Brainscape's Knowledge GenomeTM

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


See full index

Haroon flashcards > liver > Flashcards

liver Flashcards

1
Q

Describe the drug metabolism of aspirin

A

Phase I:
- Hydrolysis reaction:
Aspirin + H2O —> Salcylic acid + Ethanoic acid

Phase II:
- Conjugated with glycine or glucuronic acid
- Forms a range of ionised products which can be excreted

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

What is the metabolism reaction of alcohol

A

ADH = alcohol dehydrogenase
ALDH = aldehyde dehydrogenase

Ethanol—ADH—> acetaldehyde—ALDH—> Acetate —> CO2 + H20

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

Functions of the liver

A

(ADMIReS)
Albumin
Detoxification
Metabolism of carbs and billirubin
Immunity (Kuppfer cells)
Regulation of oestrogen levels
e
Storage (vitamins ADEK, Fe, Cu, fat)

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

Liver function tests (LFTs) - markers of liver function

A
  • Bilirubin (mainly unconjugated)
  • Albumin
  • Prothrombin time (PT/INR)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Direct markers of liver damage

A
  • Highun conjugated bilirubin
  • Low albumin
  • High PT/INR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Enzymes that show liver damage is likely

A
  • AST and ALT
  • AST:ALT usually around 1

If your AST levels are too high, it might be a sign of an injury affecting tissues other than the liver. High ALT levels may mean you have a liver injury.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Bilirubin metabolism

A

1 – Creation of Bilirubin
Reticuloendothelial cells are macrophages which are responsible for the maintenance of the blood, through the destruction of old or abnormal cells. They take up red blood cells and metabolise the haemoglobin present into its individual components; haem and globin. Globin is further broken down into amino acids which are subsequently recycled into new rbcs.

Meanwhile, haem is broken down into iron and biliverdin, a process which is catalysed by haem oxygenase. The iron gets recycled to rbcs, while biliverdin is rapidly reduced (bilverdin reductase) to create unconjugated bilirubin.

2 – Bilirubin Conjugation
In the bloodstream, unconjugated bilirubin binds to albumin to facilitate its transport to the liver. Once in the liver, glucuronic acid is added to unconjugated bilirubin by the enzyme glucuronyl transferase. This forms conjugated bilirubin, which is more soluble. This allows conjugated bilirubin to be excreted into the duodenum in bile.

3 – Bilirubin Excretion
Once in the colon, colonic bacteria deconjugate bilirubin and convert it into urobilinogen. Around 80% of this urobilinogen is further oxidised by intestinal bacteria and converted to stercobilin and then excreted through faeces. It is stercobilin which gives faeces their brown colour.

Around 20% of the urobilinogen is reabsorbed into the bloodstream as part of the enterohepatic circulation. It is carried to the liver where some is recycled for bile production, while a small percentage reaches the kidneys. Here, it is oxidised further into urobilin and then excreted into the urine.

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

What is the name of the cells responsible for fibrosis?

A

Stellate

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

Functions of the peritoneum

A

In health:
- Visceral lubrication
- Fluid and particulate absorption
In disease:
- Pain perception
- Inflammatory and immune response
- Fibrinolytic activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Risk factors for biliary tract disease

A
  • Female
  • Fat (BMI 30+)
  • Forty (+)
  • Fertile (pregnant or many children)
  • Fair

also:
- Family history
- Fatty liver disease (non-alcoholic)
- T2DM
- Haemolytic conditions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Symptoms of ascending cholangitis

A

Charcot’s triad:
- RUQ pain
- High fever
- Jaundice
Reynold’s pentad:
- Charcot’s triad + altered mental state + hypotension

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

Diagnosis of ascending cholangitis

A
  • FBC: leukocytosis
  • LFT: high conjugated hyperbilirubinaemia
  • Abdo ultrasound for CBD dilation and gallstones
  • MRCP: diagnostic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Treatment of ascending cholangitis

A
  • ERCP (bile duct clearance)
  • Laproscopic cholecystectomy once stable to prevent recurrence
  • Consider risk of sepsis
  • Empiricle while waiting Abx - co-amoxiclav
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

MRCP and ERCP

A

MRCP = Magnetic resonance cholangio-pancreatography
ERCP = Endoscopic retrogade cholangio-pancreatography

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

Murphy sign

A
  • RUQ tenderness, ask patient to take a breath in while pressing RUQ
  • Will wince or stop inspiring normally in cholecystitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Symptoms of cholecystitis

A
  • RUQ pain
  • Fever
  • Tender gallbladder
  • Referred pain to tip of right shoulder (phrenic)
  • Murphy sign positive
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Diagnosis of cholesystitis

A
  • FBC: leukocytosis + neutrophilia
  • LFT: normal
  • Abdo ultrasound shows thickened gallbladder wall 3mm≤
    and stones/sludge in and fluid around gallbladder
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Treatment for cholecystitis

A
  • Surgery within 1 week, typically done within 72 hours
  • via laproscopic cholecystectomy
  • Until then: IV fluids, analgesia, antibiotics if necessary, nothing by mouth
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Complications of cholecystitis

A
  • Sepsis
  • Gallbladder empyema
  • Gangrenous gallbladder
  • Perforation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are gall stones made from?

A
  • Cholestrol (80%)
  • Pigment
  • Or mixed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Symptoms of gallstones

A
  • Colicky or sharp pain
  • Fever
  • Jaundice
  • Dietary upset

Worse after a fatty meal, may come in episodes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Diagnosis of gall stones

A

Bloods:
- Alanine transaminase
- Bilirubin
- Amylase

Then:

First line: Abdominal ultrasound to identify gallstones

Or: MRCP (MRI scan) or CT abdomen & pelvis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Aetiology of gall stones

A
  • Cholesterol supersaturation (diet, hormones)
  • Genetic (gallbladder motility)
  • Haemoglobin turnover (haemolytic anaemia, cirrhosis, sickle cell)

10% of people have gallstones
And they acount for 30% of all acute presentations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Management of gall stones if not treating directly/straight away

A
  • NSAIDs for mild pain
  • IM diclofenac for severe pain
  • Change lifestyle
  • Decrease fat in diet
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Treatment of gallstones

A

Symptomatic OR asymptomatic and stone blocks CBD:
Elective laproscopic cholecystectomy
Radiological drain (cholesystostomy)
ERCP (endoscopy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Complications of gallstones that may also be signs

A
  • Acute cholecystitis
  • Acute cholangitis
  • Obstructive jaundice
  • Pancreatitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is it called when a gall stone is trapped in the common bile duct?

A

Choledocholelithiasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is a hernia?

