DIABETES MELLITUS

The Endocrine System

Pancreas A spongy tube-shaped organ about 6 inches

long

Located in the back of the abdomen, behind the stomach

The head of pancreas is on the right side of abdomen. It is connected to the duodenum, the upper end of the small intestine

The narrow end of the pancreas called the tail extends to the left side of the body.

Endocrine Pancreas and Exocrine Pancreas

Exocrine pancreas= secretes more than 1000 ml of digestive substances

Endocrine pancreas= involves the Islets of Langerhans Over 1 M islets has two cell types:

alpha cells secrete glucagons that stimulate glyconeolysis

beta cells secretes insulin protein metabolism

hormones are secreted to compensate bld sugar level

The organ affected in diabetes is the endocrine pancreas

The shape of this organ is unusual; it is an archipelago, with clusters of cells distributed through the pancreas

The larger islet look like small grain of the sand

Pancreas The endocrine cells are clustered in groups

within the pancreas

Pancreatic Islets – little islands of cells

Pancreatic islet cells – cells within the islets which make specific pancreatic endocrine hormones (insulin and glucagon)

Secretes their hormones (insulin) into the blood

stream and are surrounded by small blood vessels

Glucose= insulin balance Hyperglycemia

Too much glucose orToo little insulin

HypoglycemiaToo much insulin or Too little glucose

Pancreatic Endocrine Hormones

Insulin Purpose : regulate blood glucose (sugar)

in the normal range

Action – forces many cells of the body to absorb and use glucose thereby decreasing blood sugar levels

Secreted in response to : High blood glucose

Secretion inhibited by: Low blood glucose

Disease due to deficient action: Diabetes

Disease due to excess action: Hypoglycemia Insulin Shock

How insulin affects blood glucose

Insulin Aids glucose entry into the cells

Stimulates glycogenesis bld = formation and storage of glycogen (liver) glucose

level Promotes glucose catabolism

Decrease transcellular transport of glucose: Require Na for transport K for production

Therefore decreased blood glucose level. And inhibits protein and fat breakdown

Glucagon Purpose: Assist insulin in regulating blood

glucose (sugar) in the normal range.

Action: forces many cells of the body to release (or produce) glucose (increasing blood sugar)

Secreted in repose to: low blood glucose

Secretion inhibited by: High blood glucose

Disease due to deficient action: sometimes nothing, sometimes hypoglycemia

Disease due to excess action: Hyperglycemia

Glucagon Secreted by the alpha cells of the pancreatic

islet.

High blood glucose – no glucagon is secreted.

Low blood glucose (between meals, during exercise) = more and more glucagon is secreted.

Has an effect on many cells of the body, most notably in the liver.

Effect: make the liver release the glucose it has stored in its cells into the bloodstream, with the net effect of increasing blood glucose.

Below – 70 – hypoglycemia

Above 110 – can be normal (if have eaten within 2 to 3 hours)

Insulin Regulation and Release Beta cells in islets of Langerhands of

pancreas; released from pancreas as proinsulin and converted into insulin by liver

Alpha cells produce glucagon

Released continuously to maintain a blood glucose of 70 – 100 mg/dl (mg/dl means milligrams of glucose in 100 ml of blood)

Normal Regulation of Blood Glucose The human body wants blood glucose (blood

sugar) maintained in a very narrow range.

Insulin and glucagon are the hormones secreted by islet cells within the pancreas.

Diabetes A multisystem disease related to abnormal

insulin production, impaired insulin utilization, or both.

1,500 BC diabetes is already present (with polyuria and ants and fly’s in urine

250 BC Apolonius of Memphis coined diabetes and later Mellitus (Latin = honey)

Is a disorder characterized by hyperglycemia or elevated blood glucose (blood sugar)

Glucagon

Mobilization of glucose from liver

Stimulates alpha cells

Increase Bld. Glucose Decreased Blood glucose

Stimulates B- Cells Increased Uptake of glucose by

cells

Insulin

Diabetes

Condition where the blood sugar level consistently runs to high.

A chronic metabolic disorder in which the body cannot metabolize carbohydrates, fats and proteins because of lack of or ineffective use of the hormone insulin.

