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Abdo Flashcards

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1
Q

What are the causes of chronic liver disease?

A

3 commonest: Alcohol, hep B/C and nonalcoholic hepatic steatosis

Others:
Autoimmune: PBC
CHronic hepatitis
Metabolic: haemochromatosis

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2
Q

What are the complications of CLD?

A 
Portal HTN
Haemorrhage secondary to varices
Ascites 
SBP
Hepatic encephalopathy
Hepatorenal syndrome
Hepatopulmonary syndrome
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3
Q

WHat are the criteria for grading encephalopathy?

A

West-Haven criteria

0: clinically normal, small changes to memory
1: Mild confusion, euphoria, depression, short attention, impaired mental tasks
2: Drowsy, lethargy, mild disorientation, inappropriate behaviour
3: Somnolent but rousable with voice, grossly confused
4: comatose

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4
Q

How do you grade cirrhosis?

A

Modified Child-Pugh system

Looks at bilirubin, albumin, INR, ascites, encephalopathy

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5
Q

How do you classify jaundice?

A

Pre-hepatic: autoimmune haemolytic anaemia, malaria, SCD

Hepatic: acute viral hepatitis, paracetamol, alcohol

Post-hepatic: gallstones, malignancy

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6
Q

What do you know about hepatorenal syndrome?

A

Inadequate hepatic breakdown of vasoactive substances leading to excessive renal vasoconstriction. Type 1 develops rapidly and type 2 slowly
Difficult to reverse without hepatic transplantation, diagnosis of exclusion

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7
Q

How do you manage ascites in association with CLD?

A 
No added salt diet
Spironolactone
Loop diuretics next
Therapeutic drainage
Radiological procedures such as TIPS but increase risk of encephalopathy
Liver transplant
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8
Q

WHat are the causes of ascites

A 
Common:
Cirrhosis with portal hypertension
Malignancy
CCF
Nephrotic syndrome

Uncommon:
Budd-chiari syndrome
Portal vein thrombosis
Constrictive pericarditis
Malabsorption syndormes
Peritoneal mesothelioma
TB peritonitis
Myoxedema
Ovarian disease
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9
Q

What causes ascites formation in CLD?

A

Relative renal hypoperfusion causes increased renin from juxtaglomerular cells
Renin activates aldosterone
Deficient hepatic metabolism reduces aldosterone and ADH breakdown
Hypoalbuminaemia decreases oncotic pressure
The combination of salt and water retention from hyperaldosteronism and high ADH with high portal pressures causes nelt ultrafiltration of fluid into abdo cavity

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10
Q

How do you distinguish between transudate and exudate in ascites?

A

SAAG
<11g/L= exudate
>11g/L= transudate

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11
Q

What are the causes of hepatomegaly?

A

Top 3 causes:

  • CCF
  • Malignancy
  • Lymphoma

Other: malaria, hepatitis, leishmania, sarcoid

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12
Q

What scoring systems may help in evaluation of a patietn presenting with alcoholic hepatitis?

A

Maddreys discriminant function test
Mayo end stage liver disease score
Glasgow alcoholic hepatitis score

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13
Q

How would you manage a patient with acute alcoholic hepatitis?

A

Supportive: alcohol abstinence, nutrition adequate, treatment of any infection
Maddreys discrimenant function score >32 indicates treatment with steroids

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14
Q

What are the histological features of alcoholic liver disease?

A

Hepatic steatosis: accumulation of fat in liver cells (reversible)
Alcoholic hepatitis: acute inflammation and hepatocyte necrosis (reversible)
Hepatic cirrhosis- fibrosis of liver tissue

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15
Q

What clotting factor abnormalities may be assoc with amyloidosis?

A

Loss of clotting factors IX and X. Also infiltration of amyloid protein contributes to vascular fragility so significant risk of bleeding with percutaneous liver biopsy

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16
Q

What are the common and uncommon causes of isolated splenomegaly?

A

Common:

  • Chronic malaria
  • Kala-azar
  • Schistosmiasis
  • lymphoproliferative disease

Uncommon:

  • Feltys disease
  • chronic haemolytic anaemia
  • IE
  • left sided portal hypertension
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17
Q

What is the characteristic chromosomal abnormality in CML?

A

Philidelphia chromosome
Translocation (9;22)
BCR-ABL protein
Treat imatinib

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18
Q

What is feltys syndrome?

A

Triad of RA, splenomegaly and neutropenia
COmplications are recurrent infection, hypersplenism- anaemia and thrombocytopenia, skin hyperpigmentation, cutaneous ulceration

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19
Q

Why might the platelet count be reduced in alcoholic liver disease?

