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1443 Diabetic Complications
Terms in this set (65)
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
damage to blood vessels s/t chronic hyperglycemia; theories as to WHY hyperglycemia causes angiopathy are:
1) accumulation of glucose metabolism byproducts (e.g.,sorbitol) which are associated w/ nerve cell damage
2) formation of abnormal glucose molecules in basement membrane of small blood vessels, e.g., in eye and kidney
3) derangement in RBC function that leads to decrease in oxygenation of tissues.
One of the leading causes of diabetic related deaths; chronic blood vessel dysfunctions classified as macrovascular complications and microvascular complications
Angiopathy: Macrovascular complications
diseases of the large and medium sized blood vessels that occur with greater frequency and with an earlier onset in people with diabetes; includes cerebrovascular, cardiovascular, and peripheral vascular disease.
High incidence with smoking, obesity, HTN, high fat intake, and sedentary lifestyle
Angiopathy: Macrovascular Consequences
2) CVA: stroke; risks are atherosclerosis, HTN
3) CVD: women have 4-6 X increase (compared to no DM); men with DM 2-3 X increase
4) PVD: with atherosclerosis, advances more rapidly; more likely to be in smaller vessels below knee; NOT able to bypass; results in gangrene
Decrease risks: obesity, smoking, HTN, high fat intake and sedentary
Angiopathy: Microvascular complications
result from thickening of the vessel membranes in the capillaries and arterioles in response to conditions of chronic hyperglycemia;
Differ from MACROvascular in that MICRO is specific to diabetics.
Can be found throughout the body, but most commonly eyes (retinopathy), kidneys (nephropathy), and skin (dermopathy).
Microvascular: Diabetic Retinopathy
process of microvascular damage to the retina as a result of chronic hyperglycemia, presence of neuropathy, and hypertension in pts with diabetes; estimated to be most common cause of new cases of blindness in people 20-74 y.o. Classified as nonproliferative and proliferative
most common form of retinopathy; partial occlusion of small blood vessels in the retina causes microaneurysms to develop in capillary walls. Walls are so weak that capillary fluid leaks out causing retinal edema and eventually hard exudates or intraretinal hemorrhages. Vision is affected if macula is involved.
most severe form of retinpathy; involves retina and vitreous. Retinal capillaries become occluded, new blood vessels are formed to compensate and provide blood to retina.
New vessels are fragile and hemorrhage easily, producing vitreous contraction. Eventually light stops reaching the retina as the vessels become torn and bleed; patient sees red or black spots or lines
Diabetic Retinopathy: Treatments
EARLIEST and most treatable stages often produce no vision changes
1) annual eye exam
2) laser photocoagulation: destroys ischemic areas that produce growth factors that encourage neovascularization
3) blocking VEFG (vascular endothelial growth factor), which is identified in the development of retinopathy
4) vitrectomy: aspiration of blood, membrane, fibers from inside of eye
a microvascular complication associated with damage to the small blood vessels that supply the glomeruli of the kidney. Patients should be screened annually with a measurement of albumin-creatinine ratio from a urine specimen.
Risk factors include hypertension, genetic predisposition, smoking, chronic hyperglycemia.
Diabetic NEPHROpathy: Interventions
Critical to prevent/delay:
1) tight BG control
2) annual screening: GFR, serum creatinine, macro- and microalbuminuria
**in renal failure: dialysis
nerve damage that occurs because of the metabolic derangements (e.g., accumulations of sorbitol and fructose) associated with diabetes mellitus.
The two major categories:
1) SENSORY: (loss of protective sensation), which affects the peripheral nervous system,
2) AUTONOMIC: affects nearly all body systems
most common form; usually distal symmetric polyneuropathy affecting hands/feet bilaterally.
S/S include (usually worse at night):
1) loss of sensation,
2) abnormal sensation,
**Control of glucose is the only treatment, drug therapy can help control symptoms; drugs can be used for pain: capsaicin (topical), tricyclic antidepressants, SSRI (Cymbalta), antiseizure (gabapentin)
Sensory Neuropathy: Complications
1) muscle atrophy in feet/hands
2) complete or partial loss of sensitivity to temperature and touch aka loss of protective sensation (LOPS)
Sensory Neuropathy: Treatment
**Control of glucose is the only treatment,
Drug therapy can help control symptoms; drugs can be used for pain:
1) capsaicin (topical),
2) tricyclic antidepressants,e.g, amitriptyline (Elavil)
3) SSRI, e.g., duloxetine (Cymbalta),
4) antiseizure (gabapentin)
Micro- and Macrovascular: Foot & LE complications
result from combined effect of micro- and macro--; foot ulcers, amputations
Risk Factors: sensory and/or autonomic neuropathy; PAD, smoking, clotting abnormalities, impaired immune system
Autonomic Neuropathy: Complications
2) CV abnormalities: postural hypotension, painless MI
3) sexual dysfunction: impotence; erectile dysfunction
4) neurogenic bladder: retention impairment, which can lead to UTIs; can use cholinergics, e.g., bethanechol, or Crede maneuver (massage downward over bladder)
5) candidal vaginitis
complication of autonomic neuropathy; delayed gastric emptying.
