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Gen Med > Gastro + Hepatology > Flashcards

Gastro + Hepatology Flashcards

1
Q

What are the histological features of Crohn’s disease

A

Inflammation through all layers (transmural)
Forms granulomas
Increase in goblet cells
Has skip lesions

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2
Q

What are the radiological features of Crohn’s disease

A

String of kantor

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3
Q

How would someone with Crohn’s present

A 
Diarrhoea - may wake up in the night 
Non bloody diarrhoea 
Weight loss 
Upper GI symptoms - mouth ulcers 
Perianal disease - abscesses, skin tags, fistulae 
May have palpable mass in RIF 
May experience vomiting 
Systemic symptoms 
- malaise
- fever 
- night sweats 
- weight loss 
- anorexia
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4
Q

What is the appearance of the colon in Crohn’s

A

Thickened cobblestone appearance
Ulcers are deep, through all layers
May be fistulae

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5
Q

What are the extra intestinal symptoms of Crohn’s

A 
Clubbing 
Erythema nodosum
Pyoderma gangrenosum 
Conjunctivitis, episcleritis, uveitis 
Large joint arthritis 
Sacroilitis 
Ankylosing spondylitis 
Gallstones - secondary to decreased bile absorption 
Oxalate renal stones - increased calcium because bile not reabsorbed
Primary sclerosis cholangitis 
Cholangiocarcinoma 
Osteomalacia 
Amyloidosis
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6
Q

Which investigations would be done on suspected Crohn’s and what type of results would be expected

A 
Bloods 
FBC - anaemia, raised WCC (if in flare) 
CRP - may be raised 
U&Es - kidney function may be impaired,dehydration, mineral deficiencies 
LFTs

Blood and stool cultures - rule out infective cause
Stool sample - faecal calprotectin
Colonoscopy - can take biopsies, may show cobblestone appearance
MRI - asses pelvic disease

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7
Q

Where does UC affect

A

The large intestine - never extends past the ileocaecal valve unless patients get backwash ileitis
Affecting mucosa
Can affect any part of the colon but is always continuous

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8
Q

What are the features of UC

A

Diarrhoea - many times, sensation of urgency, tenesmus, bloody, mucus
Constipation and rectal bleeding - disease limited to rectum/anus
Systemic - fever, malaise, weight loss And anorexia

On examination

  • tender, distended abdomen
  • Signs of anaemia (blood loss)
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9
Q

Which investigations would be done in a patient with suspected UC

A

Bedside obs
Bloods
FBC - anaemia and inflammatory markers
CRP
U&Es - likely to be malnourished and dehydrated
Blood cultures and stool cultures - rule out pseudomembranous colitis
Faecal calprotectin - colonic inflammation

Imaging
AXR - no faecal shadows, mucosal thickening, colonic dilatation, check for perforation
Barium enema - ulceration and loss of haustral pattern
Colonoscopy and flexi sig

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10
Q

What are the extra intestinal symptoms of UC

A 
Joint pain - large joint arthritis 
Ankylosing spondylitis 
Clubbing 
Erythema nodosum - inflammation of fat cells under the skin (often shins) 
Pyoderma gangrenosum - necrotic ulcers 
Conjunctivitis, uveitis, episcleritis 
Fatty liver
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11
Q

Which laxative is used in hepatic encephalopathy

A

Lactulose - inhibits the production of ammonia in the intestine

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12
Q

What is Wilson’s disease

A

Autosomal recessive disease where copper is deposited in the liver leading to cirrhosis and hepatitis
normally presents in teenagers and early adulthood.
increased copper absorption in the intestines and decreased hepatic excretion

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13
Q

What are the signs and symptoms of wilson’s disease?

A

Kayser-Fleischer rings - copper deposits in the eyes, leading to a copper coloured ring around the iris
Blue nails
Neurological/Psychiatric - depression, psychosis, asymmetrical tremor, chorea
Osteopenia and Osteoarthritis
Myopathy incl cardiomyopathy
Pancreatitis - causing hypoglycaemia
Hypoparathyroidism
Kidney dysfunction - Renal tubular acidosis

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14
Q

What are the differentials for Wilsons disease

A 
Primary biliary cirrhosis - can lead to Copper build up
Depression and anxiety disorders 
hypothyroidism 
Diabetes 
hepatitis 
Huntingtons
Parkinsons (tremor)
MS
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15
Q

Which investigation is diagnostic of Wilsons disease and what are the other investigations

A

reduced serum caeruloplasmin (<0.1g/L)
Increased urine copper excretion
enzyme assay
Liver biopsy if other tests are inconclusive

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16
Q

how is Wilson’s disease managed?