A

Splenomegaly assoc with portal hypertension results in platelet sequestation and thrombocytopenia
Direct toxic effect of alcohol on production
Folate def may contribute

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20
Q

How would you differentiate a renal and splenic mass?

A

Characeteristics of splenic mass are:

  • Dull to percussion
  • Not ballotable
  • Palpable splenic notch
  • Palpating finger cannot get above a splenic mass
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21
Q

What are the common causes of hepatosplenomegaly?

A
  • infective
  • myelo/lymphoproliferative diseases
  • cirrhosis with portal hypertension

Less common: Wilsons, haemochromatosis, glycogen storage diseases

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22
Q

Worldwide what would be the most common cause of hepatosplenomegaly?

A

Malaria
Visceral leishmania
Schistosomiasis

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23
Q

What is meant by pre-sinusoidal portal hypertension?

A

In schistosomiasis it is causes by S.Mansoni and S.Japonicum, the eggs become trapped in portal traps where they cause granulomatous reaction and subsequent fibrosis. Synthetic function of liver maintained

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24
Q

What is the genetic basis of Wilsons disease?

A

Mutation of adenosine triphosphatase 7b (ATP7B) gene on chromosome 13
AR
Gene is key in transport of copper into secretory pathway for incoperation into copper containing enzymes.
Levels of copper containing enzymes like caerulopasmin decrease
Urinary copper is high

