Case Studies: DM Flashcards
Chronic metabolic disease resulting from either a deficiency in insulin secretion, resistance of insulin action at the cellular level or both
Leading cause of blindness, end stage kidney disease and foot/leg amputations
Seventh leading cause of death in the US
Affects 25.8 million people (8.3%) of the population - lot pop
Chronic metabolic disorder - from the deficiency in inulsin secretion or resistance of insulin or both - results in increased BG or inability regulated BG
Causes microvascular and macrovascular changes - blindness, end stage renal disease, food/leg amputations - seen often
One of leading causes of disability and death
What is Diabetes
Resulting in hyperglycemia and inability to regulate blood glucose
Chronic metabolic disease resulting from either a deficiency in insulin secretion, resistance of insulin action at the cellular level or both
No insulin is produced - has be provided for them from outside body
Autoimmune disorder
Beta cells of the pancreas are destroyed by antibodies
Onset usually occurs <30 years of age; typ Younger age than T2DM
Abrupt onset
3 P’s: Polydipsia, polyuria, polyphagia, and weight loss
Requires insulin - insulin pumps; be on sliding scale
Could be viral in etiology - Post viral infection people will develop diabetes; virus in body and brought on diabetes; does not cause diabetes
T1DM
Reduction of the cells to respond to insulin (insulin resistance) and decreased secretion of insulin from beta cells - reduction in response to insulin
Predisposing factors are obesity, physical inactivity and genetics (in family)
Onset usually occurs >50 years of age - Can be younger but typ older adults
Could have no symptoms or polydipsia, fatigue, blurred vision, vascular and neural complications
Accounts for 90% of diabetic patients - quite few pats have this
Increase in pediatric T2DM and diabetes - bad diet and less exercise - increase childhood obesity making more prevalent
T2DM
Glucose intolerance during pregnancy
Not mean will be diabetic after delivery - put at higher risk for T2DM down line
Gestational
carb/glucose (candy, juice)
Insulin (all supplies with it)
Glucameter
Water
Glucameter supplies
BP cuff
Stethoscope
Cell phone
Oxygen
Commode
Stuck in an elevator that has T1DM what 10 things want with us
Insulin
Glucameter and supplies
carbohydrate/glucose (Juice)
Narrow down to 3 for T1DM
carbohydrate/glucose (Juice) - hypoglycemia bigger emergency than hyperglycemia; have syptoms a lot quicker; take really high BG to have symptoms of hyperglycemia; when get low BG get symptoms quickly - need keep tight good BG control but not want too low; brain uses glucose and without glucose it starves - s/s of it starving
Narrow down to 1 for T1DM
Polydipsia
Polyuria
Polyphagia
3 P’s - what are they and why does it happen
Excessive thirst
Caused by dehydration
Polydipsia
Frequent and excessive urination
Caused by osmotic diuresis secondary to excessive serum glucose
Polyuria
Excessive hunger
Really high BG but not pushed into cells those cells are starving
Excessive eating
Caused by cell starvation
Polyphagia
Given in subcutaneous tissue
Do not mix long acting insulin or premixed insulin
Regimens are used to duplicate the basal and prandial release pattern of the pancreas
Can be given by a continuous subcutaneous infusion
Regular insulin is the only insulin that can be administered IV - Reg insulin only one administered via IV: insulin drip; not Lantis or Humalog
What should the nurse know about insulin
Abdomen, back of arm, buttocks, thigh
Abdomen, back of arm typ; can do other places
Ask places where would like it
Sometimes want back of arm and want break abd to get a break if take insulin all time
Given in subcutaneous tissue
Short and long acting - doing diff things - always have insulin and glucose control - but when have meals have big spikes and want prevent big spikes and big declines that causes hypoglycemia
Regimens are used to duplicate the basal and prandial release pattern of the pancreas
Externally worn pump - Can wear pump - typ T1DM
Can be given by a continuous subcutaneous infusion
To prevent hypoglycemia and if a client is having a hypoglycemic episode it is important to know what type of insulin is on board so that we know how long the hypoglycemia could occur
Rapid Acting Insulin (ex. aspart (Novolog); lispro (Humalog)); not give without having tray; need tray in front of them
Short Acting Insulin (ex. regular U100; regular U500) - regular insulin
Intermediate Acting Insulin (ex. NPH; 70/30; 50;50)
Long Acting Insulin (ex. glargine (Lantus); detemir (Levemir)) - okay if not have meal tray in front of them
Reg insulin - typ insulin drip and in area where can closely regulate it (ICU) - where need have continuous - not people who have pump - in emergency situations; going through IV; can give subQ and but only type can also go through IV
Why is it important for a nurse to know onset, peak and duration of insulin?
