Nurs 3366 - Disorders of the endocrine pancreas

What is Diabetes Mellitus?

diabetes: “passing too much urine”; mellitus: “honey-flavored”

• (DM) means “passing too much honey-flavored urine”

commonality of all DM disease presentations is that pathologic hyperglycemia is present

How do you diagnosis/monitoring of DM?

normal fasting serum glucose = 70-99

• fasting blood sugar (FBS) of ≥ 126 (on 2 separate testing occasions)

• every few months by a glycosylated hemoglobin test, AKA hemoglobin A1-C (Hgb A1c)

What is hemoglobin A1-C (Hgb A1c)?

an indirect way to measure average daily glucose levels

• a certain percentage of our hemoglobin molecules pick up glucose

  during the lifespan of the RBC

• the Hgb A1c test asks: in the last 4 months or so, what average percentage of overall Hgb molecules is composed of Hgb A1c?

What is the significance of the Hgb A1c test?

no more than about 4-6% of the total Hgb molecules should be glycosylated

• good medical therapy & diet should keep it at <7% (in diabetic, would be unreasonable to have it be totally normal)

What is Type I DM?

TOTAL lack of insulin secretion from beta cells of pancreas

• due to autoimmune destruction of beta cells

What are the S&S of Type I DM?

NO INSULIN→ glucose can’t get into cells, so accumulates in blood hyperglycemia (usually > ~200)→ exceeds renal threshold →glucosuria→glucose in the urine → draws water into urine

• polyuria (large amounts of urine)→ polydipsia (great thirst) & S&S of dehydration (dry skin, dry mucus membranes)

What are the S&S of Type I DM due to glucose not being used as an energy source?

gluconeogenesis→ high ketones in blood

• S&S such as ”acetone breath” & ketonuria

nutritional deficiency→ weight loss despite huge appetite (polyphagia), → fatigue

What is Type I diabetes “extreme state”?

diabetic ketoacidosis (DKA) - metabolic acidosis

• pH: <7.35 HCO3: <22

  PCO2: norm PaO2: norm SaO2:norm

kussmaul respirations: fast, deep breathing pattern which is a compensatory response to metabolic acidosis

if not treated, DKA can progress to diabetic coma

What is treatment for Type I DM?

ONLY definitive treatment for Type I DM is to insulin

What is Type II DM?

fat cells have decreased number of insulin receptors in cell membranes→this causes —> insulin resistance

• hyperglycemia keeps stimulating beta cells to secrete insulin;

  ie, the pancreas is in “overdrive”→ causes hyperinsulinemia

• eventually there is pancreatic beta cell fatigue; ie, the pancreas “poops out” from being in overdrive for so many years→ diminished insulin secretion

What are the S&S of Type II DM?

more subtle than Type I, because there is SOME insulin being secreted and therefore SOME glucose is allowed into the cells

• usually there is fatigue, mild polydipsia & polyuria but sometimes the first

  signs (like HTN) are that of chronic organ damage such as diabetic retinitis

• no S&Ss of metabolic acidosis

What is the Type II diabetes “extreme state”?

HHNS (AKA -- HHNK)-- hyperglycemic-hyperosmolar-nonketotic syndrome

• since the S&S of Type II DM are so insidious: glucose can slowly reach a much higher than in Type I (blood glucose of Type II usually > 400 to 900)

• characterized by very high serum osmolality (from very high number of

  glucose molecules), extreme polyuria & extreme dehydration

can progress to diabetic coma

What are the long-term problems of DM?

macroangiopathy: glucose toxicity→damage to large & medium-sized arteries → atherosclerosis in brain, heart, aorta, femoral arteries (stroke, CAD, aneurysms, PAD)

microangiopathy—damage to small vessels such as:

• retinal arterioles→ retinopathy→ blurred vision, blindness

• capillaries of kidneys -- DM is major cause of chronic renal failure

• skin—easy bruising

What are the long-term problems of DM regarding neuropathy?

peripheral neuropathy —burning, pain, itching, numbness of feet→ lack of feeling also cause increase risk of trauma and infection

autonomic neuropathy—damage to nerves of the autonomic system

• slowing of gut (gastoparesis), causing altered nutrition absorption & constipation

• “silent MI” – pain transmission during MI is dysfunctional

What is the Metabolic Syndrome?

it is a cluster of traits that SIGNIFICANTLY increases risk for CV disease:

• Type II DM with its hyperglycemia and insulin resistance

• elevated triglycerides, decreased HDL

• HTN

• abdominal obesity

What is Hypoglycemia?

defined as blood glucose <70 plus S&S

• not eating or food not absorbed

• natural hyperinsulinism (this is rare)—glucose in blood triggers over-secretion of insulin

• taking too much insulin

What are the S&S of Hypoglycemia?

shakiness, irritability, sweating are due to effects of counterregulatory hormones:

glucagon, cortisol, growth hormone, epinephrine

• let you know you need to eat (irritable, sweating, tachycardia)

• stimulate glycogenolysis & gluconeogenesis→ yields glucose

What are the hypoglycemic crisis states?

if glucose gets low enough for the brain to run out of fuel, patient can become unconscious—called hypoglycemic shock/coma or insulin coma-- and can also have seizures

What are the the differences in hypoglycemic situations & diabetic ones?

hypoglycemic: cold & clammy give me some candy

• low blood sugar

• Wet S&S

• occur much more rapidly than diabetic ones

diabetic: hot and dry, sugar high

• high blood sugar

• Dry S&S

• occur slowly compared to hypoglycemic ones

What is the tx for Hypoglycemia?

give IV glucose; or can give intramuscularly (IM) or subcutaneously (subQ)