Exam 2

What is IPE?

What is IPE?

• IPE occurs when members of two or more health care professions engage in learning with, from, and about each other to enable effective collaboration and improve health outcomes

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What is interprofessional collaborative practice?

Collaborative practice happens when multiple health workers from different professional backgrounds work together with patients, families, careers, and communities to deliver the highest quality of care across settings

What are the core competencies of IPE?

• Values/ethics: Work with individuals of other professions to maintain a climate of mutual respect and shared values

• Roles and responsibilities: Use knowledge of one’s own role and those in other professions to appropriately assess and address the healthcare needs of the patient and population served

• Interprofessional Communication: Communicate with patients, families, communities, and other health professionals in a responsive and responsible manner that supports a team approach to the maintenance of health and the treatment of diseases

• Teams and teamwork: Apply relationship building values and principles of team dynamics to perform effectively in a different team roles to plan and deliver patient/population centered care that is safe, efficient, effective, and equitable

What does a physician’s assistant do? What is their education requirement?

• Works with and diagnoses patients

• Works with physician

• Masters

What does a registered nurse do? What is their education requirement?

• Inpatient → know the most about the patient (crucial for coordination), caretaker

• Associates (pushing for bachelor’s though)

What does a occupational therapist do? What is their education requirement?

• Work with patients to regain skills of daily living

• Regain strength, shaking with Parkinson’s

• Doctorate

What does a physical therapist do? What is their education requirement?

• Work on strength to be physically active

• Doctorate

What does audiology do? What is their education requirement?

• Hearing and balance disorders

• Speech delays

• Doctorate

What does a pharmacist do? What is their education requirement?

• Handle prescriptions and equipment

• Verify prescription is okay (no interactions with other drugs)

• Resource for over the counter info

• Doctorate

What does a speech language pathologist do? What is their education requirement?

• Dysphagia, oral problems, auditory problems that affect speech or swallowing

• Masters

What does a social worker do? What is their education requirement?

• Coordinates with patients, their family, and their insurance so patient can leave safely

• Social, financial, and emotional support

• May provide transport

• Masters

What does a respiratory therapist do? What is their education requirement?

• Breathing issues → strengthen ability to breathe

• Associates

What does a radiologic technician do? what is their education?

• Specialize radiologic tests

• Associates

How much does IPE lower risk of hospitalization?

• 20-50%

• Also fewer costs

How does liver function affect mortality?

• Only need 20% of liver function to live

• Die without it though

What are the major connectors of the liver, gallbladder, and pancreas?

• Portal vein - connects them with GI tract and delivers to liver

• Sphincter of Oddi → connects pancreas to duodenum

• Common bile duct → to pancreas

• Cystic duct → gallbladder to liver

• Note: Since they are connected, a problem in one will cause problems in others

What are the hematologic functions of the liver?

• Synthesis of clotting factors: Fibrinogen; prothrombin; and factors V, VII IX, and XII

• Produces plasminogen and heparin (components of the fibrinolytic system

What are the detoxifying functions of the liver?

• Converts ammonia to urea for excretion by the kidneys

• Converts drugs, pesticides and steroid hormones to water soluble form to be excreted in the urine

• Alcohol metabolism (alcohol dehydrogenase)

• Removes bacteria and debris from blood via phagocytic action of Kupffer cells

  • Bilirubin from breakdown of RBCs, conjugated and excreted in bile

What are the phases of detoxification? How does this relate to nutrition?

• Phase 1: Toxins turned into intermediary metabolites. Some metabolites are dangerous so it is important to move to phase 2 quickly. ROS’s can also be made but can be neutralized by antioxidants

• Phase 2: Intermediary metabolites turned into excretory derivatives

• These processes all need nutrients, so eating these can increase efficiency

What are the metabolic functions of the liver for vitamins?

• Stores all fat-soluble vitamins and B12

• Synthesizes proteins for transport of vitamin A

• Converts folate to 5-methyl tetrahydrofolic acid (activation)

• Vitamin D activation (1st step) to calcidiol, then sent to kidney to become calcitriol (active form)

What are the metabolic functions of the liver for minerals?

• Stores zinc, iron, copper, and magnesium

• Synthesizes proteins for transport of iron, zinc, and copper

What are the metabolic functions of the liver for carbohydrates?

• Convert galactose and fructose to glucose

• Stores glucose as glycogen and releases it as necessary

• Coverts precursors to glucose when needed

What are the metabolic functions of the liver for lipids?

• Converts FAs to acetyl CoA to produce energy (beta-oxidation)

• SYnthesizes and hydrolyzes triglycerides, phospholipids, cholesterol, and lipoproteins

• Produces and excretes bile for digestion and absorption of fats and fat soluble vitamins

What are the metabolic functions of the liver for protein?

• Transamination and deamination reactions

• Makes serum proteins: albumin, globulins transferring, ceruloplasmin, lipoproteins, blood clotting proteins

What is the storage function of the liver?

• Flood chamber → Primary reservoir in the body

• Can store 200-400 ml of blood that can be released during blood loss

What is the bile salt cycle?

• Bile salts made in the liver from cholesterol and stored in gallbladder

• Bile salts released during digestion; 95% is reabsorbed and 5% is excreted (can increase the amount excreted by increasing soluble fiber → Method to lower cholesterol since the liver has to synthesize more bile salts)

What are the major causes of liver disease?

• Hepatotoxins (alcohol, medications in high doses, fungi toxins

• Viruses (hepatitis)

• Iron and Copper (prooxidants)

• Genetic diseases

How is liver disease diagnosed?

• Evaluation of protein metabolism

  • Serum proteins, proteins that are markers for specific liver disease

• Evaluation of detoxification and excretion capabilities

  • hepatic excretion of bilirubin → serum and urine bilirubin

  • Cholestasis tests → alkaline phosphatase, GGT (enzymes made by liver cells)

• Evaluation of enzyme synthesis

  • Hepatic enzymes → ALT, AST, LDH go up with liver cell damage

• Specific tests for viral hepatitis

• Have to look at all these markers in conjugation with one another

What are the forms of hepatitis? How are the spread?

• Hepatitis A (HAV) → fecal-oral route; symptoms resolve on own

• Hepatitis B (HBV) → transmitted via blood, blood productions, semen, and saliva; develops into cirrhosis; especially dangerous to children; need drug intervention

• Hepatitis C (HBC) → Exposure to blood or body fluids from an infected person; no vaccine; most common cause of needing a liver transplant

• Hepatitis D and E (HDV; HEV) → uncommon in US and need HBV to replicate

What are the non-hepatitis liver disease?

• NASH

• Sclerosing cholangitis

• Hemochromatosis

• Wilson’s disease

• Cirrhosis

• Non-Alcoholic Fatty liver disease

What is non-alcoholic fatty liver disease?

• Fat accumulation in liver

• Usually from obesity

• No symptoms until late stage

What is chronic hepatitis?

• Can be caused by autoimmune, viral, metabolic, or toxic (drug) reason

• Defined as a least 6 month course of hepatitis or biochemical and clinical evidence of liver disease with biopsy confirmation showing nonresolving inflammation of the liver

What is fulminant hepatitis? What can it lead to?

• Severe liver dysfunction with hepatic encephalopathy

• No previous liver disease and development of hepatic encephalopathy within 8 weeks of illness → Sudden onset

• Causes: viral hepatitis (75% of cases), chemical toxicity (drugs, mushrooms, industrial poisons)

• Can lead to: cerebral edema, bleeding, renal failure, cardiovascular abnormalities, pulmonary complications, acid-base balance disturbances, electrolyte disturbances, sepsis and pancreatitis

What is the nutrition intervention for hepatitis?

• Optimal kcal and protein to prevent catabolism and provide nutrients to regenerate liver

• NO ALCOHOL

• Small frequent feedings if needed

• Moderate fat if tolerated

What is NASH?

• An intermediate stage in non-alcoholic fatty liver disease before cirrhosis (fully reversible still)

• Accumulation of fat droplets in the hepatocytes which are surrounded by acute and chronic inflammatory cells; associated with accumulation of fibrous tissues in the liver

• Causes include drugs, inborn errors of metabolism, acquired metabolic disorders (T2DN, obesity, lipodystrophy, etc)

• Seen in 50% of bariatric surgery patients

• Most common liver disease in US adolescents

• Leading cause of mildly elevated transaminases (ALT and AST)

• Progression to cirrhosis is variable (Dependent on age, presence of obesity and T2DM)

• Treatment is often weight loss (not rapid) to decrease liver fat

What is sclerosing cholangitis?

• Chronic cholestatic liver disease with fibrosing inflammation of segment of extrahepatic bile ducts (bile builds up in the liver leading to damage)

• Progression leads to portal hypertension (high blood pressure in portal vein causing decreased blood flow to liver), hepatic failure, and cholangiocarcinoma (cancer in bile duct)

• May be an immune disorder (50-75% of patients also have IBD and 60-70% are men)

• Steatorrhea and fat soluble vitamin deficiencies occur if not treated

What is hemochromatosis?

• Inherited iron overload disease → iron toxicity (iron regulated at absorption)

• Results in hepatomegaly (increased liver size), esophageal varices (enlarged veins in the esophagus due to increased blood from the liver), ascites (fluid accumulation in abdominal cavity), etc

• If diagnosed early, phlebotomy will improve the condition

What is wilson’s disease?

• Autosomal recessive disorder with impaired biliary copper excretion

• Kayser-Fleischer rings confirm diagnosis

• Can present with acute, fulminant, or chronic active hepatitis secondary to the disease

• Neurological signs are often the first symptoms (ex. posture and gait)

• Treatment: Chelation therapy (chelate Cu so it is not absorbed), zinc supplements (compete for absorption; increase metallothionein which binds to Cu in enterocytes so that it does not go to blood), and low Cu diet (if all else fails)

• If not diagnosed until onset of fulminant failure, fatal without transplant

What is primary biliary cirrhosis?

• Caused by progressive destruction of small and intermediate-sized intrahepatic bile ducts

• 90% of patients are women

• Progresses slowly and results in cirrhosis portal hypertension and stage-liver disease (transplantation or death at this point)

• An immune-mediated disease

What is alcoholic cirrhosis?

• Most common liver disease in the US and the 9th leading cause of death in 2021

• Acetaldehyde causes damage to mitochondrial membrane structure and function

What is the alcohol intake threshold for alcoholic liver disease

40 g for men and 20g for women

What is a “drink”?

• 12-15g alcohol with legal standard of 15g

• 12 oz beer

• 5 oz wine

• 1.5 oz hard liquor

What are the 3 stages of alcoholic cirrhosis?

• Hepatic steatosis → Do not feel anything yet, only found with liver function tests of abnormal lipid panel

  • Culmination of metabolic disturbances: Increase the mobilization of fatty acids from adipose tissues, Increase in hepatic synthesis of FAs, decrease FA oxidation, increase triglyceride production, reversible with abstinence of alcohol

• Alcoholic hepatitis → Inflammatory damage

  • Hepatitis may resolve if alcohol discontinued or may progress

• Alcoholic cirrhosis → clinical symptoms of ascites, GI bleeding (esophageal varices), portal hypertension, hepatic encephalopathy, etc.

What are the clinical manifestations of cirrhosis?

• GI malabsorption and distress (early) → Less bile production

• Fatty liver with necrosis → Death of hepatocytes

• Nutritional deficiencies → Malabsorption and low intake (ex.alcohol disrupts thiamin)

• Ascites

• Wernicke-Korsikoff syndrome (thiamin deficiency from alcoholism → malabsorption and low intake)

• Esophageal varices from portal hypertension

• GI bleeding if varices burst

• Hepatic encephalopathy

What is portal hypertension/ascites? How is it treated?

• Elevated blood pressure in the portal vein leads to ascites (fluid build up in abdomen), GI bleeding from varices, encephalopathy

• Treatments:

  • Sodium restriction

  • Paracentesis (insert drain)

  • Fluid restriction if necessary (if hyponatremia)

  • Diuretics

What is Wernicke-Korsikoff Syndrome?

