Nfs 260 Exam 2

Front 1

Xerostomia

Back 1

-Dry mouth
-Dehydration--> provide more fluid
-Chemotherapy can influence salivary glands

Front 2

Dysgeusia

Back 2

-Distorted taste
*Can be caused by radiation therapy

Front 3

Ageusia

Back 3

-Inability to taste
*Can be caused by radiation therapy

Front 4

Diet modification for upper GI disease

Back 4

-Texture modification = soft, mechanized, blenderized, and liquid
-Liberal use of fluids
***Monitor oral intake by calorie count, observation, or food diary

Front 5

Phases of swallowing

Back 5

-Oral phase-chewing, formation of bolus, pushed by tongue to soft or hard palate
-Pharyngeal phase-closure of nasopharynx, protection of airways, pharyngeal peristalsis and relaxation
-Esophageal phase-passage of bolus through esophagus to stomach
**All three phases must be coordinated for success in swallowing

Front 6

Types of dysphagia

Back 6

-Neurogenic = Cerebrovascular accident, Traumatic brain injury, Neurodegenerative disease, myopathies
-Post-surgical = Anterior cervical spine surgery, Transhiatal esophagectomy, Laryngectomy
-Esophageal = GERD, Spasms, Fibrosis, Cancer, Strictures, Muscle degeneration

Front 7

One oral symptom of dysphagia can be...

Back 7

Lingual neuralgia or thrush

Front 8

Esophageal symptoms of dysphagia can be...

Back 8

-Reflux
-Bad breath
-Complaints of food (not liquid) sticking
-Discomfort at level of thyroid notch or sternum
-Swallowing difficulties are intermittent

Front 9

Dysphagia diets

Back 9

-NND-1 Dysphagia Pureed includes food of “pudding like consistency that are smooth or pureed with no lumps
-NND-2 Dysphagia Mechanically Altered includes moist and soft textured foods such as tender ground or finely diced meats, soft cooked vegetables, soft ripe or canned fruit, and some moistened cereals
-NND-3 Dysphagia Advanced includes most regular foods except very hard, sticky, or crunchy items.
***Thickened liquids are important- spoon thick, honey-like, nectar-like, and thin liquids

Front 10

Symptoms of GERD

Back 10

-Dysphagia
-Belching
-Increased salivation
-Pain,
-Heartburn
-Inflammation

Front 11

Gaviscon

Back 11

-Foam which protects the stomach to prevent reflux

Front 12

Antacids can...

Back 12

Increase LES pressure

Front 13

Prokinetics

Back 13

-Strengthens LES sphincter and makes the stomach empty faster [bethanechol (Urecholine), a cholinergic drug effecting the sympathetic nerves, metoclopramide (Reglan), a dopamine antagonist

Front 14

Causes of peptic ulcers

Back 14

-Helicobacter pylori
-Genetics = Excess pepsin, Increased parietal cell mass, Decreased secretion of mucus lining and buffers
-Nonsteroidal anti-inflammatory drugs (NSAIDs) = asprin (decreases mucus layer) and IB profuen
-Stress ulcers

Front 15

Nutrition care for peptic ulcers

Back 15

-Three moderate size meals per day vs several small meals
-Decrease consumption of spices, particularly red and black peppers when inflamed
-Increase intake of omega 3 and 6 fatty acids, which may be protective

Front 16

Drugs to help with peptic ulcers

Back 16

-Antibiotics = Flagy
-H2 blocker = Tagamet
-Cytoprotective agents = sucralfate (Carafate), synthetic prostaglandins protect mucosa

Front 17

Gastric surgery for peptic ulcers

Back 17

-Vagostomy = eliminates cholinergic simulation to reduce acid secretion (cuts vagus nerve)
-Vagotomy-Pyloroplasty = reduces acid and decreases control of peristalsis and gastric emptying (get rid of scar tissue and open pyloric sphincter)
-Billroth 1 = top half of stomach is reconnected to the duodenum
-Billroth 2 = top half of stomach is reconnected to the small bowel
-Gastric ByPass

Front 18

Post-gastrectomy diet

Back 18

-Fluids and foods withheld til GI function returns (given ice chips and water first)
-Low CHO liquids - broth, soup, unsweetened gelatin, diluted unsweetened juices, cooked cereals, or isotonic formulas or avoid clear liquids as first oral feeding and give one or two food items of protein, fat or complex CHO
-Progress to solid foods – easily cut or masticated meat, starches, and vegetables
-Highly spiced, fatty and hypertonic foods may not be well tolerated

Front 19

Early Dumping syndrome

Back 19

-Symptoms = abdominal fullness, nausea within 20 minutes of eating, flushing, rapid heart rate, faintness, sweating
-Cause = distension of small bowel due to shift in fluid from plasma into jejunum due to hypertonicity of food and decrease in peripheral vascular resistance and perhaps visceral pooling of blood.

