SANTOS, Sean Lemuel L.

[OS 215 ENDOCRINOLOGY] PRECEPTORIALS CASE REPORT

This is the case of AP, 27/M from San Andres, Manila who came in for his follow-up
appointment regarding his diabetes (since 2015, currently on insulin maintenance)

I. PATIENT HISTORY

A. History of Present Illness

December 2015 ● Px experienced weight loss, polyuria, and polydipsia observed
for 1 month prior, for which he eventually sought consult at the
clinic, as well as for concomitant fever
● Thereafter diagnosed with diabetes, given metformin and
advised lifestyle modification → observed to have regained
strength

Interim ● Followed up at the clinic every 2 weeks for 2 months, then was
referred to PGH

2017/18 ● Px was put on insulin (3x a day, 30 mins before meals currently)
○ 20U 70:30 in the morning
○ 08U of regular insulin at lunch
○ 18U 70:30 at night

2017/18 ● Px had pneumonia infection

○ Manifested as difficulty of breathing (orthopnea), back
pain
○ Given co-amoxiclav for 1 week and had a thoracentesis

2018 ● Px was brought to ER due to loss of consciousness secondary to

hypoglycemia on 2 separate occassions:
● On the first, Px was unable to eat dinner upon falling asleep after
an insulin injection and rushed to Manila Doctors
● On the second, Px was unable to eat lunch after an insulin
injection due to toxic work shift and rushed to PGH

2020-present ● Px had a total of 2 teleconsultations

February 22, 2023 ● Px came in for a check-up due to uncontrolled blood sugar
○ FBS usually around 200-300 mg/dL
○ Went to a birthday party and indulged with food (crispy
pata, rice, etc.)
○ Revealed to have elevated LDL and prescribed
atorvastatin (40mg, 1x/day)
○ Prescribed Vit B1 for occasional numbness of his arms
 SANTOS, Sean Lemuel L.

B. Past Medical History

● Diagnosed with diabetes in 2015
● Hospitalizations: pneumonia (2018), loss of consciousness d/t hypoglycemia (2018)
● (-) previous surgeries, CV events
● Past medications: metformin, insulin NPH, regular insulin, atorvastatin (OD), vit. B1 (for
pangangalay)
● Completed 2 doses of Sinovac, no boosters taken

C. Family History
● (+) diabetes in father (unknown type), (+) lung cancer in paternal grandfather
● (-) diabetes in the rest of the immediate family (mother and siblings)

D. Personal and Social History

● 2nd child to a mother of 8 children living in a compound of two houses
● Previously worked as a supervisor in Shakey’s restaurant, now works as a delivery man
since 2020
● (-) smoking
● (+) occasional drinking (“only during birthday parties/special occasions”)
● Regular physical activity (e.g., basketball 3-4x/week)
● High carbohydrate diet: prior to diagnosis, ate 4-5 cups of rice per meal and ate up to
5x/day, with predilection towards meat, specifically chicken with skin; now cuts on rice
and avoids sweeteners and sweet drinks
● Changes in sexual activity: Currently, not sexually active but has noticed erectile
dysfunction

E. Review of Systems
● (+) Myopia
● (+) Occasional numbness
● No pruritus
● No fever, malaise, poor appetite
● No chest pain, palpitations, easy fatigability, syncope, diaphoresis, edema
● No coughing or wheezing
● No congestion or rhinorrhea
● No hot or cold intolerance, polydipsia, polyuria
● No GIT pain, vomiting, constipation, diarrhea
● No muscle pain or weakness
● No headache or dizziness
 SANTOS, Sean Lemuel L.

II. PHYSICAL EXAMINATION

A. General Survey ● Pupils are equal, round and react to

● Hygiene: Clean/neat light and accommodation
● Nutrition: Well-nourished ● EOM intact
● General appearance: Relaxed ● Nares patent
● Emotional state: Calm
● Development: Well F. Neck
● Coherence: Coherent ● Supple
● Consciousness: Conscious ● No lymphadenopathy
● Orientation: Oriented ● Normal range of motion

B. Anthropometric Measurements G. Respiratory

● Temperature: 36.4 ● Normal respiratory effort
● BP: 117/90 (R) and 110/90 (L) ● No wheezing, rhonchi or rales
● HR: 84 ● Lungs clear to auscultation
● SO2: 99 bilaterally
● RR: 20
● PR: 83 H. Cardiovascular
● Weight: 52 kg ● Regular rate and rhythm
● Height: 1.62 m ● Normal S1/S2
● BMI: 19.8 (Normal) ● No murmurs, rubs and gallops

