Campugan Casas Ecarma Escobanas Endocrine Disorders

Republic of the Philippines
Cebu Normal University

Osmeña Blvd., Cebu City, 6000, Philippines
College of Nursing
Telephone No.: (+63 32) 254 4837
Email: cn@cnu.edu.ph
Website: www.cnu.edu.ph
Pathophysiology of Endocrine Disorders:

Schema and Discussions
In partial fulfillment of the requirements for the subject Psychopathophysiology of

3rd Year - Bachelor of Science in Nursing
in Cebu Normal University
Sway Marie Ecarma

Katrina Escobanas
Karla Clodeth Casas
Jay Campugan
November 2023
College of Nursing
Telephone No.: (+63 32) 254 4837
I. Cushing’s Disease
A. Schema
Figure 1. Cushing’s Disease Pathophysiology: Kidney, vasculature and muscle
Figure 2. Cushing’s Disease Pathophysiology: Liver, peripheral tissue, reproductive system, adipose
tissue, skin and connective tissue
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Figure 3. Cushing’s Disease Pathophysiology: Immune System and bone and calcium metabolism;
Diagnosis of Cushing’s Disease
B. Discussions
Definition. Cushing's disease is a hormonal disorder marked by heightened production of
adrenocorticotropic hormone (ACTH) from the anterior pituitary, resulting in an excess
release of cortisol from the adrenal glands. This often stems from a pituitary adenoma or
an overproduction of corticotropin-releasing hormone (CRH) from the hypothalamus.
Clinical Manifestations. Symptoms encompass general weakness, elevated blood

pressure, diabetes mellitus, menstrual irregularities, and psychiatric alterations. Physical
signs of elevated cortisol levels include moon facies, buffalo hump, easy bruising,
abdominal striae, obesity, facial plethora, and hirsutism.
It is noteworthy that a significant number of Cushing's disease patients do not exhibit

bitemporal hemianopsia, primarily because the majority of lesions are pituitary
microadenomas (less than 10mm in size).
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Etiology. In individuals with Cushing's disease, the presence of a pituitary adenoma is

nearly universal, although it may not be readily apparent through imaging. Nevertheless,
in rare instances, the condition may arise from diffuse corticotroph cell hyperplasia, even
without the occurrence of ectopic secretion of corticotropin-releasing hormone (CRH).
Typically, these tumors are microadenomas, measuring less than 10 mm, with only 5 to
10 percent classified as macroadenomas. Macroadenomas have a higher likelihood of
generating abnormally elevated ACTH concentrations compared to microadenomas (83%
versus 45%).
Various genetic mutations contribute to the development of these adenomas, with the
most common mutation being USP8 (ubiquitin-specific peptidase 8). These mutations
result in the abnormal expression of growth factors, which, in conjunction with ACTH,
contribute to an increase in cortisol levels.
Pathophysiology. In Cushing's disease, the frequency of ACTH production remains

constant, but the typical circadian rhythm is disrupted. The elevated levels of plasma
ACTH contribute to bilateral adrenal hyperplasia, resulting in an increased production of
cortisol. As a consequence, the normal circadian rhythm of cortisol is also disrupted.
While cortisol primarily functions as a glucocorticoid, at higher concentrations, it can

manifest mineralocorticoid activity. This can lead to hypertension and hypokalemia
through the activation of the renin-angiotensin-aldosterone system (RAAS). The RAAS
hormone system regulates plasma sodium concentrations and arterial blood pressure,
ultimately leading to hypokalemia as an indirect outcome.
Diagnosis and Laboratory Assessment. Once exogenous sources are ruled out, clinical
suspicion of Cushing’s Syndrome prompts laboratory assessment for confirming
endogenous hypercortisolism. Established diagnostic guidelines recommend two
screening tests: late-night salivary cortisol, 24-hour urine free cortisol, or low-dose
dexamethasone suppression (1 mg overnight or 2 mg over 48 hours) testing. Elevated
cortisol levels in these screenings indicate Cushing’s Syndrome.
ACTH levels help distinguish between ACTH-independent (15%-20%) and