Refrigerate insulin not in use
Insulin in use may be kept at room temperature for up to 28 days
Discard unused insulin after 28 days
Prefilled syringes are stable up to 30 days when refrigerated
Have a spare bottle of each type of insulin used on hand
Inspect the insulin before each use - look at it
Use disposable needles one time - only one time even if just for self
Follow infection control measures
What should be included in patient edu
Lantus should always be stored in a refrigerator
Multipatient vials - clean top; some pats have pens where easier for them
Insulin in use may be kept at room temperature for up to 28 days
Store upright
Prefilled syringes are stable up to 30 days when refrigerated
Cleaning with alcohol pads, washing hands and pat understands that
for insulin injections as well as blood sugar checks
Follow infection control measures
2 acute comps related to diabetes
HHS and DKA –
give fluids first; more profound dehydration typ
HHS -
Serum glucose
Osmolarity
Serum ketones
Serum pH
Serum HCO3
Serum Na+
BUN
Creatinine
Urine ketones
DKA
> 300
Serum glucose
Variable
Osmolarity
Positive at 1:2 dilutions
difference
Serum ketones
Less than 7.35
Serum pH
Less than 15
Serum HCO3
Low, normal, or high
Serum Na+
Greater than 30; elevated because of dehydration
BUN
Greater than 1.5; elevated because of dehydration
Creatinine
Positive
difference
Urine ketones
Serum glucose
Osmolarity
Serum ketones
Serum pH
Serum HCO3
Serum Na+
BUN
Creatinine
Urine ketones
HHS
> 600
Serum glucose
> 320
Osmolarity
Negative
difference
Serum ketones
Greater than 7.4
Serum pH
Greater than 20
Serum HCO3
Normal or low
Serum Na+
Elevated
BUN elevated because dehydrated
BUN
Elevated
Creatinine
Negative
Difference
Urine ketones
Fasting BG test
Glucose tolerance test
Glucosylated Hgb (Hgb A1C)
BG values
Normal range: 70-100; less than 100; older adults: levels rise 1 mg/dL per decade of age
Sig of abnorm results: levels greater than 100 but <126 = impaired fasting glucose (not fast well); >126 on at least 2 diff occasions diagnostic of diabetes (dependent on eating)
Fasting BG test
Normal range: <140
Sig of abnorm results: 140-200 impaired glucose tolerance (not diagnostic); >200 indicate provisional diagnosis (concern)
For gestational diabetes - fine afterwards but higher risk for T2DM
Glucose tolerance test
Normal range: 4-6%; levels greater than 6.5% diagnostic for DM
Sig of abnorm results: >8% poor diabetic control
Looking at over time best indicator of BG control; goal with diabetic pats with BG is keep tight BG control - not want really high/low - so least amount acute/chronic comps - imp pats know why need do it or else not follow regiment - think not imp or not impact them but does impact them and explain comps and can affect eyes, kidneys, nerves, limbs
Education is really imp for pats; can be good night before and tight blood glucose control on fasting but this tells overtime
Tell us about BG control
Glucosylated Hgb (Hgb A1C)
Microvascular
Macrovascular
What leads to these complications?
Microvascular and macrovascular comps of DM
Retinopathy
Neuropathy
Nephropathy
Microvascular
CV disease
Stroke
Peripheral vascular disease
Macrovascular
Changes to the blood vessels secondary to hyperglycemia
Changes in blood vessels leads to poor tissue perfusion and cell damage and death - lot times diabetic pats have issues in feet - harder get there because poor perfusion - smaller vessels in feet than in trunk of body
What leads to these complications?