A

Protrusion of an organ through a defect in its containing cavity. Typically bowel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Reducible vs irreducible hernias

A

Reducible - can be pushed back into place
Irreducible:
- Obstructed - intestinal obstruction
- Strangulation - intestinal ischaemia
- Incarcerated - contents fixed in sac due to size or adhesions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Curative treatment for hernias

A

Surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Other types of hernias

A
  • Umbilical (in neonates)
  • Incisional (surgical scars)
  • Epigastric
  • Obturator (Howship-Romberg sign)
  • Diastasis recti
  • Spigelian
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is a femoral hernia?

A
  • Bowel herniates through femoral cord
  • Female, mid-old age
  • Very likely to strangulate due to rigid femoral canal borders
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Symptom of femoral hernia

A

Swelling in upper thigh pointing down

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Diagnosis of femoral hernia

A
  • Abdo/pelvic ultrasound if unsure
  • BUT usually clinical (based on symptoms)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Borders of the femoral TRIANGLE

A

Sartorius laterally
Adductor longus medially
Inguinal Ligament superiorly

⛵️

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Borders of the femoral CANAL (within the femoral triangle)

A

Femoral vein laterally
Lacunar ligament medially
Inguinal ligament anteriorly
Pectineal ligament posteriorly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Rolling hiatal hernias

A
  • 20%
  • LOS stays in the abdomen
  • Part of fundis rolls into thorax
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Sliding hiatal hernias

A
  • 80%
  • LOS slides into abdomen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is a hiatal hernia?

A
  • Stomach herniates through diaphragm aperture
  • Obese women and 50+ year olds
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Symptoms of hiatal hernias

A
  • GORD
  • Dysphagia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Diagnosis of hiatal hernias

A
  • Barium swallow (diagnostic)
  • Oesophago gastro duodenoscopy
  • Chest x-ray
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is an inguinal hernia?

A
  • Spermatic cord herniates through inguinal canal
  • In males (obviously
  • History of heavy lifting/abdopressure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Direct inguinal hernias

A
  • 20%
  • In Hesselbach’s triangle
  • Medial to inferior epigastrics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Hesselbach’s triangle

A

Rectus abdominis medially
Inferior epigastric vessels superiorly/laterally
Poupart’s (inguinal) ligament inferiorly

🪦

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Indirect inguinal hernias

A
  • 80%
  • Not in Hesselbach’s triangle
  • Lateral to inferior epigastrics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Symptoms of inguinal hernias

A
  • Painful swelling in groin
  • Points along groin margin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Diagnosis of inguinal hernias

A
  • Usually clinical
  • Unsure = AUSS (CT/MRI)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Acute vs chronic pancreatitis

A

Acute
- Reversible acute inflammation of the pancreas
Chronic
- 3+ month history of pancreatic deterioration
- Irreversible pancreatic inflammation + fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Causes of acute pancreatitis

A

Idiopathic

Gallstones
Ethanol🍾🍷🍻
Trauma

Steroids
Mumps/malignancy
Autoimmune
Scorpion stings
Hypercalcaemia/hyperlipidaemia
ERCP
Drugs (azathiprine, NSAIDs, ACE inhibitors, tobacco, thiazides)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Pathophysiology of acute pancreatitis

A
  • Gall stones obstruct pancreatic secretions
  • Accumulated digestive enzymes in pancreas
  • Host defences soon overwhelmed
  • Causes autodigestion -> inflammation + enzymes leak in blood
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Symptoms of acute pancreatitis

A
  • Sudden severe epigastric pain radiating to the back (DDx: abdominal aortic aneurysm)
  • Nausea and vomiting
  • Jaundice
  • Pyrexia
  • Steatorrhoea
  • Grey Turner sign and Cullen sign
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Diagnosis of acute pancreatitis

A
  • Blood test first line: High serum amylase/lipase
  • Cxr to eclude gastroduodenal perforation
  • Abdo ultrasound -> diagnostic for gall stones; CT/MRI for extent of damage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Glasgow score for severity of acute pancreatitis

A

PaO2 < 8KPa
Age > 55
Neutrophils (WBC > 15x109/L)
Calcium > 2mmol/L
Renal urea > 16mmol/L
Enzymes (LDH > 600iu/L or AST > 200iu/L)
Albumin < 32g/L
Sugar, glucose > 10mmol/L

0-1 - mild pancreatitis
2 - moderate pancreatitis
3+ - severe pancreatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Treatment for acute pancreatitis

A
  • Rescuscitation if required
  • IV fluid
  • IV analgesia
  • IV antibiotics for infection/associated cholangitis
  • Nil by mouth
  • ERCP within 72 hours of pain onset if required
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Main complication of acute pancreatitis

A

Systemic inflammatory response syndrome (SIRS)
2 ≤ out of:
- Tachycardia (90+ bpm)
- Tachypnoea (20+ RR)
- Pyrexia (38°c <)
- High WCC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Causes of chronic pancreatitis

A
  • Alcohol (mc)

Also:
- CKD
- CF
- Trauma
- Recurrent acute pancreatitis
- Cancer
- Autoimmune

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Symptoms of chronic pancreatitis

A
  • Epigastric pain radiating to back - exacerbated by alcohol
  • Exocrine (eg: steatorrhoea) and endocrine (eg: T2DM) dysfunction
  • Pseudocysts or abscesses

DDx: Pancreatic cancer, especially of body and tail

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Diagnosis of chronic pancreatitis

A
  • Faecal elastase low (indicator of exocrine function)
  • Abdo ultrasound and CCT to detect pancreatic calcification and dilated pancreatic duct (diagnostic)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Treatment of chronic pancreatitis

A
  • Alcohol cessation
  • Dietary modification
  • Analgesia for abdo pain, first line = NSAIDs
  • Pancreatic supplements (eg: enzymes, insulin for DM)
  • ERCP or surgery if required
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Pathophysiology of primary biliary cholangitis

A
  • Intrahepatic autoimmune jaundice affecting intralobular bile ducts
  • Autoantibodies cause intralobular bile duct damage; chronic autoimmune granulomatous inflammation
  • Resulting in cholestasis -> Fibrosis, cirrhosis, portal hypertension, infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Risk factors for primary biliary cholangitis

A
  • Female
  • 40-50 years old
  • Other autoimmune disease
  • Smoking
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Complications of primary biliary cholangitis

A
  • Malabsorption of fats + vit ADEK (=steatorrhoea)
  • Ostemalacia
  • Coagulopathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Symptoms of primary biliary cholestasis

A
  • Initially often asymptomatic
  • Routine test shows high anti-mitochondrial antibodies
  • Pruritis + fatigue earliest, then jaundice, then hepatosplenomegaly, + xanthelasma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Diagnosis of primary biliary cholangitis

