• No results found

Lesson N- Diabetes.pptx

N/A
N/A
Protected

Academic year: 2020

Share "Lesson N- Diabetes.pptx"

Copied!
33
0
0

Loading.... (view fulltext now)

Full text

(1)

Diabetes Mellitus

(2)

Outline

Diabetes Mellitus 1. Types

2. Risk Factors

3. Metabolic Effects of Diabetes 4. Acute Complications

a. Hypoglycemia

b. Diabetic Ketoacidosis (DKA)

c. Hyperglycemic Hyperosmolar Nonketotic Syndrome (HHNK)

5. Chronic Complications

(3)

Objectives

At the end of the lecture, the student vocational nurse

will be able to:

Compare and contrast the two types of diabetes

mellitus

Summarize the risk factors associated with both

Describe the systemic metabolic effects of diabetes by

each body system

Formulate a nursing care plan which addresses the

physiological and psychosocial integrity, health

(4)

Diabetes Mellitus

Metabolic Disorder of the Pancreas

Affects CHO, fat, and protein metabolism; Chronic disorder

Affected people experience many debilitating and life-threatening

complications before death

Metabolic Syndrome

Abdominal obesity; HTN; Elevated LDP, triglycerides, blood glucose

levels; Low HDL

90-95% Acquire Disorder as Adults

7th Cause of Death in U.S.; 23.6 million in U.S. have DM (estimate)

Incidence increased among African Americans, Latinos, Native

Americans, Asian Americans

(5)

Diabetes Mellitus

Two major forms:

Type I

formerly called insulin-dependent diabetes mellitus (IDDM)Characterized by no insulin production by the beta cells in the

islets of Langerhans of the pancreas

Onset: childhood and adolescence

Type II

formerly called non-insulin dependent diabetes mellitus

(NIDDM)

Characterized by insulin resistance or insufficient insulin

production

(6)

Diabetes Mellitus

Prediabetes MellitusCan lead to

Type 2 diabetesHeart diseaseStroke

Impaired fasting glucose

(IFG): 100 to 125 mg/dL

Impaired glucose tolerance

(IGT): 140 to 199 mg/dL

A significant number of those

with pre-diabetes will develop the disease

Weight loss and increase

physical activity can delay or avoid onset of Type II DM

Islet of Langerhans

(7)

Diabetes Mellitus

Hyperglycemia

An elevated blood glucose level

Associated: Other disorders; ManagementPancreatitis; Adrenocortical hormones

Insulin

Functions:

Carries glucose into body cells as their preferred

source of energy

(8)

Diabetes Mellitus

Pathophysiology and Etiology

Type 1 diabetes mellitus (IDDM)

No insulin production of the islet cells, or endocrine

portion of the pancreas

Lipolysis (breakdown of fat) results in accumulation of

fatty acids and ketones (metabolic byproducts of fat metabolism)

Ketoacidosis (a form of metabolic acidosis)

Autoimmune disorder (genetic mutation causes killer

(CD8) T-cell lymphocytes to attack and destroy the insulin-producing islet cells

(9)

Diabetes Mellitus

Pathophysiology and Etiology

Type 2 diabetes mellitus (NIDDM)Inherited

Obesity causes changes in liver function

accompanied by hyperglycemia and insulin

resistance (decreased sensitivity to insulin at the tissue level)

Insufficient insulin

(10)

Diabetes Mellitus

Pathophysiology and Etiology

Type 2 diabetes mellitus (NIDDM)

Insulin resistant; Insufficient insulin; Inherited

Obesity—trigger;

Glycosuria (Caused by an excessive glucose in the blood; appears when BS level >180mg/dL)

Impaired renal threshold (kidney’s ability to

reabsorb glucose and return it to the bloodstream) • Ketonemia (increased ketones in the blood)

(11)

Diabetes Mellitus

Assessment Findings

Signs and symptoms

Polyuria (excessive urine production)Polydipsia (excessive thirst)

Polyphagia (feels hungry and eats more)Weight loss

DehydrationBlurred visionThirst

(12)

Diabetes Mellitus

Diagnostic findings

Urinary tests

presence of glucose and ketonesBlood tests

• random blood sugar, fasting blood glucose, postprandial glucose, oral glucose tolerance test

Glucometer

measures capillary blood glucose from finger stick blood

sample

Hemoglobin A1c test (glycosylated hemoglobin)

Measures amount of glucose stored in the hgb molecule

(13)

Diabetes Mellitus

Medical Management

Depends on type of diabetes

Diet and weight loss: Major component of treatmentDietary allowances (calories, percentages of CHO,

fats, and proteins)

Carbohydrate counting

Glycemic index (measures how fast CHO food raises

blood sugar)

Exercise

(14)

Insulin: Four categories

Rapid acting

Insulin lispro (Humalog)

Onset: 5-15min; Peak: 1-2hr; Duration: 3-4hrAspart (Novolog)

Onset: 5min; Peak: 1hr; Duration: 3-4hr

Short acting

Regular insulin (Humulin R, Novolin R, Iletin II Regular)Onset: 30min-1hr; Peak: 1-3hr; Duration: 6-8hr

Intermediate acting

Isophane insulin suspension (NPH, Humulin N, Novolin N)Onset: 1-1.5hr; Peak: 4-12hr; Duration: 24hr

Insulin zinc suspension (Lente)

(15)

Insulin: Four categories (cont’n)

Long acting

Extended insulin zinc suspension (Ultralente, Humulin U)Onset: 4-8hr; Peak: 8-10hr; Duration: 18-30hr

Glargine (Lantus)

