DIABETES/BILIARY

MCC NURSING

Diana Blum MSN

DEFINITION

Disorder of carbohydrate, protein, and fat

metabolism resulting from an imbalance between

insulin availability and need.

Group of metabolic diseases characterized by

increased levels of glucose in the blood

(hyperglycemia) resulting from defects in insulin

secretion, insulin action, or both

STATISTICS

•Third leading cause of death

•Becoming more common

•285 million people globally currently have– 1/3 of which are undiagnosed

•By 2030 it will exceed 438 million

•More elderly have (ages 65-74)

•Prevalent in Caucasians, African Americans, Native Americans, and

Hispanics

•Leading cause of :– Non traumatic amputations, blindness, and ESRD

WHY IS THIS HAPPENING?

_________

_________

__________

__________

WHAT ARE THE RISK FACTORS?

INSULINHORMONE

•Anabolic Hormone produced by beta cells in the islets of

Langerhans in the pancreas

•Transports and metabolizes glucose for energy

•Signals the liver to stop the release of glucose

•Prevents fat and glycogen breakdown– Enhances dietary fat storage in adipose

•Increases protein synthesis

•Controls level of glucose in blood – Regulates production of – Regulates storage of glucagon

DIABETES

Cells stop responding to insulin

Pancreas may stop producing

Both lead to Hyperglycemia and complications like

DKA and HHNS

DIABETES

PREDIABETES

Normal glucose metabolism

Obesity

Previous personal history of hyperglycemia

TYPE 1: JUVENILE

Insulin dependent(natural

level low or absent)

Autoimmune process that

destroys beta cells of the

pancreas

Genetics play role

May be triggered by virus

or toxins

TYPE 2

Non insulin dependent

Diabetes Pancreas retains some

function but resistance to insulin is a major cause Insulin becomes less

effective at stimulating glucose uptake by tissues and regulating glucose release by liver

Genetics may play role Obesity also plays a

role

Usually onset after 30

Can take oral nasal or sq

insulin

GESTATIONAL

Glucose intolerance

associated with

pregnancy 2-10% women

annually

Related to secretion of

placental hormones

which cause insulin

resistance

At risk: obese, history of

gestational diabetes,

glycosuria, stillbirth or

abortion, and fam history

TX: diet modifications,

insulin

WHAT IS THE OVERALL GOAL?

CHRONIC COMPLICATIONS TO DIABETES

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NEPHROPATHY

SIGNS AND SYMPTOMS

•3 P’s} polyuria, polydipsia, polyphagia

•Fatigue

•Weakness

•Sudden vision changes

•Tingling/numbness of hands or feet

•Dry skin

•Slow to heal wounds

•Recurrent infections

DIAGNOSIS CRITERIA

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AMERICAN DIABETES ASSOCIATION GLYCEMIC

GOALS:

HbA1C goal: <7 % (6% is upper limit for normal) without signif. HypoglycemiaPreprandial glucose: 90-130 mg/dLPostprandial (peak 11/2 hour) 180 mg/dL50% of the blood glucose values within target (70 to 140 mg/dL)No more than 30% of readings above 200 No more than 1 or 2 mild hypoglycemic episodes per 1 to 2 weeks

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ADA GLYCEMIC GOALS (CONTINUED) :LDL <100 mg/dL

Triglycerides <150 mg/dLHDL >40 for males, >50 for femalesBlood pressure: <130/80 with no signs of orthostatic hypotensionMinimal to no peripheral edemaUrinary albumin excretion <30Retention of recognition of hypoglycemia

Insulin• What is it’s most serious side

effect?_______• What can affect the

absorption of Insulin? a. _____________ b.______________ c.______________ d.______________

Insulin is inactivated by,

insulinase, an enzyme in the

liver.

MEDS

InfectionWt gainPubertyInactivityHyperthyroidism

Exercise

Renal Failure

Weight Loss

Adrenal Insufficiency

NEEDS FOR INSULIN

Increases Needs Decreases Needs

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ORAL HYPOGLYCEMIC AGENTS:NEVER GIVEN TO TYPE I

First modify diet, exercise

Second modify diet, exercise, hypoglycemic

agents

Third: Insulin added to treatment as B-cells have declined over

time

HOWEVER, those that respond BEST to oral agents are >40

years and have had diabetes Type II less than 5 years.