A
  • LFT
  • Rule out acute hepatitis by testing for HepBsAg and HVCAb
  • Serology
  • Rule out extrahepatic cholestasis via ultrasound
  • Liver biopsy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

LFT and serology results for primary biliary cholangitis

A

LFT:
- High ALP
- High conjugated bilirubin
- low albumin
Serology:
95% have anti-mitochondrial antibodies (especially M2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Liver biopsy results for primary biliary cholangitis

A
  • Portal tract infiltrate (lymphocyte + plasma cell)
  • 40% granulamatous
  • Portal tract fibrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Treatment for primary biliary cholangitis

A
  • Ursodeoxycholic acid (reduces intestinal absorption of cholesterol)
  • Colestyramine to treat pruritus
  • Consider vitamin ADEK supplements
  • May ultimately need liver transplant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Pathophysiology of primary sclerosis cholangitis

A
  • Autoimmune destruction of intra + extralobular hepatic duct
  • Blocks the flow of bile out of the liver into the intestines
  • Chronic bile obstruction eventually leads to liver inflammation (hepatitis), fibrosis and cirrhosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Risk factors for primary sclerosing cholangitis

A
  • Male
  • 40-50
  • Strong link to IBD (especially ulcerative cholitis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Presentation of primary sclerosis cholangitis

A
  • 50% asymptomatic until disease advances
  • Charcot’s sign
  • Pruritis
  • Fatigue
  • Hepatosplenomegaly
  • IBD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Diagnosis of primary sclerosing cholangitis

A
  • Cholestatic LFT
  • GS imaging: MRCP
  • Biopsy same as PBC
    Serology:
  • HBVsAg/HCVAb -ve
  • AMA -ve
  • Coelic screen anti tTG -ve
  • pANCA +ve in 33-88%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Treatment of primary sclerosing cholangitis

A

Conservative:
- Colestyramine for pruritis
- Fat soluble ADEK
- ERCP to dilate and stent structures
- Consider liver transplant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Risk factors for alcoholic liver disease

A
  • Chronic alcohol
  • Obesity
  • Smoking
  • Female gender
  • Genetic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Stages of alcoholic liver disease

A

steatosis (fatty liver, undamaged)

alcohol hepatitis (w/ mallory bodies)

alcohol cirrhosis (micronodular)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Symptoms of alcoholic liver disease

A
  • Early stages may be asymptomatic
    Later:
  • Chronic liver failure symptoms
  • Alcohol dependency
  • Hepatomegaly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Assessing alcohol dependency

A
  1. Alcohol use disorder ID test: 10 questions
  2. Questionnaire with CAGE questions (>2 = dependent!)
    - Should you cut down?
    - Are people annoyed by your drinking?
    - Do you feel guilty about drinking?
    - Do you drink in the morning? (eye opening)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Diagnosis of alcoholic liver disease

A

Bloods
- LFT shows liver damage
- High GGT-
- (gamma-glutamyl transferase (GGT) test measures the amount of GGT in the blood. GGT is an enzyme found throughout the body, but it is mostly found in the liver. When the liver is damaged, GGT may leak into the bloodstream. High levels of GGT in the blood may be a sign of liver disease or damage to the bile ducts)
-
- AST:ALT > 2
- Macrocytic and megaloblastic anaemia
Biopsy to confirm extent:
- Mallory cytoplasmic inclusion bodies
- Inflammation and necrosis in alcoholic hepatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Conservative treatment for alcoholic liver disease

A
  • Healthy diet, lower BMI
  • Stop alcohol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Pharmacological treatment for alcoholic liver disease

A
  • Consider steroids short term (Maddrey’s discriminant value of 32)
  • IV thiamine (Vit B1) so you don’t develop Wernicke Korsakoff syndrome
  • Could also give folate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Surgical treatment for alcoholic liver disease

A
  • Consider liver transplant for ESLF cases-end stage liver failure
  • Must have abstained from alcohol for 3+ months
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Complications of alcoholic liver disease

A
  • Pancreatitis
  • Hepatic Encephalopathy
  • Ascites
  • HCC= Hepatocellular carcinoma
  • Mallory-weiss tear
  • Wernicke Korsakoff syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Pathophysiology of ALD

A
  • Alcohol dehydrogenase enzymes and cytochromes (2 ways of metabolism)

Alcohol dehydrogenase and acetaldehyde dehydrogenase reduce nicotinamide adenine dinucleotide (NAD) to NADH (reduced form of NAD). Excessive NADH in relation to NAD inhibits gluconeogenesis and increases fatty acid oxidation, which in turn promotes fatty infiltration in the liver.

oxidative stress promotes hepatocyte necrosis and apoptosis in these patients. Free radicals can also induce lipid peroxidation, which can cause inflammation and fibrosis. The alcohol metabolite acetaldehyde, when bound to cellular protein, produces antigenic adducts and induces inflammation.

  • Risk of forming reactive O2 species, more overload = more O2 species
  • Eventual scar tissue around central veins, adding to portal hypertension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Delirium tremens+ treatment

A
  • Alcohol stimulates GABA receptors and inhibits glutamate receptors
  • Chronic alcohol leads to upregulation of glutamate receptors and downregulation of GABA receptors
  • Treat wirh IV Chlordiaepoxide or diazepam
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Alcohol units

A
  • 1 unit = 8g/10ml pure alcohol
  • Recommended no more than 14 units a week for both men and women

Equation:
strength (ABV) x volume (ml)
dividedby
1000

              1000
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Alcohol withdrawal

A

6-12 hours: tremours, sweating, headaches
12-24 hours: hallucination
24-48 hours: seizures
24-72 hours: delirium tremens (medical emergency)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Gilbert’s syndrome

A
  • Most common in males
  • T1DM
  • Autosomal recessive
  • Most common cause of hereditary jaundice
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Pathophysiology of Gilbert’s syndrome and Crigler Najjar syndrome

A
  • Autosomal recessive
  • Deficient or abnormal UGT (UDP101), reducing UGT activity
  • Causes an excess in unconjugated hyperbilirubinaemia

(In Crigler Najjar, UGT is completely gone)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Presentation of Gilbert’s syndrome

A
  • 30% asymptomatic
  • Typically males around 20
  • May present with painless jaundice at a young age
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Symptoms of Crigler Najjar syndrome

A
  • More severe than Gilbert’s
  • Jaundice
  • Nausea and vomiting
  • Lethargy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Treatment of Gilbert’s and Crigler Najjar syndrome

A
  • Gilbert’s: Usually no need
  • CN: Phototherapy to break down unconjugated bilirubim
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Complications of Crigler Najjar syndrome

A
  • More severe progression chances
  • Can die from kernicterus in childhood
  • Kernicterus is accumulation of bilirubin in the basal ganglia, causing severe neurological deficits
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

What do all types of hepatitis show?

