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Phase 2 > LIVER / GI > Flashcards

LIVER / GI Flashcards

1
Q

What does autoimmune hepatitis require for diagnosis

A

Biopsy - presence of plasma cells and lymphocytes in portal tracts

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2
Q

Investigations for chronic liver disease

A

1.Bloods:
LFT - can indicate if it is a more liver or biliary picture (biliary alk phos + GGT), prothrombin time

Serology - Hep B, C, EBV, CMV, IgGs - autoimune

FBC - infection, lympocytes

Biochem - tells you metabolic causesIron (haemochromatosis), Cu (wilsons), alpha trypsin 1 deficiency

U&Es - tell you if there are any problems with fluid balance and overload to liver

2.Imaging
Ultrasound to rule out gallstones
Can use CT, MRI to confirm if -ve but suspicion

3.Biopsy
If needed, based on blood results, eg to confirm autoimmune, NAFLD

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3
Q

What would you see on biopsy for primary sclerosing cholangitis (PSC)

A

Periductal “Onion skin” fibrosis around the hepatic ducts/ bile duct - see strictures

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4
Q

What would you see on biopsy for primary biliary cholangitis (PBC)

A

See granulomas in wall of bile duct

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5
Q

What would you see on biopsy for autoimmune hepatitis

A

Lymphoplasmacytic infiltrate (plasma cells around portal tracts)

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6
Q

Cause of autoimmune hepatitis

A

Unknown - affects you or middle aged women predominantly. May present with signs of autoimmune disease + hepatitis signs

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7
Q

Which autoimmune cause of liver failure overlaps with IBD

A

Primary sclerosing cholangitis - 70% of pt also have colitis. This of this as a vasculitis overlap as well- ANCA associated

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8
Q

Which autoimmune disease in liver failure responds to steroids

A

Autoimmune hepatitis

PBC + PSC don’t respond

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9
Q

Describe a clinical scenario of primary biliary cholangitis

A 
Female, young - middle aged
Liver/ Biliary + Autoimmune symptoms, itching, mild jaundice, joint pains, fatigue
Bloods - biliary + - alk phos, liver enzymes ok
Albumin - normal
Raised IgM
AMA + (95% of pts)
US - normal 
Serology - no infection
Biopsy, granulomas in biliary wall 
Limited response to steroid
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10
Q

Presentation of fatigue & itching

A

Primary biliary cholangitis

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11
Q

Treatment of PBC, PSC

A

ursideoxycholic acid

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12
Q

Gene associated with haemochromatosis

A

HFE

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13
Q

Treatment of haemochromatosis

A

Venesection

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14
Q

Before starting anticoagulants or anti-thrombotic drugs what blood test should be done

A

LFT - check the patient isn’t at risk of haemorrhage or that metabolism may be altered

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15
Q

Liver cancer most commonly occurs in patients with what liver pathology/ disease stage

A 
Cirrhosis 
Higher risk:
Hep B, C (advanced to cirrhosis)
Haemochromatosis
Lower risk - alcoholic FL, autoimmune diseases
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16
Q

What screening should be done on any patient with liver cirrhosis

A

Hepatocarcinoma screening - 50% produce alpha fetoprotein

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17
Q

Liver cancer is most commonly primary or secondary

A

Secondary

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18
Q

Causes of primary liver cancer

A

Cirrhosis - hepatitis and haemochromatosis causes

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19
Q

What is a common asymptomatic chronic liver disease

A

Non alcoholic fatty liver (non alcoholic steatohepatitis)

May pick this up through a routine LFT

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20
Q

What is the difference between non-alcoholic fatty liver and non-alcoholic steatohepatitis

A

NAFL is fat deposits and inflammation over the liver. NASH is fat, inflammation and fibrosis (more advanced liver disease than NAFL)
Need to do biopsy to distinguish between these - important clinically as fibrosis means the pt is closer to cirrhosis. NASH important cause of ‘cryptogenic’ cirrhosis.

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21
Q

Treatment of non alcoholic fatty liver

A

Weight loss

Few effective drug treatments

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22
Q

Pathology of alpha 1-antitrypsin deficiency

A

Enzyme that inhibits protein breakdown, if deficient, get increased protein breakdown, eg like in emphysema.
Protein cant be transported out of liver.
Build up in liver - get inflammatory response, see eosinophils on histology
Deficiency in blood.