A 
Pencillamine - chelates copper 
Avoid alcohol and hepatotoxic drugs 
Low copper diet 
regular checks for the KF ring to ensure its reducing 
Screen first degree relatives
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17
Q

What is primary biliary cirrhosis?

A

Chronic liver disorder commonly seen in middle aged women

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18
Q

What is the pathophysiology of PBC?

A

Autoimmune condition
Interlobular ducts become damaged by chronic inflammatory disease process causing progressive cholestasis may eventually progress to cirrhosis

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19
Q

What are the clinical features of PBC?

A 
Early: fatigue, pruritus
Right upper quadrant pain
Steatorrhoea and darker urine
Cholestatic jaundice
hyperpigmention especially over pressure points 
Xanthalasmas 
Clubbing 
Hepatosplenomegaly 
May progress to liver failure
20
Q

What investigations should be done in suspected PBC?

A

LFTs - ALP likely to be raised due to cholestasis
Autoantibody testing - automitochondrial antibodies present in >95% of affected patients (M2 subtype)
Serum IgM will be raised
TFTs - patients often develop thyrotoxicosis
USS and CT of gallbladder and liver

21
Q

How is PBC managed?

A

Antihistamines for pruritus
Cholestyramine or colestipol will sequester bile salts and also help with pruritis – rifampicin might work if these do not
Ursodeoxycholic acid helps to slow disease progression
Steroids can be used to suppress the autoimmune process

22
Q

What is haemochromatosis

A

Autosomal recessive disease - often presents >30 years
Patients have a deficiency in Hepcidin - an iron regulatory hormone - leading to increased intestinal absorption of iron
iron then accumulates in the liver, sking and pancreas (bronzed diabetic)

23
Q

What are the clinical features of haemochromatosis

A

Fatigue, weakness, arthralgia, amenorrhoea and erectile dysfunction
Liver: stigmata of liver disease, hepatomegly, cirrhosis
Bronze skin pigmentation
Diabetes
Cardiac failure - secondary to cardiomyopathy
hypogonadism - 2nd to cirrhosis and pituitary dysfunction - hypogonadotrophic hypogonadism

24
Q

Which complications of haemochromatosis is reversible

A

Skin pigmentation

Cardiomyopathy

25
Q

Which investigations are performed if haemochromatosis is suspected

A

fasting transferrin saturation and ferritin before genetic testing

26
Q

What are some causes of liver failure

A

Alcoholic liver disease
Primary biliary cirrhosis

Infection: Hepatitis B, C. Cytomegalovirus,

Epstein Barr Virus. TB, yellow fever 
Haemochromotosis 
Autoimmune hepatitis 
Alpha-1-antitrypsin deficiency 
Wilsons disease 
Fatty liver disease 
Hepatocellular carcinoma

Drug induced: Paracetamol OD, Halothane, Isoniazid (treatment for TB)

Venous Occlusion

27
Q

How does hepatic encehalopathy occur in liver disease?

A

Build up of ammonia as liver is unable to clear it. Ammonia is in blood and enters the brain. It is converted to glutamine by astrocytes which causes an osmotic imbalance. Fluid moves into the brain
cerebral oedema - confusion

28
Q

What is the grading of hepatic encephalopathy

A

grade 1 - irritability
grade 2 - confusion, inappropriate behaviour
grade 3 - incoherent, restless
grade 4 - coma

29
Q

Which screening test is used first line in patients suspected to have coeliac disease

A

Tissue transglutaminase antibodies

30
Q

how do you work out alcohol content

A

alcohol units = volume (ml) x % / 1000

31
Q

What is rifaximin used for?

A

Prophylaxis of hepatic encephalopathy. antibiotic that modulates gut flora resulting in decreased ammonia production

32
Q

In which IBD is bloody diarrhoea more common?

