Nurb 360 Lifespan: Diabetes

Front 1

Diabetes Melittus

Back 1

group of disorders that have glucose intolerance in common (syndrome) characterized by hyperglycemia from defects in insulin action or secretion

Acutely= hyperglycemia
Chronic= macro and microvvascular complications

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Pancreas

Back 2

Endocrine gland= insulin

Exocrine gland= external digestive enzymes

Front 3

How many units of insulin does the pancreas secrete?

Back 3

40-50/day

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Alpha cells
(pancreas)

Back 4

secrete glucagon (liver glucagonlysis= increase blood sugar)

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Beta cells

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(majority of cells) secrete insulin= decrease blood sugar

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Delta cells

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Secrete somatostatin= regulates insulin and glucagon

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Catabolic hormones

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Glucagon, GH, and catecholamines= (break down) increase blod glucose

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Anabolic Hormones

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Insulin=promote glucose uptake (decreases blood glucose levels by facilitating the transport of glucose into the cells

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Gluconeogenesis

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The process of glucose metabolism in the liver from non-carbohydrate sources such as amino acids (proteins)

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Gluconeogenesis stimulated by?

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glucocorticoids, glucagon, epinephrine, and growth hormone

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6 functions of Insulin?

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1. Lowers blood sugar
2. Increases glycogen synthesis
3.Stores dietary fat
4. Inhibits glycogenolysis
5. Helps transport amino acids
6. Increases K+ uptake

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Glycogen

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primary storage form of glucose in the liver and muscles

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Glucagon function

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Binds to receptors in liver -> glucose which is being stored in the form of glycogen (glycogenolysis). as these stores become depleted liver makes additonal glucose via (gluconeogenesis)

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Somatostatin

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Released by delta cells

Inhibit growth hormone and insulin

Lowers blood sugar

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Amylin

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Secreted at same time as insulin by Beta cells

Thought to help insulin work betters
Slows rate of gastric emptying
Suppress action of glucagon

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Hypoglycemic

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Less than 80mg%

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Hyperglycemic

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Greater than 120mg%

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Type 1 DM

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Body does not produce insulin

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Type 2 DM

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Insulin resistance and secretory deficit

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Other types of diabetes

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1. Gestational (increases the risk for type II later

2. Secondary to other conditions: MODY (maturity onset diabetes)

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Fasting plasma glucose test (FPG)

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Fasting glucose between 100- 125 mg/dl = prediabetic
Equal or greater than 126 = diabetes

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Oral glucose tolerance test (OGTT)

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Glucose level measured after fast and two housr after drinking glucose rich beverage
120-199 mg/dl = prediabetes
200 or greater = diabetes

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Hgb A1c (glycosylated hemoglobin)

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Measure of plasma glucose over time by measuring glucose bound to hemoglobin

Ideal glycemic control < 7%
Non-diabetic 4-6%

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Incidence and onset of Type I and II

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Type I= 10% 11-13 yrs (onset)

Type II= 90% increaes after 40 (pima indians and Findland)

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Cause of type I DM

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Gene (chrom 6) <-> environment interaction
autoimmunity (triggered by a virus?)
Both beta and alpha cells abnormal= decrease insulin and increase glucagon

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Cause of type II DM

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Cause ?
risk factors= obesity (apple shape), family history, minorities, female, and metabolic syndrome

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MODY

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Maturity-onset diabetes of youth- has a high correlation as an autosomal dominant disorder

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Signs and symptoms of type I DM

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Polydispsia (thirst); polyuria (urination); polyphagia (hunger)
weight loss, fatigue

Abrupt presentation- usually DKA

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Diabetic ketoacidosis

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Glucose is unavailabe, the body breaks down fatt, by product is ketone bodies

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Signs and symptoms of type II DM

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Vague with slow onset

Most common: pruritus, recurrent infections, prolonged wound healing, fatigue, visual changes, and paresthesias

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For every 1 point reduction in the hemoglobin A1C

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The risk of developing microvascular complications decrease by 40% for both types of DM

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What effect does exercis have on insulin absorption

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Increased the rate of absorption

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Absorption rates for injection sites of insulin?

