Med Surg: Class 4:

Diabetes Mellitus

 

Class 4

 

Insulin vs. Glucagon, GH, epinephrine, cortisol

 

Glucagon – turns glycogen and fat into fuel

 

insulin – moving glucose and nutrients into cells

 

Type 1 – autoimmune dx, destroys beta cells

  • some genetic and environmental factors contribute to this
  • onset is not always young
  • scandinavian countries have the highest rates.
  • antibodies that can be tested for to diagnose DM1
    • GAD antibodies
    • insulin autoantibodies
    • c-peptide levels

 

type 2 DM

  • factors that contribute to insulin resistance:
    • genetic factors
    • diet
    • obesity
    • physical inactivity
  • if both parents have DM2 the child has a 50% chance of getting DM2
  • Progressive decline of Beta cell function

 

Gestational DM

  • DM that is diagnosed during pregnancy and leaves after
  • 20% of pregnant woman will get this
  • HPL – human placental lactogen, increases glucose levels to allow the baby to get more glucose
    • If there is too much glu the baby can become too fat and cause birth issues

 

secondary DM

  • chronic pancreatitis
  • Hormonal disorders
    • cushing’s disorder
    • acromegaly
  • cystic fibrosis
  • down syndrome
  • drug induced
    • nicotinic acid
    • HIV meds
    • anti rejection meds – prograph
    • glucocorticoids – dexamethasone
    • chemotherapy –

 

Diagnose DM2 (above these normal ranges)

  • A1c 5.7-6.5%
  • fasting plasma glucose 100-125 mg/dL
  • 2 hour PG 140 – 199 mg/dL in the OGTT

 

Prevention

  • metformin decreases chance by 30%
  • metformin + lifestyle is a decrease of 60% chance

 

Inpatient glu targets

  • non ICU
  • pre meal >140
  • random > 180
  • ICU
    • 140-180

 

Diabetes Meds

 

  • Metformin
    • reduction of insulin resistance, decrease liver glu production
    • PO route
    • S/E: gastrointestinal discomfort
    • if creatinine is above 1.5 risk of renal disease
  • Sulfonureas (glyburide, glipizide)
    • stim insulin production
    • S/E: hypoglycemia
  • Meglitinides
    • short term insulin secretion
  • thiazolidinediones (pioglitazone Actos)
    • reduction of insulin resistance
    • gain about 10 lbs of water weight
    • use with caution in CHF and liver Dx
    • 4 week onset, bone loss
  • SGLT2 inhibitors (invokana Canagliflozin) (jardiance Empagliflozin)
    • reduce renal glu reabsorption and increase secretion
    • S/E: weight loss, UTI
  • Incretin mimetics (bayetta bid) (bydureon 1x week)
    • stim insulin secretion, suppress glucagon, slows gastric emptying
    • GLP- Agonist
    • S/E: weight loss, N/V/D

 

Insulin

  • Basal insulin (best injected in the abdomen)
    • Long acting (detemir and glargine)
      • no peak duration of 24hr
    • intermediate acting (NPH)
      • peak 6-12hr duration of 12-20hr
  • bolus insulins (given after the meal to be sure that they ate it. the injection can go any where you can pinch an inch)
    • rapid acting (humalog, Novolog) 5-15min onset
    • short acting (regular (humulin, Novolin) 30-60min onset

 

  • Insulin pumps
    • rapid acting insulin that is infused all day to replace the basal. when the person eats they put in their blood sugar and amount of carbs about to eat.
    • there are also sensors that can track the glucose level in the blood using and sensor that needs to be calibrated with a finger stick BID. This is very helpful with trending the glucose level.
    • Nursing considerations
      • the person needs to be alert and oriented to use it
      • double check what the person is telling you about the pump
      • still use finger stick in the hospital as a double check because we are liable
      • still a SQ catheter injection to deliver the medication

 

Acute complications:

 

  • Diabetic acidosis
    • increase in ketone acid from the body breaking down fat rapidly
    • Labs
      • glucose >250
      • CO2 <15
      • Anion Gap [Na – (Cl + HCO3)] increased (acidic) 
    • almost always in people with DM1
    • s/s: n/v, polyuria, polydipsia, kussmaul respirations, tachycardia

 

  • HHNK
    • higher blood glucose than with DKA
    • spill glucose in urine
    • more common in DM2
    • same treatment as DKA

 

Hypoglycemia

  • treatment
    • Glucagon to increase hepatic glucose release
    • Epinephrine to reduce glucose uptake and increase hepatic glu production
  • s/s HTN, diaphoresis, unique to the person and there may be no symptoms
  • hypoglycemia unawareness – lowers the level that the hypoglycemia is felt by the person

 

Long term complications

 

Retinopathy

  • blood vessels are damaged
  • create black spots in vision
  • nonproliferative – occurs in about 10 years
  • Proliferative – neovascularization, from retinal hypoxia
  • macular edema –

macular edema

Glaucoma

cataracts

 

Nephropathy

  • stage 1 functional change gfr increases (GFR >90)
  • Stage 2 glomerular damage (GFR 60-89)
  • stage 3 overt nephropathy (GFR 30-59)
  • Stage 4 severe nephropathy (GFR 15-29)
  • Stage 5 end stage need dialysis (>15)

 

  • need a renal diet low potassium, refined foods ( doesn’t mesh well with DM diet)

 

Neuropathy

  • first painfull then painless once the nerve is full glycosylated
  • fall risk, (have bad proprioception)

 

Autonomic neuropathy

  • Gastrointestinal – gastroparesis
    • anorexia, nausea, vomiting
    • diagnosis from radioactive food(eggs) visualised by medical scintigraphy

 

  • cystopathy
    • cannot sense full bladder
  • ED
    • Poor blood flow (most meds do not work because it just works to increase blood flow not nerve response)
  • female sexual dysfunction  

 

Cardiovascular disease

 

  • from increased platelet aggregation, decreased fibrinolytic activity, HTN, Hyperlipidemia
  • s/s: are not common MI s/s and can be “silent”
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