Front 20

Intermediate dumping syndrom

Back 20

-Symptoms = abdominal bloating, increased flatulence, crampy abdominal pain, and diarrhea between 20 minutes and 1 hour after eating
-Cause = likely due to increased malabsorption of carbohydrates and other foodstuffs and the subsequent fermentation of the substrates entering the colon

Front 21

Late Dumping syndrome (Alimentary Hypoglycemia)

Back 21

-Symptoms = reactive hypoglycemia occurring 1-3 hours after a meal, perspiration, anxiety, weakness, shakiness, hunger, and difficulty concentrating.
-Cause = rapid digestion and absorption of food causes increased blood glucose which leads to exaggerated insulin levels and subsequent decline in blood glucose (hypoglycemia).

Front 22

Nutrition care for dumping syndrome

Back 22

-High protein, moderate fat foods with calories for weight maintenance. Complex CHO are included
-Fibrous foods slow upper GI transit and increase viscosity
-Lie down and avoid activity after meals
-Large amounts of liquids with meals may hasten GI transit but adequate fluids should be consumed in small amount throughout the day
-Use limited hypertonic, concentrated sweets
-Avoid lactose in milk and ice cream, cheese and yogurt may be tolerated

Front 23

Achalasia

Back 23

-Incomplete LES relaxation, increased LES tone, and lack of peristalsis of the esophagus (inability of smooth muscle to move food down the esophagus) in the absence of other explanations like cancer or fibrosis

Front 24

Dyspepsia

Back 24

-Chronic or recurrent pain in the upper abdomen, upper abdominal fullness and feeling full earlier than expected when eating

Front 25

Causes if GI malabsorption

Back 25

-Impairment of mechanical digestion
(Poor dentition or lack of dentures, Gastrectomy in individuals with PUD or cancer, Gastroparesis, Vagotomy of PUD)
-Impairment of chemical digestion
(Pancreatic disease)
-Impairment of solubilization
(Inadequate amount of bile salts)
-Decrease in absorptive surface area
-Impaired fatty acid esterification

Front 26

% and type of people lactose intolerant

Back 26

More that 90 percent of Africans and Asian-Americans are lactase deficient

Front 27

Normal patients excrete how much fat?

Back 27

less than 7 grams fat per day

Front 28

Clinical Manifestations of fat malabsorption

Back 28

-Failure to thrive, growth retardation, fatigue, especially in infants, children, and adolescents
-Calcium malabsorption resulting in bone pain, tetany, osteomalacia, and increased risk of fractures

Front 29

Vitamin deficiencies associated with fat malabsorption

Back 29

-Vitamin A: night blindness, hyperkeratosis
-Vitamin D: hypocalcemia, osteoporosis, osteomalacia
-Vitamin K: prolongation of prothrombin time, easy bruisability
-Vitamin E: hemolytic anemia, axonal degeneration

Front 30

Check for these antibodies to determine if someone has Celiac's disease

Back 30

-anti-tTg
-EMA

Front 31

Gluten

Back 31

-Peptide fractions of proteins found in wheat (glutenins and gliadin), rye (secalinus), and barley (hordeins).

Front 32

Celiac's can be associated with...

Back 32

-Dermatitis herpetiformis
-Muscle and joint pain
-Thyroiditis
-Type 1 diabetes

Front 33

Nutrition care for Celiac's

Back 33

-Consider use of omega-3 fatty acids
-Vitamin and mineral supplementation, especially vitamin D and calcium

Front 34

IBS

Back 34

Abdominal pain or discomfort that occurs in association with altered bowel habits over a period of at least 3 months.
***Can be either diarrheal, Constipation, or mixed forms

Front 35

What can happen if one goes off of the gluten free diet?

Back 35

-Other autoimmune complications can occur such as arthritis

Front 36

Nutrition care of IBS

Back 36

-Psyllium
-Probiotics
-Avoidance of gas producing foods

Front 37

Inflammatory Bowel Disease (IBD)

Back 37

-An autoimmune, chronic inflammatory condition of the gastrointestinal tract.
***Crohn’s Disease and Ulcerative Colitis

Front 38

Course of IBD

Back 38

-Remissions with exacerbations
-Progressive

Front 39

Drug therapy for IBD

Back 39

-Corticosteroids- anti-inflammatory
-Aminosalicylates- anti-inflammatory
-Immunosuppressants- cyclosporine, azathioprine
-Antibiotics- metronidazole
-Anti-TNF- infliximab

Front 40

Surgery for IBD

Back 40

-May be used to repair strictures or remove portions of diseased bowel.
-50-70% of people with Crohn’s disease undergo surgery.
-See recurring need for surgery
-20% of people with ulcerative colitis have a colectomy

Front 41

Vitamin/mineral deficiencies which may lead to...