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23
Q

Vascular cause of acute liver injury

A

Hepatic vein occlusion due to thombosis
Causes: underlying thrombotic disorder (Budd-Chiari syndrome), chemotherapy (dont know why)
Congestion causes acute or chronic liver injury
Presents with abnormal LFT, ascites, acute liver failure
Treatment - anticoagulation, or shunt
Liver transplant is patient develops liver failure

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24
Q

Causes of liver disease

A

Drugs
Alcohol
Virus - hepatitis B, C, D & E, CMV, EBV
Autoimmune - ANA, AMA related
Metabolic - haemachromatosis, wilsons, alpha trypsin one deficiency
Vascular - hepatic vein occlusion

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25
Q

Common causes of acute liver disease

A 
Adverse drug reaction (30% of all presentations)
Alcohol hepatitis (stand alone, or +CLD)
Viral - hep B or C 
Autoimmune hepatitis 
Hepatic vein occlusion
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26
Q

Common causes of chronic liver disease

A 
Alcoholic fatty liver
Non-alcoholic fatty liver (metabolic syndrome)
Hepatitis B or C
Autoimmune
Metabolic - haemochromatosis etc
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27
Q

Presentation (symptoms) of acute liver injury

A

Jaundice
Malaise
Nausea
Anorexia

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28
Q

Presentation (symptoms) of chronic liver injury

A

Ascites
Malaise
Oedema
Haematesis

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29
Q

Signs of chronic liver disease

A

Spider naevi
Palmar erthyema
Leuconychia - White nails with (from low albumin)
Terry’s nails - 2/3 white, distal 1/3 reddened
Clubbing
hepatomegaly

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30
Q

Itching is more common with unconjugated or conjugated billirubin

A

conjugated, t/f more or a sign in obstructive jaundice rather than haemolytic

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31
Q

What is cholestatic jaundice

A

Jaundice with dark urine and pale stools

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32
Q

What is biliary pain

A

Right upper quadrant pain, can radiate to shoulder

More common after a meal, lasts a couple of hours

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33
Q

Define cirrhosis

A

Irreversible liver damage. Large thick bands of fibrous tissue deposited between portal tracts and central vein - bridging fibrosis. Nodular regeneration in between.
Loss of normal hepatic architecture.

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34
Q

Causes of cirrhosis

A

Alcohol - chronic use
Chronic hepatitis B or C infection
Metabolic genetic disorders - haemochromatosis etc
Hepatic vein events - Budd-Chiari
Non-alcoholic steatohepatitis
Autoimmune - all 3
Drugs - amioderone, methyldopa, methotrexate

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35
Q

Signs of liver failure

A 
Bleeding - coagulopathy (failure of clotting factor synthesis)
Encephalopathy 
Odema
Sepsis 
Spontaneous bacterial peritonitis
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36
Q

Signs of portal hypertension

A

Ascites
Splenomegaly
Oesophageal varices - umbilical varices

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37
Q

Causes of biliary disease

A

Gallstones - anywhere in biliary tree

Autoimmune - PBC, PSC

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38
Q

Causes compensation in cirrhosis

A 
Dehydration
Constipation 
Covert alcohol use
Infection
Opiate over use
GI bleed
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39
Q

GI non diarrhoea disease

A

Salmonella, Typhoid (enteric fever), gastritis, peptic ulcer disease, acute cholecystitis, peritonitis, amoebic liver abscess

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40
Q

What is the secretory antibody of the intestines

A

SIgA - secretory IgA

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41
Q

List some common diarrhoea GI infections

A

Bacterial - e coli, shigella, cholera, H pylori, whipples, Aeromonas (gram -ve bacteria in water)
Viral - rotavirus, noravirus
Parasite - cryptosporidium (water dwelling), cycospora (fresh fruit)
Worms - schistosomiasis
Travel - travellers diarrhoea
Antibiotics - Clostridium difficile
Whipple’s disease - gram positive bacteria

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42
Q

Explain how rotavirus damages the body/ is pathogenic. What are its virulence factors

