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Medical Surgical GI Exam 3 > Diabetes Mellitus > Flashcards

Diabetes Mellitus Flashcards

1
Q

What is Normal insulin metabolism

A

Produced by B -cells in islets of Langerhans of Pancreas
Released continuously into bloodstream in small increments with larger amounts released after food
Stabilizes glucose level in range of 70 to 120 mg/dL

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2
Q

Normal Insulin Secretion

A
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3
Q

Type 1 Diabetes Mellitus Etiology and Pathophysiology

A

Autoimmune destruction of β-cells
Total absence of insulin
Genetic predisposition and viral exposure
Idiopathic diabetes
Latent autoimmune diabetes in adults (LADA)- Older adult who are not obese

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4
Q

Type 1 Diabetes Mellitus Onset of Disease

A

Autoantibodies are present for months to years before symptoms occur
Manifestations develop when pancreas can no longer produce insulin—then rapid onset with ketoacidosis
Necessitates insulin
Patient may have temporary remission after initial treatment

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5
Q

Type 2 Diabetes Mellitus

A

Formerly known as adult-onset diabetes (AODM) or non–insulin-dependent diabetes (IDDM)
Most prevalent type (90% to 95%)
Risk factors: overweight, obesity, advancing age, family history

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6
Q

Type 2 Diabetes Mellitus Etiology and Pathophysiology

A

Pancreas continues to produce some endogenous insulin
Insulin insufficient or poorly utilized
Multiple etiologic factors
Obesity is greatest risk factor
Genetic component increases insulin resistance and obesity

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7
Q

Four major metabolic abnormalities

A

Insulin resistance
Decreased insulin production by pancreas
Inappropriate hepatic glucose production
Altered production of hormones and cytokines by adipose tissue (adipokines- They interfere with absorption of glucose)

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8
Q

Type 2 Diabetes Mellitus Onset of Disease

A

Gradual onset
Hyperglycemia may go many years without being detected
Many times discovered with routine laboratory testing

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9
Q

Altered Mechanisms in Type 1 and Type 2 Diabetes

A
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10
Q

Type 2 Classic symptoms

A

Polyuria (frequent urination)
Polydipsia (excessive thirst)
Polyphagia (excessive hunger)
Weight loss
Weakness
Fatigue

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11
Q

Type 2 Nonspecific symptoms

A

Classic symptoms of type 1 may manifest
Fatigue
Recurrent infection
Recurrent vaginal yeast or candidal infection
Prolonged wound healing
Visual changes

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12
Q

Diagnostic Studies

A

Hemoglobin A1C level: 6.5% or higher
Fasting plasma glucose level: higher than 126 mg/dL
Two-hour plasma glucose level during OGTT: 200 mg/dL (with glucose load of 75 g)
Classic symptoms of hyperglycemia with random plasma glucose level of 200 mg/dL or higher

Fructosamine
Reflects glucose levels past 1-3 weeks
Autoantibodies

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13
Q

Hemoglobin A1C test

A

Glycosylated hemoglobin: reflects glucose levels over past 2 to 3 months
Used to diagnose, monitor response to therapy, and screen patients with prediabetes
Goal: less than 6.5%

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14
Q

Goals of diabetes management

A

Decrease symptoms
Promote well-being
Prevent acute complications
Delay onset and progression of long-term complications
Need to maintain blood glucose levels as near to normal as possible

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15
Q

Patient teaching

A

Nutritional therapy
Drug therapy
Exercise
Self-monitoring of blood glucose
Diet, exercise, and weight loss may be sufficient for patients with type 2 diabetes
All patients with type 1 require insulin

