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S3 - Pathophysiology > Hepatic, Biliary, and Pancreas > Flashcards

Hepatic, Biliary, and Pancreas Flashcards

1
Q

PART 1

A

PART 1

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2
Q

Functions of the hepatic system (liver)?

  • Conversion and excretion of ______ and _________
  • Sole source of ________ and other plasma proteins
  • Produces ____ (500-1500 mls./day)
  • Synthesizes ______ factors
  • Absorbs and processes nutrients from the ___
  • _________ (drugs, ETOH and toxins)
  • _________ (glycogen, vitamins, iron)
  • Synthesizes ____________
A
  • bilirubin and ammonia
  • albumin
  • bile
  • clotting factors
  • gut
  • detoxification
  • storage
  • cholesterol
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3
Q
  • The liver reciever approximately __% of _________ even though it makus up only approximately 2-3% of total body weight.
  • The _______ vein provides approximately / of blood supply while the hepatic artery provides the rest.
A
  • 25%, CO

- portal vein, 2/3

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4
Q

What is the functional unit of the liver?

A

Liver Lobule

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5
Q

What are some S/Sx of hepatic disease?

A
  • GI symptoms (N/V, Diarrhea, Constipation, Heartburn, Abdominal Pain, GI Bleeding)
  • Edema/Ascites
  • Dark Urine (bilirubin)
  • Light/clay colored stools
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6
Q

What causes the urine to become dark with hepatic diseases?

A

Breakdown of hemoglobin produces bilirubin. Excess bilirubin in urine presents as dark urine and suggests liver damage.

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7
Q

Other S/Sx of hepatic disease:

  • _____ _________ quadrant abdominal pain
  • ___________ involvement (confusion, muscle tremors, sleep disturbances)
  • Hepatic ______________ (abnormal development of bone)
  • _________
  • Skin changes such as _______ and bruising
A
  • right upper quadrant
  • neurologic involvement
  • osteodystrophy
  • osteoporosis
  • jaundice
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8
Q

Jaundice is a _______, not a _________.

A

-symptom not a disease

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9
Q

Jaundice:

  • _________ break down product of RBC in macrophages
  • ________ discoloration of the skin, sclerae, and mucous membranes.
  • Increased bilirubin production. Decreased processing of bilirubin.
  • Hepatocyte dysfunction (hepatitis, hepatic disease, tumor), bilirubin accumulation.
  • Impaired bile flow: caused by mechanical damage due to some obstruction of biliary tree
A
  • Bilirubin

- Yellow

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10
Q

What is the treatment of Jaundice?

A
  • resolve underlying disease
  • return to normal color suggests resolution
  • then activity and exercise can be resumed
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11
Q

What are the S/Sx of neurologic involvement in hepatic diseases?

A
  • Confusion
  • Sleep disturbances
  • Muscle tremors
  • Hyper reactive reflexes (ammonia)
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12
Q

Describe how the neurological system can be affected with hepatic disease.

A
  • Ammonia converted into urea in the liver.
  • Ammonia comes from the degredation of amino acids.
  • Ammonia is then catabolized by the liver generating urea.
  • Decreased urea production leads to ammonia accumulation in the blood and neurological symptoms.
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13
Q

What is flapping tremor?

A
  • Elicited by attempted wrist extension while the forearm is fixed.
  • Is the most common neurological abnormality associated with liver failure.
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14
Q

MSK pain location with hepatic disease tends to refer where?

A

Posterior thoracic pain (interscapular, R shoulder/upper trap/subscapular)

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15
Q

Hepatic _____________ is an abnormal development of bone/osteoporosis in individuals with chronic liver disease and leads to ___________/__________.

