CASE

STUDIES ON
MAJOR
CONCEPTS
FLUID AND ELECTROLYTE IMBALANCE
 HYPONATREMIC DEHYDRATION
By: ALCE
Case Scenario – A previously healthy 11-year-old white boy presents to the emergency department with a 3-day history of nausea, anorexia,
weakness, abdominal pain, and an episode of vomiting. He has no history of fever, diarrhea, constipation, respiratory or urinary symptoms, or use
of laxatives or diuretics.
History of Present Illness – Physical examination reveals a thinly built boy with signs of dehydration (sunken eyes and slightly dry mucous
membranes) and generalized skin hyperpigmentation, especially noticed on the extensor surfaces of the fingers of both hands. He is afebrile, with
capillary refill time of less than 2 seconds, blood pressure of 94/68 mm Hg, and a heart rate of 116 beats/min. His weight is 32 kg (70.5 lb) (weight
loss of 6% in the previous 3 days). Findings on the rest of the physical examination are normal. Initial laboratory evaluation reveals the following
values: sodium, 118 mEq/L (118 mmol/L) (reference range, 136–145 mEq/L [136–145 mmol/L]); potassium, 6.1 mEq/L (6.1 mmol/L) (reference
range, 3.5–5.1 mEq/L [3.5–5.1 mmol/L]); chloride, 92 mEq/L (92 mmol/L) (reference range, 101–111 mEq/L [101–111 mmol/L]); blood urea
nitrogen, 109 mg/dL (38.9 mmol/L) (reference range, 0–48 mg/dL [0–17.1 mmol/L]); and serum creatinine, 0.81 mg/dL (71.6 μmol/L) (reference
range, 0.1–1.0 mg/dL [8.8–88.4 μmol/L]). He has mild metabolic acidosis (pH 7.33; bicarbonate, 18 mEq/L [18 mmol/L]), and he is normoglycemic
(glucose, 94 mg/dL [5.22 mmol/L]). His complete blood cell count and liver enzyme, uric acid, lactate dehydrogenase, and C-reactive protein
levels are within normal limits. Results of urine drug screen also are negative.
He is diagnosed as having hyponatremic dehydration and is given an intravenous bolus of 20 mL/kg of isotonic (0.9%) sodium chloride solution.
He is hospitalized for monitoring and further evaluation. Right after hospitalization, he develops hypotension and is administered another bolus of
normal saline solution. His blood pressure does not improve, and he is, therefore, started on inotropic support with dopamine.
Additional laboratory evaluation reveals the cause of fluid-resistant hypotension and abnormal laboratory results.
Pathophysiology

Hyponatremia results from the inability of the kidney to excrete a water load or excess water intake. Water
intake depends upon thirst mechanism. Thirst is stimulated by increase in osmolality. Thirst is sensed by
osmoreceptors located in the hypothalamus and leads to the release of anti-diuretic hormone
(vasopressin) from the posterior pituitary. Antidiuretic hormone acts on the V2 receptors located at the
basolateral aspect of the collecting duct cells and leads to increased aquaporin expression on the luminal
aspect of the collecting duct cells which increases water absorption and abolishes thirst.
Concept Map

Causes
Causes
Diuretics
Diuretics
CHF
CHF
SIADH
SIADH
High
High levels
levels of
of of
of ADH
ADH
Dehydration
Dehydration
Risk
Risk Factors
Factors Signs and Symptoms
••Age
Age ••Nausea
Nausea andand vomiting
vomiting
••Diuretics
Diuretics ••Headache
Headache
••Conditions
Conditions that
that decrease
decrease ••Confusion
Confusion
your
your body's water
body's water excretion
excretion ••Loss
Loss of
of energy,
energy, drowsiness
drowsiness
••Intensive
Intensive physical
physical activities
activities and
and fatigue
fatigue
••Restlessness
Restlessness and
and irritability
irritability