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16
Q

Insulin Categorized according to onset, peak action, and duration

A

Rapid-acting
Short-acting
Intermediate-acting
Long-acting

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17
Q

Examples of rapid acting

A

Humalog

Novalog

Apidra

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18
Q

Examples of short acting

A

Humalin R

Novalin R

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19
Q

Examples of Intermediate Acting

A

NPH

Humulin N

Novolin N

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20
Q

Examples of long acting

A

Lantus

Levemir

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21
Q

Rapid acting onset, peak, duration

A

onset: 10-30 minutes
peak: 30 minutes- 3 hours
duration: 3-5 hours

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22
Q

Short acting onset, peak, duration

A

Onset: 30 min- 1 hour

Peak: 2-5 hours

Duration: 5-8 hours

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23
Q

Intermediate acting onset, peak, duration

A

Onset: 1.5-4 hours

Peak: 4-12 hours

Duration: 12-18 hours

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24
Q

Long acting onset, peak, duration

A

Onset: 0.8-4 hours

Peak: No pronounced peak

Duration: 24+ hours

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25
Rapid-acting (bolus)
Lispro, aspart, glulisine ***Onset of action 15 minutes Injected within 15 minutes of mealtime***
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Short-acting (bolus)
Regular with onset of action 30 to 60 minutes ***Injected 30 to 45 minutes before meal*** Onset of action 30 to 60 minutes
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(Basal) Background Insulin
Used to control glucose levels in between meals and overnight
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Long-acting (basal)
Insulin glargine (Lantus) and detemir (Levemir) Released steadily and continuously with ***no peak action Administered once or twice a day Do not mix with any other insulin or solution***
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Intermediate-acting insulin
NPH Duration 12 to 18 hours Peak 4 to 12 hours ***Can mix with short- and rapid-acting insulins*** Cloudy; must agitate to mix
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Combination Insulin Therapy
Can mix short- or rapid-acting insulin with intermediate-acting insulin in same syringe Provides mealtime and basal coverage in one injection Commercially premixed or self-mix
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Storage of insulin
Do not heat/freeze ***In-use vials may be left at room temperature up to 4 weeks*** Extra insulin should be refrigerated Avoid exposure to direct sunlight, extreme heat or cold ***Store prefilled syringes upright for 1 week if two insulin types; 30 days for one***
32
Administration of insulin
Typically given by subcutaneous injection Regular insulin may be given IV Cannot be taken orally Absorption is fastest from abdomen, followed by arm, thigh, and buttock ***Abdomen is preferred site Do not inject in site to be exercised- Can have altered peak times*** Rotate injections within one particular site
33
Insulin pump- While doing assessment check for pump
Continuous subcutaneous infusion Battery-operated device Connected to a catheter inserted into subcutaneous tissue in abdominal wall Program basal and bolus doses that can vary throughout the day Potential for tight glucose control
34
Problems with insulin therapy
Hypoglycemia Allergic reaction Lipodystrophy- The SQ tissue gets atrophied from constant injections
35
Somogyi Effect
Somogyi effect- Will have high BS in the AM- Giving to much insulin causing BS to drop Rebound effect in which an overdose of insulin causes hypoglycemia Release of counterregulatory hormones causes rebound hyperglycemia A bedtime snack, a reduction in the dose of insulin, or both
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Dawn Phenomenon
Dawn phenomenon- Hyper glycemic- Check BS between 0200-0400 Morning hyperglycemia present on awakening Due to release of counterregulatory hormones in predawn hours Increase in insulin or an adjustment in administration time
37
Oral Agents
Work on three defects of type 2 diabetes Insulin resistance Decreased insulin production Increased hepatic glucose production Can be used in combination
38
Biguanides
Metformin (Glucophage)- Do not give somenof the oral ones. They interfere with contrast media Reduce glucose production by liver Enhance insulin sensitivity Improve glucose transport May cause weight loss Used in prevention of type 2 diabetes Withhold if contrast medium is used ***Withhold if patient is undergoing surgery or radiologic procedure with contrast medium*** Day or two before and at least 48 hours after Monitor serum creatinine Contraindications Renal, liver, cardiac disease Excessive alcohol intake
39
Sulfonylureas
↑ Insulin production from pancreas Major side effect: hypoglycemia Examples Glipizide (Glucotrol) Glyburide (Micronase, DiaBeta, Glynase) Glimepiride (Amaryl)
40
Meglitinides
↑ Insulin production from pancreas Rapid onset: ↓ hypoglycemia ***Taken 30 minutes to just before each meal*** Should not be taken if meal skipped Examples Repaglinide (Prandin) Nateglinide (Starlix)
41
α-Glucosidase Inhibitors
“Starch blockers” Slow down absorption of carbohydrate in small intestine Take with first bite of each meal Example Acarbose (Precose) Miglitol (Glyset)
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Thiazolidinediones
* Most effective in those with insulin resistance * Improve insulin sensitivity, transport, and utilization at target tissues * Examples –***Pioglitazone (Actos)- Can cause myocardial infarction*** ***–Rosiglitazone (Avandia)- Increase risk of blood cancer*** •Rarely used because of adverse effects
43
Dipeptidyl Peptidase–4 (DDP-4) Inhibitor
Blocks inactivation of incretin hormones ↑ Insulin release ↓ Glucagon secretion ↓ Hepatic glucose production Examples (gliptins) Sitagliptin (Januvia) Saxagliptin (Onglyza) Linagliptin (Tradjenta)