A

Interface necrosis
“Piecemeal necrosis” on histology (don’t ask wjhat it looks like bc idk)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Pathophysiology of autoimune hepatitis

A
  • Chronic inflammation of the liver - aka: lupoid hepatitis, very rare
  • T helper cell mediated response vs hepatocytes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Risk factors for autoimmune hepatitis

A
  • Female:male, 4:1
  • Nitrofurantoin use
  • Other autoimmune diseases
  • Viral hepatitis
  • HLA DR3 or DR4
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Type 1 autoimmune hepatitis

A
  • Adult females
  • 80% of cases
  • ANA - antinuclear antibody (found in many other autoimmune diseases but very specific for Type 1 autoimmune hep)
  • ASMA - antismooth muscle antibody
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Type 2 autoimmune hepatitis

A
  • Young females
  • Rarer
  • ALC-1 (antiliver cystosol)
  • ALKM-1 (antiliver-kidney microsome)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Presentation of autoimmune hepatitis

A
  • 25% asymptomatic
  • Many = jaundice, fever, hepatosplenomegaly
  • Anorexia
  • Lupus-like rash
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Treatment for autoimmune hepatitis

A
  • Corticosteroids - prednisolone
  • Immunosuppressants - azathioprine
  • Hep A+B vaccination (depending on cause)
  • Last resort - consider transplant
99
Q

Pathophysiology of viral hepatitis

A

Inflammation of the liver as a result of viral replication within hepatocytes

100
Q

Virus types of Hepatitis

A
  • All are single-strand RNA
  • Apart from Hep B, which is double-strand DNA
101
Q

Which hepatitis needs to be notified to Public Health England?

A

All

102
Q

Which types of hepatitis have 100% immunity after infection?

A

A & E

103
Q

Acute vs chronic hepatitis

A
  • Acute: First 6 months of liver inflammation
  • Chronic: Any inflammation beyond 6 months
104
Q

Spread of Hep A

A
  • Faeco-oral spread
  • Fly vectors
  • Picornavirus
105
Q

Risk factors for Hep A

A
  • Overcrowding
  • Poor sanitation
  • Shellfish
  • Travel - endemic in Africa, Asia, South America, Middle East
106
Q

Pathophysiology of Hep A

A
  • Incubation for 2 weeks
  • Replicates in liver, excreted in bile
  • Self limiting within 6 weeks (having it/vaccine gives 100% immunity)
  • Acute, mild
107
Q

Symptoms of Hep A

A

Prodromal phase (1-2 weeks):
- Malaise
- Nausea and vomiting
- Fever
Then:
- Jaundice - dark urine + pale stools
- Hepatosplenomegaly
- Skin rash

108
Q

Diagnosis of Hep A

A
  • Bloods: High ESR + leukopenia
  • LFT: Bilirubin high when there is jaundice
  • Serology:
    HAV IgM = acutely infected
    HAV IgG = chronically infected
109
Q

Treatment of Hep A

A
  • Supportive (treatment often not required)
  • Travellers vaccine available
110
Q

Complications of Hep A (Rare)

A

Fulminant liver failure😶‍🌫️

111
Q

Spread of Hep B

A
  • Needles (needlestick injury, tattoo, IVDU)
  • Sexual
  • Vertical (mother -> child)
  • Horizontal (between children)

Blood borne and found in semen and saliva

112
Q

Risk factors for Hep B

A
  • IVDU
  • MSM
  • Dialysis patients
  • Healthcare workers
  • Present worldwide
113
Q

Symptoms of Hep B

A
  • Similar to Hep A
  • 1-2 weeks prodrome
  • Then jaundice (dark urine + pale stools), hepatomegaly, uticaria-hives, arthralgia- joint pain
114
Q

Pathophysiology of Hep B and incubation period

A
  • Acute infection infects hepatocyte, cellular response usually clears it
  • Incubation 1-6 months
115
Q

Serology chart for Hep B

A

HBsAg: acute, chronic, can be carrier

Anti HBsAg: cleared, vaccine

IgM Anti HBcAg: acute

IgG Anti HBcAg: chronic, carrier, cleared

116
Q

Hepatitis B antigens and antibodies diagram

A

Surface antigen: HBsAg. +ve = infection. Vaccine = HBsAg

E antigen: HBeAg. Released during replication. +ve = acute phase. high level = high infectivity

Core antigen: HBcAg. not in blood. Middle of virus(core)

Surface antibody: HBsAb. response to HBsAg. +ve = vaccinated or infected

E antibody: HBeAb. Response to HBeAg. +ve = been through active phase - immune response

Core antibody: HBcAb. response to HBcAg.

IgM is higher in acute infection and lower in chronic.
IgG with positive and negative HBsAg= past infection

117
Q

Treatment for Hep B

A
  • Peginterferon alfa-2a
  • Antiviral therapy
  • IV Igs for neonates
118
Q

Complications of Hep B

A
  • 5-10% of cases progress to chronic liver failure + HCC risk
  • HBV-associated decompensation with HCC has the worst prognosis
  • 90% cases in children become decompested and associated with poor prognosis. TRANSPLANT
119
Q

Spread of Hep C

A

Blood-borne and bodily fluids

  • IVDU
  • Flavivirus
  • IVDU more than vertical/sexual transmission
  • More common in the UK, again common in Africa
120
Q

Symptoms of Hep C

A
  • Often acutely asymptomatic, allowing it to become chronic later on
  • Few patients with flu-like symptoms
  • Chronic causes a sow progressive fibrosis over years + hepatosplenomegaly
121
Q

Diagnosis of Hep C

A
  • LFTs
  • Serology:
    HCVRNA = current infection/diagnoses acute infection
    HCVAb = presents within 4-6 weeks of infection, if present after 6 months then it’s chronic
122
Q

Treatment of Hep C

A

Direct acting antivirals, expensive 💸
- NS5A-inhibitor (acivir)
- NS5B-inhibitor (buvir)
- Previr

123
Q

Complications of Hep C

A

30% cases progress to chronic liver failure (cirrhosis and HCC risk)

124
Q

Spread of Hep D

A
  • Intravenous drug use
  • Sexually transmitted
125
Q

Pathophysiology of Hep D

A
  • Acute + chronic (like Hep B)
  • Dependant on surface antigen of Hep B to replicate, makes Hep B more likely to progress to cirrhosis/HCC
  • Clinically indistinguishable from acute Hep B
126
Q

