Care of Pats with DM Flashcards
Lot care directly related to mitigating comps - helping to limit amount comps pats with diabetes have
All considered emergencies; most often admitted to hospital
Diabetic Ketoacidosis (DKA)
Hyperglycemic-hyperosmolar state (HHS)
Hypoglycemia
***All considered medical emergencies
Acute comps of DM
Insulin deficiency and acidosis
Diabetic Ketoacidosis (DKA)
Insulin deficiency and severe dehydration
Hyperglycemic-hyperosmolar state (HHS)
Too much insulin or too little glucose/intake to compensate for that
Hypoglycemia
Caused by changes in blood vessels in tissue and organs - integrity of blood vessels impaired with diabetes and because of that not getting all O2 and blood supply to certain areas (kidney, retina) and causes cell damage, ischemia and eventually death
Vascular changes result from:
Changes in blood vessels lead to poor tissue perfusion and cell damage and death
Two types vascular areas affected:
Macrovascular
Microvascular
Chromic comps of DM
Hyperglycemia thickens basement membranes and causes organ damage
Hyperglycemia affects cell integrity
Vascular changes result from:
Macrovascular
Microvascular
Two types vascular areas affected:
Cardiovascular disease
Cerebrovascular disease
Peripheral vascular disease
Risk factors of hypertension, obesity, dyslipidemia and sedentary lifestyle increase risk of these complications - expenetialy increase risk of macrovascular changes
Big Focus for Nursing should be on decreasing modifiable risk factors - high cholesterol, HTN, obesity, increase exercise
Macrovascular
Increased issues with this
Pats die from this
Increased risk for this Myocardial Infarction; Increased risk for this Heart Failure
Increased risk for any embolic event
Higher risk dysrhythmias if survived MI; heart muscle effected so see HF
Cardiovascular disease
Increased issues with this
Pats die from this
2-4 times higher risk for stroke
Cerebrovascular disease
Increased issues with this
Peripheral artery disease (vascular changes, increased risk for developing wounds); Leg uclers - esp in LE; Do develop get extensions that develop rapidly because not having blood supply so harder to heal
Peripheral vascular disease
Retinopathy
Neuropathy
Nephropathy
Microvascular
Vessels in retina damaged and so leak resulting in retinal hemorrhage and not allow blood supply to get there and lead to blindness; because leaking beading increase risk for rupture; sometimes eye make new tiny vessels to compensate for that but high risk for rupturing but damage to tiny vessel in back of eye
Without retina cannot see - lot pats have issue
Also form plaque; increased risk for macular degeneration
Caused by damage to the retinal vessels causing leaking and retinal hypoxia
Retinopathy
Progressive deterioration of nerves
Either have Loss in sensation (numbness/tingling) or muscle weakness - innervation not there to innervate muscles
Caused by blood vessel changes that cause nerve hypoxia
Can affect all areas of the body (extremities, organ sys: GI (delayed gastric emptying and reflux), cardiac, urinary)
Any area of body
Neuropathy
Kidney issues
Changes in kidney - high BG - causes damages to blood vessels in kidney which then causes hypoxia to kidneys and not getting blood supply need and start damaged
Change in kidney that decreases function and causes kidney failure
Chronic high blood glucose causes damage to blood vessels in kidneys causing leaking and hypoxia
Kidneys allow filtration of larger particles that should not go through through which damage the kidneys further
Cause scarring; narrowing blood vessels and other comps causing kidneys be further hypoxic and lead to kidney failure
HTN - higher risk for kidney issues
Nephropathy
Values use diagnose diabetes and see how well diabetics doing in regards to controlling disease
Fasting BG test
Glucose tolerance test
Glucosylated Hgb (Hgb A1C)
BG values
Depending on pat fasting
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
Do check for gestational diabetes; dependent on pat - specific on how prep
Normal range: <140