A
  1. Following ingestion, rotaviruses infect the epithelial cells of the small intestine, mainly the jejunum. (Rotaviruses are resistant to acid pH).
  2. Histologically, there is shortening and atrophy of the villi, flattening of the epithelial cells, and denuding of the microvilli.
  3. This decreases the surface area of the small intestine, and limits production of digestive enzymes such as the disaccharides, normally synthesized by cells of the brush border.
  4. The patient suffers a malabsorptive state in which dietary nutrients such as sugars are not absorbed by the small intestine.
  5. This results in a hyperosmotic effect causing profuse diarrhoea
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43
Q

How does Rotavirus cause disease to the host

A

By modification of host cell structure and function of intestinal villi and microvilli.
Shortening and atrophy of villi, flattening of epithelial cells

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44
Q

Why is brush border important

A

Absorption - location of enzymes that catalyse disaccharides (maltose) to glucose for absorption. Na+ channels on enterocytes for secondary transport of glucose.

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45
Q

Commonest cause of gastroenteritis in adults

A
  1. Virus - norovirus

2. Food poisioning - bacterial, campylobacter jejuni

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46
Q

What age group does Rotavirus affect nearly all of?

A

Children under 4 years

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47
Q

What is the most common risk of rota virus vaccine in children

A

Intussusception

48
Q

Bacteria that causes gastroenteritis from reheated food

A

Bacillus cereus

49
Q

What is the organism most likely to cause vomitting and diarrhoea <6hours after eating

A
  1. Staph aureus - finger food

2. Bacillus cereus - re-heated foods (rice)

50
Q

List the time course of symptoms for common bacterial causes of foodborne diarrhoea

A 
Staph A: 6 hours or less
Bacillus cereus: <6 - 16 hours (think would present w/in a day)
Salmonella: 1-3 days
Campylobacter jejuni: 1-3 days
Shigella: 1-3 days
Vibro parahaemolyticus: 1-3 days
E coli (w/ shiga toxin, EHEC): 5 days
51
Q

Common food causes of diarrhoea

A

Dairy, meats (uncooked), salads
Uncooked foods - fruits
Finger foods - staph aureus

52
Q

What foods is EHEC (enterohaemorrhagic e coli; O157) associated with? What symptoms differentiate this from other forms of E Coli infection and what are the complications

A

Beef & milk.
Bloody diarrhoea. No fever. Adult.
Can develop HUS - haemolytic uremic syndrome
Shiga toxin gets into microvasculature endothelium and damages cells. This promotes thrombi to form. As RBCs pass through damaged microvessles, they are lysed = haemolytic (schistocytes). They are also killed with taken into thombus. Glomerular capillaries are mainly effected = uremic.
Shiga toxin, endothelial injury, thrombi, lyse RBCs, glomerulus capilliaries.

53
Q

Infectious causes of bloody diarrhoea

A

E Coli 0157
Shigella
Campylobacter jejuni
(ESC)

54
Q

What pathogen is most likely cause of travellers diarrhoea. What are it’s virulence factors (toxins) and how does it cause diarrhoea?

A
  1. ETEC - ecoli ; 2. EAEC (enteroaggregative- EAST toxin)
    Toxins = heat labile toxin (LT); heat stable toxin (ST); pilli
    Both toxins upregulate (stimulate the activation of) the CFRT (cystic fibrosis transmembrane regulator) channel
    Get more CRFT channels = increased movement of Cl out of cell into lumen. Electrolyte movement means that water follows.
    NB. Cl is transported into enterocyte from circulation with Na+ and K+, so if increase movement of Cl into lumen, get water loss from circulation to provide this.
55
Q

What toxin is associated with EHEC, what is its virulence factor

A

Shiga like toxin + T3SS (syringe like protein secretion system - basically secretes something - enzymes?, called ‘effectors’ - that mess up actin & myosin in the enterocyte, and use enterocyte microfilaments to form a pedestal for bacteria to sit on, this gives it really good attachment to lining of the SI.
Attachment with T3SS compromises the lining on enterocytes & ion and nutrient absorption (Na+) = water stays in lumen and more moves in from circulation because of hyperosmolarity in lumen.
Enters endothelium, causes injury and initiates thrombus formation.
NOT invasive. Ecoli remains on surface of enterocyte, system effects caused by Shiga toxin.

56
Q

What group are mainly affected by EIEC - enteroinvasive e coli.
How do these e coli get into enterocytes?
What are the symptoms?