C. Integument I. Abdominal
● General color: Normal ● Soft, non-distended; non-tender;
● Lesions/Rashes: Absent normal bowel sounds; no masses
● Texture: Smooth ● Injection site at lower right quadrant
● Moisture: Normal
● Temperature: Normal J. Extremities
● Normal tone and range of motion
D. Nails ● Strength and sensation intact
● Color: Pink ● Capillary refill < 2s
● Nail plate: Convex ● 2+ dorsalis pedis pulse bilaterally
● Capillary refill: < 2 sec (Normal)
● Texture: Smooth K. Neurology
● Inflammation: Negative ● (-) CN deficits (CN1, CN5 not tested)
● Alert and oriented
E. HEENT ● Reflex symmetric
● Normocephalic ● Sensation normal
● Atraumatic ● Gait normal
 SANTOS, Sean Lemuel L.

III. COMPREHENSIVE FOOT EXAMINATION

A. Relevant Medical History

● Myopia (R: 20/50 and L: 20/70)

B. Current History
● No change in foot or feet since last evaluation
● No current ulcer or history of a foot ulcer
● No pain in calf muscles when walking that is relieved by rest

C. Initial Survey
● Normal gait and posture
● No foot deformities

D. Foot Exam
● Nails are not thick, too long, ingrown or infected with fungal diseases
● No toe deformities, bunions, charcot foot, foot drop, prominent metatarsal heads or
amputation
● L and R posterior tibial pulses and dorsalis pedis pulses are present
● Skin not thin, fragile, shiny and hairless
● Probable evidence of callus formation on L hindfoot
○ No signs of pre-ulceration
○ No blood or discharge on the socks or hose

E. Sensory Foot Exam

● Normal vibratory, proprioception, and 10g monofilament sensation
● 2+ ankle reflexes

F. Risk Categorization: Low-Risk Patient

● Intact protective sensation
● No prior foot ulcer
● No foot deformity
● Pedal pulses present
● No amputation

G. Footwear Assessment
● Patient wears appropriate shoes
● Patient does not need diabetic shoes/inserts

H. Education
● Patient demonstrates appropriate foot care
 SANTOS, Sean Lemuel L.

IV. IMPRESSIONS AND DIFFERENTIAL DIAGNOSIS

Differentials Reasons to Rule In Reasons to Rule Out

Type 1 Diabetes Mellitus ● Elevated blood glucose

levels
● Early age of onset
● Normal BMI
● Insulin therapy controlled
blood glucose levels
● Family history of diabetes
● High carbohydrate diet

Type 2 Diabetes Mellitus ● Elevated blood glucose ● Patient is not old

levels ● Patient is not
● Family history of diabetes obese/overweight
● High carbohydrate diet ● Metformin was not
effective

Hyperthyroidism ● (+) Weight loss ● (-) goiter

● (+) Frequency of urination

V. BASIS FOR PRIMARY DIAGNOSIS

The primary diagnosis is Type 1 Diabetes Mellitus. The patient exhibited polyuria, polydipsia
and unexplained weight loss which rules in both diabetes and hyperthyroidism. However, there
is an absence of both goiter and the classical signs of hyperthyroidism such as excessive
sweating, tachycardia, diarrhea, and tremors among others, which rules out the condition. The
presence of risk factors such as high-carbohydrate diet and family history of diabetes further
rules in diabetes although the latter favors type 2 more than type 1. However, the early age of
onset, normal BMI and the ineffectiveness of metformin, and the requirement of insulin as 1st
line treatment heavily favors the diagnosis of Type 1 DM sinnce Type 2 DM is more commonly
seen in the adult and obese population, and metformin should be generally effective as a first
line of treatment.

VI. PATHOPHYSIOLOGIC CORRELATION

Based on the information from the patient history and physical examination, the primary working
impression is Type 1 Diabetes Mellitus–a chronic condition wherein autoantibodies attack the
insulin-producing pancreatic beta cells which leads to insulin insufficiency (Kasper et al., 2019).
Since the patient presented the classical signs of hyperglycemia (weight loss, polyuria, and
polydipsia), the evidence appears to point towards a primary diagnosis of diabetes.

In diabetes, blood glucose is unable to enter the peripheral tissues such as the adipose and
muscle tissues. As a result, these tissues use their stored alternative sources of energy in order
to maintain their normal metabolic functions. Adipocytes metabolize fatty acids through lipolysis
while the muscles use proteins through proteolysis. As a result, the body loses fats and proteins
which leads to weight loss (Jiang et al., 2020).

