2.3 Nutrition and Fluid Balance, Endocrine Flashcards
Type I Diabetes
Type I Diabetes (10-15%)
Auto-immune= body attacks beta cells in pancreas that produce insulin.
Occurs before age of 30 (usually)
No insulin is produced.
Type II Diabetes
Type II Diabetes (85-90%)results from
Risk Factors: obesity, family hx, inactivity, middle age or older (can develop younger ages)
Insulin resistance (overweight people)
Inadequate insulin production (lean people)
A combination of both
Hyperglycemia signs and symptoms
POLYDIPSIA POLYURIA POLYPHAGIA WEIGHT LOSS FATIGUE Frequency of infections Rapid onset Insulin dependent Early onset
Polyuria
Cause:
Effect:
Polyuria
Cause: High blood sugar causes water to enter intravascular space
Effect: Increased intravascular fluid causes increased urine output= electrolyte imbalances.
Blood Glucose >180 glucose is excreted in urine “glucosuria”.
Polydipsia
Cause:
Effect:
Polydipsia
Cause: Increase urine output causes dehydration
Effect: Mouth becomes dry and thirst sensors activated
Polyphagia
Cause:
Effect:
Polyphagia (excessive hunger)
Cause: Glucose can’t enter cells to provide energy when insulin not present or ineffective.
Effect: Energy production decreases = stimulates hunger= in hopes of providing body with energy = glucose still can’t enter cell to provide energy = body breaks down fats and proteins to restore energy = person loses weight.
DM Monitoring
Capillary Glucose Monitoring:
- Frequency of monitoring individualized
- Isopropyl alcohol, food residue & some lotions will alter the results.
HGB A1C or HBA1C or Glycosylated hemoglobin (A1C)
- Represents average glucose level during 2-3 month period. (Kees p. 225)
- A1C ≥ 6.5% diagnostic for diabetes (new 2014 guidelines)
Hypoglycemia signs and symptoms
Sudden onset: Blood glucose < 60 mg/dL
Symptoms: anxiety, shaky, irritability, tachycardia, difficulty thinking, poor concentration, slurred speech, blurred vision, decrease LOC, seizures, coma, pale cool skin, sweaty.
Hypoglycemia treat
Treat: Needs sugar!
Alert? Oral juice, glucose gel/tabs, reg soda
Unresponsive? IV D50
Brain requires glucose!
Hypoglycemia in Elderly
What does an insulin reaction look like in an older patient?
Speech Disorder
Slurring
Confusion
Disorientation
Not the typical diaphoresis and clammy skin
Hypoglycemia vs. stroke
Hypoglycemia can produce symptoms similar to a stroke
Blurred vision
Weakness, dizziness
Slurred speech
All suspected strokes should receive hypoglycemia treatment, just in case
Many strokes have been “cured” this way
Diabetic Ketoacidosis
what is it
A state of insulin deficiency resulting in hyperglycemia and an accumulation of ketones in the blood. Fat stores used for energy results in metabolic acidosis
Diabetic Ketoacidosis
Causes/ risk factors
Causes/ risk factors:
Sick or infection (most frequent)
Decrease or omission of insulin.
Occurs in Type 1 DM
Diabetic Ketoacidosis Labs
Labs: Ketones elevated in blood or urine. Blood glucose >250 PH <7.30 Bicarb<15
Diabetic Ketoacidosis Symptoms
Symptoms Lethargy, coma Kussmaul’s respirations Warm, dry, poor turgor Fruity breath from ketones Hypotension
Somogyi Phenomenon what is it
Is a combo of hypoglycemia in the night with rebound hyperglycemia in the morning.
Caused by too much insulin
Hyperglycemia = more insulin =hypoglycemia =secretion of counter-regulatory hormones (epinephrine, cortisol, glucagon, growth hormone = hyperglycemia =more insulin = cycle repeats
Treat by slowly reducing insulin
More common in Type I DM
Dawn Phenomenon what is it
Rise in blood glucose between 4-8 AM that is not a response to hypoglycemia.
Cause unknown: thought to be r/t nocturnal release of counter-regulatory hormones that increase blood sugar
Can occur both DM I and II
Correct with timing of insulin or increase of dose
Complications of DM- hyperglycemia
Hyperglycemia from impaired glucose & insulin resistance invokes an inflammatory process in vascular endothelial lining causing complications:
Complications of DM
Macrovascular
Macrovascular:
Manifested thru atherosclerosis results in HTN, CAD, PVD, Cerebral & Carotid artery damage
Complications of DM
Microvascular
Microvascular:
Basement membrane of smaller blood vessels & capillaries thickens eventually leading to decreased tissue perfusion.
Complications of DM
Retinopathy
Retinopathy- micro-vascular damage & hemorrhage lead to scarring of retina. Leading cause of blindness in DM.
Complications of DM
Nephropathy
Nephropathy: thickening of basement membrane of glomeruli impairing renal function.
Complications of DM
Neuropathy
Neuropathy- thickening of blood vessels that supply nerve endings. Causes change in sensation (numbness/tingling), pain (ache, burn, shooting, cold) Teach importance of visually inspecting feet/legs daily to look for injury
Diabetic Foot Care teaching
Teach Daily foot inspection avoid crossing legs Non-restrictive shoes & good quality socks Do not self-treat foot problems Avoid dry skin, cracks, infections Podiatrist evaluation Buy shoes late afternoon- feet @ largest
Management of Diabetes
DIET
EXERCISE
MEDS
Insulin Administration
Preferred site is Abdomen- allows most rapid absorption.
