Documente Academic
Documente Profesional
Documente Cultură
Submitted by:
GENERAL DATA
• Name: M.L., Sr.
• Sex: Male
• Age: 73 years old
• Birthdate: September 20, 1945
• Civil Status: Widower
• Educational Attainment: Elementary Graduate
• Occupation: Previously a Farmer (approximately 40 years)
• Nationality: Filipino
• Religion: Roman Catholic
• Place of Residence: Barangay Agutayan, Dueñas, Iloilo
• Blood Type: AB (+)
• Sources of Data: M.L., Sr.; E.L. (2nd child); M.L., Jr. (7th child)
Previous On-hand Medical Records
• Reliability: 90%
• Date of Admission: January 7, 2019 (9 AM)
• Room Number: METC, BED 2
• Handedness Right-Handed
B. Blood Chemistry
• FBS: ↑ 216 mg/dl • Triglycerides: ↑ 4.67 mmol/L
• Uric Acid: ↑ 584 umol/L • HDL: ↓ 1.3 mmol/L
• Creatinine: ↑ 123.44 U/L • LDL: ↑ 5.09 mmol/L
• Cholesterol: ↑ 8.51 mmol/L • SGPT: ↑ 49 IU/L
On the day of admission, still with body weakness and blurring of vision.
A. IMMUNIZATION HISTORY
Completed, as claimed by the 2nd child.
B. CHILDHOOD ILLNESS
Unrecalled
C. ADULT ILLNESS
Patient is a known diabetic diagnosed last 2016, however, he is non-compliant to his maintenance med-
ications such as Gliclazide and Metformin. He also has monthly checkups.
Diabetes (+)
Hypertension (-)
Pneumonia (-)
Hepatitis (-)
HIV (-)
Tuberculosis (-)
Cancer (-)
Asthma (-)
Allergies (-)
D. SURGICAL HISTORY AND HOSPITALIZATIONS
▪ 2017: Patient was admitted because of complaint of chest pain. A tumor in the kidney was also found as
claimed by his 7th child.
▪ July 2018: Patient was requested an ultrasound for his abdominal pain
E. PSYCHIATRIC HISTORY
None
F. SCREENING/LABORATORY TESTS
July 2018: Ultrasound result showed:
▪ Fatty liver
▪ Hepatic Nodules Vs Complex Cysts, unchanged
▪ Renal Cysts,Bilateral
▪ Distal Abdominal Aorta Fusiform Aneurysm
▪ Normal Gallbladder, Pancreas, Spleen, Urinary Bladderand Prostate
January 4, 2018: Complete laboratory workup (CBC, Cholesterol, FBS, etc.)
Results showed:
▪ High level of fasting blood sugar, as claimed by his 7th child
G. FAMILY HISTORY
There is no family history of diabetes, hypertension, hepatitis, asthma, HIV, TB, congenital defects, al-
lergies, psychiatric problems, cancer, or familial diseases. His wife died of leukemia at 50 years old.
Hematuria /
Suprapubic pain /
Hesitancy /
Dribbling /
Musculoskeletal
Muscle/joint pain /
Arthritis /
Backache /
Fever /
Chill /
Rash /
Muscle Weakness /
Stiffness /
Limitation of activity /
Neurologic
Dizziness /
Loss of consciousness /
Seizure /
Sensory loss /
PHYSICAL EXAMINATION
General Survey
▪ Patient was lying on bed, awake, responsive.
▪ IV line was inserted on right hand.
Vital Signs
Temperature: 37.0 0 C
Pulse rate: 72 bpm
Respiratory rate: 21 cycle per minute
Blood Pressure: 90/60 mmHg
HEENT
Head
▪ Head was normocephalic.
▪ No wounds, scars or rashes noted.
▪ No palpable masses or tenderness.
▪ Hair is white in color, evenly distributed.
Eyes
▪ Eyebrows are symmetric noted to be white.
▪ Eyelids showed no edema or lesions.
▪ Eyes open to stimuli.
