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Adv. Med Surg > Diabetes > Flashcards

Diabetes Flashcards

1
Q

What is Diabetes?

A

*Chronic disorder of impaired carbohydrate, protein, and lipid metabolism caused by a deficiency of insulin

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2
Q

What are the functions of Insulin? (6)

A

*Transports and metabolizes GLUCOSE for energy
*Stimulates storage of glucose in the liver and muscle as GLYCOGEN
* Signals the liver to stop the release of glucose
*Enhances storage of FAT in adipose tissue
*Accelerates transport of AMINO ACIDS into cells (PROTEIN SYNTHESIS)
* Inhibits the breakdown of stored glucose, protein, and fat
*↑ fat, ↑ cholesterol

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3
Q

CLASSIFICATIONS OF DIABETES? (5)

A

 Type 1 diabetes (Insulin dependent, onset early, autoimmune)
 Type 2 diabetes (Insulin resistant)
 Gestational diabetes (GDM)
 Prediabetes
 Diabetes associated with other conditions or syndromes (pancreas, corticosteroids)

-Insulin produced by islet of Langerhans and beta cells within the pancreas → damaged cells don’t produce enough insulin

-Corticostroids ↑ blood sugar → insulin resistance

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4
Q

How do you know if you’re Prediabetic?
What Tests? (3)

A
  • Impaired glucose intolerance (IGT) [mostly during pregnancy]
    • Two-hour oral glucose tolerance test (OGTT):
      140 to 199 mg/dL

*Impaired FASTING glucose (IFG) [Non-pregnancy]
* Fasting glucose level: 100 to 125 mg/d

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5
Q

Name 4 things about Type 1 Diabetes

A

Type 1 Diabetes (insulin-dependent) →
*autoimmune disorder → no insulin produced
*(requires insulin)
*Onset is ACUTE
*Usually BEFORE 30 years old

Type 1 diabetes is characterized by the destruction of pancreatic beta cells that require exogenous insulin

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6
Q

Risk Factors of type 1 Diabetes
(7/12)*

A

*Family history Obesity
Hx of gestational DM *HDL< 35
45 yrs + *Triglycerides > 250
*GENETICS Pre-hx IFG LEVELS HIGH
*Early Onset (CHILDHOOD)
*Possible IMMUNOLOGIC(AUTOIMMUNE) or
*ENVIRONMENTAL (viral or toxins) factors
Race (African, Hispanic, Asian, Native American, Pacific Islander/Native Hawaiian)

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7
Q

CLINICAL MANIFESTATIONS OF TYPE 1 DM (ASSESSMENT)

A

*Polyuria: increased urination
*Polydipsia: Increased thirst
*Polyphagia: Increased appetite
*Weight loss
*fatigue
Hyperglycemia
*Blurred vision/VISION CHANGES
Tingling/numbness in hands/feet (Parasteshia)
*Absent of minimal insulin production
*Islet cell antibodies-Present at onset
*INSULIN REQUIRED FOR ALL DM1

**Type 1 may have sudden weight loss, nausea, vomiting, and abdominal pain if DKA (diabetes ketoacidosis) has developed **

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8
Q

Diagnosis Criteria for Diabetes

A

*Fasting Blood Sugar → ≥ 126mg/dL
(no caloric intake for at least 8 hrs)

*Random Glucose → ≥ 200 w/symptoms of DM

*2hr Oral Glucose (OGTT) 2-hour postload (75 g)
→ ≥ 200 mg/dL [Normal 140-199]

*Hgb A1C →6.5 % or higher

  • Glycosylated hemoglobin – reflects glucose level over *2-3mos although, hgb stays attached to glucose up to 120 days.
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9
Q

A1C LEVELS AND GOAL

A

Normal A1C is below 5.6% (GOAL)
PREDIABETES → 5.7-6.4%
DIABETES → 6.5% OR HIGHER

-A1C is used to diagnose, screen, and monitor treatment response
Diabetic goal is 1% below initial A1C

  • Glycosylated hemoglobin – reflects glucose level over *2-3mos as a % of total Hgb although, Hgb stays attached to glucose up to 120 days.