Classified into three primary types: o Type I, IDDM,

Juvenile Onset Diabetes.

o Type II, NIDDM, Adult-onset Diabetes

o Gestational DM (GDM)

Diabetes Occur When the pancreas does not produce any insulin

(type I) or

The pancreas produces very little insulin, or

When the body does not respond appropriately to insulin, a condition called “insulin resistance.” (Type II or GDM)

Predisposing Factors Stress

o Stimulates secretion of epinephrine, norepinephrine, glucocorticoids= increases CHO

Heredityo Strongly associated with type II DM

Obesityo Adipose tissues are resistant to insulin,

therefore glucose uptake by the cells is poor. (lack of physical activity or exercise)

Viral Infection

o Increase risk to autoimmune disorder

Autoimmune Disorderso More associted with type I DM.

Womeno Multigravida with large babies

Signs and Symptoms of Pre-Diabetes

Very often there are no signs or symptoms

It is often discovered during a routine physical with basic screening for fasting blood glucose levels.

Normal level – below 100 mg/dl

100 to 125 mg/dl – this indicates impaired fasting glucose or pre-diabetes.

Over 126 mg/dl – most likely means a diagnosis of Type 2 diabetes

Criteria for Diagnosis of DM Symptoms of DM plus casual plasma

glucose concentration > 200mg/dl (11.1 mmol/L)

o Casual is defined as any time of day without regard to time since last meal.

o The classic symptoms of DM include poyluria, polydipsia, and unexplained weight loss, or 3 P’s

Fasting Plasma glucose of >126 mg/dl (7.0 mmol/L)

o Fasting is defined as no caloric intake for at least eight hours or

o Fasting blood glucose – 10 – 12 hours NPO

2 hour post prandial glucose >200mg/dl during an OGTT.

o OGTT should be performed as described by the WHO using glucose load containing the equivalent of 75g (non-pregnant) of anhydrous glucose dissolved in water.

o 100 g for pregnant women

o OGTT – Oral Glucose Tolerance

Test

o 140 – 199 mg/dl = pre-diabetic stage

o Normal OGTT <140mg/dl

Characteristics of Type 1 Diabetes Usually occurs before the age of 30 but may

occur at any age.

Most common in children. Peak incidence: puberty (around 10 – 12 years in girls and 12 – 14 years old in boys)

Quick onset with thirst, frequent urination, weight loss developing and worsening over days to weeks

Usually no known family history

No major risk factors; risk is increased if there is a strong family history

Insulin shots required to control diabetes – absolute insulin deficiency because the pancreas do not have islets of langerhans

Blood glucose levels are sensitive to small changes in diet, exercise, and insulin dose

Ketosis prone

DM Type 1 causes Caused by insulin deficiency Formerly known as “juvenile onset” or

“insulin dependent diabetes mellitus” (IDDM)

Environmental factors; virus, toxin, stress.

Hyperglycemia as the result of autoimmune destruction of pancreatic B-cells.

When 80-90% of the beta-cells are destroyed, over symptoms occur.

Type I diabetes1. The stomach changes food into glucose

2. Glucose enters the bloodstream

3. The pancreas makes little or no insulin

4. Little or no insulin enters the bloodstream

5. Glucose builds up in the blood stream

T ype I d iabetes A ssessment Onset: rapid or suddenly and very severely

(usually over a few weeks)

Major symptoms:o Being exceptionally thirsty and

hungry

o Dry mouth

o The need to urinate often

o Enuresis (bed wetting)

o Weight loss (even though you may be hungry and eating well)

o Feeling weak and tired (Fatigue)

Minor Symptomso Dry skino Skin infectionso Poor wound healingo Candidal vagintis (adolescent girls)o Manifestations of DKA

Diagnostic Evaluation Random blood glucose >200mg/dl Fasting blood glucose 126mg/dl or greater

Pathophysiology of DM Type I Triggering factor is viral infection that causes

autoimmune response of the body

Autoimmune response results in to destruction (80 – 90%) of the beta cells in the pancreas which resulted into decrease insulin production which results to hyperglycemia.

