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DAVAO MEDICAL SCHOOL FOUNDATION, INC.

– COLLEGE OF MEDICINE
Department of Internal Medicine

Name: MEEVIE LOVE D. TOLEDO


Batch/Sec@on: NMD 3 Date: NOVEMBER 27, 2020

DAY 2 ACTIVITY

InstrucFons:
● Strictly use Harrison’s Principles of Internal Medicine 20th ediFon, Bate’s Guide to Physical ExaminaFon and History Taking, or Clinical PracFce Guidelines as your reference in answering this case. You
may also use the official textbooks used by other departments.
● Indicate the name of the book, chapter and page number in the reference column. Failure to write the reference will incur deducFon from the total grade.
Case:

M. M., is 55-year-old male, market vendor, from Agdao, Davao City

Chief complaint: weight loss

The pa@ent was apparently well un@l 8 months prior to consulta@on, he started no@cing that his pants were geCng gradually loose despite his good appe@te. This was associated with weakness. There
was no consulta@on done.
Three months prior to consulta@on, the pa@ent has been having frequent urina@on where he passes large volume of urine, and that he usually wakes up from sleep to urinate. The condi@on was
associated with excessive thirst for which he used to drink plenty of water. The condi@on was tolerated. No consulta@on was done. No medica@ons were taken.
Four weeks prior to consulta@on, the pa@ent noted onset of @ngling sensa@on and numbness of both hands and feet. S@ll, no consulta@on was done. No medica@ons were taken.
Two weeks prior to consulta@on, due to worsening weight loss, the pa@ent decided to weigh himself and noted 62 kilograms weight from 70 kilograms (10 months ago prior to the onset of the
condi@on). The persistence of the condi@on prompted the pa@ent to seek for medical care. Hence, this consulta@on.

Past medical history • claimed that he has no diabetes, no hypertension, no asthma


• no known food and drug allergies
Family history • father is diabe@c and hypertensive
• mother is hypertensive
Personal and social • smokes one pack of cigare]e every day
history • occasionally drinks alcohol

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DAVAO MEDICAL SCHOOL FOUNDATION, INC. – COLLEGE OF MEDICINE
Department of Internal Medicine
Review of systems • denies history of heat intolerance, tremor, bowel changes
• denies chest pain, orthopnea, PND
• denies cough, hemoptysis, rise of temperature in the a^ernoon

Physical ExaminaFon Findings


General Survey Vital Signs Skin HEENT Neck
BP 110/70
HR 94 bpm Neck supple
PERRLA, pupil diameter 3mm bilaterally
Awake, coopera@ve, coherent RR 16 cpm, not labored Nega@ve for rash or other lesions Trachea midline
Anicteric sclera
Not in respiratory distress T 37.1 C Warm to touch No palpable nodes
No nasal drainage
Good skin turgor and mobility No vein disten@on
Fundoscopy: see image
Ht 5’5’’ No neck mass
Wt 61 kgs

Lungs Heart Abdomen Genitalia/Rectum ExtremiFes Neuro


Equal chest expansion
PMI at 5th ICS, 7cm from
Resonant
the midsternal line
Ausculta@on: see a%ached Normoac@ve bowel sounds DRE reveals good sphincter ton, no
Ausculta@on: see a%ached
file So^, nontender, masses, no tenderness, empty CNs II-XII intact
file No clubbing, cyanosis, nor edema
nondistended rectal vault, and no blood on the Muscle strength = 5/5 all extremi@es
Pulses 2+ bilateral in all extremi@es
No guarding, no rebound examining finger See Babinski examina@on below
Intact ROM
case 21 lung tenderness Normal sized prostate without See DTR below
case 21 heart No bruits, no masses nodules, asymmetry
sounds.mp3
sounds.mp3

Babinski Interpret

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DAVAO MEDICAL SCHOOL FOUNDATION, INC. – COLLEGE OF MEDICINE
Department of Internal Medicine

2020-08-10-21-56-28. Negative Babinski sign


mp4

Double click the icon to play the short clip


This examination is necessary because the
patient is already experiencing tingling
Is this examination necessary? Justify. sensation and numbness of both hands and
feet and this test would elicit if there are any
CNS lesion affecting the corticospinal tract.

Deep Tendon Reflexes Interpret

Normal and symmetric biceps,


brachioradialis, triceps, and patellar reflexes.
Diminished achilles tendon reflex.

Yes, this test is necessary because it will


provide information about the extent of
Is this test necessary? Justify.
peripheral neuropathy the patient is
experiencing.

3
DAVAO MEDICAL SCHOOL FOUNDATION, INC. – COLLEGE OF MEDICINE
Department of Internal Medicine

Is this a normal or an abnormal


Fundoscopy IdenFfy and describe the labeled items
finding?

Macula and Fovea. No hard exudates or


1 abnormal spots noted. No signs of macular Normal
degeneration noted.

Optic cup. The disc outline is sharp and


yellow-orange in color. The physiologic cup is
located centrally and yellowish-white in color.
2 Normal
Its diameter from side to side is less than half
that of the disc. No signs of papilledema, or
atrophy noted.
Retinal vein and artery. The arteries are light
red and smaller than veins. The light reflex is
bright. The veins are dark red and larger. The
3 Normal
light reflex is absent. No hemorrhages, tiny
red spots or microaneurysms noted. No
neovascularization noted.

Is this examina@on necessary? Jus@fy. Yes, this examination is necessary because retinopathy is also one of the microvascular
complications of Diabetes mellitus along with neuropathy and nephropathy.

