most common)
Monitor electrolytes
Increase caloric dietary intake - Has no insulin
Monitor CBG - Characterized by the destruction of the
Standby vasopressors basi mag addisonian crisis pancreatic beta cells (the one that produces
pagid siya insulin, yet not functioning in DM 1)
Increase Na in diet - Combined genetic, immunologic, and
Decrease K in the diet possibly environmental factors are thought
to contribute to beta-cell destruction
DIABETES MELLITUS - Events that lead to destruction are not fully
understood
Diabetes: a group of metabolic diseases - DKA (diabetic ketoacidosis) is a metabolic
characterized by hyperglycemia resulting from derangement that occurs most commonly in
defects in insulin secretion, insulin action or both persons with DM type 1 and results from a
(CDC, 2020) deficiency of insulin
Number of people >20y.o diagnosed with diabetes - Hyperglycemia, ketosis, metabolic acidosis
increases yearly - Commonly preceded by a day or more of
Rate of prediabetes is steadily increasing among polyuria, polydipsia, nausea, vomiting, and
adults fatigue with eventual stupor and coma if not
Can cause: nontraumatic amputations, ESKD, treated
blindness and death - The breath has a characteristic fruity odor
Patients diagnosed with DM who are hospitalized bcos of ketones in the bloodstream that
with COVID-19 have been found to have a higher diffuses in the breath using pulmonary
rate of intubation and mortality circulation

Insulin is a hormone secreted by beta cells which

are one of the 4 types of cells in the islets of
Langerhans in the pancreas
- An anabolic hormone (ga store)
- During fasting, the pancreas continuously
releases a small amount of insulin;
glucagon is released when blood glucose
levels decrease, stimulating the liver to
release stored glucose
 Clinical Manifestations
Healthy
- Insulin molecules binds with the glucose to Depend on the level of hyperglycemia
allow it to enter the cells and will become Classic (3P’s):
glycogen as fuel storage polyuria, polydipsia, and polyphagia
Fatigue
Diabetic 1 Weakness
- No insulin bcos beta cells is damage Sudden vision changes
- Bcos it cannot enter the cell it stays in the Tingling or numbness in hands or feet
bloodstream causes hyperglycemia Skin lesions that are slow to heal
Recurrent infections
DM TYPE 2
- Occurs more commonly among people >30
years old and who have obesity
- Incidence is rapidly increasing in younger
people
- Resistant ang insulin sa cells - indi mag
baton ang cells sang insulin
- 2 main problems: insulin resistance and
impaired insulin secretion
- To overcome insulin resistance and to
prevent the buildup of glucose in the blood,
increased amounts of insulin must be
secreted to maintain the glucose level at
normal or slightly elevated
- Insulin resistance may also lead to
metabolic syndrome (pseudo syndrome)

HYPERGLYCEMIC HYPEROSMOLAR
SYNDROME (HHS)

HHS is a serious condition in which hyperosmolality

and hyperglycemia predominate, with alterations of
the sensorium
Ketosis is usually minimal or absent
Persistent hyperglycemia causes osmotic diuresis,
which results in loses of water and electrolytes -
kidney has threshold few mg of glucose; liver
cannot filter it causes glycosuria -> will cause
osmotic dialysis; more concentrated urination
causes lose of water and electrolytes
Assessment and Diagnostics
To maintain an osmotic equilibrium, water shifts
from extracellularly
FBS
RBS
2H postprandial glucose
HbA1c
Lipid profile
S. Crea
Urinalysis
ECG

Treatment
Goal: normalize insulin activity and blood glucose
to reduce the development of complications
No cure for DM only can be controlling blood
glucose level and improve insulin resistance
Nutritional therapy 50-60% carbs - low glycemic
index; gradually increases blood sugar
Exercise 3-4 times a week with caution
250 mg/dL prone to DKA
Oral antidiabetic agents (sulfonylurea)
Insulin therapy

Nursing Intervention

Patient education - compliance to medication

Diet
Educate about the complication
Importance of foot care
Importance of exercise
Disturbances in Musculoskeletal Function

Musculoskeletal system
● Composed of bones, joints, muscles, tendons, ligaments, and bursae
● Major functions: support and protection and motion
● Other functions: maintain body temperature (increases metabolic rate), facilitates
circulation (improves venous return to the heart), reservoir for immature blood cells and
essential minerals
● MSK disorders and injuries directly affect the quality of life of an individual
● Has vascular and nerve supplies.

