5.2- Diseases of the Liver and Pancreas Flashcards
(49 cards)
1
Q
What 3 tests check liver function?
A
- Hepatocellular damage
- aminotransferases (ALT/AST)
- gamma glutamyl transpeptidase (y-GT)
- Cholestasis ( bile ducts)
- bilirubin
- alkaline phosphatase; suggests cholestasis or bone breakdown
- Synthetic function (APG)
- albumin
- prothrombin time (clotting)
- glucose
2
Q
What is jaundice?
A
yellow pigmentation of the skin and sclera caused by accumulation of bilirubin in tissue
- clinically detectable when bilirubin>40umol/L
- normal range <22 umol/L
3
Q
How do you classify jaundice?
A
1) Prehepatic ( haemolytic)
2) Hepatic (parenchymal)
3) Post-hepatic (cholestatic); backup of bilirubin in blood
4
Q
What is the cause of jaundice?
A
disruption of the normal metabolism of bilirubin
May arise from any:
- Excessive bilirubin production because of increased haemolysis ( pre-hepatic)
- Reduced capacity of liver cells to secrete unconjugated bilirubin into blood; hepatic/intra-hepatic
- obstruction to drainage of bile, causing backup of bilirubin into liver ; post-hepatic
5
Q
What is bilirubin?
A
- breakdown product of RBCs
- unconjugated biliirubin is bound to albumin in blood
- bilirubin is conjugated in the liver ie bound to glucoronic acid+becomes water soluble
- excreted in bile into duodenum
- de-conjugated into urobilinogen
- urobilinogen oxidised to form urobilin and stercobilin, which go into faeces
6
Q
Once formed, what happens to urobilinogen?
A
- it gets oxidised in the duodenum to form urobilin and stercobilin, which leave in the stool
- trace of urobilinogen also gets reabsorbed into the eneterohepatic circulation:
and then re-excreted in bile
-also goes to kidneys and colour them yellow
7
Q
What is pre-hepatic jaundice?
A
- because of excessive haemolysis due to anything
- liver is unable to cope with excess bilirubin
LAB FINDINGS:
1) Unconjugated hyperbilirubinaemia: (because bilirubin is unconjugated before it gets to the liver)
ie high amounts, is pre-hepatic jaundice
2) Reticulocytosis: immature RBCs (pre-hepatic jaundice)
3) Anaemia
8
Q
What are the causes of pre-hepatic jaundice?
A
ie anything that causes haemolysis
- Inherited:
- RBC membrane defects
- Haemoglobinopathies eg sickle cell
- metabolic defects
- Congenital hyperbilirubinaemias
-Gilbert’s syndrome- common a lack of function in the enzyme that conjugates bilirubin
- Crigler-Najjar syndrome-rare
- Dubin Johnson syndrome-rare
- Acquired:
- immune
- mechanical
- infections
- drugs eg NSAIDS, cephalosporins, nitrafurantoin
9
Q
What is hepatocellular jaundice?
A
ie hepatic/ intra-hepatic jaundice
- deranged hepatocyte function
- cell necrosis→inability to metabolise or excrete bilirubin
- happens w cholestasis ie slow sloppy movement of bile
10
Q
What are the lab findings of hepatocellular jaundice?
A
- mix of unconjugated and conjugated hyperbilirubinaemia
- increased liver enzymes ie AST/ALT, reflects liver damage
- same or increased ALP; causes cholestasis and swollen cells (alkaline phosphatase)
- abnormal clotting
11
Q
Name 9 causes of hepatocellular jaundice?
A
- Congenital
- Hepatic inflammation
- Autoimmune hepatitis
- Alcohol
- Drugs eg paracetamol
- Cirrhosis
- Hepatic tumours
- Haemochromatosis-depositions of Fe
- Wilson’s disease- depositions of Cu
12
Q
What is post-hepatic/cholestatic/jaundice?
(OBSTRUCTIVE JAUNDICE)
A
- Obstruction of biliary system; can be intrahepatic or extrahepatic
- passage of conjugated bilirubin locked
13
Q
What are the lab findings of post-hepatic/obstructive jaundice?
