SILLIMAN UNIVERSITY MEDICAL SCHOOL

SUBMITTED TO: DR. SHERWIN TIAMZON, MD

SUBMITTED BY: Diones, Mitchelle Noelle Q.
Escabarte, Belle T.
Galura, Merianne Joy S.
Gener, Jashen dela Rosa
Giangan, John Kevin C.
Jakosalem, Kim G.
REPRESENTATIVE CASE
1) IDENTIFYING DATA: J.V. 73 y/o male, married Roman Catholic, former construction worker, from Valencia, Negros Oriental
2) CHIEF COMPLAINT: epigastric pain and vomiting
3) MEDICAL HISTORY

A)HISTORY OF PRESENT ILLNESS:

Three weeks PTA, patient had onset of body weakness associated with episodes of dizziness. No consult done, no medication
taken.

2 weeks PTA, patient had episodes of epigastric pain, pain scale 7-8/10. Burning in character, non-radiating, aggravated by food
intake and temporarily relieved by antacid (Kremil-S).

1 wee PTA, patient noted persistence of body weakness now associated with decreased in appetite.

1 day PTA, patient had 2 episodes of post prandial vomiting ~ 50-75 cc with blood streaked vomitus prompting admission.

B) PAST MEDICAL HISTORY:

(+) Diabetes Mellitus for 4 years
Maintenance meds: Glimiperide 3 mg AC breakfast, Pioglitazone 30 mg pc lunch
(+) gouty arthritis x 4 years, self-medicated with Diclofenac 50 mg and Naproxen 500 maximum of 2
(+) BPH maintaining Dudasteride 500 mcg every other day

C)FAMILY HISTORY:
(+) DM type 2
(+) Hypertension
(-) BA
(-) Cancer

D)PERSONAL AND SOCIAL HISTORY:

Patient is a former construction worker, smoker for 20 pack years, quit smoking for 10 years. He is occasional alcoholic beverage
drinker (4 bottles of beer) for ~ 10-15 year. Last alcohol intake 2 months PTA. He is non-allergic to food and medication.
REVIEW OF SYSTEMS PHYSICAL EXAMINATION
General Survey: (-) weight loss (-) fever General Survey: awake, coherent, afebrile, and not in acute respiratory distress
HEENT: not indicated Vital Signs: BP: 120/80 mmHg HR 85 bpm: Weight: not
Chest and Lungs: (-) cough, (-) dyspnea indicated
Cardiovascular: (-) palpitation (-) chest pain RR: 22 cpm Temp: 36.4 oC O2 sat: 98%
Gastrointestinal: denies history of melena Skin: (+) pallor (-) jaundice
nor hematochezia Chest/ Lungs: (+) pale palpebral conjunctivae, anicteric sclera, pale lips, moist
Musculoskeletal: recurrent L shoulder and tongue; (-) tonsillopharyneal congestion
knee pains Cardiovascular: equal chest expansion, (+) fine rales at both basal area; PMI 5th
Genitourinary: not indicated intercostal space, regular rhythm, (-) murmur
Peripeheral Vascular: not indicated Abdomen: flat, normoactive bowel sounds, soft, non-tender
CNS: not indicated Genitourinary: not indicated
Extremities: weak pulses, (+) erythematous L shoulder and L knee joint, warm
touch, (+) tenderness
