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Nur 3010 exams > Diabetes > Flashcards

Diabetes Flashcards

1
Q

what is diabetes

A

group of metabolic diseases characterized by hyperglycemia
- 1/3 cases undiagnosed

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2
Q

devastating complications of diabetes

A
  • physical, social, economic consequences
  • leading case of non-traumatic amputations
  • leading cause of end stage kidney disease
  • 7th cause of death in US
  • leading cause of new blindness in adults 18-64yrs
  • increased risk of ED visits and hospitalizations
  • increased risk for covid and being hospitalized, intubated, or dying from covid

MOST IMPORTANT: education, self management

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3
Q

pathophysiology of diabetes: insulin (what, when, actions (3))

A
  • hormone secreted by beta cells, which are in the islets of langerhans in the pancreas
  • secreted when we eat (but for other reasons) to move glucose from blood -> muscles, liver, fat cells

actions (MAIN):
1) transports and metabolized glucose for energy
2) stimulated storage of glucose in the liver and muscles (in form of glycogen)
3) enhances storage of dietary fat in adipose tissue
other:
- signals liver to stop release of glucose
- accelerates transport of amino acids (derived from dietary protein) into cells
- inhibits the breakdown of stored glucose, protein, fat

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4
Q

diagnosis of diabetes mellitus

A
  • A1C (gold standard) > or = 6.5%

other:
- fasting plasma glucose = 126 mg/dL
- two hour plasma glucose level 200 mg/dL or more during oral GTT
- patients with classic symptoms of hyperglycemia or hyperglycemic crisis, random plasma glucose level of 200 mg/dL or more

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5
Q

pre-diabetes

A
  • mild hyperglycemia (not at cut off yet)
  • encourage health diet, exercise, and weight control
  • NON PHARM INTERVENTIONS ONLY
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6
Q

pre-diabetes = metabolic syndrome (what, measurements)

A

includes pre diabetes but also covers:
- obesity
- disorders of adipose and insulin resistance

measurements:
- abdominal adiposity: waistline >40in men, >35 in women
- triglyceride >150
- BP >130/80
- fasting blood glucose > 100mg/dL
- strongly associated with peripheral vascular & heart disease

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7
Q

types of diabetes (2)

A

1) type 1: beta cell destruction, usually leading to absolute insulin deficiency (minority, hard to control, total destructive beta cells)
2) type 2: progressive insulin secretory defect in addition to insulin resistance (body wants lots of insulin, decreased supply)

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8
Q

other subcategories of diabetes

A
  • gestational diabetes: all women should be tested at 24-28 weeks of gestation with an oral glucose tolerance test, goal <140mg/dL
  • LADA (latent autoimmune diabetes in adults) - type 1
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9
Q

glycated hemoglobin/A1C goal

A
  • targets change based on population
  • goal: <7% for vast majority of diabetes
    (if pregnant) <6.5%
    (if life expectancy 10-15%) <8%
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10
Q

type 1 diabetes (%, what, type, manifestations)

A
  • 5-10%
  • B cells no longer secrete insulin
  • autoimmune disease
  • diabetic ketoacidosis (DKA): first manifestation of disease for children and adolescents
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11
Q

type 1 diabetes mangement

A
  • insulin is required to keep Type 1 DM patients alive
  • 2 types of insulin required:
    1) Basal (continuously acting insulin)
    2) Bolus (single dose)
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12
Q

basal insulin (what, controls, rates)

A
  • continuously acting insulin
  • controls glucose levels that would otherwise increase secondary to glycogenolysis (release of glycogen) by the liver (glycogen always being released into bloodstream no matter what)
  • insulin pump basal rates: inject continuously, 24/7 once programmed, long acting insulin (Lantus, Levemir)
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13
Q

bolus insulin

A
  • single doses
  • control carbohydrate intake and subsequent glucose release into the bloodstream
  • insulin pump bolus: programmed by user before meals, rapid acting (Novolog, Humalog) injections in non pump users
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14
Q

type 2 diabetes (%, who, type, what)

