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Pathophysiology final exam review > Lecture 13- Hepatic, Biliary, and Pancreatic > Flashcards

Lecture 13- Hepatic, Biliary, and Pancreatic Flashcards

1
Q

What are some common hepatic system functions?

A

-Conversion and excretion of bilirubin
-Detoxification of drugs, ETOH, and toxins thus lowering load on immune system
-Storage for glycogen, vitamins, iron
-Synthesizes cholesterol
-Sole source of albumin and other proteins
-Produces bile

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2
Q

What is the functional unit of the liver?

A

Liver lobule

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3
Q

What are some signs and symptoms of hepatic disease?

A

-N/V, Diarrhea, Constipation, Heartburn, Abdominal pain, GI bleeding
-Edema/Ascites (limited albumin synthesis)
-Dark urine (impaired bilirubin degradation)
-Light/clay colored stools (impaired bile secretion)
-Right upper quadrant abdominal pain
-Skin changes such as jaundice an bruising
-Neurologic involvement (confusion, sleep disturbances, muscle tremors, hyperactive reflexes

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4
Q

What type of musculoskeletal issues can be seen with hepatic disease and what is the cornerstone of liver care?

A

-thoracic pain (inter scapular, R shoulder, R upper trap, R subscapular)
-Hepatic osteodystrophy- abnormal development of bone/osteoporosis
severity of hepatobiliary disease dictates bone problems

Rest is the cornerstone of liver care, thinking of activity instead of formal exercise

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5
Q

What are some changes associated with aging and the liver?

A

-decrease in size and weight

-increased processing time

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6
Q

How does the liver heal after damage? Is this a quick process?

A

Healing involves complete parenchymal regeneration or scarring or a combination

This does occur quickly

but if there is chronic hepatic injury, there can be fibrosis (cirrhosis)

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7
Q

What are the different types of hepatic responses to insult?

A

-Inflammation (hepatitis)- can be result of liver damage or cause
-Degeneration- Occurs in response to a toxic or autoimmune insult
-Necrosis- Response to any injury
-Fibrosis- result of any severe hepatic injury and does not go away, cirrhosis is fibrosis of the entire liver.

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8
Q

What is Jaundice?

A

This is a symptom not a disease

-Hemolysis or excessive destruction of RBCs
-Decreased processing of bilirubin
-Hepatocyte dysfunction (hepatitis, hepatic disease, tumor)
-Impaired bile flow

This is treated by treating the underlying disease, return to normal skin color suggests a resolution of the disease

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9
Q

What is Cirrhosis?

A

The progressive, patterned loss of healthy tissue in the liver; replacement of damaged tissue with fibrotic tissue

-Final common pathway of progressive inflammatory and/or necrotic damage to the liver

Results in partitioning of the liver, and significant loss of liver function associated with loss of 80-90% of liver function

Makes the liver tissue hard and lumpy

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10
Q

What are some clinical implications of Cirrhosis?

A

-Osteoporosis
-Impaired posture
-Impaired muscle performance
-Loss of balance
-Deconditioning
-Ascites/bilateral edema of feet and ankles
-Blood loss

Rest to reduce metabolic demand on the liver is recommended.

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11
Q

What is portal hypertension?

A

The portal vein delivers venous blood from the GI tract to the liver, the liver then delivers this blood to inferior vena cava.

Portal hypertension describes elevated pressure within the portal system.

Vascular resistance and blood flow are the two important factors contributing to the development of portal hypertension

consequence of cirrhosis induced blockage of portal blood flow and occurs in drainage system that enters portal vein.

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12
Q

What are some consequences of portal hypertension?

A

Ascites: from increase hydrostatic venous pressure
-Splenomegally: from venous congestion of the spleen
Hemmrrhoids- from venous congestion of the large bowel
Venous hums- continuous noises audible in patients with portal hypertension

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13
Q

What is hepatic encephalopathy?

A

Potentially irreversible, decreased level of consciousness in people with severe liver disease

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

Insidious onset-progressive worseing of symptoms

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14
Q

Symptoms of hepatic encephaolopathy?

A

Depression, personality changes, impaired attention, drowsiness, sleep disorders, ataxia, asterixis, hyperreflexia
-marked confusion, incoherent speech, muscle rigidity

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15
Q

Implications for the PT of hepatic encephalopathy?

A

-Patient safety
-impaired motor and sensory integrity, impaired mobility, balance
-impaired arousal
-Risk for pressure ulcers secondary to malnutrition, immobility, edema

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15
Q

What is ascites?

A

An abnormal accumulation of fluid in the peritoneal cavity

this is associated mostly with cirrhosis

caused by increased hydrostatic venous pressure (portal hypertension) and back up of blood

Implications: accompanying impaired cardiac and respiratory function, lymphedema, integumentary disorders, malnutrition, muscle degradation

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16
Q

What is Hepatitis?

A

An infection by one of the several viruses with specific affinity for the liver (A, B, C, D, E)

acute or chronic inflammation of the liver

chronic hepatitis: viruses, medications, metabolic abnormalities, autoimmune disorders, idiopathic

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17
Q

Are most people with hepatitis symptomatic? How is it diagnosed?

A

Most people with chronic hepatitis are asymptomatic, symptoms when they appear are nonspecific

It is diagnosed through serologic testing (specific Ab, liver function tests, liver biopsy)

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18
Q

What is the prognosis of hepatitis?

A

This depends on the presence of liver comorbidities and the development of cirrhosis
Occurrence of liver cancer or cirrhosis hastens the progression

survival for compensated hepatitis is good 90%> 5 years,

survival for uncompensated hepatitis is extremely low (variceal bleeding, ascites, hepatic encephalopathy)

require a liver transplant

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19
Q

What is fulminant hepatitis?

A

A viral liver disease that progresses in the course of a few weeks from onset of symptoms to hepatic encephalopathy

rapid hepatic failure

characterized by massive liver parenchyma necrosis and liver size (atrophy)

occurs after infection with certain hepatitis viruses, alcoholic hepatitis, or drug induced liver injury

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20
Q

What is Hepatitis A? (HAV)

A

It is formerly known as “infectious hepatitis”
spread by close personal contact or oral-fecal contamination of water and food

Benign and self limiting disease

high risk of acute infection, but most with acute disease recover with no lasting liver damage

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21
Q

What is hepatitis B? (HBV)

A

formerly known as serum hepatitis
formerly known as “serum hepatitis”​

Spread parenterally by transfusion, needle sticks, IV drug use/shared needles, dialysis, sexual contact, bodily fluid​

At risk: Healthcare workers who come in contact with blood​

Acute symptoms: See above​

Most persons with acute disease recover with no​ lasting liver damage; acute illness is rarely fatal​

15 - 25% of chronically infected persons develop chronic liver disease

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22
Q

What is hepatitis C?

A

Leading cause of chronic liver disease​

Transmitted by contact with blood of an infected person, primarily through contaminated needles, sexual contact, needle sticks​

Acute illness is uncommon​

75%–85% of newly infected persons develop chronic infection. 5-20% develop cirrhosis​

15%–25% of newly infected persons clear the virus​

Annual mortality: 12K

23
Q

What is hepatitis D and E?

A

Hepatitis D​

Only occurs in people who are also infected with the Hepatitis B virus​

Has both acute and chronic forms​

Hepatitis E​

uncommon​

enterically transmitted, water-borne mild disease occurring mostly in Africa and Asia

24
Q

Other common causes of Liver disease?

A

Drug- and toxin-induced liver disease​

Dose-related meaning that if enough drug is administered, there will be liver damage​

drugs include acetaminophen, tetracycline, anti-neoplastic agents; alcohol

alcoholic induced liver damage , 10 million americans are alcoholics and about 10-15% will develop cirrhosis

what happens?
Direct mitochondrial damage due to acetaldehyde production from ethanol metabolism​

Fatty 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

25
Q

Other causes of liver disease continued

A

Hemachromatosis​

Wilson’s disease (copper overload)​

Hereditary alpha-1 antitrypsin deficiency: results in cirrhosis​

Reyes’s syndrome: Fatty liver and develop acute encephalopathy. Develops after acute viral illness. Aspirin administration to children​

Prolonged obstruction in the biliary tree​

Liver carcinomas/mets from colon, lung or breast

26
Q

What is the biliary system?

A

Creates, moves, stores, and releases bile into the duodenum

Gallbladder-
Saclike organ attached to the inferior surface of the liver​

Stores and concentrates bile, which drains to it from the liver​

35-100 ml storage capacity for bile-yellowish green fluid (bile salts, cholesterol, bilirubin​

Bile ducts → hepatic ducts → cystic duct

27
Q

What are most biliary diseases attributed to?

A

gallstones (cholelithiasis) or inflammation of gallbladder (cholecystitis)

28
Q

What is Cholelithiasis ?

A

“Gallstone disease”​

One of the most common GI diseases in the US and a major reason for abdominal surgery​

Occurs when stones form in the bile and move into the biliary tract

29
Q

How do gall stones form, what are they made of, and how do they cause obstruction/pain?

A

Stones form in the gall bladder​

Form when the composition of the bile changes​

Cholesterol stones (80% of all cases)​

Bilirubin salt stones (20% of all cases)​

75% of patients with stones are asymptomatic​

25% of patients with stones become symptomatic​

Physically obstruct ducts → distension of bladder​

Muscles in the duct contract onto the stones→ pain​

Cystic duct most frequent site of obstruction

30
Q

What are symptoms of gall stones?

A

abdominal pain, R upper quadrant
-abdominal tenderness and muscle guarding
-pain may radiate to shoulder and upper back or midback/scapula

Diagnosed with ultrasound and treated with surgery (cholecystectomy)

31
Q

What are some risk factors for gallstones?

A

age
genetics
decreased physical activity
obesity
poor lipid profile
RA
TPN
liver disease
Biliary structures
DM

32
Q

How can PTs help manage?

A

PT management includes breathing exercises, turning, coughing, wound splinting, compression stockings, early activity to prevent clot formation and increase early intestinal motility

33
Q

What are the different types of cells of the pancreas?

A

Alpha cells (endocrine): Secrete glucagon, 25% of the cells​

Beta cells (endocrine): Secrete insulin, 50-70% of the cells​

Delta cells (endocrine): Secrete somatostatin (growth hormone)​

Acinar cells: Responsible for the production, storage and regulated secretion of digestive enzymes [lipases, proteases, trypsinogen and amylase

34
Q

What is pancreatis?

A

An inflammation of the pancreas​

May result in the autodigestion of the pancreas​

Acute form, chronic form​

A systemic disease

35
Q

Details of acute pancreatitis

A

May involve surrounding organs​

Causes:​

Gallstones (obstruction of the common bile duct)​

Chronic ETOH consumption​

Inappropriate activation of trypsinogen​

Symptoms:​

Pain, N&V, anorexia​

Abdominal pain: cardinal symptom of acute pancreatitis; sharp & severe; position changes do not alleviate the pain

36
Q

What are some 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

37
Q

Details of chronic pancreatitis?

A

Characterized by the development of irreversible changes in the pancreas 20 to chronic inflammation​

Chronic abdominal pain, opioid abuse, decreased appetite, wt. loss poor quality of life​

Epigastric (upper central region of the abdomen) pain with radiation to the back​

Pain relieved by knee to chest or bending forward​

Diabetes

38
Q

What is Pancreatic cancer?

A

Adenocarcinoma (cancer that starts in the glands that line the inside of an organ); ​

> 55 YOA​

Head of the pancreas (70%); blockage of pancreatic duct​

More common in blacks than whites​

Diagnosed most often as advanced disease​

Wt. loss, pain and jaundice​

Impaired posture​

Impaired muscle performance, ROM​

Intractable back pain

39
Q

Function of the exocrine pancreas?

A

constitutes 80% of the pancreas

cells are in grape like clusters called acini

the cells contain digestive enzymes that are exocytosed into the lumen of the acinus

linked to a duct system that conducts through pancreatic duct, common bile duct, and into duodenum.

enzymes such as trypsinogen, lipases, amylase, etc.

also cells are source of bicarbonate, which acts to neutralize acidity of the chyme in the GI system

40
Q

Phases of pancreatic exocrine function

A

Cephalic Phase: Sight of food, mediated by vagus nerve​

Gastric phase​

Release of gastrin in response to stomach distension​

Stimulates release of zymogen granules into pancreatic ducts

Intestinal phase​

Low pH induces intestine to release secretin ​

Presence of fatty acids and peptides stimulate the release of cholecystokinin (CCK) from the small intestine​

These hormones stimulate the release of pancreatic juices

40
Q

Causes of acute pancreatitis?

A

gallstones and alcoholism

both act to block important ducts

41
Q

What is involved with the endocrine pancreas?

A

Called the Islets of Langerhans​

Constitutes 1-2% of the pancreas​

Receives 15% of the pancreatic blood flow​

Islets house 3 types of cells​

Alpha cells (A cells): Secrete glucagon​

Beta cells (B cells): Secrete insulin​

Delta cells (D cells): Secrete somatstatin​

Innervated by the autonomic nervous system

41
Q

What is type 1 diabetes mellitus?

A

Replaces Juvenile-onset or Insulin Dependent (IDDM) diabetes mellitus​

Accounts for 5-10% of all cases of DM​

Type IA​

Autoimmune destruction of B cells resulting in an insulin deficiency​

Type IB​

Insulin deficiency with no evidence of autoimmune disease​

Patients are on indefinite insulin therapy

42
Q

What are some actions of insulin?

A

Stimulates cellular uptake of glucose​

Reduces circulating levels of glucose​

​

Stimulates glycolysis and glycogenolysis​

Stimulates cellular uptake of amino acids​

Is an anabolic hormone​

​

Stimulates the uptake of glucose by fat cells and its conversation into fats​

​

Favors the immediate use of glucose and the storage of glucose​

​

Stimulates cell growth and synthesis of new mRNA’s

43
Q

Long term complications from type 1 diabetes?

A

CV disease, stroke, kidney failure, foot ulcers, retinal defects

44
Q

Clinical features of DM?

A

Polyuria​

Excessive urination/clear the excess glucose​

Polydipsia (excessive thrist)​

​

Polyphagia​

Excessive catabolism leads to negative energy balance and increased food intake​

Weight loss​

Excessive catabolism​

Ketoacidosis​

Secondary to increased protein catabolism

45
Q

Diagnosing diabetes?

A

Symptoms of diabetes plus casual plasma glucose concentration ≥200 mg/dl (11.1 mmol/l). Casual is defined as any time of day without regard to time since last meal. The classic symptoms of diabetes include polyuria, polydipsia, and unexplained weight loss. ​

or​

FPG ≥126 mg/dl (7.0 mmol/l). Fasting is defined as no caloric intake for at least 8 h.​

or​

2-h postload glucose ≥200 mg/dl (11.1 mmol/l) during an OGTT.

46
Q

Diagnosing diabetes continued

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 (the diagnosis must be confirmed, as described below).​

​

FPG = fasting plasma glucose​

IFG = Impaired plasma glucose

47
Q

What is type 2 diabetes?

A

Type II diabetes​

Replaces Adult-onset or Non-insulin Dependent Diabetes Mellitus (NIDDM)​

Accounts for 80-90% of all cases of DM​

Is reaching epidemic proportions in this country (metabolic syndrome)​

Can reflect an insulin deficiency and/or insulin resistance​

Patients may or may not be on insulin therapy​

Life style disorder: Inactivity and/or obesity

48
Q

Details of glycemic control?

A

Defined by Hb A1C levels​

Glycosylated hemoglobin​

Measure of glucose control ​

​

Optimal level < 7% or 7 g/dl​

Normal levels < 6 % or 6 g/dl​

Monitored at least biannually​

​

Reduction of Hb A1C levels from 8% to 7 %​

14% decrease in all cause mortality & incidence of MI’s

risk of adverse event is very high with increased a1c levels

important that patients know this

49
Q

What is metabolic syndrome?

A

components include:
Dyslipdemia​

Hypertension (Increased Na retention)​

Abdominal obesity​

Insulin resistance (elevated glucose levels, impaired glucose tolerance)​

Proinflammatory state​

Prothromboic state (increased risk for clot formation)​

A large waist is 35 inches or more in a woman and 40 inches or more in a man.

50
Q

Diabetic retinopathy

A

Slow in developing​

5- 20 yrs to appear​

​

Type II​

21% been found to have retinopathy at time of first diagnosis​

After 20 yrs. 60% of type II’s will have retinopathies​

​

Progression can be slowed with appropriate glycemic control

51
Q

Diabetic nephropathy

A

Diabetes most common cause of ESRD​

Responsible for approximately 40% of all cases​

​

20-30 % of all diabetics will develop ESRD​

​

Blacks and Hispanics are at greater risk than non-Hispanic whites​

​

Glycemic control and HTN control reduce risk and slows progression of nephropathy

52
Q

Diabetic neuropathy

A

Damage to nerves​

Involves both motor and sensory nerves​

Often involves lower extremities​

Can involve autonomic nerves​

​

Characterized by:​

Loss of sensation​

Sensation of numbness, tingling, burning​

Muscle weakness (weakness in the tibialis anterior)​

Foot drop

Pathophysiology final exam review (1 decks)

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