DM Med Surg

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  1. What are the risk factors for developing DM?
    • Over 45 y/o
    • Over ideal body weight (obesity)
    • Close family member with diabetes
    • African American, American Indian or Hispanic Heritage
    • Gestational DM
    • HTN
    • CAD
    • Sedentary Lifestyle
    • Polycystic Ovary Disease (POS)
  2. Explain what happens to glucose in the liver
    • Liver stores the extra glucose (1/3 of the body's glucose) by turning glucose to glucagon by glycogenesis
    • When the body needs more sugar, the liver converts glucagon into glucose by glycogenolysis
    • If there is no more glucagon in the liver, proteinlysis and then lipolysis will occur
  3. Where are glucagon and insulin created?
    • Both are created in the islets of langerhorn in the pancreas
    • Glucagon is created in the Alpha cells
    • Insulin is created in the beta cella
  4. What does insulin release look like throughout the day?
    • A small basal rate of insulin is secreted throughout the day under normal circumstances
    • A Prandial dose is released with food
    • Together, this keeps blood glucose (BG) below 120 mg/dL
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  5. How does insulin act as a transporter?
    • It transports and metabolizes glucose into the cell
    • Stimulates the storage of glucose and enhances storage of fat
    • Promotes triglyceride storage
    • Accelerates transport of amino acids into cells
  6. What counterregulatory hormones work against insulin to increase BG?
    • Glucagon
    • Epinephrine
    • Growth Hormone
    • Cortisol
    • These are secreted during fasting or periods of stress
  7. How does the stomach effect BG?
    • If stomach empties too fast, it does not absorb enough glucose from food
    • Incretin hormones (GLP-1) secreted in stomach prevent hyperglycemia after meals
  8. What are the macrovascular complications of DM?
    • CVA
    • MI
    • Atherosclerosis
    • CAD
    • HTN
    • Hyperlipidemia
    • PVD
    • The high BG irritates the blood vessels and large swings dilate and restrict blood vessels causing damage
  9. What are the microvascular complications of DM?
    • The thickening of vessel membranes of capillaries and membranes causes damage
    • Retinopathy
    • Nephropathy
    • Sensorimotor autonomic neuropathy
  10. Describe DM retinopathy
    • Major cause of blindness in the US
    • Venous Beading: dilation and constriction of bloos vessels look like links of sausage
    • NonVasularization Retinopathy: neovascularization, but new vessels are weak and bleed
    • Proliferative Retinopathy: structural obstructions causing poor circulation. No new vessels.
  11. What causes nephropathy and what is the first s/s?
    • Nephropathy is from chronic high BG causing renal HTN
    • leading cause of ESDK in the US and often need dialysis
    • Microalbumia in urine is often the first s/s
    • 24 hour albumin/creatinine clearance to diagnose
  12. How does DM cause neuropathy?
    • Hyperglycemia causes nerve hypoxemia through blood vessel changes
    • As the axon and myelin sheath are damaged, the nerve impulses are no longer transmitted
  13. What are the autonomic and Peripheral manifestations of DM neuropathy?
    • Autonomic: hypoglycemic unawareness, bladder problems, constipation, dysphagia, erectile dysfunction, changes in temperature adjusting
    • Peripheral: numbness and inability to feel pain or temperature change, tingling or burning sensation (dysesthesias), sharp jabbing pain which may be worse at night, sever pain to the lightest touch, muscle weakness, complications with foot care
  14. What is the difference in causes between T1DM and T2DM?
    • T1DM: often caused by genetics, an autoimmune disease or virus. ¬†ICA and ICAA antibodies are present in labs
    • T1DM: caused by obesity and stress
  15. What differentiates T1DM from T2DM?
    • T1DM: Beta cells do not produce any insulin at all. Diagnosed commonly before 30 y/o. They are dependent on outside source of insulin
    • T2DM: Normally a gradual onset as pancreas does not produce enough insulin, patient becomes insulin resistant or produces too much glucose. May end up on insulin along with lifestyle changes
  16. What is syndrome X?
    • It is diagnosed when 3 of the following exist for a genetic predisposition to DM:
    • Triglyceride level of 150 or higher
    • HDL of over 40
    • Blood Pressure 130/85 or higher
    • fasting Glucose 110 mg or higher
  17. What are the diagnostic labs for DM?
    • Fasting Plasma Glucose: 126 mg/dL or higher on 2 or more occasions
    • Glucose Tolerance: >200 mg/dL 2 hours from receiving glucose
    • Casual Glucose: >200 mg/dL with s/s of hyperglycemia
    • A1C: normal range is 4-6% and tells of glucose control over the last 3-4 months
    • Urine: may be checked for ketones, a marker of lipolysis
  18. What are the three Ps of hyperglycemia?
    • Polyuria
    • Polydyspia
    • Polyphagia
  19. What is whipples triad of hypoglycemia?
    • S/S of low blood glucose
    • A low plasma glucose (below 70 mg/dL)
    • Correction after plasma glucose is raised
  20. What are the S/S of hypoglycemia?
    • Tremors
    • Tachycardia
    • Diaphoresis
    • Dizziness¬†
    • Anxiety
    • Blurred vision
    • Aggrivated or upset
    • Hungry
    • Weak or tired
    • Confusion
    • Seizures
    • Loss of Conciousness
  21. What are the S/S of Hyperglycemia?
    • Polydyspia
    • Polyuria
    • Polyphagia
    • Tired
    • Blurry Vision
    • Dry skin
    • Nonhealing wounds
  22. What is the nursing intervention for hypoglycemia?
    • Give glucagon tab, 4 tsps of sugar or 15g carbs to bring up BG
    • If this does not work, admin 1mg of glucagon subcut, give IV or 25-50mL D50W
  23. Describe DKA
    • DKA has a sudden onset
    • Extreme Hyperglycemia
    • Pancreas is producing no insulin and sugar is unable to get into cells. Hypoglycemic cells trigger for more sugar from protein and then lipids, driving the BG sky high
    • Ketones are a biproduct of lipolysis and put the body into a metabolic acidosis
  24. What are the s/s of DKA?
    • Polyuria, polydispia, polyphagia
    • tachycardia
    • fruity breath
    • ketones in urine
    • kussmaul's resps (very deep and rapid to blow off CO2)
    • Dehydration
    • Hypotension
  25. What are the interventions for DKA?
    • Assess ABCs, LOC, electrolyte and BG level
    • Correct volume depletion with NSS at high rate (watch for cerebral edema if D51/2NSS is given as it is hypotonic)
    • IV insulin therapy
    • Potassium Replacement by IV (only for a short period, as then it can spring into hyperkalemia)
  26. Describe Hyperglycemic Hyperosmolar State (HHS)
    • gradual onset
    • Increased blood osmolarity state by extreme hyperglycemia (causing dehydration, seizures, coma, hemiparesis and aphasia)
    • Body produces some insulin to prevent metabolic acidosis (no ketones in urine)
  27. What are the nursing interventions for HHS?
    • Fluid replacement at high volume (1L 1/2NSS over 1 hr)
    • Assess neuro status and monitor for cerebral edema
    • IV insulin after fluid replacement
    • Replace and monitor electrolytes
  28. What should a patient with DM do if they become ill?
    • Take insulin or oral agents as prescribed
    • Test BG q4hrs
    • Report BG of >300 to HCP
    • Test for ketones in urine, contact HCO if positive
    • If n/v/dd occur, take fluids q30min and if not tolerated call HCP
  29. What is a diabetic diet?
    • Count calories
    • Protein 15-20%
    • Sat Fat <7%
    • Carbs 45-65%
    • Fiber 25g/day
    • Sodium <2.4 g/day
    • Watch alcohol intake (only take with food)
  30. What is the number of carbs the DM patient needs to keep in mind?
    • 15g of carbs = 1 slice of bread or 1/2 cup of ice cream
    • Patients may be able to subsitute foods, but must count carbs
    • 2000cal diet has 250g carb per day
  31. How can exercise help the DM patient?
    • It lowers BG by increasing the uptake in skeletal muscle and fat
    • If Bg is over 250, do not exercise as the body cannot absorb this sugar and the BG will continue to rise
    • Exercise decreases obesity, HTN, cholesterol and other risk factors/comorbidities for DM
  32. What is the somogyi effect?
    • Due to giving insulin, the BG drops significantly at night and undetected hypoglycemia can take place during sleep
    • The body tries to compensate and rebound hyperglycemia with DKA occurs
    • Treatment is to have a snack before bed and to reevaluate insulin to prevent bottoming out
  33. What is the dawn phenomenon?
    • Hyperglycemia upon awakening due to growth hormones at night
    • Treatment is to change time of insulin admin or increase dose
  34. Describe an insulin pump
    • If BG is well controlled, a patient may use an insulin pump
    • The pump gives a basal rate and the patient can provide a prandial dose at meals
    • Patient must check BG reguarly
    • Catheter in subcut tissue is rotated every 3 days
Card Set:
DM Med Surg
2014-03-24 01:46:36
LCCC Diabetes Nursing Med Surg

for exam 2
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