A
  • 90-95%
  • majority of patients are adults, but with increasing child obesity, there is increase incident in children (r/t high processed foods being stored in adipose tissue)
  • associated with metabolic syndrome
  • imbalance between insulin production and use (inadequate insulin response VS. insulin resistance syndrome or combination of both
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15
Q

type 2 diabetes mangement

A
  • can range from diet to PO meds to Insulin and other subQ agents
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16
Q

hyperglycemia

A

(>125 fasting, >180 2 hours post prandial)
- common in both T1 and T2
- most won’t show s/sx until 200-300+

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17
Q

hyperglycemia s/sx

A
  • 3 P’s (polyuria (urinating a lot), polydipsia (drinking lots of fluids), polyphagia (cells starving)
  • fatigue
  • weakness
  • sudden vision changes
  • tingling or numbness in hands or feet
  • dry skin, skin lesions, or wounds that are slow to heal
  • recurrent infections
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18
Q

what causes blood sugar to go up or down?

A

carbohydrates

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19
Q

hypoglycemia

A

(BS <70)
- common in T1, less T2
- not everyone will have s/sx

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20
Q

hypoglycemia s/sx

A
  • diaphoresis
  • anxiety
  • confusion
  • slurred speech
  • hunger
  • irritability
  • pale skin
  • fatigue
  • irregular/fast pulse
  • dizziness
  • shakiness
  • headache
  • blurred vision
  • fainting
  • MAIN CONCERN: seizures, coma, death
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21
Q

hypoglycemia mangement (non pharm, pharm, home)

A

NON PHARMACOLOGICAL
- prevention with education
- rule of 15’s: carbohydrates 15g of fast-acting/concentrated (no fat/protein, OJ, pop, sugar, candy, glucose tabs), recheck BG in 15 minutes

PHARMACOLOGICAL
- glucagon 1 mg given IM or
- Dextrose 50% in water (D50W) 25-50 mL IV

HOME
- glucagon IM or intranasal (baqsimi)

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22
Q

physical exam findings diabetes mellitus

A
  • BP (control)
  • BMI
  • funduscopic exam (retinal) and visual activity: visit ophthalmologist yearly
  • foot exam (lesions, signs of infection, pulses): self exams (daily, wounds, cuts, bruises)
  • skin examination (lesions, insulin injection sites): acanthuses nigricans (discoloration of skin folds), lipodystrophy (fat distribution patterns)/hypertrophy
  • neurologic examination (sensory- checking for paresthesia with monofilament test)
  • oral examination (dental health)
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23
Q

lipohypertrophy (LH)

A
  • dense tissue formed in an area repeatedly injected with insulin, due to the anabolic effect of insulin causing local fat cells to enlarge and proliferate
  • rotate injections
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24
Q

diagnostic labs diabetes mellitus (5 + acute exacerbation labs)

A
  • hemoglobin A1C: surrogate for glucose control over past 3-4 months, reflects life of red blood cell (normal <5.7, diabetic goal <7%)
  • WBCs: may be elevated during acute exacerbations of disease
  • Basic metabolic panel: renal function (BUN/Cr will increase in the setting of chronic uncontrolled blood glucose), electrolytes (K+)
  • lipid panel: risk stratification (statin, control diet)
  • C peptide: reflects presence of insulin production, elevations may occur in setting of insulin resistance, reductions may occur when we don’t make enough insulin

acute exacerbation labs:
- ketones: presence in blood or urine indicates anaerobic metabolism S/D to absolute lack of insulin, may also see pH drawn arterially if ketones are present
- anion gap: difference between positively and negatively charged ions (normally 4-12 mmol/L), elevations can be seen in setting of metabolic acidosis (too high = indicates metabolic acidosis)

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25
Q

other diagnostic labs (urine)

A

urine (normally, no protein in urine)
- protein: <150mg is normal, may see elevations in diabetic populations with kidney disease “proteinuria”
- can be done as a point of care “UA” or 24 hour urine sample (not often done unless kidney disease)

24 hour urine:
- may be done yearly in patients with nephropathy/kidney issues
- started in morning after first void/emptying bladder (6:15)
- collect and refrigerate every void after start time
- collection would end at same time following day (6:15)

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26
Q

self management - blood glucose monitoring (SMBG)

