Diabetes mellitus Flashcards
alpha cells produce what
glucagon
beta cells produce what
insulin
Insulin promotes:
- glucose production, use, and storage
- hypoglycemia (and moves K+ back in cells) and glucagon promotes hyperglycemia
what type of agent is glucose and what is the action
osmotic
diuresis and fluid and F&E loss
what is diabetes and what are the types
- Chronic multisystem disease characterized by hyperglycemia from abnormal insulin
production, no insulin
production, impaired insulin use, or all. - Without insulin, glucose builds up in the blood causing
hyperglycemia - Type 1, Type 2, gestational, and secondary
clinical manifestations of DM
- Polyuria - osmotic agent - diuresis
- Polydipsia - excreted fluid - now thirsty
- Polyphagia - no energy from glucose so need energy from food
- Dehydration, weight loss, fatigue,
weakness, vision changes,
tingling/numbness if hands/feet, dry
skin, lesions that are slow to heal,
and recurrent infections
medical management of DM
- Nutrition
- Exercise
- Glucose Monitoring
- Medication
- Education
Acute Complications of Diabetes Mellitus
- Arise from events associated with
hyperglycemia (DKA and HHS) and
hypoglycemia (also referred to as
insulin reaction). - Hypoglycemia worsens rapidly and
constitutes a serious threat if action is
not immediately taken. - All require emergency treatment and
can be fatal!!!
glucose levels for hypoglycemia
Blood glucose falls below range of 50-60 mg/dL
treatment to increase blood glucose
Epi and glucagon
(using the autonomic nervous system) by stimulating liver
causes of hypoglycemia
overdose of diabetes medication (peak),
inadequate food intake,
increased exercise without food,
improper administration of insulin,
decreased food intake/missed meals,
increased insulin sensitivity,
decrease glucose production with alcohol consumption,
rapid hypoglycemia (in treatment of DKA & HHS),
nocturnal hypoglycemia,
can happen anytime
***More deadly than the other complications of DM
Hypoglycemia clinical manifestations
- Diaphoresis
- Tremor
- Hunger
- Tachycardia
- Palpitation
- Anxiety
- Cool, clammy skin
- CNS:
– Headache
– Confusion
– Memory lapses
– Numbness of lip and mouth
– Slurred speech
– Impaired coordination
– Emotional changes
– Irrational/combative behavior
– Diplopia
– Drowsiness
complications/severe s/s of hypoglycemia
disoriented behavior, seizures, difficulty arousing
from sleep, loss of consciousness
* Symptoms can occur suddenly and vary
relative hypoglycemia
The client seemingly has a glucose WNL, but is lower than their usual high numbers
The client frequently has a blood glucose level in low range of normal and are symptomatic when it falls below 50
hypoglycemic unawareness
Normal compensatory response fails to cause symptoms; hypoglycemia without warning
hypoglycemia treatment
Can be quickly reversed
Treatment depends on LOC, ability to eat, setting, & glucose level
Immediately check glucose upon symptom onset
“Rule of 15” ONLY IF ALERT!!!
* Give 15-20 g simple carb
– 3-4 glucose tablets
– 4-6 oz of fruit juice or reg soda
– 6-10 hard candies
– 2-3 teaspoons of sugar/honey
* Recheck in 15 min
* If still low, repeat procedure
* Notify MD after 2-3 failed tries
* Once glucose WNL, provide a snack or meal to prevent recurrent hypoglycemia
* explore causes
* prevention education
hypoglycemic treatment for unresponsive patient
- 20-50 mL IV 50% Dextrose at rate of 10 mL/min (instant results)
- No IV, not alert, & can’t swallow? glucagon IM or SQ
- Turn on side for risk of aspiration
- Teach family/friends/coworkers how to use
what is diabetic ketoacidosis
Absence or markedly inadequate amount of insulin
* Characterized by uncontrolled hyperglycemia from profound insulin deficiency
* Just because they are hyperglycemic, doesn’t mean they are in DKA!
* Commonly occurs in type 1 DM
Untreated, the patient becomes comatose as a result of dehydration, electrolyte imbalance, and acidosis. If the condition is not treated, death is inevitable.
causes of DKA
insufficient/missed doses of insulin,
physical/emotional stress, illness, infection
four key issues of DKA
hyperglycemia, ketosis,
metabolic acidosis, and dehydration
patho of DKA
- Lack of glucose in the cell causes the body to attempt to obtain energy by rapid breakdown of fat fat breakdown that ketones (acidic by-products)
- Increased ketones leads to ketosis
- Ketosis alters pH balance metabolic
acidosis - Glucose is an osmotic agent and blocks the reabsorption of water osmotic diuresis dehydration and loss of F&E
- Severe depletion of sodium, potassium**, chloride
- Potassium can be increased with metabolic acidosis
clinical manifestations of DKA
- Hyperglycemia: polyuria, polyphagia,
polydipsia - Glucose 300-500
- Dehydration
- Blurred vision
- Abdominal pain with anorexia, nausea,
and vomiting - Acetone in breath sweet, fruity odor
- Kussmaul respirations to reverse
acidosis - Mental status changes
diagnostics for DKA
- Glucose > 250 mg/dL
- ABG: pH < 7.30, bicarb <16
- Moderate to large ketones in
urine and serum - Glycosuria
- Increased anion gap
- Abnormal K, NA, and chloride
anion gap for DKA
- Difference between the measured serum cations (Na) and anions (Cl and HC03) in ECF (p. 87)
Helps determine source of acidosis and remaining anions in blood - Normal: 8-12 mmol/L
- Increases in metabolic acidosis with acid gain (DKA, lactic acidosis)
- Elevations in the amount of anions changes the pH of the. blood/serum, decreases pH, & creates a more acidic
environment - May alert the HCP to the presence of a metabolic acidosis that might not be apparent on first glance of the arterial blood gas values.