▪ Pupils are black
▪ They were equally round and reactive to light and accommodation.
▪ Positive direct and consensual reflexes on both eyes.
▪ Clear sclerae; pinkish in color bulbar and palpebral conjunctiva
▪ No discharges or tearing noted.
▪ No lesions, lacerations or scars noted.
Ears
▪ Ears are normal in size and symmetrical.
▪ No discharges, lumps, or lesions noted.
▪ Poor response to whispered voice.
!7
Nose
▪ Nose was midline, patent, no visible redness, and no discharges seen.
▪ Septum is at the midline; no nasal flaring noted.
▪ Mucous membranes pink and moist.
▪ No lesions or swelling noted.
▪ No pain or tenderness in frontal and maxillary sinuses upon palpation.
Lungs
• Symmetrical with good expansion. No use of accessory muscles noted.
• No tenderness upon palpation.
• No lagging sign noted; lungs resonant; breath sounds vesicular.
• No crackles, wheezes, or rhonci; no adventitious breath sounds heard upon auscultation.
Cardiovascular
• Adynamic precordium; Point of Maximal Impulse at 5th Intercostal Space Mid-Clavicular Line.
• Carotid pulse, brachial pulse, & radial pulse palpable.
• No heaves or thrill noted upon auscultation; no abnormal heart sounds or murmurs heard upon auscultation.
Abdomen
• Round; symmetrical; warm to touch; no bruise, erythema and jaundice noted; no dilated vein, rashes, striae
noted; umbilicus contoured downward, midline, no inflammation and ventral hernia noted.
• Normoactive bowel sounds (12-22) heard on right lower quadrant; no borborygmy and bruits noted
• No direct and rebound tenderness noted; negative in fluid wave test; negative for Rovsing’s sign; no Cullen’s
and Grey Turner signs noted.
Musculoskeleteal
• Upper Extremities
• Symmetrical and warm to touch.
• IV line inserted on the right metacarpal. No swelling, deformities, muscle atrophy, fasciculations,
or abnormal positioning noted. Dislocations on joints are not noted.
• No pain upon palpation of bony landmarks.
• Brachial and Radial pulses are palpable.
• Lower Extremities:
• Symmetrical and warm to touch. Foot pads are wrapped with a moist towel.
• No wounds, swelling deformities, atrophy or abnormal positioning noted on both extremities.
• Femoral, Popliteal, and Dorsalis Pedis pulses are palpable. Can distinguish light touch or sharp
objects on both feet.
MUSCLE STRENGTH
Left Right
Genitourinary
Not assessed
Nervous System
Mental status: Patient is conscious, eyes open spontaneously, cooperative and answers questions when
asked. Patient is oriented to time, place and his surroundings.
Motor: Patient is able to move all limbs against resistance. Able to keep balance when standing still
with hands at the side. Able to keep balance when walking.
CRANIAL NERVES
CN 1: Olfactory CN I olfactory:
Intact, able to distinguish smell of rubbing alcohol.
CN 2: Optic CN II Optic:
Able to point to the moving finger of examiner.
Vision is blurry when reading letters unless directly
in front of the patient.
CN 5: CN V: Trigeminal:
Patient can discern light touches on forehead,
Trigeminal
cheeks, and chin; blinks when corneas are
touched by cotton
CN 11: CN XI Accessory;
Able to move neck and shoulders against resis-
Accessory
tance muscle strength of 5/5.
DIABETES MELLITUS
Diabetes Mellitus is a chronic disease due to the pancreas’ deficient production of insulin or by the
ineffectiveness of the insulin produced. The cause may be either both acquired or an inherited one. These defi-
ciencies leads to increased levels of glucose concentrations in the blood, that may eventually damage different
systems of the body. The increased levels of glucose may damage the blood vessels of kidneys, eyes or even
neuropathy when left untreated.
