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Abdominal Flashcards

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1
Q

Causes of clubbing

A

C: cardiac. subacute infective endocarditis. cyanotic heart disease. atrial myxoma.
L: lungs. lung abscess. empyema.
U: ulcerative colitis.
B: biliary cirrhosis.
B: bronchogenic carcinoma (most commonly small cell)
I: idiopathic.
(N: not COPD)
G: gastrointestinal. malabsorption (e.g. coeliac disease) Crohn disease.

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1
Q

What is the mode of inheritance of Peutz-Jeghers syndrome?

A

Autosomal dominant
Caused by mutations in the STK11 which is a tumour suppressor gene.

Causes polyps + melanocytic macules.

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2
Q

What are the manifestations of Peutz-Jeghers syndrome?

A

Dark-coloured freckling on oral mucosa.

Polyps within the GI tract which may be complicated by bleeding, obstruction and chronic pain.

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3
Q

What is the mode of presentation of HHT (Osler-Weber-Rendu syndrome)

A

Recurrent epistaxis in childhood with red spots on lips / tongue / fingertips + FH of disease
Characterised by multiple telangiectasia.
The patient is at risk of haemorrhage from AV malformations, particularly pulmonary + cerebral.

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4
Q

What is the mode of inheritance of HHT? (Osler-Weber-Rendu syndrome)

A

Autosomal dominant.
More than 80% of cases are due to mutations in ENG or ACVRL1 genes.

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5
Q

Most common causes of CLD in the Western world?

A

Alcohol
Chronic viral hepatits B and C
NAFLD
Autoimmune hepatitis
Metabolic conditions: Wilson’s, haemochromatosis

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6
Q

What are the reversible causes of hepatic encephalopathy?

A

Alcohol, drugs, GI haemorrhage, infection, constipation

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7
Q

Name some complications of CLD.

A

Portal hypertension
Haemorrhage
Ascites
SBP
Hepatic encephalopathy
Hepatorenal syndrome
Hepatopulmonary syndrome

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8
Q

What do you understand by decompensated CLD? What are the factors which can lead to decompensated CLD?

A

The liver can compensate for a significant amount of hepatocyte injury, but can decompensate as a result of ongoing liver injury or additional stress.

Precipitating factors: alcohol intake, untreated chronic active viral hepatitis, GI bleed, large salt intake, sepsis, constipation, dehydration.

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9
Q

How does decompensated CLD present clinically?

A

Clinically, decompensated CLD presents with: ascites, encephalopathy, hepatorenal syndrome, coagulopathy, jaundice

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10
Q

How do you grade severity of hepatic encephalopathy?

A

West Haven criteria:

Grade 0: clinically normal but with small changes in memory
Grade 1: mild confusion, short attention span, disordered sleep
Grade 2: drowsiness, lethargy, mild disorientation
Grade 3: somnolent but rousable, grossly confused and disorientated
Grade 4: comatose, no response to verbal / painful stimuli

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11
Q

How do you grade severity of cirrhosis?

A

Modified Child-Pugh system - classes correspond to 1-year survivals

Class A (5-6 points) - 100% 1y survival
Class B (7-9 points) - 80% 1y survival
Class C (10-15 points) - 50% 1y survival

Parameters measured: encephalopathy stage, bilirubin, INR, ascites, albumin

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12
Q

How do you classify causes of jaundice?

A

Pre-hepatic: excessive breakdown of RBCs e.g., haemolytic anaemia, malaria, hereditary haemoglobinopathies

Hepatic: due to hepatocyte injury e.g., acute viral hepatitis, paracetamol, alcohol, hypoxic / ischaemic

Post-hepatic: due to obstruction of bile flow e.g., gallstone obstruction, pancreatic head malignancies

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13
Q

Tell me about hepatorenal syndrome.

A

Results from inadequate hepatic breakdown of vasoactive substances, leading to excessive renal vasoconstriction.

It can develop rapidly (type I) or slowly (type II).

Mimics pre-renal impairment.

As the kidneys attempt to conserve maximum salt and water in response to perceived hypovolaemia, the patient produces low volumes of highly concentrated urine that is low in sodium.

It is usually diagnosis of exclusion, having ruled out obstruction, sepsis and nephrotoxic meds.

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14
Q

How is ascites investigated?

A

The protein level of ascites is measured to determine whether ascites is of a transudative or exudative cause. The serum ascites albumin gradient (SAAG) is an accurate test for diagnosis of the cause.