• Severe thiamine deficiency due to alcoholism (alcohol interferes with absorption and lower intake)

• Disordered consciousness → seem drunk when they are not

• Ocular disturbances → eye moving back and forth, optic disc edema

• Ataxia → Loss of coordination

What is hepatic encephalopathy? What are the clinical signs?

• Cognitive dysfunction precipitated by GI bleeding (from esophageal varices), fluid and electrolyte abnormalities, uremia, infection, etc.

• Clinical signs: Fectore hepaticus (”Breath of death” → really bad breath because liver is not metabolizing toxins so they are sent to the lungs), changes in EEG, increased blood ammonia in some (not always a good measure)

What are the stages of hepatic encephalopathy?

• Stage 1: mild confusion, other mental changes (personality, intellectual)

• Stage 2: drowsiness, lethargy, asterixis (hand flapping)

• Stage 3: somnolent (sleepy) by rousable

• Stage 4: coma

What are the theories of pathogenesis of hepatic encephalopathy?

• Accumulation of toxins (i.e. ammonia) that eventually reach brain

• False neurotransmitters → BCAAs down (used in brain, muscle, heart when gluconeogenesis and ketogenesis are depressed, AAAs up released by muscle proteolysis but synthesis of liver protein are depressed)

  • Also due to ammonia and decreased gluconeogenesis

• Increased neuro inhibitory substances in blood and brain → synergistic neurotoxin hypothesis

  • Also due to ammonia (binds to gaba receptors)

What are the nutrition implications of cirrhosis?

• Early satiety from ascites (use more dense foods, small frequent meals, liquid meal replacements, add oil or protein powder)

• Impaired nutrient digestion and absorption

• Increased energy expenditure (due to dysfunctional gluconeogenesis, FA release, and general inefficient energy use)

• Hypoglycemia due to hyperinsulinemia or hyperglycemia due to gluconeogenesis dysfunction and possible pancreas dysfunction

What are the energy needs for cirrhosis?

• 35-40 kcal/kg

What are the protein needs for cirrhosis?

1.2-1.5 g/kg

What are the general nutrition interventions for cirrhosis?

• Fat less than 30% for steatorrhea

• Restrict sodium for ascites

• Supplement vitamins and minerals for deficiencies (ex. vitamin D and thiamin)

• Other considerations: enteral feeding; soft diet for patients with esophageal varices (decrease chance of bursting)

What are the protein recommendations for cirrhosis/hepatic encephalopathy?

• Protein is controversial but at least .8g/kg

• Nelms says no restriction due to malnutrition up to 1.6 g/kg

• If all else fails use special BCAA formulas

What are the fat recommendations for cirrhosis/hepatic encephalopathy?

• May need replacement with MCT oil (not digested with bile)

• If large stool losses may need to go to low fat diet, but if that does not work (diarrhea continues) go back to 20-40%

What are the carbohydrate recommendations for cirrhosis/hepatic encephalopathy?

• May see glucose intolerance (insulin resistance due to pancreas dysfunction)

• Hypoglycemia may also occur (especially after alcohol ingestion) due to lack of gluconeogenesis in the liver

What are the electrolytes and fluid recommendations for hepatic encephalopathy?

2 g sodium and 1-1.5 liter fluid restriction if fluid overload

What are the types of medications used for cirrhosis/hepatic encephalopathy?

• Broad spectrum antibiotics- kills bacteria that convert urea to ammonia

• Lactulose- acidifies colonic contents, retaining ammonia as ammonium (increases rate of conversion) and causes diarrhea (fluid loss is okay since there is usually fluid overload)

What is the monitoring and evaluation of hepatic encephalopathy?

Tolerance to feedings, amount of nutrients consumed, dry and non-dry weight changes (see fluid changes too), laboratory values, and cognitive status

How does CF affect the body?

• Reduces Cl transport → Reduced Na and water transport → increase viscosity of mucus secretions in epithelial cells → obstruct ducts and impair functions of many organs

• Lungs: sticky mucus dehydrated the airway surface liquids and obstructs lung function leading to decreased lung function; also causes recurrent respiratory infections

  • CF is regarded as a pulmonary disease because most CF patients die of pulmonary complications

• Sweat glands: Cl levels are abnormally high; used for diagnosis

• Pancreas: Sticky mucus causes PI and CFRD

• Liver: Liver disease and biliary cirrhosis

• Male infertility (CBAVD)

How does malabsorption occur in patients with CF? How is it treated?

• Occurs in cases with PI but not in PS (PS have longer life expectancy)

• Pancreatic ducts are obstructed resulting in greatly reduced enzymes and bicarbonate secretions; eventually cells are destroyed

• Treated with pancreatic enzyme replacement therapy (PERT)

How does CF related diabetes occur (CFRD)?

• As CF progresses, the endocrine function of the pancreas is lost and less insulin is secreted

What is the earliest onset of CF? How common is it?

• Meconium ileus → neonatal intestinal obstruction presented at time of birth

• Caused by blockage in terminal ileum with dehydrated meconium

• Present in 20% of patients; 80% need surgery

What is distal intestinal obstruction syndrome (DIOS)?

The equivalent of MI that occurs at older ages

When does PI usually occur?

Typically in infancy

When do CF patients develop lung diseases?

• Lungs of infants with CF are structurally and functionally normal at birth

• Lung disease is often mild in early childhood and progressively declines during adolescence

What are the nutritional consequences of CF?

PI → Malabsorption → kcals and nutrients lost in stools → Unable to meet energy and nutrient requirement → poor growth and nutrient deficiencies

What is the best indicator of nutrition in children with CF?

• Growth

• Both BMI and weight are near the 50th percentile, but height trends lower

What are the indicators of growth?

Weight-for-age, height-for-age, BMI percentile (>2 years); weight-for-length (<2 years)

What is FEV1?

FEV1 stands for Forced Expiratory Volume in one second. It is a measure of the maximum amount of air that a person can forcefully exhale in one second after taking a deep breath. It is typically used as a measure of lung function to diagnose and monitor respiratory diseases

What are the levels of lung function?

• Normal lung function = >90% FEV1

• Mild Lung disease = 70-89% FEV1

• Moderate Lung disease = 40-69%

• Severe lung disease = <40%

How does lung function decline in CF?

• FEV1 normal at 6-10 years old

• About 80% FEV1 by 20y

• 70% FEV1 by 30y

• Decline is 1-2% FEV1 → with this rate, by 50y FEV1 will be 50% or lower

What is bacteria is measured most aggressively in patients with CF? Why?

• Pseudomonas aeruginosa (PA)

• Causes FEV1 to decrease at a much faster rate

• By age 20, nearly half of CF patients have PA colonized in airway

What are the top two causes of death in CF?

1. Respiratory complications

2. Transplant complications

What is the life expectancy with CF?

• About a quarter die before their mid 20s and about half die in their early 30s

• Life expectancy is about 45y

How have the prospects for patients with CF changed?

• Life expectancy expanded by 15y

• Less lung function complications

Why is CF not diagnosed at birth or soon after? When can it be diagnosed at birth?

• There are little to no pulmonary symptoms

• Primary symptoms are loose/watery stools, which is common in breast fed infants

• Even if infants show malabsorption symptoms and/or poor growth, the first suspected cause is often milk intolerance or allergy

• Exception is MI

What are factors leading to suspicion of CF?

• MI

• Steatorrhea

• Poor growth or failure to thrive

• Frequent respiratory infections

• Family history of CF

• Positive NBS

What is the history of newborn screening (NBS) for CF?

• Before screening was implemented, CF diagnosis was usually made in late infancy, after growth failure has occurred

• 1994- WI and CO implemented NBS

• 2009- guidelines made

• 2010- all states implemented CF NBS

What is a sweat chloride test? How is it interpreted?

• First step in CF diagnosis after a positive screening

• Measures sweat chloride by pilocarpine iontophoresis

• Pilocarpine and a little electrical stimulation is applied to small area of the arm to stimulate sweat production and sweat is collected on filter paper or gauze

• Interpretation

  • <29 mmol/L = no CF

  • 30-59 mmol/L = CFSPID

  • 60 mmol/L = CF

What is NBS? What is the Goal? How is it performed?