The disease is generally divided into two principal forms, Type 1 which is insulin dependent or Type 2
which is the non-insulin dependent form of the disease. Type I Diabetes although previously known as juvenile-
onset diabetes, this may also develop in adults. It is an autoimmune condition where antibodies attack the pan-
creas and destroys the insulin-secreting beta cells in the islets of Langerhans.
DIFFERENTIAL DIAGNOSES
HYPEROSMOLAR HYPERGLYCEMIC STATE (HHS)
Hyperosmolar hyperglycemic state (HHS) is a metabolic complication of diabetes mellitus that is charac-
terized by severe hyperglycemia, extreme dehydration, hyperosmolar plasma, and altered consciousness. This is
primarily seen in individuals with type 2 diabetes mellitus and develops within several weeks. Insulin levels in
HHS are inadequate to facilitate glucose utilization by insulin-sensitive tissues, but are adequate enough to pre-
vent lipolysis and ketogenesis. It presents with polyuria, weight loss, decreased oral intake, mental confusion,
lethargy, profound dehydration, hypotension, tachycardia, and altered mental status. Individuals however do not
present with nausea, vomiting, abdominal pain, and Kussmaul respiration. Risk factors for HHS include old age,
poor kidney function, poor diabetes management, infection, heart problems, and certain medications. Diagnosis
of HHS include a plasma glucose of level of >600 mg/dl and increased plasma osmolality >320 mOsm/kg with-
out ketoacidosis.
DKA is a serious complication of diabetes that occurs when the body produces high levels of blood acids
called ketones. The condition develops when the body can't produce enough insulin. Insulin normally plays a key
role in helping sugar (glucose) a major source of energy for the muscles and other tissues that enter the cells.
Without enough insulin, the body begins to break down fat as fuel. This process produces a buildup of acids in
the bloodstream called ketones, eventually leading to diabetic ketoacidosis if untreated.
STROKE
A stroke occurs when the blood supply to part of your brain is interrupted or reduced, depriving brain
tissue of oxygen and nutrients. Within minutes, brain cells begin to die. It may be caused by a blocked artery
(ischemic stroke) or the leaking or bursting of a blood vessel (hemorrhagic stroke). Some may experience only
a temporary disruption of blood flow to the brain (transient ischemic attack, or TIA) that doesn't cause perma-
nent damage.
About 80 percent of strokes are ischemic strokes. Ischemic strokes occur when the arteries to the brain
become narrowed or blocked, causing severely reduced blood flow (ischemia). While, Hemorrhagic stroke occurs
when a blood vessel in the brain leaks or ruptures. Brain hemorrhages can result from many conditions that af-
fect the blood vessels.
HYPOGLYCEMIA
Hypoglycemia is characterized by a reduction in plasma glucose concentration to a level that may induce
symptoms or signs such as altered mental status and/or sympathetic nervous system stimulation. This condition
typically arises from abnormalities in the mechanisms involved in glucose homeostasis. The most common cause
of hypoglycemia in patients with diabetes is injecting a shot of insulin and skipping a meal or overdosing insulin.
RULE IN RULE OUT
CANCER
A disease in which abnormal cells divide without control and can invade nearby tissue. Cancer cells can
also spread to other parts of the body through the blood and lymph system. A serious disease that is caused
when cells in the body grow in a way that uncontrolled and not normal, killing normal cells and often causing
death.
ANEMIA
A condition that develops when your blood lacks enough healthy red blood cells or hemoglobin. Anemia
happens when there is a decrease number of circulating red blood cell in the body. It is the most common blood
disorder in the general population.
PITUITARY TUMOR
Pituitary tumors are abnormal growths that develop in your pituitary gland. Some pituitary tumors result
in too many of the hormones that regulate important functions of your body. Some pituitary tumors can cause
your pituitary gland to produce lower levels of hormones. Most pituitary tumors are noncancerous (benign)
growths (adenomas). Adenomas remain in your pituitary gland or surrounding tissues and don't spread to other
parts of your body.