44
Diabetes Nutritional Therapy
Counseling Education Ongoing monitoring Interdisciplinary team with registered dietitian as lead
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Diabetes Nutritional Therapy: Type 2 DM
ADA healthy food choices for improved metabolic control Emphasis on achieving glucose, lipid, and blood pressure goals Weight loss Nutritionally adequate meal plan with ↓ fat and CHO Spacing meals Regular exercise ***Carbohydrates Minimum of 130 g/day*** Fruits, vegetables, whole grains, legumes, low-fat milk Monitor with CHO counting, exchanges, or experienced-based estimation
46
Glycemic index
Term used to describe rise in blood glucose levels after carbohydrate-containing food is consumed High glycemic index foods increase glucose levels faster http://www.glycemicindex.com
47
Fats
Limit saturated fats to less than ***7% of total calories Limit cholesterol to less than 200 mg/day*** Two or more servings of fish per week to provide polyunsaturated fatty acids ***Protein should make up 15% to 20% of total calories***
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Alcohol
Limit to moderate amount Consume with food to reduce risk of nocturnal hypoglycemia
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Fiber
Fiber-Recommendation: 25 to 30 g/day
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•Carbohydrate counting
Serving size is 15 g of CHO Typically 45 to 60 g per meal Insulin dose based on number of CHOs consumed Patient teaching essential
51
Diabetes Exercise
Start slowly after medical clearance Monitor blood glucose Glucose-lowering effect up to 48 hours after exercise Exercise 1 hour after a meal Snack to prevent hypoglycemia Do not exercise if blood glucose level exceeds 300 mg/dL and if ketones are present in urine
52
Common manifestations of hypoglycemia
Shakiness Palpitations Nervousness Diaphoresis Anxiety Hunger Pallor Altered mental functioning Untreated hypoglycemia can progress to loss of consciousness, seizures, coma, and death Hypoglycemic unawareness lack of counterregulatory hormones No warning signs/symptoms until glucose level critically low
53
Hypoglycemia Tx
Check blood glucose level ***Treatment: rule of 15- 15 grams of carbs recheck in 15 minutes*** In acute care settings ***Fifty percent dextrose, 20 to 50 mL, IV push*** ***Glucagon, 1 mg, IM or subcutaneously***
54
Self-Monitoring of Blood Glucose
Patient teaching How to use, calibrate When to test Before meals Two hours after meals When hypoglycemia is suspected During illness- BS can increase Before, during, and after exercise
55
Ambulatory and home care teaching
Overall goal is to enable patient or caregiver to reach an optimal level of independence Use services of certified diabetes educator (CDE) Establish individualized goals for teaching Include family and caregivers Assess patient’s ability to perform SMBG and insulin injection Assess patient/caregiver knowledge and ability to manage diet, medication, and exercise therapy Teach manifestations and how to treat hypoglycemia and hyperglycemia Frequent oral care ***Foot care- Check their feet daily, Don’t go barefoot, Cut their nails straight Travel needs- Time change. Keep your watch to your regular time to keep your medications on track, Have someone with you. Know what your hypoglycemia symptoms are and carry snacks.***
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Chronic Complications Diabetic Retinopathy
Microvascular damage to retina Most common cause of new cases of adult blindness Nonproliferative: more common, early stage Proliferative: more severe
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•Nonproliferative
Partial occlusion of small blood vessels in retina causes microaneurysms
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Proliferative
Involves retina and vitreous humor New blood vessels formed (neovascularization): very fragile and bleed easily Can cause retinal detachment
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Diabetic retinopathy
Initially no changes in vision ***Annual eye examinations with dilation to monitor*** Maintain glycemic control and manage hypertension
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Chronic Complications Diabetic Retinopathy Tx
Laser photocoagulation Most common Laser destroys ischemic areas of retina Vitrectomy Aspiration of blood, membrane, and fibers inside the eye Drugs to block action of vascular endothelial growth factor (VEFG)
61
Chronic Complications Diabetic Nephropathy
Damage to small blood vessels that supply the glomeruli of the kidney Leading cause of end-stage kidney disease Risk factors Hypertension Genetics Smoking Chronic hyperglycemia Annual screening If albuminuria present, drugs to delay progression: ACE inhibitors Angiotensin II receptor antagonists Control of hypertension and tight blood glucose control: imperative Nerve damage due to metabolic derangements of diabetes Of patients with diabetes, 60% to 70% have some degree of neuropathy Reduced nerve conduction and demyelinization Sensory or autonomic
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Sensory neuropathy
Loss of protective sensation in lower extremities ***Major risk for amputation- Do to poor foot care***
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Distal symmetric polyneuropathy
Most common form Affects hands and/or feet bilaterally Loss of sensation, abnormal sensations, pain, and paresthesias
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Treatment for sensory neuropathy
Tight blood glucose control Drug therapy Topical creams Tricyclic antidepressants Selective serotonin and norepinephrine reuptake inhibitors Antiseizure medications
65
Autonomic neuropathy
Sexual function Erectile dysfunction Decreased libido Vaginal infections Neurogenic bladder → urinary retention Empty frequently, use Credé’s maneuver Medications Self-catheterization
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Medical Surgical GI Exam 3 (21 decks)

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