• Testing newborns in their first days of life for specific disorders and conditions that can cause serious health problems if not treated in infancy or childhood

• Early detection and treatment to prevent or reduce intellectual and physical disabilities and life-threatening illnesses

• NBS is performed by obtaining infants blood via heel prick onto a Guthrie card used to do numerous biochemical tests and genetic analyses

  • There a 5 spots on the card containing .4 ml dried blood with 5-10 ug of DNA

How is NBS done for CF? What is a positive screen?

• Tier 1

  • Biochemical test: Immunoreactive Trypsinogen (IRT)

  • Trypsinogen is normally present in the pancreas and not blood

  • Trypsinogen in the blood is higher in CF due to pancreatic damage

  • Positive screen = IRT > 170 ug/ml

• Tier 2

  • Done if tier 1 is positive

  • DNA analysis of a certain number of CFTR mutations

• Note: Positive NBS does not mean CF → Sweat test for diagnosis

  • Ex. elevated IRT present in premature infants

What is CFSPID? What is the follow-up?

• CF Screen Positive, Inconclusive Diagnosis (Sweat test 30-59mmol/L)

• AKA CF-related metabolic syndrome

• NBS only screens for a certain number of mutations, so follow up looks for all 250 mutations that can cause CF or sequences the entire CFTR gene

What are the other tests for CFTR function not common to the US?

• Nasal potential difference test

• Intestinal current measurement

• Not diagnostic

What is cholecystitis and what is the MNT?

• Inflammation that goes away on its own

• A low fat diet is recommended after an attack

What is cholelithiasis? What is the etiology?

• Gallstones

• Etiology → abnormal proportions of cholesterol and bile acids

How is cholelithiasis diagnosed?

Diagnosed by ultrasound, HIDA scan (tracer), and ERCP (endoscopy and fluoroscopy)

How is cholelothiasis treated?

• Gallbladder is removed

• Before surgery: Low fat diet with 25-30% fat for stimulation and drainage of the biliary tract

• After surgery: No diet needed after removal (basal bile from liver is usually sufficient)

What is choledocholithiasis?

Obstruction of duct (due to a stone possibly)

What is biliary atresia?

• Lack of gallbladder and bile duct

• Usually caused by a blockage after birth where these need to be removed

What are the two major functions of the pancreas?

• Endocrine → make insulin, glucagon, and somatostatin

• Exocrine → secretes digestive enzymes and bicarbonate into the GI tract

What are the major diseases of the pancreas?

• Acute pancreatitis → Sudden or slow onset that eventually resolves (sometimes on its own)

• Chronic pancreatitis → Continually have acute pancreatitis issues and underlying inflammation

  • Seen with alcohol abuse

• Pancreatic cancer (treated differently)

What can cause pancreatitis?

Gallstones, medications, metabolic disorders, etc.

What is pancreatitis? What are the signs and symptoms?

• Inflammation of the pancreas where there is autodigestion and cellular necrosis of the pancreas due to enzymes being activated outside of the GI tract (also causes hemorrhage pancreatic tissue)

• Less digestion enzymes and bicarbonate is secreted (may need acid inhibitors)

• Characterized by edema, cellular exudate (inflammatory cells), fat necrosis, lab values showing and increase in serum amylase, and severe pain

What are the most common causes of pancreatitis?

Alcohol abuse and biliary tract disease

Why does alcohol abuse lead to pancreatitis?

Leads to an increase precipitation of stones in the biliary tract and pancreas

What is the whipple procedure? What is the MNT?

• Surgery used to treat tumors in the pancreas, duodenum, or bile duct

  • Ex. for a pancreatic tumor the part of the pancreas, the gallbladder, and some of the duodenum are removed

• MNT: Small frequent meal s(5-6 a day) to not overload the GI system; high kcal and high protein foods, avoid fluids with meals

  • Pancreatic enzymes may be used for issues with gas and bloating (may be temporary or life long)

How do you nutritionally assess pancreatitis?

• Anthropometrics - focus on weight history (malabsorption and low intake) and body composition (LBM)

• Dietary history - what foods are causing pain, alcohol intake

• Labs - blood glucose, TGs, hematocrit, hemoglobin, WBC