Diagnosis of Hep D

A

Manifests as co-infection IgM HDV + IgM HBV

127
Q

Treatment and complications of Hep D

A
  • Treat Hep B
  • Can also use inteferons but not that good lol
128
Q

Spread of Hep E

A
  • Faeco-oral (undercooked pork)
  • Water
  • Dogs
  • Calicivirus
129
Q

More on Hep E

A
  • Usually self limiting acute hepatitis (95% are asymptomatic)
  • Commoner than Hep A in the UK (endemic)
  • Common in Indo-China
130
Q

Complications of Hep E

A
  • Can cause chronic disease in immunosuppressed
  • Can cause fulminant liver failure:
    Normal mortality 1-2%
    Pregnant ladies 10-20% !!!
131
Q

Diagnosis of Hep E

A

Serology:
HEV IgM = acute infection
HEV IgG = recovery, only chronic in immunocompromised patients

132
Q

Treatment of Hep E

A
  • Supportive, self limiting
  • Vaccine only in China! 🇨🇳
133
Q

Primary vs secondary liver cancer

A

Primary
- Less common
- Cancer that originates in the liver
- Hepatocellular carcinoma (90%) and cholangiocarcinoma (10%)
- There are also benign primary tumours
Secondary
- More common
- Cancer that originates outside of the liver and metastasises to the liver

134
Q

Types of benign primary tumours

A
  • Hepatic adenoma
  • Focal nodular hyperplasia
  • Haemangioma - most common, seen in infants as “strawberry mark” on skin within first few weeks of life 🍓
135
Q

What does cholangiocarcinoma arise from

A
  • The biliary tree
  • Typically adenocarcinomas
136
Q

Risk factors for cholangiocarcinoma

A
  • Parasitic flukeworms
  • Biliary cysts
  • IBD
  • Primary sclerosing cholangitis
137
Q

Symptoms of cholangiocarcinoma

A
  • Abdominal pain
  • Weight loss
  • Puritis
  • Fevers
  • COURVOISER sign (but pancreatic cancer is usually more comon)you have jaundice and a gallbladder that is enlarged but is not painful.

🌌late constellation of symptoms as tumour is slow growing🌌

138
Q

Diagnosis of cholangiocarcinoma

A
  • LFT: high bilirubin, high ALP
  • High CEA and CA19-9
  • First line = imaging: abdominal ultrasound + CT
  • ERCP (imaging of biliary tree) - invasive but can be therapeutic and diagnostic
139
Q

Treatment of cholangiocarcinoma

A

Majority of cases inoperable as patients present very late

140
Q

What does hepatocellular carcinoma (HCC) arise from?

A

Liver parenchyma

141
Q

Risk factors of HCC

A
  • Chronic hepatitis virus - C and B
  • Decompensated liver cirrhosis
142
Q

What does HCC metastasise to?

A
  • Lymph nodes, bones, lungs
  • Via haematogenous spread (hepatic/portal veins)
143
Q

Symptoms of HCC

A
  • Signs of decompensated liver failure (jaundice, ascites, HE…)
  • Signs of cancer (TATT, unexplained weight loss, nausea, vomiting…)
  • May have irregular hepatomegaly
144
Q

Diagnosis of HCC

A
  • High serum AFP
  • Imagine: first line ultrasound, CT for confirmation
  • Biopsy is diagnostic but often avoided to prevent seeding of tumour elsewhere
145
Q

Treatment for HCC

A
  • Surgical resection of tumour
  • In decompensative cirrhosis -> liver transplant
  • Prevantative: Hep B vaccineas hep b can cause hcc
146
Q

What is pancreatic cancer?

A
  • Adenocarcinoma (in most cases) of the exocrine pancreas
  • Of ductal origin
  • Typically affects the head of the pancreas
147
Q

Risk factors for pancreatic cancer

A
  • Males
  • 60+
  • Smoking
  • Alcohol
  • DM
  • Family history/genetics (PRSS-1 gene mutation)
  • Chronic pancreatitis
148
Q

What parts of the pancreas does pancreatic cancer usually target?

A
  • Head - 60%
  • Body - 25%
  • Tail - 15%
149
Q

Presentation of pancreatic cancer of the head

A

Courvoisier sign
- Painless jaundice
- Pale stools + dark urine
- Palpable gall bladder

150
Q

General presentation of pancreatic cancer

A
  • Epigastric pain radiating to the back, worse at night (relieved sitting forward)
  • Trousseau sign - migratory thrombophlebitis
  • Weight loss and anorexia
  • Recent diagnosis of DM
  • Nausea
  • Vomiting
  • Constipation
151
Q

Referral for pancreatic cancer

A
  • Over 40 + jaundice - 2 week wait referral for suspected cancer pathway
  • Over 60 + weight loss + one other symptom - direct access CT scan within 2 weeks
152
Q

Management of pancreatic cancer

A
  • Mainly palliative due to very poor prognosis, 5 year survival rate of 3%
  • Surgery (Whipple’s procedure) + post-op chemo if no mets
153
Q

Diagnosis of pancreatic cancer

A
  • CT scan and histology from a biopsy
  • CA19-9 tumour marker (non-specific)
  • CT TAP scan (thorax, abdomen pelvis) for staging
154
Q

Ammonia

A
  • Neurotoxic - causes irreversible brain damage
  • Because it stops the Krebs cycle
155
Q

Symptoms of liver failure

A
  • RUQ pain
  • Hepatomegaly
  • Jaundice
  • Nausea and vomiting
  • Ascites
  • Bruising or muscle wasting
156
Q

Aetiology of acute liver failure

A
  • Viral: Viral hepatitis, CMV, EBV
  • Autoimmune hep (more chronic)
  • Drugs: paracetamol overdose, alcohol, ecstasy
  • HCC
  • Metabolic: Wilson’s, haemochromatosis, A1ATD
  • Budd Chiari syndrome
157
Q

Fulminant liver failure

A
  • Rare syndrome of massive multiacinar necrosis
  • Rapid
  • Caused by paracetamol overdose in 50% of cases in the UK
158
Q

Types of fulminant liver failure

A

Hyperacute - Hepatic encephalopathy within 7 days of jaundice
Acute - Hepatic encephalopathy within 8-28 days of jaundice
Subacute - Hepatic encephalopathy within 5-26 weeks of jaundice

159
Q

Pathophysiology of acute liver failure

A
  • Declined liver function
  • Liver loses regeneration/repair ability -> irreversibly damaged
  • In patient with previously normal liver
160
Q

West Haven criteria grades 1-4 of hepatic encephalopathy

A
  1. Altered mood, sleep problems
  2. Lethargy, mild confusion, asterixis, jaundice
  3. Marked confusion, solmonence, ataxia
  4. Comatose
161
Q