ACTH-dependent (70%-80%) causes. ACTH-independent etiologies (adrenal adenomas,
carcinomas, or hyperplasia) are identified by adrenal gland CT or MR imaging with
suppressed ACTH levels. Normal or elevated ACTH levels indicate ACTH-dependent
causes.
For ACTH-dependent cases, cortisol suppression after high-dose dexamethasone, cortisol

and ACTH responses to CRH stimulation, and pituitary MR imaging revealing an
adenoma (40%-60% of cases) suggest Cushing's Disease (CD), requiring pituitary
surgery. Patients with discordant test results or negative pituitary MR imaging undergo
inferior petrosal sinus sampling to determine pituitary adenoma presence in CD cases.
ACTH-dependent cases not suppressing with high-dose dexamethasone or stimulating
cortisol production may have an ectopic ACTH-secreting tumor (10%-15%). Body
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imaging typically identifies and localizes these tumors, such as pulmonary and other
carcinoid tumors.
Differential Diagnosis. The differential diagnosis for Cushing disease includes Cushing
syndrome, ectopic ACTH secretion, exogenous corticosteroid use, pseudo-Cushing
syndrome, or physiologic hypercortisolism.
Complications. If left untreated, Cushing disease can cause complications such as:
● Osteoporosis, potentially leading to pathological fractures, commonly affecting
foot bones and ribs.
● Hypertension.
● Type 2 diabetes mellitus.
● Infections due to compromised immune response.
● Decreased muscle mass.
● Depression and other psychological issues.
II. Pheochromocytoma
A. Schema
Figure 4. Pathophysiology of Pheochromocytoma.

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B. Discussions
Definition. Pheochromocytoma is a rare tumor that typically originates in the adrenal
glands, located atop each kidney. Usually, pheochromocytoma manifests in one adrenal
gland, though instances of tumors developing in both glands are possible. These glands
consist of distinct layers, each responsible for producing various hormones. The central
region of the adrenal glands, known as the adrenal medulla, produces hormones like
epinephrine and norepinephrine which are essential for regulating heart rate and blood
pressure.
When there is pheochromocytoma, there is an abnormal overproduction of these

hormones, leading to potential health issues. Individuals with this type of tumor may
experience symptoms such as high blood pressure and headaches. Left untreated, a
pheochromocytoma can inflict severe or life-threatening damage on other bodily systems.
It underscores the importance of timely diagnosis and intervention to manage the
hormonal imbalance and avert potential complications.
Etiology. The etiology of pheochromocytoma is complex, encompassing both sporadic

and hereditary factors. While a notable proportion of cases occur spontaneously, the
majority are linked to genetic factors. Hereditary pheochromocytoma is frequently
associated with specific genetic syndromes, notably Multiple Endocrine Neoplasia type 2
(MEN 2), comprising subtypes MEN 2A and MEN 2B. Von Hippel-Lindau syndrome,
characterized by mutations in the VHL tumor suppressor gene, is another hereditary
condition wherein pheochromocytomas can manifest. In sporadic instances,
tumorigenesis may result from somatic mutations in diverse genes. The pathogenesis
involves chromaffin cells, which produce catecholamines such as epinephrine and
norepinephrine. The abnormal overproduction of these hormones by pheochromocytoma
gives rise to symptoms like hypertension, palpitations, and excessive sweating. Early
diagnosis is pivotal, often necessitating genetic testing in suspected hereditary cases. This
proactive approach is crucial for effective management, aiming to prevent complications
associated with hormonal excess.
Pathophysiology. In pheochromocytoma, disruptions in genetics and sporadic DNA

mutations interfere with proteins associated with tumor suppression or oncogenesis,
resulting in uncontrolled proliferation of chromaffin cells in the adrenal medulla. The
formation of adenomas prompts the excessive secretion of catecholamines, including
epinephrine and norepinephrine, detectable in both plasma and urine through elevated
metanephrine levels.
The overproduction of catecholamines sets off a cascade of physiological effects.