-Anemic patients have ↓ HgbA1c d/t ↓Hgb –>
check fructosamine levels

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10
Q

KEY FACTORS (6/8) of Type 2 DM?
WHAT IS IT?

A

*Insulin resistance d/t impaired beta cell
function results in
*DECREASED INSULIN PRODUCTION
Islet cell antibodies= ABSENT
-onset over age 30 years,
*increasing in children, obesity
-Slow, progressive glucose intolerance: Many times discovered with routine testing and elderly pts.
**Treated initially with DIET & EXERCISE
*Oral hypoglycemic agents initially- may need to convert to insulin or use both (METFORMIN)

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11
Q

CLINICAL MANIFESTATIONS OF
T2DM (7/12)*

A

*** “Three Ps”: Polyuria; Polydipsia;
Polyphagia
*Weight loss, fatigue, weakness,
*vision changes, tingling or numbness in hands
or feet, dry skin, skin lesions or
wounds that are slow to heal,
*recurrent vaginal yeast or
*candidal infection

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12
Q

RISK FACTORS FOR
METABOLIC SYNDROME? (3/6)

HOW MANY DO YOU NEED TO BE AT RISK TO BE POSITIVE?

A
  • *Metabolic syndrome
    -(3/5 risk)-
    *FBS >100,
    *abdominal obesity (waist)
    ((M) waist >40” ; (F)>35”
    *BMI >30),
    *hypertension (≥130/85),
    *Low HDL (<40 (M); <50 (F) or
    *High Triglycerides (>150)

*CAD,
-Previously identified (IFG) impaired
fasting glucose,
*hx of GDM
*babies > 9 pounds
-Prediabetic patients
* African Americans, Asian Americans, Hispanics, Native Hawaiians or other Pacific Islanders, and Native Americans

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13
Q

Five Components of DM management
[MENPE]

A
  1. Nutritional therapy
  2. Exercise
  3. Monitoring
  4. Pharmacologic therapy
  5. Education

The goals of diabetes management(= balance diet)
 Reduce symptoms
 Promote well-being
 Prevent acute complications of hyperglycemia, and
 Prevent or delay the onset and progression of long-term complications

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14
Q

Dietary Management Goals for DM

A

*Carbohydrates: 50%-60% of total calories;
*emphasize whole grains
*Fat: 20% to 30%, with <10% from
saturated fat and <300 mg cholesterol,
-Two or more servings of fish/week to provide polyunsaturated fatty acids
*Protein: 10% to 20% of total calories,
-Fiber: 25 -30g daily *
*Alcohol (inhibits gluconeogenesis): ↓BS
Limit to moderate amount
**(1-2 drinks/day [W=1 drink/M=1-2], drink w/ food,
do not omit regular meal
[12 oz= beer/15 oz= liquor/5 oz= wine]

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15
Q

EXERCISE PRECAUTIONS FOR DM

A

*Monitor glucose before, during, and after exercise
* *Exercise with elevated blood sugar levels (>250 mg/dL) &
*KETONES in urine should be AVOIDED (type 1 DM)
*↓ BS; Aids in weight loss; ↓ cardiovascular risk
-↓ insulin resistance and BG
-Insulin secretion normally decreases w/ exercise; it does not occur in patients on exogenous insulin
should eat a 15g carbohydrate snack before moderate exercise to prevent HYPOGLYCEMIA
* Glucose-lowering effect of exercise lasts up to 48 hours
* Effect of strenuous activity makes body perceive “stress” causing release of counter-regulatory hormones and temporary increased glucose; makes
condition worse
* Get medical clearance; start slowly and
progress to goal:
**Exercise stress test for patients > age 30 who have
2 or > risk factors is recommended

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16
Q

What are 4 ways to monitor Glucose/insulin Levels?