Back 41

-Growth delay in children and adolescents
-Anemia
-Infection
-Poor wound healing
***50% IBD patients have deficiencies

Front 42

Causes of malnutrition from IBD

Back 42

-Poor appetite
-Increased nutrient requirements secondary to an increase in resting energy expenditure from...
--Inflammation
--Necrosis/regeneration of epithelium
--Fever, sepsis
--Surgery

Front 43

IBD increased nutrient losses

Back 43

-Reduced absorption due to disease and possible resection
-Bacterial overgrowth-absorptive efficacy
-Decreased absorptive surface area
-Decreased absorption of vitamin B12
-Decreased bile salt availability and production
-Increased transit time resulting in diarrhea
-Anemia secondary to
-----Decreased absorption of iron, folate, vitamin B12
-----Active GI bleeding

Front 44

Vitamin/mineral supplements for IBD

Back 44

-Patients may need 1 to 5 times the RDA
-Heal resection-patients require intramuscular injections of vitamin B12 for life
-Iron supplements required if iron deficiency anemia present
-Calcium and vitamin D supplements required with chronic corticosteroid use
-Folic acid supplements required with chronic Sulfasalazine use

Front 45

Low fiber in IBD

Back 45

-Decrease the possibility of obstruction
-Minimize physical irritation to the inflamed bowel
-Reduce stool weight and frequency
-Slow rate of intestinal transit time

Front 46

Fat controlled diets

Back 46

-Purpose--> Used to relieve symptoms of diarrhea, steatorrhea, flatulence, abdominal pain.
-Characteristics--> 50 g allows 6 oz meat or substitute and 3-5 fat equivalents (5 g)
25 g allows 4 oz meat or substitute and one fat equivalent

Front 47

Ostomy Diets

Back 47

-Purpose = Nutritionally adequate and minimizes unpleasant odors, risk of obstruction and excessive output
-Diet = Low fat, limit insoluble fiber, high soluble fiber helps to increase food transit time and thicken stool

Front 48

Types of hepatitis

Back 48

1. Hepatitis A virus transmitted by fecal-oral route, called infectious hepatitis, vaccine available, does not cause chronic hepatitis
2. Hepatitis B and C virus transmitted blood, semen and saliva, associated with chronic liver disease and liver cancer
3. Hepatitis C is associated with chronic active hepatitis, liver cirrhosis, and liver cancer
4.Hepatitis D (formally non-A, non-B) is toxic to functional liver cells and may be related to HAV and HBV)
5. Hepatitis E is often due to toxic liver injury from carbon tetrachloride or acetaminophen overdose and has 80-90% mortality

Front 49

Symptoms of hepatitis

Back 49

-Phase 1- fever, arthralgia (joint pain), arthritis, rash, angioedema (rash underneath the skin)
-Phase 2-malaise (uneasiness), fatigue, myalgia (muscle pain), anorexia, nausea, vomiting,
-Phase 3- jaundice
-Phase 4-jaundice and other symptoms subside

Front 50

Fulminant Hepatitis

Back 50

-Severe liver dysfunction accompanied by hepatic encephalopathy
-Causes include viral hepatitis, chemical toxicity (acetaminophen, poisonous mushrooms, industrial poisons)
-See cerebral edema, coagulopathy, bleeding, cardiovascular abnormalities, renal failure, pulmonary problems, acid –base disturbance, sepsis, and pancreatitis

Front 51

Chronic Hepatitis

Back 51

-6 month course of hepatitis or biopsy confirmation
-Possible causes are autoimmune, viral, metabolic, medicines or toxins
-Symptoms-fatigue, sleep disorders, jaundice, muscle wasting, ascites, edema, hepatic encephalopathy, splenomegaly, palmar erythema, and spider angiomata

Front 52

Treatment of hepatitis

Back 52

-Drugs used for viral infections
1. Interferon alfa
2. Second generation nucleoside analogues (lamivudine) - antiviral drugs
-Rest
-Nutrition care: Good nutrition, fluids, frequent small meals, difficult due to anorexia. 3000 kcal per day, 1-1.2 g protein/kg, vitamin K, potassium and sodium important with diarrhea

Front 53

Stages of alcoholic liver disease

Back 53

-Hepatitic steatosis (fatty liver)
-Alcoholic hepatitis
-Alcoholic Cirrhosis (Laennec’s)
***Third leading cause of death in middle aged Americans

Front 54

Diagnosis (things tested and show increased levels) for alcoholic liver disease

Back 54

-Bilirubin (end products of bile that can be found in the blood which cause jaundice)
-alkaline phosphatase
-serum AST (aspartate aminotransferase) = enzyme in the liver that should not be found in the bloodstream
***Hepatic steatosis is reversible with abstinence from alcohol

Front 55

Nutrition care for alcoholic liver disease

Back 55

-Kcal and protein important
-Vitamin supplement with B12, folate, thiamin, pyridoxine, A, D
-Mineral supplement with zinc, magnesium, calcium, phosphorus

Front 56

Effects if inadequate protein

Back 56

-Fluid flows out into the body (edema)

Front 57

What decreases if the liver is not functioning?