Sig of abnorm results: 140-200 impaired glucose tolerance (not diagnostic); >200 indicate provisional diagnosis (concern)
Glucose tolerance test
More and more used in acute care and community
Indication of how pats BG over period time; glucose attaches to Hgb gives avg BG over 120 days - lifespan RBC; good clue on how pats with diabetes doing
Higher level higher BG been
Correlate with what avg BG been
Normal range: 4-6%; levels greater than 6.5% diagnostic for DM
Sig of abnorm results: >8% poor diabetic control - commonly used and imp blood work for DM pat; not matter if eat before lab draw because do when come in
Glucosylated Hgb (Hgb A1C)
Related to initial hyperglycemia/comps secondary to hyperglycemia
Risk for injury related to hyperglycemia - hypoglycemia, neuropathy, nephropathy, retinopathy, pain related to diabetic neuropathy (main things look at for diabetic pats)
Potential for impaired wound healing related to endocrine and vascular effects of diabetes
Risk for injury related to diabetic neuropathy
Acute pain and chronic pain related to diabetic neuropathy
Risk for injury related to diabetic retinopathy-induced reduced vision
Potential for kidney disease related to impaired kidney circulation
Potential for hypoglycemia
Potential for diabetic ketoacidosis
Potential for hyperglycemic-hyperosmolar state and coma
Planning and priorities
What want at end of care for DM pats
Main priority: Maintaining blood glucose in expected range decided by provider and preventing acute and chronic complications of DM are the primary outcomes - help pat self manage DM so have as min comps related to it as possible; prevent comps and maintain BG within range supposed to be and if do that should help with comps
Performs treatment regimen as prescribed
Follows recommended diet
Monitors blood glucose/suger using correct testing procedures
Seeks health care if blood glucose levels fluctuate outside of recommended parameters
Meets recommended activity levels - exercise always big
Uses drugs as prescribed
Maintains optimum weight
Problem-solves about barriers to self-management
Expected outcomes
Nutrition
Exercise
Blood glucose monitoring
Medications
Interventions
Worried about BG and concerned about what eating so nutrition huge
Dietician should be involved and collab with them; if not have them refer them to someone outpat so can absorb info and not in stressful situation; make sure getting resources outpat setting
Should be individualized
45-65% carbohydrates - “carb counting” (more pop esp if BG harder control, dose insulin based on carbs eating for each meal) - oftentimes with insulin give basal dose then give based on high BG or meals eating; very specific; pop in all settings
15-20% protein (if normal kidney function); make sure only if no nephropathy; if probs with kidneys cut back
Limit saturated fats and cholesterol - high cholesterol increases risk for macrovascular changes - keep cholesterol as low and same with triglycerides
Watch alcohol intake (can lead to hypoglycemia) - way works on liver - suppresses release of glucose; oftentimes BG go down with alcohol; if do drink eat in moderation so not have issues with alcohol
Need to take patient preferences and culture into consideration
Nutrition
Help regulate blood glucose and increases insulin sensitivity; more receptive to insulin - huge for T2DM
Important in weight loss for DM 2
Should monitor blood glucose and watch for injury - increase BG if already stressed and also drop it so monitor closely; careful with injury because harder to heal
More cognisent
Exercise
Very important in self care - Very imp to monitor BG - indication how doing with care; teach how check BG and make sure have equiment
Target goals are individualized - BG to be; provider and goals
Frequency depends on drug regimen - frequency of treatments
Accuracy is essential - make sure BG accurate
Ensure proper technique - where on finger checking it
Continuous glucose monitoring (inserted in sub-q tissue) - insulin pumps
Blood glucose monitoring