Skeletal system:
● 206 bones in a normal adult
● 300+ bones before infusion in infancy
ga angot
● Axial (forms the base; where vital organs are placed–skull etc.) and appendicular
skeleton (extremities)
● Cancellous bone, cortical bone
carpal, tarsals
● Long bones, flat bones, irregular bones, sesamoids (patella; acts as a pulley)
● Periosteum, endosteum largest sesamoid; better pull of
● Joints and articular cartilage water

growth plates occur

metaPhysis- growth plates spongy appearance
● Cancellous bone (may pores na inside sang
bone; loosely pack cells; soft), cortical bone (shaft;
more densely pack; hard)
● Periosteum (protective covering or membrane;
attaches blood supply), endosteum (inner part) of bone
● Articular cartilage- acts as a cushion or
protection in joints.; white shiny part

Muscular system:
Contributes to motion
● Flexion and
extension
● Internal and
external rotation
● Abduction and
adduction
● Circumduction
● Inversion and
eversion

Assessment IPPA (InPaPeA)

● Gait (inspection) how the patients walk
○ Normal or limping gait or ga piang
● Spinal curvature (posture)
○ Cervical and lumbar curvature are
normally lordotic posture– the
convexity is facing anteriorly
tubang ang ulbo
preggy pt spine curvatures
 ○ Thoracic and sacral curvature are normally kyphotic–the convexity of the
curvature is facing posteriorly. pa buktot
inspection ● Deformities, lesions (obvious upon inspection)
palpation ● Tenderness, crepitations, masses- note location, size, consistency (palpation)
● ROM, strength (special)
● Sensation
● Tissue viability (capillary refill time in less than 2 seconds- normal)

Diagnostic modalities
● Blood studies
● Radiography
● CT Scan
● MRI
● UTZ
● EMG, NCV
● DEXA scan
● Bone scan
● Arthrocentesis
● Arthroscopy
● Biopsy

Trauma
● Traumatic injuries: tissue damage of varying severity that occur suddenly from external
forces
● May be blunt (wala pelas, doesn’t have clean cut) or penetrating (may blood)
● May or may not be life-threatening
● E.g. contusions, lacerations/ incisions, abrasions (scrapes), avulsions, fractures,
dislocations
Fracture
● A break in the continuity of the bone; cortical break with corresponding damage to
surrounding soft tissue.
○ Radio dense part- cortex
○ Radio loosen part- medullary canal
● May be open or close
● Fracture–there is a break in the cortex, due to a break in the bone–there will be bleeding
on it called fracture hematoma.
○ Open fractures warrant admission for surgical debridement and antibiotics
○ Close fracture- doesn't have a cut penetrating outside
● Fracture bleeding- oozing, fat globules (oily)
○ Dress appropriately
○ Apply a splint
○ Send to a tertiary institution (ASTP)
● Venous bleeding- not oily/ fat globules
● Regular wound bleeding- pressure could stop the bleeding
● May be complete or incomplete

Dislocation
● No break in the continuity of the cortex. ONLY Complete separation of 2 bones from their
articulation
○ May be simple( wala bale) or complex (fracture dislocation; nautod pag dislocate)
● Subluxation: partial separation
● Dislocation: Complete separation/ distraction

Clinical manifestations:
 ● May have an obvious deformity (especially for dislocation)
● Pain and tenderness (acute)
● Swelling and hematoma
● Limitation in ROM (range of motion is affected)
● If ma ipit ang nerves
○ +/- paresthesias
○ +/- pulselessness

Complications (emergency)
● Nerve or vascular damage
● Malunion- bale nga nag ayo pero wala na align sakto
● Nonunion- bale that does not heal yet no pain
● Infection
● Acute Compartment syndrome- increased intracompartmental pressure that will lead to
localized ischemia and subsequent necrosis
○ Caused by the expansion of intracompartmental contents that makes the muscle
swell inside, tissue and maybe there is an external swelling. This is due to ACS
kay mahugot ang blood supply sa sulod.
○ Recognized by: 5Ps
■ Pain- out of proportion of the injury. Unrelieved by analgesic. High
intensity of pain. Elicit pain by passive stretching of the compartment.
■ Pallor
■ Pulselessness
■ Poikilothermia- temperature of a dead body (yame)--- ang temp nya
gafollow sa temperature sang surrounding.
■ Paresthesia- Paresthesia refers to a burning or prickling sensation that is
usually felt in the hands, arms, legs, or feet, but can also occur in other
parts of the body. If may naipit na nerve
■ Paralysis- due to dead nerve supply
● Fat embolism syndrome- fat globules could escape to the circulation and might block the
pulmonary circulation (pruritus, chest pain or DOB)