Reference
Question/Task Answer
(Source, page no.)
Was your HPI output the same or
almost the same with your instructor? My HPI output is almost the same as my instructor’s. I still need to improve on it because there are minor details
that I forgot to include. There are data in the HPI that need to be clarified further, like if it’s the first time of the
Do you need to improve on it? Are there
patient to experience these symptoms; if the patient went on a diet prior to the manifestation of weight loss; if
any data in the HPI that you think needs the patient drank a lot of water prior to polyuria; if his urine has a presence of blood; and informations about
to be clarified in the HPI? And what signs and symptoms of other microvascular complications.
were these?

4
DAVAO MEDICAL SCHOOL FOUNDATION, INC. – COLLEGE OF MEDICINE
Department of Internal Medicine
Given the history and physical Harrison’s Principles of
examination, what is now your working Internal Medicine 20th
impression of this case? ● Diabetic neuropathy secondary to Diabetes mellitus type 2 ed., chapters 396 and
398; pages 2853, 2858,
and 2879
What are the nonmodifiable risk factors Harrison’s Principles of
of this patient? ● Age
Internal Medicine 20th
● Family history of diabetes ed., chapter 396; page
2853
What are the modifiable risk factors of Harrison’s Principles of
this patient? ● Cigarette smoking
Internal Medicine 20th
● Obesity ed., chapter 398; page
2870
Calculate the patient’s latest BMI? Bates’ Guide to Physical
Classify. Examination and History
BMI = 22.38 (normal weight) Taking 12th edition;
Chapter 4, pages 116
and 123
Calculate the patient’s BMI prior to the Bates’ Guide to Physical
onset of his complaint? Classify. Examination and History
BMI = 25.6 (overweight) Taking 12th edition;
Chapter 4, pages 116
and 123
Explain the pathogenesis of the This is a manifestation of microvascular complication, which is a result of chronic hyperglycemia. The peripheral
numbness and tingling sensation of the nerves are supplied by small arteries called vasa nervorum, that is why numbness and tingling sensation are in both
patient. hands and feet. Since the mechanism(s) by which hyperglycemia leads to diverse cellular and organ dysfunction is
unknown. These are some of the hypothesis: 1.) epigenetic changes happen in affected cells due to hyperglycemia;
2.) advanced glycosylation end products (AGEs) are formed because of hyperglycemia, which bind to specific cell
Harrison’s Principles of
surface receptor that can lead to cross-linking of proteins, accelerated atherosclerosis, glomerular dysfunction,
Internal Medicine 20th
endothelial dysfunction, and altered extracellular matrix composition; and 3.) hyperglycemia: a) increases glucose
ed., chapter 398; page
metabolism via the sorbitol pathway related to the enzyme aldose reductase; b.) increases the formation of
2876-2877
diacylglycerol, leading to activation of protein kinase C, which alters the transcription of genes for fibronectin, type
IV collagen, contractile proteins, and extracellular matrix proteins in endothelial cells and neurons; and/or c.)
increases the flux through the hexosamine pathway, which generates fructose-6- phosphate, a substrate for O-
linked glycosylation and proteoglycan production, leading to altered function by glycosylation of proteins such as
endothelial nitric oxide synthase.

5
DAVAO MEDICAL SCHOOL FOUNDATION, INC. – COLLEGE OF MEDICINE
Department of Internal Medicine
Explain the pathogenesis of the weight Insulin is a major anabolic hormone, so its deficiency results in a catabolic state that affects not only glucose
loss despite good appetite. metabolism but also fat and protein metabolism. Unopposed secretion of counterregulatory hormones (glucagon,
growth hormone, epinephrine) also plays a role in these metabolic derangements. The assimilation of glucose into
muscle and adipose tissue is sharply diminished or abolished. Not only does storage of glycogen in liver and muscle
Robbins and Cotran
cease, but also reserves are depleted by glycogenolysis.

Pathologic Basis of
Disease 9th edition;
With a deficiency of insulin the scales swing from insulin promoted anabolism to catabolism of proteins and fats.
Chapter 24; page 1113
Proteolysis follows, releasing gluconeogenic amino acids that are removed by the liver and used as building blocks
for glucose. The catabolism of proteins and fats tends to induce a negative energy balance, which in turn leads to
increasing appetite. Despite the increased appetite, catabolic effects prevail, resulting in weight loss and muscle
weakness.
Explain the pathogenesis of the Robbins and Cotran
frequent urination. The resultant hyperglycemia exceeds the renal threshold for reabsorption, and glycosuria ensues. The glycosuria Pathologic Basis of
induces an osmotic diuresis and thus polyuria, causing a profound loss of water and electrolytes. Disease 9th edition;
Chapter 24; page 1113
Explain the pathogenesis of the Robbins and Cotran
The obligatory renal water loss combined with the hyperosmolarity resulting from the increased levels of glucose in
increased water intake. Pathologic Basis of
the blood tends to deplete intracellular water, triggering the osmoreceptors of the thirst centers of the brain. In this
Disease 9th edition;
manner, intense thirst (polydipsia) appears.
Chapter 24; page 1113

Make a video demonstra@on on how to properly execute the following examina@ons:


1. Cranial Nerve Examina@on
2. Babinski
You may look for a partner inside your residence. If you don’t have a partner, improvise. You may use a dummy in some examina@ons or you may act as the pa@ent. Wear mask.
For this video ac@vity, you are expected to:
● Do the examina@on correctly based on your prior knowledge on how to execute the maneuver
● Provide proper instruc@ons to the pa@ent as you proceed with the examina@on
● Do the examina@on as how you would execute it to your real pa@ent
Follow this video outline:
1. Introduce yourself properly to your preceptor (no need to build rapport for this ac@vity)
2. Proceed with the examina@on (no need to explain to the preceptor)
To submit the video, upload it in google drive then copy the shareable link and paste the link below. Make sure you have turned on the link from google drive.

Paste the link of the video in


the next blank column

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