WHICH 2 ARE MAINLY FOR DM1 patients?

A
  1. Self-Monitoring Blood Glucose (SMBG) using at home device
  2. Continuous Glucose Monitoring System (CGMS) used by type 1 DM
  3. Urine Ketone Strips – Type 1 DM w/ Blood sugar ≥ 240 when under stress (illness/gestational DM) → [DKA]
  4. Hgb A1C – every 2-3 months (GOAL 5.6% or lower)
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17
Q

RAPID-ACTING INSULIN
GENERIC/TRADE (3)

ONSET, PEAK, DURATION

A

LISPRO (HUMALOG)
ASPART(NOVOLOG)
GLULISINE (APIDRA)

ONSET-10-30 MIN [INJECT within 15 min of meal]
PEAK: 30 MIN-3 HRS [1 HOUR]
DURATION: 3-5 HOURS [4-5 HOURS -PPT]

**Injected within 15 minutes of mealtime;
duration 4-5 hours

PREVENTS POST-MEAL HYPERGLYCEMIA

“15 minutes feels like an hour during 4 rapid responses”

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18
Q

SHORT-ACTING INSULINS (2)

ONSET, PEAK, DURATION

A

REGULAR (HUMULIN R, NOVOLIN R)

ONSET: 30 MIN-1 HOUR (Injected 30 to 45 min b4 meal)
PEAK: 2-5 Hours (2-4 hours PPT)
DURATION: 5-8 HOURS

Injected 30 to 45 minutes BEFORE meal; Peak 2-4 hrs

PREVENTS POST-MEAL HYPERGLYCEMIA

“Short-staffed nurses went from 30 patients to(2) 8 patients”

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19
Q

INTERMEDIATE-ACTING INSULIN (2)

ONSET, PEAK, DURATION

A

NPH (HUMULIN N, NOVOLIN N)

-NPH is cloudy and can be mixed w/ REGULAR OR SHORT → given at BEDTIME to control fasting AM BS
DONT SKIP LUNCH-INSULIN IS PEAKING

ONSET: 1.5-4 HOURS [2]
PEAK: 4-12 HOURS [8]
DURATION: 12-18 HOURS [16]

“Nurses Play Hero TO(2) EIGHT 16 year olds”

20
Q

Long Acting Insulin (3)

ONSET, PEAK, DURATION

A

GLARGINE (LANTUS) [BASAL, “PEAKLESS”]
DETEMIR (LEVEMIR)
DEGLUDEC (TRESIBA)

DO NOT MIX LONG ACTING INSULINS
Onset 1&1/2 hrs [ppt]
*CLOSEST TO BODYS NATURAL INSULIN d/t peakless”

ONSET: 0.8-4 HOURS [2]
PEAK: BASAL, “PEAKLESS”, rarely to none peak
DURATION: 16-24 hours [24]

“The TWO LONG nursing shifts NEVER PEAKED but lasted 24 HOURS”

21
Q

INHALED INSULIN (1)

ONSET, PEAK, DURATION

A

AFREZZA

RAPID ACTING, no COPD, $$$

ONSET:12-15 MIN RAPID ACTING
PEAK: 60 MIN [1 HOUR]
DURATION: 2.5-3 HOURS

22
Q

INSULIN PUMP USE & TEACHING

A

Insulin pump use: continuous subQ insulin (rapid or regular) infusion at a basal rate and bolus before meal/ Change set and site every 2 to 3 days

23
Q

Storage of insulin/rotating sites

A

In-use vials/pens may be left at room
temperature up to 4 weeks (28 days)
*Extra insulin/pens should be REFRIGERATED *
-Avoid exposure to direct sunlight, extreme heat or cold/
-No freezer
-Abdomen is preferred site
-Do not inject in site to be exercised *
-Systemic rotation within one
anatomical area –not to use the same
site more than once in a 2-3 week
period (to prevent lipodystrophy) *