A
  • hepatic osteodystrophy

- osteopenia/osteoporosis

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16
Q
  • Healing of the liver occurs _______ with complete parenchymal regeneration or scarring or a combination.
  • ________ hepatic injury results in fibrosis (cirrhosis).
A
  • quickly

- Chronic

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17
Q
  • ______ is a late stage of scarring (fibrosis) marked by degeneration of cells, inflammation, and fibrous thickening of tissue. It is typically a result of alcoholism or hepatitis.
  • It is a progressive, patterned loss of healthy tissue which is replaced with _______ tissue.
  • Significant loss of liver function is associated with loss of __% or more of liver function.
A
  • Cirrhosis
  • fibrotic
  • 80%
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18
Q

Practice implications for Cirrhosis:

  • Osteoporosis
  • Impaired ________
  • Impaired ________ performance/weakness
  • Loss of ___________
  • Deconditioning
  • Ascites/bilateral edema of feet/ankles
  • Blood loss
  • _____ to reduce metabolic demand on the heart is recommended.
A
  • posture
  • muscle
  • balance
  • REST
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19
Q

Portal Vein:

  • A vein conveying blood to the liver from the _____, ________, ________, __________, and ___________.
  • Carries about __% of the blood going to the liver.
  • Conducts blood to ________ _____ in the liver i.e. not a true vein.
  • The ______ vein and _______ arteries deliver blood to the liver.
A
  • liver from the spleen, stomach, pancreas, gall bladder, and intestines
  • 75%
  • capillary beds
  • portal vein and hepatic arteries
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20
Q

Portal Hypertension:

  • Portal hypertension is defined as an increase in hepatic sinusoidal blood pressure > __ mm
  • ________ and abnormal liver architecture combine to form mechanical barriers to blood flow in the liver increasing the resistance and blood pressure in the hepatic portal system
  • What contributes to this hypertension- probably ________ and accompanying fibrosis; compression of arteries.
A
  • 6mm
  • fibrosis
  • cirrhosis
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21
Q
  • Increased portal pressure causes a __________ flow of blood back into the stomach, spleen, large and small intestine, rectum, and esophagus.
  • The result of this are varices back upsteam, what is varices?
A
  • retrograde

- an abnormally dilated vessel with a tortuous course (congestion)

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22
Q

Describe these consequences of portal hypertension:

  • Ascites
  • Spleenomegally
  • Hemorrhoids
  • Varices
A
  • Ascites- from increased hydrostatic venous pressure
  • Spleenomegally- enlargement of the spleen caused by venous congestion in spleen
  • Hemorrhoids- from venous congestion in the bowel
  • Varices- esophagus, stomach, rectum, or umbilical area
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23
Q

Hepatic __________ is a potentially irreversible decreased level of consciousness in people with severe liver disease. What is it thought to be caused by?

A
  • Hepatic Encephalopathy

- Thought to be caused by elevated blood ammonia and altered neurotransmitter status in the brain.

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24
Q

Describe how Hepatic Encephalopathy occurs.

A
  • Ammonia is created by bacteria in the colon from the metabolism of protein and urea.
  • Ammonia is absorbed into the portal blood system and transported to the liver where it is converted into urea
  • But the diseased liver cannot metabolize the ammonia
  • Blood ammonia levels go up impairing cognitive and motor function at the level of the brain
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25
Q

What are the S/Sx of Hepatic Encephalopathy?

A
  • Depression, personality changes, impaired attention
  • Drowsiness, sleep disorders, ataxia, asterixis, slurred speech, hyperreflexia
  • Marked confusion, incoherent speech, muscle rigidity
  • STUPOR, DECEREBRATE POSTURING, POSITIVE BABINSKI, DILATED PUPILS
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26
Q

Hepatic Encephalopathy Implications for the PT:

  • Patient _______
  • Impaired ______ and _______ integrity
  • Impaired arousal
  • Risk for pressure ulcers secondary to malnutrition, immobility, edema
A
  • safety

- motor and sensory

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27
Q
  • ________ is an abnormal accumulation of fluid in the peritoneal cavity and is associated mostly with _______ and accompanying ______ _________.
  • How is it managed?
A
  • Ascites, cirrhosis and portal hypertension

- Paracentesis, albumin comsumption, diuretics, sodium and fluid restriction

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28
Q

Ascites Implications:

  • Accompanying impaired _______ and _________ function
  • ___________
  • ________ disorders
  • Malnutrition
  • Muscle degradation
A
  • cardiac and respiratory
  • lymphedema
  • integumentary
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29
Q

PART 2

A

PART 2

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30
Q
  • Hepatitis is an __________ condition of the liver caused by _______ by one of several viruses with specific affinity for the liver (A,B,C,D,E).
  • Infection can result in _____ or ________ inflammation of the liver.
  • What are some other viruses that can cause hepatitis?
A
  • inflammatory, infection
  • acute or chronic
  • Epstein-Barr, CMV (cyto-megalovirus)
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31
Q
  • Most people with chronic hepatitis are __________.