A
  • blood glucose monitoring is a cornerstone of diabetes management
  • recommended that SMBG occurs when circumstances call for it: AC/HS (before meals, bedtime), before driving, before/after exercise, before/after intercourse, before/after exams, etc.
  • goal: 70-130 between meals, <180 after meals
  • continuous glucose monitors: CGMs (automatically check BG Q5 minutes)
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27
Q

self management - continuous glucose monitors

A
  • used for insulin dependent (IDDM) and non-insulin dependent (NIDDM) diabetes mellitus
  • consist of a “sensor” that is injected into the subQ tissue and communicates data to an external receiver (smartphone, insulin pump, stand-alone device) to give glucose readings every 5 minutes
  • NOT FDA APPROVED FOR INPATIENT USE
  • sensor INTERACTS with Tylenol
  • may be used to make treatment decisions
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28
Q

self management - nutrition (MNT, goals, other indications)

A
  • medical nutrition therapy (MNT): nutritional therapy prescribed for management of diabetes usually given by registered dietician (diet to improve glucose levels)
  • nutritional management of diabetes goals:
    1) BG levels normal range
    2) keep lipid levels within ideal ranges
    3) BP levels normal range

other:
- prevent slow rate of development of chronic complications of diabetes
- address individual nutrition needs, taking into accounting personal/cultural preferences and willingness to change
- maintain pleasure of eating by only limiting food choices when indicated by specific evidence

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29
Q

self management - nutrition meal plan

A

focuses on percentages of calories that come from carbs, proteins, fats
- carbs: 50-60% total caloric intake
- proteins: 10-20% (limit amount of saturated fats to 10%)
- fats: 20-30%
- fiber: 28g/day
- TIP: fiber dramatically reduces amount of carbs absorbed into blood

don’t have to know percentages

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30
Q

2 ways to look at nutritional therapy

A

1) dietary “servings/exchanges”
- generally reserved for T2 DIABETES
- great for patients who are taking PO anti diabetics or take a set amount of bolus insulin for meals
- “ADA” diet: exchange lists

2) carb counting
- indicated for T1 DIABETES
- works with “insulin intensive therapy” utilizing “insulin to carbohydrate” ratios
- allows patients more flexibility provided they understand how to dose insulin accordingly

31
Q

outpatient with intensive insulin therapy

A

carbohydrate counting: GOAL for outpatient diabetic mangement
- prescribed insulin to carb ratio (ex: 1 unit per 9 grams carbs)

32
Q

iclicker: how much serving for tropical Burt peep with 27 grams of carbs (1 unit/9g carbs)

A
  • 3 units
33
Q

glycemic index

A
  • fiber, protein, and fats slow absorption of carbohydrates
  • Raw or Whole Foods tend to have slower response than cooked, chopped, or pureed food
  • eat whole fruits rather than juices (juices have no fiber)
34
Q

self management - nutrition (alcohol, artificial sweeteners, misleading food labels)

A

alcohol
- pure alcohol (vodka, whiskey) can lower BG and mask s/sx hypoglycemia
- alcohol in beer, mixed drinks, seltzers, etc. has loads of sugar
- REC: check blood frequently, small amount mixed drinks

artificial sweeteners
- have potential to increase insulin production in T2 diabetics which can result in weight gain and further resistance

misleading food labels
- big difference between “sugar free” and “no sugar added”, learn to read food labels
- no sugar added (no extra sugar added but still loads of natural occuring sugar) < sugar free (0.5g sugat total)

35
Q

self management - exercise

A
  • exercise is great for blood glucose control + cardiac risk reduction (30m/day)
  • exercise REDUCES blood glucose by: potentiating insulin, increasing uptake of glucose by the muscles
  • exercise INCREASES blood glucose when: stimulating SNS (high intensity workouts, competitive sports, marathon)
  • very important to monitor blood glucose before, during, and after exercise, especially during a new regimen (may require additional food prior to exercise)
36
Q

pharmacologic - insulin (2 types of regimens)

A
  • based on blood glucose monitoring
  • 2 types of regimens:

1) conventional - fixed dosing requiring fixed meal plans
- ex: sliding scale, prandial dosing
- better for type 2 DM
- inpatient setting, easier to control, not as sensitive to carbs

2) intensive - insulin is adjusted spontaneously
- insulin to carb ratio (1 unit / 10g carbs)
- takes into account activity levels, stress, etc.
- promotes tight control
- better for type 1 DM

37
Q

generic: lisper, aspart, fast aspart, glulisine (trade, onset, peak, duration)