Hyponatremia
 HYPOKALEMIA
By: ADUNA

A 40 y.o. male present to the emergency department with a chief complain of weakness all over his body. 
Chief complain: Weakness all over the body
Past: Father has a hypertension and diabetes. His mother has liver cancer. Client stated that 10 years ago, he developed bilateral
lower extremity weakness. Laboratory evaluation showed hypokalemia. Since then, he has been receiving potassium supplement, but
his serum potassium has remained low or low normal. He did not experience further episode of weakness. He denied vomiting,
diarrhea, palpitation, tremor or excessive sweating. He also denied use of over the counter medications or supplements.
Present: Patient works as a driver for food delivery. He experiences weakness every now and then but he thought that he was only
tired so he just ignore it. But the following day he couldnt help himself to get up and his body are all weak.
Pathophysiology

Hypokalemia can occur as a result of decreased potassium intake or increased potassium loss. Decreased potassium
intake rarely results in hypokalemia due to the ability of the kidneys to effectively minimize potassium excretion. However,
reduced intake can be a contributor to hypokalemia in the presence of other causes, such as malnutrition or diuretic
therapy. Cellular uptake of potassium is promoted by alkalemia, insulin, beta-adrenergic stimulation, aldosterone and
xanthines, such as caffeine. Most cases of hypokalemia result from gastrointestinal (GI) or renal losses. Renal potassium
losses are associated with increased mineralocorticoid-receptor stimulation such as occurs with primary hyperreninism and
primary aldosteronism. Increased delivery of sodium and/or non-absorbable ions (diuretic therapy, magnesium deficiency,
genetic syndromes) to the distal nephron can also result in renal potassium wasting. GI losses are a common cause of
hypokalemia with severe or chronic diarrhea being the most common extrarenal cause of hypokalemia. (Reference:
Pathophysiology and management of hypokalemia, Robert Unwin, 2011).
Concept Map
 THIRD DEGREE BURN
By: BAYAUA
Case Scenario: A 58-year-old female patient was activated as a Level 1 trauma alert after being involved in a house explosion with
resultant fire. She was awake and alert with no loss of consciousness at the scene but sustained significant thermal injuries per
EMS report. She was intubated pre-hospital for “airway protection” out of concern for inhalation injury with facial burns. The patient
shows decrease in her Fluid and Electrolytes Values. While a large, third degree burn certainly elicits a significant morbid response
in many observers, spending significant time managing the burn wounds while neglecting potential internal hemorrhage will
invariably lead to a delay in treatment and worse outcomes.

History Of Present Illness: Patient was activated as a Level 1 trauma alert after being involved in a house explosion with resultant
fire. She was awake and alert with no loss of consciousness at the scene but sustained significant thermal injuries per EMS report.
She was intubated pre-hospital for “airway protection” out of concern for inhalation injury with facial burns. Orally intubated with
bilateral breath sounds, mildly tachycardic in the 100s, moderately hypertensive in the 160s/90s, with readily apparent full-thickness
burns to the face, neck, anterior torso, bilateral arms, and bilateral legs. Secondary survey and imaging revealed no further injuries.
Pathophysiology

Burn wound is characterized by an inflammatory reaction leading to rapid oedema formation, due to increased microvascular permeability,
vasodilation and increased extravascular osmotic activity. These reactions are due to the direct heat effect on the microvasculature and to chemical
mediators of inflammation. The earliest stage of vasodilatation and increased venous permeability is commonly due to histamine release. Damage
to the cell membranes partly caused by oxygen-free radicals released from polymorphonuclear leucocytes would activate the enzymes catalyzing
the hydrolysis of prostaglandin precursor (arachidonic acid) with rapid formation of prostaglandin as the result. Prostaglandins inhibit the release of
norepinephrine and may thus be of importance in modulating the adrenergic nervous system which is activated in response to thermal injury. The
morphological interpretations of the changes in the functional ultrastructure of the blood barrier following thermal injury seem to be an increase in
the numbers of vacuoles and many open endothelial intercellular junctions. Furthermore changes of the interstitial tissue after burn trauma are of
great importance. The continuous loss of fluid from the blood circulation within the thermally damaged tissue causes increased hematocrits levels
and a rapid fall in plasma volume, with decreased cardiac output and hypoperfusion on the cellular level. If the fluids are not adequately restored
burn shock develops. Furthermore, the burn wound provides a vast area of entry of surface infection with a high risk of septic shock.
Concept Map
The patient shows
decrease in her She was intubated
Fluid and pre-hospital for
Electrolytes Values “airway protection”
  out of concern for
A 58-year-old female inhalation injury
patient was activated with facial burns.
as a Level 1 trauma THIRD DEGREE BURN
alert after being
involved in a house
explosion with
resultant fire