CNS: not indicated
PRIMARY WORKING IMPRESSION
DIAGNOSIS RULE IN RULE OUT
Peptic ulcer disease ID: Male CANNOT BE RULED OUT
HPI:
(+) burning epigastric pain aggravated by food intake and
 temporary relied with antacid intake
(+) episodes of post prandial vomiting with blood-streaked
volume
PE:
(+) pallor
(+) pale palpebral conjunctivae, anicteric sclera, pale lips, moist
tongue
PMH:
(+) Smoker
(+) Alcoholic
(+) NSAID intake
III. DIFFERENTIAL DIAGNOSIS
DIAGNOSES RULE IN RULE OUT
Gastritis ID: 73 y/o PMH:
HPI: (-) previous mucosal injury
(+) burning epigastric pain aggravated by food intake and (-) signs and symptoms of
temporary relied with antacid intake blood loss/anemia
(+) vomiting
(+) decreased appetite
PE:
(+) pallor
(+) pale palpebral conjunctivae, anicteric sclera, pale lips
PMH:
(+) NSAID intake
GERD ID: 73y.o. male HPI:
HPI: (-) heartburn
(+) burning epigastric pain aggravated by food intake (-) dysphagia
PE: (-) regurgitation
(+)fine rales at both basal area (-) cough
(-) chest pain
(-) hoarseness
Pancreatitis ID: 73 y.o. male HPI:
HPI: (+) burning, non-radiating
(+) epigastric pain epigastric pain
(+) vomiting with blood-streaked vomitus PE:
(+) decreased appetite (-) fever
PE: (-) tachycardia
(+) pallor (-) hypotension
(+) pale palpebral conjunctivae, anicteric sclera, pale lips (+) non-tender abdomen
(+)erythematous L shoulder and L knee joint (-) jaundice
PMH:
(+) Diabetes Mellitus
(+) Smoker
(+) Alcoholic
Myocardial Infarction ID: 73 y.o. male HPI:
HPI: (-) chest discomfort
(+) epigastric pain (-) anxiety
(+) body weakness (-) cough
(+) vomiting (-) diaphoresis
PE: PE:
(+) pallor (-) fever
(+) pale palpebral conjunctivae, anicteric sclera, pale lips
(+) RR: 22 cpm
(+) fine rales at both basal area
(+) weak pulse on extremities
PMH:
(+) Diabetes Mellitus
Family Hx:
(+) Hypertension
Esophagitis HPI: HPI:
(+) epigastric pain (-) heartburn
 (+) vomiting with blood-streaked vomitus (-) dyspepsia
(+) decreased appetite (-) water brash
(-) bloating
(-) fullness
(-) cough
IV. RATIONAL LABORATORY & DIAGNOSTIC TESTS
PATIENT NORMAL
LAB. TEST INTERPRETATION/NECESSITY AVAILABILITY COST
RESULTS VALUES
HEMATOLOGY
Complete Blood Count CBC is routinely done in every SUMCFI, HCH, P220
patient since it gives the physician NOPH, and
Hemoglobin the needed information about the other
4.6 g/dL (1st 13-18 hematologic picture, prognosis, private
hospital day) g/dL response to treatment, and recovery laboratories
9.6 g/dL (2nd of the patient. In here, patient’s
hospital day) result shows decreased hemoglobin
Hematocrit 8.3 g/dL (3rd and hematocrit either because of
hospital day) less intake or GI loss through
9.6 g/dL (7th bleeding.
hospital day)