adequate sample; using correct and all supplies needed; calibrate machine; BG monitoring - need teach pats how use monitor because one first things need know how do if new diabetics; go over machines: ensure able do it and see; use good infection control, cleaning it and not sharing equipment
Accuracy is essential - make sure BG accurate
All patients with type 1 DM will require insulin
Patients with type 2 DM may require medication (antidiabetic drugs or insulin) if they do not achieve blood glucose control with diet and exercise - some may need oral insulin; vary with pat and how able control BG
Medications
Shorter-acting drugs (ex. glipizide (Glucotrol))
Longer-acting drugs (ex. glyburide (Diabeta); glimepiride (Amaryl))
Metformin (Glucophage)
Other common medications
Drug therapy for DM
Increases insulin secretion - T2DM (producing some but not very much)
Better for patients with irregular eating - not eating reg time
Preferable in older patients or decreased/diminished kidney, liver or cardiac function
Take around meal time and need know BG before taking them
Shorter-acting drugs (ex. glipizide (Glucotrol))
Increases insulin secretion - T2DM (producing some but not very much)
Daily dosing is better for adherence: once a day
Longer-acting drugs (ex. glyburide (Diabeta); glimepiride (Amaryl))
Very common for diabetic pats
Reduced hepatic glucose production and increases tissue sensitivity to insulin - more able pull glucose into cells
Should not be used with anyone with kidney disease
can cause lactic acidosis in patients with renal insufficiency - be aware of s/s of that: malaise, fatigue, muscle pain, changes in LST, abd discomfort
Upset stomach - take with food
Needs to be held for 48 hours after administering any contrast media or surgery - make sure kidney func back up to where needs to be and contrast dyes toxic on kidneys and want make sure good before start med again
Metformin (Glucophage)
Exenatide (Byetta, Bydureon) – SQ (sim to insulin) - frequent; given before meals bid; respond well to it
Acarbose (Precose) – PO; commonly seen
Pioglitazone (Actos) - PO
Sitagliptin (Januvia) - PO; commonly seen
Either increase sensitivity to insulin or increase secretion of insuli
Other common medications
Given in subcutaneous tissue
Do not mix long acting insulin or premixed insulin - some do mix
Regimens are used to duplicate the basal and prandial release pattern of the pancreas - Insulin doing in T1DM is body has certain basal insulin and releases more insulin based on when eat - prandial release pattern - with insulin given to pats give base dose (long acting) and give bolus doses around meal time; BG high and when eating body needs insulin so can handle glucose
Can be given by a continuous subcutaneous infusion of insulin
Insulin admin
Give it: Abdomen (best place and absorbs quickest), back of arm, buttocks, thigh - fat tissue; want rotate spots within area (such as within abd)
Given in subcutaneous tissue
Externally worn pump - monitor and insulin pump
Need lots of education - pats have that know LOT - need tons edu; well-versed on it; know what doing with it because high risk
Can be given by a continuous subcutaneous infusion of insulin
Need know type insulin giving, when works, peaks, duration - because if pats goes hypoglycemic tells how long going to last and how going to treat it
Rapid Acting Insulin (ex. aspart (Novolog); lispro (Humalog))
Short Acting Insulin (ex. regular U100; regular U500)
Intermediate Acting Insulin (ex. NPH; 70/30; 50;50)
Long Acting Insulin (ex. glargine (Lantus); detemir (Levemir))
Types insulin (Chart 64-8)
Work fastest; peak fastest; last shortest amount of time
Rapid Acting Insulin (ex. aspart (Novolog); lispro (Humalog))
Second fastest
Short Acting Insulin (ex. regular U100; regular U500)
Basal dose then do rapid or short acting in between/for meals during day
Long Acting Insulin (ex. glargine (Lantus); detemir (Levemir))
Injection site
Absorption rate
Injection depth
Timing of injection
Mixing insulin
Factors affecting insulin absorption
Absorption fastest in the abdomen