DM Type II Characteristics Usually develops in middle age or alter

(Adult diabetes onset) and tends to be hereditary

Most common type

Patient is overweight at the time of diagnosis

Sometimes referred to as “adult-onset diabetes”

Has started to appear in children because of the rise in obesity in young people (children and adolescents)

Obesity

Being overweight can lead to high blood pressure and related complications

Blood vessel damage (atherosclerosis)

Heart attack or heart failure

Kidney failure

Obesity increases a person’s risk of illness and death due to diabetes, stroke, coronary artery disease, hypertension, high cholesterol and kidney and gallbladder disorders, Obesity may increase the risk for some types of cancer.

DM Type II Characteristics Increased prevalence in some ethnic groups:

Asian Americans, African Americans, pacific islanders, Asian Americans, Hispanic/Latino

Not prone to ketoacidosis until late in course or with prolonged hyperglycemia

May or may not have symptoms of hyperglycemia.

May also have extreme tiredness, blurred vision, delayed healing, numbness and tingling of the hands and feet, recurring infection.

Children between the ages of 10-19 that have one or more of the following are at an increased risk;

o Family historyo Member of certain ethnic populationo Overweighto Sedentary lifestyle

Types 2 Diabetes Symptoms Sometimes, people with Type II diabetes

don’t’ notice any symptoms or the symptoms are experienced gradually.

Asymptomatic but symptoms are gradual:They include:

o Blurry visiono Cuts or sores that are slow to heal o Itchy skin, yeast infections

o Increased Thirsto Dry Moutho Need to urinate often o Leg pain

Causes of Diabetes: Impaires insulin production Insulin resistance

Blood Sugar Illustration1. Stomach converts food to glucose2. Glucose enters bloodstream3. Pancreas produces insulin4. Glucose enters body effectively5. Glucose levels in balance

Diabetes Mellitus Type II1. The stomach changes food into glucose2. Glucose enters the bloodstream 3. The pancreas makes insulin4. Insulin enters the bloodstream 5. Glucose can’t get into the cells of the

body. Glucose builds up in the blood vessels

Gestational Diabetes Mellitus (GDM)

Triggered by pregnancy

Hormone changes during pregnancy can affect insulin’s ability to work properly, resulting in high blood glucose levels.

Over 25 years old

Above their normal body weight before pregnancy

Family history of diabetes or

Hispanic, black, Aboriginal, or Asian

GDM Causes Insulin resistance due to pregnancy Genetic predisposition Gestational diabetes affects about 4% of all

pregnant women.

It begins when hormones form the placenta make the mother insulin resistant

Many women who have gestational diabetes develop type 2 diabetes years later.

Their babies are also at some risk for developing diabetes later in life.

GDM Characteristics CHO intolerance during pregnancy

o 1 hour screen using a 100g oral glucose load (performed between 24th and 28th

week of gestation unless otherwise indicated)

o If the 1 hour screen for glucose is >140 mg/dl (>7.8 mmol/L) a full diagnostic 100g, 3 hour OGTT is indicated.

Usually blood glucose level returns to normal after child birth, however, has an increased risk of developing type II DM.

Diagnostic Tests

Fasting Plasma Glucose Test (FPG) o Confirmed by repeat testing on another day

o When over symptoms of hyperglycemia (polyuria, polydipsia, and poylphagia) co-exist

o Normal: 70 to 100 mg/dl

o 100 – 125 mg/dl pre-diabetic stage (check BS q 3 mos)

o Glucose level exceeding 126mg/dl (7.0 mmol/L) Signals diabetes

o DM: a 140mg/dl for 2 readings

Random or casual Plasma Glucose Measurement

o Measurement exceeding 200mg/dl (11.1 mmol/L) plus manifestation of diabetes

o Casual is defined as any time of day without regard to the time of the last meal.

Two-Hour OGTT (Oral Glucose Tolerance Test)

o Non-pregnant = 75gms. oTest for 2 hours after glucose rich drink after

FBS

oNormal: less than 140 mg/dl

o140 – 199 mg/dl – pre-diabetic stage

o 200 mg/dl signals diabetes

oDone in out-patient basis

o Important: (no stress; regular diet)

1 hour, 2 hour, 3 hour OGTTo Done when results of FBS/2 hour

PPBS are borderline (high normal)

HgbA1c – Glycohemoglobin or glycosylated hemoglobin

o Normal fasting blood sugar after 120 days; because sugar is attached to RBC

Most accurate Normal (7 and below)

Type I Diabetics will typically have hemoglobin A1C determined every 3 to 4 months.

