Art + Sci Unit 9

Diabetes mellitus

a multi system disease related to abnormal insulin production (absent or insufficient) and/or impaired insulin utilization

Possible causes of diabetes

- genetics

- autoimmunity

- viruses

- environmental factors

Types of diabetes

- 1 and 2 (most common)

- gestational

- prediabetes

- secondary

Insulin

- produced by beta cells in the Islets of Langerhans in the pancreas

- released continuously into bloodstream in small increments; larger amounts released after food

- stabilizes glucose range to 4-6 mmol/L

Insulin function

facilitates glucose transport from bloodstream across cell membrane to cytoplasm of cell; decreases blood glucose

Insulin after meals

- increased levels in blood

- stimulates storage of glucose as glycogen in liver and muscle

- inhibits gluconeogenesis

- enhances fat deposition, increases protein synthesis

Type 1 diabetes mellitus

- autoimmune destruction of beta cells by T cells = insufficient insulin production

- autoantibodies present for months-years before clinical symptoms; can cause significant reduction of beta cell function before manifestations occur

- will require exogenous insulin to sustain life

Onset of DM1 manifestations

develop when pancreas can no longer can no longer produce insulin; rapid onset, ketoacidosis

Prediabetes

a condition in which the blood sugar level is higher than normal, but not high enough to be diagnosed as diabetes

- impaired fasting glucose (6.1-6.9)

- impaired glucose tolerance/plasma glucose levels (7.1-11)

Prediabetes symptoms

- usually asymptomatic but damage already occurring to heart and blood vessels

- watch for polyuria, polyphagia, polydipsia

Type 2 diabetes mellitus

- most prevalent

- usually 35+ yrs of age, majority overweight

- the pancreas continues to produce some endogenous insulin, but insufficient amount or poorly utilized by tissues

Risk factors for DM2

- obesity, adipose tissue

- genetic mutations leading to insulin resistance or risk for obesity

Major metabolic abnormalities

1. insulin resistance

2. decreased ability of pancreas to produce insulin

3. inappropriate glucose production from liver

4. alteration in production of hormones and adipokines

Insulin resistance

the inability of the cells to respond to insulin; receptors are either unresponsive or insufficient in number

- results in hyperglycemia

Decreased ability of pancreas to produce insulin

beta cells fatigued from compensating, beta cell mass lost

Inappropriate glucose production from liver

in which the liver's response of regulating release of glucose is haphazard

- not a primary factor in development of DM2

Alteration in production of hormones and adipokines

play a role in glucose and fat metabolism; contribute to patho of DM2

Adiponectin and leptin

two main adipokines believed to affect insulin sensitivity

Metabolic syndrome

cluster of abnormalities that increase the risk for cardiovascular disease and diabetes; characterized by insulin resistance

- ex. HTN, dyslipidemia, insulin resistance, dysglycemia

Risk factors for metabolic syndrome

abdominal obesity, sedentary lifestyle, urbanization and westernization, certain ethnicities

Type 2 diabetes mellitus onset

gradual onset, person may go for many years with undetected hyperglycemia

- osmotic fluid/electrolyte loss from hyperglycaemia may become severe > hyperosmolar coma

Secondary diabetes

a type of diabetes caused by another disease or certain drugs or chemicals; usually resolved when underlying condition treated

Drugs that may cause secondary diabetes

corticosteroids (prednisone), phenytoin (Dilantin), atypical antipsychotics (clozapine)

Conditions that may cause secondary diabetes

schizophrenia, Cushing's, hyperthyroidism, immunosuppressive therapy, parenteral nutrition, cystic fibrosis

DM1 clinical manifestations

- polyuria, polyphagia, polydipsia

- weight loss, weakness, fatigue

DM2 clinical manifestations

- nonspecific, may have 3 Ps

- fatigue

- recurrent infection, recurrent yeast or monilia infection

- prolonged wound healing

- visual changes

Methods of diagnosis of DM

1. A1C > 6.5%

2. fasting plasma glucose > 7

3. random/casual plasma glucose measurement > 11.1 + classic symptoms

4. 2-hour oral glucose tolerance test level > 11.1 earn a load of 75 g is used

Hemoglobin A1C test

shows the amount of glucose attached to Hgb molecules over RBC lifespan

- used a DM diagnostic test, useful in determining glycemic levels over time

Normal A1C

< 6%; reduced risk of retinopathy, nephropathy, neuropathy

Goals of DM management

- Decrease symptoms

- Promote well-being

- Prevent acute complications

- Delay onset and progression of long-term complications

Interprofessional care of DM

- patient teaching, self-monitoring of blood glucose

- nutritional therapy

- medication therapy

- exercise

Exogenous insulin

Insulin from an outside source

Required for type 1 diabetes

Prescribed for patient with type 2 diabetes who cannot control blood glucose by other means

Oral agents for DM

work on insulin resistance, decreased insulin production, and increased hepatic glucose production

Nutritional therapy for DM1

- meal plan based on individual's usual food intake and is balanced with insulin and exercise patterns

- insulin regimen managed day to day

Nutritional therapy for DM2

- emphasis on achieving glucose, lipid, and BP goals

- calorie and fat intake reduction

Protein

- contributes 15-20% of total energy consumed

- diabetic neuropathy: limit intake to 15% of energy

Fats

- contributes less than 35% of energy

- reduce saturated fats and trans fats to less than 9% of energy intake

- reduce polyunsaturated fat to less than 10% of energy intake; include foods rich in polyunsaturated omega-3 fatty acids and plant oils