Assessment and diagnostics

● Plain radiography
● CT Scan
● MRI
● Arthroscopy

Medical/ surgical treatment

● Pain control
● Immobilization
● Close reduction - using cast or splint
● ORIF - by the use of screws
● External fixation - by using antenna “kudal” ila extremities
initial management
Nursing interventions
● Assess trauma patient ABC (airway, breathing, circulation)
● Bleeding control
● Assess pulse, motor, sensory (neurovascular status)
● Immobilize the extremity (splint- should put accordingly: encompass 1 joint above and 1
joint below– cover both joint para di maghulag ang fracture sa tunga); splint the extremity
where it lies, kung ano tsura nya pagkita mo, maintain that position in splinting, di na
pagtadlunga before e splint.
For arterial bleeding/ excessive bleeding
● Pressure pack to stop bleeding and put a bandage. Not too tight nga mapatay ang
extemity

If gagwa tul’an
1. Irrigate with normal saline (or other isotonic solution)
2. Betadine should not be put on the bone (kay mapatay ang tul’an), ONLY around the
wound.
3. Cover the wound with moist gauze( normal saline ang e basa sa gauze)
4. Cover with dry gauze
5. Put with an elastic bandage
6. Apply splint

Basic sprains
RICE
● Rest (avoid weight bearing)
● Ice (to avoid swelling and acute compartment syndrome)
● compress
● Elevate

Infection
Risk factors:
● Poor nutritional status (esp. For pt who has hypoproteinemia)
● IV drug users (using needles)
● Immunocompromise
● Infection at remote sites

Osteomyelitis
Inflammation of the bone caused by an infecting organism
● Most common: S. aereus
Infection of bone characterized by progressive inflammatory destruction (old bone: sequestrum)
and apposition of new bone (new bone: involucrum)
Duration:
● Acute: <2 weeks
● Subacute: 2 weeks- 6 weeks
● Chronic: >6 weeks

Mechanism of infection
● Exogenous: direct inoculation
● Hematogenous

Most response
Pyogeric- creating pus
Nonpyogenic di kaya sng immune response

Pathophysiology
1. Hematogenous bacteria’s seeding or direct inoculation
2. Inflammatory reaction of bone
3. Local ischemic necrosis
4. Abscess formation try to contain sa infection; pus collection
5. Increased medullary pressure
6. Cortical ischemia ipit ang cortex
7. Escape of pus into subperiosteal space
8. Subperiosteal abscess (cloace- gadrain sang pus in the presence of ulcerations)
 9. Sequestrum formation; chronic osteomyelitis

Clinical manifestations
● Fever
● Tachycardia
● Diaphorisis
● Body malaise
● erythema
● pain/tenderness
● Swelling
● Warmth around the affected area
● Skin ulceration (chronic)

Assessment and diagnostics

● CBC- infection parameter
● ESR- infection parameter
● CRP- infection parameter
● Plain radiograph- to detect Sequestrum
● Technetium 99 bone scan- to detect areas with high metabolic activity
● MRI- to detect surrounding soft tissue edema and surrounding Sequestrum and
involucrum
● Aspiration- to take abscess and send for culture and biopsy
● Biopsy
● Culture

Treatment
● Supportive care
● Antibiotics
● Debridement (removal of devitalized tissue), curettage (scrape), sequestrectomy
(removal of dead bone)
● Antibiotic beads (look like rosary beads)
hydration
Nursing intervention
Dependent nursing intervention- pre-meds, antibiotics PRN
Independent nursing intervention
Bed rest
Provide comfort
Wound care and good hygiene
Increase OFI to improve hydration status
High protein diet
Vitamin C

Discharge:
Encourage compliance with antibiotics
Teach wound dressing
Use of ambulation aids

Septic arthritis hip and knee

Results from bacterial invasion of a joint space which can occur through:
● Hematogenous spread
● Direct inoculation from trauma or surgery
● Contiguous spread from an adjacent site of osteomyelitis or cellulitis
Considered an orthopedic emergency
The lower extremity weight-bearing joints are predominantly affected by (61% to 79%); however,
any joint can be involved, and multiple joint infections do occur