Do not give in legs prior to exercise- increases absorption rate and chance of hypoglycemic event.
If mixing insulin must draw up “clear before cloudy” (regular then NPH). Avoids contamination of NPH into regular insulin vial.
Do not massage site after injection- interferes with absorption.
Teach pt that exercise lowers insulin requirements; seek consultation prior to exercise program.
Insulin Administration tips
Tips to decrease pain with injection: Allow alcohol to dry on skin 1st Room temp insulin Don’t reuse needles Quick penetration and removal of needle at same angle.
Noninsulin Hypoglycemic Agents
Metformin
Metformin (Biguanides):
Reduces FBG (fasting blood glucose) & postprandial (after eating) hyperglycemia.
Often suspended during hospitalization r/t increased risk of lactic acidosis
Stopped prior to and 48 h after use of contrast media & surgery r/t risk of renal failure.
Low risk of hypoglycemic events
Noninsulin Hypoglycemic Agents
Sulfonylureas
Sulfonylureas glipizide (Glucotrol), glyburide (Micronase), glimepirde (amaryl)
Treat type 2 DM in non-obese people not controlled by diet alone.
Stimulate pancreatic cells to secrete more insulin making peripheral tissues more sensitive to insulin.
Usually suspended during hospitalizations r/t dose adjustments must be made slowly.
Not useful in acute illness.
Common side effect hypoglycemia compounded by NPO status.
Teaching: Sick Day rules
M- Monitor blood sugar levels more frequently
D- Do not stop taking insulin
C- Check urine for ketones if glucose >240
B- Be careful with over-the-counter medications
H- Have a game plan & ask for help if needed
F- Force fluids (8 oz. each hour)
C- Call provider if unable to eat >24h, vomiting /diarrhea >6 h, urine ketones mod/lg for >4h
ADRENAL GLAND FUNCTION Medulla
Medulla (inner portion of adrenal gland)
Epinephrine and Norepinephrine
ADRENAL GLAND FUNCTION Cortex
Cortex (outer portion) Produces hormones essential to life.
Mineralcorticoids (release controlled by renin when b/p or Na is low)
Glucocorticoids (cortisol & cortisone) released in time of stress affect CHO metabolism & regulates glucose use in body tissues.
Androgens- sex hormones
Loss of cortex hormones=death
Cushing’s Syndrome
what is it
treated
Excessive cortisol produced
Chronic disorder
Taking corticosteroids long time= increased risk.
Treated: meds to suppress cortisol or adrenalectomy
Cushing’s Syndrome
Excess cortisol effects
Excess cortisol effects:
Fat deposits abdomen, under clavicle, upper back “buffalo hump”
Moon face
Muscle weakness/wasting r/t change in protein metabolism.
Loss of collagen & connective tissue
Thinning of skin, abdominal striae (stretch marks)
Poor wound healing, frequent infections
Altered glucose metabolism sometimes causing DM
Emotional changes (depression/ psychosis)
Cushing’s Disease Diagnostics labs
Increased levels: Serum cortisol Sodium Glucose Urine free cortisol
Decreased levels:
Potassium
Cushing’s Disease Diagnostics
Treatment
Treatment:
Meds to suppress activity of adrenal cortex (Mitotane, aminoglutethimide)
Adrenalectomy
Addison’s Disease what is it
Adrenal insufficiency - Cortisol deficiency
Autoimmune most common cause
Slow onset s/s occur after 90% adrenal function lost.
Deficient cortisol effects:
Sodium is lost & potassium retained
Extracellular fluid depleted and blood volume decreased
Addison’s Disease S/S
S/S:
Postural hypotension & syncope, dysrhythmias
Dizziness, confusion, lethargy, emotional lability
Weakness, muscle wasting
Hyperpigmentation of skin
Hyperkalemia, hyponatremia, hypoglycemia
Addison’s Disease Diagnostics labs
Decreased levels of:
Serum cortisol levels
Blood glucose levels
Serum sodium levels
Increased:
Serum potassium levels
Addison’s Disease
Teaching and treatment
Treatment:
Meds to replace corticosteroids and mineralocorticoids
Hydrocortisone (Cortef & others)
Fludrocortisone (Florinef)
Prednisone, dexamethasone, methylprednisolone
Steroids suppress immune system
Teach: meds needed for rest of life, diet low K+ high Na+ and protein.
Addisonian Crisis
Life threatening acute adrenal insufficiency caused by major stressors (surgery, acute illness, trauma)
Abruptly withdrawn from corticosteroid meds or hemorrhage into adrenal glands
Addisonian Crisis s/s
S/S (develop rapidly): high fever, weakness, severe penetrating pain in abdomen/lower back/legs, severe vomiting, diarrhea, hypotension, circulatory collapse, shock and coma.
Addisonian Crisis treatment
Treatment: rapid IV replacement of fluids and glucocorticoids. Fluid balance generally restored in 4-6 hours.
Adrenal Gland Hormones
3 “S’s”
Sugar: glucocorticoids (cortisol and cortisone), effect carbohydrates by regulating the glucose
Salt: mineralocorticoids (aldosterone), Na and water, regulate BP, part of renin angiotensin aldosterone systems
Sex: androgens (male hormones, DHEA, testosterone)