A
  • trade: Humalog, Novolog (rapid)
  • onset: 3-15 minutes
  • peak: 45-75 minutes
  • duration: 2-4 hours
38
Q

generic: regular (IV w/ NS)

A
  • trade: fast (used for hyperglycemia with DKA)
  • onset: 30 minutes
  • peak: 2-4 hours
  • duration: 5-8 hours (when regular insulin is given IV, onset within minutes, but duration is only 15 minutes)
39
Q

generic: NPH (what, trade, onset, peak, duration)

A
  • cheapest on the market for no insurance
  • trade: intermediate
  • onset: 2 hours
  • peak: 4-12 hours
  • duration: 8-18 hours, with usual duration of action around 12 hours
40
Q

generic: insulin glargine

A
  • trade: Lantus (long)
  • onset: 2 hours
  • peak: no peak (no big risk hypoglycemia)
  • duration: 20 - >24 hours
41
Q

generic: insulin determir

A
  • trade: Levemir (long)
  • onset: 2 hours
  • peak: 3-9 hours
  • duration: 6-24 hours
42
Q

pharmacologic - insulin - conventional (3) (most commonly seen inpatient settings and w/ type 2 DM

A

sliding scale: <350/400 = call provider
- BG 151-200: 1 unit
- BG 201-250: 2 units
- BG 251-300: 3 units..etc
- if eating when giving insulin, give same amount

prandial dosing: patient to control BS
- 10 units Humalog (rapid) per meal, 3 times a day + sliding scale if eating

plus: basal dosing (20 units Lantus or Levemir daily)

43
Q

pharmacologic - insulin - intensive (better for Type 1 DM) (3)

A

multiple factors: need to keep glucose within range and account for carb intake

1) correction factor: amount of insulin required to achieve target BG
- correction factor 1 unit per every 20mg/dL above target BG
- ex: if bg is 240, goal is 100, correction factor is 7 units (7x20 = 140 or 240-100=140/20 = 7)

2) insulin to carb ratio: amount of insulin required to accommodate carb intake
- insulin to carb ratio: 1 unit per 10 carbs
- ex: if patient was eating a Big Mac with fries (148g carb) -> 15 units of insulin (15x10)
- ex: piece of toast with 2 eggs (15g bread) -> 2 units insulin (10x2)

3) plus: basal dosing once or twice daily to accommodate the livers release of glycogen
- ex: 20 unit Lantus or Levemir daily

44
Q

iclicker: 50 units Lantus, NPO, how much insulin do you give?

A
  • all 50 units bc it’s long acting (basal dosing = long acting), hold short acting
45
Q

pharmacologic - insulin delivery

A
  • subQ injection: seen in hospitals
  • insulin pens: small, prefilled cartilage that eliminates need to draw up a syringe
  • insulin pumps: external, continuous infusions of subQ insulin that is externally worn, eliminates need for basal insulin as the pumps delivers continuous low dosing rapid acting to mimic basal preparation
  • inhaled preparations: afrezza - not common, not used in hospitals, considered ultra rapid acting (1 minute onset)

how to: inject air into vile to remove air, then pull back. orange cap

46
Q

complications of insulin therapy (6 + dawn phenomenon, insulin waning, somogyi effect)

A
  • storage issues (no hot car)
  • local allergic reactions (rare)
  • systemic allergic reactions (rare)
  • insulin lipodystrophy
  • resistance to injected insulin
  • morning hyperglycemia: dawn phenomenon, insulin waning, somogyi effect)

1) dawn phenomenon: release in cortisol in morning, increases BS
2) insulin waning: basal insulin at same time in morning, doesn’t last 24 hours, hyperglycemia (lantus dosing)
3) somogyi effect: hypoglycemia, SNS -> release glycogen -> blood stream -> wake up d/t hypoglycemia

47
Q

pharmacologic - non insulin interventions

A

1st line: metformin (glucophage)
- most common ADR: GI upset
- additional risk of lactic acidosis in critically ill patients
- not used in hospitals
- teach: take after meals to remove ADRs, cause kidney injury with contrast (not much evidence yet)