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O R A L H Y P O G LY C E M I C A G E N T SN E V E R G I V E N T O P R E G N A N T W O M E N A S

C A N D E P L E T E I N S U L I N F R O M T H E F E TA L PA N C R E A S

1. Sulfonylureas: promote insulin release from Bcells tolbutamide glyburide glipizide gluimepirideAdverse effects: wt gain, hyperinsulinemia, hypoglycemia NOT to be admin. To those with hepatic/renal insufficiency as causes delayed excretion resulting in hypoglycemia

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2. Meglitinide “postprandial glucose regulator” repaglinide nateglinideWork like sulfonylurea but rapid onset and short durationVery effective in early release of insulin following a mealVery effective with metformin Take 1 to 30 minutes ACCaution with hepatic impairmentCauses wt gainHypoglycemia a factor but less than sulfonylureas

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O R A L H Y P O G LY C E M I C A G E N T S :I N S U L I N S E N S I T I Z E R S

Biguanides

METFORMIN (increases glucose uptake thereby

decreasing insulin resistance)

Does NOT promote Insulin secretion

hypoglycemia is way less than sulfonylureas (only

occurs if caloric intake not enough)

IT CAN REDUCE HYPERLIPIDEMIA

THE ONLY ORAL AGENT PROVEN TO DECREASE CV

MORTALITY !!

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Metformin:

- pt usually loses wt due to loss of appetite

- needs to be discontinued for pt needing IV

contrast for diagnostic study

- should not be used with pts on heart failure

meds causes increased risk of lactic acidosis

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O R A L H Y P O G LYC E M I C A G E N T S :Α - G LU C O S D A S E I N H I B I T O R S

- take at beginning of the meal- delays digestion of carbohydrates thereby decreasing glucose absorption Acarbose Miglitol - do not stimulate insulin release - do not cause hypoglycemiaMajor side effects: - flatulence, diarrhea, abd crampingDO NOT USE WITH PT WITH INFLAMMATORY BOWEL DISEASE, COLONIC ULCERATION, INTESTINAL OBSTUCTION

DAWN PHENOMENON:

early-morning

hyperglycemia caused by

decreased effectiveness of insulin

& increased secretion of growth

hormone & other hormones

overnight.

What can be changed in the insulin

dosing to prevent this??

COMPLICATIONS

Somogyi Effect• Hypoglycemia

occurs in the middle of the nite

• Glucose is released from liver

• Sugar level increases while sleeping.

• Pg 1681

ACUTE COMPLICATIONS

Diabetic Ketoacidosis (DKA): - hyperglycemia induced crisis - precipitated by stress, infections, MI trauma, alcohol, dehydration, electrolyte loss

- non-compliance - S/S: abd pain, vomiting, Kussmaul respirations, acetone breath, - severely dehydrated - may be alert, lethargic, comatose TREATMENT: fluids, K+, regular Insulin, treatment of cause, ICU

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Hyperosmolar Hyperglycemic State (HHS)nonketotic - less common than DKA - insulin level is too low to prevent hyperglycemia but high enough to prevent fat breakdown - Profound dehydration - mental status changes, hyperosmolarity, - extreme hyperglycemia (>600 mg/dL) - no ketoacidosis -precipitated by: acute stress (dehydration, infections) OFTEN FATAL -hypotension, tachycardia, seizuresDX: BMP, CBC, ABG

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COMPLICATIONS OF HHS:

•Cerebral infarct & MI

•Mesenteric thrombosis

•Pulmonary embolism

•DIC

•Cerebral edema

•CHF

•ARDS

•rhabdomyolysis

TEACHING OPPORTUNITY

Nutrition management

Exercise

Exams

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P R O B L E M S W I T H E X E R C I S E F O R D I A B E T I C S :

Screen for retinopathy first since strenuous exercise may

precipitate vitreous hemorrhage or retinal detachment

Pts with eye involvement must avoid physical activity that

involves straining, jarring, valsalva-like maneuvers

Those with CVD, >35 yrs, autonomic neuropathy, PVD,

microvascular disease need cardiovascular evaluation and stress

test before exercise program

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EXERCISE (CONTINUED)Repetitive exercises on insensitive feet will cause ulcerations

NO to treadmill, jogging, prolonged walking, step exercise

Recommend: swimming, bicycling, rowing, chair exercises, arm

exercises, other non-wt-bearing

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EXERCISE (CONTINUED)Aerobic activity: - swim, walk, run as this promotes utilization of glucose as the fuel, desirable for CV health, hypertension, lipid profiles, circulation, wt loss Recommended: - 150 minutes/week of moderate (50 to 70 % of max heart rate) - 90 min/week of vigorous (70% of max heart rate)EXERCISE 3 days/week with no more than 2 consecutive days without exercise

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Anaerobic activity:

- wt lifting (avoided) unless approved by

cardiologist and ophthalmologist

- if approved:

- 3x/week, targeting all major muscle

groups

ELECTROLYTE MANAGEMENT

Phosphate is not recommended to be replaced

Calcium and Magnesium may be

Potassium shifts from intracellular to extracellular

placing them at risk for ____?