Type II Diabetics will often require measurements less often (twice a year)

o HgbA1Co Normal : less than 6.5 %o Excellent: 6.5 – 7.5 %

o Good: 7.5 – 8.5 %o Fair: 8.5 – 9.5 %o Poor: Greater than 9.5 %

Acute Complications of Diabetes Mellitus

Diabetic Ketoacidosis (DKA, Type 1)

Hyperglycemia

Causes: infections overeating underdose of insulin stress surgery

Assessment: 3 P’s Cardinal signs of DM

Polyuria Polydipsia Polyphagia

Warm, flushed dry skin Soft eyeballs Tachycardia Nausea and vomiting Abdominal pain Kussmaul’s breathing (deep rapid

breathing) Fruity odor of breath Urine (+) CHO

Ketones ketonuria

Altered LOC

Above normal glucose levelHyperkalemia initially then becomes hypokalemiaMetabolic acidosisHyponatremia

Management: Patent airway Oxygen therapy NSS+ regular insulin/ IV D10 W once CHO reaches 250

mg/dl KCl/ slow IV drip, once urine output

is adequate Monitor bld sugar Patient teaching:

Causes Signs and symptoms Prevention Management

Hypoglycemia( INSULIN SHOCK)

Causes: Omission of meals Overdose of insulin Strenuous exercise G.I upset

Assessment Restlessness Hunger pangs Yawning Weakness Tremors Pallor Diaphoresis Cold, clammy skin Headache Dizziness Faintness Tachycardia Abdominal pain Blurred vision Slurred speech Urine (-) CHO

No ketonuria Altered LOC

Management:

Simple sugars per orem 3 -4 oz regular softdrink 8 oz fruit juice 5-7 pcs. Lifesaver’s candies 3- 4 pcs hard candies 1 tbsp sugar 5 mls pure honey/ Karo syrup 10-15 grams CHO

D5050 (D50W) 20-50 ml/ IV pushMonitor bld sugarPatient teachingCauseS and sxPreventionManagement

Hyperosmolar Hyperglycemic Nonketotic syndrome

o Slightly rapid respirationo No breath odoro Markley elevated bld glucose levelo Hypernatremia o Negative ketonemia, traces onlyo Normal Serum Potassium o Lacks metabolic acidosis

Chronic Complications of Diabetes Mellitus

Diabetic Retinopathy

Diabetic Nephropathy

Neuropathy

Complications of the foot and lower extremity

Integumentary complications

Infection

Amputation due to prolong wound healing

Peripheral vascular disease

Heart disease

Neurogenic bladder

Renal failure/ nephropathy

Decrease libido

Impotence

Clinical Impact of diabetes Mellitus The leading cause of new case of end stage

renal disease

A 2 to 4 fold increase in cardiovascular risk /disease

Leading cause of new cases of blindness in working-aged adults

The leading cause of non-traumatic lower extremity amputations

Brain is ischemic stroke

Nurisng Mngt of DM:Diet, drugs, exercise, Education

NURSING INTERVENTIONS for DM

Nursing management for DM IIAssessment

Evidence of polyuria, polydipsia, polyphagia

Current weight and head –to-toe assessment

Blood glucose level before each meal and at bedtime

Any ketones or albumin in the urine

Monitor urine for keotnes if the patients is ill or if glucose is above 240 mg/100ml

Observe for hypoglycemia caused by over treatment of insulin

Review BG diaries for level of control and need for insulin adjustment.

Obtain a complete, medical, drug and allergy history, including symptoms and duration.

Determine when the client was diagnosed with diabetes and if others in the family are also diabetic.

If patients are diabetic, ask the client to identify prescribed treatment regimen and when intake of food and self-administered drugs last.

Serum electrolyte, cholesterol, lipid, triglycerides, BUN and creatinine

Look for physical changes associated with diabetes

o V/S especially BP in lying, sitting and standing positions, peripheral pulses, temperature of the extremities, inspection of extremities for edema or changes in color.

Monitor of potential cerebral edema when fluid replacement is initiated for DKA.

Weight daily while patient is on IVF replacement.