-Inject 1 to 1.5” apart within the anatomical area

-Best place to inject is ABD → Arms → Thighs → Butt

24
Q

Oral Antidiabetic Agents:

Manifestation/SE/Nursing Interventions/Education

A

Used for type 2 DM who require more than diet & exercise

  • Major side effect: hypoglycemia
  • Nursing interventions: monitor blood glucose for →hypoglycemia and other potential side effects
  • Patient Education
  • Combinations of oral drugs may be used
25
Q

ORAL MEDICATIONS GIVEN FOR T2DM

[2 CLASSES, 4 MEDICATIONS]

A

*2nd - Gen Sulfonylureas → (MOA) stimulate beta cells to secrete insulin→ taken w/ meals, will ↓BS → HYPOGLYCEMIA

-Glipizide (Glucotrol)

-Glyburide (Micronase)

-Glimepiride (Amaryl)

*Biguanides → inhibits the production of glucose by the liver/ increase body tissue sensitivity to insulin

-Metformin (Glucophage)

26
Q

2ND GEN SULFONYLUREAS

MOA/EDUCATION/SE

A

*2nd - Gen Sulfonylureas → (MOA) stimulate beta cells to secrete insulin→ taken w/ meals, will ↓BS → HYPOGLYCEMIA

*Glipizide (Glucotrol) → Beta-blockers (-olol) will mask hypoglycemic symptoms (double check BS)

*Glyburide (Micronase) → If mixed with alcohol → Disulfiram (Antabuse) effect → will make you sick

*Glimepiride (Amaryl) → Sulfa Allergy → Do not use

27
Q

Biguanides -
Metformin (Glucophage):

[MOA/EDUCATION/SE]

A

*Biguanides → (MOA) inhibits production of glucose by liver/ increase body tissue sensitivity to insulin

*Produces GI issues → upset stomach w/diarrhea
*Lactic acidosis → metabolism changes from aerobic
to anaerobic producing lactic acid
*Monitor Kidney function d/t acute kidney failure from
metformin

  • SE: GI disturbances (tests with iodine =
    increase in LACTIC ACIDOSIS)

-Metformin and Iodinated contrast dyes leads →
lactic acidosis OR acute kidney failure [MONITOR KIDNEY]

Must STOP 48 hrs before/after PROCEDURES/SURGERIES until renal function returns to normal

-Iodine is naturally toxic → requires NPO → will cause diuretic effect + nephrotoxic agent
*Dehydration + iodine = kidney unable to filter lactic → Lactic Acidosis

28
Q

Acute Complications of Diabetes (3)

A

o Hypoglycemia
o DKA
o Hyperglycemic hyperosmolar syndrome (HHS)

29
Q

What is Morning Hyperglycemia (Insulin Waning)

and its treatment?

A

↑ BS from bedtime to morning

Tx: increase evening NPH/long-acting insulin or add a
dose of NPH before dinner

30
Q

WHAT IS Somogyi Effects and its tx?

A

*Hypoglycemia around 2-3 am d/t a sudden drop in BS causes body to think it is stressed → cortisol, catecholamines released →
*Rebound morning hyperglycemia (7am)around 3 am a sudden drop in BS causes body to think it is stressed → cortisol, catecholamines released → by morning 7am, → sugar is really high (usually caused by too much NPH at bedtime)

*Tx: ↓ evening bedtime NPH dose or add a bedtime snack –
-Ask pt to wake up and record 2 or 3am blood sugar levels

31
Q

Dawn Phenomenon

A
  • Pre-breakfast hyperglycemia (5-8 AM) d/t nocturnal
    growth hormone (*common in young adolescents);

*Treatment- change dinnertime NPH → bedtime,
↑ (NPH) the current dosage

32
Q

Hypoglycemia MANIFESTATIONS

A

blood sugar lower than 70 → too much insulin, medication, exercise, or not enough food

*Adrenergic symptoms (mild <60) → sweating, tremors, tachycardia palpitations, nervousness, hunger