Pathophysiology
1. Systemic bacteremia/ direct inoculation
2. Spreads throughout the synovium and synovia fluid
3. Hyperemia and infiltration with polymorphonuclear leukocytes that rapidly increase over
the next several days
4. Activation of enzymes from the acute inflammatory response, production of toxins and
enzymes by bacteria, and stimulation of T. lymphocytes
5. Collagen is exposed to collagenases and the mechanical properties of the articular
cartilage are altered
6. Destruction of articular cartilage (4-6 days after infection)
7. Complete destruction occurs at– 4 weeks

Risk factors:
● Rheumatoid arthritis
● Osteoarthritis
● Prosthetic joint
● Low socioeconomic status
● Intravenous drug abuse
● Alcoholism
● Diabetes
● Previous intraarticuular corticosteriod injection
● Cutaneous ulcers

Clinical manifestations
● Joint pain and swelling
● Area is warm to touch
● Fever
● Refusal to use involved extremity

Assessment and diagnostics

● CBC- inflammatory parameters
● ESR- inflammatory parameters
● CRP- inflammatory parameters
● Joint fluid studies-
● Imaging
● Kochers criteria- to assess for the presence of Septic arthritis
■ 1 point each, the higher the score, the higher the probability that the
patient is having a septic arthritis
○ Fever > 38.5C
○ WBC > 12,000
○ ESR >40mm/s
○ Refusal to bear weight

Treatment
● Antibiotic therapy
● Pain management
● Arthrocentesis tempo immobilization
● Arthrotomy and debridement
● Temporary immobilization (knee-knee immobilizer; ankle-splint)

Nursing interventions
 ● Provide comfort
● Pain control
● Supportive therapy
● Encourage compliance with immobilization (needs time to heal)
● Drain attach to post-op- monitor drain output (amount, characteristics)

Necrotizing fasciitis
● Flesh-eating bacteria
● A life-threatening infection that spreads along the soft tissue planes
● Risk factors: immune suppression, bacterial introduction
● Has a mortality rate of 32%- correlates with time to surgical interventions

Inflammatory reaction in the soft tissue creates thrombosis in the capillaries

Thrombosis leads to local ischemia to necrosis of the soft tissues

Clinical manifestations
● Localized abscess or cellulitis with rapid progression
● Toxic looking patient
● Fever, chills
● Tachycardia
● Severe pain
● Skin bullae
● Discoloration
● Swelling
● Subcutaneous emphysema (crepitus)

Assessment and diagnostics

The higher the score, the higher the chance that the patient is having necrotizing fasciitis
● CBC- part of the diagnostic criteria called LRINEC SCORE
● CRP- part of the diagnostic criteria called LRINEC SCORE
● S.Na- part of the diagnostic criteria called LRINEC SCORE
● S.Crea- part of the diagnostic criteria called LRINEC SCORE
● Blood glucose- part of the diagnostic criteria called LRINEC SCORE
● Biopsy, gram stain, and culture- get a specimen or blood for biopsy, gram, and culture

Treatment
● Antibiotic therapy
● Emergency radical debridement

Nursing interventions
● Look out for the development of septic shock; monitor VS ( hypotension, tachypneic,
tachycardic, hyperthermic)
● Ensure patent IV line
Post-op
● Monitor still for septic shock (VS and MIO)
● Check dressing
● Ensure pt comfort
● Diet; high protein, vit c
● wound hygiene
● CBG monitoring

Inflammatory and metabolic disorders

Gout
Most common form of inflammatory arthritis
3-4 M is more than :F
Incidence increases with age, BMI, alcohol consumption, HTN, and diuretic
Patients with gout have an increased risk for CV diseases

Oxidize by xanthin oxidace

1. Purine
2. Hypoxanthine
3. Xanthin
4. Uric acid
Uricase (enzyme not present in human) metabolize uric
acid into its inactive form allantoin

Clinical manifestations
● Acute gouty arthritis
● Tophi
● Gouty nephropathy
● Uric acid urinary calculi

Assessment and diagnostics

● Pain, swelling, redness, and warmth, without the presence of infection
○ The manifestations usually awaken the patient at night
○ Self-limiting even without medication; madula after 7-19 days pero gabalik balik.
○ Preceded by a night of binge drinking or binge eating of red meats or organ
meats
● Synovial fluid polarized light microscopy
● Uric acid levels (may be falsely low during gouty attacks)
○ Clinical check-up should be a week after the flare-up to have accurate result
● 24h urinary uric acid
● S.Crea- check kidney function