48
Q

oral agents affects type 2 diabetes

A
  • decrease glucose absorption in intestines
  • decrease hepatic glucose output in liver
  • increase peripheral glucose uptake in muscles
  • decrease glucagon secretion, increase insulin secretion
49
Q

sick days

A

1) patient still need to take insulin when they are ill/not eating
- basal
- bolus insulin to treat hyperglycemia
- check B/S more often
2) If sick (vomiting, not eating, febrile) check blood often (Q4Hours)
3) seek emergency care if:
- unable toe at for 24 hours
- trouble breathing
- constant hypoglycemia
- changes in mental status

50
Q

medical emergencies: DKA (what, who, manifests, causes)

A
  • life threatening complication of DM
  • typically affects patients with type 1 diabetes but can affect patients with type 2 diabetes
  • absolute insulin deficiency
  • can’t metabolize macronutrients normally -> anaerobic metabolites
  • manifests with: severe hyperglycemia, metabolic acidosis & fluid and electrolyte imbalances (S/D anaerobic metabolism)
  • illness causes elevation of counter-regulatory hormones (growth hormone, cortisol, epinephrine, glucagon -> makes the sugar go higher)
51
Q

causes of DKA

A
  • infection
  • inadequate insulin therapy (big cause!)
  • severe illness (CVA, MI, pancreatitis)
  • alcohol abuse
  • trauma
  • drugs
  • sudden discoloration of insulin (underserved patients, pump failure)
  • present in DKA with initial diagnosis DM type 1, some type 2 DM can develop in catabolic stress associated with severe critical illness
52
Q

s/sx DKA

A
  • polyuria
  • polydipsia
  • marked fatigue/weakness
  • blurred vision
  • headache
  • orthostatic hTN, frank hTN, weak, rapid pulse
  • anorexia, N/V
  • abdominal pain
  • kussmaul respirations - acetone breath (fruity odor) with hyperventilation (with very deep, but not labored reparations)
  • lethargic or comatose
53
Q

diagnostics DKA (4)

A
  • blood glucose levels 250-800 mg/dL (not that high relative to HHNK/HHS)
  • serum bicarbonate (0-15 mEq/L) -> acidosis
  • pH (6.8-7.3) -> acidosis

carbon dioxide (PaCO2 10-30 mmHg):
- reflects respiratory compensation
- ketone bodies in blood and urine
- sodium and potassium may be low, normal, or high, depending on amount of dehydration present
- increased levels of creatinine, blood urea, nitrogen (BUN), and hematocrit may also be seen with dehydration

54
Q

DKA interventions non pharm + pharm

A

NON-PHARMACOLOGICAL
- prevention (NUMBER 1)
- loads of education: patient who go into DKA will generally be discharged as soon as they are no longer acidotic

PHARMCOLOGICAL
1) correcting dehydration: 0.9% NS then switch to D5W, when sugar drops too low, we add dextrose to allow for continued delivery of insulin
2) treating hyperglycemia: with regular insulin via IV
3) correcting electrolyte: disturbances and acidosis, monitor K+ (can drop with insulin)

55
Q

medical emergency: hyperglycemic hyperosmolar syndrome (type, what, causes)

A
  • blood glucose way higher than DKA, patient is sicker
  • seen with Type 2 DM
  • insulin deficiency initiated by an illness that raises the demand for insulin while ketosis is usually absent
  • persistent hyperglycemia causes osmotic diuresis: losses of water and electrolytes, dehydration leading to severe hypernatremia and increased osmolarity, dehydration also further concentrates glucose (worsening hyperglycemia)
56
Q

HHS s/sx (5)

A
  • hypotension
  • profound dehydration (dry mucous membranes, poor skin turgor)
  • tachycardia
  • hallucinations S/D to cerebral hydration
  • variable neurologic signs (alteration of consciousness, seizures, hemiparesis)
57
Q

HHS diagnostics (6)

A
  • blood glucose >600 mg/dL (much higher in reality, 1200 mg/dL)
  • electrolytes (hypernatremia, hyperkalemia)
  • BUN
  • CBC
  • serum osmolality >350 mOsm/kg (S/D glucose)
  • arterial blood gas analysis (rule out acidosis)
58
Q

HHS interventions

A

NON PHARM
- prevention

PHARM
- correcting dehydration: 0.9% NS
- treating hyperglycemia
- correcting electrolyte disturbances and acidosis (acidosis is rare in these cases, monitor K+)

