DM I Flashcards by Leslie Mancini

Pancreas

endocrine function

Islet of Langerhans cells – secretes hormones and hormone-like messengers

Insulin
Secreted by beta cell in response to rising concentrations of glucose

Glucagon
Secreted by the alpha cells in response to decreasing concentrations of glucose

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pancreas

exocrine function

Digestive enzymes
Secreted by acinar cells

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general

Affects ~34.2 million (10.5%) people in the United States
Seventh-leadingcause of death (79,000 deaths annually)

Chronic condition characterized by disordered metabolism and inappropriate hyperglycemia due to:
Deficiency in insulin production or
Resistance to insulin’s action

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uncontrolled disease leads to

blindness, limb amputation, kidney failure, and vascular and heart disease

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types(4)

Type I diabetes mellitus
5-10% of cases

Type II diabetes mellitus
~90% of cases

Gestational diabetes mellitus (5-7% of pregnancies)

Secondary diabetes
Drug- or chemical-induced diabetes (glucocorticoids use)
Complications of other diseases affecting the pancreas (pancreatitis)

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Diabetes Mellitus – Type I

general and autoimmune process

Results from T-cell immune-mediated destruction of insulin-producing pancreatic islet cells over months to years → complete lack of insulin

Autoimmune process (95%)
Glutamic acid decarboxylase (GAD) antibodies - most common in adults
Insulin autoantibodies (IAA) – most common in children
Idiopathic (5%)

dont need to know antibodies just that you need 2 or more

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DM I

Age of incidence

Commonly arises in children and young adult
Most commonly diagnosed at ages 4–6 years, with 2nd peak in early teenage years
Incidence and prevalence are increasing

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DM I

susceptibility

Gene mutation: HLA-linked (HLA-DQ, HLA-DR3, andHLA-DR4)

Associated with other autoimmune conditions

Environmental factors: drugs and chemical toxins, viral infections, dietary factors

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DM I

Patho
Stage 1

Asymptomatic
Characterized by normal fasting glucose, normal glucose tolerance, and the presence of ≥ 2 pancreatic autoantibodies

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DM I

Pathi
Stage 3

Evidence of diabetes, defined by hyperglycemia with clinical symptoms

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DM I

Patho
Stage 2

Asymptomatic
Characterized by pancreatic autoantibodies (usually multiple)
Dysglycemia: impaired fasting glucose, impaired glucose tolerance, or an abnormal HbA1c

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DM I

Clin Man

Characteristic symptoms of hyperosmolality (increase glucose in the bloodstream) and hyperketonemia (lipolysis)
Polyuria
Polydipsia
Polyphagia
Fatigue
Blurry vision
Weight loss

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DM I

DKA

May present urgently with diabetic ketoacidosis (DKA) – 1/3 of pediatric patients
Usually precipitated by a “tipping” event (viral illness, trauma, emotional stress)
Abdominal pain
Vomiting
Fruity “acetone” breath

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DM I

Urinalysis

Glucosuria, ketonuria, microalbuminuria(sign of kidney damage, hopefully dont see)

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DM I

Labs: insulin, random glucose, anything else?

↓ Serum insulin level

Random plasma glucose
≥200 mg/dL with symptoms of hyperglycemia → diabetes

Diabetes-related autoantibodies

DM I

Fasting plasma glucose (FPG)

No calorie intake for at least 8 hours
≥126 mg/dL on more than 1 occasion → diabetes
100-125 mg/dL → impaired fasting glucose tolerance (↑ risk for diabetes/ prediabetes)

DM I

2-hour plasma glucose during a 75-gram oral glucose tolerance test (OGTT)

≥200 mg/dL → diabetes

DM I

hemoglobin A1C

Indirect measure of average blood glucose levels over an 8-12 weeks

Multiple factors can affect A1C levels: age, race, genetic background, recent blood transfusion, chronic alcohol use, RBS disorders, chronic liver disease

≥ 6.5% → diabetes

not as reliable, especially if someone is presenting with DKA

better for monitoring

DM I

Measure C-peptide

Measured in blood or urine (24-hour collection)
Released from the pancreas with insulin production

