Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Jess GI > 5.2: Liver and pancreatic disease > Flashcards

5.2: Liver and pancreatic disease Flashcards

1
Q

In alcoholic liver disease, what is the basis of an enlarged abdomen, liver and spleen?

A

Destruction of normal liver architecture through cirrhosis reduces the liver’s production of albumin and the passage of blood flow through the liver - increasing pressure in the portal venous system. Since the portal system has no valves, this will raise the pressure in the splanchnic vasculature draining into it (causing spleenomegaly). A higher hydrostatic>oncotic pressure results in fluid leaking into the peritoneal cavity causing ascites.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What causes portosystemic anastomoses and what can happen as a result of this?

A

When the pressure/resistance in portal flow exceeds the pressure in the systemic veins, portal venous blood is diverted via the poro-systemic venous anastomoses which can become varicose as they enlarge

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What term is used to describe the radiating dilated (varicose) veins seen on a patient’s abdomen

A

Caput medusa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Name three general types of liver function tests that can be done

A
  1. Hepatocellular damage; ALT/AST, y-GT (y-glutamic transpeptidase)
  2. Cholestasis (decrease in bile flow due to impaired secretion or obstruction); bilirubin (and alkaline phosphatase can suggest this)
  3. Test the liver’s function; albumin, prothrombin time, glucose
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

When is jaundice clinically detectable? Name the three ways jaundice is classified

A

> 40micromol/L

Classified three ways:

  1. Prehepatic (hemolytic - abundant unconjugated bilirubin in the blood)
  2. Hepatic (problem with the liver, cannot secrete and/or conjugate bilirubin)
  3. Post hepatic (cholestatic, obstruction to drainage so bilirubin can’t leave the liver)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are three potential lab findings of prehepatic jaundice?

A
  1. Unconjugated hyperbilirubinaemia
  2. Reticulocytosis; immature RBCs (many new ones being formed to try to compensate for the excessive breakdown)
  3. Anemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Name two inherited, one congenital and three acquired causes of pre-hepatic jaundice

A

Inherited: Hemoglobinopathies (i.e thalassemias, sickle cell, etc), metabolic defects
Congenital: Gilbert’s syndrome (benign, lack of function of the enzyme that conjugates bilirubin)
Acquired: drugs, burns, infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What happens in hepatic jaundice and what are two potential complications?

A

Liver cannot manage the bilirubin its getting, leads to cell necrosis and can cause some cholestasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Name four possible lab findings in hepatic jaundice

A
  1. Mixed unconjugated and conjugated hyperbilirubinemia: (unconjugated trying to get in, but if liver is partially working will have some conjugated)
  2. Raised AST/ALT: reflects liver damage
  3. Increased alkaline phosphatase: can reflect a degree of cholestasis
  4. Abnormal clotting
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Name five causes of hepatocellular/hepatic jaundice

A
  1. Alcohol (can cause cirrhosis)
  2. Hepatic tumours
  3. Drugs (i.e paracetsamol)
  4. Wilson’s disease
  5. Hemochromatosis; hereditary where iron is despoted in the tissues leading to liver damage, diabetes and bronzer discolouration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is characteristic of post-hepatic jaundice?

A

Obstruction of the biliary system so conjugated bilirubin cannot enter the duodenum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are six potential lab findings of post-hepatic jaundice?

A
  1. Conjugated hyperbilirubinemia
  2. Dark urine; bilirubin in it
  3. Pale stools; bilirubin in it (steatorrhea)
  4. No urobilinogen in the urine (as it cannot enter the bowel and be converted/deconjugated)
  5. Increase in ALT/AST; liver damage
  6. Increase in canalicular enzymes (ALP); partly due to general cholestasis/everything is backed up
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are four intrahepatic and four extrahepatic causes of post-hepatic jaundice?

A

Intrahepatic (due to hepatic swelling)

  1. Hepatitis
  2. Drugs
  3. Cirrhosis
  4. Biliary cirrhosis (little bile ducts are blocked)

Extrahepatic (obstruction distal to the bile canaliculi)

  1. Gallstones
  2. Biliary stricture
  3. Carcinoma (esp. in the head of the pancreas)
  4. Pancreatitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is Courvoisier’s law?

A

In the presence of a non-tender palpable gallbladder, painless jaundice is unlikely to be caused by gallstones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Are you normally able to palpate gallstones?

A

No as they usually form over a long period of time as a result of a SHRUNKEN fibrotic gallbladder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Why does a gallbladder usually become enlarged?