- How is it diagnosed?

A
  • asymptomatic

- symptoms, physical exam, blood test

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32
Q

What are the symptoms of viral hepatitis?

A
  • N/V
  • poor appetite, wt loss
  • weakness
  • jaundice, dark urine
  • pale or clay-colored stool
  • fatigue
  • most people have vague or no symptoms at all
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33
Q

Viral Hepatitis Prognosis:

  • Depends on ______ of hepatitis, presence of liver ___________ and development of ________.
  • Occurence of liver cancer and/or cirrhosis _______ the progression.
  • Mod-to-severe _______ consumption.
A
  • type, comorbidities, cirrhosis
  • hastens
  • ETOH
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34
Q

Hepatitis A:

  • Formerly known as “_________ hepatitis”
  • Spread by close personal contact or oral-fecal contamination of water and food, poor hand hygeine, shared use of oral utensils.
  • Hepatitis A is _______ and ____-________
  • Most persons with _______ disease recover with no lasting liver damage; rarely fatal
  • ______ contagious
  • preventable with __________
A
  • “infectious hepatitis”
  • benign and self-limiting
  • acute
  • highly
  • vaccine
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35
Q

Hepatitis B:

  • Formerly known as “_______ hepatitis”
  • Spread by blood transsfusions, needle sticks, IV drug use/shared needles, dialysis, sexual contact, exchange of body fluid.
  • Considered a ____ because it is transmitted via sexual intercourse
  • Incubation period about ___ days
  • Most persons with ______ disease recover with no lasting liver damage; rarely fatal
A
  • “serum hepatitis”
  • STD
  • 90
  • acute
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36
Q
  • Who is most at risk for Hepatitis B?
  • __-__% of chronically infected persons develop chronic liver disease.
  • Is there a vaccine?
A
  • healthcare workers who come in contact with blood
  • 15-25%
  • Yes
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37
Q

Hepatitis C:

  • Leading cause of ________ liver disease transmitted by contact with blood of an infected person.
  • ______ illness is uncommon.
  • __-__% of newly infected persons develop a chronic infection. __-__% develop cirrhosis.
  • __-__% of newly infected persons clear the virus.
  • Is there a vaccine?
A
  • chronic
  • acute
  • 75-85%, 5-20%
  • 15-25%
  • No
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38
Q

What is the treatment of Hepatitis C?

A
  • Interferon-stimulates the immune system to attack the virus
  • Ribavirin-anti-viral drug used in tandem with interferon
  • New direct acting antiviral agents (curative, 8-12 week course of oral medication)
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39
Q

Who should be tested for Hepatitis C?

A
  • Recieved organ transplant before 1992
  • Have ever injected drugs
  • Recieved blood product used to treat clotting problems that was made before 1987
  • Born between 1945 and 1965
  • Have had long term kidney dialysis
  • Children born to HCV-positive mothers
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40
Q

What is autoimmune Hepatitis?

A

Immune reaction launched against cellular material in liver.

41
Q

What are some other viral causes of Hepatitis?

A
  • CMV
  • Epstein-Barr
  • Yellow Fever
42
Q

Other Causes of Liver Disease:

  • _____ and _____-induced liver disease.
  • ______ liver (fat accumulations -> inflammation -> scarring (cirrhosis)
  • ______ abuse
A
  • drug-induced and toxin-induced
  • fatty
  • ETOH
43
Q

10 million Americans are alcoholics and about 10-15% of theses will develop cirrhosis.
-Describe this pathogenesis.

A
  • Mitochondrial damage occurs
  • Excessive fat content in the liver leads to inflammation which degeneration of hepatocytes
  • Degenerated hepatocytes can stimulate an autoimmune reaction that causes further damage: alcoholic “hepatitis”
  • Nutritional-deficit injury: occurs because most alcoholics do not eat right
44
Q

PART 3

A

PART 3

45
Q

What is the biliary system?

A

Transportation route for bile into the duodenum with a storage site in the gallbladder.