Orally intubated
apparent full- with bilateral breath
thickness burns to sounds, mildly
the face, neck, tachycardic in the
anterior torso, 100s, moderately
bilateral arms, and hypertensive in the
bilateral legs 160s/90s
 HYPERCALMCEMIA
By: BERNABEO

Case Scenario: A 37-year-old Caucasian female presented to the UPMC Endocrine Genetics Clinic in 2019 for evaluation and
management of hypercalcemia and hyperparathyroidism. She had previously undergone parathyroid surgery at an outside institution
in 2013 for presumed primary hyperparathyroidism (pHPT). Since then, her serum calcium remained elevated in the range of 10.4–
11.1 mg/dL with concomitant non suppressed parathyroid hormone (PTH) levels ranging from 66–178 pg/mL.

History of Present Illness: After she undergone a parathyroid surgery for presumed primary hyperparathyroidism her serum calcium
remained elevated in the range of 10.4 – 11.1 mg/dL.

Family history: Was notable for lung cancer in her paternal grandfather, leukemia in her maternal grandfather, and stomach cancer in
her paternal grandmother. She had no allergies. She was not taking any medications or over-the-counter supplements.
Pathophysiology

Calcium concentration is regulated by plasma membrane calcium receptor, PTH and its receptor, calcitonin and its receptor, and by
the actions of vitamin D on kidneys, bone, and intestines. PTH mobilizes calcium directly by enhancing bone resorption, and
indirectly, by stimulating one alpha-hydroxylase which increases vitamin D3 production, in turn, leading to increased absorption of
calcium from the gut and increased bone resorption. Primary hyperparathyroidism is due to a solitary adenoma or diffuse
hyperplasia of the gland. In this condition, there is an abnormal set point in the relation between calcium and PTH levels and
calcium-independent PTH secretion. The principal pathophysiologic alteration in severe hypercalcemia accompanying
hyperparathyroidism and malignancy is enhanced osteoclastic bone resorption. Hypercalcemia impairs renal mechanisms
that lead to sodium and calcium excretion; PTH and PTHrP acting on renal tubules enhance further calcium reabsorption.
Concept Map:

SIGNS & SYMPTOMS RISK FACTORS

Loss of appetite Nausea & vomiting People with a family

Women in their history of
50s hyperparathyroidism

Confusion,
The need to drink
disorientation,
more fluid &
& difficulty
urinate more
thinking

