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Diabetes - Diabetic Ketoacidosis & Hyperosmolar Hyperglycemia Syndrome
Terms in this set (33)
lack of enough insulin and cell deprivation of glucose causes stimulation of hepatic conversion of glycogen into glucose resulting in elevated BG
type of glucose level caused by
1) too much food,
2) too little diabetic medications,
4) emotional/physical stress,
5) poor absorption of insulin
**counterregulatory hormones released when stress, illness persist
1) polyuria: osmotic diuresis (glucose in renal tubules cannot be reabsorbed; consequent hyperosmolarity and osmotic pressure results in more water in tubules)
2) polyphagia followed by lack of appetite,
3) polydipsia: hyperosmolarity of blood causes thirst as cells release more water into circulation
5) blurred vision,
8) abdominal cramping
9) dry, warm, itchy skin
**do NOT exercise if BG 250 mg/dL (stress hormones released) and ketones (Type 1); do NOT exercise if >300 mg/dL (Type 2)
2) drink water
3) eat less CHO at meals
**contact HCP if BG >250 mg/dL two-three times in one week
1) do NOT stop taking medication
2) check BG more frequently
3) clear liquids until no more nausea
low blood glucose (<70 mg/dL); occurs when there is too much insulin in proportion to available glucose in the blood; counterregulatory neuroendocrine hormones are released in response: suppress insulin, promote glucagon and epinephrine.
**If untreated: loss of consciousness, seizures, coma, death
1) alcohol intake without food,
2) too little food or skipping meals
3) too much diabetic medication
4) too much exercise,
5) mismatch of medications and food,
6) weight loss without medication adjustment,
MILD: sweating, tremor, tachycardia, palpitation, nervousness, hunger
MODERATE: poor concentration, numb lips/tongue, HA, light-headedness, slurred speech, irrational/combative behavior, visual disturbances
SEVER: disorientation, loss of consciousness, difficult to arouse, seizures, coma
**Can mimic alcohol intoxication.
***use of beta blockers interferes with recognizing the symptoms
condition in which pt does not experience warning signs/symptoms of hypoglycemia until glucose reaches critical point; related to autonomic neuropathy
RULE of 15:
1) check blood glucose for levels < 70 mg/dL
2) ingestion of 15-20g of a simple (fast-acting) carbohydrate: glucose tablets, 4 oz of juice, 1 T of honey, 4-6 oz soda
***NO CANDY BARS/COOKIES: treatment with fats s/b avoided b/c the fat will slow absorption of sugar. Avoid overtreatment.
3) Recheck glucose 15 minutes after treatment. If no significant improvement after two to three doses, 1 mg of glucagon by IM/SQ injection (deltoid preferred)
4) Administer complex CHO (starch) + protein after recovery
ACUTE CARE SETTINGS: 20-50 mL of 50% dextrose IVP
1) regular pattern of exercise and eating
2) regular BG testing and insulin adjustment
3) always have a simple sugar
4) wear an ID bracelet so others will be aware in emergency
5) TEACH prevention and instruct to call HCP when BG <70 mg/dL two-three times in one week
Diabetic Ketoacidosis (DKA); aka diabetic acidosis/diabetic coma
caused by profound deficiency of insulin and is characterized by hyperglycemia, ketosis, acidosis, and dehydration.
When circulating supply of insulin is insufficient, glucose can't be properly used for energy, so the body breaks down fat as a secondary source of fuel, creating ketones.
Most likely to occur in Type 1, but may be seen in Type 2 in conditions of severe illness/stress when pancreas cannot meet the extra demand for insulin.
Precipitating factors include illness, infection, inadequate insulin dosage, undiagnosed type 1 diabetes, poor self-management, and neglect. If untreated, death is inevitable.
acidic by-products of fat metabolism that can cause serious problems when they become excessive in the blood.
An acute insulin deficiency and glycogenolysis, in conjunction with glyconeogenesis cause hyperglycemia.
1) Hyperglycemia leads to osmotic diuresis, leading to fluid volume deficit causing hemoconcentration eventually causing hypovolemic shock, renal failure, and hypoxia.
2) Fats are incompletely metabolized causing ketone body production that also leads to osmotic diuresis.
3) As the body becomes more acidic potassium leaves the cells and is replaced with hydrogen ions.
4) As hypoxia worsens lactic acid builds up contributing to the acidosis.
5) insulin deficiency impairs protein synthesis and causes protein degradation, resulting in nitrogen losses (amino acids contain NH2)
1) EARLY: may present as lethargy, weakness
2) dehydration resulting in poor skin turgor, dry mucous membranes,
4) orthostatic hypotension;
5) Abdominal pain accompanied with nausea, vomiting.
6) Kussmaul respirations,
7) acetone noted on breath (fruity);
DKA: Lab Findings
1) glucose > 250,
2) arterial blood pH < 7.3,
3) serum HCO3 < 16,
4) moderate to large ketones in urine/blood.
5) high anion gap (normal = 8-12 mEq/L)
Anion Gap: Relationship to Metabolic Acidosis
Formula is (Na+) - (Cl and HCO3), but not all cations and anions are measured;
normally unmeasured anions (albumin, phosphates, sulfates, organic acids) EXCEED unmeasured cations (Mg, Ca, other minerals), thus the ANION GAP
normal AG = 8-12 mEq/L
Metabolic acidosis is usually associated with a HIGH anion gap, HOWEVER normal anion gap may occur if chloride is retained (hyperchloremic metabolic acidosis)
symptom seen in DKA; rapid, deep breathing associated with dyspnea. Body's attempt to reverse metabolic acidosis through exhalation of excess CO2.
