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Department of Internal Medicine: Day 2 Activity
Department of Internal Medicine: Day 2 Activity
– COLLEGE OF MEDICINE
Department of Internal Medicine
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:
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.
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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
Babinski Interpret
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Department of Internal Medicine
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DAVAO MEDICAL SCHOOL FOUNDATION, INC. – COLLEGE OF MEDICINE
Department of Internal Medicine
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?
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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.
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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