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Flashcards in week 9- diabetes Deck (44)
1

Diabetes Mellitus

• 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.

2

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

3

type 1

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.

4

type 2

Cellular resistance to insulin.
-Genetic component
-Obesity
-Age

5

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.

6

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).

7

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.

8

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

9

tyoe 1 treatment

Blood glucose monitoring
Insulin, Exercise
Dietary management - balancing CHO intake to insulin and exercise

10

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,
VOMITING, NAUSEA

11

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)

12

“Three Ps”

Polyuria
Polydipsia
Polyphagia

13

Diabetes MellitusDiagnosti
c Studies

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

14

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
Ideal goal
CDA ≤7.0%
Normal range is

15

DIETARY CONCERNS Goals:

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.

16

see slide

26 42 43

17

Distribution of Calories

• CHO
– Upwards to 60%
• Protein
– 10-20%
• Fats
– Some say

18

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

19

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

20

exercise

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.

21

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.

22

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.

23

Exogenous insulin

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

24

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)

25

Problems with insulin therapy

Hypoglycemia
Allergic reaction
Lipodystrophy
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)

26

Drug TherapyOral Agents

• Work on three defects of type 2 diabetes
– Insulin resistance
– Decreased insulin production
– Increased hepatic glucose production

27

Complication of DiabetesAcute

1. Diabetes Ketoacidosis (DKA)
2. Hyperosmolar Hyperglycemic nonketotic syndrome (HHS)
3. Hypoglycemia

28

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

29

Etiology of DKA

Incorrect or missed insulin dose
Incorrect insulin administration
Undiagnosed Type 1 diabetes
Illness
Trauma
Surgery

30

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

31

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
Orthostatic hypotension

Kussmaul breathing- deep rapid breathing in order to rid the body of excess CO2 and reduce the acidotic state

32

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

33

Emergency therapyInitial

• 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

34

Initial Tx

• 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

35

Ongoing assessment

Monitor v/s, LOC, O2 sat, cardiac rhythm,
Urine output
Breath sound for evidence of fluid overload
Serum glucose
Serum potassium
pH

36

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).

37

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

38

3. Hypoglycemia(Insulin reaction)

Abnormally low Blood Sugar
Blood sugar 2.7mm falls to

39

Etiology of hypogkycemia

Too much insulin or Oral hypoglycemic agent
Too little food
Excessive physical activity

40

S&S of Hypoglycemia

Sweating
Weakness
Dizziness
Anxiety
Nausea
Hunger
palpitations
Head ache
Tiredness
Trembling
Tingling
Vision changes
Confusion
drowsiness
Difficulty concentrating
Difficulty speaking



41

Tx of Hypoglycemia

• In adults mild –moderate should be treated with 15 g of carbohydrate
• Preferably glucose or sucrose tablets OR
• Solution
• 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

42

Acute Complications

• Nursing management DKA/HHS
o Patient closely monitored
 Administration
o IV fluids
• Insulin therapy
• Electrolytes
 Assessment
• Renal status
• Cardiopulmonary status
• Level of consciousness

Patient closely monitored
Signs of potassium imbalance
Cardiac monitoring
Vital signs

43

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

44

Skin & Foot Care

• Hygiene is very important
• Wash feet daily; pat dry
• Check feet daily for cuts, or blisters
• Cut nails to contour of toe
• Wear clean cotton socks(never barefoot)
• Break in new shoes carefully
• Guard against frostbite
• Lanolin can be helpful (not between toes)