Onset: 2-4hr; Peak: none; Duration: >24hr

Insulin mixtures

Humulin 50/50

Onset: 15min; Peak: 2-4hr; Duration: 20-22hrHumulin 70/30

Onset: 30min; Peak: 7-12hr; Duration: 16-24hrNovolin 70/30

Onset: 30min; Peak: 3-8hr; Duration: 10-16hrHumalog 75/25

(16)

Diabetes Mellitus

Medical Management

Types of Insulin

Human, beef, pork

Administration of insulin

Dosage:

U-100; Type

IV

Subcutaneous;

Lipoatrophy

Lipohypertrophy

Insulin pen

(17)

Diabetes Mellitus

Medical Management

Oral antidiabetic agents-type 2 Sulfonylureas and meglitinides

“insulin releasers”

Stimulates pancreas to secrete more insulinBiguanides and thiazolidinediones

“insulin sensitizers”

Help tissues use available insulin more efficientlyAlpha-glucosidase inhibitors into glucose

Breaks down complex CHOAdjuvant drugs

Glucose-regulating functionPancreas transplantation

(18)
(19)

Acute Complications:

Diabetic Ketoacidosis (DKA)

Pathophysiology and Etiology

Occurs when there is an acute insulin deficiency or an

inability to use whatever insulin the pancreas secretes

Brittle (unstable) diabetes

Noncompliance with treatment; Infection Acidotic state; Coma

Assessment Findings

Weakness; Thirst; Anorexia; Vomiting; Drowsiness;

Abdominal pain; Kussmaul respirations; Low BP

Blood glucose 300-1000mg/dL; Urine test; Laboratory

(20)

Diabetic Ketoacidosis (cont’n)

Medical Management

Main goals

Reduce the elevated blood glucose

Correct fluid and electrolyte imbalances

Clear the urine and blood of ketones

IV Insulin; Glucose

Isotonic fluid

Potassium replacements

(21)

Hyperosmolar Hyperglycemic Nonketotic

Syndrome (HHNKS)

Pathophysiology and Etiology

Hyperglycemia without ketosis

Results from serious illness; DiuresisBlood glucose >500

pH normal range (7.35-7.45)

Assessment Findings

Hypotension; Mental changes

Extreme thirst; Dehydration; TachycardiaFever; Neurologic signs

(22)

Hyperosmolar Hyperglycemic Nonketotic

Syndrome (cont’n)

Diagnostic Findings:

Blood glucose

Serum potassium, sodium

Serum osmolarity

Medical Management

Insulin administration

Correction of fluid and electrolyte imbalances

CVP

(23)

Hypoglycemia

Pathophysiology and Etiology

Hyperinsulinism

blood glucose <60 mg/dLContributing factors:

Diet; Exercise; Alcohol

Assessment Findings

Signs and symptoms:

Nausea; Drowsiness; Hunger; Malaise; Excessive

perspiration; Confusion; Coordination difficulty; Personality or behavior changes

Diagnostic Findings:

(24)

Hypoglycemia (cont’n)

Medical Management

Administration of 15 to 20 g of simple

carbohydrate as soon as possible

Glucagon

IV administration of 50% glucose

Complex carbohydrates

(25)

Chronic Complication:

Peripheral Neuropathy

Pathophysiology and Etiology

Pathologic changes in nerves

Develops 10 or more years after the onset of DMPoor glucose control

Decreased blood circulation to nerve tissue Motor neuropathy

When motor nerves are affected, the muscles weaken and

atrophy

Sensory neuropathy

Leads to paresthesias (abnormal sensations such as

prickling, tingling, burning, or needle-like pain) – Autonomic neuropathy

(26)

Peripheral Neuropathy (cont’n)

Assessment Findings

Signs and symptoms:

Pain; Swollen feet; Disturbing sensations; Digestive, urinary,

and sexual dysfunction; Dizziness; Smaller skeletal muscles

Diagnostic findings: Neurologic examination;

Screening test; Electromyography

Medical Management

Diet; Exercise; Pain relief measures

Drug therapy; Antibiotic therapy; Drugs to reverse diabetic

neuropathies

(27)

Diabetic Nephropathy

Pathophysiology and Etiology

Progressive decrease in renal functionGlomerular deterioration

Five stages:

Stage I Hyperfiltration, Glomerular hypertrophy; 10 yrs afterStage II Microalbuminuria; 15 yrs after dx of DM

Stage III Gross albuminuria; 15 yrs

Stage IV Advanced dysfunction; 15-20 yrsStage V End-stage renal failure; 20-25 yrs

Assessment Findings:

Swollen feet and hands; Gradually increasing BP;

(28)

Diabetic Nephropathy (cont’n)

Diagnostic Findings:

Serum creatinine test; Renal creatinine clearance test

Medical Management:

Control blood glucose levels, hypertension

Drug therapy; Dietary protein reduction; Smoking

cessation

(29)

Diabetic Retinopathy (cont’n)

Pathophysiology and Etiology

Vascular changes in retina

Develops 10 or more years after

onset of diabetes

Types

Nonproliferative

Proliferative—blindness

Assessment Findings

(30)

Diabetic Retinopathy (cont’n)

Medical Management

Laser photocoagulationVitrectomy

ACE inhibitor

Nursing Management

Encourage therapeutic regimen for tight glucose controlClient education

Complications of diabetes

(31)

Vascular Disturbances

Pathophysiology and Etiology:

Thickening of arterial walls

Coronary artery diseaseHyperlipidemia

Assessment Findings:

Cool extremities; Leg cramps; Gangrene; Skin ulcers;

Myocardial infarctions

Diagnostic Findings:

Laboratory tests

Angiography

(32)

Vascular Disturbances (cont’n)

Medical and Surgical Management:

Lipid-lowering measures

Vasodilators

Platelet aggregation reduction drugs

Amputation

Insulin

(33)

Reference

Timby, B. & Smith, N. (2010). Introductory

References

Related documents