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25
What are the clinical manifestations of Wilsons disease?
GI: chronic active hepatitis, fulminant hepatitis, chronic liver disease Neuro: tremor, parkinsonism, dysdiadokokinesis, chorea, dystonias, chroeoathetosis, ataxia, epilepsy Psychiatric: Psycosis, personality change, intellectual impairment Opthalmological: Kayser Fleisher rings in Descemets membrane, sunflower cataracts MSK: osteopenia, arthropathy, chondrocalcinosis Renal: Fanconi syndrome, nephrocalcinosis Cardiac: cardiomyopathy Haematological: haemolytic anaemia
26
What are the biochemical features of Wilsons disease and what are the limitations of these tests?
Low serum caeruloplasmin High urinary copper Both copper and caeruloplasmin are acute phase reactants so should be interpreted in context
27
How might somebody present with PBC?
Asymptomatic Intense pruritis and lethargy RUQ pain easy bruising Female, age 40-50yrs
28
What signs would you look for in PBC?
``` Scratch marks Jaundice Orbital xanthelesmata and skin xanthomas Hepatosplenomegaly signs of CLD Sings of other autoimmune conditions eg systemic sclerosis and autoimmune thyroiditis ```
29
What is the natural history of PBC?
Anti mitchondrial antibodies are directed against mitochondrial enzyme complex M2. AMA is positive in 90% Disease progression is so slow that often not affected during lifespan but once symptomatic unlikely to survive >2yrs
30
What treatment options are currently available for PBC?
General measures- alcohol avoidance, fat soluble vitamins ADEK Ursodeoxycholic acid: reduces cholestasis and improves liver function tests however has little effect on symtpoms/prognosis Cholestyramide- for itching Liver transplant
31
What are the early features of haemochromatosis?
Fatigue Arthralgia Sexual dysfunction
32
What are the later features and complications of haemochromatosis?
Hepatic cirrhosis- chronic liver disease- hepatomegaly T1DM Bronze skin discolouration (you can tell because there is no tan line!) Cardiomyopathy- often dilated with arrythmias Chondrocalcinosis
33
What is the typical genetic abnormality found in haemochromatosis?
AR One of the most common heritable genetic conditions in northern europe- prevalence 1/200 Most common allelle is C282Y on HFE gene
34
Can you name a cause of accelerated iron accumulation in patients with primary haemochromatosis?
Alcohol may accelerate it
35
What are the difficulties screening for haemochromatosis?
Serum ferritin, iron and Saturation may be increased in other causes of cirrhosis particularly alcohol and hep c Phenotypically women have less severe disease due to menstrual losses More than one mutation in HFE gene and mutations inn other genes so a negative screen does not rule it out.
36
How would you treat somebody with primary haemochromatosis?
``` MDT input Avoid alcohol and iron supplements Weekly phlebotomy to reduce iron stores Desferrioxamine can be used Liver transplant in those with advanced cirrhosis ```
37
How might somebody that has had a liver transplant present?
Complication of immunosuppression - Infectious disease- typical or atypical - Malignancy- BCC, SCC, bowel - metabolic complications- post transplant diabetes - CV complications- IHD, CVD, acute rejection Transplant dysfunction- rejection or recurrent disease Surgical complications in early post op period: biliary leak or hepatic/portal vein thrombosis
38
What are the causes of end stage liver disease?
Alcohol abuse Viral hepatitis Autoimmune (PBC, autoimmune heptaitis) Cryptogenic cirrhosis
39
What is the common cause of liver transplantation?
Alcohol
40
Is a liver transplant ever indicated for cirrhosis from chronic hepatitis C
Yes it is now an accepted indication
41
What are the criteria for referral to a liver unit for transplantation?
The Kings College hospital criteria are divided into: paracetamol induced - arterial lactate >3,5 after 4hrs resuscitation - Or pH <7.3 or arterial lactate >3.0 12hrs after resuscitation - Or all 3 of: INR >6.5, Cr >300, encephalopathy (grade 3 or 4) Non-paracetamol induced - Arterial lactate >3.5 4hrs after resuscitation - INR >6.5 - Or any 3 of: INR >3.5, age <10yrs or >40yrs, bili >300, jaundice >7 days, aetiology being drug reaction
42
What immunosuppressive drug regimens are currently in use for liver transplant?
Steroids in combination with a calcineurin inhibitor such as tacrolimus or ciclosporin and an antiproliferative agent such as mycophenolate mofetil
43
What other forms of liver support are available?
``` MARS system (Molecular adsorbents recirculation system)- 2 circuits- 1st exposed to albumin to bind toxins and ammonia and 2nd the albumin is removed ECLAD (extracorporeal liver assist devices) ``` Heterotopic liver transplant- implantation of a lobe of allogenic liver
44
What are the extra abdominal features of IBD?
Clubbing Uveitus Large and small joint arthropathies and sacroilitis Skin disease- pyoderma gangrenosum, erythema nodusum Peripheral oedema from hypoalbuminaemia Cushiongoid from steroid therapy
45
What are the differences between Crohns and UC?
Crohns - skip lesions - any part of bowel- mouth to anus - transmural (full thickness) inflammation - Granulomas UC - continuous - Colon+ backwash ileitis - superficial inflammation - crypt abcesses
46
How might a patient with IBD present to emergency department?
- bloody diarrhoea worsening over several days | - de novo presentation may be difficult to distinguish from bacterial gastroenteritis
47
What are the criteria for grading severity of IBD?
Truelove and Witts criteria - Mild: < 4 stools per day, no systemic disturbance, normal ESR - Moderate: > 4 stools per day with minimal systemic disturbance - Severe: >6 stools per day with blood and evidence of systemic disturbance evidenced by fever, tachycardia, anaemia or ESR >30
48
How would you induce remission in UC and Crohns?
Crohns - steroids (budesonide if not tolerated) + azathioprine/mercaptopurine + inflixumab/adalimumab UC - aminosalicylates (topical if proctitis) - Steroids if severe + ciclosporin
49
How would you maintain remission in UC and Crohns?
Crohns - Azathioprine or mercaptopurine (only use methotrexate in those who needed it to induce remission) UC - Aminosalicylates (mesalazine, sulphasalazine) + azathioprine
50
What are the complications/extra-abdominal features of Crohns and UC?
Crohns - erythema nodusum - pyoderma gangrenosum UC - Primary sclerosing cholangitis - toxic megacolon - osteoporosis - colon canacer