59
Q

diabetic macrovascular complications (what, types (3), management)

A
  • results from thickened sclerotic vessel walls that are prone to atherosclerosis
  • 3 main macrovascular complications: coronary artery disease (MI), cerebrovascular disease (CVA), peripheral vascular disease (PAD)
  • mangement: prevention with aggressive modification, reduction of risk factors, control blood glucose and blood pressure, eliminate other RF’s -> smoking, ETOH, drug abuse
60
Q

diabetic microvascular complications (what, types (2))

A
  • results from capillary basement membrane thickening
  • 2 main microvascular complications: diabetic retinopathy (eyes - vision changes, distortions, blurred, cobwebs, sometimes none), kidney disease
61
Q

microvascular complications - retinopathy (s/sx, management)

A

s/sx:
- visual distortion, loss of central vision
- painless
- blurry vision, floaters, cobwebs in some
- only mild vision changes in others

management:
- control blood sugar, cessation of smoking, control blood pressure to slow progression
- argon laser photocoagulation OR hemostasis injections (bleeding spot eyes, inject -> eyeball)
- nursing education: follow up ophthalmologist, mild retinopathy is not directly related to A1C or glycemic control

62
Q

microvascular complications - nephropathy (s/sx, diagnostics, management)

A

s/sx:
- hypoglycemic episodes may result (either from glucose wasting or impaired insulin clearance)

diagnostics:
- microalbuminuria (>30mg/24 hour)
- BUN and creatinine elevations

management:
- prevention through avoiding nephrotoxins
- control blood sugar, cessation of smoking, control blood pressure to slow progression (ACE-I, ARBs)
- nursing education
- low sodium, low protein diet
- monitor glucose levels, decrease insulin
- dialysis or transplant with ESRD

63
Q

diabetic neuropathy

A
  • group of diseases that affect all types of nerves, including: peripheral (sensorimotor, autonomic, spinal nerves)
64
Q

peripheral neuropathy (what, s/sx, management)

A
  • affects distal portions of the nerves, especially the nerves of the lower extremities

s/sx: paresthesia, numbness, burning sensation (esp. at night), decreased sensation and proprioception, Charcot joint foot, decrease in deep tendon reflexes

management: insulin therapy, control blood glucose levels to delay onset, slow progression, pain management PRN (gabapentin - neuropathic pain)

65
Q

autonomic neuropathy (what, s/sx, management)

A
  • related largely to the cardiac, gastrointestinal, and urinary systems

s/sx:
- cardiac: slight tachycardia, orthostatic hypotension, silent MI
- GI tract: delayed gastric emptying/gastroparesis
- urinary: neurogenic bladder
- misc: hypoglycemic unawareness, sexual dysfunction

management:
- modifying risk factors (control blood glucose, blood pressure)
- diet changes
- meds for symptom management

66
Q

foot problems diabetics (what, neuropathy, peripheral vascular disease, immunocompromised)

A

combo assault on lower extremities

neuropathy: nerve damage
- loss of pain, pressure sensation
- increased dryness, fissuring of the skin (s/d decreased sweating)
- motor neuropathy results in muscular atrophy, which may lead to changes in shape of foot

peripheral vascular disease:
- poor circulation of the lower extremities contributes to poor wound healing and development of gangrene
- circulation impairment

immunocompromised:
- hyperglycemia impairs ability of specialized leukocytes to destroy bacteria, leading to lowered resistance to certain infections

67
Q

Charcot foot

A
  • weakening of bones in feet coupled with neuropathy, resulting in fractures and morphologic changes in the feet
  • difficult to treat, requires expensive serial casting over a period of months to years where the patient is non-ambulatory

TIP: encourage foot care ALWAYS

68
Q

special issues in hospitalized diabetic patient: surgery

A

during period of physiologic stress, glucose levels tend to increase, because levels of stress hormones (epinephrine, norepinephrine, glucagon, cortisol, growth hormone) increases
- if hyperglycemia is not controlled during surgery: osmotic diuresis (excessive loss of fluids and electrolytes), DKA, delayed wound healing and increased risk for infection

hypoglycemia: if surgery is delayed beyond morning in a patient who received a morning injection of intermediate acting insulin

frequent blood glucose monitoring: essential throughout pre and post operative periods