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Abdomen and arm = most rapid

Thigh = intermediate

Buttocks = slowest

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Liperhypertrophy

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Development of scar tissue = decreased insulin absorption

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Fast-acting insulin

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Humalog, Novalog (need to know the onset, peak, and duration

Great for picky eaters, give after meals based on the number of carbs

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Long-acting insulin

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Lantus
Taller, skinnier vial
"poor man's pump" 24 hour duration, similar to basal rate (never peaks)

Low ph (burns); can't be mixed with other insulins

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Cost of Insulin pump supplies and injectable insulin / month

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$300 - $400

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When do you refrigerate insulin?

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If vial unopened

Never Freeze

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Blood glucose target ranges (mg/dl)

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Under age 2, 100-250

2-5, 100-220

6-16, 80-180

Over 16, 80-120

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Hypoglycemia symptoms

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"Low and clammy"
Sympathetic response = tachycardia, palpitations, diaphoresis, tremors, pallor, anxiety
Neuroglycopenia response = headache, confusion, irrability, poor judgement, blurred vision, hunger seizures

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What causes hypoglycemia?

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1. Too much insulin
2. Not enough carbs
3. Activity and exercise

(can be very acute)

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If there is a doubt between hyper and hyp, which do you treat for?

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Always treat for hypo

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How to treat for hypoglycemia?

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Give 15 grams of fast-acting carbs

Follow with a complex carb, if it will be one hour before next meal/snack

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What do you do for loss of consciousness or seizure activity?

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Glucagon, converts the glycogen in the liver to glucose

(if in hospital = D50W, or D25W for children)

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What to do when ketones are present?

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Push sugar-free fluids to flush out the ketones

Rest and quiet activities, as body thinks it does not have enough insulin

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Carb counting

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1 carb = 15 grams of carbohydrate

15 grams of carbohydrate = 1 carb

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Signs that could indicate DKA

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N/V
Fruity odor breath
Deep, rapid respirations (kussmaul)
Decreasing LOC
Moderate or high urinary ketones
Persistent hyperglycemia

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Dawn phenomena

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Diagnosed via 3AM BS

Insulin wears off (3AM BS normal) -> increased BS on awakening -> more insulin at bedtime tx

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Somogyi effect

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Too muc insulin at bedtime -> hypoglycemia (at 3AM BS) -> rebound hyperglycemia -> treatment with increased insulin is bad (give snack at bedtime and/or less insulin)

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Prediabetes

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Known as impaired glucose tolerance or impaired fasting glucose
BS: 100-126
OGTT: 140-199

(will develop type II diabetes in approx 10 years if don't change lifestyle

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Secondary diabetes

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Genetic defects (Downs)
Hormonal (hyperthyroidism)
Congenital
Pancreatic disorders
Drug therapy (steroids)
Metabolic

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Major difference between MODY and type II

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MODY= 1 gene

Type II DM= multiple genes

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Metabolic Syndrome
characteristics

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Abdominal obesity waist 40 (men), 35 (women) or more
Elevated B/P (> 130/85)
Elevated triglycerides (> 150)
Elevated FBS
Insulin resistance

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Hyperglycemic Hyperosmolar Nonketonic Syndrome
characteristics

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Fluid loss
No ketones
Elevated BS
Blood osmolarity >300
CNS changes

Tx= IV bolus insulin, restore F & E

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Chronic complications
(macrovascular)

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Increased BS -> chronic hypoxia due to altered RBC function -> hear comensates -> increase BP (and associated problems)

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Chronic complications
(microvascular)

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Diabetic retinopathy (legal blidness 25 x more common)
Nephropathy (leading cause of renal failure; tx ACE inhibitors)
Neuropathy - increased BS is causing demylenation of nerves