Excessive activation of G protein-coupled receptors involved in catabolic metabolic
processes may induce hyperglycemia, weight loss, and fatigue. Simultaneously, episodic
hyperactivity of the sympathetic nervous system manifests in symptoms such as panic,
tremors, anxiety, profuse sweating, tachycardia, palpitations, pallor, increased blood
pressure (either sustained or paroxysmal), and headaches.
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Complications arising from the intermittent hyperactivity of the nervous system, triggered
by the surplus catecholamines, can include severe outcomes such as heart attacks, strokes,
or even death. This intricate interplay of genetic factors and molecular disruptions
underscores the complexity of pheochromocytoma pathophysiology, necessitating
vigilant monitoring, early detection, and prompt intervention to mitigate potentially
life-threatening consequences.
Complications. Most complications associated with pheochromocytoma stem from the

heightened blood pressure resulting from the excessive production of catecholamines.
Hypertension poses a risk to various organs, particularly the cardiovascular system, brain,
and kidneys. This vascular damage can precipitate severe conditions, including heart
disease, strokes, kidney failure, and ocular nerve complications. Another potential
complication involves the development of malignant tumors. In rare instances, a
pheochromocytoma may display cancerous traits, with the malignant cells potentially
spreading to different parts of the body. Typically, cancerous cells originating from a
pheochromocytoma or paraganglioma tend to metastasize to the lymphatic system, bones,
liver, or lungs.
Clinical manifestations. The primary manifestation of a pheochromocytoma is elevated

blood pressure, which may be consistently high or intermittent. In some cases, the tumor
can induce dangerously high blood pressure, albeit this is an uncommon cause. It
becomes a consideration when conventional medications prove insufficient in managing
hypertension.
Less frequent symptoms may manifest, particularly during periods of stress or positional
changes, and can vary among individuals. These symptoms may encompass a rapid pulse,
the sensation of a fast or fluttering heartbeat (palpitations), a forceful heartbeat,
headaches, nausea, vomiting, clammy skin, trembling (tremors), and feelings of anxiety.
Diagnosis. To diagnose pheochromocytoma, a series of diagnostic tests including

laboratory examinations such as a urine test and a blood test are done to measure
epinephrine, norepinephrine, or their derivatives in the patient's system. If indicative
results from laboratory assessments suggest the potential presence of pheochromocytoma,
the diagnostic process advances to imaging tests such as CT scans, MRIs,
M-iodobenzylguanidine (MIBG) imaging, and Positron Emission Tomography (PET). In
cases where an adrenal gland tumor is incidentally discovered during unrelated imaging,
supplementary tests are likely to further evaluate the tumor.
Genetic testing may be recommended to ascertain if the pheochromocytoma is linked to

an inherited disorder. This information is crucial for multiple reasons, including
considerations for associated conditions, screening for other medical issues, and
implications for treatment decisions or sustained health monitoring. Test outcomes may
also prompt the necessity of screening other family members for the presence of
pheochromocytoma or related conditions.
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Nursing management. The nursing care for individuals with pheochromocytoma adopts
a collaborative and comprehensive approach, offering support across the diagnostic,
therapeutic, and ongoing care phases.
➔ Preoperative Care:
● Blood Pressure Monitoring: Consistently monitoring blood pressure is
crucial for promptly identifying hypertensive crises, enabling necessary
medication adjustments to maintain a safe blood pressure range.
● Fluid Balance: Ensuring adequate hydration is imperative to prevent
hypovolemia during surgical procedures.
➔ Postoperative Care:
● Hemodynamic Monitoring: Continuous vigilance over vital signs,
including blood pressure, heart rate, and oxygen saturation, is pivotal
during the postoperative period.
● Pain Management: Effectively addressing postoperative pain is critical,
given its potential to trigger the release of catecholamines, exacerbating
hypertension.
● Fluid Management: Diligent monitoring of fluid balance is essential to
prevent both volume depletion and overload.
➔ Education and Support:
● Patient Education: Delivering comprehensive education on the condition,
medications, and the importance of adherence.
● Lifestyle Modification: Emphasizing the significance of lifestyle
changes, including a low-sodium diet and avoidance of triggers that may
stimulate catecholamine release (e.g., specific foods, stress).
➔ Psychosocial Support: Providing emotional support and addressing anxiety,
recognizing that stress can trigger symptoms.
➔ Follow-up and Surveillance:
● Regular Monitoring: Ensuring scheduled follow-up appointments for
continuous monitoring of blood pressure, biochemical markers, and
imaging studies.
● Genetic Counseling: Facilitating referrals for genetic counseling to assess
the risk of hereditary forms and discuss family screening.
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III. Diabetes Insipidus