A
- conjugated hyperbilirubeinaemia
- bilirubin in urine ie dark ( bc of backup through liver intoblood; gets excreted into urine instead)
- pale stools ie steatorrhoea
- no urobilinogen in urine ie no bilirubin enters bowel so is not converted to urobilinogen
- increased canalicular enzymes ie ALP ( indicator of cholestasis/blockage of bile)
- raised ALT and AST bc of backing into liver
14
Q
What are the causes of post-hepatic jaundice? ( Intrahepatic and Extrahepatic)
A
INTRAHEPATIC:hepatocyte swelling (HDCP)
- hepatitis
- drugs
- cirrhosis
- primary biliary cirrhosis
EXTRAHEPATIC: obstruction distal to bile canaliculi (GBC)
- gallstones
- biliary structure
- carcinoma in:
- head of pancreas
- ampulla
- cholangiocarcinoma ie bile duct
- porta hepatis lymph nodes
15
Q
What is Courvoisier’s law for post-hepatic jaundice?
A
- in the presence of a non-tender palpable gallbladder, painless jaundice is unlikely to be caused by gallstones
- GB is often more enlarged when there is biliary obstruction over a shorter period of time eg malignancy
-tender GB seen in:
- acute cholecystitis; tender and distended w a mucocele or empyema related to gallstones
16
Q
Recap: What are the 3 types of jaundice?
A
HOT LIVER
Pre-hepatic- Haemolytic
Hepatic- Obstruction
Post hepatic- cholestatic ie tumour
17
Q
What is hepatitis?
A
- inflammation of the liver*
- can be acute or chronic
- Acute hepatocyte breakdown; causes Aminotransferase release (AST/ALT) and jaundice
- Prolonged/chronic damage:
- synthetic failure*
- low albumin*
- low clotting factors*
18
Q
What are the causes of Hepatitis?
A
- infections-viral
- Toxins ie alcohol/haemochromatosis/ Wilson’s disease/drugs
- Autoimmune
19
Q
What is viral hepatitis and what are the types?
A
- Hepatitis A:
-goes in via the faecal-oral route ie contaminated water+ usually acute
6F’s: faeces, flies fluid, field, fluids, fingers, food
- Hepatitis B:
- blood/body flluids/ vertical spread eg cervical transmission
- acute and chronic; may progress to cirrhosis
- Hepatitis C:
- blood spread
- involves chronic liver disease, cirrhosis and hepatocellular carcinoma
20
Q
State the pathology and complications of alcoholic liver disease
A
- Pathology:
fatty change
alcoholic hepatitis
cirrhosis
- Complications: (6)
- hepatocelluar carcinoma
- liver failure bc of cirrhosis
- Wernicke-Korsakoff syndrome
- Dementia
- Encephalopathy
- Epilepsy
21
Q
What is liver cirrhosis?
A
- liver cell necrosis, causes nodular regeneration and fibrosis
- increased resistance to blood flow
- deranged liver function
22
Q
What are the causes of liver cirrhosis?
A
- alcohol
- hepatits B/C
- non-alcoholic fatty liver disease
- primary biliary cirrhosis
- autoimmune hepatitis
- haemachromatosis
- Wilson’s disease
23
Q
Name some clinical features of liver cirrhosis.
A
-LIVER DYSFUNCTION:
- jaundice
- anaemia
- Dupuytren’s contracture
- palmar erythema
- bruising
- Portal hypertension
- Spontaneous bacterial peritonitis
24
Q
What is defined as portal hypertension?
A
- portal venous pressure> 12 mmHg due to intrahepatic or extrahepatic portal venous compression/ occlusion
CAUSED BY:
- Obstruction of the portal vein; blood backs up and opens up channels to other places
- Obstruction of flow withun the liver ie cirrhosis
25
What investigations do you conduct for liver cirrhosis? (6)
* check for normal raised ALT/AST
* increased ALP
* increased bilirubin
* decreased bilirubin
* deranged clotting
* check for low Na
26
How do you manage liver cirrhosis? (STT)
* Stop drinking
* Treat compliations
* Transplantation
27
Name 5 clinical manifestations of portal hypertension?
* splenomegaly
* spider naevi
* ascites
* oesophageal/ rectal varices
* caput medusa
28
What are the different ducts near the liver and GB?
