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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
15
16
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
23
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
24
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
29
33
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.
34
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
37
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
38
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 !!
39
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
40
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
45
COMPLICATIONS OF HHS:
•Cerebral infarct & MI
•Mesenteric thrombosis
•Pulmonary embolism
•DIC
•Cerebral edema
•CHF
•ARDS
•rhabdomyolysis
TEACHING OPPORTUNITY
Nutrition management
Exercise
Exams
48
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
49
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
50
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
51
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
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