A. Schema
Figure 5. Pathophysiology of Diabetes Insipidus.
B. Discussions
Definition. Diabetes insipidus is a rare disorder characterized by the inability of the body
to properly regulate water balance. This condition is distinct from diabetes mellitus,
which involves abnormalities in insulin function and blood glucose regulation.
The fundamental aspect of diabetes insipidus revolves around the antidiuretic hormone
(ADH), also known as vasopressin. ADH is produced by the hypothalamus and released
by the posterior pituitary gland. Its primary function is to regulate water reabsorption in
the kidneys, influencing the concentration of urine and maintaining water balance in the
body. In diabetes insipidus, there is a dysfunction either in the production or response to
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ADH. This dysfunction results in the kidneys being unable to reabsorb water properly,
leading to the excretion of large quantities of diluted urine. Consequently, individuals
with diabetes insipidus experience polyuria (excessive urination) and develop
compensatory polydipsia (excessive thirst).
There are two main types of diabetes insipidus:
- Central Diabetes Insipidus (CDI)

- Nephrogenic Diabetes Insipidus (NDI)
Clinical Manifestations:
- Polyuria: Individuals with DI excrete abnormally large volumes of urine (more

than 3 liters per day), leading to frequent urination.
- Polydipsia: Excessive thirst is a compensatory mechanism to replace the fluids
lost through polyuria.
- Dehydration: Despite increased fluid intake, dehydration can occur due to the
inability to conserve water.
- Electrolyte Imbalances: Sodium imbalances, particularly hyponatremia, can lead
to neurological symptoms such as confusion and seizures.
Etiology:
Central Diabetes Insipidus (CDI):
- Cause: Insufficient production or release of ADH.

- Etiology: Often related to damage or dysfunction in the hypothalamus or pituitary
gland.
- Common Causes: Head trauma, tumors, infections, autoimmune diseases
affecting the pituitary, and certain medications.
Nephrogenic Diabetes Insipidus (NDI):
- Cause: Kidneys fail to respond to ADH.

- Etiology: Can be inherited (genetic mutations) or acquired (kidney damage due to
drugs, electrolyte imbalances, or chronic diseases).
- Common Causes: Certain medications (e.g., lithium), kidney diseases, and
electrolyte imbalances.
Pathophysiology:
Antidiuretic Hormone (ADH):
- ADH, produced by the hypothalamus and released by the posterior pituitary.

- It regulates water balance by increasing the permeability of the renal tubules to
water, allowing for its reabsorption.
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Central DI Pathophysiology:
- In CDI, there is a lack of ADH production or release.

- This can be due to damage to the hypothalamus or pituitary gland, disrupting the
synthesis or release of ADH.
- Without sufficient ADH, the kidneys cannot concentrate urine, leading to the
excretion of large volumes of dilute urine.
Nephrogenic DI Pathophysiology:
- In NDI, the kidneys do not respond to ADH

- This insensitivity is often caused by genetic mutations or acquired factors that
affect the responsiveness of renal tubules to ADH.
- Even if ADH is present, the kidneys cannot reabsorb water effectively, resulting
in excessive urine production.
Diagnosis. To differentiate between central diabetes insipidus (CDI) and nephrogenic

diabetes insipidus (NDI), several tests are commonly employed. These tests help assess
the underlying cause of the disorder, whether it is a deficiency in antidiuretic hormone
(ADH) production or a failure of the kidneys to respond to ADH.
Fluid Deprivation Test:
- Purpose: Assess the body's response to dehydration.

- Procedure: The patient abstains from fluid intake, and urine and blood samples
are collected at regular intervals.
- Interpretation: In CDI, urine output remains high, and urine remains dilute
despite dehydration; In NDI, there may be a decrease in urine output and an
increase in urine concentration in response to dehydration.
Desmopressin (DDAVP) Test:
- Purpose: Differentiate between CDI and NDI by assessing the response to

synthetic ADH (desmopressin).
- Procedure: Desmopressin, a synthetic ADH, is administered, and urine and blood
samples are collected.
- Interpretation: In CDI, there is a positive response with increased urine
concentration; In NDI, there is little to no response because the kidneys are
insensitive to ADH.
Water Loading Test:
- Purpose: Evaluate the kidneys' ability to concentrate urine in response to excess

fluid intake.
- Procedure: The patient consumes a large volume of water, and urine samples are
collected.
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- Interpretation: In CDI, there is a limited increase in urine concentration; In NDI,

urine remains dilute even with excess fluid intake.
Measurement of Urine and Blood Osmolality:
- Purpose: Assess the concentration of solutes in urine and blood.