A

Due to pathologies causing biliary obstruction over a shorter period of time (i.e like a malignancy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is hepatitis? When is it considered acute vs chronic and what lab signs would indicate for each?

A

Inflammation of the liver

Acute: if it’s less than 6 months (may see signs of jaundice and raised ALT/AST)

Chronic: >6 months
Liver failure, low albumin and low clotting factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are three main causes of hepatitis?

A
  1. Viral infection
  2. Toxins; alcohol, drugs (paracetamol), Wilson’s (copper), hemochromatosis (iron)
  3. Autoimmune
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How might you acquire each of the three main types of viral hepatitis? Do they tend to cause acute or chronic inflammation and what are three potential complications of the third type?

A

Hep A: fecal-oral, mostly acute

Hep B: body fluids/blood and vertical spread, acute or chronic - may progress to cirrhosis

Hep C: blood spread

  1. 50% chronic liver disease
  2. 30% cirrhosis
  3. 5% hepatocellular carcinoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Other than Hep A,B and C, name four other viral infections that may lead to hepatitis

A

Hep D (if there is also a Hep B infection), Hep F (similar to Hep A), EBV, CMV,

21
Q

What are the three pathological steps in alcoholic liver disease, when does it become irreversible?

A
  1. Fatty change
  2. Alcoholic hepatitis
  3. Cirrhosis - irreversible
22
Q

Name five complications of alcoholic liver disease

A
  1. Liver failure
  2. Dementia
  3. Epilepsy
  4. Encephalopathy
  5. Hepatocellular carcinoma
23
Q

What are the three most common causes of liver cirrhosis? Name the three major clinical features

A

Top 3 causes: alcohol, Hep B/C, non-alcoholic fatty liver disease

Major clinical features

  1. Liver dysfunction; jaundice, anemia, bruising, dupuytrens, palmar erythema
  2. Portal hypertension
  3. Spontaneous bacterial peritonitis
24
Q

Name five potential lab findings you may see in a patient with liver cirrhosis, how can it be managed?

A

Investigations: High AST/ALT, high bilirubin, low albumin, deranged clotting, high ALP (suggests cholestasis)

Management: stop drinking, treat complications and transplant

25
Q

List six general signs/symptoms of liver disease

A
  1. Jaundice
  2. Palmar erythema
  3. Spider naevi
  4. Gynecomastia
  5. Edema; hypoalbuminia
  6. Dupuytren’s contracture
26
Q

What are two major causes of portal hypertension?

A
  1. Obstruction to the portal vein (even pancreatic cancer can do this)
  2. Obstruction of flow within the liver, i.e cirrhosis
27
Q

Name 6 clinical manifestations of portal hypertension

*including the three sites of portal-systemic anastomoses and the resulting varicies/clinical signs

A
  1. Caput medusa (Periumbilical vein anastomoses; superior and inferior epigastric veins)
  2. Ascites
  3. Spider naevi
  4. Esophageal varicies
  5. Rectal varies (Hemorrhoids)
  6. Splenomegaly
28
Q

What are the four major pathological processes causing diseases of the gall bladder and biliary tree

A
  1. Obstruction
  2. Infection
  3. Inflammation
  4. Neoplasia
29
Q

What is cholelithiasis? What are the five classic predispositions and name 6 risk factors. What is the most common symptom?

A

Gallstones; female, fat, forty, fertile and fair

Risk factors: FH, sudden weight loss, loss of bile salts (i.e part of the small bowel removed as bile salts are usually resorbed here), diabetes, OC

Most commonly asymptomatic

30
Q

List three types of gallstones you can have and their respective characteristics

A
  1. Pure cholesterol, tend to be solitary
  2. Pigment stones (bilirubin stones), tend to be multiple small and black
  3. Mixed - 80%
31
Q

Describe the character of the pain felt in gallstones, where can it radiate, how long is it usually felt and how can it be resolved?

A

Biliary colic, sudden onset of epigastric/RUQ pain that radiates to the back and lasts 15 min-24 hours. Usually resolves spontaneously or with analgesics

32
Q

Other than pain, name three other more minor complications that can arise from gallstones?

A
  1. Gallbladder contractions; attempting to release contents past the stone
  2. Impact of stone in the cystic duct
  3. Associated nausea and vomiting
33
Q

What are three major complication of gallstones?