Back 57

-Digestion
-Metabolism

Front 58

Process of cirrhosis from alcoholic liver disease

Back 58

Liver cells are stable (last long and not a high turnover)-->Liver makes new cells when other are destroyed (damaged cells aren't completely gone)-->new cells grow around scar tissue-->causes decreased blood flow or new cells do not function because they are too far from the blood supply-->cirrhosis
**Causes malabsorption of fats (not enough bile)

Front 59

Hepatic encephalopathy

Back 59

Changes of brain function from liver not being able to metabolize nutrients properly. Improperly broken down nutrients then get into the blood

Front 60

Alcohol dehydrogenase reactions

Back 60

-H+ ions formed can develop hypoglycemia and high TGL (fatty liver)
-High levels of uric acid = gout

Front 61

Alcohol decrease absorption of...

Back 61

-Thiamin
-Folate
-Vitamin B12.

Front 62

Ascites

Back 62

-Fluid found in the abdominal cavity caused by alcoholic fatty liver disease

Front 63

Nutrition management of alcoholic liver disease

Back 63

-Increased energy, small frequent meals
-Sodium restriction in fluid retention
-Fluid restriction for hyponatremia
-Carbohydrate controlled for hyperglycemia

Front 64

Symptoms of cirrhosis

Back 64

-Dyspepsia
-Spider angiomata
-Palmar erythema

Front 65

Manifestations of cirrhosis

Back 65

-Portal hypertension, esophageal varices, ascites, edema, CNS dysfunction (hepatic encephalopathy), renal insufficiency and osteopenia, -Increased serum AST and BSP(sulfobromophthalein)

Front 66

Impaired hepatic function causes...

Back 66

-Decreased synthesis of clotting factors
-Decreased storage of macro and micronutrients
-Decreased protein synthesis

Front 67

Treatment for impaired hepatic function

Back 67

-Diuretic drugs: spironolactone, amiloride, Lactulose, neomycin-reduce ammonia
-Procedures for portal bleeding-Shunts, banding,tamponade
-Procedures for ascites-paracentesis
-Monitoring blood glucose

Front 68

Stages of portal systemic encephalopathy

Back 68

-Grade I - mild confusion, agitation, decreased attention
-Grade II - disorientation, drowsiness
-Grade III - inability to compute, rage, paranoia
-Grade IV - coma

Front 69

Causes of portal systemic encephalopathy

Back 69

-Impaired ammonia detoxification by liver and becomes toxic to brain
-Increased aromatic amino acids leading to false neurotransmitters
-Other possible causes: short chain fatty acids, mercaptans, phenols (synnergistic neurotoxins), Zn deficiency
***end products of nitrogen metabolism (ammonia) are toxic to the brain-->replace branch chain amino acids leading to false neurotransmitters

Front 70

Nutrition care for portal systemic encephalopathy

Back 70

-Foods high in BCAA (Dairy and vegetable protein--->fiber increase excretion of N)

Front 71

Liver transplant

Back 71

-Immunosuppressant drugs cause hyperglycemia-decrease simple sugars
-Corticosteroids can increase Na retention-limit Na to 2-4 g/day

Front 72

Biliary Dyskinesia

Back 72

spasm or improper opening of sphincter of Oddi

Front 73

Cholelithiasis

Back 73

Gallstones
***female, fat, forty, fair, fertile

Front 74

Choledocholithiasis

Back 74

Stones in common bile duct

Front 75

Cholecystitis

Back 75

inflammation of gallbladder or common bile duct

Front 76

Cholestasis

Back 76

sludgelike buildup in gallbladder due to lack of stimulation or release of bile

Front 77

Cholangitis

Back 77

Inflammation of bile duct

Front 78

Medium chain fatty acids

Back 78

Can be eaten when gallbladder is not functioning properly
*MCFA do not form micelles

Front 79

Nutrition care for gallbladder disease

Back 79

-In acute cholecystitis, use low-fat diet, progress to diet with few condiments and gas forming vegetables
-In chronic cholecystitis, use fat (25% of calories)/calorie controlled (weight reduction) diet, adequate CHO and fiber
-In cholelithiasis, high fiber, low calories