- Interpretation: In CDI, urine osmolality remains low despite dehydration; In NDI,
urine osmolality may be normal, but blood osmolality tends to be elevated due to
the body's inability to conserve water.
MRI or CT Imaging:
- Purpose: Identify structural abnormalities in the brain, especially the

hypothalamus and pituitary gland.
- Interpretation: CDI may be associated with structural abnormalities in the
hypothalamus or pituitary gland;NDI is generally not associated with such brain
abnormalities.
Genetic Testing:
- Purpose: In cases of suspected NDI, genetic testing may be considered to identify

specific mutations associated with the condition.
Complications:
- Dehydration: Excessive urination leads to fluid loss, increasing the risk of

dehydration. This could lead to thirst, weakness, dark urine, and, in severe cases,
hypovolemic shock.
- Electrolyte Imbalances: Increased urine output can cause imbalances, especially
low sodium levels. This could lead to neurological symptoms like confusion and
seizures due to severe electrolyte disturbances.
- Impaired Thermoregulation: Fluid imbalance affects the body's ability to regulate
temperature. This could lead to difficulty managing body temperature, increased
risk of heat-related issues.
- Mental Health Impact: Chronic thirst and urination can lead to psychological
distress. This could lead to emotional issues, stress, and anxiety affecting overall
well-being.
- Impact on Renal Function: Chronic high urine output may stress the kidneys.
This could lead to increased risk of kidney dysfunction over time in severe cases.
- Secondary Effects on Endocrine System: Disruption of the
hypothalamus-pituitary-kidney axis can impact other hormonal systems. This
could lead to possible effects on other hormones regulated by the pituitary gland.
Treatment and management:

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- Desmopressin (DDAVP): Mechanism: Synthetic form of antidiuretic hormone

(ADH); Indication: Central diabetes insipidus (CDI) to replace deficient ADH;
Administration: Oral, intranasal, or intravenous depending on severity;
Monitoring: Regular assessment of urine output and osmolality.
- Hydration: Prevent dehydration due to excessive fluid loss, especially during
warm weather or increased physical activity.
- Treatment of Underlying Causes: CDI Causes: Address underlying issues such as
head trauma, tumors, or infections; NDI Causes: Manage conditions contributing
to kidney dysfunction (e.g., adjust medications causing NDI).
- Thiazide Diuretics (in NDI): Mechanism: Enhance renal tubular responsiveness
to ADH; Indication: Nephrogenic diabetes insipidus (NDI); Monitoring:
Electrolyte levels, especially sodium, to prevent imbalances.
- Low-Sodium Diet (in NDI): Minimize the risk of hypernatremia.
Nursing Management:
- Monitor fluid intake and output; Electrolytes and weight

- Vital Sign Monitoring: Regular monitoring, especially in cases where
dehydration can impact blood pressure.
- Neurological Assessment: Assess for signs of confusion, restlessness, or altered
mental status indicating electrolyte imbalances.
- Patient Comfort and Safety: Thermoregulation: Ensure a comfortable
environment to prevent temperature-related complications; Fall Prevention:
Implement measures to prevent falls, especially in cases of dehydration affecting
stability.
- Patient Support: Psychosocial Support: Address emotional aspects, as chronic
conditions can impact mental well-being; Education: Provide thorough education
about the condition, medications, and the importance of follow-up care.
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IV. Syndrome of Inappropriate Antidiuretic Hormone (SIADH)

A. Schema
Figure 4. Pathophysiology of SIADH.
B. Discussions
Definition. Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) is a
medical condition marked by the abnormal overproduction of antidiuretic hormone
(ADH), also referred to as vasopressin. ADH is pivotal in maintaining water balance by
directing the kidneys to reabsorb water. In contrast to Diabetes Insipidus, where there is
insufficient ADH production, SIADH is characterized by an unregulated and
inappropriate surge in ADH levels. This results in the kidneys retaining excessive
amounts of water, disrupting the normal fluid balance in the body.
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Etiology. The multifaceted etiology of Syndrome of Inappropriate Antidiuretic Hormone