Where inject affects how absorbed
Teach to rotate around a site but not to another site
Injection site
In any particular affected by type of insulin, amount (larger amount takes longer to absorb), local heat, massage, exercise, or scarring (cannot feel it so less painful but not absorb as well)
Absorption rate
Affect it
90 degree angle usually always given (thinner patients may need to inject at a 45-degree angle to avoid IM injection and absorb much faster vs subQ)
Injection depth
How close given to meal
Timing of injection
Sometimes 2 insulins mixed together not absorb as if were give 2 sep shots at same rate; got onset of short-acting and duration of longer-acting so harder to judge with mix; make sure before inject that swirling it to make sure fully mixed
Response to mixed insulin may differ from the response to the same insulins given separately
Mixing insulin
A sig amount to edu
Refrigerate insulin not in use - can refrigerate insulin before opened and once opened keep out fridge for 28 days and then throw away after 28 days
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 and extra needles; not reusing needles - imp: painful and injection not effective
Inspect the insulin before each use
Use disposable needles one time
Follow infection control measures: swabbing top of vial
Drawing up own insulin: can do it themself: can see it: magnifiers and help them with; ones can dial in dose - easier if issues with fine motor; whatever utilizing make sure can effectively use it/someone designated to be caregiver can
Patient edu-insulin
Lantus should always be stored in a refrigerator
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
Transplantation of the pancreas (cadaver donor)
Islet cell transplantation
Surgical interventions
Not lot whole lot
Almost all pancreas transplants are done to treat Type 1 diabetes
Requires lifelong drug (immunosuppressive) therapy to prevent rejection - issues with infection later on
Seen often with kidney transplants
Considered in patients with diabetes and end-stage kidney disease who have had or plan to have a kidney transplant
Complications are common (ex. infection, rejection, cancer)
Transplantation of the pancreas (cadaver donor)
Transplant some beta cells - not common
Considered experimental
Islet cell transplantation
High risk for injury: peripheral neuropathy: issues with foot care because of that are; foot issues/wounds common reasons why diabetics come into hospital; really bad wound
Foot injury is the most common complication of diabetes leading to hospitalization
There is an increased risk for wound progression that could eventually lead to amputation - very serious
Most lower extremity amputations are preceded by foot ulcers
Make sure shoes fit; check for sensation and mobility
Assess the patient for risk for diabetic foot problems
Assess the foot
Cleanse and inspect feet daily
Wear properly fitting shoes
Avoid walking in bare feet
Wear clean, dry socks daily - not wear socks with seams that could put pressure that might not notice
Trim toenails properly - big; done specific way
Report non-healing breaks in the skin of the feet to the health care provider - taken care of right away
Reducing risk for injury-peripheral neuropathy/foot care
for status of circulation
for evidence of deformity
for loss of strength
for loss of protective sensation
Assess the foot
Neuropathic pain big issue for diabetic pats; not typ pain; results from damage anywhere along the nerve
Manifestations for diabetic pats - cannot describe it well or describe it as pain
Pharmacologic agents to manage neuropathic pain:
Managing pain - diabetic neuropathy
Tingling, numbness, loss of proprioception in lower extremities
Burning
Muscle cramps
Piercing or stabbing pain
Metatarsalgia (walking on marbles)
Allodynia (pain from normal nonpainful stimuli) - pain feels more than should be because all nerve damage
Hyperalgesia (exaggerated pain response)
Manifestations for diabetic pats - cannot describe it well or describe it as pain
Gabapentin (Neurontin) - anticonvulsant meds; for seizures; more for neuropathic pain now