15.1 % (1st 36.0-45.0

hospital day) %
29.6 % (7th
hospital day)
BLOOD CHEMISTRY
Na+ 132 meq/L 135-145 Serum electrolytes are used to aid in SUMCFI, HCH, P600
K+ 4.9 meq/L mEq/L the assessment of fluid balance of NOPH, and
3.4-5.0 the patient since she is experiencing other
mEq/L changes in bowel movement for the private
past few months. The patient has laboratories
hypokalemia and hyponatremia
which could be because of either less
intake, GI loss through bleeding or
due to vomiting.
Albumin 2.9 g/dL 3.5-5.5 Albumin is one of the two main SUMCFI, HCH, P290
g/dl protein factions of blood. It functions NOPH, and
in maintaining oncotic pressure and other
in transportation of bilirubin, fatty private
acids, drugs, hormones, and other laboratories
substances that are insoluble in
water. The patient presented with
hypoalbuminemia which is also an
indication for peptic ulcers. Low
serum albumin levels are associated
with poor prognosis of wound
healing and peptic ulcer bleeding.
Uric acid 8.8 mg/dL 3.5-7.2 Elevated amounts of serum uric acid SUMCFI, HCH,
mg/dL (hyperuricemia) become deposited NOPH, and
in joints and soft tissues and cause other
gout, an inflammatory reaction to private
the urate crystal deposition. In here, laboratories
the patient’s results showed
hyperuricemia. This explains the
gouty arthritis that the patient has.
Creatinine 1.8 mg/dl 0.6-1.2 Because creatinine is continually and SUMCFI, HCH, P170
easily excreted by the renal system, NOPH, and
increased levels indicate a slowing of other
the glomerular filtration rate. private
Creatinine is thus a very specific laboratories
 indicator of renal function, revealing
the balance between creatinine
formation and excretion. The patient
laboratory result showed increase in
creatinine which indicates upper
gastrointestinal bleeding and
impaired kidney function. This can
also increase due to dehydration
because the patient is also vomiting.
Blood Urea Nitrogen 38mg/dL 7-18 Elevated urea nitrogen in the SUMCFI, HCH, P210
mg/dL bloodstream is called “azotemia.” NOPH, and
However, the value is nonspecific as other
to cause and thus may be a result of private
either prerenal, renal, or postrenal laboratories
causes. Prerenal causes may be
grouped under factors that result in
inadequate renal circulation or
conditions resulting in abnormally
high levels of blood protein. Renal
causes are those of impaired renal
filtration and excretion of urea
nitrogen. Postrenal causes are lower
urinary tract obstructive conditions
that result in diffusion of urea
nitrogen in dormant urine back into
the bloodstream through the
tubules. The patient has an elevated
BUN, this could be due to degraded
blood being absorbed in the
gastrointestinal tract because there
is bleeding already which was
caused by the ulcer.
Na+ 132 meq/L 135-145 Serum electrolytes are used to aid in SUMCFI, HCH, P600
K+ 4.9 meq/L mEq/L the assessment of fluid balance of NOPH, and
3.4-5.0 the patient since she is experiencing other
mEq/L changes in bowel movement for the private
past few months. The patient has laboratories
hypokalemia and hyponatremia
which could be because of either less
intake, GI loss through bleeding or
due to vomiting.
IMAGING STUDIES
EGD Endoscopic This is the preferred diagnostic test in the SUMCFI 5000-
(Esophagogastroduodeno finding of evaluation of patients with suspected PUD. It is 9500
scopy) bleeding 1.5cm highly sensitive for the diagnosis of gastric and
gastric ulcer, duodenal ulcers, allows for biopsies and cytologic
antrum. brushings in the setting of a gastric ulcer to
differentiate a benign ulcer from a malignant
lesion. EGD detected the patient to have gastric
ulcer, also this procedure can be used in treating
peptic ulcer through sclerotherapy injection
which was done to the patient that could help in
stopping the bleeding.
PATHOPHYSIOLOGY
PLEASE SEE ATTACHED PATHOPHYSIOLOGY ON THE LAST PAGE. THANK YOU.
V. THERAPEUTIC MANAGEMENT
FINAL DIAGNOSIS
DIAGNOSIS RULE IN RULE OUT
Upper GI bleeding secondary to CC: Epigastric pain and vomiting CANNOT BE RULED OUT
bleeding peptic ulcer disease Hx: (+)body weakness, (+)dizziness,
 epigastric pain; pain scale 7-8/10,
burning in character, non-radiating,
aggravated by food intake and
temporarily relieved by antacid, (+)
decreased appetite, (+)post prandial
vomiting with blood streaked vomitus,
(+)DM, long term NSAID intake, smoker,
alcoholic,
PE: (+)pallor
LABS:
Decreased hemoglobin and hematocrit,
hyperuricemia, increased creatinine,
BUN, decreased albumin, decreased
serum sodium and potassium levels.
ENDOSCOPY:
Bleeding 1.5cm gastric ulcer, antrum and
control of bleeding by injection
sclerotherapy done.
LIST OF PROBLEMS THERAPEUTIC OBJECTIVES
1. Bleeding 1. Stop the bleeding, identify and treat the
2. Epigastric pain underlying cause.
3. Fluid and electrolyte imbalance 2. Relieve the patient from epigastric pain related to
4. Nausea and vomiting the disease condition.
5. Body weakness 3. Replace and maintain lost fluid and electrolyte
6. Decreased appetite levels caused by vomiting and GI bleeding.
7. Joint pains 4. Restore patient’s appetite and improve energy
8. Azotemia level.
9. Hyperglycemia (DM type 2) 5. Alleviate joint pains
6. Improve urinary functioning
7. Monitor and maintain blood sugar level
ADVICE AND INFORMATION NON-PHARMACOLOGIC MANAGEMENT
1. Include patient’s family or significant others in the 1. Admit patient in the ward under my care.
management of the patient. 2. Secure patient’s consent
2. Educate patient and his family on his present health 3. Start IV infusion of PNSS to run @ 3L/day
condition, signs and symptoms, pathophysiology and the 4. Labs:
complications which may result if the case will be left CBC, Blood typing, Electrolytes: Na+, K+, Ca++,
untreated. H. pylori test, RBS, HbA1c, stool exam, lipid
3. Emphasize on the role of alcohol, NSAIDs, and smoking on profile, Liver enzymes: SGPT, SGOT, Urinalysis,
the development of the patient’s disease Blood uric acid, Creatinine, Troponin T+I,
4. Inform patient on proposed treatment course and possible CKMB, Amylase, Lipase, 12 Lead ECG
intervention. Educate regarding the 5. Initiate Oxygen therapy at 2LPM
benefits of drugs to be taken and the possible side effects or 6. Put patient on NPO
adverse reactions to watch-out for. 7. Insert NGT open to drain (Gastric lavage)
5. Let the patient and his family know the urgency of the 8. Secure 3 liters of PRBC then transfuse
diagnostic procedures and medical interventions (such as 9. Schedule for EGD
upper GI series and endoscopy, blood transfusions) that the 10. Monitor vital signs every 4 hours and record.
patient may undergo for diagnosis, treatment, and biopsy. 11. Monitor intake and output every shift and record.
6. Obtain informed consent for the diagnostic procedure and 12. Refer accordingly
disclose to the patient and family the results.
7. Educate patient and his family about the dietary and 
lifestyle changes he is going to make, with the adjustments
to be made by the family.
8. Encourage on importance of good lifestyle practices such as
avoidance of smoking and alcoholism, and consuming a
healthy diet that does not aggravate symptoms.
9. Emphasize importance of follow-up check-ups and
monitoring.
10. Point out to the patient and his family to refer
abnormalities observed immediately to the
physician in charge for prompt evaluation and
management
PHARMACOLOGIC MANAGEMENT
DRUG NAME EFFICACY SAFETY SUITABILITY
Proton Pump Inhibitors
Esomeprazole Suppresses gastric acid Watch out for headache Prophylaxis for GI bleeding due to
secretion by inhibiting and any symptoms of GI gastric erosions.
H+/K+ ATPase in the upset.
gastric parietal cell. It
is the S-isomer of
omeprazole.
Omeprazole It blocks the final step Watch out for GI Prophylaxis for GI bleeding due to
(Prosec) in gastric acid disturbances particularly gastric erosions.
secretion by specific diarrhea; skin rashes and
inhibition of H+/K+ headache.
ATPase enzyme system
present on the
secretory surface of
the gastric parietal cell.
Both basal and
stimulated acid are
inhibited.
Antacids
Al Hydroxide+Mg Hydroxide Neutralizes gastric Should not be used in Commonly used antacids,
(Maalox) acid; increases gastric chronic renal failure combination of both aluminium and
pH patients because of magnesium hydroxide that avoid side
possible effects such as constipation and
hypermagnesemia, and phosphate depletion.
aluminium may cause
chronic neurotoxicity in
these patients
Al Hydroxide+ Mg Hydroxide + Aluminum hydroxide: Should not be used in Commonly used antacids,
Simethicone Neutralizes stomach chronic renal failure combination of both aluminium and
(Mylanta) hydrochloride to form patients because of magnesium hydroxide that avoid side
AICI3 salt plus water, possible effects such as constipation and
Increases gastric pH hypermagnesemia, and phosphate depletion.
Magnesium hydroxide: aluminium may cause
Promotes bowel chronic neurotoxicity in
excavation by causing these patients
osmotic retention of
fluid, forms
magnesium chloride
when reacts with
hydrochloric acid
Simethicone: Disperses
and prevents gas
pockets in the GI
system by decreasing
surface tension of gas
bubbles
Al Hydroxide+Mg Hydroxide Neutralizes gastric Should not be used in Commonly used antacids,
(Maalox) acid; increases gastric chronic renal failure combination of both aluminium and
pH patients because of magnesium hydroxide that avoid side
possible effects such as constipation and
hypermagnesemia, and phosphate depletion.
aluminium may cause
chronic neurotoxicity in
these patients