A

UC

33
Q

In which IBD is weight loss more common

A

Crohns

34
Q

What are the features of Crohns Disease?

A 
Diarrhoea
Weight loss
Affects mouth to anus 
Mouth ulcers 
Perianal disease - skin tags and ulcers
Skip lesions 
Abdominal mass palpable in RIF 
inflammation down to the serosa therefore prone to stritures, fistulas and adhesions
35
Q

What are the features of UC?

A 
Bloody diarrhoea 
Abdominal pain in LLQ
Tenesmus - feeling of not being empty after defecation
No inflammation past the submucosa 
Crypt abcesses 
granulomas are infrequent
36
Q

What are the extra-intestinal complications in Crohns?

A 
Gallstones - reduced bile absorption 
Oxalate renal stones - increases the loss of calcium in the bile nd calcium binds oxalate
Erythema Nodusum 
Pyoderma gangrenosum 
Arthritis 
Episcleritis
Osteoporosis
37
Q

What are the extra intestinal features in UC?

A 
Primary sclerosing cholangitis 
Uveitis 
Erythema Nodusum 
Pyoderma gangrenosum 
Arthritis 
Episcleritis
Osteoporosis
Colorectal cancer
38
Q

A patient with UC is given a barium enema and a AXR is taken what does it show?

A

Loss of haustrations
Lead pipe colon
Superficial ulceration
Pseudopolyps

39
Q

What is the pathophysiology behind alcoholic fatty liver disease?

A

Excess alcohol consumption generates NADH and this causes more fatty acids to be produced and less NAD+ means there is less fatty acid oxidation
The fat is then deposited in the hepatocytes

40
Q

What is the pathophysiology of Alcoholic Hepatitis

A

Inflammation of hepatocytes
Mallory Hyaline bodies are found in the liver - damaged intermediate filaments
Reduced hepatic function therefore uncojugated bilirubin builds up and less albumin produced –> jaundice and ascites
Portal hypertension due to damage to hepatocytes

41
Q

What is the final stage of ALD and what are the complications?

A

Cirrhosis
- portal HTN –> caput medusa, oesphageal varices, haemorrhoids and splenomegaly
Coagulation disorders - increased prothrombin time. Liver produces factors 2, 7, 9 and 10
Ascites - movement of fluid and low albumin
Hepatic encephalopathy - increased levels of ammonnia
Hepatorenal syndrome
Thrombocytopenia - due to splenomegaly causing sequestration of platelets

42
Q

What is hepatorenal syndrome?

A

Life threatening condition that causes renal failure in patients with liver cirrhosis
Portal hypertension causes splanchnic vasodilation therefore decreased circulating blood volume so RAAS activated –> renal vasoconstriction

43
Q

What would be the findings in the blood results?

A

AST: ALT ratio is greater than 2:1
RBC macrocytosis
Elevated GGT, Bilirubin and ALP
Folate level is decreased due to decreased intestinal absorption
Anaemia
U&Es - Mineral deficiencies
Clotting - PT increased and INR increased

44
Q

If cirrhosis is suspected what types of imaging can be used?

A

Abdo Ultrasound - useful to aid biopsy

Fibroscan - check degree of fibrosis

45
Q

How is ALD managed?>

A

Stop drinking
withdrawal medication to stop drinking - - Chlordiazepoxide (oral), Lorazepam (IM) – for withdrawal symptoms
Disulfriam - nausea and vomiting if pt drinks whilst taking this
Corticosteroids - helps reduce hepatic inflammation
Lactulose - increases gut motility and prevents ammonia from building up
Vitamins and mineral replacement - thaimine to prevent wernickes-korsakoff
for ascites - spironolactone
Drain fluid is ascites are very large
Monitor weight to ensure fluid is coming off

46
Q

What is CAGE

A

Have you ever thought about Cutting down
have people Annoyed you when they have asked about your drinking
do you ever feel Guilty about your drinking
Do you ever use alcohol as as Eye opener i.e. to get going in the morning

47
Q

What is the pathophysiology of hepatic encephalopathy

A

Ammonia builds up in the blood and enters the brain
It is converted to glutamine by astrocytes and causes a fluid imbalance
Fluid then shifts into the brain –> cerebral oedema this puts pressure on the brain

Gen Med (10 decks)

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