Front 80

Litholytic therapy

Back 80

use of chenodeoxycholic and ursodeoxycholic acid to dissolve small stones and prevent new formation. Need at least 6 mo. therapy

Front 81

Extracorporeal lithotripsy

Back 81

Use of shock waves to break up gallstones

Front 82

Laparoscopic cholecystectomy

Back 82

gallbladder removal via use of a laparoscope

Front 83

Cholecystectomy

Back 83

surgical removal of gallbladder

Front 84

Types of pancreatitis

Back 84

-Acute pancreatitis-autodigestion due to obstruction of the pancreatic duct. Seen with gallstones, alcohol abuse, biliary tract disease and trauma
-Chronic pancreatitis-fibrotic, necrotic disease with decreased enzymatic processes, often caused by excessive alcohol
**involves inflammation with edema, fat necrosis, and cellular exudate

Front 85

Nutrition care for pancreatitis

Back 85

-Acute pancreatitis-NPO with IV hydration (pain medication used), some success seen with nasoenteric feedings (low fat = less stimulation of pancreas), advance to clear or full liquids. Progress to a light, low fat diet in six feedings
-Chronic pancreatitis-low to moderate in fat, moderate protein, high CHO. Six small feedings. Check alcohol consumption. Avoid alcohol, gastric stimulants (coffee, tea, spices) and use pancreatic enzyme replacement (Viokase, Pancrease, Cotazym

Front 86

Type 1 diabetes

Back 86

-5-10% of cases
-Can be caused by autoimmune disorder (may see autoantibodies in serum)
-Seen in lean persons experiencing thirst (polydipsia), excessive hunger (polyphagia), weight loss, and frequent urination (polyuria)
-Characterized by hyperglycemia, electrolyte imbalance, and ketoacidosis
-Treated with careful planning of diet coordinated with insulin and exercise

Front 87

Gestational diabetes

Back 87

-Glucose intolerance first recognized during pregnancy
-Screening should occur between week 24 and 28 of gestation
-May lead to increased fetal morbidity

Front 88

Diagnosis criteria for diabetes

Back 88

-Fasting plasma glucose level ≥126 mg/dl
-Casual plasma glucose level ≥200 mg/dl
-Glucose tolerance test with 75 g (100 g for pregnant women) of administered glucose and measurements made at 2 hr ≥ 200 mg/dl

Front 89

How much insulin to provide to someone with diabetes

Back 89

-6 units/kg of body weight

Front 90

Blood glucose target range (non pregnant adults)

Back 90

-Pre-meal glucose = 90-130 mg/dl
-Two hour post-meal glucose = >180 mg/dl
-Bedtime glucose = 100-160 mg/dl
-Hemoglobin a1c = < 7%

Front 91

Lipid and blood pressure ranges for normal individuals

Back 91

-LDL = <100mg/dl
-HDL (Men) = >40 mg/dl
-HDL (Women) = >50 mg/dl
-TGL = <150 mg/dl
-Blood pressure = <130/80 mm Hg

Front 92

Sugar alcohols and non-nutritive sweeteners with regards to diabetes

Back 92

-May be consumed with daily intake levels established by FDA

Front 93

Fat recommendations for diabetes

Back 93

-Limit dietary cholesterol to < 200 mg/day
-Consume two or more servings of fish per week to provide omega-3 fatty acids

Front 94

Protein's effect on diabetes

Back 94

-Can increase insulin response without increasing plasma glucose concentration
***Don’t use protein to treat acute or prevent nighttime hypoglycemia

Front 95

Triad

Back 95

-Metabolic syndrome
-Coronary heart disease
-Diabetes Mellitus

Front 96

Micro-nutrients with regards to diabetes

Back 96

No clear evidence to support vitamin and mineral supplements, antioxidant or chromium supplements

Front 97

Pre-meal insulin

Back 97

-Amount of carbohydrate in the meal does not effect glycemic control, if premeal insulin is adjusted appropriately
-Premeal insulin algorithms are valid; variations in carbohydrate do not modify basal ultralente insulin
-Variations in meal glycemic index, fiber, fat, or caloric intake do not influence premeal insulin

Front 98

Insulin dose: T1DM with trace to small amounts of ketones or T2DM with BMI =/<27

Back 98

0.3-0.5 units/kg actual body weight

Front 99

Insulin dose:T1DM with moderate to large amounts of ketones or T2DM with BMI =/>27

Back 99

0.5-0.7 units/kg actual body weight

Front 100

Insulin dose:T2DM with oral hypoglycemic medications

Back 100

0.1-0.3 units/kg ideal body weight

Front 101

1500 rule

Back 101

-1500/total daily insulin = insulin sensitivity or the amount 1 unit of insulin will lower blood glucose
***amount of insulin to bring blood glucose back to goal