DKA: Potassium imbalances
Ketonuria causes cation elimination, e.g., K+ and also Na, Mg, because ketones are ANIONS; body is attempting to maintain electrical neutrality;
Initially loss d/t to osmotic diuresis and/or vomiting
1) obtain serum K+ before insulin tx (insulin causes K+ to enter cells)
2) if hypokalemic, start K+ replacement therapy
DKA: Treatment Goals
1) correct dehydration
2) correct electrolyte imbalances
3) correct acidosis
DKA: Initial Treatment
1) check ABC; administer O2 via NC
2) start IV access with large bore catheter
3) start fluid resuscitation
4) start insulin drip
DKA: Dehydration Correction
1) 0.9% NS or .45 % NS given at 1L/hr. until B/P returns to normal and urine output is 30-60 ml/hr.
**overinfusion, esp. w/ hypotonics, cause sudden serum Na drops that can lead to cerebral edema
2) Insulin withheld until fluid resuscitation is started because insulin allows water to enter the cell along with glucose and can lead to a depletion of vascular volume.
**Initial insulin bolus is given and then continuous regular insulin drip at 0.1 U/kg/hr is started.
**need to drop BG by 36-54 mg/dL/hour--rapid drops can cause cerebral edema
3) Once blood glucose levels reach 250 mg/dl, 5% dextrose may be added to the fluid regimen to prevent hypoglycemia. Monitor potassium levels throughout the treatment.
***Potassium can fall rapidly as insulin drives potassium into the cells.
4) Potassium is added to the IV solution when urine output is normal. Administer sodium bicarbonate if severe acidosis (ph< 7.0)
DKA: Electrolyte Correction
Aim is tor replace ECF/ICF water and to correct deficits: Na, Cl, HCO3, K, PO4, Mg and nitrogen
1) administer K+ AFTER first getting serum K+ level
2) monitor serum K+ frequently
3) monitor heart with ECG
Hyperosmolar Hyperglycemic Syndrome (HHS)
life threatening syndrome that can occur in diabetics who produce enough insulin to prevent DKA but not enough to prevent severe hyperglycemia, osmotic diuresis, and ECF depletion.
**Less common than DKA
**often in pts over 60 y.o. w/ Type 2.
Causes are UTI, pneumonia, sepsis, any acute illness, newly diagnosed type 2 diabetes. Glucose can get quite high before diagnosis. Often r/t impaired thirst sensation and/or functional inability to replace fluids
1) severe hyperglycemia (greater b/c no ketogenesis) which results in profound fluid loss (osmotic diuresis)
2) profound dehydration
3) decreased Na, K and phosphorus
As fluid loss continues, eventually hypovolemia occurs:
1) decreased renal perfusion leads to anuria
2) hypotension leads to hypoxia and lactic acid increase (anaerobic metabolism)
3) hemoconcentration leads to hyperviscosity and thrombosis
**shock, seizures, coma and death if not corrected
HHS: Laboratory Finding
1) BG >600 mg/dL
2) increased serum osmolality (275-295 mOsm/kg is normal)
3) ketones absent/minimal in serum and urine
Client requires greater fluid replacement than DKA, but similar treatment:
1)45% or 0.9 % NS at a rate that is dependent on cardiac status and degree of fluid volume deficit. Total loss 6 to 12 L.
2) Regular insulin bolus given by IV bolus, followed by infusion after fluid replacement therapy is instituted to aid in reducing the hyperglycemia.
3) When blood glucose levels fall to approximately 250 mg/dl, IV fluids containing glucose is administered to prevent hypoglycemia.
4) Electrolytes are monitored and replaced as needed
MONITOR: CV and respiratory; renal function; LOC; electrolytes; I & O; skin turgor
DKA & HHS: Principal Difference
HHS usually has enough circulating insulin so that ketoacidosis does not occur
Type 1 Diabetes
More common in young, but can occur at any age. Signs and symptoms are abrupt, but disease process may be present for several years. Associations between specific human leukocyte antigens, HLA-DR3 and HLA-DR4 & as many as 20 genes influence susceptibility. Environmental factors are virus, toxins. Nutritional status thin, catabolic state. Symptoms thirst, polyuria, polyphagia, fatigue, weight loss. Ketosis prone at onset or during insulin deficiency. Diet management essential; insulin required
Type 2 Diabetes
Usually age 35 yr or older but can occur at any age, Incidence is increasing in children. Onset is insidious, may go undiagnosed for years. Genetic tendency but no relationship to HLA, majority of cases are polygenic. Environmental factors obesity, lack of exercise. Nutritional status obese or possibly normal. Symptoms frequently none, fatigue, recurrent infections. Ketosis resistant except during infection or stress. Diet management essential; oral agents or insulin or injectables
DM: Acute Complications
Diabetic Ketoacidosis, Hyperosmolar Hyperglycemic Syndrome (HHS), Hypoglycemia
What DM patients will not respond to glucagon injection for hypoglycemia?
Patients with minimal glycogen stores will not respond to glucagons. These include patients with alcohol-related hepatic disease, starvation, and adrenal insuffiency
Why do type 2 diabetics not usually develop ketosis?
Usually sufficient insulin is present to block ketogenesis
Diabetics: Why does renal failure occur?
Microangiopathy in the kidney causes diffuse glomerulosclerosis that affects the basement membranes of all glomerular capillaries. The basement membranes become thickened and leaky.
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