H2-Blockers
Cimetidine H2 receptor Cimetidine has weak Significantly inhibit basal and
antagonist; blocks H2 antiandrogenic side stimulated acid secretion, with
 receptors of gastric effects resulting in similar ulcer-healing rates are
parietal cells, leading reversible gynecomastia achieved, this class of drug is often
to inhibition of gastric and impotence. Other used for treatment of active ulcers
secretions. side effects include (4-6 weeks) with combination with
confusion and elevated antibiotics at eradicating H. pylori
levels of serum
aminotransferase,
creatinine and serum
prolactin
Ranitidine H2 receptor Patients may develop Significantly inhibit basal and
(Zantac) antagonist; blocks H2 tolerance to H2 blockers. stimulated acid secretion, with
IV-50mg q8hr receptors of gastric Reversible systemic similar ulcer-healing rates are
parietal cells, leading toxicities include achieved, this class of drug is often
to inhibition of gastric pancytopenia, used for treatment of active ulcers
secretions. neutropinea, anemia, and (4-6 weeks) with combination with
thrombocytopenia antibiotics at eradicating H. pylori.
Are more potent H2 receptor
antagonist than cimetidine.
H. pylori agents
Bismuth subsalicylate Antimicrobial anti- Can cause black stool,
(Kaopectate) inflammatory action; constipation or
antisecretory effect. darkening of tongue The combination of bismuth,
Tetracycline Inhibits bacterial Causes rashes and,very metronidazole, and tetracycline was
(Astisite) protein synthesis by rarely, hepatotoxicity the first triple regimen found
binding with 30s and and anaphylaxis effective against H.pylori
possibly 50s ribosomal
subunits
Metronidazole Inhibits nucleic acid Encephalopathy,
(Flagyl) synthesis by disrupting seizures, aseptic
DNA and causing meningitis, and
strand breakage. neuropathies reported
with increase dose and
chronic therapy
Cytoprotectives
Sucralfate Act by several Toxicity from thi8s drug Forms ulcer adherent complex;
(Carafate) mechanisms by is rare, with constipation protects ulcer from acid, pepsin and
promoting a trophic being most common, It bile salts.
action by binding should be avoided in
growth factors such as patients with chronic
EGF, enhancing renal insufficiency to
mucosal defences and prevent aliminum-
repair induced neurotoxicity.