RULE IN RULE OUT
DIABETES INSIPIDUS
Diabetes Insipidus (DI) is a rare disorder of the posterior pituitary that is characterized by a deficiency
of antidiuretic hormone (ADH) or vasopressin which helps regulate amount of fluid in the body. The decrease in
ADH causes a decrease in water reabsorption in the renal tubules and decreases intravascular fluid volume. This
leads to increased serum osmolality and excessive urine output. Patient would present with excessive thirst even
after drinking fluids and excretion of large volume of dilute urine. Other signs of DI include nocturia, bed-wet-
ting, fever, difficulty sleeping, unexplained weakness, muscle pains, irritability, lethargy, vomiting, diarrhea, and
it can interfere with appetite causing weight loss. Patient may also have electrolyte imbalance and may become
dehydrated. Risk factors included head injury, surgeries, familial tendencies, infections, vascular problems, and
some drugs. Tests that can verify this diagnosis include your urinalysis and water deprivation test.
Carbon monoxide poisoning occurs when carbon monoxide builds up in your bloodstream. When too
much carbon monoxide is in the air, your body replaces the oxygen in your red blood cells with carbon monox-
ide. This can lead to serious tissue damage, or even death.
Carbon monoxide is a colorless, odorless, tasteless gas produced by burning gasoline, wood, propane,
charcoal or other fuel. Improperly ventilated appliances and engines, particularly in a tightly sealed or enclosed
space, may allow carbon monoxide to accumulate to dangerous levels.
▪ This blood test indicates your average blood sugar level for the past two to three months. Normal levels
are below 5.7 percent, and the result between 5.7 and 6.4 percent is considered prediabetes. An A1c
level of 6.5 percent or higher on two separate tests means you have diabetes.
❖ RANDOM BLOOD SUGAR TEST
▪ Blood sugar values are expressed in milligrams per deciliter (mg/dL), or millimoles per Liter (mmol/L).
Regardless of when you last ate, a sugar level is 200mg/dl (11.1 mmol/L) or higher suggests diabetes,
especially if you also have signs and symptoms of diabetes, such as frequent urination and extreme
thirst.
❖ FASTING BLOOD SUGAR TEST
▪ A blood sample is taken after an overnight fast. A reading of less than 100mg/dL (5.6 mmol/L) is nor-
mal. A level from 100-125 mg/dL (5.6 to 6.9 mmol/L) is considered prediabetes.
▪ If your fasting blood sugar is 126 mg/dL (7 mmol/L) or higher on two separate tests, you have diabetes.
▪ This test is less commonly used than the others, except during pregnancy. You’ll need to fast overnight
and then drink a sugary liquid at doctor’s office. Blood sugar levels are tested periodically for the next
two hours.
▪ A blood sugar level less than 140 mg/dL (7.8 mmol/L). a reading between 140 and 199 mg/dL (7.8
mmol/L and 11.0 mmol/L) indicates prediabetes. A reading of 200 mg/dL (11.1 mmol/L) or higher after
two hours suggests diabetes.
MANAGEMENT
The goals in caring for patients with diabetes mellitus are to eliminate symptoms and to prevent, or at
least slow, the development of complications. Microvascular (ie, eye and kidney disease) risk reduction is ac-
complished through control of glycemia and blood pressure; macrovascular (ie, coronary, cerebrovascular, pe-
ripheral vascular) risk reduction, through control of lipids and hypertension, smoking cessation, and aspirin ther-
apy; and metabolic and neurologic risk reduction, through control of glycemia.
Aggressive glucose lowering may not be the best strategy in all patients. However, in this case, glucose
lowering medications is important. Individual risk stratification is highly recommended. In patients with ad-
vanced type 2 diabetes who are at high risk for cardiovascular disease, lowering HbA1c to 6% or lower may in-
crease the risk of cardiovascular events.
