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Clinical Profile Physical Findings

 45 y.o  Hypotensive
 Male  Tachycardic
 Farmer, resides in Palo, Leyte  Tachypneic
 Sudden localized, burning, epigastric pain PRS 7/10,  Afebrile
nonradiating, aggravated by food intake slightly re-
lieved by Aluminum-magnesium hydroxide
 Normal oxygen saturation
 Body malaise  Orthopneic
 Dizziness  In respiratory distress
 Recurrent burning, localized epigastric pain PRS 9/10,  Poor capillary refill
aggravated by food intake slightly relieved by Alumi-  Lips & Mucosa: Pale
num-magnesium hydroxide  Gums: Pale pink
 Melena  Epigastric direct tenderness (+)
 2019: Acute gouty arthritis  Presence of tarry stool on gloves after DRE.
 Fond of coffee Pivot: Melena

Ddx: Esophageal Varices Ddx: Upper GI malignancy Ddx: Acute gastritis Peptic Ulcer Disease Ddx: Schistosomiasis Ddx: Hemorrhagic & erosive
gastropathy
(Gastric vs Duodenal Ulcer)
R/I: R/I: R/I: R/I: R/I: R/I:
Melena Male Melena Farmer Possibility of NSAID abuse
Dizziness Epigastric pain Recurrent burning pain in Gastric Duodenal Endemic in Palo
epigastric area Alcoholic
Generalized pallor Melena Abdominal Pain
Symptoms of Anemia Melena
Body malaise Diarrhea Burning epigastric Burning epigastric Melena
(generalized pallor, slow pain pain Abdominal pain
Tachycardia Body weakness Tachycardic Pain precipitated
capillary refill) by food intake
Tachypnea Generalized Pallor Hypotensive R/O:
Melena Tachycardic R/O:
Low diastolic blood pressure 10 pack-year smoker Poor Hypotensive No rash
socioeconomic Melena No dyspepsia
R/O: status Poor
No itchiness No nausea
R/O: R/O: Heavy coffee socioeconomic No fever & chills
No nausea drinker status No vomiting
No hematemesis Absence of mass Smoker Heavy coffee No cough
No hematemesis Possibility of NSAID drinker No loss of appetite
No known liver disease No unintentional weight loss abuse Smoker No muscle pain
No bloated abdomen No fever
No easy bruising No early satiety Possibility of No enlarged liver
No indigestion R/O: NSAID abuse
No jaundice No Nausea & vomiting No disturbance of No hematuria
sleep d/t pain R/O:
No syncope No indigestion Pain is alleviated Cannot totally rule
No seizures
No ascites No dysphagia by food intake out No hematochezia

Admitting diagnosis: Peptic ulcer disease

Pathophysiology

Inhibition of COX-1 in GIT


leads to reduction of
prostaglandin secretion &
cytoprotective effects in
Frequent Coffee intake Skips Meals Farmer Poor socioeconomic Status Possible abuse of NSAIDS gastric mucosa w/c in-
creases susceptibility to
mucosal injury

Irritation to gastric mucosa Acid & Pepsinogen release w/ Chronic H. pylori infection Production of urease that
vagal response to increased stress catalyzes hydrolysis of urea
to ammonia

Increased gastrin secretion

Increased gastric acid production

Weakness, body malaise

Epigastric Pain Damage/Erosion of the mucosa Inflammation

Ulcer detection:
To r/o other causes : Formation of Ulcers  Barium studies of proximal GIT:
appearance of discrete ulcer wall
Liver function tests: normal craters
Amylase: normal
Lipase: normal  Upper endoscopy : presence of a
Gastrointestinal bleeding Dehydration well-demarcated break in the
mucosa that may extend into the
muscularis propria of
Iron deficiency anemia
the duodenum
Melena Tachycardia Hypotensive

Note: H. pylori infection:


Hypotension Tachypnea  Rapid urease test : positive
 Serology (H.pylori test) : positive
CBC: Stool exam:  Stool antigen: Positive
RBC: decreased
WBC: normal
Hgb: decreased No ova or parasite seen
Hct: decreased
MCHC: decreased
MCV: decreased Reduced urinary output
RDW: increased Raised creatinine
Platelet: decreased
NLMEB: normal Reduced eGFR
Increased urea:creatinine ratio
Iron studies: Electrolytes :
Serum iron: decreased NaKCl: increased
Transferrin/TIBC: increased Urinalysis:
Transferrin saturation: decreased Increased urine S.G
Ferritin: decreased
Soluble transferrin receptor: increased

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