Constipation &
Depression
abdominal pain
 HYPOMAGNESEMIA
By: COCUSA
A 65-year-old male with medical history of hypertension, diabetes mellitus, hyperlipidemia, remote stroke, and severe gastroesophageal refl ux presented
to his Veteran Affairs (VA) clinic with 2 days of generalized abdominal pain, nausea, and watery diarrhea (6-8 episodes over 24-h). His medications
included amlodipine, aspirin, vitamin D, lisinopril, metformin, pravastatin, and omeprazole (20 mg daily for 1.5 years). He had no history of neck surgery,
remote or recent alcoholism, starvation, diuretic use, thyroid disease, chronic diarrhea, steatorrhea, or malabsorption. To he was sent VA emergency
department (ED) and laboratory [Table 1][3] showed hypomagnesemia at 0.0 mg/dL, hypocalcaemia at 7.9 mg/dL (1.98 mmol/l), and sinus tachycardia
(120 beats/min) and right bundle branch block (RBBB) with prolonged QT on electrocardiogram (ECG). He left the ED against medical advice due to
agitation. He had normal SMg 5 months earlier
Laboratory studies at our institution revealed severe hypomagnesaemia at 0.52 mg/dL (normal 1.7–2.7 mg/dL), hypocalcaemia at 7.6 mg/dL and
hypophosphatemia, hypokalemia, elevated serum creatinine (SCr) and creatinine phosphokinase (CPK level), and anion gap metabolic acidosis with
lactic acidosis Urinalysis revealed mild hyaline cast without ketones. Fractional sodium excretion was 0.39% and urine to plasma creatinine ratio was 167
suggesting prerenal azotemia. 24-h urinary magnesium (24 hUMg) was 265 mg (with urinary volume was 5300 mL) and SMg level normalized to 2.17
mg/dL (0.89 mmol/l) on day 3 (after receiving 8 g of intravenous [IV] magnesium sulfate). After aggressive hydration, electrolyte repletion and sedation,
the acidosis, CPK levels, and SCr normalized. His diarrhea resolved on the 2nd day. Electroencephalogram and magnetic radiographic imaging of the
brain were unremarkable.In the ICU, he received esomeprazole for gastrointestinal (GI) prophylaxis. After 8 days of unsuccessful supplementation with IV
magnesium sulfate (total of 23 g), esomeprazole was changed to famotidine 20 mg IV twice daily. He was continued on oral magnesium oxide 400 mg 3
times daily for 5 days. He received furosemide on day 5-7. SMg and calcium levels remained normalized after oral magnesium was discontinued.
Repeated ECG converted to sinus rhythm. Subsequently, patient was discharged home and seen at clinic without any significant neurologic deficits and
with normal laboratory
Pathophysiology
Magnesium is the second-most abundant intracellular cation and, overall, the fourth-most abundant cation. It plays a
fundamental role in many functions of the cell, including energy transfer, storage, and use; protein, carbohydrate, and fat
metabolism; maintenance of normal cell membrane function; and the regulation of parathyroid hormone (PTH) secretion.
Systemically, magnesium lowers blood pressure and alters peripheral vascular resistance.
 
Almost all enzymatic processes using phosphorus as an energy source require magnesium for activation. Magnesium is
involved in nearly every aspect of biochemical metabolism (eg, DNA and protein synthesis, glycolysis, oxidative
phosphorylation). Almost all enzymes involved in phosphorus reactions (eg, adenosine triphosphatase [ATPase]) require
magnesium for activation. Magnesium serves as a molecular stabilizer of RNA, DNA, and ribosomes. Because magnesium
is bound to adenosine triphosphate (ATP) inside the cell, shifts in intracellular magnesium concentration may help to
regulate cellular bioenergetics, such as mitochondrial respiration.
 
Extracellularly, magnesium ions block neurosynaptic transmission by interfering with the release of acetylcholine.
Magnesium ions also may interfere with the release of catecholamines from the adrenal medulla. Magnesium has been
proposed as an endogenous endocrine modulator of the catecholamine component of the physiologic stress response.
 Concept Map
Signs and Symptoms of hypomagnesemia
 Convulsions.
 Apathy. Treatment  whole grain cereal
 Muscle cramps.
 Hyperreflexia.
Diet: magnesium-rich foods include:  soymilk
 Acute organic brain syndromes.
 Depression.
 Generalized weakness.  spinach  black beans
 Anorexia.
Complications  almonds  whole wheat bread

 Seizures  cashews  avocado

 cardiac arrhythmias (abnormal heart patterns)  peanuts  banana

 coronary artery vasospasm

 sudden death
 DIARRHEA
By: DELA CRUZ

Case Scenario: A mother of 3-year-old child presents to the clinic with a chief complaint of loose stools of 5-6 episodes per day, nausea
and pain in the abdomen. He denies any episodes of fever, weight loss, fatigue, night sweats, or chills. He also denies any
hematochezia or hematemesis.
History of Present Illness
- As per patient’s informant the child was in usual state of health 1 day back when she started with pain in the abdomen with an
episode of loose stools during the day.
- Followed by loose stools 5-6 episode in 2-3 hours with nausea.
- Pain was colicky in nature involving whole abdomen..
Pathophysiology

