DIABETES MELLITUS TYPE 1

DIABETES MELLITUS TYPE 1 LIPASE

 It makes up 5% to 10% of all DM cases.  An enzyme the body uses to break down fats in food so
 Also known as “Juvenile Onset” Diabetes they can be absorbed in the intestines.
 Because it is diagnosed in young patients who  Lipase is produced in the pancreas, mouth, and stomach.
are younger than 30 years old.  Digestion of Lipids (Fats)
 Occurs at a very young age; as young as 10
 Another name for it is “Insulin-dependent Diabetes”
 With this type of DM, the pancreas doesn't make
insulin or makes very little insulin.
 This type is also known as “Brittle DM”
 Blood sugar swings can be severe and frequent.
 Type 1 DM is Ketosis-prone
 Because people with type 1 diabetes don't have
insulin, they cannot metabolize ketones, which
are gradually flushed through urine in people
without the disease.
 For people with type 1 diabetes, ketosis can
result in an accumulation of ketone acids in their
bloodstream known as diabetic ketoacidosis
(DKA).
BETA CELLS
 Responsible for the production of insulin
 Cells that make insulin, a hormone that controls the level
of glucose (a type of sugar) in the blood.

INSULIN
 The major purpose of insulin is to regulate the body's
energy supply by balancing micronutrient levels during the
fed state.
 Insulin is critical for transporting intracellular glucose to
insulin-dependent cells/tissues, such as liver, muscle, and
adipose tissue.
 Insulin is a polypeptide hormone mainly secreted by β
cells in the islets of Langerhans of the pancreas.
CAUSES OF TYPE 1 DIABETES  The hormone potentially coordinates with
 Hereditary Predisposition glucagon to modulate blood glucose levels;
 Autoimmune Diseases insulin acts via an anabolic pathway,
 Viruses and Infections
 Autoimmune Destruction of Beta Cells ALPHA CELLS
 Damage or Removal of the Pancreas  Responsible for the production of glucagon
 Unfavorable Environmental Factors  These release glucagon, which elevates blood glucose
 Drugs and Chemical Toxins
 Endocrine Diseases GLUCAGON
 A hormone that works with other hormones and bodily
ANATOMY AND MECHANISMS functions to control glucose levels in the blood.
 It comes from alpha cells found in the pancreas and is
closely related to insulin-secreting beta cells.
 Glucagon increases your blood sugar level and prevents it
from dropping too low
 It breaks down fats
 Responsible for lipolysis

HOW GLUCOSE IS STORED

 The body has 3 Storage Bins for Glucose
1. Muscle
2. Adipose Tissue
3. Liver
 These three areas are the primary sites of energy storage.

AMYLASE
 An enzyme that helps the body to digest carbohydrates.
 Its main function is to hydrolyze the glycosidic bonds in
starch molecules, converting complex carbohydrates to
simple sugars.
 Digestion of Carbohydrates

TRYPSIN
 It is an enzyme that helps us digest protein.
 In the small intestine, trypsin breaks down proteins,
continuing the process of digestion that began in the
stomach.
 Metabolism of Protein

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 GLUCOGENESIS
 Formation of glucose in the liver
 In other sources, it is called gluconeogenesis
 The process of making glucose (sugar) from its own Further complications could lead to shock, coma, and death.
breakdown products or from the breakdown products of
lipids (fats) or proteins.
 Gluconeogenesis occurs mainly in cells of the liver or
kidney.

GLYCOLYSIS
 Process in which glucose is broken down to produce
energy

PATHOPHYSIOLOGY

DEAMINATION
 The removal of an amine group from a molecule.
 Deaminases
 Enzymes which catalyse this reaction.
 In the body, deamination takes place primarily in the liver.
 However, glutamate is also deaminated in the
kidneys.
 This refers to the process by which amino acids are
broken down if there is an excess of protein intake.
 The amino group is removed from the amino acid and
converted to ammonia.
Healthy Vs. Diabetic

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 EENT Blurred vision, acetone smell