A

Children
Get in using T3SS and invasins - invasin is an effector that causes ulceration and allows e coli to move into cell.
Occure in large intestine, not small intestine.
Symptoms - dysentery. Bloody diarrhoea, fever, abdo pain.

57
Q

What group is EPEC most common in, what is its virulence factor and symptoms

A

Common in children < 1 year
Virulence = T3SS, adhesion
Symptoms = watery diarrhoea

58
Q

List the different types of E Coli that cause gastroenteritis

A

ETEC (enterotoxigenic) - travellers
EHEC (enterohaemorrhagic) - food borne, milk beef
EIEC (enteroinvastive) - Large intestine, children, dysentry
EAEC (enteroaggregative) - travellers
EPEC (enteropathogenic) - P = paediatric, children <1
DAEC
UPEC - uro-pathogenic - UTI, mainly women

59
Q

List some causes of gallstones

A

Depends where the gallstones are.
If in hepatic ducts - could be because of too much cholesterol (bile is made up of water, fats - cholesterol, bilirubin, and bile salts - any imbalance in these could cause a stone).
Too much bilirubin - think of haemolytic (pre-hepatic) and hepatic causes - cirrhosis, fatty liver etc

If in bile duct, could be because of primary biliary cholangitis or primary sclerosing cholengitis, bc of obstruction in the bile duct and stasis.

60
Q

What are the commonest compositions of gallstones

A

Cholesterol

Calcium carbonate

61
Q

Common pathogens of peritonitis

A

Surgical
2° bacterial peritonitis due to to perforation or trauma; polymicrobial with gut flora

Spontaneous bacterial peritonitis (SBP)
complication of ascites in cirrhosis, E coli and other GNB, S. pneumoniae,

Paediatric in absence of ascites
S. pneumoniae and other streptococci

Infection 2° peritoneal dialysis
with Staph. aureus , coagulase negative staphylococci or other skin flora, E. coli, , P. aeruginosa or other gram negative bacteria

Pelvic inflammatory disease (PID)
As complication of chlamydial or gonococcal sexually transmitted infection (STI) in young women

Tuberculous

62
Q

What is charcot’s triad

A

Fever
RUQ Pain
Jaundice

63
Q

List some examples of non-infectious causes of peritonitis

A

Foreign body post surgical
endometriosis
pancreatitis

64
Q

What is Reynolds pentad

A

Charcot’s triad, plus:
Hypotension
Confusion/altered mental state

65
Q

What does MRCP stand for

What does ERCP stand for

A

Magnetic resonance cholangiopancreatography

Endoscopic retrograde cholagiopancreatography

66
Q

When is an MRCP or ERCP used

A

Looking for gallstones

Use if ultrasound not shown anything but have clinical suspicion

67
Q

What investigations should be done in a patient who you suspect has ascending cholangitis

A

Abdominal ultrasound
MRCP, ARCP if ultrasound -ve or unclear
Bloods - LFTs

68
Q

What is the management of ascending cholangitis

A 
IV fluid 
IV antibiotics
ERCP to remove stone
Stenting
Laproscopic cholecystecomy
Open surgical exploration/drainage/percutanous cholangiography
69
Q

Is bile sterile

A

Yes
Commensal bacteria of the gut is prevented from infecting bile by flow
When flow is partially or fully obstructed by gallstone then gut bacteria can colonise bile, cause cholangitis and ascend biliary tree to liver

70
Q

What would be the signs and symptoms of biliary sepsis

A 
RUQ pain
Jaundice 
Fever
Hypotension
Confusion/ altered mental state
71
Q

What are the signs and symptoms of acute cholecystitis, how does this clinical presentation differ from biliary colic (gallstones) and ascending cholangitis

A

RUQ pain
Fever - would differentiate from gallstones
Bloods - LFT, FBC - raised inflammatory markers - differentiate from gallstones

No jaundice - if ascending cholangitis would have jandice

72
Q

Risk factors for acute cholecystitis

A

Diabetes

Obesity

73
Q

Common bacterial cause of gastritis and peptic ulcers

Risk factor for gastric carcinoma

A

Helicobacter Pylori

74
Q

What are the pathogenic mechanisms of H Pylori

A

Synthesizes urease which produces ammonia. Ammonia damages the gastric mucosa = ulcer.
Ammonia can also increase (neutralise) pH making stomach more hospitable to other pathogens