Presentation of acute liver failure and their diagnosis

A
  • Jaundice - hyperbilirubinaemia
  • Coagulopathy - raised PT/INR over 1.5
  • Hepatic encephalopathy - EEG
  • Extent of liver damage: biopsy GOLD STANDARD

Top 3 are main characteristics

162
Q

Diagnosis of acute liver failure

A
  • Bloods
  • Imaging
  • Microbiology
163
Q

Bloods for acute liver failure

A
  • LFTs show liver damage (High bilirubin, low albumin, high PT/INR)
  • High serum AST + ALT
  • High NH3
  • Low glucose
164
Q

Imaging for acute liver failure

A
  • EEG to grade HE
  • Abdominal ultrasound to check for Budd Chiari syndrome
165
Q

Microbiology for acute liver failure

A
  • To rule out infections
  • Blood culture, urine cultire, ascitic tap
166
Q

Treatment of acute liver failure

A
  • ITU, ABCDE, fluid, analgesia
  • Treat underlying cause and complications
167
Q

Treatments for complications of liver failure

A
  • High ICP: IV mannitol
  • HE: Lactulose (increases NH3 excretion)
  • Coagulopathy: Vit K
  • Ascites: Diuretics, esp spironolactone
  • Sepsis: Sepsis 6 pathway
168
Q

Cause of failure with lung pathology

A

Alpha 1 antitrypsin deficiency

169
Q

Risk factors for chronic liver failure

A
  • Alcohol
  • Obesity
  • T2DM
  • Drugs
  • Inherited metabolic diseases/existing autoimmunity
170
Q

Assessing prognosis and requierd treatment for chronic liver disease

A

✨Child-Pugh score✨
- Considers bilirubin, ascites presence, serum albumin, PT/INR, hepatic encephalopathy
A: 100% 1 year survival
B: 80% 1 year survival
C: 45% 1 year survival

171
Q

End stage liver failure

A
  • Decompensated cirrhosis
  • A high risk factor for developing hepatocellular carcinoma
172
Q

Presentation of chronic liver failure

A
  • Same as acute +
  • Portal hypertension
  • Oesophageal varices
  • Caput medusae- the appearance of a network of painless, swollen veins around your bellybutton
  • Spider naevi- dilation of preexisting central arterioles from which numerous thin-walled capillary branches radiate like red spider legs, carrying away freely flowing blood
  • Palmar erythema- a rare condition that makes the palms of the hands turn red.
  • Gynecomastia
  • Clubbing 🕺
  • Fetor hepaticus - chronic bad breath due to liver
  • Dupuytren contracture- an abnormal thickening of tissues in the palm of the hand. The thickened tissues may develop into a hard lump. Over time it can cause 1 or more fingers to curl (contract) or pull in toward the palm.
173
Q

Diagnosis of chronic liver failure

A
  • Liver biopsy to determine extent (fibrosis vs cirrhosis)
  • LFT, imaging, ultrasound, ascitic tap culture
174
Q

Treatment of chronic liver failure

A
  • Prevent progression (decrease alcohol and BMI, avoid drugs)
  • Consider liver transplant if decompensated liver failure
  • Manage complications
175
Q

Progress of chronic liver failure

A

hepatitis/ cholestasis —> fibrosis (reversible damage) —-> cirrhosis (irreversible) —> compensated (some extent of liver function) OR decompensated (ESLF)

176
Q

Aetiology of chronic liver failure

A
  • ALD (Most common)
  • NAFLD
  • Viral: Hep B, C, D
  • Budd Chiari syndrome
  • Drugs
  • Autoimmine
  • PBC + PSC
177
Q

Pathophysiology of liver cirrhosis

A
  • The result of chronic inflammation and damage to liver cells
  • When liver cells are damaged, they are replaced with scar tissue, fibrosis, and nodules within the liver
  • Increased resistance leading to portal hypertension
178
Q

Aetiology of liver cirrhosis

A
  • Alcoholic liver disease (most common cause in developed world)
  • Non-alcoholic fatty liver disease
  • Hepatitis B
  • Hepatitis C
179
Q

Complications of liver cirrhosis

A
  • Ascites
  • Portal hypertension
  • Varices
  • Jaundice
  • Spider naevi + caput medusae
  • Coagulopathy
  • Hypoalbuminaemia -> oedema
  • Portosystemic encephalopathy
  • Hepatorenal and hepatopulmonary syndromes
180
Q

Diagnosis of liver cirrhosis

A
  • LFTs show liver damage (most accurate)
  • FBC: thrombocytopenia
  • ALT, AST, ALP are all deranged
  • Definitive = liver biopsy
181
Q

Treatment for liver cirrhosis

A
  • Definitive = liver transplant
  • Conservative: fluids, analgesia, alcohol abstinence, good nutrition
  • Treat complications
182
Q

Compensated vs decompensated cirrhosis

A

Compensated - liver is able to override ability to function

183
Q

Pathophysiology of alpha 1 antitrypsin (A1AT) deficiency

A
  • Autosomal recessive muttion of serdina-1 gene (protease inhibitor) on chromosome 14 causes deficiency of A1AT
  • A1AT normally inhibits NE-neutrophil elastase, NE degrades elastic tissue
    Lungs:
  • Degrades elastic tissue
  • Alveolar duct collapse
  • Air trapping
  • Characteristic panacinar emphysema
    Liver:
  • Soon becomes fibrotic; cirrhosis + HCC risk
  • A1AT is made by the liver so fibrotic will make synthetic liver function even worse - catch 22
184
Q

Presentation of A1AT deficiency

A
  • Young/mid aged man with little to no smoking history but COPD-like symptoms
    Lung symptoms:
  • Dyspnoea
  • Chronic cough
  • Sputum production
  • Barrel chest - chest becomes expanded in size
  • Pink puffer- fast, labored breathing may cause their skin to appear red or pink temporarily
    Liver symptoms:
  • Jaundice
185
Q

Diagnosis of A1AT deficiency

A
  • Serum A1AT < 20mmol/L
  • Barrel chest on exam, cxr shows hyperinflated lungs
  • CT = panacinar emphysema
  • LFT shows obstruction (FEV1:FVC < 0.7)
  • Genetic testing
186
Q

Treatment for A1AT deficiency

A
  • If smoking, stop
  • Manage ephysema, eg: inhalers (SABAs and LABAs)
  • Consider hepatic decompensation patients for liver transplant
187
Q