_HYPOKALEMIA_.

Bicarb is only replaced in life threatening

situations( acidosis <6.9)

•HYPOGLYCEMIA/INSULIN SHOCK

•1) The person will be sweating, clammy,

pale, trembling and feel weak.

•2) Ask the person what he needs and get it

for him or her.

•3) Feed the person a quickly absorbed

sugar such as fruit juice, honey or a soft

drink. Do not attempt to feed a person who

has lost consciousness.

W H AT D O Y O U D O I F T H E YB E C O M E U N C O N S C I O U S B E F O R E A B L E

T O F E E D A C A R B / J U I C E , E T C. ?

•Dextrose 50% 

•(D 50)

•25gm/50ml - 1 ampule 

•  Usual Dose:  1 amp Action:  Provides

glucose calories for metabolic needs

Indications:  Hypoglycemia, Use with

insulin for hyperkalemia Precautions: 

Monitor blood glucose, can cause

thrombosis in small veins. 

BILIARY TRACT

ASSESSMENT Present illness: digestive disturbance, pain, meals,

aggravating and relieving factors

PMH: GB dx, pregnancy, surgery, meds

Fam Hx: GB dx

System: pruritis, indigestion, fat intolerance,

dyspepsia, n/v, light colored stools, dark urine

HEPATITIS

JAUNDICE

Hepatitis A(HAV)

Hepatitis B

(HBV)

Hepatitis C(HCV)

Hepatitis D(HDV)

Hepatitis E(HEV)

What is it? HAV is a virus that causes inflammation of the liver. It does not lead to chronic disease.

HBV is a virus that causes inflammation of the liver. The virus can cause liver cell damage, leading to cirrhosis (scarring of the liver) and cancer.

HCV is a virus that causes inflammation of the liver. This infection can lead to cirrhosis and cancer.

HDV is a virus that causes inflammation of the liver. It only infects people with HBV.

HEV is a virus that causes inflammation of the liver. It is rare in the United States. There is no chronic state.

Incubation period 15 to 50 days. Average 30 days.

45 to 160 days. Average 120 days.

2 to 25 weeks. Average 7 to 9 weeks.

2 to 8 weeks.

2 to 9 weeks. Average 40 days.

How is it spread? Transmitted by fecal/oral route, through close person-to-person contact or ingestion of contaminated food and water.

Contact with infected blood, seminal fluid, vaginal secretions, contaminated needles, including tattoo/body piercing tools. Infected mother to newborn. Human bite. Sexual contact.

Contact with infected blood, contaminated IV needles, razors and tattoo/body piercing tools. Infected mother to newborn. NOT easily spread through sex.

Contact with infected blood, contaminated needles. Sexual contact with HDV-infected person.

Transmitted through fecal/oral route. Outbreaks associated with contaminated water supply in other countries.

Hepatitis A(HAV)

Hepatitis B

(HBV)

Hepatitis C(HCV)

Hepatitis D(HDV)

Hepatitis A(HAV)

Hepatitis B

(HBV)

Hepatitis C(HCV)

Hepatitis D(HDV)

Symptoms

May have none. Adults may have light stools, dark urine, fatigue, fever and jaundice (yellowing of the skin).

May have none. Some people have mild flu-like symptoms, dark urine, light stools, jaundice, fatigue and fever.

Even fewer acute cases seen than any other hepatitis. Otherwise same as HBV.

Same as HBV. Same as HBV.

Treatment of chronic disease

No specific treatment.

Interferon and anti-virals.

Interferon (peginteferon) along with the antiviral ribavirin.

Interferon. Supportive.

Who is at risk? Household or sexual contact with an infected person or living in an area with HAV outbreak. Travelers to developing countries, men who have sex with men and IV and non-IV drug users.

Infant born to infected mother, having sex with infected person or multiple partners, IV drug users, emergency responders, health care workers, men who have sex with men, household contacts of chronically infected persons and dialysis patients.