46
Q
  • _____ is a dark green to yellowish fluid produced by the liver.
  • What is the purpose of bile?
  • What does biliary obstruction cause?
A
  • Bile
  • Helps emulsify the lipids in food. This process greatly increases surface area for the action of the enzyme pancreatic lipase.
  • Prevents the flow of bile to the duodenum resulting in accumulation of bile in the blood and causing jaundice.
47
Q
  • Bile is moved to the gall bladder through the right and left _________ ducts which join to form the common hepatic duct. Bile must then move through the _______ duct to reach the gall bladder.
  • The common hepatic duct joins with the cystic duct to form the ______ _____ duct.
  • The _________ duct joins the common bile duct and the common bile duct continues on to enter the ___________.
A
  • hepatic ducts, cystic duct
  • common bile duct
  • pancreatic duct, duodenum
48
Q
  • What is the function of the gallbladder?

- Movement of bile to and from the gallbladder is via ________ action of muscles in the cystic duct.

A
  • Stores and concentrates bile by absorbing water through the wall of the gallbladder.
  • peristaltic
49
Q

Most common biliary diseases are due to either _______ (___________) or __________ of the gallbladder (___________).

A
  • gallstones (cholelithiasis)

- inflammation (cholecysstitis)

50
Q

__________ is a “gallstone disease” and is one of the most common GI diseases in the US and a major reason for abdominal surgery.

A

Cholelithiasis

51
Q

What are the risk factors for gallstones?

A
  • Age
  • Genetics
  • Decreased physical activity
  • Obesity
  • Poor lipid profile
  • RA
  • TPN (total parenteral nutrition)
  • Liver disease
  • Gastric bypass surgery
  • DM
52
Q
  • Gallstones form in the ___________ and form when the composition of _____ changes.
  • ________ stones make up 80% of all cases while ________ salt stones make up the other 20%.
  • 75% are __________, while 25% become ___________.
A
  • gall bladder, bile
  • cholesterol (80%), bilirubin salt (20%)
  • asymptomatic, symptomatic
53
Q

What is the most frequent site of obstruction with gall stones?

A

-cystic ducts

54
Q

What are the symptoms of cholelithiasis (gall stones)?

A
  • Abdominal pain
  • R upper quadrant
  • Abdominal tenderness and muscle guarding
  • Pain may radiate to shoulder and upper back
  • 50% with symptomatic gall stones will have a recurrent episode
55
Q
  • How are gall stones diagnosed?

- What is the treatment of gall stones?

A
  • ultrasound

- surgery (cholecystectomy)

56
Q

What are the implications for a therapist when talking about gall stones?

A

Physical activity may play an important role in the prevention of symptomatic gallstones disease.

57
Q

What are the usual post-op exercises for any surgical procedure?

A
  • breathing
  • bed positioning
  • coughing wound splinting if needed
  • compressive stockings and leg exercises
58
Q

Cholelithiasis (gall stones) Implications for PT:

  • Physical activity may play an important role in the prevention of __________ gallstone disease in up to a third of all cases.
  • Laparoscopic cholecystectomy
  • Many individuals still experience referred pain to the right shoulder for __-__ hours.
  • Usual postoperative care-breathing, turning, coughing, wound splinting, compressive stockings, and leg exercises
A
  • symptomatic

- 24-48

59
Q

What is a complication of gall stones defined as calculi in the common bile duct that can cause pancreatis?

A

Choledocholithiasis- calculi in the common bile duct, can cause pancreatitis.

60
Q

PART 4

A

PART 4

61
Q

Pancreas Gross Anatomy:

  • Found in the __________.
  • Extends from behind the ________ to the left upper abdomen near the spleen.
  • Drains into the inner curvature of the ___________.
  • _______ ______ drains the organ, joining with the common bile duct which in turn drains into the duodenum.
A
  • abdomen
  • stomach
  • duodenum
  • Pancreatic duct
62
Q

The pancreas functions both as an _______ and ________ gland.

A
  • endocrine

- exocrine

63
Q
  • What is an endocrine gland?

- What is an exocrine gland?

A
  • Endocrine- Ductless glands that secrete their products, hormones, directly into the blood.
  • Exocrine- Glands that secrete substances onto an epithelial surface by way of a duct.
64
Q

In regards to the pancreas as an endocrine gland, it secretes ______ and ________ hormones.

A

-insulin and glucagon

65
Q

________ is a peptide hormone that regulates the metabolism of carbohydrates, fats, and protein by promoting the absorption of glucose from the blood into liver, fat, and skeletal muscle cells. It is calorie _________.