Hyperglycemia affects cells integrity
Lot BG overtime - damaging vessels
Changes to the blood vessels secondary to hyperglycemia
Tight BG control - manage BG
*Maintaining blood glucose in expected range and preventing acute and chronic complications of diabetes
Best way to prevent complications is to keep tight control of blood glucose
What is our primary goal for clients diagnosed with diabetes?
Foot care imp in pats with diabetes
Harder time with healing - harder time with wound healing - think about BG all time with healing
Foot injury is the most common complication of diabetes leading to hospitalization
Assess the foot
Cleanse and inspect feet daily - using mirrors or sig other do it
Wear properly fitting shoes
Avoid walking in bare feet
Wear clean, dry socks daily
Trim toenails properly - big deal if ingrown toenail; cut by someone
Report non-healing breaks in the skin of the feet to the health care provider - emphasizing why so imp with pats
Peripheral neurpathy/foot care
Increased risk for wound progression that could eventually lead to amputation
Most lower extremity amputations are preceded by foot ulcers - not want amputation and not strives for and complicates lift and want avoid - can do prosthetics
Foot injury is the most common complication of diabetes leading to hospitalization
for status of circulation - check pedal pulses - sometimes diminished - not have circ is prob; look for circ
for evidence of deformity
for loss of strength
for loss of protective sensation - cannot feel if cut foot and not know about it and gets progressively worse and ends up hospital; not want walk barefoot; wear well fitting shoes and socks; might not able feel if something hot/cold on feet
Really assessing them and proper tools to that
Assess the foot
Neuropathic pain results from damage anywhere along the nerve
Manifestations
Pharmacologic agents to manage neuropathic pain: - might be used for something else; know why pat on that and investigate what used for
Peripheral neuropathy/managing pain
Tingling, numbness complain about, loss of proprioception in lower extremities - cannot tell where it is and when walking run into things
Burning
Muscle cramps
Piercing or stabbing pain
Metatarsalgia (sensation of walking on marbles)
Allodynia (pain from normal nonpainful stimuli) - something someone might think not as painful
Hyperalgesia (exaggerated pain response)
Manifestations
Oxycodone not work for them for nerve pain
Gabapentin (Neurontin) - anticonvulsant; neuropathic pain
Pregabalin (Lyrica) - neuropathic pain
Duloxetine (Cymbalta) - neuropathic pain
Pharmacologic agents to manage neuropathic pain: - might be used for something else; know why pat on that and investigate what used for
Need get Regular eye exams - yearly
Appropriate eyewear
Might need Reading aids - have to draw up insulin; glucose meters where it is read out to them
need make sure getting ocular pressures done
Adaptive devices for administering insulin - dexterity to give self insulin
Specialized adaptive equipment for blood glucose monitoring
Retinopathy
Want to Control hypertension
Correct hyperlipidemia - keeping lipid and cholesterol numbers under control imp
Kidney function evaluation:
If microalbuminuria develops:
Smoking cessation - always want do
Drug therapy for nephropathy
Nephropathy
Annual serum creatinine level/BUN; GFR - looking at these
Annual test for microalbuminuria in specific patients
Kidney function evaluation:
Control BP and blood glucose - high BP damage blood vessels in kidneys and not working properly and stop remove waste and extra fluid in body - want make sure keep good BP and BG control
Restrict dietary protein
Avoid nephrotoxic agents including contrast dyes - when using dyes
Promptly treat UTI’s - all infections
Prevent dehydration
If microalbuminuria develops:
Angiotensin-converting enzyme (ACE) inhibitors (ACEIs)
Angiotensin receptor blockers (ARBs)
Drug therapy for nephropathy
Reduce level of albuminuria and progression of kidney damage
Angiotensin-converting enzyme (ACE) inhibitors (ACEIs)
Block action of angiotension, blood vessels enlarge and BP decreased
Help with BP management and helping not develop nephropathy and kidney damage
Angiotensin receptor blockers (ARBs)