Secretion (SIADH) encompasses a pivotal root cause associated with impaired or
damaged nervous system function. This impairment reverberates into the endocrine
system, affecting the secretion and production of antidiuretic hormone (ADH).
Conditions such as brain injuries, infections, and malignancies influence the intricate
balance of ADH production and regulation, which manifests SIADH.
Among these factors is the correlation with malignancies, where postoperative scenarios
following brain and thoracic surgeries may act as precipitating events for SIADH.
Additionally, the intake of certain medications, including antidepressants, antipsychotics,
and select anti-seizure drugs, introduces an additional layer of complexity. These
medications, by altering ADH levels, contribute to the development of SIADH. The
comprehensive understanding of these diverse etiological components is paramount for
accurate diagnosis and effective management of SIADH.
Pathophysiology. The presented etiological factors, when left unchecked and untreated,
lead to uncontrolled Antidiuretic Hormone (ADH) production, giving rise to Syndrome of
Inappropriate Antidiuretic Hormone (SIADH).
In response to elevated ADH levels, Aquaporins—integral proteins in the cell walls of the
convoluted tubules and collecting ducts—facilitate increased fluid retention by regulating
water movement within cells. The intensified ADH presence prompts the release of
additional aquaporins, contributing to decreased blood osmolality.
Within the nephron's principal cell, ADH binds to receptors, enhancing water movement
and fostering water retention. This elevated water reabsorption from the collecting ducts
to the bloodstream results in decreased urine volume and diluted blood sodium levels,
ultimately leading to Hyponatremia. This condition arises due to the primary dilution of
sodium caused by retained water in the bloodstream, leading to the excretion of more
sodium in the urine.
In situations of increased blood volume, the stretching of the heart's muscle walls triggers
heightened Atrial Natriuretic and B-type natriuretic release. Sodium reabsorption occurs,
causing hypotonic concentration gradients. This process leads to neuronal swelling,
bursting, and death, contributing to Cerebral Edema. Neurocognitive effects, such as
mood swings, confusion, seizures, and potential comatose states, manifest as a result.
Seizures and Cerebral Edema elevate intracranial pressure, initiating complications that
may lead to fatal outcomes if untreated.
Additionally, the decrease in plasma sodium osmolarity impairs the firing of action
potentials, affecting motor neurons, the hypothalamus, and the medulla. Clinical
manifestations include tremors, muscle cramps, headaches (a key indicator of decreased
sodium levels), and nausea, directly correlating with increased intracranial pressure. The
intricate cascade of events underscores the critical importance of addressing SIADH to
prevent severe neurocognitive complications and potential fatality.
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Diagnosis and Laboratory Assessment. The diagnosis of Syndrome of Inappropriate

Antidiuretic Hormone Secretion (SIADH) involves a comprehensive approach, starting
with a thorough clinical assessment that considers the patient's medical history, recent
illnesses, medications, and presenting symptoms, including nausea, headaches, confusion,
and seizures. Laboratory tests play a crucial role, examining serum sodium levels, serum
osmolality, urine osmolality, and urinary sodium concentration. The fluid restriction test,
restricting fluid intake to observe the body's response, helps confirm the diagnosis by
revealing the kidneys' continued concentration of urine even with limited fluid. Imaging
studies, such as CT or MRI scans, are employed to identify potential tumors or
abnormalities in the brain or chest contributing to excessive antidiuretic hormone release.
Additionally, the evaluation extends to identifying and addressing underlying causes,
including medication review and investigation for tumors. The response to treatment,
particularly the improvement of hyponatremia with appropriate interventions, further
supports the accurate diagnosis of SIADH. This diagnostic process ensures a
comprehensive understanding of the condition, guiding effective management strategies.
Complications. Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH)