Pregabalin (Lyrica) - anticonvulsant meds; for seizures; more for neuropathic pain now
Duloxetine (Cymbalta) - antidepressant; effective
Pharmacologic agents to manage neuropathic pain:
Ensure have these taken care of
Reducing risk for injury by reducing BG as much as can
Regular eye exams - yearly
Appropriate eyewear if needed
Reading aids
Adaptive devices for administering insulin - impaired vision and check BG, admin insulin, draw it up in tiny syringes, are magnifiers or switch to pen or get prefilled syringes; also have talking meters so easier time checking BG
Specialized adaptive equipment for blood glucose monitoring
Reducing risk for injury-sig impaired vision
Kidney damage big issue for diabetic pats
Control hypertension - damage to kidney occurs is big issue - keep under control
Correct hyperlipidemia - keep down
Kidney function evaluation:
If microalbuminuria develops:
Smoking cessation
Drug therapy for nephropathy - having albumin in urine
Reducing risk for injury - diabetic nephropathy (big comps want prevent)
Monitor all of these: Annual serum creatinine level/BUN; GFR
Annual test for microalbuminuria in specific patients - urine tested for albumin; check beginning kidney damage so do other interventions so limit amount of damage to kidney
Kidney function evaluation:
Control BP and blood glucose
Restrict dietary protein
Avoid nephrotoxic agents including contrast dyes
Promptly treat UTI’s
Prevent dehydration; make sure staying hydrated
Monitor on all of this and take care of it before proceeds further
If microalbuminuria develops:
Helps with lot comps; constricts vessels in kidneys when smoke
Smoking cessation
Angiotensin-converting enzyme (ACE) inhibitors (ACEIs)
Angiotensin receptor blockers (ARBs)
Drug therapy for nephropathy - having albumin in urine
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 to block kidney damage
Angiotensin receptor blockers (ARBs)
Treatments do higher risk for this
Skin
Dehydration
Respirations
Mental status
Symptoms
Glucose
Ketones
Hypoglycemia
Cool, clammy, sticky
Skin
Absent
Dehydration
No particular/consistent change
Respirations
Anxious, nervous, irritable, mental confusion, seizures, coma: issues with this
Mental status
Weakness, double vision, blurred vision, hunger, tachycardia, palpitations
Symptoms
Less than 70
Glucose
Negative
Ketones
Issue with this if DM
Skin
Dehydration
Respirations
Mental status
Symptoms
Glucose
Ketones
Hyperglycemia
Warm, moist
Skin
Present
Dehydration
Rapid, deep
Kussmal type/respirations: rapid and deep
Acetone odor (fruity odor) to breath
Respirations
Varies from alert to stuporous, obtunded, or frank coma: issues with this quickly; irritable at first, not quite right progress if not treated to coma
Mental status
Issues with blurred vision, tachycardia
None specific for DKA
Acidosis; hypercapnia; abdominal cramps, N/V
Dehydration: decreased neck vein filling, orthostatic hypotension, tachycardia, poor skin turgor
Symptoms
> 250
Glucose
Positive - body trying break down other things to get glucose and produces the ketones in body
Ketones
Not want pat be here
Prevention is the best treatment! - check BG, not giving too much insulin, making sure eating
Avoid:
Treatments:
Hypoglycemia treatment
Excess insulin
Deficient intake or absorption of food
Exercise
Alcohol intake - give hypoglycemia because impact on liver because stops releasing glucose
Avoid:
For patients who can tolerate oral intake: - awake and alert
For patients who can not tolerate oral intake: - not want cause aspiration
Frequent checks of PBG following treatment
Follow protocols of health system/hospital
Treatments:
Take 15-20 grams of oral glucose if PBG<70 - tab, gel, orange juice, candy, marshmallows
Take 30 grams of oral glucose if PBG <50
Repeat in 15 minutes after initial treatment if glucose remains low
For patients who can tolerate oral intake: - awake and alert
Give to self at home and convert glycogen in liver to glucose and increase BG
