EXAM 3 Flashcards
Diabetes type 1
- autoimmune dysfunction
- an inadequate production of insulin
- early-onset (age < 30 years), genetic predisposition, race/ethnicity
Diabetes type 2
- body cell’s cannot respond to the production of insulin regardless of making it.
- more common
-obesity, age>30 years, hypertension, smoking alcohol, HDL<35 mg/Dl or triglycerides> 250 mg/dl, or history of gestational diabetes or babies over 9 pounds
Functions of insulin
❖ Transports and metabolizes glucose for
energy
❖ Stimulates storage of glucose in the liver
and muscle as glycogen
❖ Signals the liver to stop the release of
glucose
❖ Enhances storage of dietary fat in adipose
tissue
❖ Accelerates transport of amino acids into
cells
❖ Inhibits the breakdown of stored glucose,
protein, and fat
LADA
-Subtype of diabetes in which progression of autoimmune beta cell destruction in the pancreas is slower than in types 1 and 2 diabetes
-clinical manifestation of LADA shares the features of types 1 and 2 diabetes.
Metabolic syndrome
-Elevated waist circumference (greater or equal to 88 cm for women, greater or equal to 102 cm for men)
-Elevated triglycerides (greater or equal to 150 mg/dl) or drug treatment for elevated triglycerides
-low HDL cholesterol (< 40 mg/dl for men, <50 mg/dl for women) or drug treatment for low HDL
-elevated blood pressure (systolic greater or equal to 130 mm Hg or diastolic greater or equal to 85 mm Hg) or hypertensive drug treatment
-elevated fasting glucose (greater or equal to 100 mg/dl) or drug treatment for elevated glucose
Diabetes mellitus type 1 S/S
- Polyuria, polydipsia, polyphagia
-fatigue, weakness, vision changes, tingling or numbness in hands or feet, dry skin, skin lesions or wounds that are slow to heal, recurrent infections, fruity breath
-kussmaul respiration
-type 1 may have sudden weight loss, headache, nausea, vomiting or abdominal pain
Type 1 diabetes features
Onset: sudden
Age at onset: mostly in children
Body habits: Thin or normal
Ketoacidosis: common
Auto antibodies: usually present
Endogenous insulin: low or absent
Type 2 diabetes
Onset: gradual
Age at onset: Mostly in adults
Body habits: Often obese
Ketoacidosis: Rare
Auto antibodies: absent
Endogenous insulin: Normal, decreased or increased
Optimal HgbA1c levels for management of diabetes
less than 6.5%-8% would be optimal
Target goal: 7%
Insulin Therapy
Rapid acting- lispro
short acting - regular insulin
Intermediate acting - NPH insulin
Long acting: Glargine insulin
Nursing actions for diabetes
-observe client perform administration
-monitor for hypoglycemia
-Dosages can be adjusted for exercise, fasting procedures, diet
-Rotate the injection site to prevent lip hypertrophy
- inject at 90 angle (45 if thin)
-no need to aspirate for blood
-rapid or short acting (clear) drawn up first, then long acting (cloudy)
-wear medi alert
Methods of insulin delivery
-Traditional subq injections
-Insulin pens
-jet injectors
-Insulin pumps
-Future: implantable insulin pumps, artificial pancreas systems
Complications of insulin therapy
-local allergic reactions
-systemic allergic reactions
-insulin lipodystrophy
-resistance to injected insulin
-hypoglycemia
-Morning hyperglycemia
hypoglycemia s/s
-shaky
-fast heartbeat
-sweaty
-dizzy
-anxious
-hungry
-blurry vision
-weak or tired
-headache
-nervous or upset
hyperglycemia s/s
-extreme thirst
-frequent urination
-dry skin
-hunger
-blurred vision
-drowsiness
-nausea
management of hypoglycemia
-give 15 to 20 g of fast-acting, concentrated carbohydrate
-three or four glucose tablets
-glucose gel, 6-10 hard candies
-4 to 6 ounces of juice or regular soda (not diet soda)
-Emergency measures; if the patient cannot swallow or is unconscious
-subq or im glucacon (1 mg)
-25 to 50 ml of 50% dextrose solution IV
Oral antidiabetic agents focuses
-used for patients with type 2 diabetes who require more than diet and exercise alone
-combinations of oral drugs may be used
-major side effect: hypoglycemia
-Nursing interventions: monitor blood glucose for hypoglycemia and other potential side effects
-patient education
Biguanide (metformin)
counter insulin resistance (especially decrease hepatic glucose output)
sulfonylureas (glimepiride, glidazide, glyburide/gilbenadmine, glipizide)
Stimulate insulin secretion
Meglitinides (repaglinide, nateglinide)
Simulate insulin secretion (faster onset and shorter duration of action than sulfonylureas)
Gliptins (sitagliptin, vildagliptin, saxagliptin)
Increase prandial insulin secretion
thiazolidinediones (pioglitazone, rosiglitazone)
increase insulin sensitivity (especially increase peripheral glucose utilization)
a-Glucosidase inhibitors (acarbose, miglitol, voglibose)
Slow rate of carb digestion
Exercise
-Lower blood glucose-exercise only when levels are between 80-250
-If more than 1 hour passed since eating and planning high intensity work out, consume a carbohydrate snack first
-Ketones in urine- don’t
-Check BS more often
-Benefits: Aids in weight loss, easing stress, and maintaining a feeling of well-being. It also lowers cardiovascular risk
Exercise precautions
-insulin normally decreases with exercise; patients on exogenous insulin should eat a 15 g carbohydrate snack before moderate exercise to prevent hypoglycemia
-patients with type 2 diabetes not taking insulin or an oral agent may not need extra food before exercise
-potential post-exercise hypoglycemia
-need to monitor bg levels more often
gerontologic considerations
Foot care
-Wash daily
-Dry well especially between toes
-feel for bumps or temperature changes
-look between toes; check each toenail
-file toenails straight across
-check for dry cracked skin
-examine bottom of the feet
-track what you find
SICK days
(SUGAR): check your bg level ever 2 to 3 hrs necessary
(INSULIN): always continue to take ur insulin even when you are sick to avoid DKA
(CARBS): Make sure you take in enough carbs and drink enough fluids. If your glucose level is high, stick with sugar-free drinks. If ur glucose level is low, drink carb-containing drinks.