A
  • Insulin

- conserving

66
Q

_________ is a peptide hormone, produced by alpha cells of the pancreas. It functions to raise the concentration of glucose and fatty acids in the bloodstream. It favors energy __________.

A
  • Glucagon

- utilization

67
Q

What is the exocrine gland function of the pancreas?

A

Secretes HCO3- and a number of digetive enzymes into the pancreatic duct which in turn conducts these molecules to the epithelial lining of the duodenum.

68
Q
  • What region of the pancreas contains its endocrine cells?

- What are the 3 types of cells it houses and their function?

A

-Islets of Langerhans

  • Alpha Cells (A cells): secrete glucagon
  • Beta Cells (B cells): secrete insulin
  • Delta Cells (D cells): secrete somatostatin (growth hormone-inhibiting hormone GHIH)
69
Q

Insulin secretion is regulated by circulating _______ levels.

A

glucose

70
Q

Actions of Insulin:

  • Stimulate cellular uptake of _________ thus reducing the circulating levels.
  • Stimulates __________ and ___________ which favor the utilization of available glucose.
  • Inhibits ____________ and ______________ which inhibits the storage of glucose.
  • Stimulates cellular uptake of amino acids.
A
  • glucose
  • glycolysis and glycogenolysis
  • gluconeogenesis and glycogenolysis
71
Q

Insulin is an ___________ hormone.

A

anabolic

72
Q

Insulin favors the immediate use of glucose and the _________ of glucose.

A

storage

73
Q

What has the opposite effect of insulin and is released from A cells in response to declining insulin levels? It works to increase the concentration of glucose and fatty acids in the blood stream. It is a ________ hormone.

A
  • glucagon

- catabolic

74
Q

What are the exocrine functions of the pancreas?

A
  • Digestive enzymes ESSENTIAL for processing food.

- HCO3 neutralizes the acidic pH of the gastric juices.

75
Q

_______ _______ are the specialized organelle in pancreatic acinar cells for digestive enzyme storage.

A

Zymogen granules

76
Q

What exocrine enzymes are secreted by the pancreas?

A
  • Proteases (digest proteins and peptides to single amino acids)
  • Pancreatic lipase (digests triglycerides, monoglycerides, and FFAs)
  • Amylase
77
Q

Zymogens are a storage form of digestive enzymes, do they have catalytic activity?

A

Not until they are transformed.

78
Q
  • _____ _________ occurs when there is an abnormal activation of digestive enzymes within the pancreas.
  • It results in the ____________ of the pancreas.
A
  • Acute Pancreatitis

- autodigestion

79
Q

What are some causes of Acute Pancreatitis?

A
  • Gallstones
  • Chronic ETOH consumption
  • Idiopathic
  • Pancreatic cancer
  • Drugs
80
Q

What are the symptoms of Acute Pancreatitis?

A
  • Pain, N/V, anorexia

- Abdominal pain (sharp and severe), position changes do not alleviate the pain

81
Q
  • Pancreatitis can be _____ or _______.
  • It is a _______ disease (hyperglycemia, hypoxemia, kidney failure, hypovolemia and shock, jaundice and portal vein thrombosis)
A
  • acute or chronic

- systemic

82
Q

What is the treatment of Acute Pancreatitis?

A
  • IV fluids
  • analgesics
  • NPO/stop feeding the patient
  • Severe pancreatitis: Admission to ICU
83
Q

What are the PT implications for Acute Pancreatitis?

A
  • Presents with back pain.
  • Pancreatic scarring may occur and limit trunk extension.
  • Don’t feed the patient if NPO.
  • Bed positioning: side-lying, knee-chest position with a pillow pressed against the chest or sitting with trunk flexed.
84
Q

PART 5

A

PART 5

85
Q

Chronic Pancreatitis:

  • Characterized by the development of __________ changes in the pancreas secondary to chronic inflammation.
  • Chronic _________ pain, ______ abuse, decreased apetite, weight loss, poor QOL.
  • _________ pain with radiation to the back.
  • Pain relieved by knee to chest or bending forward.
  • Diabetes
A
  • irreversible
  • abdominal pain, opioid abuse
  • epigastric
86
Q

Pancreatic Cancer:

  • Adenocarcinoma >__ yo.
  • 70% of blockage occurs at the ______ of the pancreas.
  • More common in _________.
  • Diagnosed as an advanced disease.
  • Wt loss, pain, jaundice.
  • Impaired ________, _______ performance, and ROM.
  • Intractable ____ pain.
A
  • 55 yo
  • head of the pancreas
  • blacks
  • posture, muscle performance, and ROM
  • back pain
87
Q

What is a whipple procedure?