Monitor for tachycardia with DHN and related to K imbalances.

Monitor insulin injection sites o Watch for signs of

lipohypertrophy (localized tissue buildup from giving injections in the same site)

o Observe for signs of irritation; avoid injection site for several weeks if these occur.

o Observe skin for signs of hypersensitivity reactions to insulin and notify doctor immediately

o Changes in the skin over insulin injection sites, impaired skin areas that appear to be healing poorly; ulcerations or evidence of skin or soft-tissue infection.

o Visual acuity and last date of ophtlamic examination

Decreased visual acuity and visual changes such as blurred vision

o Muscle atrophy, weakness, or loss of sensation

Nursing Interventions

Infective Therapeutic regimen Management1. Assess current level of knowledge related to disease

process.

2. Describe the disease process and treatment recommendations

3. Discuss the lifestyle changes that may be required to control the disease process

4. Describe possible chronic complications

5. Plan individualized exercise program with the patient.

6. Review steps to prevent hyperglycemia and hypoglycemia

7. Review insulin administration (if used); have patient give return demonstration of insulin injection.

Fatigue1. Assist the patient in assigning priority to

activities to accommodate energy levels.

2. Monitor for signs and symptoms of hyperglycemia: polyuria, polydipsia, polyphagia, weakness, lethargy, malaise, blurring of vision or headache.

3. Anticipate situations in which insulin requirements will increase (e.g. time of stress, illness)

4. Facilitate diet and exercise regiment

5. Restrict exercise if blood glucose levels are >250 mg/dl

Risk for Infection1. Observe extremities for color, warmth,

swelling, pulses, texture, edema and ulcerations.

2. monitor skin for excessive dryness and moistness

3. Promote sufficient nutritional intake

4. Encourage fluid intake

5. Increase fiber in diet (inhibits glucose absorption in the intestines), complex CHO and complex sugar (in vegetables and fruits)

6. Encourage rest periods

7. Encourage increased mobility and exercise

8. Teach patient and family about signs and symptoms of infection And ask for return demonstration) and when to report them to health care provider

Supportive care: administer IVF as ordered during periods

of DHN from vomiting and diuresis

Management of Diabetes

Diet/Nutrition Exercise Education Medication (OHA/ insulin injection)

Goals of Diabetes management Gylcemia – A1C <7% ADA; <6.5% AACE Hypertension: <130/80 mm Hg Dyslipidemia

o LDL: <100 mg/dl (<70 mg/dl in very high risk)

o HDL: men >45 mg/dl; women 55>mg/dl

o Triglycerides: <150 mg/dl

Prothrombotic State – ASA Rx (81 – 325 mg/day)

o People with dm + CVDo People >40 years of age with DM

+> other CV risk factor

Cigarette Smoking – cessation

Management of Diabetes Education must be synonymous and

simultaneousA. Monitoring

Blood glucose Glycosylated hemoglobin

B. Primary treatment Overall goals; near normal

BG, optimal lipid level, maintain reasonable weight, prevent chronic complications

1. Diet and weight control 2. Hypoglycemic agents (OHA)

ABC’s of diabetes

ABC’s of DM should be the #1 goal of all diabetics

A for A1C: your A1C checks tell you the average blood glucose levels for the past 2 or 3 months. It’s the blood check with a memory

Goal: less than 7%

Bis for blood pressure: when blood pressure is high, your heart has to work harder.

Target BP = less than 130/80 mm Hg

Cis for cholesterol: your cholesterol levels tells the amount of fat in the blood

A. HDL Cholesterol, help protect your heart

B. LDL cholesterol, can clog your blood vessels and lead to heart disease

C. Triglyceride are another kind of blood fat that raises risk for stroke and MI

D. Target LDL – less than 100 Triglyceride – less than 150 HDL – less than 40

ABC’s of Diabetes Proper daily management of keeping blood glucose near

normal levels can significantly lower the risk and progression of eye, kidney, nerve and cardiovascular complications and improve over all quality of life.

Weight control is a very important factor in diabetes management

A 10 – 15 pound loss can help reach blood pressure, blood glucose and cholesterol goals.

Effective diabetes management usually includes drug therapy tighter with lifestyle changes, such as regular physical activity, a healthy diet and dietary supplementation with an effective product.