can give rise to a spectrum of complications, with the foremost concern being the
development of hyponatremia. This condition, marked by abnormally low sodium levels,
manifests in various neurological symptoms, ranging from nausea and headaches to
seizures and potential coma in severe cases. Notably, the excessive retention of water
induced by SIADH can lead to cerebral edema, characterized by the swelling of brain
tissue. This, in turn, contributes to increased intracranial pressure, posing a significant
risk for complications such as brain herniation. The neurological impact extends to
neurocognitive effects, including mood swings and altered mental status, and may result
in seizures, respiratory distress, and permanent neurological damage if left untreated. In
extreme cases, the complications associated with SIADH can escalate to a
life-threatening scenario, underscoring the importance of early recognition,
comprehensive management, and diligent monitoring to prevent severe consequences.
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Campugan Casas Ecarma Escobanas Endocrine Disorders

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Campugan Casas Ecarma Escobanas Endocrine Disorders

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Republic of the Philippines

Cebu Normal University

Pathophysiology of Endocrine Disorders:

In partial fulfillment of the requirements for the subject Psychopathophysiology of

Sway Marie Ecarma

Figure 1. Cushing’s Disease Pathophysiology: Kidney, vasculature and muscle

Clinical Manifestations. Symptoms encompass general weakness, elevated blood

It is noteworthy that a significant number of Cushing's disease patients do not exhibit

Etiology. In individuals with Cushing's disease, the presence of a pituitary adenoma is

Pathophysiology. In Cushing's disease, the frequency of ACTH production remains

While cortisol primarily functions as a glucocorticoid, at higher concentrations, it can

ACTH levels help distinguish between ACTH-independent (15%-20%) and

For ACTH-dependent cases, cortisol suppression after high-dose dexamethasone, cortisol

Figure 4. Pathophysiology of Pheochromocytoma.

When there is pheochromocytoma, there is an abnormal overproduction of these

Etiology. The etiology of pheochromocytoma is complex, encompassing both sporadic

Pathophysiology. In pheochromocytoma, disruptions in genetics and sporadic DNA

The overproduction of catecholamines sets off a cascade of physiological effects.

Complications. Most complications associated with pheochromocytoma stem from the

Clinical manifestations. The primary manifestation of a pheochromocytoma is elevated

Diagnosis. To diagnose pheochromocytoma, a series of diagnostic tests including

Genetic testing may be recommended to ascertain if the pheochromocytoma is linked to

III. Diabetes Insipidus

Figure 5. Pathophysiology of Diabetes Insipidus.

There are two main types of diabetes insipidus:

- Central Diabetes Insipidus (CDI)

- Polyuria: Individuals with DI excrete abnormally large volumes of urine (more

Central Diabetes Insipidus (CDI):

- Cause: Insufficient production or release of ADH.

Nephrogenic Diabetes Insipidus (NDI):

- Cause: Kidneys fail to respond to ADH.

Antidiuretic Hormone (ADH):

- ADH, produced by the hypothalamus and released by the posterior pituitary.

- In CDI, there is a lack of ADH production or release.

- In NDI, the kidneys do not respond to ADH

Diagnosis. To differentiate between central diabetes insipidus (CDI) and nephrogenic

Fluid Deprivation Test:

- Purpose: Assess the body's response to dehydration.

Desmopressin (DDAVP) Test:

- Purpose: Differentiate between CDI and NDI by assessing the response to

Water Loading Test:

- Purpose: Evaluate the kidneys' ability to concentrate urine in response to excess

- Interpretation: In CDI, there is a limited increase in urine concentration; In NDI,

Measurement of Urine and Blood Osmolality:

- Purpose: Assess the concentration of solutes in urine and blood.

- Purpose: Identify structural abnormalities in the brain, especially the

- Purpose: In cases of suspected NDI, genetic testing may be considered to identify

- Dehydration: Excessive urination leads to fluid loss, increasing the risk of

Treatment and management:

- Desmopressin (DDAVP): Mechanism: Synthetic form of antidiuretic hormone

- Monitor fluid intake and output; Electrolytes and weight

IV. Syndrome of Inappropriate Antidiuretic Hormone (SIADH)

Figure 4. Pathophysiology of SIADH.

Etiology. The multifaceted etiology of Syndrome of Inappropriate Antidiuretic Hormone

Diagnosis and Laboratory Assessment. The diagnosis of Syndrome of Inappropriate

Complications. Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH)

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