Front 102

500 rule

Back 102

-500/total daily insulin = CHO: insulin ratio or the amount of CHO 1 unit of insulin will cover
***amount of insulin to cover CHO’s eaten

Front 103

Priority in Type 2 diabetes

Back 103

-Improving blood glucose control ***higher priority than weight loss

Front 104

Prevention of type 2 diabetes

Back 104

-Physical activity
-Sustained weight loss of 8 to 15 lb

Front 105

Variables not associated with Coronary artery disease in UKPDS

Back 105

-BMI
-Waist-hip ratio
-Decreased physical activity
-Raised insulin concentrations

Front 106

Benefits of exercise for type 2 diabetes

Back 106

-Activates intracellular Glut 4 glucose transporters improving peripheral glucose uptake
-Suppresses hepatic glucose production
***Most effective in persons with BG <200 mg/dL or with impaired glucose tolerance

Front 107

Acceptable Daily Intake (ADI)

Back 107

The amount that can be safely consumed on a daily basis over a person’s lifetime without adverse effects
*Includes a 100-fold safety factor

Front 108

Sources of carbohydrate

Back 108

-Starches
-Fruits
-Milk
-Desserts
***One carbohydrate serving = 15 grams of carbohydrate

Front 109

CHO counting recommendations

Back 109

-3 to 4 servings per meal for women
-4 to 5 for men
-1 to 2 for snacks

Front 110

Level 1 (Basic) CHO counting

Back 110

Introduces the concept of carbohydrate counting and emphasizes consistent amounts of carbohydrate at meals and snacks.

Front 111

Level 2 (Intermediate) CHO counting

Back 111

Focuses on relation-ships between food, medication, activity, and blood glucose level and introduces the concept of how to make adjustments based on blood glucose patterns.

Front 112

Level 3 (Advanced) CHO counting

Back 112

Teaches patients who use multiple daily injections of insulin or insulin pumps how to match short-acting insulin to carbohydrate using carbohydrate-to-insulin ratios.

Front 113

Formula for determining g of CHO

Back 113

-g CHO per serving X number of servings/serving size = CHO in your serving
-Total g CHO/15 g = total CHO choices
***ignore sugar grams

Front 114

Types of insulin medications

Back 114

-Rapid-acting- Aspart or Lispro
-Short-acting: regular
-Intermediate-acting: NPH (8-10 hrs after injection = peak)
-Long-acting: Ultralente and Glargine (Lantus)

Front 115

Hyperosmolar hyperglycemic nonketotic syndrome (HHNK)

Back 115

-Caused by not taking insulin appropriately-->becomes sick (body has no ketones)-->urinate a lot to get rid of extra glucose--> electrolyte imbalance and dehydration
**Person can collapse and look like in a coma
**Acute in type 2 (type 1 most likely has ketones)

Front 116

Hyperglycemia/Diabetic Ketoacidosis (DKA)

Back 116

-Caused by inadequate insulin for glucose utilization, fats form (metabolize fat to feed starving cells) and ketone bodies are produced (will be in the liver and blood stream) causing acidosis, polyuria occurs; treat with insulin, fluid, electrolytes
**Seen in type 1 diabetes
**Will have sweet smelling breath from ketones
**Will breath deeply and rapidly = kussmaul breathing
**Acute

Front 117

Hypoglycemia or insulin reaction

Back 117

-See shakiness, sweating, palpitations, hunger, mental confusion, slurred speech, lethargy, unconsciousness; treat with 15-20 g CHO and recheck blood glucose in 15 min. May need to readminister CHO
**Acute

Front 118

Which type of diabetes uses oral medications?

Back 118

-Type 2
*Need insulin in the body to increase production

Front 119

Long term complications of diabetes

Back 119

-Dyslipidemia-elevated lipids in blood
-Hypertension
-Retinopathy-aneurisms and decreased blood flow to the eye, may lead to blindness
-Nephropathy-poor or blocked blood flow to the kidneys cause uremic complications
-Neuropathy-poor or blocked blood flow to the nervous system particularly peripheral arteries with tingling sensations and loss of feeling

Front 120

Dawn phenomena

Back 120

High glucose levels in the morning after fasting overnight
**Seen in type 2 diabetes

Front 121

Lipid decreasing blood flow in diabetes is the cause...