Fibre

approx 30-50 g/day

Carbohydrates

45-60% of energy

- less than 10% of daily energy should come from sugar

Glycemic index

term used to describe rise in blood glucose levels after carb-containing food is consumed

- should be considered when a meal plan is formed

DM nursing diagnoses

- inadequate health management

- potential for injury

- potential for unstable blood glucose levels

- potential for peripheral neurovascular dysfunction

Acute complications of DM

diabetic ketoacidosis, hyperosmolar hyperglycaemic syndrome, hypoglycaemia

Diabetic ketoacidosis

caused by profound deficiency of insulin; most commonly in DM1

- hyperglycaemia, ketosis, acidosis, dehydration

Precipitating factors of DKA

Illness

Infection

Inadequate insulin dosage

insulin omission

Undiagnosed type 1 diabetes

When supply of insulin is insufficient...

glucose cannot be properly used for energy and body breaks down fat stores = ketones

Ketones

by-products of fat metabolism

- alter pH, causing metabolic acidosis

- excreted in urine

- electrolytes become depleted

S&S of DKA

Polydispia, polyuria, polyphagia, dehydration, fruity breath, kussmaul breathing

Kussmaul respirations

Deep, rapid breathing; usually the result of an accumulation of certain acids when insulin is not available in the body.

DKA treatment

- airway management, O2 admin

- correct fluid/electrolyte imbalance; IV infusion NaCl

- insulin therapy (withheld until fluid resuscitation begun; bolus > continuous infusion)

Hyperosmolar hyperglycaemic syndrome

life-threatening, less common than DKA, often in DM2

- enough circulating insulin that DKA does not occur

- neurological manifestations occur because of increased serum osmolality

- requires greater fluid replacement than DKA

HHS lab values

Blood glucose >34 mmol/L

Increase in serum osmolality

Absent/minimal ketone bodies

Assessment of HHS and DKA

assess renal status, cardiopulmonary status, LOC, signs of K+ imbalance

Hypoglycemia

low blood glucose

- occurs when too much insulin in proportion to glucose in the blood or blood glucose < 4 mmol/L

- untreated, can lead to loss of consciousness, seizures, coma, death

Hypoglycemia manifestations

anxiety, diaphoresis, tremors, hunger, pallor, palpitations

Hypoglycemic unawareness

no warning S&S, increased risk for decreased blood glucose levels; often related to autonomic neuropathy

Causes of hypoglycemia

mismatch in timing of food intake and peak action of insulin or oral hypoglycemic agents

Hypoglycemia treatment

15-20 g of simple carb; juice, soft drink, Life-Savers > recheck blood sugar after 15 mins

Hypoglycemia treatment if unable to swallow

1 mg glucagon IM or SUBQ (beware rebound hypoglycemia) or 20-50 mL 50% dextrose IV push

Chronic complications of DM

macrovascular and microvascular

Macrovascular angiopathy

disease of large/medium blood vessels promoted by altered lipid metabolism seen in diabetes (but not always specific to diabetes)

Microvascular angiopathy

results from thickening of vessel membranes in capillaries and arterioles in response to chronic hyperglycemia; is specific to diabetes

Diabetic retinopathy

microvascular damage to the retina caused by chronic hyperglycemia

- nonproliferation vs proliferative

Nonproliferative retinopathy

most common form; partial occlusion of small blood vessels in the retina causes micro aneurysms > capillary fluid leaks out > retinal edema and hart exudates or intraretinal hemorrhages

Proliferative retinopathy

the most severe form; involves the retina and vitreous; when retinal capillaries become occluded, the body compensates by forming new blood vessels to supply the retina with blood; these new blood vessels are fragile and hemorrhage easily > vitreous contraction > retinal detachment

Diabetic retinopathy treatment

laser photocoagulation, vitrectomy, anti-vascular endothelial growth factor meds

Laser photocoagulation

laser destroys ischemic areas of retina and prevents further visual loss

Vitrectomy

aspiration of blood, membrane, and fibres inside the eye

Diabetic nephropathy

microvascular damage to glomerular capillaries due to high blood sugar of diabetes mellitus

- leading cause of end-stage renal disease

Prevention of diabetic nephropathy

tight glucose and BP management (ACEs and ARBS), yearly screening for microalbuminuria and serum creatinine

Diabetic sensory neuropathy

macrovascular damage to peripheral nerves due to diabetes; loss of sensation, abnormal sensations, pain, paresthesias to hands/feet; can cause atrophy, ulcers

Autonomic neuropathy

can affect nearly all body systems

- complications: gastroparesis (delayed gastric emptying), cardiovascular abnormalities, neurogenic bladder

Diabetic dermopathy

damage to skin; reddish brown, round or oval patches

Acanthosis nigricans

dark, coarse, thickened skin

Necrobiosis lipoidica diabeticorum

red-yellow lesions; skin becomes shiny, revealing tiny blood vessels

Infection in DM

defect in mobilization of inflammatory cells; impairment of phagocytosis by neutrophils and monocytes

Sulfonylureas and meglitinides

drugs that increase insulin secretion

Biguanides or thiazolidinediones

drugs that enhance insulin sensitivity by decreasing insulin resistance