Can produce anorexia, nausea, vomiting, reflux, and persistent feelings of fullness. Can trigger hypoglycemia by delaying food absorption.
neuropathic arthropathy; results in ankle and foot changes that ultimately lead to joint dysfunction and foot drop. Occurs gradually and promotes abnormal distribution of weight over the foot, increasing chances of developing a foot ulcer as new pressure points emerge.
integumentary complication in diabetes; dark, coarse, thickened skin predominantly seen in flexures and on the neck.
necrobiosis lipoidica diabeticorum
integumentary complication associated with type 1 diabetes, usually appears as red-yellow lesions with atrophic skin that becomes shiny and transparent revealing tiny blood vessels under the surface; must be protected from injury and ulceration
integumentary complications associated with type 1 diabetes; probably autoimmune in nature and forms partial rings of papules often on the dorsal surface of hands and feet.
ACE inhibitors (lisinopril) and angiotensin II receptor antagonists (losartan)
Inhibits angiotensin-converting enzyme resulting in decreased plasma angiotensin II. Delays progression of neuropathy in patients with diabetes, treats hypertension. Watch for hypotension. Blood glucose must be tightly controlled in patients with diabetic neuropathy.
Depletes the accumulation of pain-mediating chemicals in the peripheral sensory neurons. Relief of neuropathic pain. Apply cream 3-4 times a day. Symptoms will increase at the start of therapy. Relief of pain is attained in 2-3 weeks.
Tricyclic antidepressants (amitriptyline—Elavil)
Inhibit the reuptake of norepinephrine and serotonin, which are neurotransmitters believed to play a role in transmission of pain through the spinal cord. Relief of neuropathic pain. Antidepressant. Can cause sedation, dry mouth and suicidal thoughts.
Selective serotonin and norepinephrine reuptake inhibitors (duloxetine—Cymbalta)
Increases levels of serotonin and norepinephrine , improving the body's ability to regulate pain. Relief of neuropathic pain. Antidepressant. Can cause nausea and vomiting, dizziness, dry mouth and headache.
Antiseizure (gabapentin—Neurontin, pregabalin—Lyrica)
Decreases the release of neurotransmitters that transmit pain. Anticonvulsant action is unknown. Relief of neuropathic pain. Prevents seizures. Can cause dizziness, somnolence and peripheral edema.
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.
LOPS (Loss of protective sensation)
occurs with sensory neuropathy. Because this is a major risk factor for lower extremity amputation, annual screening using a monofilament should be done. Insensitivity to a 10-g Semmens-Weinstein monofilament has been shown to greatly increase the risk for diabetic foot ulcers that can lead to amputations.
13 Interventions: Diabetic Foot Care
1) Pat feet dry gently, especially between toes.
2) Examine feet daily.
3) Use lanolin on feet to prevent dryness and cracking. Do not use between toes. Use mild foot powder on sweaty feet. Powder feet never shoes.
4) Do not use commercial remedies to remove calluses or corns. 5) Cleanse cuts with warm water and mild soap and cover with clean dressing. Do not use iodine, alcohol or adhesives.
6) Report non healing sores to health care provider.
7) Cut toenails STRAIGHT across. Soak before cutting.
8) Separate over lapping toes with cotton or lamb's wool.
9) Never go barefoot. Slippers with soles. No open toes. Break shoes in gently.
10) Wear clear absorbent socks cotton, white or colorfast. Do not wear clothing that leaves impressions.
11) Do not use heating pads or hot water bottles.
12) Avoid feet in dependent position.
13) Guard against frost bite
Diabetics: Why Prone to Infection?
1) loss of sensation (neuropathy)
2) defect in the mobilization and function of inflammatory cells
3) impaired phagocytosis by neutrophils and monocytes.
4) decreased circulation
5) pathogens proliferate more rapidly
6) patient ignorance of predisposition
Diabetics: Psychological Considerations
1) increased rates of depression
2) higher rates of eating disorders
3) higher rates of anxiety
Diabetics: Gerontological Considerations
1) prevalence increases with age
2) hypoglycemia unawareness is more common
3) glucose intolerance
4) delayed psychomotor function could interfere with management
5) patient's desire to treat may change
6) more comorbidities
SO: recognize limitations in physical activity, manual dexterity and visual acuity; educate accordingly to needs and slower pace
Diabetics: Annual Exam Components
1) dilated eye exam
2) inspection of feet and extremities
5) kidney function
6) lipid profile
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