Diarrhea is the reversal of the normal net absorptive status of water and electrolyte absorption to
secretion. Such a derangement can be the result of either an osmotic force that acts in the lumen to
drive water into the gut or the result of an active secre­tory state induced in the enterocytes. In the
former case, diarrhea is osmolar in nature, as is observed after the ingestion of nonabsorbable
sugars such as lactulose or lactose in lactose malabsorbers. Instead, in the typical active secretory
state, enhanced anion secretion is best exemplified by enterotoxin-­induced diarrhea
Concept Map

Signs and Symptoms Risk Factors

Loose, watery poor water

stools storage practices
Mucus in the
stool
low economic
Urgent need to have a status
bowel movement
DIARRHEA lack of
education
Abdominal cramps
not treating water in
the home
Abdominal pain
 

Bloating Nausea
 HYPOMAGNESEMIA
By: MUNGCAL
Case Scenario: The patient was a 57-year-old Caucasian male. He was an ex-smoker and reported normal alcohol
consumption. His medical history included coronary artery disease, hypertension and gastrointestinal reflux. He had been
diagnosed with type 2 diabetes mellitus back in 1996. At the time he got the diabetes diagnosis, he reported that his stools for
many years had tended to be a little loose. However, he described it as a minor problem, the main annoyance being the
passing of loose stools once every morning. Initially he was treated with glipizide (a SU drug). Metformin was added in 1999.
The dose had been gradually increased, and since 2004 he had been taking 1 g with breakfast and 0.5-1 g with supper. He
had no known complications to his diabetes.
History of Present Illness: He was admitted to the Medical Ambulatory in March 2008 because of carpal and calf spasms, pain
(especially in the legs), paresthesias of the lips, hands and feet, and malaise. His GP had diagnosed hypomagnesemia,
hypocalcemia and hypokalemia. When seen in the Medical Ambulatory, he reported a substantial diarrhoea problem which
had lasted a long time. He did not recall exactly when the diarrhoea had become a problem, but at least he remembered that it
was after the introduction of metformin in 1999. When asked about any relation between the diarrhoea and the introduction of
metformin or increase of metformin dose, he had not noticed any such relation. The last months before his admission in March
2008 his diarrhoea had worsened even more. These months he had been passing loose stools on average four times a day.
Sometimes he had observed some mucilage in the stools. His additional medication included glimepirid (a SU drug),
metoprolol, isosorbide mononitrate, ramipril, atorvastatin, clopidogrel, aspirin, and lansoprazol.
Pathophysiology
 
 High serum calcium
 Increased acetylcholine release
 Increased neuromuscular irritability
 Increased sensitivity to acetylcholine at the myoneural junction
 Diminished threshold of excitation for the motor nerve
 Enhanced myofibril contraction
 Hypomagnesemia
Concept Map

SIGNS AND
RISK
SYMPTOM
FACTORS
DEFINITION S
 
Hypomagnesemia—serum levels of Convulsions.
alcoholism
congestive heart
magnesium levels below the usual Apathy.
failure
Muscle cramps.
reference range of 1.5 to 2.5 mg/dL—can diabetes

result from decreased intake, redistribution

of magnesium from the extracellular to the Hyperreflexia. chronic diarrhea
hypokalemia
intracellular space, or increased renal or Acute organic brain
syndromes. hypocalcemia
gastrointestinal loss. It can be acquired or Depression. malnutrition