Anyone who had a blood transfusion or organ transplant before 1992, health care workers, IV drug users, dialysis patients, infants born to infected mother and having multiple sex partners.

IV drug users, men who have sex with men, dialysis patients, healthcare workers, infants born to infected mothers and those having sex with a HDV infected person.

Travelers to developing countries, especially pregnant women.

Hepatitis A(HAV)

Hepatitis B

(HBV)

Hepatitis C(HCV)

Hepatitis D(HDV)

Prevention Get a hepatitis A vaccine.

Take immune globulin within two weeks of exposure.

Wash hands with soap and water after going to the toilet.

Use household bleach to clean surfaces contaminated with feces, such as changing tables.

Practice safe sex.

Get a hepatitis B vaccine.

Take immune globulin within two weeks of exposure.

Practice safe sex.

Clean up infected blood with bleach and wear protective gloves.

Don't share razors, toothbrushes or needles.

Don't inject street drugs.

Don't get a tattoo or body piercing.

Practice safe sex.

Clean up spilled blood with bleach. Wear gloves when touching blood.

Don't share razors or toothbrushes.

Don't inject street drugs.

Don't get a tattoo or body piercing.

Get a hepatitis B vaccine to prevent HBV infection.

Practice safe sex.

Avoid drinking or using potentially contaminated water.

Wash your hands with soap and water after going to the toilet.

Hepatitis A(HAV)

Hepatitis B(HBV)

Hepatitis C(HCV)

Hepatitis D(HDV)

CIRRHOSIS

12th leading cause of death

Irreversible

Causes: hepatitis, rt heart failure, ETOH

Alcohol is most common in USA

S/S: gradual, fatigue, weakness, anorexia, wt loss,

VIT D deficiency

PORTAL HTN

Result of scarring of liver

Normal is 3mmHG increases to 10mmHG

Portal veins carry blood from GI tract

Causes varices or thin walled veins being prone to

rupture and ascites

CHOLELITHIASIS

Gallstones in biliary tract

If stone can’t pass it causes

obstruction

2 stone types: cholesterol and pigmented

s/s: fever, N/V, abd pain, right shoulder pain, back pain,

restlessness after meals, jaundice, pruritis, clay colored stools,

dark urine, deficiencies in vitamin A, E, D, K

Diagnostics: abd x-ray, US, MRI, FLP, ERCP,

TX: LAP- Chole, provide rest, IVF, NG Sxn, Antibx, low fat liquid

diet immediately after episode avoiding eggs, cream, pork, fried

foods, cheese, rich dressings, gas forming veggies, and alcohol.

BILIARY DYSKINESIA•Motility disorder of the GB

•Uncommon

•S/S: episodic epigastric or

RUQ pain, N/V

•Pain occurs after fatty meal

•Dx: serum bilirubin amylase,

lipase, AST, ALT,CBC

•Tx: surgery, low fat diet,

meds (ursodial or chenodiol),

lithotripsy, herbal goldenseal

ASSESSMENTPresent illness: general well being, digestive problems, painPMH: abd trauma, abd disorders, surgery, metabolic disorders, medsFAM HX: pancreatic disordersSystem: pruritis, resp distress, n/v, abd painFunctional: diet, ETOH useExam: restlessness, flushing, diaphoresis, low grade fever, tachycardia, tachypnea, hypotension, jaundice, dryness, scratches, abd distention, tenderness, hypoactive bowel tones, abd discoloration

PANCREATITIS

•Inflamed pancreas from activation of potent pancreatic enzymes within the pancreas, mainly trypsin

– Acute or chronic•Causes: ETOH, viral infections, peptic ulcer dx, cysts, renal fx, hyperparathyroidism, trauma, surgery, etc•S/S: abd pain, severe vomiting, flushing, cyanosis, dyspnea, low grade fever, tachycardia and tachypnea, hypotension, distended abd, absent bowel tones = ileus, shock

PANCREATIC CANCER

Spreads quickly• 75% are adenocarcinomas at

head of pancreas43920 new cases each yr in USA

• Many cases are men in 60sRisk factors: smoking, pancreatitis, high fat dietDx: Spiral CT is the most accurate toolS/S:pain, jaundice, liver enlargement, wt loss, glucose intolerance, anorexia, vomiting, weakness, diarrhea

• The most common sign is painless progressive jaundice

Tx: surgery, pain meds, tube feedings, post op radiation, chemoNSG DX: pain, fear, skin integrity, disturbed body image

THE END

Questions