75
Q

What is the treatment for H Pylori infection

A

PPI to lower acid level that is irritating ulcers - eg. omeprazole
Antibiotics - H Pylori is a gram negative rod
Clarithromycin (macrolide, ribosome inhibitor)
+ Amoxicillin (bacterial cell wall inhibitor)

76
Q

Risk factors for H Pylori infection

A

Age - more likely to have living as commensal

77
Q

Describe the routes of parthenogenesis of H Pylori infection and possible outcomes

A
  1. Normal/ slightly increased gastric acid = no disease (due to differences in bacterial strain and/ or genetics) H pylori is not a harmful commensal
  2. Increased gastric acid production - bc of ammonia and drive to change ph (dont really know if true)
    - > causes peptic ulcers
  3. Lower ph bc of ammonia
    - >causes gastric cancer
78
Q

What is diverticulitis

A

Infection of diverticula - out pouchings of the colon, these alone arent a disease or may not cause problems, they from because of weak spots in the colon wall. When they become infected = diverticulitis

79
Q

Causes of peptic ulcer disease

A

H Pylori
NSAIDs (cox-1 inhibitors, = inhibit prostaglandin synthesis, required for mucus production, decreased = reduced mucosal barrier = ulcer).
Bile salts - duodenal reflux

80
Q

GI infections that cause dysentery (diarrhoea + blood)

A 
C Diff
Campylobacter jejuni 
Amoebic dysentery 
Shigella
E coli - EHEC &amp; EIEC
Yersinia entrocolitis
81
Q

List some non diarrhoeal GI infections

A 
Gastritis - H pylori infection
Staph A - finger food
Bacillus cereus - finger food
Yersinia entercoliticia 
Ascending cholangitis - risk of biliary sepsis 
Cholecystitis
Amoebic liver abscess
Peritonitis
82
Q

Signs of ascending cholangitis

A

Charcots triad

83
Q

What empirical antibiotics would you give for appendicitis

A

Co-amoxiclav or cephalosporin (if penicillin allergy, eg cefuroxime): cell wall target
+ Metronidazole: intracellular target

84
Q

What empirical antibiotics would you give for ascending cholangitis

A

IV Co-amoxiclav - dont know why

85
Q

What foods is salmonella associated with

A

Chicken & eggs

86
Q

What food is campylobacter associated with

A

meats

87
Q

What food is EHEC associated with

A

beef

milk

88
Q

What foods is staph A associated with

A

any finger food

89
Q

what advice would you give to a patient who has diarrhoea and is taking the oral contraceptive pill

A

To count the days she has diarrhoea as missed pill day and to use alternative contraception

90
Q

Which IBD condition is associated with an increased risk of uveitis, iritis, episcleritis and ankylosing spondylitis

A

Ulcerative colitis

91
Q

Name some pathological differences between Crohn’s and UC

A

Crohn’s can affect whole GI tract
UC - large bowel only

Crohn’s has patchy distribution across mucosa and is transmural, non caseating granulomas
UC - continuous distribution with ulcers, only usually affects mucosea and submucosa

Crohns’ - malabsorption syndrome bc it mainly affects SI
UC - electrolyte imbalances bc affects large bowel

92
Q

Which IBD has the most systemic complications

A 
Ulcerative colitis
Liver - inflammation &amp; PSC
Skin - skin abscesses 
Eyes - uveitis etc
Joints - ank sponds
93
Q

Commonest cause of infectious gastritis

A

H Pylori

94
Q

Causes of gastritis

A

Acute = alcohol (binge), NSAID, asprin, reflux (duodenal), stress (ischemia)
Chronic = H Pylori, autoimmune (pernicious aneamia), chemical - NSAIDS, asprin, corticosteroids, bile reflux (secondary to gastrectomy - bilous vomitting)
Others: Coeliac gastritis, Eosinophillic - associated with Scleroderma and Lupus, Granulomatous - associated with crohns

95
Q

What are the two commonest causes of peptic ulcers, what are the commonest sites of peptic ulcers and age groups

A

Causes - H Pylori, NSAIDS
Duodenal (most common)
Gastric (less common, more common in elderly)
Peptic ulcers more common in elderly

96
Q

Complications of peptic ulcers

A

Haemorrhage- posterior surface of duo & gastroduodenal artery commone place. If haemorrhage in stomach = haematemesis, if duodenum = melaena
Perforation - peritonitis