Treatment
● Colchicine- manage pain
● NSAIDs- manage pain
● Xanthine oxidase inhibitors- e.g. allopurinol, febuxostat
● Uricosuric agent- urinates uric acid e.g. probenecid
● Corticosteroids- to modulate the inflammatory reaction
● Lifestyle changes- low purine diet, low fat diet, avoid binge drinking and smoking,
exercise
Nursing intervention
● Patient Education regarding the lifestyle
○ Low purine diet
○ Decrease red meat
○ Decrease organ meat
○ Decrease processed meat, legumes
○ Decrease fat in the diet
○ Avoid binge drinking
○ Avoid smoking
○ Educate regarding disease process for compliance
● The more frequent attack, the closer intervals

Osteoporosis
● Most prevalent bone disease in the world
● BMD T-score <-2.5Standard Deviation
○ Osteopenia- low but does not reach -2.5
○ “penia”- kulang mineralization sang bone
● May occur as primary or secondary osteoporosis
● Hereditary
● Prolonged steroid use
● Thyroid medication prolonged

Mas laban ang ginabreak (osteoclast) nga bone kaysa sa gina build up nga bone (osteoblast).

Clinical manifestations
● Asymptomatic in the early stages
● Back pain- collapse of vertebral body seen in elderly
● Loss of height- collapse of vertebral body seen in elderly
● Fragility fractures- e.g. hip fracture esp. for elderly, wrist fracture or colles fracture,
vertebral body compression deformities.
Assessment and diagnostics
● DEXA scan
● Conventional radiographs

Treatment
● Vit D and Ca supplementation
● Bisphosphonates- can be oral or parenteral.
○ Ex. risedronate
○ orally; has a side effect of esophageal ulcerations
■ remain upright after taking the med atleast 30min-1hr
■ take med with full glass of water
■ take before breakfast/ on empty stomach
■ given once a week
■ take med on the same day each week; pwede palagsan if mamiss ang
dose
■ Ensure safety/ full precautions
■ Increase calcium in diet
■ Exposure to sunlight to convert steroid in the body to vit D
■ Teach weight-bearing exercises (walking, light jogging, etc); this activity
apply stress to the bone and stress stimulate bone formation more than
bone resorption
■ Proper positioning
○ Post-op PHA
■ Pillow between both legs for dislocation precaution
● Avoid hip flexion of more than or beyond 90 degrees
● Avoid hip internal rotation and hip adduction
 ■ Teach to use ambulation aids
■ Wound care
● RANKL inhibitors- ginaguba ang ngipun ngipun sang osteoclast, thus preventing
resorption. Ex. denosumab (prolia)
● Selective estrogen receptor modulators- raloxifene
● PTH analogues- teriparatide
Parathyroid hormone acts to resolve calcium to the bone to increase serum levels of calcium
however, there were studies that showed pathologic continuous exposure to PTH such as in
hyperparathyroidism amuna nga gahabog habog kay ginasuyop nya lng ang calcium nga
ginahatag sa bloodstream
Normal parathyroid function and just take PTH analogues, intermittent lng daw ang exposure ta
sa PTH hormone, this would create a paratoxical effect than the PTH. It will stimulate more
absorption of calcium by the bone than resorption.

Osteoarthritis
● A non-inflammatory degenerative disorder of the joints
● Most common degenerative joint disease
○ May be primary or secondary
○ Elderly
● Due to a history of fractures or septic arthritis
● Often begins in the third decade of life and peaks between the 5th and 6th decades
Pathophysiology

Articular cartilage facilitate gliding

Synovial fluid aids in lubrication in joints and cushion

Osteoarthritis
Articular cartilage degenerate along with the formation of the subchondral cyst and bone spurs
(osteophytes)

Clinical manifestations
● Pain aggravated by movement and relieved by rest
● Stiffness
● Functional impairment
 ● May cause bony enlargements in the PIP- proximal interphalangeal joint and the DIP-
distal interphalangeal joint (Bouchard’s and Heberden’s nodes)

Assessment and diagnostics

Plain radiographs

In normal joint- there is joint space

Osteoarthritis- with increasing grade, the joint space becomes narrower

Treatment
Goal: decrease pain and stiffness; improve mobility if possible
● Orthotics/ ambulation aids
● Weight reduction
● TENS
● NSAIDs as needed
● Arthroplasty- removal and change of joint only in severe case of osteoarthritis

Nursing interventions
● Patient education
● Non-weight-bearing exercise (swimming)
● Proper use of orthotics
● Rest as needed
● Take NSAIDs as needed, not as maintenance to avoid peptic ulcer disease
● Seek consultation to a joint specialist or arthroplasty surgeon for evaluation for joint
replacement