GB responsible for storage and passage of bile from liver to duodenum
Pathological processes which cano happen (OIIN)
- Obstruction
- Inflammation
- Infection
- Neoplasia
29
What are gallstones?
cholelithiasis
(fair, fat, fertile, female and forty)
30
What are the risk factors for getting gallstones? (6)
* increasing age
* positive family history
* sudden weight loss eg after obesity surgery
* loss of bile saltsl eg ileal resectiom, terminal ileitis
* oral contraception
* diabetes
31
What are the 3 types of gallstones?
* **MIXED:** cholesterol w calcium and bile pigments
* **PURE CHOLESTEROL:** usually solitary, up to 5cm
* **PIGMENT STONES( BILIRUBIN STONES):** calcium bilirubinate, multiple, small and black
32
Name 5 complications of gallstones?
* Biliary colic
* Cholecystitis
* Ascending cholangitis
* Obstructive jaundice
* Acute pancreatitis
33
What is biliary colic?
* happens in cystic duct; impaction of stone in the cystic duct
* gallbladder contraction happens to try and get rid of obstruction
* sudden onset of epigastric/ RUQ pain that radiates to the back
* lasts from 15 mins-24 hours; resolves spontaneously or w analgesics
* associated nausea and vomiting
34
What is cholecystitis?
inflammation of the gallbladder
* impaction of stone in cystic duct
* RUQ pain and fever
* sepsis
* local peritonism
* raised WBC count
* gall bladder mass
* raised attacks may become chronic
35
How is cholecystitis managed?
* analagesia
* NBM- nil by mouth
* IV antibiotics and fluids
* surgery: **laparoscopic cholecystectomy**
36
What is ascending cholangitis?
* inflammation/infection of the common bile duct
* bacteria ascend from the CBD junction with the duodenum
* bile duct is already partially obstructed by gallstones
* LIFE THREATENING
37
How does ascending cholangitis present and how can it be managed?
Presents with:
**Charcot's triad:**
***-RUQ pain***
***-Obstructive jaundice***
***-Fever, shock, confusion***
Manage with:
- resuscitate
- IV broad spectrum antibiotics
- surgery; **Endoscopic drainage of common bile duct**
38
What is pancreatitis?
* inflammation of the pacnreas
* inflammatory process caused by effects of enzymes released from pancreatic acini
* can be acute or chronic
39
Differentiate between acute and chronic pancreatitis?
**Acute pancreatitis:** -oedema, haemorrhage, necrosis
(OHN)
Chronic pancreatitis: fibrosis and calcification (FC)
40
What are the causes of acute pancreatitis?
GET SMASHED
* **Gallstones**
* **Ethanol**
* Trauma
* Steroids
* Mumps
* Autoimmune
* Scorpion bite
* **Hyperlipidaemia**
* ERCP/ iatrogenic
* Drugs
41
What is the pathogenesis of acute pancreatitis?
* **Duct obstruction**; juice and bile reflux
* **Acinar damage;** from reflux or drugs
* **Protease** leaking out from tissue destruction
* **Lipase** from fat necrosis
* **Elastase** from blood vessel destruction
42
What are the clinical signs of acute pancreatitis?
* sudden severe epigastric pain
* penetrates to the back
* vomiting
* steadily decreases over 72 hours
43
How is acute pancreatitis treated?
* supportive; **drip and suck; IV fluids and NG tube**
* **fluid balance**
44
What biochemical changes do you see in acute pancreatitis?
* **high amylase**
* **low calcium**
* **high glucose**
* **high ALP/ bilirubin**
45
What is chronic pancreatitis?
* **parenchymal destruction, fibrosis, loss of acini and duct stenosis**
* **Chronic alcoholism**; CF, inherited, biliary disease
46
What are the clinical signs of chronic pancreatitis?
* **pain**
* **malabsorption; weight loss, steatorrhoea**
* **jaundice**
* **DM**
47
What are the risk factors of pancreatic carcinoma?
* smoking
* over 60 yrs
* high fat diet
* alcohol
* chronic pancreatitis
* DM
* FHx
48
What are the clinical features of pancreatic carcinoma?
late presentation, early metastases and poor survival rates
-normally a ductal adenocarcinoma, mostly in the head of pancreas
* initially asymptomatic
* painless progressive obstructive jaundice
* nausea and vomiting
Symptoms:
* **pain**
* **weight loss**
* **malabsorption**
* **diabetes**
* **carcinomatosis**
49
How is pancreatic carcinoma managed?
* surgery
* chemotherapy
* palliative