Pathophysiology of haemachromatosis

A
  • Autosomal recessive mutation of HFE gene (chromosome 6)
  • Excess Fe uptake by transferrin-1 and low hepcidin synthesis (hepcidin regulates Fe homeostasis)
  • Fe accumulation and fibrosis of liver (+ pancreas, kidney, heart, skin, ant. pituitary)
188
Q

Normal Fe vs Fe in haemochromatosis

A
  • Normal: 3-4g
  • Haemochromatosis: 20-30g
189
Q

Risk factors for haemochromatosis

A
  • Male
  • 50s
  • Genetics
  • Can be due to excess transfusions (secondary)
190
Q

Symptoms of haemochromatosis

A
  • Fatigue
  • Joint pain
  • Hypogonadism (due to anterior pituitary damage)
  • Slate grey/bronze skin
  • Liver cirrhosis symptoms
  • Osteoporosis
  • Heart failure
191
Q

Gross Fe overload triad

A
  • Bronze statue skin
  • Hepatomegaly
  • T2DM
192
Q

Diagnosis of haemochromatosis

A
  • Fe studies
  • Genetic test
  • Liver biopsy (assess degree of damage with Perl’s Prussian blue stain)
193
Q

Fe studies results in haemochromatosis

A
  • High serum Fe
  • High ferritin
  • High transferrin saturation
  • Low total iron-binding capacity
194
Q

Treatment of haemochomatosis

A
  • First line: Venesection 3-4 times a year for life
  • If contraindicated; desfernoxamine (chelation therapy)
  • Lifestyle, decrease Fe in diet, avoid fruits
195
Q

Pathophysiology of Wilson’s disease

A
  • Autosomal recessive mutation of ATP7B gene on chromosome 13
  • Impaired biliary copper excretion and transport bound to caeruloplasmin
  • Excess Cu accumulation in liver, basal ganglia and cornea
196
Q

The three features of Wilson’s disease

A

Hepatic
- Chronic hepatitis
- Liver cirrhosis
Neurological
- Assymetrical parkinsonism
- Memory issues
- Dysarthria (difficulty speaking because the muscles you use for speech are weak) and dystonia - movement disorder that causes the muscles to contract involuntarily
- Depression
- Full psychosis
Opthamological
- Kayser-Fleischer rings - Cu deposits in in cornea, greenish brown ringed appearance

197
Q

Diagnosis of Wilson’s disease

A
  • 24 hour urine Cu tests: low serum copper and caeruloplasmin
  • AST:ALT >4.5
  • Liver biopsy - High Cu, hepatitis
  • MRI brain: cerebellar + basal ganglia degeneration
198
Q

Management of Wilson’s disease

A
  • 1st line - D-Penicillinamine (Cu chelation, lifelong)
  • Diet change: avoid food high in Cu, shellfish, mushroom
  • Last resort -> liver transplant
199
Q

Risk factors for NAFLD

A
  • Obesity
  • T2DM
  • Hypertension
  • Hyperlipidaemia
  • Middle aged onwards
  • Family history
  • Drugs (NSAIDs, amiodarone)
200
Q

Stages of NFALD

A
  1. Hepatosteatosis (NAFLD)
  2. Non-alcoholic steatohapatitis (NASH)
  3. Fibrosis
  4. Cirrhosis
201
Q

Symptoms of NAFLD

A
  • Typically asymptomatic, findings are incidental
  • If v.severe, present with signs of liver failure
202
Q

Diagnosis of NAFLD

A
  • first line Deranged LFTs (High PT/INR, low albumin, high bilirubin) high everything else
  • AST:ALT < 1
  • FBC: thrombocytopaenia, hyperglycaemia
  • Enhanced liver fibrosis blood tests if fibrosis suspected (comes under lft) ELF
  • Abdominal ultrasound to confirm
    Fib 4 score (second line)
  • Assess risk of fibrosis using non-invasive method
203
Q

Enhanced liver fibrosis blood test for assessing fibrosis

A
  • Measure three markers - HA, PIIINP and TIMP-1
  • <7.7 = none-mild fibrosis
  • ≥7.7 - 9.8 = moderate fibrosis
  • ≥9.8 = severe fibrosis
204
Q

FIB-4 score for assessing fibrosis

A

> 2.67 = advanced -> refer to hepatology specialist

205
Q

Management of NAFLD

A
  • Weight loss
  • Exercise
  • Control diabetes, blood pressure and cholesterol
  • Stop smoking
  • Avoid alcohol
  • Vitamin E to improve liver function
  • Pioglitazone to decrease insulin resistance
206
Q

Complications of NAFLD

A
  • HE
  • Ascites
  • HCC
  • Portal hypertension
  • Oesophageal varices
207
Q

Treatment for paracetamol overdose

A
  • Activated charcoal within 1 hour of ingestion - Sticks to paracetmol to ensure it’s not absorbed (adsorption), decreases all intestinal absorption
  • Followed by IV N-Acetyl Cysteine - Increases availability of glutathione to get rid of excess NAPQI
208
Q

Paracetamol metabolism

A
  • 95%: Phase II conjugation -> excreted
  • 5%: Phase I conjugation -> NAPQI (hepatotoxic) -> Phase II conjugation -> glutathione (antioxidant) -> excreted
209
Q

How does paracetamol overdose work?

A
  • Shunting phase 1 pathway as phase 2 is too saturated
  • Glutathione depleted
  • Hypertoxicity of NAPQI in liver and inflammation
210
Q

Pathophysiology of ascites

A

Accumulation of fluid in the peritoneal cavity

211
Q

How can liver cirrhosis cause ascites?

A
  • Hypoalbuminaemia (reduced plasma oncotic pressure)
  • Portal hypertension (increased hydrostatic pressure)
  • Renal water retention

Cirrhosis is the most common cause of ascites (50% of patients develop ascites within 10 years

212
Q

Aetiology of ascites

A
  • Cirrhosis (70%)
  • Malignancy
  • Heart failure
  • TB
  • Pancreatitis
213
Q

Symptoms of ascites

A
  • Abdominal distension (severe = risk of SBP!)
  • Pain/discomfort = malignant
  • Signs of liver disease
  • May have jaundice and puritis
  • Shifting dullness
214
Q

Treatment of ascites

A
  • Treat underlying cause
  • Diuretic to increase Na+ excretion (spironolactone) + socium restriction
  • Paracentesis -which a needle is inserted into the peritoneal cavity to obtain ascitic fluid (or indwelling drain for smaller volume)
  • Peritoneovenkus shunting - relieves ascites by transferring fluid through a one-way valve from the peritoneal cavity into the superior vena cava.
215
Q

Diagnosis of ascites

A
  • Shifting dullness on exam
    Imaging: x-ray, uss, CT abdomen
    Ascitic tap:
  • Cytology (WCC counts) + MC+S
  • Protein measurement: transudate + exudate
216
Q

Transudate testing for ascites

A
  • <30g/L protein (low)
  • Serum albumin ascitic gradient is <11g/L
  • Clear fluid
  • Fluid due to high hydrostatic pressure - portal htn, budd chiari, constructive pericarditis, CHF, nephrotic syndrome
217
Q

Exudate testing for ascites

A
  • ≥30g/L protein (high)
  • Serum albumin ascitic gradient is ≥11g/L
  • Cloudy fluid
  • Fluid due to inflammation mediated exudation, or low oncotic pressure - malignancy, peritonitis, pancreatitis
218
Q

What is SAAG?