Back 121

-Of long term effects of high blood glucose levels

Front 122

Whipple's triad

Back 122

-Hypoglycemia

Front 123

Fasting hypoglycemia

Back 123

-Seen with insulin treated diabetes when no food is consumed
-Seen in serious underlying conditions like hormone deficiency or tumorigenesis

Front 124

Nutrition care for hypoglycemia

Back 124

-Avoid caffeine
-Small frequent meals, usually 5-6/day with complex CHO, fiber and protein source as each meal

Front 125

Addison's disease

Back 125

-Insufficiency of the hormones of the adrenal cortex
-Less mineralcorticoids (aldosterone)
1. Increased excretion of Na, Cl, water
2. Decreased extracellular fluid
3. Acidosis
4. K retention
5. Lower blood volume, less cardiac output
-Less glucocorticoids (cortisol)
1. Decreased gluconeogenesis
2. Hypoglycemia

Front 126

Symptoms of Addison's disease

Back 126

-Weight loss
-Fatigue
-Dehydration
-Diarrhea or constipation
-Anorexia
-Nausea
-Vomiting
-Abdominal pain
-Pigmentation on knees, elbows, and palmar creases
***#1 treatment is to replace hormones

Front 127

Cushing Disease

Back 127

***Opposite of Addison's
-Buffalo trunk = fat pads on shoulders
-Kyphosis = curvature of the back
-Hirsutism = facial hair for women
-Moon face or red face
-Infertility
-Muscle weakness and fatigue
Increase in total body fat mass
-Osteoporosis and amenorrhea
-Mobilization of aa = loss of protein
***Change diet to treat

Front 128

Hypothyroidism, Myxedema, Gull’s Disease, Cretinism

Back 128

-Deficiency of thyroxine or triiodothyronine
-Symptoms: lower metabolic rate - increased weight, increased blood cholesterol, decreased cold tolerance, dry skin, lethargy, depression
-Treatment: thyroid extract

Front 129

Hyperthyroidism, Grave’s Disease

Back 129

-Overactive thyroid
-Symptoms: weight loss and wasting, goiter, increased glucose metabolism, preferential use of fat; in older patients, atrial fibrillation or congestive heart failure may occur
Treatment: Antithyroid drugs (can destroy parts of the thyroid), Radioiodine, Partial thyroidectomy

Front 130

Percutaneous Transluminal Coronary Angioplasty

Back 130

Slender balloon tipped tube-a catheter-from an artery in the groin to a trouble spot in an artery of the heart. The balloon is then inflated, compressing the plaque and dilating (widening) the narrowed coronary artery so that blood can flow more easily. This is often accompanied by inserting an expandable metal or plastic stent. Stents are wire mesh tubes used to prop open arteries
**Plaque can build around the stent and reduce blood flow again--> caused by high lipids

Front 131

Atherectomy

Back 131

Procedure similar to PTCA, but plaque is removed by high-speed drill.

Front 132

Laser Angioplasty

Back 132

Procedure similar to PTCA, but the catheters uses a laser that is able to remove enough plaque to permit the balloon to be inflated in order to dilate the stenosis

Front 133

Percutaneous transmyocardial revascularization (PTMR)

Back 133

Catheter and laser are directed through artery in the leg to the heart. Small holes within the blocked vessel that are created by the laser increase blood flow to the heart

Front 134

Coronary Artery Bypass Graft

Back 134

Surgical procedure that uses the saphenous vein or internal mammary artery to “bypass” the blocked vessel

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Ischemic heart disease

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Heart disease characterized by inadequate blood supply to the heart

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Unstable angina

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chest pain occurs at rest

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Myocardial infarction

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-Ischemia causes muscle damage which causes leakage of cellular contents debris into the blood
**Heart attack (can happen anywhere in the heart)
**Can check for contents and debris in the blood to see if MI occurred

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Cardiac biomarkers of ischemic heart disease

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-Creatine kinase
-Lactate dehydrogenase isozyme
-Cardiac troponin T

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Recommendations for Na after surgical procedures for atherosclerosis

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-Not a severly restricted Na diet

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Angina treatment

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-Diet =Calories ideal for weigh, Small frequent feedings, Control hyperlipidemia
-Drugs = Nitroglycerin = increase oxygen to the heart to decrease pain and symptoms
***DOES NOT help with blockage
***Increases epinephrine and vasodilation

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Myocardial Infarction treatment

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-Use oxygen, aspirin, morphine (reduce the work of the heart and relax)
-Non-caffeine clear liquids→soft diet, frequent meals
-Follow TLC Diet

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What is the strongest risk factor for peripheral artery disease?