SAAG >11g/l - transudate (cirrhosis, cardiac failure, nephrotic syndrome)
SAAG <11g/l - exudate (malignancy, pancreatitis, TB)

Would also measure: neutrophil count and microscopy / culture (SBP), amylase (pancreatitis), and cytology (malignancy).

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15
Q

What are the indications for liver transplant in an adult?

A

Acute: paracetamol poisoning, other drugs, acute hepatitis, EBV and CMV infections.

Chronic: alcoholic liver disease, PBC, PSC, chronic viral hepatitis, Wilson’s disease, Budd-Chiari syndrome, hepatic malignancy.

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16
Q

How do you manage ascites in association with CLD?

A

Low-salt diet, spironolactone, furosemide.
If these measures fail, can perform therapeutic paracentesis.
TIPSS may help to relieve portal hypertension.
Liver tx is a curative procedure for end-stage disease when medical management fails.

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17
Q

Causes of ascites?

A

Common: cirrhosis with portal HTN, malignancy, CCF, nephrotic syndrome

Uncommon: Budd-Chiari syndrome, portal vein thrombosis, constrictive pericarditis, malabsorption, TB peritonitis, myxoedema, ovarian diseases

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18
Q

How would you distinguish between transudative and exudative ascites in patients with low serum albumin?

A

By using the serum ascites albumin gradient (SAAG)

A low gradient <11g/L indicates loss of protein into the ascites - EXUDATE
A high gradient >11g/L indicates TRANSUDATE

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19
Q

What is the differential diagnosis of generalised lymphadenopathy?

A

Lymphoproliferative disease: CLL, ALL, Hodgkin’s and NH lymphoma
Viral disease: HIV, EBV, CMV
Other infections: TB, brucellosis and toxoplasmosis
Inflammatory disease: SLE, RA, sarcoidosis

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20
Q

How are Hodgkin’s and Non-Hodgkin’s lymphoma differentiated pathologically?

A

Through the presence of Reed-Sternberg cells in Hodgkin’s lymphoma. These are characteristic binucleate cells found on light microscopy of a biopsy.

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21
Q

What are ‘B symptoms’ in lymphoma and what are their significance?

A

These include weight loss, unexplained fever and night sweats.

B symptoms are included in the Ann Arbor staging classifications of NHL and HL, and indicate a poorer prognosis.

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22
Q

Tell me about CLL.

A

Monoclonal proliferation of lymphocytes.
Most commonly suspected from routine bloods, with a high WCC.
Staged by the Binet system, and cytogenetic testing can give info on how the disease is likely to progress, therefore guiding treatment.
Stage A disease can be managed with a ‘watch and wait’ approach, more advanced disease requires chemotherapy and MABs.
Complications of CLL include bone marrow failure, haemolytic anaemia, chest infections and acute transformation to diffuse large B-cell lymphoma.

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23
Q

Top 3 causes of hepatomegaly?