The patient was also reported to be polyphagic although he mentioned that he was already
 SANTOS, Sean Lemuel L.

eating too much even before the symptoms of polyuria, polydipsia and weight loss started to
become apparent. Nonetheless, his already excessive eating pattern prior to diagnosis might
have masked his polyphagia when he began to have symptoms. In diabetes, polyphagia occurs
because when the body triggers the sensation of hunger when it is unable to utilize the glucose
in the blood (Fournier, 2000).

Meanwhile, polyuria occurs because the kidneys fail to reabsorb the excess glucose that is
filtered from the blood. This excess glucose drags so much water with them that the body
begins produce too much urine at a fast rate. This excessive urination lowers the blood volume
triggering a thirst sensation and consequently resulting to polydipsia (Burmazovic et al., 2018).

Hyperthyroidism can be initially ruled out because there is no goiter and absence of classical
signs such as heat intolerance, unprovoked anxiety and palpitations, diarrhea, and tremors
among others.

There are certain risk factors that contribute to the development of diabetes. Among these are
family history of diabetes, obesity, and a high carbohydrate diet. Both Type 1 and Type 2 DM
have a significant genetic component with Type 1 DM having a 30-70% concordance and Type
2 DM having a 70-90% concordance in identical twins (Kasper et al., 2019). Obesity is more
often linked to Type 2 rather than Type 1 DM. As mentioned previously, Type 1 DM is due to a
defect in insulin secretion. On the other hand, Type 2 DM is generally and initially due to a
defect in insulin sensitivity.

In Type 2 DM, glucose molecules in the blood are unable to enter the peripheral tissues
because their insulin receptors respond less to insulin in the blood. Normally, when insulin binds
to its receptors, a signalling pathway is activated which eventually leads to the insertion of
GLUT4 molecules into the membrane of its target cells. One of the factors that contribute to
insulin resistance is obesity. In obese individuals, there is an excess of fatty acid molecules
stored in adipocytes and used by tissues as a source of energy. Once the tissues become
reliant on fatty acids, by some unknown mechanism, their insulin receptors become resistant to
insulin and they become less reliant on glucose. As a result, glucose remains in the blood–a
state of hyperglycemia (Kahn & Hull, 2006).

In this patient, the evidence seems to be pointing towards Type 1 rather than Type 2 DM
because based on his physique and BMI, he is not overweight/obese and does not seem to
have too much fat in the body which would otherwise predispose him to Type 2 DM. His normal
BMI suggests a problem of insulin secretion rather than insulin action, thereby favoring the
diagnosis of Type 1 DM.

The patient’s high-carbohydrate diet appears to be an aggravating and not a causative factor in
the development of Type 1 DM. The insulin production in the pancreas might have already be
deteriorating early-on during the asymptomatic stage. When the glucose intake suddenly
spiked, it created a shortage of available insulin because the demand overwhelmed the body’s
supply of insulin.

Nonetheless, a high-carbohydrate diet could also predispose a person to develop Type 2 DM.
When there is excessive blood glucose, the beta cells of the pancreas initially compensates by
producing more insulin. However, as they release insulin, they also release amylin which, over
time, accumulates within the zone of beta cells, hardens the beta cells and reduces their
capacity to produce insulin, eventually leading to beta cell exhaustion (Kanatsuka et al., 2018).
However, this pathology occurs for a long period of time and is therefore seen among older
 SANTOS, Sean Lemuel L.

individuals, which is inconsistent with the condition of the patient who became symptomatic at
the age of just 15 years old. In fact, the age of onset is one of the distinguishing features of the
two types of DM, with Type 1 DM having an early age of onset and Type 2 DM occuring
commonly in the adult years (Kasper et al., 2019).

The medication of the patient provides proof of the type of diabetes that he has. As mentioned
in the history, the patient was initially prescribed metformin–an insulin sensitizer that is used to
treat Type 2 DM. After some time, the patient still experienced hyperglycemic episodes,
indicating that the problem is not insulin action. When he was finally prescribed with insulin, he
was finally able to control his blood sugar, indicating an insulin secretion problem. In fact, the
insulin medication was so effective in lowering his blood glucose levels that he had two
hypoglycemic episodes (eventually leading to temporary loss of consciousness) when he forgot
to eat food after injecting insulin. This occurs because the brain solely relies on glucose as an
energy source. When an already reduced blood glucose is taken up by the cells due to insulin
influx, the brain gets deprived of glucose and malfunctions as a result—manifesting in the form
of neurological symptoms such as fainting as experienced by the patient (Cryer, 2007).

