DM I Flashcards
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
pancreas
exocrine function
Digestive enzymes
Secreted by acinar cells
DM
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
DM
uncontrolled disease leads to
blindness, limb amputation, kidney failure, and vascular and heart disease
DM
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)
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
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
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
DM I
Patho
Stage 1
Asymptomatic
Characterized by normal fasting glucose, normal glucose tolerance, and the presence of ≥ 2 pancreatic autoantibodies
DM I
Pathi
Stage 3
Evidence of diabetes, defined by hyperglycemia with clinical symptoms
DM I
Patho
Stage 2
Asymptomatic
Characterized by pancreatic autoantibodies (usually multiple)
Dysglycemia: impaired fasting glucose, impaired glucose tolerance, or an abnormal HbA1c
DM I
Clin Man
Characteristic symptoms of hyperosmolality (increase glucose in the bloodstream) and hyperketonemia (lipolysis)
Polyuria
Polydipsia
Polyphagia
Fatigue
Blurry vision
Weight loss
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
DM I
Urinalysis
Glucosuria, ketonuria, microalbuminuria(sign of kidney damage, hopefully dont see)
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
Tx
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 duringpuberty
Individuals withinfectionsor other acute medical conditions
Acute stress situations
Starting dose can be adjusted up or down every few days based on bloodglucose
DM I
Administration → basal + bolusinsulin
Basalinsulin (40-50% of total daily insulin dose)
↓ Hepaticglucoseproduction
Helps achieve normoglycemia in thefasting state
Long-actinginsulin
Bolusinsulin
Prandial (pre-meal)insulincovers theglucoseincrease after food intake
Short- or rapid-actinginsulin
Rapid-acting insulin
Start working in 12–30 minutes, peaks in 1-3 hours
Glulisine(Apidra)
Lispro(Humalog)
Aspart (NovoLog)
Short-actinginsulin:
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 ininsulin pumps fortype 1 diabetes
Long-actinginsulin
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
Regularweight and BP checks at each follow-up visit
Lab testing of HbA1clevels to evaluateglucosecontrol and efficacy of therapy - Target goal: < 7%
Every 6 months if HbA1cis at target goal
Every 3 months if HbA1cis above target goal
Annual microalbumin:creatinine ratio urine test
Start an ACE inhibitor for patients with albuminuria to protect kidneys
Lipid testing annually:
Triglycerides, totalcholesterol, 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)