hereditary.
 KWASHIORKOR
By: OMLANG
A 5-month-old Orang Asli baby boy was referred to the visiting Family Medicine Specialist by a nurse for failure to thrive because his serial weight gain was
unsatisfactory. He was born full term with a birth weight of 2.42 kg. His weight continued to rise through the second month but began to fall below the -2SD in
the third month and below the -3SD in the ffth month, as shown in Figure 1. Over this period, he was assumed to be thriving, as neither parent noticed any
physical changes. He had a good appetite and normal bowel function. He was breastfed exclusively until he reached two months, at which point the mother
stopped breastfeeding due to inadequate milk supply. He was then fed sweetened condensed milk, water, and occasionally plain rice. He had no known
medical illness.
After a clinical examination, his vital signs were found to be normal. His weight was 4.5kg (< -3SD) and his length was 57cm (< -3SD). He had prominent round
cheeks resembling a cherubic appearance. (Figure 2). Tere were no signs of pallor, severe wasting, dehydration, or dysmorphic features. However, there was
pitting edema visible in both lower limbs (Figure 3). Other examinations uncovered nothing of note. A developmental assessment showed that he is able to lie
prone in the supine position and able to bear weight while standing. He exhibited no monosyllabic babbling.
Past Medical History: He was urgently referred to the hospital for severe acute malnutrition, as kwashiorkor was highly suspected. Laboratory investigations
revealed a normal full blood count, but low serum protein and albumin levels. He was started on initial refeeding with F-75, the “starter” formula, for one week
before being given F-100, the “catch-up” formula. Emotional and sensory stimulation was provided throughout inpatient care. He was discharged after about
one month to the outpatient clinic for a nutritional rehabilitation program. His frst monthly follow-up showed that he was doing well; within six months, his weight
had normalized.
Pathophysiology:

Kwashiorkor is characterized by peripheral edema in a person suffering from starvation. Edema results from a loss of fluid balance
between hydrostatic and oncotic pressures across capillary blood vessel walls. Albumin concentration contributes to the oncotic
pressure, allowing the body to keep fluids within the vasculature. Children with kwashiorkor were found to have profoundly low
levels of albumin and, as a result, became intravascularly depleted. Subsequently, antidiuretic hormone (ADH) increases in
response to the hypovolemia, resulting in edema. Plasma renin also responds aggressively, causing sodium retention. These
factors contribute to the edema.
Kwashiorkor is also marked by low glutathione (antioxidant) levels. This is thought to reflect high levels of oxidant stress in the
malnourished child. High oxidant levels are commonly seen during starvation and are even seen in cases of chronic inflammation.
One measure at reversal would be improved nutritional status and sulfur-containing antioxidants. There is also an experimental
theory proposing that alterations in the microbiome/virone contribute to edematous malnutrition, however, further studies are
required to understand the mechanism.  
 Concept Map: • Conditions that interfere with
protein absorption such as cystic • Peripheral pitting edema that
fibrosis. begins in dependent regions and
• Dietary changes for management proceeds cranially.
Kwashiorkor of milk allergies in infants and • Abdominal distension
children • Round face
• Diets that are low in protein such • Subcutaneous fat retention with
as a vegan diet loose inner inguinal skin folds
•Parasites such as intestinal worms
Signs & Symptoms

 Peripheral pitting edema that begins in dependent regions and proceeds cranially

 Marked muscle atrophy

 Abdominal distension (with/without dilated bowel loops and hepatomegaly)

 Round face (prominence of the cheeks, or “moon facies”)

RISK FACTORS
 Thin, dry, peeling skin with confluent areas of scaling and hyperpigmentation  Conditions that interfere with protein absorption such as cystic fibrosis
 Dietary changes for management of milk allergies in infants and children
 Dry, full, hypopigmented hair that falls out or is easily plucked  Diets that are low in protein such as a vegan diet
 Drought or famine
 Hepatomegaly (from fatty liver infiltrates)  Infections that interfere with protein absorption
 Limited food supply, as may occur during political unrest
 Growth retardation  Parasites such as intestinal worms
 Poor education about proper nutrition
 Psychic changes (anorexia, apathy)  Prolonged hospitalization or residence in a nursing home
 Skin lesions/dermatitis (perineum, groin, limbs, ears, armpits)

 Subcutaneous fat retention with loose inner inguinal skin folds

 
 SYMPTOM OF INAPPROPRIATE ANTI DIURETIC
HORMONE
By: ONIA

Case Scenario: Mrs SP, 86 years of age, is a nursing home resident who was admitted to hospital following an unwitnessed fall.
She had been feeling unsteady on her feet for the past week, but her mental state and vital signs were normal, and there were no
neurological deficits on examination.