A. Pharmacologic Therapy
Early initiation of pharmacologic therapy is associated with improved glycemic control and reduced long-
term complications in type 2 diabetes. Drug classes used for the treatment of type 2 diabetes include the follow-
ing:
• Biguanides
• Sulfonylureas
• Meglitinide derivatives
• Alpha-glucosidase inhibitors
• Thiazolidinediones (TZDs)
• Glucagonlike peptide–1 (GLP-1) agonists
• Dipeptidyl peptidase IV (DPP-4) inhibitors
• Selective sodium-glucose transporter-2 (SGLT-2) inhibitors
• Insulins
• Amylinomimetics
• Bile acid sequestrants
• Dopamine agonists
Biguanides
Metformin is the only biguanide in clinical use. Metformin has proved effective and safe. A nested case-
control analysis found that, as with other oral antidiabetic drugs, lactic acidosis during metformin use is very rare
and is associated with concurrent comorbidity.
Metformin lowers basal and postprandial plasma glucose levels. Its mechanisms of action differ from
those of other classes of oral antidiabetic agents; metformin works by decreasing hepatic gluconeogenesis. It
also decreases intestinal absorption of glucose and improves insulin sensitivity by increasing peripheral glucose
uptake and utilization.
Patients on metformin have shown significant improvements in hemoglobin A1c and their lipid profile,
especially when baseline values are abnormally elevated. In addition, metformin is the only oral diabetes drug
that reliably facilitates modest weight loss. In the UKPDS, it was found to be successful at reducing macrovascu-
lar disease endpoints in obese patients.The results with concomitant sulfonylureas in a heterogeneous popula-
tion were conflicting, but overall, this drug probably improves macrovascular risk.
Sulfonylureas
Sulfonylureas (eg, glyburide, glipizide, glimepiride) are insulin secretagogues that stimulate insulin re-
lease from pancreatic beta cells and probably have the greatest efficacy for glycemic lowering of any of the oral
agents. However, that effect is only short-term and quickly dissipates. Sulfonylureas may also enhance peripher-
al sensitivity to insulin secondary to an increase in insulin receptors or to changes in the events following insulin-
receptor binding.
Sulfonylureas are indicated for use as adjuncts to diet and exercise in adult patients with type 2 diabetes
mellitus. They are generally well-tolerated, with hypoglycemia the most common side effect. The first-generation
sulfonylureas are acetohexamide, chlorpropamide, tolazamide, and tolbutamide; the second-generation agents
are glipizide, glyburide, and glimepiride. The structural characteristics of the second-generation sulfonylureas
allow them to be given at lower doses and as once-daily regimens.
Meglitinide derivatives
Meglitinides (eg, repaglinide, nateglinide) are much shorter-acting insulin secretagogues than the sul-
fonylureas are, with preprandial dosing potentially achieving more physiologic insulin release and less risk for
hypoglycemia. Although meglitinides are considerably more expensive than sulfonylureas, they are similar in
their glycemic clinical efficacy.
Alpha-glucosidase inhibitors
These agents delay sugar absorption and help to prevent postprandial glucose surges. Alpha-glucosidase
inhibitors prolong the absorption of carbohydrates, but their induction of flatulence greatly limits their use. They
should be titrated slowly to reduce gastrointestinal (GI) intolerance.
Thiazolidinediones
TZDs (eg, pioglitazone [Actos], rosiglitazone [Avandia]) act as insulin sensitizers; thus, they require the
presence of insulin to work. They must be taken for 12-16 weeks to achieve maximal effect.
These agents are used as monotherapy or in combination with sulfonylurea, metformin, meglitinide,
DPP-4 inhibitors, GLP-1 receptor agonists, or insulin. They are the only antidiabetic agents that have been
shown to slow the progression of diabetes (particularly in early disease).
Glucagonlike peptide–1 agonists
GLP-1 agonists (ie, exenatide, liraglutide, albiglutide, dulaglutide) mimic the endogenous incretin GLP-1;
they stimulate glucose-dependent insulin release, reduce glucagon, and slow gastric emptying. The use of a
GLP-1 in addition to metformin and/or a sulfonylurea may result in modest weight loss. Animal data suggest that
these drugs prevent beta-cell apoptosis and may in time restore beta-cell mass. The latter property, if proven in
humans, would have tremendous therapeutic potential.