97
Q

Causes of peptic ulcers

A

Blood supply - ischemia
Acid production - H Pylori
Mucin production - NSAIDs, asprin, H Pylori

98
Q

Cause of coeliac’s disease

A

Adenovirus type 12 infection + genetic susceptibility (HLA dq2, dq8, B8)

99
Q

What auto-antibodies are associated with coeliacs disease

A

Anti-gliadin, Anti-transglutaminase, Anti-endomysial in 90% of patients

100
Q

What are the pathological changes of coeliacs disease

A

Villus atrophy

Crypt hyperplasia

101
Q

How is coeliac’s diagnosed

A

Bloods - auto antibodies (90% of pts)
Biopsy - histological changes
Response to gluten free diet - clinical improvement can be achieved within 48 hours of diet change and full remission can be achieved

102
Q

What are the symptoms/ features of malabsorption

A

Weight loss
Changes in bowel habit/ stools
Anaemia

103
Q

List the different pathology of malabsorption

A
  1. Insufficient intake
  2. Problem with intraluminal digestion (pancreas problem, biliary obstruction)
  3. Insufficient surface area (coeliacs, crohns - resection, Giardia)
  4. Deficiency in digestive enzymes - lactose intolerance, bacterial overgrowth (brush boarder)
  5. Defective epithelial transport - bile reabsorption
  6. Lymphatic obstruction - lymphoma, TB
104
Q

Symptoms of coeliac’s disease

A

Malabsoption symptoms if severe, if milder, bloating and indigestion

105
Q

Risk factors for GORD

A 
Obesity 
Hiatus hernia
Increased gastric fluid volume
Smoking 
Alcohol 
Hot drinks
Caffeine 
Patient age
106
Q

Pathology of GORD

A

Anything that increases abdominal pressure relative to lower oseophageal pressure.
Obesity, pregnancy, delayed gastric emptying, hiatus hernia.
Lower sphincter opens - acid, pepsin reflux - squamous epithelium damaged - inflammation - repair - fibrosis - may get metaplasia to goblet cells - Barrett’s oseophagus - 1% lifetime risk of adenocarcinoma.

107
Q

What is bacterial overgrowth

A

Upper small intestines are sterile. Stasis of luminal contents (eg in systemic sclerosis) gives bacterial in lower intestines more opportunity to grow. Impairs brush border enzymes = malabsorption

108
Q

What is the most common type of volvulus

A

Sigmoid, then cecal

109
Q

What are the commonest types of bowel obstruction and their causes

A
  1. Small intestine adhesion - cause previous surgery
  2. Small intestine inflammation - cause crohn’s, inflammation - stricture - obstruction
  3. Large bowel obstruction - colorectal cancer - most often in rectum
110
Q

What are the most common cancers in the UK

A

Breast
Prostate
Lung
Bowel

111
Q

What is the main type of colorectal cancer

A

Adenocarcinoma

112
Q

What stages do cells go through before coming cancerous

A

hyperplasia - metaplasia (change to other differentiated cell, eg goblet to squamous) - dysplasia - change to undifferentiated (abnormal) cells - carcinoma in situ - invasion - metastasis

113
Q

What investigations should you do for peritonitis

A

Bloods - FBC, U&E, LFT, culture
Imaging - ARX, CT
In primary - sample ascities fluid and culture

114
Q

What measure in ascities fluid is 100% indicative of SPB

A

ascities lactate >250 mg/dL

115
Q

What is the pathology of haemochromatosis

A

Human haemochromatosis protein mutation (HFE gene). This protein regulates expression of hepcidin (with some interaction of transferrin gene as well)
Basically, the mutation leads to decreased expression of hepcidin, which = unregulated absorption of Iron = increased serum irom = deposit in tissues, heart, pancrease, liver etc = fenton reactions (generate free radicals) = tissue damage = organ failure. Main one to think about is heart failure and liver failure.

116
Q

Describe iron metabolism

A

Absorption into enterocytes via haem transporters or metal transporter (Fe2+), movement out of enterocyte via ferroportin (hepcidin regulated) -> binds to transferrin -> liver or macrophage for storage -> taken in by transferrin receptor. Released from macrophage or liver cell by ferroportin (hepcidin regulated).

Phase 2 (12 decks)

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