Subcutaneous Injections of Insulin Develop a systematic plan for giving insulin

injection S.C. about 1 inch (2.5 cm) apart. o ARMS. Begin below the deltoid

muscle and end 1 handbreadth above the elbow, Begin at the midline and progress outward laterally, using the external surface only.

Nursing Responsibilities in Insulin Therapy

Route: Subcutaneous- slow absorption

less painful IV- DKA (an emergency) SC- 90 degree thin 3/8” , obese: 1/2”, 5/8” Do not massage site of injection

Administer insulin at room temperature Cold insulin lipodystrophy

Rotate the site of injection To prevent lipodystrophy. Lipodystrophy

inhibits insulin absorption

Store vial of insulin in current use at room temperature

Other vials should be refirgertaed

Gently roll vial in between the palms to redistribute insulin particles

DO NOT shake; bubule make it difficult to aspirate exact amount

Observe for side-effects:Localized: Induration or redness Swelling Lesion at the site Lipodystrophy

Generalized:

Edema Sudden resolution of Hyperglycemia retention of

water Hypoglycemia Somogyi phenomenon

Prolonged Doses of insulin

therapy s. CHO levels Stress responses

are triggered Counterregulatory hormones are secreted

(EPI, NE,GLucocorticoid)

REBOUND HYPERGLYCEMIA

Dawn’s Phenomenon NOrmoglycemia during the night 12mn- 3am

GH secretion

Hyperglycemia 6-8 am

INSULIN Therapy

Onset: how long it takes for the insulin to start

lowering blood glucose?

Peak time: time after injection when the insulin is the most

effective at lowering blood glucose

Duration: how long the insulin keeps lowering blood

glucose?

FOUR Main Types of INSULIN available

Rapid-acting= clear insulinRegular Intermediate acting-cloudyLong-acting- cloudy

There are also pre-mixed insulins

The intermediate acting insulin with regular insulin and are convenient for people who need to use both

Generic Name/Brand name

Onset Peak Duration

Rapid actingHumalog (Liepro)

<15min

1-2 hrs

3-4 hrs

Novolog <15 min

1-2 hrs

3-4 hrs

Apidra <15min

1-2 hrs

3-4 hrs

RegularHumulin R ½ hr 2-3

hrs3-6 hrs

Novolin R ½ hr 2-3 hrs

3-6 hrs

Intermediate acting (NPH)Humulin N 2-4 hrs 4-10

hrs10-16 hrs

Novolin N 2-4 hrs 4-10 hrs

10-16 hrs

Long actingUltraLente 2 hrs 16-

20hrs24 hrs

Long acting analogGlargine (Lantus)

1 hr No peak

20-24 hrs

Detemir (Levemir)

¾ hr 6-8 hrs (minimal peak action)

Up to 24 hrs

Intermediate actingNPH or Lente 2 hrs 6-8

hrs12-16 hrs

Long acting 2 hrs 16-20 hrs

24+ hrs

MIXTURENPH 70 U & regular 30 U

½ hr 4-8 hrs

24 hrs

NPH 50 U & regular 50 U

1/2 4-8 24

UltraLente(injected 15 mins after meal)

Glargine (Lantus)Should not be given with pregnantNot be mix with other insulin

Follow these 2 rules for proper site rotation Same general location at the same

time each day Rotate within each injection site

Bleeding at the Injection Site do not rub the spot maintain light pressure with your finger to

prevent bruising if a bruise does appear don’t use that injection

site again until the bruise is gone

Insulin Injection sitedeltoidOuter armAbdomenHip areaThighButtocks

Abdomen with exception of a circle with 2 inches below the navel

Keep insulin at room temperaturePut a label when the insulin is openAdverse reaction: rashes, itchiness

Where should you inject? you can inject insulin in the several places on

your body insulin injected near the stomach works fastest insulin injected into the thigh works slowest works medium on the arm

How to store?1. use the whole bottle for 30 days2. if don’t use the whole bottle refrigerate all of the time3. don’t keep insulin in the freezer4. keep at least extra bottle

TIPS administering insulin NPH

Should not be mix with Lente insulin

When rapid-acting insulin is mixed with either an intermediate or long-acting insulin, the mixture should be injected within 15 mins before a meal

Rapid-acting insulin can be mixed with NPH, lente and ultra-lente

Syringes and Needles Some people reuse the syringe It is also wise not to use alcohol

to clean the used needle Never share syringe Check your bld glucose 1 to 2

hrs after your injection, or sooner if s/sx of hypoglycemia

Discard needle if it is noticeably dull

If reused store at room temperature; do not refrigerate

Side-Effects and Cautions

Induce hypoglycemia as a result of intermittent excesses in insulin production and release.