Indicates how much insulin is being made by the body
Low levels indicate insulin deficiency (type 1 DM)
High levels indicateinsulin resistance (type 2DM)

when you produce insulin you also produce C peptide

DM I

Diabetes education

initially and then on a yearly basis

How to monitor glucose levels
Fasting
Near meals (before and/or after)
With signs and symptoms ofhypoglycemiaor hyperglycemia
How to administer insulin
Signs of disease progression
Beneficial lifestyle changes

DM I

Beneficial lifestyle modifications

Nutritional and dietary requirements (dietitian)
Instruction on carbohydrate counting and insulin –to-carbohydrate ratio (1:15)
Regular exercise
Weight losswith reduced caloric intake if overweight or obese

Smoking cessation to decrease the risk of comorbid complications

(15 g of a carbohydrate = one carb serving; 1 unit of insulin for 1 carb serving)

DM I

No cure for diabetes

Insulin replacement required for the treatment of type 1 DM
Comes in multiple preparations: rapid-acting, short-acting, and long-acting
Administered by subcutaneous injection or by infusion pump

should have glucagon for if glucose is too low

DM I

Self-monitoring or continuous glucose monitoring

Increasing use of continuous glucose monitoring systems (DexCom)
Measures glucose concentrations continuously in the interstitial fluid for 7-14 days
Glucose data can be transmitted to a smartphone or to the screen of an insulin pump
Directional arrows indicate the rate and direction of change of glucose levels
Alerts can be set for dangerously low or high glucose values

# DM I initial dose of insulin

Total daily dose of 0.2–0.6 units/kg/day; some people may require up to 0.7 units/kg/day May need increased dosing for: Adolescents during puberty Individuals with infections or other acute medical conditions Acute stress situations Starting dose can be adjusted up or down every few days based on blood glucose

# DM I Administration → basal + bolus insulin

Basal insulin (40-50% of total daily insulin dose) ↓ Hepatic glucose production Helps achieve normoglycemia in the fasting state **Long-acting insulin** Bolus insulin Prandial (pre-meal) insulin covers the glucose increase after food intake **Short- or rapid-acting insulin**

Rapid-acting insulin

Start working in 12–30 minutes, peaks in 1-3 hours Glulisine (Apidra) Lispro (Humalog) Aspart (NovoLog)

Short-acting insulin:

Starts working in 30-60 minutes, peaks at 2-4 hours Rapid-acting and short-acting insulins are used in combination with longer-acting insulins or in insulin pumps for type 1 diabetes

Long-acting insulin

Starts working in 2-4 hours, duration of action 17–24 hours Glargine (Lantus) Detemir (Levemir)

# DM I Dawn Phenomenon

In the early morning hours, hormones **(growth hormone, cortisol, and catecholamines) cause the liver to release large amounts of glucose** into the bloodstream In diabetic patients, the body does not produce enough insulin causing **high blood sugar in the morning** (before eating) If the **blood sugar level is normal or high at 2 a.m. to 3 a.m., it is likely the dawn phenomenon** Avoid carbohydrate snacks late in the evening

# DM I Somogyi Effect

If the **blood sugar level drops too low in the early morning hours,** hormones (growth hormone, cortisol, and catecholamines) are released to reverse the low blood sugar level In diabetic patients who takes **insulin and do not eat a bedtime snack their blood sugar level can drop during the night** and the body will releasing hormones that raise the blood sugar level causing hyperglycemia **If the blood sugar level is low at 2 a.m. to 3 a.m., suspect the Somogyi effect**

# DM I Clinician monitoring

Regular weight and BP checks at each follow-up visit Lab testing of HbA1c levels to evaluate glucose control and efficacy of therapy - **Target goal: < 7%** Every 6 months if HbA1c is at target goal Every 3 months if HbA1c is above target goal Annual microalbumin:creatinine ratio urine test Start an **ACE inhibitor for patients with albuminuria** to protect kidneys Lipid testing annually: Triglycerides, total cholesterol, HDL, and LDL with **goal < 100 mg/dL** Annual eye exam Annual foot exam Prophylactic vaccines (influenza, pneumococcal) Regular dental exams

# DM I Complications | acute/chronic

Acute Hypoglycemia Hyperglycemia, including diabetic ketoacidosis Chronic Nephropathy Neuropathy Retinopathy Coronary artery disease Peripheral arterial disease CVA/TIA Diabetic foot disease (foot ulcers and amputations)