Endocrine Flashcards
Diabetes Mellitus (DM)
A metabolic disease resulting from the breakdown in the ability of the body to either produce and/or utilize insulin, resulting in inappropriate hyperglycemia.
DM type 1 and DM type 2
Diabetes type 1
Previously known as insulin dependent or juvenile diabetes.
Most commonly seen in caucasians and diagnosed before age 20.
Genetic predisposition.
Virtual absence of circulating insulin.
Positive autoimmune antibodies with the presence of Human Leukocyte Antigen (HLA-DR3 or HLA-DR4) and having antibodies against Glutamic Acid Decarboxylase (GAD-65) and Islet cell antibodies (ICA)
Ketone development usually occurs, tyoically seen with type 1 and not type 2.
Believed to be the restul of an infectious or toxic environment insult to pancreatic B cells o genetically predisopsed persons.
S/S of type 1 DM
Polyuria
Polydipsia
Polyphagia
Nocturnal ensuresis
Weight loss
Weakness/fatigue
Labs/diagnostics for type 1 and type 2
Serum fasting (at least 8 hours) blood glucose of >= 126 on more than one occasion OR
Random plasma glucose >=200 with signs of hyperglycemia (polyuria, polydipsia and weightloss) OR
Plasma glucose >=200 measured 2 hours after a glucose tolerance test OR
A1C >=6.5
Type 2 DM will not have ktones in blood/urine.
Management of type 1 DM and type 2
Treatment plans for all diabetics must be highly individualized.
Analyze baseline studies: Onset of age, obesity, cardiac risk factors, presence of ketones, diagnostic markers, cholesterol/triglycerides/EKG, renal studies, baseline physical exam.
- Type 1:
Optimal insulin regimens is a basal insulin + mealtime boluses of a rapid acting or sort acting insulin.
-Basal insulin: delievered daily or twice daily of an intermediate acting (NPH) or long acting (detemir) or continuous subq insulin infusion via a pump using a rapid acting insulin preparation (lispro).
-Mealtime boluses + additional insulin used to correct additional hyperglycemia. - Type 2: Therapy should begin with weight control for obses pts, Dietary treatment with guidelines, Exercise.
-After third failure of fasting blood glucose, pt has diagnosed DM type 2.
-Starter drug is Metformin, if dose >1G then can add a GLP-1 agonist due to increased side effects (dulaglutide, semaglutide).
Somogyi Effect
Nocturnal hypoglycemia develops stimulating a surge of counter regulatory hormones (somogyi means opposite) which raises blood sugar.
Note that the pt is hypoglycemia at 0300 but rebounds with an elevated blood glucose at 0700.
Treatment: Reduce or omit the bedtime dose of insulin.
Dawn Phenomenon
Results when tissues become desensitized to insulin nocturnally.
Note that the blood glucose becomes progressively elevated throughout the night, resulting in elevated glucose levels at 0700.
“The dawn is rising”
Treatment: Add or increase the bedtime dose of insulin
Diabetes Type 2
Previously known as non-IDDM or adult onset DM.
Most common DM in U.S.
Usually seen in adults >45
* Circulating insulin exists enough to prevent ketoacidosis but is inadequate to meet the pts insulin needs.
* Caused by either tissue insensitivity to insulin or an insulin secretory defect resulting in resistance and/or impaired insulin production.
Not linked to antigen/antibodies.
Associated with metabolic syndrome, previously known as Syndrome X.
Metabolic syndrome
These are characteristics that set someone up for sudden cardioembolic death namely stroke and MI.
Also sets someone up for having DM.
1.) Waist circumference: >= 40 inches in men and >=35 inches in woman.
2.) BP>=130/85
3.) Triglycerides >=150
4.) FBG >=100
5.) HDL <40 in men and <50 in women
Needs 3 to diagnose metabolic syndrome.
1.) Liklely to be diabetic if you have 3 of these
2.) Risk of sudden cardioembolic death is increased.
S/S of DM type 2
Insidious onset of hyperglycemia, pt may be asymptomatic.
Polyuria
Polydipsia
Overweight
Reccurent vaginitis is often the first symptom in women
Peripheral neuopathies
Blurred vision
Chronic skin infections, including pruritis.
Types of insulin
- Rapid acting:
-Lispro, aspart
-Onset ~15 minutes
-Peaks ~90 minutes
-Duration ~3 hrs - Short acting:
-Regular, humulin
-Onset ~ 30 minutes
-Peaks ~ 2 hours
-Duration ~ 8 hours - Intermediate acting:
-NPH
-Onset ~ 2 hrs
-Peaks ~ 6 hrs
-Duration ~ 24 hrs - Long acting:
-Detemir, glargine
-Onset ~ 1 hr
-Peaks ~ no peak
-Duration ~ 24 hrs
Metformin
Biguanide
The drug of choice as a starter dug for most pts with DM type 2.
Lowers basal and postprandial glucose levels by affecting glucose absorption and hepatic gluconeogenesis.
May cause some weight loss and reduces LDLs, may cause lactic acisosis (caution against excessive alcohol ingestion).
D/C 1-2 days before recieving contrast.
Black box warning of lactic acidosis.
GLP-1 agonist
Dulaglutide, semaglutide (dosed once weekly, most popular)
Mimics endogenous incretin glucagon like peptide (GLP-1); stimulates glucose dependent insulin release, reduce glucoagon, and slow gastric emptying.
Used with metformin or sulfonylurea may cause modest weight loss.
Black box warning of thyroid cancer
RIsk evaluation and mitigation strateies program (REMS): pancreatitis.
Diabetic Ketoacidosis (DKA)
A state of intracellular dehydration as a result of elevated blood glucose levels.
Often is an acute complication of type 1 DM, although type 2 DM pts can get this if they’ve lost >90% of B cell function.
Hyperglycemia increases serum osmolality causing a shift of intracellular water into the intravascular space.
Characterized by hyperglycemia, hyperkalemia and low pH.
S/S of DKA
Polyuria including nocturia, polydipsia, weakness/fatigue, N/V, Kussmauls breathing, altered LOC, fruity breath, orthostatic hypotension with tachycardia, poor skin turgor, hypothermia unless infection is present.
Lab/diagnostics of DKA
Hyperglycemia (>250)
Ketonemia/ketouria
Markered glycosuria
Acidosis
Low HCO3 (22-32)
Low serum CO2 (40-50)
Elevated hct/BUN/Cr
Hyperkalemia
Leukocytosis
Hyperosmolality (275-295, or 2x sodium)
Increased anion gap (7-17)
Serum osmolality equation
2[Na+K]+glucose/18
Management of DKA
Protect the airway, administer O2
Isotonic fluids at least 1L in first hour then 500ml/hr after.
If glucose >500 then use 1/2NS after first hour for intracellular hydration.
When glucose falls >250 change to D51/2NS to prevent hypoglycemia.
Insulin bolus of 0.1u/kg then drip of 0.1u/kg/hr (IV). If glucose does not fall by 10% after first hour then repeat bolus.
If pH<7.1 then correct severe acidosis with bicarb drip.
Do not treat hyperkalemia
Hyperosmolar Hyperglycemic State (HHS)
State of greatly elevated serum glucose, hyperosmolality and severe intracellular dehydration without ketone production.
Usually occurs as a complication of DM type 2
Patients cannot produce enough insulin to prevent severe hyperglycemia, osmotic diuresis and extracellular fluid depletion.
S/S of HHS
Polyuria
Weakness
Changes in LOC (may be most obvious presenting sign)
Hypotension
Tachycardia
Poor skin turgor