Can induce weight gain, mainly as a result of edema and reduction of the osmotic diuresis caused by hyperglycemia

Other side-effects are: abdominal upset, headache and hypersensitivity reactions.

Sulfonylureas are potentially teratogenic impairment of liver or kidney function increase the risk of hypoglycemia, and are contraindications.

Contra indication: impaired liver and kidney function

Oral Hypoglycemic

How hypoglycemics drug works? act as endogenous insulin

stimulate pancreas to produce more insulin

prevent liver from manufacturing glucose from glucagon

stimulate muscle uptake of glucose

inhibit breakdown of foods to simple sugar in out delaying absorption

Oral hypoglycemia

1.BiguanidesMechanism of actionIn hyperinsulinemia, biguanides can lower fasting levels of insulin in plasma

Prevent liver from manufacturing glucose from glycogen

Therapeutic uses may be derive from their tendency to reduce gluconeogenesis in the liver and as a result, reduces the level of glucose in the bld, tends to make the cell of the body more willing to absorb glucose already present in the blood stream, and there again reducing the level of glucose in the plasma.

metformin (Glucophage)

Available: 500 mg, 800 mg, 1000 mg

first line drug of choice for DM, treatment of type 2 Diabetes particularly in overweight and obese people and those with normal kidney fx

evidence suggest it may be the bets choice for people with heart failure

does not induce hypoglycemia (when taken alone) mechanism: reduce

gluconeogenesis it makes the cell more

willing to absorb glucose

SE: hyperactivity, diarrhea, dyspepsia, (occurring 30%) lactic acidosis

2. SUlfonylureasActs by increasing insulin release from the beta cells in the pancreas First generation Second GenerationAcetohexamideChlorpropamideTolbutamideTolazamide

GlipizideGlictazideGlibendamide (glyburide)Gliquidone

Third Generation GlimepirideDisadvantageIneffective where there is absolute deficiency of insulin production such as in type 1 Diabetes or past pancreatectomy

Side EffectsWeight gain, mainly as a result of edema and reduction of the osmotic diuresis caused by hyperglycemiaOther S.E Abdominal upsetHeadache, hypersensitivity reactions

Side EffectsInduce hypoglycemia(As a result of intermittent excesses in insulin production and release)

Sulfonylureas

Caution potentially teratogenic

Increase the risk of hypoglycemia

impairment of the liver and kidney fx

Contraindicated with:Impaired liver and kidney fx Pregnant women3. ThiazolidinedionesThese drugs work buy sensitizing muscle and fat cells to accept insulin more readilyActos (pioglitazone) and Avandia (rosiglitazone) are the only two thiazolidinediones marketed today.

4. Alpha- Glucosidase Inhibitors

Glyset (miglitol) and Precose (acarbose) –two most prescribed alpha-glycosidase inhibitors (aka “starch blockers”)

These medications need to be taken at the beginning of each meal so that they can work to slow digestion, which in turn slows the rise of glucose in the blood

Often prescribed in conjunction with other diabetes medications May cause diarrhea or gas.

5. Meglitinides Similar to the alpha-glucosidase inhibitors in that they

are taken before each meal

Stimulate the pancreas to produce more insulin in relationship to how much glucose is in the blood

Brand names are Prandin (repaglinide) and Starlix (nateglinide)

Can be used in combination with some other oral medications for increased effectiveness.

DPP-4 Inhibitors New oral medication called

Januvia (sitagliptin phosphate) has been approved by the FDA for management of type 2 diabetes.