*Central nervous system (moderate <40) → inability to concentrate, headache, confusion, memory lapses,
slurred speech, drowsiness (all involve the head)

*Severe Hypoglycemia (severe <20) → disorientation, seizures, loss of consciousness, death

33
Q

Hypoglycemic Unawareness

A

No warning signs/symptoms [ASYMPTOMATIC] until glucose level critically low
* R/T autonomic neuropathy and lack of counterregulatory hormones
Beta-adrenergic blocking agents
* Patients at risk→ elderly should keep blood glucose levels somewhat higher

34
Q

Management of Hypoglycemia (ALERT PT.)

(15/15 RULE)

A

Give 15 g of fast-acting, concentrated carbohydrate
* Three or four glucose tablets/ 8 oz of low-fat milk
* 4 oz of juice or regular soda (not diet soda) =1/2 cup
* 6 saltine crackers/ 3 graham crackers *

Retest blood glucose in 15 minutes; retreat if < 70 mg/dL; (repeat 2 times if <70)
* If glucose remains low after 2 to 3 times; call HCP or EMS
*
*Treat with 25–50 mL 50% dextrose IV or glucagon 1 mg subQ or IM *
**Provide a snack with PROTEINS AND CARBS unless the patient plans to eat a meal within 30 to 60 minutes

35
Q

Management of Hypoglycemia
(UNCONSCIOUS AND HOSPITAL/ER)

(15/15 RULE)

A

-If the patient cannot swallow or is unconscious:
* SubQ or intramuscular glucagon 1 mg
*May repeat in 10 min if pt remains unconscious
* If regain consciousness-
**Provide a snack with PROTEINS AND CARBS unless the patient plans to eat a meal within 30 to 60 minutes

  • Hospital or emergency room: 25–50 mL *50% dextrose *(D50W) *solution IV
  • Ensure IV patency (very irritating to vein)
36
Q

CLINICAL S/S & MANIFESTATIONS OF
Diabetic Ketoacidosis (DKA)

A

*MOSTLY Type 1 DM PATIENTS *

**Hyperglycemia/Dehydration/Acidosis (Ketosis) **
↑BS ↑Ketones ↑Acidosis (with dehydration)= DKA

Manifestations include
polyuria, polydipsia, blurred vision, weakness,headache, anorexia,
abdominal pain (cramps), nausea, vomiting, diarrhea, acetone breath, hyperventilation with Kussmaul respirations and mental status changes, dry & warm skin (dehydration), sunken eyes.

37
Q

SICK DAY RULES

A
  • Physical and emotional stress causes increased glucose secondary to counterregulatory hormones
    *Do not eliminate insulin doses when nausea and vomiting occur *
    Frequent self-monitoring blood glucose
  • If glucose is greater than 240 mg/dL, check urine for ketones every 3 to 4 hours * Two consecutive glucose levels greater than 300 mg/dL or moderate to high urine
    ketone levels should be reported to HCP

PT. EDUCATION ON SICK DAY RULE

38
Q

ASSESSMENT OF DKA (LAB VALUES)

A
  • Blood glucose levels *>300 *to 1,000
  • Severity of DKA is not only due to blood glucose level

    Ketoacidosis is reflected in low serum bicarbonate, low pH;
    low PCO2 reflects respiratory compensation (Kussmaul’s respirations) * Ketone bodies in blood and urine++
    ↑BUN/Cr –↑due to dehydration [BUN 10-20]
    ↑ K+ = Acidosis (H+ ↑) – K+ leaves cell to exchange with H+ - hyperkalemia
    -Electrolytes vary according to water loss and level of hydration
39
Q

treatment for DKA

& what do you monitor for ?