69
Q

special issues in hospitalized diabetic patient: self care issues

A

for pts who are actively involved in diabetic self management (esp. insulin dose adjustment” -> relinquishing control over meal timing, insulin timing, and insulin dosage can be particularly difficult and anxiety provoking
- ex: insulin should be taken 15 min. before eating (but not usually done)
- educate patient and discuss care with them to ease anxiety

  • patient may fear hypoglycemia and express much concern over possible delays in receiving attention from the nurse if hypoglycemic symptoms occur or may disagree with a planned dose of insulin
  • nurse acknowledge that patient’s concern and involves the patient in the plan of care asap
70
Q

special issues in hospitalized diabetic patient: hyperglycemia

A

a number of factors may contribute to hyperglycemia
- changes in usual treatment regimen (ex. increased food, decreased insulin, decreased activity)
- medications (ex. corticosteroids, used in treatment of a variety of inflammatory disorders)
- IV dextrose, which may be part of the maintenance fluids or may be used for the administration of antibiotics and other meds, without adequate insulin therapy
- overly vigorous treatment of hypoglycemia
- inappropriate withholding of insulin or inappropriate use of “sliding scale”
- mismatched timing of meals and insulin (ex. postmeal hyperglycemia may occur if short-acting insulin is given immediately before or even after a meal)

71
Q

special issues in hospitalized diabetic patient: hypoglycemia

A

factors that may contribute to hypoglycemia
- overuse of sliding scale regular insulin, particularly as supplement to regularly scheduled, twice daily short, and intermediate acting insulins
- lack of changes in insulin dosage when dietary intake is changed (ex. NPO diet)
- overly vigorous treatment of hyperglycemia (ex. giving too frequent successive doses of regular insulin before the time of peak insulin activity is reached), resulting in cumulative effect
- delayed meal after administration of lispro, aspart, or glulisine insulin (patient should eat within 5-15 min after insulin administration)

72
Q

special issues in hospitalized diabetic patient: alterations in diet

A

dietary medications commonly prescribed during hospitalization require special consideration for patients who have diabetes
- NPO: ensure that usual insulin dosage has been changed. these changes may include eliminating the rapid insulin (still basal)
- CL: diabetes receive more simple carbohydrate foods, such as juice and gelatin desserts, than are usually included in the diabetic diet and will cause rapid rise in glucose
- Enteral TF: tub feeding formulas contain more simple carbohydrates and less protein and fat than the typical meal plan for diabetes
- Parenteral: patients receiving parenteral nutrition may receive both IV insulin and SQ (sometimes insulin may be added to TPN - continuous insulin)

73
Q

special issues in hospitalized diabetic patient: hygiene

A

nurses caring for hospitalized patients with diabetes must focus attention on oral hygiene and skin care. careful assessments of the oral cavity and the skin are important with implementation of prevention measures
- increased risk for periodontal disease: nurse should assist with dental care BID
- chafing and fungal infections tend to occur: nurses should assist in keeping the skin clean and dry, esp. in areas of contact between two skin surfaces (ex. groin, axilla, under the breasts)
- the nurse should ask about symptoms of neuropathy, such as tingling and pain or numbness of feed and assess DTR
- as with any patient confined to bed, nursing care must emphasize the prevention of skin breakdown at pressure points. the heels are particularly susceptible to breakdown because of loss of sensation of pain and pressure associated with sensory neuropathy
- feed should be cleaned, dried, lubricated with lotion (not between toes) and inspected frequently. if the patient is in the supine position, pressure on heels can be alleviated by elevating lower legs on a pillow, with the heels positioned over edge of the pillow

74
Q

special issues in hospitalized diabetic patient: stress

A

increase in stress hormones lead to an increase in glucose levels, esp. if intake of food and insulin remain unchanged. in addition, during periods of emotional stress, people with diabetes may alter their usual pattern of meals, exercise, and medication. this can contribute to hyperglycemia or even hypoglycemia
- physiologic stress, such as infections and surgery, contributes to hyperglycemia and may precipitate DKA or HHS
- emotional stress related to hospitalization for any reason can also have a negative impact on diabetic control
- learning strategies for minimizing stress and coping with stress when it does occur are important aspects of diabetes education

Nur 3010 exams (13 decks)

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