Januvia lowers blood sugar levels by blocking an enzyme knows as dipeptidyl peptides IV or DPP-4

Prescribed for type 2 diabetes only

Does not need to be taken with a meal

Side effects include upper respiratory infection, sore throat and headache

Januvia is processed through the kidneys,

Renal function should be assessed before taking Januvia

Pulmonary Insulin Exubera 300-400 “u” of insulin;

only 10%a is absorb but very effective

Diabetic Food Pyramid

Diet Consult with dietician to provide energy

needs of the patient o Low caloric diet specially if obese

20% CHON, 30% HCHO, 50% CHO

High Fiber diet- inhibits glucose absorption in the intestines

Complex carbohydrates

o 3 Meals, 2 snacks (AM/PM snacks) 5x/day (small meals,

frequent)

o More vegetable in the diet 1 cup of vegetable =16 cal.

(more than half of the plate)

3 fruits/day (3 servings only) e.g. 1 small apple, 1 small orange, 1 slice of mango.

Artificial Sweeteners are allowed (at least 5 sachets a day)

o Equalo Splendao Sweet and Low (Saccharin) should

not be given with pregnant women or even with PKU

Sticking to a meal plan and eating well-balanced meals leads to better diabetes management . there are several benefits:

o Weight controlo Meeting nutritional needso Control of blood glucose levelso Lowering high blood pressureo Reducing cholesterol levels

Exercise Exercise has a number of benefits – both for

you and your overall health. You’ll not only control your weight and lower your blood sugar level, but you’ll also feel better about yourself. And there are even more advantages of keeping fit:

Benefits: Increased energy Control cholesterol Decrease Weight management Self control

After obtaining a complete medical check-up, talk to your doctor about what kinds of activities is right for you. This is especially important if you:

o Are over 35 y/oo Have had diabetes for more than ten

yearso Have had any complications of

diabeteso Have heart disease or are at high

risk for ito Have proliferative diabetic

retinopathy

o Haven’t’ exercised in a long time.

Plan active weekends. Skip the elevator and take the stairs

Park at the far end of the parking lot and walk to the office or store

Walk a few blocks before getting on your bus, and get off a few blocks before your stop

Take a break from your desk to stretch and go for a walk.

Before lunch, go for a brisk 10-minute walk

Get outdoors – rake your leaves, was your car, push a lawn mower.

Increase uptake of glucose by the cells Decrease insulin requirements Allows additional sources of CHO (snacks) Maintain IBW, serum CHO, and serum lipids

Done 1 -2 hours pc to prevent hypoglycemia

Regular pattern, rather than sporadic – to maintain stable serum CHO levels.

Try to avoid immediately exercising the part of your body where you have injected insulin. For example, don’t’ inject into your leg just before bicycling, or into your arm just before a game of tennis, or into your abdomen before doing sit-ups.

Normal and target blood glucose ranges Normal blood glucose levels in people who do not have diabetes

Upon waking (fasting)- 70 – 110

After Meals – 70- 140 

Target blood glucose levels in people who have diabetes

Before meals – 90 – 130

1 to 2 hours after the start of a meal – less than 180

Hypoglycemia (low blood glucose) – 70 or below

Pathophysiology

Lack of insulin staying in the

plasma

Glucose is unable to enter fat or muscle

cells

Polyphagia (increase appetite)

Liver release Glucose

Increased Blood Sugar

(Hyperglycemia)

Glycosuria

Increased Osmotic Pressure

Polyuria

As more and more water is lost from the blood stream into the urine, water is drawn from the cells. Dehydration results and the person feel thirsty

Polyuria DHN Thirst (Polydipsia)

The Glucose is in the wrong place because insulin is not available to help glucose enter fat and muscle cells. Cells still need fuel for energy and the body begins to breakdown CHON and fat to be used as energy

Increased CHON

breakdown for energy

Muscle Wasting

Weakness Weight Loss

Fat stores used for energy

Increased fatty acids

Ketonemia

Kidney Lungs

Ketonuria Acetone Breath

Acidosis Coma

Kussmaul Breathing

Simplified

Lack of Insulin

Glucose unable to enter fat and

muscle cells

Abnormally increased appetite (polypahgia)

Hyperglycemia Glycosuria Polyuria DHNThirst

Coma

Body CHON used for Energy

Body Wasting

Weakness

Weight Loss

Stored Fat used for energy Ketonemia Acidosis

Coma

Kusmaul’s Breathing

Ketonuria