A

Congestive cardiac failure
Malignancy
Lymphoma

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24
What scoring systems may help in the evaluation of a patient presenting with acute alcoholic hepatitis?
Maddrey's discriminant function test to predict prognosis in alcoholic hepatitis. The Mayo End Stage Liver Disease (MELD) score - predicts survival probability over 90 days. The Glasgow alcoholic hepatitis score on day 1 has an overall accuracy of 81% when predicting 28-day outcome.
25
How would you manage a patient with acute alcoholic hepatitis?
Mainstay of treatment is supportive: abstinence from alcohol, adequate nutrition, treatment of infection. Liver biopsy may be indicated to confirm the diagnosis. Maddrey's discriminant function score of >32 is an indication for treatment with steroids (40mg prednisolone).
26
What are the histological features of alcoholic liver disease?
Hepatic steatosis - accumulation of fat in liver cells Alcoholic hepatitis - acute inflammation and hepatocyte necrosis Hepatic cirrhosis - fibrosis of liver tissue
27
What clotting factor abnormalities may be associated with hepatic amyloidosis?
Hepatic amyloidosis is associated with the loss of clotting factors 9 and 10. Infiltration with amyloid protein contributes to vascular fragility - significant risk of bleeding if percutaneous biopsy is performed.
28
What are the causes of massive splenomegaly?
'MMM' Myelofibrosis CML Malaria / Visceral leishmaniasis
29
What are the most common causes of isolated splenomegaly worldwide?
Chronic malaria Kala-azar Schistosomiasis
30
What is the characteristic chromosomal abnormality in CML and what signal transduction pathway is this associated with?
The Philadelphia chromosome is the hallmark of CML, found in 90% of cases. Cytogenetically results from a chromosomal translocation t(9;22). Results in an altered bcr-abl protein which increases tyrosine kinase activity. This activates proteins which speed up cell division and inhibit DNA repair.
31
Tell me about Felty's syndrome.
Felty's syndrome is: splenomegaly, RA and neutropaenia. Frequency of Felty's increases with duration of RA. People with this syndrome are at risk of infection due to neutropaenia. Complications of Felty's include: recurrent infection, hypersplenism causing anaemia and thrombocytopaenia, skin hyperpigmentation and cutaneous ulceration.
32
Why might the platelet count be reduced in alcoholic liver disease?
Splenomegaly associated with portal HTN results in platelet sequestration and thrombocytopaenia. Direct toxic effect of alcohol on production + function of platelets. Platelet count of <50 is an indication for platelet transfusion in the presence of bleeding, particularly from varices.
33
How would you differentiate between a splenic and a renal mass?
4 characteristics of a splenic mass (not present with renal mass) - CNPD 'cannot percuss daintily' Cannot get above it Not ballotable Palpable notch Dull to percussion
34
What is the function of the spleen?
Removal of old/damaged RBCs Storage of platelets B- and T-lymphocyte-mediated immune function
35
What advice should be given to a patient undergoing a splenectomy?
Preoperative vaccinations: pneumococcal, influenza, meningococcus Lifelong prophylactic penicillin Annual influenza vaccine Wear medic alert bracelet Sick day rules
36
What are the indications for a splenectomy?
Hypersplenism (ITP) Mass effect of spleen Traumatic rupture Haematological malignancies Congenital haemolytic anaemias (hereditary spherocytosis)
37
Tell me about polycythaemia rubra vera.
Primary polycythaemia, due to a fault in the bone marrow. Results in uncontrolled RBC proliferation, often due to a mutation in the JAK2 gene. PRV usually presents with raised Hb, or with thrombosis, headache, sweating and itch. Investigation is initially with an FBC, if PRV suspected, would test for JAK2 mutation. Management is targeted at lowering thrombosis risk. Includes venesection, aspirin and myelosuppression. JAK2 inhibitors are under trial. A major complication, alongside thrombosis, is transformation to AML.
38
What is the ddx of hepatosplenomegaly?
'CMLVII' Chronic liver disease with portal hypertension Myeloproliferative disease: CML, AML Lymphoproliferative disease: CLL, HL and NHL Viral disease: EBV, CMV, HIV Inflammatory disease: sarcoidosis Infiltrative disease: amyloidosis, glycogen storage disease
39
What are the myeloproliferative disorders?
A group of conditions caused by abnormal myeloid stem cell proliferation in the bone marrow. RBCs: PRV WCCs: CML Platelets: essential thrombocytopaenia Fibroblasts: myelofibrosis
40
Tell me about amyloidosis.
A multisystem disease that results from extracellular deposition of abnormal proteins. 2 main types: Amyloid L and Amyloid A AL mainly occurs on its own, can be seen alongside myeloma. Mainly dx on biopsy, can treat its complications (e.g., renal transplant). AA mainly occurs in conjunction with other inflammatory disorders and infections (such as RA). Diagnosed by biopsy. Condition often improves with tx of underlying inflammatory disorder.
41
What is the genetic basis of Wilson's disease?
The genetic abnormality in Wilson's is a mutation of the ATP7B gene. The gene is a key element in copper transportation. Mutation of this gene leads to accumulation of free copper in hepatocytes, followed by spill over into the serum / urine. The levels of caeruloplasmin decrease.