B. Dietary Modifications
For most patients, the best diet is one consisting of the foods that they are currently eating. Attempts to
calibrate a precise macronutrient composition of the diet to control diabetes, while time-honored, are generally
not supported by the research. Caloric restriction is of first importance. After that, individual preference is rea-
sonable.
Modest restriction of saturated fats and simple sugars is also advised. However, some patients have re-
markable short-term success with high-fat, low-carbohydrate diets of various sorts. It is stressed out that weight
management in general and is flexible regarding the precise diet that the patient consumes. Also, a diet com-
posed of foods that are within the financial reach and cultural milieu of the patient.
C. Activity Modifications
Most patients with type 2 diabetes mellitus can benefit from increased activity. Aerobic exercise im-
proves insulin sensitivity and may improve glycemia markedly in some patients.
Structured exercise training of more than 150 minutes per week is associated with greater HbA1c reduc-
tion; however, physical activity helps lower HbA1c only when combined with dietary modifications.
It is advised that the patient should choose an activity that he/she is likely to continue such as walking.
Walking is accessible to most patients in terms of time and financial expenditure.
A previously sedentary patient should start activities slowly. Older patients, patients with long-standing
disease, patients with multiple risk factors, and patients with previous evidence of atherosclerotic disease should
have a cardiovascular evaluation, probably including an imaging study, prior to beginning a significant exercise
regimen.
Balducci et al showed that a supervised, facility-based exercise training program, when added to stan-
dard treatments for type 2 diabetes mellitus, yields better results than does simply counseling patients to exer-
cise.
A randomized, controlled trial by Church et al emphasized the need to incorporate both aerobic and re-
sistance training to achieve better lowering of HbA1c levels. Aerobic exercise alone or in combination with resis-
tance training improves glycemic control, circulating triglycerides, systolic blood pressure, and waist circumfer-
ence. The impact of resistance exercise alone, however, remains unclear.
Loimaala et al found that long-term endurance and strength training resulted in improved metabolic
control of diabetes mellitus and significant cardiovascular risk reduction, compared with standard treatment.
However, exercise training did not improve conduit arterial elasticity.
D. Laboratory Monitoring
E. Prevention of Type 2 Diabetes Mellitus
Guidelines from the American College of Clinical Endocrinologists for the prevention of type 2 diabetes mellitus in
patients at risk recommend the following measures:
• Weight reduction
• Proper nutrition
• Regular physical activity
• Cardiovascular risk factor reduction
• Aggressive treatment of hypertension and dyslipidemia
F. Lifestyle improvement
The Diabetes Prevention Program (DPP) trial has shown that modest lifestyle changes (eg, 4-5% sus-
tained weight reduction for approximately 3 y) reduce the risk for diabetes in patients at high risk by 58%. Eight
health-care facilities participated in an instructive study of group-based lifestyle intervention that should help
other agencies/states emulate strategies used to affect positive lifestyle changes for the prevention of diabetes.
In an 11-year, population-based cohort study of over 200,000 men and women without evidence of dia-
betes, heart disease, or cancer at baseline, good lifestyle decisions in combination significantly reduced the risk
of developing diabetes. For each additional positive lifestyle factor (eg, with regard to diet, physical activity, or
smoking) in the low-risk group, the odds for diabetes were 31% lower.
Yeh et al found that although cigarette smokers are at increased risk for type 2 diabetes, smoking cessa-
tion leads to higher short-term risk. In this prospective cohort study in 10,892 middle-aged, nondiabetic adults,
1254 persons developed type 2 diabetes during 9 years of follow up.
The adjusted hazard ratio of incident diabetes among persons in the highest tertile of pack-years was
1.42, compared with persons who had never smoked. However, in the first 3 years after quitting smoking, the
hazard ratio was 1.73; the risk then gradually decreased, disappearing completely at 12 years. Yeh et al recom-
mended that smoking cessation in smokers at risk for diabetes be coupled with strategies for prevention and
early detection of diabetes.