Cardio Tachycardia

GIT Nausea, vomiting, abdominal pain

GUT Polyuria, glycosuria, nocturia, ketonuria

MSK Muscle wasting

KUSSMAUL’S BREATHING
 Or also known as Kussmaul’s Respiration
 Hyperventilation to excrete excessive ketones in the body.
 Deep, rapid breathing

REMEMBER!
- Proteins should not be broken.
- Normal pH = 7.35 to 7.45
- Type 1 is prone to ketosis
CLASSIC SIGNS OF DM – TYPE 1 o Excessive breakdown of fats = ↑Ketones
 Polyuria
- DKA = 300 to 800 mg / dL
 Increased urination
 Polyphagia
DIAGNOSTIC OR LABORATORY FINDINGS
 Increased thirst
 Normal Blood Sugar Level: 60 to 100 mg/dL
 Polydipsia
 Increased hunger
FASTING BLOOD SUGAR (FBS)
 > 126 mg/dl x 2
 Measures your blood sugar after an overnight fast
 A fasting blood sugar level of 99 mg/dL or lower is normal.
RANDOM BLOOD SUGAR OR RBS (CASUAL)
 >200 mg/dl
 It is the testing of the blood sugar level at any time or
random time of the day.

GLYCATED HEMOGLOBIN (A1C) TEST

 Normal Value: < 5.7%
 Abnormal/Diabetic Value: > 6.5%
 It measures the amount of glucose (sugar) in your blood.
 The test is often called A1c, or sometimes HbA1c.
 It is done every 3 months.
 It is usually the preferred test for assessing glycemic
control in people with diabetes.

OTHER SIGNS AND SYMPTOMS OF DM – TYPE 1 MANAGEMENT

 Weight Loss  Education
 Fatigue  Nutrition
 Increased frequency of infections  Activity
 Rapid onset  Insulin
 Insulin dependent  Self-monitoring Blood Glucose (SMBG)
 Familial tendency
 Peak incidence from 10 to 15 years old EDUCATION
 Educate the patient about the condition’s pathophysiology,
signs and symptoms, and complications.

NUTRITION AND DIET

 Objectives of Nutritional Therapy in DM
 Control of total caloric intake to attain or maintain
reasonable weight.
 Control of blood glucose to maintain health and
prevent complications.
 Address individual nutritional needs.
 Normalization of lipids and BP to reduce the risk
for CVDs.
 Modify lifestyle as needed to treat obesity,
hyperlipidemia, CVDs, etc.

SYSTEM SYMPTOMS
Lethargy, fatigue, polydipsia, polyphagia,
CNS
confusion
Systemic Weight loss

Respi Kussmaul’s breathing, hyperventilation

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 SMBG
 An approach whereby people with diabetes measure their
blood sugar (glycemia) themselves using a glycemic
reader (glucose meter).
 Based on the reading, they can adjust or check the effect
of their treatment (diet, exercise, insulin, antidiabetics,
stress management).

MONITORING KETONES IN URINE

< 0..6 Normal

0.6 – 1.0 Slightly High
HDL 1.0 – 3.0 Moderately High
 High Density Lipoprotein > 3.0 Very High
 Known as the Good Cholesterol
 It absorbs cholesterol in the blood and carries it back to
the liver.

LDL
 Low Density Lipoprotein
 Known as the Bad Cholesterol
 Makes up most of your body’s cholesterol.
 High levels of LDL cholesterol raise your risk for heart
disease and stroke.
ACTIVITY
 Lowers blood sugar by increased uptake of glucose by
muscles improving insulin utilization
 Improves circulation, improves muscle tone, and promotes
weight reduction
 Eases stress and maintains the feeling of wellbeing
 It alters lipid concentration
 ↑ HDL, ↓LDL, ↓ Total cholesterol and triglycerides
 In monitoring the patient’s activity, make sure not to let
them exercise at the insulin’s peak.
 This could lead to hypoglycemia.
 Exercise is not started if BS is >250 mg/dl
 ↑glucagon, catecholamine, growth hormone

INSULIN
 Inject insulin either 2, 3, or 4 times a day.

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