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-Diabetes

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Heart Failure/Congestive Heart Failure Treatment

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-Oxygen
-Strong Diuretics-->decrease fluid around the heart
-Limit activity-->to spare oxygen
-Na - 2000 mg/day
-Energy - 30-50% above basal
-Fluid restriction - 1000-1200 ml/day
-Co-enzyme Q (less is produced when there is damage to the heart)

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Heart Failure/Congestive Heart Failure

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-Heart loses inability to work as a muscle
-Heart attack causes damage to valves-->can decrease ejection rate causing parts of the body not getting enough nutrients and oxygen

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Congestive

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Fluid around the heart caused by the inability of the heart to function

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Cardiac cachexia

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-Progressive and extreme loss of both fat and lean tissue in a patient with prolonged myocardial insufficiency (heart is not acting as a pump to supply the body)
-Increased BMR due to enlarged heart and increased breathing
-Anorexia-->difficult to give a heart transplant to low weight people
-Nausea
-Vomiting
-Malabsorption
-Protein = Not absorbed in the GI tract because it will be affected first (rapid turnover of GI cells)

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Drug therapies for cardiac cachexia

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-Anticoagulants = blood thinners (aspirin, warfarin-->decrease platelet aggrigation) May interact with herbs and certain supplements
-Antihypertensives = ACE inhibitors, alpha-adrenegic blockers, beta blockers, calcium channel blockers, aldosterone and Na balance, diuretics
-Antilipidemics = bile acid sequestrants (cholestyramine = resin drugs), fibric acids (gemfibrozil), HMG CoA reductase inhibitors a (lovastatin or simvastin), nicotinic acid, statin drugs (lipitor)
-Cardiac Glycosides = digitoxin, digitalis (helps the heart contract harder)

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Cardiac transplant considerations

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-Immuno suppressive drugs (can cause hyperglycemia)-->so body doesn't reject the organ
-Long-term metabolic effect - weight gain, glucose intolerance

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When lung function is normal the levels are...

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-PO2 (75-100 mm Hg)
-PCO2 (35-45 mm Hg)
-pH (7.35-7.45)
-O2 sat (94-100%)
-bicarbonate (22-26 mEq/liter

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Malnutrition related to lung function

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-Decreased function of parenchyma (reproducing cells) of the lungs, wasting of respiratory muscles, and reduced ventilatory drive

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Chronic Obstructive Pulmonary Disease – COPD

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-A disease that limits airflow through either inflammation of the lining of the bronchial tubes or destruction of the alveoli
***Distruction of exchange

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Emphysema

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-type I COPD
-Destruction of the alveoli characterized by dilation and destruction of the air spaces distal to the terminal bronchioles, destruction of the alveolar membrane and loss of bronchi elastic recoil. Symptoms: Over inflation, collapse and dypsnea (shortness of breath).

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Chronic bronchitis

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-Type 2 COPD
-Characterized by inflammation and narrowing of the lumen of the bronchi. Symptoms: excessive mucus, productive cough, infection, and bronchospasm.

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Carbonic acid

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-Releases H+ ions and gets rid of CO2
***How the body deals with acd-base balance

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What are the two things that deal with acid-base balance in the blood?

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-Lungs
-Kidneys = form bicarbonate and ammonia

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What happens to the lungs when someone is extremely malnurished?

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-Lung function decreases

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Management of COPD

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-Drugs: antibiotics, bronchodilators, mucolytic agents, steroids, leukotriene inhibitors
-Increased BMR -->feed too much makes lungs work harder
-Increase protein (be mindful of respiratory quotient)
***repletion without overfeeding

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Respiratory quotient numbers

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-CHO = 1.0
-Protein = 0.8
-TGL = 0.7

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Adult Respiratory Distress Syndrome (ARDS)

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-Respiratory failure resulting from an acute insult to the lungs that occurs when the respiratory system is no longer able to perform its normal function
-Due to those that directly cause injury to the lung, such as pneumonia, aspiration, or an inhalation injury, or those that result in indirect injury precipitated by events outside the lung, such as sepsis, trauma, or pancreatitis
**Multiple organ dysfunction syndrome

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Diagnosis of ARDS

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Blood gases =
-O2<60 mm Hg (Normal 80-100)
-CO2>50 mm Hg (Normal 35-45)
-pH<7.3 (normal 7.35-7.45) = acidosis
**hopefully go back to normal function after provided a respirator and nutrients

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Weaning off respirator

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-Use parenteral, enteral, transitional diets. Need 1/2 calories from new feeding before decreasing old. Soft diets are best for patients first consuming an oral diet as throat is often sore from tube.
-Calories - maintenance level REE X 1.2-1.4 or RDI energy equations
-Protein - 1.5-2.0 g/kg/day

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What reduces wound healing?

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Hyperglycemia

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Bronchial asthma

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-A chronic inflammatory disorder of the airway involving many cells and cellular elements, such as mast cells, eosinophils, T lymphocytes, macrophages, neutrophils, and epithelial cells. Inflammation is the primary problem thought to be primarily immunoglobulin E (IgE) mediated.
-Signs: wheezing, breathlessness, chest tightness, coughing
-Obesity seems to be associated with asthma
-Nutritionally adequate diet, antioxidants especially vitamin C