A

-Done to remove a tumor in the head of the pancreas, ampulla, or the first part of the duodenum.

What is resected?

  • Head of pancreas
  • Gallbladder
  • End of common bile duct
  • Ampulla
  • Duodenum
  • Possible part of stomach
88
Q

DM Type I:

  • Accounts for __-__% of all cases of DM.
  • Type IA = ?
  • Type IB = ?
  • Regardless of the type, these patients are on indefinite _______ therapy.
A
  • 5-10%
  • Type IA = Autoimmune destruction of B cells resulting in an insulin deficiency.
  • Type IB = Insulin deficiency with no evidence of autoimmune disease.
  • insulin
89
Q

What are the complications that can arise from DM Type I?

A
  • Diabetic ketoacidosis
  • Hyper- and hypoglycemia
  • Coma induced by hypoglycemia
90
Q

What is diabetic ketoacidosis?

A

Accelerated degredation of fatty acids -> formation of ketones -> lowers blood pH

91
Q

What are the clinical features of DM?

A
  • Polyuria- Excessive urination/clear the excess glucose.
  • Polydipsia- Excessive thirst.
  • Polyphagia- Excessive appetite.
  • Weight loss- Excessive fat catabolism.
  • Ketoacidosis- Secondary to increased fat catabolism.
92
Q

DM Diagnostic Values:

  • What is the normal fasting glucose levels?
  • What is the IFG (impaired fasting glucose) levels?
  • What is the provisional diagnosis of diabetes levels?
A
  • FPG <100 mg/dl (5.6 mmol/l) = normal fasting glucose
  • FPG 100–125 mg/dl (5.6–6.9 mmol/l) = IFG (impaired fasting glucose)
  • FPG ≥126 mg/dl (7.0 mmol/l) = provisional diagnosis of diabetes

FPG = fasting plasma glucose

93
Q

What is the optimal Hb A1C level?

A

<7% or g/dl

94
Q

DM Type II:

  • Acounts for __-__% of all cases of DM.
  • Is reaching epidemic proportions in this country.
  • Can reflect an insulin ________ and/or _________.
  • Patients may or may not be on insulin therapy.
A
  • 80-90%

- deficiency and/or resistance

95
Q

_______ syndrome is a pre-diabetic syndrome. What are the components of it?

A

Metabolic Syndrome

  • Dyslipidemia
  • HTN (increased Na retention)
  • Abdominal obesity
  • Insulin resistance
  • Proinflammatory state
  • Prothrombin state
  • Large waist (>35in women, >40in men)
96
Q

Diabetic Retinopathy:

  • Diabetic Retinopathy can take __-__ years to appear.
  • __% been found to have retinopathy at time of diagnosis.
  • After 20 years, __% of type IIs will have retinopathies.
  • Progression can be slowed with glycemic control.
A
  • 5-20
  • 21%
  • 60%
97
Q

Diabetic Nephropathy:

  • Diabetes is the most common cause of ______, responsible for approximately __% of all cases.
  • 20-30% of all diabetics will develop ESRD.
  • ________ and ______ control reduce risk and slows progression of nephropathy.
A
  • ESRD
  • 40%
  • glycemic and HTN control
98
Q

Diabetic Neuropathy:

  • Involves damage to nerves (______, ______, and _________).
  • Often involves ______ extremities.
  • Characterized by loss of sensation; sensation of numbness, tingling, and burning; and ______ weakness.
A
  • sensory, motor, and autonomic
  • lower
  • muscle weakness
99
Q

___________ ________ ______ Syndrome is an inflammatory syndrome characterized by varying degrees of bone and joint disorganization secondary to underlying neuropathy, trauma, and perturbations of bone metabolism

A

Diabetic Charcot Foot Syndrome

S3 - Pathophysiology (14 decks)

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