History of Present Illness: Her past medical history included osteoporosis, hypertension, gastro-esophageal reflux disorder (GERD)
and depression. Mrs SP was on multiple medications, including escitalopram for depression, telmisartan for hypertension,
controlled‑release oxycodone/naloxone for chronic back pain, oxybutynin for urinary urge incontinence, simvastatin, pregabalin for
sciatica, omeprazole for GERD and six-monthly denosumab injections for osteoporosis.

Vital Signs: BP: 130/70      HR: 86     RR: 20    Temperature: 36.5C    O2Sat: 94%
 
Plasma Sodium: 125 mmol/dL POTASSIUM: 3.6mmol/L BUN: 30mg/ dL Creatinine: 0.8mg/dL SERUM OSMOLALITY: 270
mosm/kg
Pathophysiology

Initial injury stimulates neurons in supraoptic and paraventricular nuclei

of hypothalamus> ADH hypersecretion and increased aquaporins at
collecting ducts> diluted blood> Free water clearance inhibition leading
to water retention and extracellular volume expansion> decreased
aldosterone> suppression of plasma renin activity> decreased sodium>
SIADH
Concept Map

SYMPTOM OF INAPPROPRIATE ANTIDIURETIC HORMONE

SIGNS AND SYMPTOMS RISK FACTORS

- Low urine output - Small lung CA/ Nasopharyngeal CA/ Pancreatic Malignancy/
- High level of ADH Lymphoma/ Sarcoma
- Hyponatremia - Desmopressin/ SSRIs/ Carbamazepine/ Tricyclic Antidepressants/
- Overhydrated Phenothiazines/ Haloperidol/ Vincristine
- Retain too much fluid - Hereditary

TREATED WITH
- Restrict fluid intake as first line treatment
- Second-line treatments include increasing solute intake with 0.25–0.50 g/kg per day of
urea or a combination of low-dose loop diuretics and oral sodium chloride
- Use of lithium, demeclocycline, or vasopressin receptor antagonists is not
recommended.
 
By: PANOPIO
By: PERENA
 DUODENAL ULCER
By: SANTOS
Case Scenario: A 45-year-old man presents with a 2-month history of epigastric abdominal pain. He describes the pain as burning and says that it occurs
at night or early in the morning. The patient has found that eating food generally improves these symptoms. The patient admits to having had similar
symptoms intermittently during the past several years, and over-the-counter H2 antagonists have always resolved his symptoms. He denies any weight
loss, vomiting, or melena. He has no family history of significant medical problems. The patient’s physical examination reveals a normal head and neck,
and cardiopulmonary examinations show no abnormalities. The abdomen is nondistended, minimally tender in the epigastrium, and without masses. A
rectal examination reveals Hemoccult-negative stool. Laboratory studies reveal normal values for the white blood cell (WBC) count, hemoglobin and
hematocrit levels, platelet count, electrolyte levels, serum amylase level, and liver function tests.
History of Present Illness: A 45 year old man has sign and symptom consistent with peptic ulcer disease. The patient has self-medicated with H2-receptor
antagonists in the past with success, but the symptom are currently unrelieved with medication.
The case involves a 45-year-old man with “burning” epigastric pain that improves with eating. This scenario suggests a diagnosis of PUD that is refractory
to medical management. However, whenever such a patient is encountered, the initial step should be to evaluate for other disease processes (ie,
pancreatitis, gastric malignancy, biliary colic). In this case, upper gastrointestinal (GI) endoscopy is indicated to assess the ulcer disease, as well as the
esophagus, stomach, and duodenum. When indicated, ultrasonography and computed tomography (CT) imaging of the abdomen may be useful to help
identify pathology in the upper abdomen. When it is confirmed that the patient is indeed suffering from PUD, it is important to question the patient to see if
he has been compliant with the medical therapy. Failure of optimal medical therapy may be influenced by the presence of H pylori, high gastrin levels, or
noxious stimuli such as nonsteroidal anti-inflammatory drugs (NSAIDs)
Pathophysiology
Concept Map