A
  1. Ascending cholangitis - inflammation/infection of the common bile duct. Bacteria can ascend with the duodenum
  2. Cholecystitis - inflammation of the gallbladder
  3. Sepsis (resulting from an infection)
  4. Localized peritonism
  5. Obstructive jaundice
  6. Acute pancreatitis (if there is blockage/inflammation of the pancreatic duct)
34
Q

How are gallstones managed?

A
  1. Analgesia
  2. IV fluids or antibiotics
  3. Surgery (cholecystectomy)
35
Q

What is the significance of Charcot’s triad?

A 
Indicative of ascending cholangitis
1. RUQ pain
2. Jaundice (obstructive jaundice) 
3. Fever 
\+ shock and confusion
36
Q

How is ascending cholangitis managed?

A

Life threatening:

Resuscitate, IV braid spectrum antibiotics, surgery to drain the CBD

37
Q

What is the pathogenesis of acute pancreatitis and what does the GETSMASHED acronym stand for?
*include which specific enzymes are involved

A

Enzymes released from pancreatic acini trigger an inflammatory response leading to acinar damage and duct stenosis (which can cause obstruction - which may lead to bile and acid reflux and severe constant upper abdominal pain which commonly radiates to the back. The activation of these enzymes may occur as a result of duct obstruction, infection or hyper-stimulation of the pancreatic secretions (often done by alcohol)
-enzymes include protease (tissue destruction), lipase (fat necrosis), elastase (blood vessel destruction)

Causes of acute pancreatitis: (most common are top 2) 
Gallstones
Ethanol
Trauma
Steroids
Mumps
Autoimmune
Scorpion bite
Hyperlipidemia
ERCP
Drugs
38
Q

What are four clinical signs of acute pancreatitis

A
  1. Cullen’s sign: superficial edema and bruising
  2. Grey Turner’s sign: bruising of the flank
  3. Sudden severe epigastric pain (a result of duct obstruction) that penetrates to the back
  4. Vomiting
39
Q

How is acute pancreatitis managed? What is the most notable biochemical change?

A

Treatment is supportive; IV fluids, gastric tube to rest the bowel so the pancreas isn’t constantly trying to produce more enzymes with no fluid

Most notably raised amylase

40
Q

What is characteristic of chronic pancreatitis? What are three causes and four clinical presentations?

A

This chronic inflammatory disease causes destruction of the pancreatic tissue (loss of acini and duct stenosis) and fibrosis

Causes: most commonly alcohol, CF, biliary disease

Clinical: pain, malabsorption (pancreas isn’t producing the necessary enzymes, steatorrhea), diabetes (as the endocrine system is damaged), jaundice (if the common bile duct is blocked)

41
Q

What is the prognosis of a pancreatic carcinoma discuss three reasons why? How does early metastasis affect treatment options?

A

Poor prognosis; vague and late presentation, local spread can involve many structures, resection is complicated and largely non curative.

Early metastasis means only 10-20% are suitable for surgery (many given chemo and palliative care)

42
Q

Where in the pancreas do pancreatic carcinomas typically form and what happens as a result of this?

A

70% in head of pancreas which means your more likely to have symptoms (i.e if common bile duct is blocked = obstructive jaundice and the associated symptoms)

43
Q

What are four clinical features of pancreatic carcinomas

A
  1. Painless progressive obstructive jaundice
  2. Nausea and vomiting
  3. Initially asymptomatic
  4. Weight loss (malabsorption)
44
Q

What is the reason behind ‘biliary colic’ pain?

A

Occurs if the gallstone moves to the gall bladder neck or ducts

45
Q

Name three benefits of performing a transcutaneous ultrasound to investigate (i.e pancreatic cancer)

A

Painless, no radiation, non-invasive

46
Q

What potential therapeutic advantage does endoscopic retrograde cholangiopancreatogoraphy (ERCP) have over other investigate techniques?

Name two potential side effects of this technique

A

Involves the use of an endoscope to introduce contrast medium into the biliary tree and pancreatic system. Since you cans pass forceps and diathermy stuff through the endoscope you can potentially enlarge the sphincter of Oddi and remove gallstones from the common bile duct

Side effects: infection, perforation of biliary tree

47
Q

Name two tumour markers that can be useful in the diagnosis of pancreatic carcinoma

A
  1. Carcinoembryonic antigen (CEA)

2. Ca 19-9

48
Q

Name four risk factors for pancreatic carcinomas and identify the most common one.

(For bonus, name to other specific to diet/lifestyle)

A
  1. smoking (most common)
  2. > 60
  3. Chronic pancreatitis
  4. Diabetes
    + high fat diet, alcohol

Jess GI (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions