Flashcards in week 9- diabetes Deck (44)
• Not a single disease, but a group of disorders.
– Abnormal glucose homeostasis
• Normal glucose = 3.9 - 6 mmol/L.
– Decrease in insulin production.
– Decrease in activity of insulin.
– Disordered metabolism of CHO, proteins, and fats.
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 the storage of dietary fat in adipose tissue
• Accelerates transport of amino acids into cells
• Inhibits the breakdown of stored glucose, protein, and fat
Type I:Destruction of Beta cells-autoimmune mediated. Approx. 5% of children with type I diabetes have a first or second degree relative with Type I. The child inherits a susceptibility to the disease rather than the disease itself. Viral component: exposure to congenital rubella and enterio virus may have a higher risk of developing the disease.
Cellular resistance to insulin.
DM Type I Characteristics
• Any age, most often young.
• Abrupt onset
• Thin, catabolic state
• Polydipsia, polyuria, polyphagia, fatigue
• Requires insulin, ketoacidotic if absent.
• Vascular & neurologic complications >5yrs old.
Genetics: If one child has DM1 then other siblings have 5-10% chance of getting DM1. 45% if sibling is identical twin. If father has DM, then children will have 4-6%. If mother has DM, then children have a 2-3%(double that of father) of getting DM.
DM Type II Characteristics
• Any age, but age is usually >35yrs
• Onset is gradual
• Obese or normal in appearance
• Oral agents effective
• Insulin required in 30-40%
• Mild or no symptoms
• Ketosis if infected, or stressed
• Vascular, and neurologic complications.
• 90% of people with DM have type II.
• Inherited defect in insulin receptors and postreceptors of cells.
• Insulin resistance triggers increased insulin output by pancreas, thus resistance may begin 3-4 decades prior to patient becoming symptomatic.
• Excessive hepatic glucose production causes hyperglycemia(even while fasting) (>27-55mmol/L).
DM Type II genetics
Genetics: 100% in monozygotic twins. Siblings have 7-14% chance, Both parents = 15-45% risk for children, 50% chance of passing defective gene to one’s children.
High risk groups: African decent, Hispanic, Asian, South Asian, Aboriginal (1 in 2). Caucasians have lowest rate.
Age: half of cases are older than 55yrs.
type 1 manis
Polydipsia, polyuria, recent wgt. loss but maybe overweight, short
duration of symptoms, initial period of decrease insulin requirement but will need insulin for survival, ketosis, KA on presentation on 30%-40% of cases- continued risk for DKA
tyoe 1 treatment
Blood glucose monitoring
Dietary management - balancing CHO intake to insulin and exercise
type 2 manis
Obese, little or no wgt. gain or may be significant wgt. loss, acanthosis, nigricans, long duration of sysptoms, polyuria, polydipsia may be mild or absent
Glucoseuria w/o ketourea in 33% of case on initial presentation
KA on initial presentation in 5%-25% of cases, HTN
Lipid disorder, excessive wgt. gain and fatigue d/t insulin resistance
Other: acne, menstrual disturbance,
type 2 therapy
Diet with decreased c
calories and low fat foods
Decrease sedentary activity time or increase
routine physical activity
Blood glucose monitoring
Oral medication (Metformin to improve insulin sensitivity)
Four methods of diagnosis
1.AIC ≥ 6.5%
2..Fasting plasma glucose level ≥ 7 mmol/L
3.Random or casual plasma glucose measurement ≥11 mmol/L plus classic symptoms
4.Two-hour OGTT level ≥11.1 mmol/L when a glucose load of 75 g is used
Hemoglobin A1C test
Hemoglobin A1C test
Recommended to be used as a diagnostic test
Useful in determining glycemic levels over time
Shows the amount of glucose attached to hemoglobin molecules over RBC life span
Approximately 120 days
Regular assessments required
Normal range is
DIETARY CONCERNS Goals:
Maintenance of normal blood glucose levels by balancing food intake with insulin or oral meds with activity levels.
Achievement of optimal serum lipid levels.
Controlled food intake to maintain normal weight, growth and development, metabolic needs during illness, or pregnancy/lactation.
Prevention and treatment of acute/ chronic complications of illness.
Improved overall health.
26 42 43
Distribution of Calories
– Upwards to 60%
– Some say
Alcohol and DM
• ETOH in moderation will not have impact on b-d sugars
– Careful re. Mixes, and sugar content of wine.
• ETOH in large amounts is dangerous
– Interferes with gluconeogenesis (proteins)
• B-d sugars can decrease into danger zone
– May mask S+S of hypoglycemia
• Person may not receive treatment
– Energy not used is converted into fat.
– May potentate glucose-lowering agents
• Decreased BS r/t decreased gluconeogenesis
• ETOH can be converted into disulfiram
Alcohol Teaching Points
Drink only if sugars well controlled
Don’t drink on an empty stomach
If dinner is late, eat fruits/veggies or starches
Don’t omit food if using insulin
Avoid sweet mixes, or wines
If dancing, eat more food
Wear a visible identification
An exercising cell needs less insulin
Pt. Must plan ahead for exercise
>1hr after meal, or 10-15g CHO snack
1-2 extra fruits, and veggies choice
For q45 minutes – 1hour of strenuous exercise, pt must consume additional 10-15g CHO
Blood sugars should be well controlled before strenuous exercise is considered.
Illness and DM
Check blood or urine at least 4x qd
Check urine for glucose and ketones q void. High glucose with ketones is more serious than without ketones.
More short acting insulin if BS >13, and ketones in urine.
Do not stop taking insulin
Fluid balance important
Soft diet, liquid CHO helpful
Glucagon for severe insulin reaction, go to ER after initial treatment.
Pts need at least their regular dose of insulin, even if Vomiting and Diarrhea. May require additional regular insulin to compensate.
Recommend pt seek medical help if Vomiting >1-2 days (for test). Reality is if no food or drink in 4hours, then seek medical help.
Precautions for Surgery
• 15-20 u per hour may need to be given to offset the stress of surgery, and corticosteroid therapy
1. Diabetic patients should preferably be operated on first on a list and, where possible, morning lists are preferable to afternoon lists.
2. Blood glucose monitoring should be hourly while a diabetic patient is starved. A patient on an infusion should be monitored hourly until stable and then as indicated.
3. If a blood glucose falls below 3 as measured by an approved meter, repeat the measure immediately and obtain a laboratory blood glucose if the BG remains below 3 mmol/L.
4. If the BG is > 17 mmol/L, surgery should not be undertaken that day unless the condition is serious or life-threatening. Expert advice is strongly advised and the patient should be referred to a physician. It is usually possible to get the diabetes adequately controlled so that the patient is fit for surgery within one or two days.
5. Insulin infusions should be prescribed on the insulin chart. A change in the scale used requires the infusion be represcribed. 10% glucose (+/- potassium) should be prescribed on the fluid balance chart.
6. Plasma potassium should be checked at least 8 hourly during insulin infusions.
7. Metformin carries a risk of lactic acidosis and should be discontinued perioperatively.
Insulin from an outside source
Required for type 1 diabetes
Prescribed for patient with type 2 diabetes who cannot control blood glucose by other means
Types of insulin
– Human insulin
• Only type used today
• Prepared through genetic engineering
– Common bacteria (Escherichia coli)
– Yeast cells using recombinant DNA technology
– Insulins differ with regard to onset, peak action, and duration.
• Characterized as rapid-acting, short-acting, intermediate-acting, long-acting
– Different types of insulin may be used for combination therapy.
– Rapid-acting analogue (clear): lispro (Humalog), aspart (NovRapid), and glulisine (Apidra)
– Short-acting (clear): regular
– Intermediate-acting (cloudy): NPH
– Extended long-acting: glargine (Lantus), detemir (Levemir)
Problems with insulin therapy
Somogyi effect (Somogyi effect
Rebound effect in which an overdose of insulin causes hypoglycemia
Usually during hours of sleep
Counterregulatory hormones released
Rebound hyperglycemia and ketosis may occur.)
Dawn phenomenon (Characterized by hyperglycemia present on awakening in the morning
Due to release of counterregulatory hormones in predawn hours
Growth hormone/cortisol possible factors)
Drug TherapyOral Agents
• Work on three defects of type 2 diabetes
– Insulin resistance
– Decreased insulin production
– Increased hepatic glucose production
Complication of DiabetesAcute
1. Diabetes Ketoacidosis (DKA)
2. Hyperosmolar Hyperglycemic nonketotic syndrome (HHS)
1. Diabetic Ketoacidosis (DKA)
A severe metabolic, electrolyte, & fluid imbalances
Life threatening condition that occurs in pts with Type 1 diabetes
May also be seen in pts with Type 2 diabetes
Body uses fat and protein stores for energy
Etiology of DKA
Incorrect or missed insulin dose
Incorrect insulin administration
Undiagnosed Type 1 diabetes
Characteristic S&S of DKA
Vomiting > 2x in 6 hrs
> 5 diarrheal stools in 24 hrs
Illness (viral or other) and unable to eat
Change in mental status(leh, restles, conf)
Temp >38.9c for 12 hrs
Glucose > 17mmol/L on two readings or > 10 mmol/L with moderate to large ketones (BS 16-44)
Large ketones, acetone breath
Rapid, weak pulse
Characteristic S& S of DKA
Evidence of bacterial infection (eg. Fever & drainage)
Difficulty breathing (Kussmaul resp - deep rapid breathing in order to rid the body of excess CO2 and reduce the acidotic state)
Decreased urine output/ frequency
Dysuria or evidence of UTI
Kussmaul breathing- deep rapid breathing in order to rid the body of excess CO2 and reduce the acidotic state
Assessment of DKA
Blood glucose levels vary between 16.6 and 44.4 mmol/L
Severity of DKA is not related to blood glucose level
Ketoacidosis is reflected in low serum bicarbonate and low pH; low PCO2 reflects respiratory compensation
Ketone bodies in blood and urine
Electrolytes vary according to water loss and level of hydration
• Ass- patent airway
• O2 as prn
• IV access (large bore catheter)
• IV fluid replacement with N/S until BP stabilize & urine output > 30-60mls/hr
• Begin Insulin(Regular) drip 0.1u/kg as needed
• Rehydration with IV fluid
– Note: rehydration leads to increased plasma volume and decreased K+; insulin enhances the movement of K+ from extracellular fluid into the cells
• Admin KCL IV to correct
• Admin Na bicarb IV if severe acidosis Ph
Monitor v/s, LOC, O2 sat, cardiac rhythm,
Breath sound for evidence of fluid overload
2. Hyperosmolar Hyperglycemic nonketotic Syndrome (HHNS)
Def: A life threatening syndrome that can occur in pts. with diabetes who are able to produce enough insulin to prevent DKA but not enough to avoid severe hyperglycemia, osmotic diuresis, and extra cellular fluid depletion. (Lewis p. 1361).
Characteristic of HHNS
• Can occur in type I or type 2 pts
• More common in type 2 esp. elderly pts.
• Precipitated by physiologic stress(infect, CVA, MI, Sx)
• Slow onset- over days
• BS usually >33.3 mmol/L
• Normal pH
• Serum & urine ketones- absent
• Serum Osmolarity- > mOsm/L
• Bicarb- normal
• Elevated BUN& Creat
• Mortality 10-40%
• Care similar to DKA
3. Hypoglycemia(Insulin reaction)
Abnormally low Blood Sugar
Blood sugar 2.7mm falls to
Etiology of hypogkycemia
Too much insulin or Oral hypoglycemic agent
Too little food
Excessive physical activity
S&S of Hypoglycemia
Tx of Hypoglycemia
• In adults mild –moderate should be treated with 15 g of carbohydrate
• Preferably glucose or sucrose tablets OR
• Eg. 15 mls (3 tsp) or 3 packets of table sugar dissolved in H2O
• 175 mls. (3/4 cup) of orange or regular soft drink
• Six (6) Life Savers (1=2.5 g CHO)
• 15 mls. ( 1 tablespoon) of honey
• Wait 15 mins, retest BS & retreat with another 15 g CHO if results
• Nursing management DKA/HHS
o Patient closely monitored
o IV fluids
• Insulin therapy
• Renal status
• Cardiopulmonary status
• Level of consciousness
Patient closely monitored
Signs of potassium imbalance
Long-Term Complications of Diabetes
• Macrovascular complications
o Accelerated atherosclerotic changes
o Coronary artery disease, cerebrovascular disease, and peripheral vascular disease
• Microvascular complications
o Diabetic retinopathy and nephropathy
• Neuropathic changes
o Peripheral neuropathy, autonomic neuropathies, hypoglycemic unawareness, pseudomotor neuropathy, and sexual dysfunction