-(KETONES): Check ur blood or urine ketone levels every 4 hrs. Take rapid-acting insulin if ketones are present. Remember to drink plenty of water to flush out ketones out of ur system.
Acute complications of Diabetes
-hypoglycemia
-DKA
-Hyperglycemic hyperosmolar syndrome (HHS)
-Comparison of DKA and HHS
DKA (Type 1) s/s
-Dry and high sugar 250-500 +
-Keytones and Kussmaul resp.
-Abominal pain
-Acidosis Metabolic ph 7.35 or less
HHNS (type 2) s/s
-highest sugar OVER 600+
-Higher fluid loss (extreme dehydration)
- Head Change-Neurological Manifestations “Confusion”
- NO abdominal Pain, NO ketones (NO ACID, NO KUSSMAUL)
-Slower onset and stable potassium
DKA
-Absence or inadequate amount of insulin resulting in abnormal metabolism of carb, protein, and fat
-Clinical features
- hyperglycemia, dehydration, Acidosis, 3 Ps, Abdominal pain, N/V, profound weakness, blurred vision, headache, orthostatic hypotension, fruity breath, mental status changes
Common causes of DKA
-infection (pneumonia, UTI, skin, abdominal)
-Infraction (MI, stroke, bowel infarction)
-infant on board (pregnancy)
-indiscretion (dietary nonadherence)
-insulin deficiency (insulin pump failure or nonadherence)
LAB assessment of DKA
-Blood glucose levels between 250-800 mg/dl
-Ketoacidosis low serum bicarbonate, low pH; low PCO2
-electrolytes vary due to degree of dehydration
-BUN: greater than 30
-creatinine greater than 1.5
-Hct: Increased
-NA: below, within or above;
K: Within or above
Ketones in blood and urine
hyperglycemic hyperosmolar syndrome
-hyperosmolar hyperglycemia is caused by a lack of sufficient insulin; ketosis is minimal or absent
-hyperglycemia (greater than 600) causes osmotic diuresis, loss of water and electrolytes, hypernatremia, and increased osmolality = profound dehydration
Manifestations: 3 Ps, orthostatic hypotension, Tachycardia, weight loss, neurologic signs caused by cerebral dehydration
Lab assessment of HHS
-Blood glucose levels greater than 600 mg/dL
-ABGs: absence of acidosis; pH greater than 7.4; bicarb greater than 20mEq/L
-Electrolytes vary due to the degree of dehydration
-BUN: greater than 30
-Creatinine greater than 1.5
-HCT: increased
-NA: normal or below
-K: normal to high d/t dehydration
-Ketones absent
Long-term complications of diabetes
-Macrovascular (accelerated atherosclerotic changes)
* coronary artery disease, cerebrovascular disease, stroke, MI, peripheral vascular disease
-Microvascular
*microangiopathy; diabetic retinopathy, nephropathy
-Neuropathic
*peripheral neuropathy, autonomic neuropathies, hypoglycemic unawareness, neuropathy, sexual dysfunction
Pituitary gland
- The master gland
- Regulated by the hypothalamus
- Divided into two lobes
- Posterior pituitary
- Anterior pituitary
Anterior pituitary Disorders
ACTH- Adrenocorticotropic hormone
Too much → Cushing’s disease
Too little → Addison’s disease
GH- Growth hormone
Too much → gigantism and acromegaly
Too little → dwarfism
Posterior pituitary Disorders
ADH- Antidiuretic hormone
Too much → SIADH
Too little → DI
Adrenal Gland
Adrenal medulla
- Functions as part of the autonomic nervous system
Catecholamines: epinephrine and norepinephrine
Adrenal cortex
- Glucocorticoids
- Cortisol affects glucose, protein and fat metabolism; responds to stress; affects the immune system
Mineralocorticoids
- Aldosterone increases sodium absorption and potassium excretion in the kidney
Blood Cortisol levels
Higher levels in the morning
- Peak between 0400 and 0800
Lowest levels around midnight or 3 to 5 hours after
the onset of sleep
The 4 pm lab value should be 1/3 to 2/3 of the 8
am value
8:00 am: 5 to 23 mcg/dL
4:00 pm: 3 to 13 mcg/dL
Addison’s disease (Adrenocortical insufficiency)
Damage or dysfunction of the adrenal cortex → decreased aldosterone
and cortisol
Primary Addison’s disease
Idiopathic autoimmune dysfunction- most common
TB
Histoplasmosis
Adrenalectomy
Cancer metastasis
Radiation
Secondary Addison’s Disease
Not producing enough pituitary hormone: tumors, inflammation, etc.
Pituitary cancer
Radiation to the brain
Steroid withdrawal