Symptomatic Medications
Antipasmodics
Hyoscine-N-butylbromide Hyoscine-N- Hyoscine-N- For Acute GI, biliary and
(Buscopan) butylbromide, a known butylbromide does not genitourinary spasm including
antispasmodic enter central nervous biliary and renal colic
substance, It relieves system.
pain by acting on the
muscle spasm which
causes pain.
Antiemetics
Metoclopramide Blocks dopamine Adverse effects: Management of nausea and vomiting
(Clometide) receptors and extrapyramidal associated w/varous GI disorders, in
serotonin receptors symptoms, restlessness, GERD and gastric stasis.
and sensitizes tissues sedation and headache
to acetylcholine;
increases upper GI
motility but not
 secretions; increases
lower esophageal
sphincter tone

P-DRUGS
DRUG NAME EFFICACY SAFETY SUITABILITY COST
Omeprazole It blocks the final step Watch out for GI Prophylaxis for GI bleeding Inj40mg
(Prosec) in gastric acid disturbances due to gastric erosions. (+10mL amp
IV-40mg q12-24hr secretion by specific particularly diluent) 1’s
inhibition of H+/K+ diarrhea; skin (P463.00/vial)
ATPase enzyme rashes and
system present on the headache.
secretory surface of
the gastric parietal
cell. Both basal and
stimulated acid are
inhibited.
Al Hydroxide+Mg Neutralizes gastric Should not be Commonly used antacids, 60mLx1’s
Hydroxide acid; increases gastric used in chronic combination of both (P92.21/bottle)
(Maalox) pH renal failure aluminium and magnesium
patients because hydroxide that avoid side
PO 2-4 tsp suspension QID of possible effects such as constipation
20min-1hour after meals hypermagnesemia, and phosphate depletion.
&at bedtime and aluminium
may cause chronic
neurotoxicity in
these patients
Ranitidine H2 receptor Patients may Significantly inhibit basal and Inj 25mg/mL
(Zantac) antagonist; blocks H2 develop tolerance stimulated acid secretion, (amp)5x1’s
IV-50mg q8hr receptors of gastric to H2 blockers. with similar ulcer-healing (P930.60/box)
parietal cells, leading Reversible rates are achieved, this class
to inhibition of gastric systemic toxicities of drug is often used for
secretions. include treatment of active ulcers (4-
pancytopenia, 6 weeks) with combination
neutropinea, with antibiotics at
anemia, and eradicating H. pylori.
thrombocytopenia Are more potent H2 receptor
antagonist than cimetidine.
Bismuth subsalicylate Antimicrobial anti- Can cause black The combination of bismuth,
(Kaopectate) inflammatory action; stool, constipation metronidazole, and
525mg antisecretory effect. or darkening of tetracycline was the first
PO q6hr for 14 days tongue triple regimen found
effective against H.pylori
Tetracycline Inhibits bacterial Causes rashes
(Astisite) protein synthesis by and,very rarely,
500mg binding with 30s and hepatotoxicity and
PO q6hr for 14 days possibly 50s anaphylaxis
ribosomal subunits
Metronidazole Inhibits nucleic acid Encephalopathy, 500mgx100’s
(Flagyl) synthesis by seizures, aseptic (P2172.50)
250mg disrupting DNA and meningitis, and
PO q6hr for 14 days causing strand neuropathies
breakage. reported with
increase dose and
chronic therapy
Sucralfate Act by several Toxicity from Forms ulcer adherent 100’s
(Carafate) mechanisms by thi8s drug is rare, complex; protects ulcer from (P4262.40/pack)
1g PO q6hr initially; promoting a trophic with constipation acid, pepsin and bile salts.
maintenance: 1g PO q12hr action by binding being most
growth factors such common, It should
 as EGF, enhancing be avoided in
mucosal defences and patients with
repair chronic renal
insufficiency to
prevent aliminum-
induced
neurotoxicity.
Hyoscine-N-butylbromide Hyoscine-N- Hyoscine-N- For Acute GI, biliary and Inj 20mg
(Buscopan) butylbromide, a butylbromide does genitourinary spasm (amp) 10x 1’s
1amp IV q6hr PRN known antispasmodic not enter central including biliary and renal (P1265.00/box)
substance, It relieves nervous system. colic
pain by acting on the
muscle spasm which
causes pain.

Metoclopramide Blocks dopamine Adverse effects: Management of nausea and 10vials

(Clometide) receptors and extrapyramidal vomiting associated (P2203.65)
1amp IV q8hr PRN serotonin receptors symptoms, w/varous GI disorders, in
and sensitizes tissues restlessness, GERD and gastric stasis.
to acetylcholine; sedation and
increases upper GI headache
motility but not
secretions; increases
lower esophageal
sphincter tone
VI. MONITORING AND FOLLOW-UP
1. Follow-up after 1 week for signs and symptoms of complications, response and adherence to pharmacologic
management.
2. Monitor laboratories: CBC, serum electrolytes, RBS, urinalysis.
3. Assess for adherence to diet and lifestyle modification.

VII. PRESCRIPTION WRITING

BELLE T. ESCABARTE MD BELLE T. ESCABARTE MD

Silliman University Medical Center Silliman University Medical Center

Patient: J.V Date: 12-1-15 Patient: J.V Date: 12-1-15

Address: Valencia , Negros Oriental Age/Sex: 73 y/o/ male Address: Valencia , Negros Oriental Age/Sex: 73 y/o/ male

BELLE T. ESCABARTE MD BELLE T. ESCABARTE MD

Lic. No. 017626 Lic. No. 017626
 REFERENCES:
BELLE T. ESCABARTE MD
Silliman University Medical Center  Bickley, A. et. Al. (2009).Bates’ guide to physical
examination and history taking. 10th ed.
Patient: J.V Date: 12-1-15  Fauci, A. et Al. (2012). Harrison’s principles of
Address: Valencia , Negros Oriental Age/Sex: 73 y/o/ male internal medicine. 18th ed. NY: McGraw-Hill medical
publishing division.
 Hammer, G. D., & McPhee, S. J. (2010).
Pathophysiology of disease: an introduction to
clinical medicine. 7th ed. NY: McGraw Hill companies.
 Wilson, D. D. (2008). McGraw-Hill's manual of
laboratory and diagnostic tests. NY: McGraw Hill
companies.
 MedScape. November 29, 2015. www.medscape.com
 Philippine Drug Price Reference Index.(2013).
NCPAM(Department of Health).

BELLE T. ESCABARTE MD
Lic. No. 017626