51
Causes of epigastric mass
Carcinoma of stomach or pancreas Abdominal aortic aneurysm Lymphoma Caudate lobe of liver
52
Causes of right iliac fossa mass
``` Crohns disease Caecal carcinoma Ileocaecal mass including amoebic abcess, ileocaecal TB, appendicular mass Ovarian tumour Renal transplant ```
53
Causes of left iliac fossa mass
``` Carcinoma of sigmoid colon Diverticular mass Faecal mass Ovarian tumour Renal transplant ```
54
How is ADPKD inherited and how and when would you recommend screening?
AD Mutation in PKD1 on chromosome 16 and PKD2 on chromosome 4 Screening with US but does not rule out if <30yrs US criteria if positive FH - <30yrs- at least 2 unilateral or bilateral renal cysts - 30-59yrs- at least 2 cycts in each kidney - >60yrs- at least 4 cysts in each kidney Supported by pancreatic and hepatic cysts if no FH - Bilateral renal enlargement and cysts or - Presence bilateral renal and hepatic cysts - no manifestations of other disease
55
Name some extra renal manifestations of ADPKD
``` Cysts in other organs Intracranial berry aneurysms Polycythaemia (excess erythropoietin release) Hypertension (excess renin release) Cardiac valve disease (MV prolapse) Diverticular disease Aortic aneurysm Abdominal wall hernias ```
56
Name some organs that contain cysts in ADPKD
Kidneys Liver Pancreas Arachnoid cysts
57
Name some causes of abdominal pain in patients with ADPKD?
Infected cyst Haemorrhage into cyst Some conditions occur in higher frequency in patients with ADPKD and can cause abdo pain: - Diverticulitis/diverticular perforation - Nephrolithiasis - Strangulated/incarcerated hernia - ruptured AAA - Tuberous sclerosis complex
58
What signs do you look for in somebody with a renal transplant?
Oblique scar in iliac fossa + mass below Signs of immunosuppression - Increased skin pigmentation - Multiple skin warts - Premature aging of skin - Skin malignancy or evidence of previous exicision - Sun cream or hat by bed - Fine tremor of ciclosporin toxicity or tacrolimus - Gingival hypertrophy- ciclosporin Signs of ESRF or RRT- peritoneal or haemodialysis Evidence of aetiology of native kidney - ADPKD - Diabetic- BM stick marks, lipodystrophy from insulin injections - Hearing aids- Alports syndrome or aminoglycoside induced nephropathy with ototoxicity - Facial lipodystrophy assoc with mesangiocapillary GN type 2 - If no evidenc of underling cause then likely GN Functional status of the transplant - HTN - Fluid overload - Current evidence of dialysis - phosphate binders by bed
59
What are the complications of chronic kidney disease?
``` Anaemia- EPO Hyperparathyroidism- initially secondary (hyperplasia of parathyroid due to low calcium and have low/normal calcium) then tertiary (hypercalcaemia) Hyperphosphataemia (due to insuffient removal of phosphate by kidneys, worsens hyperparathyroidism)- 1st line is calcium acetate as phosphate binder Renal bone disease Uncontrolled hypertension Uraemic encephalopathy, pericarditis Fluid overload Amyloidosis secondary to dialysis ```
60
What are the commonest causes of end stage renal failure?
Diabetes mellitus ADPKD Chronic Glomerulonephritis Hypertension in Afro-Caribbean population
61
What are the complications of transplanting a patient with Alports syndrome?
Defect in type IV collage so a new transplant exposes them to antigens they have not encountered before. The subsequent antibody response against this antigen may result in some patients developing anti-glomerular basement membrane disease
62
Name some opportunistic infections assoc with renal transplantation
CMV Pneumocystis jiroveci EBV BK virus ( common polyomavirus which lies dormant in renal tract and can cause ureteric stenosis and interstitial nephritis JC virus ( causes progressive multifocal leucoencephalopathy)
63
Why are the kidneys transplanted into the pelvis?
Good blood supply Space Proximity to bladder for anastomosis Easy access for biopsy/nephrostmy
64
What are the commonest causes of death in a patient with a renal transplant?
Cardiovascular: accelerated CVD is a feature of all patietns with renal disease Infection due to immunosuppression is 2nd
65
What are some causes of a distended abdomen?
Fat Faeces Foetus Flatus and Fluid
66
Name the surface markings of aorta
Lies in epigastrum, just to left of midline and bifurcates at L4/5
67
What is peutz Jeghers syndrome?
Characeterised by the appearance of benign haemartomas in GI tract accompanied by mucocutaneous pigmented macules over hands, feet and lips. Presents at screening, with intersussception or malignancy disease
68
What is the inheritance of Peutz-Jeghers syndrome?
AD | mutation in gene STK11 which is tumour suppressor gene
69
WHat are the complications of HHT?
Anaemia Recurrent epistaxis GI haemorrhage from telangiectasia and AVM in bowel HIgh output cardiac failure as result of large AVM SOB and haemoptysis as result of lung AVMs Stroke and SAH- cerebral AVMs
70
What are the common sites of AVM in HHT?
Brain, lung, liver, bowel, spine
71
What is the genetic basis for HHT?
AD | Number of genes described
72
What is Heyde's disease?
Association between aortic stenosis and colonic angiodysplasia Mild form of von willebrands disease due to sheer stresses around aortic valve which increase the breakdown of large molecules of vWF resulting in consumptive deficiency Often improves with AVR
73
What are the signs of kidney- pancreas transplant?
May have 2 scars in iliac fossa or midline scar | Look for signs of functioning pancreas- no finger prick marks or injection site marks
74
How is the pancreas drained when transplanted and what are the complications?
Old pancreatic transplants were bladder drained, urinary amylase could be used to monitor for early signs of graft pancreatitis . Route of drainage was complicated by reflux pancreatitis, persistant haematuria, recurrent UTIs, metabolic acidosis (bicarb loss) Now most perform primary enteric drainage
75
Can you name some complications of post transplant immunosuppression?
Infections Malignant disease- BCC, SCC, post transplant lymphoproliferative disorder CVD Chronic transplant injury- ciclosporin and tacrolimus nephrotoxic Morphological changes- cushingiod, acne vulgaris
76
What are the indications for a liver and kidney transplant?
Usually hep B/C with assoc glomerulonephritis or cryoglobulinaemia (not usually hepatorenal syndrome as with liver transplant the renal function is potentially reversible)

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