Diabetes, in general, and type 1 DM, in particular, can lead to various complications such as
infections, hypercholesterolemia, retinopathies and neuropathies to name a few. In this case,
the patient once had a pneumonia infection 2 to 3 years after being diagnosed with diabetes.
Excess glucose molecules in the blood combines with basement membrane proteins of blood
vessels (Lee et al., 2022) and activates the protein kinase C pathway, causing blood vessel wall
thickening (Lien et al., 2021). This results to decreased vascular supply and thus, a decreased
delivery of immune cells to sites of infection (Kasper et al., 2019).

Furthermore, the patient was also found to have elevated LDL in 2023. In diabetes, excess
glucose molecules can combine with lipids to form modified (glycated) LDLs that can lodge in
the intima of blood vessels and eventually accumulate to form atheromatous plaques (Poznyak
et al., 2020). For this reason, the patient was prescribed atorvastatin—an HMG-CoA reductase
inhibitor that prevents the conversion of HMG-CoA to mevalonate which is the rate-limiting step
in cholesterol synthesis in the liver. Decreased cholesterol synthesis consequently leads to
enhanced synthesis of LDL receptors which are essential in sequestering excess LDLs in the
blood (Kasper et al., 2019).

Myopia is another possible diabetic complication that is present in the patient. In diabetes, lens
cells and fibers take up enormous amounts of glucose which triggers the enzyme aldose
reductase to convert them into sorbitol. However, as sorbitol accumulates, water from the
aqueous humor is abstracted leading to lenticular swelling and thus, to increased lens
curvature: manifesting as myopia (Kaštelan et al., 2018).

The patient also presents neuropathic complications such as erectile dysfunctions, numbness,
and probable evidence of callus formation on the left hindfoot. Erectile dysfunction might also be
a vascular complication and this can be confirmed if the patient is responsive to
phosphodiesterase inhibitors such as Sildenafil (Defeudis et al., 2021). Numbness is a sensory
neuropathy while possible callus formation is a motor neuropathy. By some unknown
mechanism, diabetic neuropathies might be due to the following reasons: reduction in
neurofilament, nerve ischaemia, demyelination, degeneration and reduced Schwann cell-axonal
transport (Feldman et al., 2019).
 SANTOS, Sean Lemuel L.

VII. MANAGEMENT

A. DIAGNOSIS

In diagnosing patients suspected to have diabetes, blood glucose can be measured to establish
the diagnosis. Criteria for the diagnosis of DM is as follows: (1) Fasting blood sugar (FBS) of at
least 120 mg/dl and/or (2) Random blood sugar (RBS) of at least 200 mg/dl and/or (3)
Hemoglobin A1C of at least 6.5% and/or (4) 75g OGTT of at least 200 mg/dl.

Serum C-peptide measurement can also be done to further rule-in type 1 DM and confirm the
need for insulin therapy in the presence of an elevated glucose level. Isulin and serum
C-peptide are both derived from the same polypeptide. Absence of C-peptide suggests absence
of insulin as seen in type 1 DM.

Antibody markers for type 1 DM may also be ordered to confirm whether there are antibodies
that are attacking the beta cells of the pancreas. These include islet cell, insulin and glutamic
acid decarboxylase antibodies. Lipid profile measurements can be ordered to detect if there is
dyslipidemia–a risk factor and a concomitant problem in DM.

Physical examination such as fundoscopy and foot exam may also be performed to detect any
presence of retinopathies and/or neuropathies, respectively.

B. TREATMENT

Since the patient appears to have type 1 DM, the primary therapy is insulin. Thus, the patient
should continue taking his short-acting insulin 30 minutes before every meal. The patient is also
advised to have a consistent physical activity of at least 30 minutes of moderate intensity
exercise every other day and adhere to a medical nutrition therapy plan by lowering intake of
high glycemic index foods and having a consistent meal plan.

For his other diabetes-related conditions, the patient should continue his intake of atorvastatin
as prescribed to control his dyslipidemia and to prevent the development of macrovascular
complications such as myocardial infarction, stroke and peripheral artery disease. He should
also continue with his intake of Vitamin B complex for occasional numbness and may take
Sildenafil for erectile dysfunction as needed. The patient is also advised to wear corrective
lenses for his near-sightedness and complete his immunization for prevention of infections.

Finally, the patient should be given psychosocial support and diabetes management education.
He should be given counseling for any psychological distress, be linked to diabetes support
groups, and be taught on how to have a glycemic and therapeutic goal, and how to perform a
daily foot examination.
 SANTOS, Sean Lemuel L.

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