Glucagon subcutaneous or intramuscular - short acting - follow up if good response with food to keep BG up; continually monitor because can go back down because can go back down to make sure not go back down
50% Dextrose intravenous - short acting - follow up if good response with food to keep BG up; continually monitor because can go back down because can go back down to make sure not go back down
For patients who can not tolerate oral intake: - not want cause aspiration
T1DM come in with
Uncontrolled hyperglycemia - key, metabolic acidosis - key, increased production of ketones
Aciditic because body breaking down other things than glucose for energy and increased production of ketone bodies and causes lot CM
Sudden onset
Precipitating factor: infection, stress, inadequate insulin intake (not doing insulin regiment appropriate); have infection or stress increases insulin needs so pushes into DKA
Manifestations:
Emergency and typ straight to ICU
Monitor:
Treatment:
Diabetic ketoacidosis
Ketosis (increased production of ketone bodies causes this which is an acidosis: have: Kussmaul respirations (RR trying blow off CO2 - get rid acid so better balance with pH); ketones produce fruity breath; nausea; abdominal pain)
Dehydration and electrolyte loss/imbalance
Manifestations:
Airway - acidosis
LOC/mental status
Hydration (VS; I&O) - rehydrate
Electrolytes (assess for S/S of hypokalemia-fatigue, malaise, confusion, muscle weakness, shallow respirations, abdominal distention or paralytic ileus, hypotension, and weak pulse)
Monitor:
Priority is give IV fluids to get BG back under control then give IV fluids so adequately hydrated then look at electrolytes if needed
Regular insulin by continuous IV infusion
Replace potassium (ensure urine output is at least 30 mL/hr) - common electrolyte imbalance (it being low) for these pats
IV Sodium Bicarbonate (used only for severe acidosis) - body’s working recover from acidosis may need to give something alkalotic to get acidosis under control
Treatment:
Hyperglucemic episode - T2DM
Hyperosmolar (increased blood osmolarity) state caused by hyperglycemia
Gradual onset
Precipitating factor: dehydration; infection; poor fluid intake
Higher BG with this than DKA
Big emergency situation
Manifestations:
Monitor:
Treatment:
Hyperglycemic-hyperosmolar state (HHS)
Lot Neurological symptoms-seizures, myoclonic jerking, reversible paralysis
Severe dehydration and electrolyte loss - more profound dehydration
No ketone bodies
Manifestations:
Airway
LOC/mental status
Hydration (VS; I&O)
Electrolytes (assess for S/S of hypokalemia-fatigue, malaise, confusion, muscle weakness, shallow respirations, abdominal distention or paralytic ileus, hypotension, and weak pulse)
Monitor:
IV fluids of NS if shock or severe hypotension, otherwise IV fluids of ½ NS - hydration most imp because can go into shock from dehydration and HTN
Assess/watch for signs of cerebral edema (abrupt changes in mental status, abnormal neurological signs, coma) - all fluid replacement
IV insulin is administered only after fluids have been replaced
Treatment:
Serum glucose
Osmolarity
Serum ketones
Serum pH
Serum HCO3
Serum Na+
BUN
Creatinine
Urine ketones
DKA
High
>300
Serum glucose - DKA
Variable
Osmolarity - DKA
Positive at 1:2 dilutions
Serum ketones - DKA
Because has ketones will have lower pH
Less than 7.35
Serum pH - DKA
Because severe acidosis
Less than 15
Serum HCO3 - DKA
Low, normal, or high
Serum Na+ - DKA
Both dehydrated
Greater than 30; elevated because of dehydration
BUN - DKA
Both dehydrated
Greater than 1.5; elevated because of dehydration
Creatinine - DKA
Positive
Urine ketones - DKA
Serum glucose
Osmolarity
Serum ketones
Serum pH
Serum HCO3
Serum Na+
BUN
Creatinine
Urine ketones
HHS
Significantly high
>600
Serum glucose - HHS
High - causing severe dehydration - diuresising from high osmolarity
>320
Osmolarity - HHS
Not in serum or urine
Negative
Serum ketones - HHS
Greater than 7.4
Serum pH - HHS
Greater than 20
Serum HCO3 - HHS
Normal or low
Serum Na+ - HHS
Both dehydrated
Elevated
BUN - HHS
Both dehydrated
Elevated
Creatinine - HHS
Negative
Urine ketones - HHS