A
  • Serum albumin ascites gradien
  • SAAG >1.1g/dL = portal hypertension, suggesting nonperitoneal cause of ascites
219
Q

Classification of ascites

A

Stage 1: Detectable only after careful examination/uss
Stage 2: Easy detectable but relatively small volume
Stage 3: Obvious, not tense ascites
Stage 4: Tense ascites (large)

220
Q

Prehepatic jaundice

A
  • Unconjugated hyperbilirubinaemia due to increased RBC breakdown
  • Mainly caused by haemolytic anaemias
  • Urine bilirubin negative and urobilinogen high
221
Q

Intrahepatic jaundice

A
  • Conj/unconj hyperbilirubinaemia, may be mixed
  • Dark urine - raised bilirubin in urine and raised bile salts, decrease in urobilinogen
  • Parenchymal disease: HCC, ALD/NAFLD, hep, hepatotoxic drugs (eg: rifampicin), Gilbert syndrome, Crigler-Najjar syndrome
222
Q

Post hepatic jaundice

A
  • Conjugated hyperbilirubinaemia due to biliary obstruction
  • Pale stools + dark urine as bilirubin can’t reach GI tract and builds up in urine
  • Caused by biliary tree pathologies (eg: choledocholelithiasis, cancers)
  • High bilirubin and low urobilinogen in urine
223
Q

What is jaundice?

A
  • aka: icterus
  • Yellowing of skin/eyes/mucous membranes due to accumulation of conjugated or unconjugated bilirubin
  • Sign of liver dysfunction
224
Q

Four signs to look for when a patient presents with jaundice

A
  • Courvoisier sign
  • Charcot triad
  • Reynold’s pentad
  • Murphy sign
225
Q

Investigations for jaundice

A
  • Bloods
  • LFTs
  • First line imaging - ultrasound

Normally:
- No bilirubin in urine
- Urobilinogen in urine

226
Q

Biliary tree pathology

A
  • Choledocholithiasis
  • Pancreatic cancer
  • Cholangiocarcinoma
  • Mirizzi syndrome
  • Drug induced cholestasis
  • Autoimmune (PBC+PSC)
  • GALLSTONES
227
Q

Pathophysiology of oesophageal varices

A
  • Portal hypertension results in collateral blood shunting to gastroesophageal veins
  • Typically small, become oesophageal varices at the cardia and lower oesophagus
228
Q

Presentation of haemorrhage of oesophageal varices

A

Haematemesis (vomiting blood)

DDx: Mallory-Weiss tear
- Tear in oesophageal mucosa
- Very acute history
- Increased abdominal pressure

229
Q

Diagnosis of oesophageal varices

A

Oesophagogastroduodenoscopy

230
Q

Acute treatment for oesophageal varices

A

Acutely:
- Resus until haemodynamically stable
- Consider blood trasfusion (Hb < 70g/L or <80g/L w cardiac comorbidity)

231
Q

Stopping bleeding of oesophageal varices

A
  1. IV terupressin (SST is CI)
  2. Variceal banding
  3. Transjugular intrahepatic portosystemic shunt - decreases portal pressure by diverting blood to other larger veins, SE = hepatoencelopathy
232
Q

Preventing bleeding of oesophageal varices

A
  • Non-selective beta blocker (eg: propanolol) + nitrates
  • Repeat variceal banding
  • Last resort: liver transplant (decompensate cirrhosis)
233
Q

Pathophysiology of portal hypertension

A
  • Normal pressure in portal vein = 5-8mmHg
  • Cirrhosis = increased resistance to flow, leads to splanchnic dilation and compensatory increased CO
  • Fluid overload in portal vein (10+ = bad, 12+ = very bad)
234
Q

Causes of portal hypertension

A

Prehepatic: Portal vein thrombosis
Intrahepatic: Cirrhosis (mc in UK), schistomiasis (mc worldwide)
Post hepatic: Budd chiari, RHS heart failure, constrictive pericarditis

235
Q

Symptoms of portal hypertension

A
  • Mostly asymptomatic
  • Present when oesophageal varices rupture
  • (90% of portal hypertension cases develop oesophageal varices, 1/3 of these rupture)
236
Q

Primary and secondary peritonitis

A

Primary
- Ascites
- Spontaneus bacterial peritonitis (infection) (mc)
Secondary
- Underlying cause, eg: bile, malignancy

Peritonitis can also be classified as acute or chronic

237
Q

Bacterial causes of SBP

A
  • Gram -ve = e.coli + klebsiella (colliform rods)
  • Gram +ve = stap.aureus (cocci)
238
Q

Chemical causes of SBP

A
  • Bile
  • Old clotted blood
  • Ruptured ectopic pregnancy
  • Intestinal perforation
    (which get ultimately infected)
239
Q

Presentation of SBP

A

Sudden onset severe abdo pain (and shoulder tip pain) then collapse + septic shock, fever
- Rigidity helps pain (DDx: renal colic)
- Poorly localised -> more localised

+ ascities usually

Symptoms and signs of underlying conditions

240
Q

Treatment of SBP

A
  • Treat underlying cause; IV fluid + IV antibiotics
  • Urinary catheterisation + GI decompression
  • IV Broad spectrum antibiotic therapy
  • Analgaesia
  • Surgery = peritoneal lavage
241
Q

Complications of SBP

A
  • Septicaemia if not treated early
  • Subphrenic/pelvic abscesses
  • Paralytic ulcers
242
Q

What is spontaneous bacterial peritonitis?

A

Peritonitis (infection of the peritoneum), that happens without a hole or a tear.
Ascitic fluid is affected

243
Q

Diagnosis of SBP

A
  • Ascitic tap shows neutrophilia
  • Cultures (mc+s) show causative organism
  • High ESP and CRP
  • Exclude pregnancy as cause (b-hCG test) and bowel obstruction (abdo xR)
  • Cxr shows air under diaphragm -> indicates perforated colon

Haroon flashcards (10 decks)

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