A

Ensure patent airway; administer O2
Rehydration with IV fluid: VAD (Vascular Access Device) –0.9 NS (or 0.45 % saline) and when glucose level reaches 250 mg/dL, 5% to 10% dextrose is added to the fluid regimen to prevent hypoglycemia, as well as a
sudden drop in glucose that can be associated with cerebral edema.
Reverse acidosis
-IV continuous infusion (0.1 U/kg/hr) of regular insulin after bolus (10 Units)
Restoring electrolytes: hypokalemia is the major concern
-Note: rehydration leads to increased plasma volume and decreased K+,
insulin enhances the movement of K+ from extracellular fluid into the cells

Monitor
* Blood glucose and renal function/UO: restore urine output to 30 to 60 mL/hr
* EKG and electrolyte levels—K+–> cardiac monitoring
* VS, lung assessments, signs of fluid overload

40
Q

Hyperglycemic Hyperosmolar Syndrome

A

HHS Caused by a *lack of sufficient insulin; ketosis
is minimal or absent *
* It often occurs in patients older than 60 years w/
type 2 diabetes
High mortality rate: often occurs in elderly with no known history of DM or
type 2 DM

Precipitating factors: UTIs, pneumonia, sepsis, acute illness, Newly diagnosed type 2 diabetes

Hyperglycemia (> 800 mg/dL) causes osmotic diuresis with loss of water and electrolytes; hypernatremia, and increased osmolarity occur with dehydration
and glycosuria

41
Q

MANIFESTATIONS OF HHS

A

hypotension, profound dehydration, tachycardia,
and variable neurologic signs D/T cerebral dehydration

42
Q

TREATMENT OF HHS (5)

A

same as DKA (insulin is not as critical)

Rehydration,
Insulin administration –less critical role in the treatment
*Monitor fluid volume and electrolyte status *
Correct underlying precipitating cause

43
Q

Long-Term Complications of Diabetes

A

Tight glucose control can prevent/minimize complications

Macrovascular complications
* Accelerated atherosclerotic changes
CAD, CVA, PVD (peripheral vascular disease)
disease

* Microvascular complications: kidney and eyes
Diabetic retinopathy: Most common cause of new cases of
adult blindness -needs annual exam
Nephropathy: Leading cause of end-stage kidney disease-
B assess for microalbuminuria – if present, use ACE-I or ARB

 Neuropathic changes- Tingling and numbness in extremities
* Peripheral neuropathy- Major risk for amputation
* Autonomic neuropathies - hypoglycemic unawareness, sexual dysfunction,
Gastroparesis (delayed gastric emptying), painless myocardial infarction, Neurogenic bladder (→ urinary retention)

44
Q

Foot Complications

A

*Sensory neuropathy and PAD are major risk factors for amputation *
* Smoking increases risk
Sensory neuropathy → loss of protective sensation → unawareness of injury
* Monofilament screening (Pg. 1496- Figure 51-10) * Peripheral artery disease
* ↓ Blood flow, ↓ wound healing, ↑ risk for infection

Patient teaching to prevent foot ulcers
(***Chart 51-10-Foot Care)
* Proper footwear
* Avoidance of foot injury
* Skin and nail care
*Daily inspection of feet
* Prompt treatment of small problems

45
Q

EDUCATION ON FOOT (10)

A
  1. control DM
  2. DAILY INSPECTION → use mirror to see bottom
  3. wash/ dry feet daily → dry between toes, warm water
  4. cream on bottom of feet → not between toes
  5. smooth corns/callus with pumice stone softly
  6. trim nails → straight across
  7. wear shoes/socks always → white socks, protect your feet (cotton socks) can see if its bleeding
  8. protect your feet from temp changes
  9. elevate your feet, do not cross your legs, wiggle toes, move your ankles
  10. report any injuries

Buy shoes in the afternoon when feet are more swollen, break in shoes slowly 2 or 3 hrs at a time to reduce the r/o blisters

46
Q

Peripheral artery disease (PAD) Nursing Interventions (3)

A
  • ↓ Blood flow, ↓ wound healing, ↑ risk for infection

EDUCATION ON Foot care

Adv. Med Surg (8 decks)

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