42
What are the biochemical features of Wilson's disease and what are the limitations of these tests?
High urine copper levels, low serum caeruloplasmin. Both copper and caeruloplasmin are acute phase reactants and increase in the presence of an acute phase response.
43
What are the most frequent presenting complaints of PBC?
Asymptomatic in many patients and diagnosed incidentally. Pruritus and fatigue are most common, some experience RUQ pain. Impaired bile production leads to impaired absorption of fat-soluble vitamins and easy bruising.
44
What is the natural history of PBC?
Female:male ratio is 9:1. AMA is positive in 90% of patients with PBC. Symptomatic patients are unlikely to survive >2 years, but if asymptomatic then disease progression is so slow that lifespan is unaffected.
45
Can you name some conditions that might mimic PBC?
Autoimmune hepatitis and PSC. Granulomas in the liver may suggest cholestatic sarcoidosis but AMA is usually absent in this condition.
46
What treatment options are available for PBC?
General: alcohol avoidance, vitamin ADEK supplementation. Medical: ursodeoxycholic acid, cholestyramine Surgical: liver tx in advanced cases
47
What is the genetic abnormality found in haemochromatosis?
Prevalence of 1 in 200 in people of northern European extraction. Disease has variable penetration, most common allele is the C282Y allele in the HFE gene.
48
Can you name a cause of accelerated iron accumulation in patients with primary haemochromatosis?
Alcoholism may accelerate iron accumulation.
49
What are the difficulties with screening for haemochromatosis?
Serum haematinics may be increased in other causes of cirrhosis. The underlying diagnosis can be resolved by liver biopsy. Ferritin is also an acute phase reactant and can be raised in other conditions. Females have milder and later onset than males (due to menstruation), can result in delayed diagnosis. More than one mutation in the HFE gene exists - can make genetic analysis difficult.
50
How would you treat someone with primary haemochromatosis?
MDT approach - multiple organ systems affected. Mainstay of treatment is avoidance of alcohol and iron. Weekly therapeutic phlebotomy. Desferrioxamine (iron chelator) can be used to reduce iron stores. Liver transplant in advanced cirrhosis.
51
What is the most common indication for liver transplant?
Alcoholic liver disease.
52
Is a liver transplant indicated for cirrhosis from chronic hep C infection?
Yes, this is now an indication for liver transplantation.
53
What is the overall survival following liver transplant?
Around 60% over 15 years.
54
What are the criteria for referral to a liver unit for transplantation?
The King's College Criteria help identify patients at higher risk of death who should be referred for urgent liver tx: Lactate >3.5 4 hours after resuscitation OR INR >6.5 OR any 3 of: INR >3.5, age <10 or >40, serum bili >300, jaundice >7 days, aetiology being a drug reaction
55
What immunosuppressants are currently in use for liver transplants?
Corticosteroids Tacrolimus / ciclosporin Mycophenolate mofetil (MMF)
56
How do you differentiate between Crohn's and UC?
The main differentiating factors are the sites and extent of inflammation across the bowel wall. CD affects any part of the GI tract from mouth to anus and has 'skip lesions' whereas UC is just the colon and continuous. CD causes transmural inflammation, whereas UC causes superficial inflammation. Histologically, CD causes granulomas, whereas UC causes crypt abscesses.
57
What are the extra-intestinal manifestations of IBD?
Skin: erythema nodosum, pyoderma gangrenosum, aphthous ulceration Joints: seronegative arthritides Eye: uveitis, scleritis, episcleritis, conjunctivitis Hepatobiliary: PSC, cholangiocarcinoma Renal: oxalate stones
58
What screening tests should you consider before initiating biological therapies?
History and examination Hepatitis serology HIV test CXR T-spot test for TB
59
What biological agents are available for treatment of IBD?
UC: infliximab and golimumab CD: infliximab and adalimumab Vedolizumab (novel agent) for both diseases for pts who fail first-line treatment.
60
What are Truelove and Witts' criteria?
Used to assess severity of a flare of IBD, and to guide intervention. Mild: <4 stools / day, no systemic disturbance and normal ESR Moderate: >4 stools/day, minimal systemic disturbance Severe: >6 stools/day with bloods and evidence of systemic disturbance (fever, tachycardia, anaemia or ESR >30)
61
Current treatment strategies for Crohn's disease?
Mesalazine 4g/day for mild disease Oral / IV steroids for severe disease Azathioprine as steroid-sparing agent Infliximab in refractory disease Surgery if medical therapy fails Antibiotics if infection suspected Maintenance: stop smoking, remission treatment with MTX, AZA or infliximab
62
How would you manage acute colitis?
In acute flare, aim is to induce remission. In remission, focus changes to preventing relapses with maintenance therapy. Mild/moderate disease: mainstay is corticosteroid therapy. Mesalazine is an effective topical agent for distal disease. Severe acute disease requires IV steroids and close monitoring (toxic megacolon).
63
When would you consider ciclosporin in a patient with a severe exacerbation of UC?
IV hydrocortisone remains the mainstay of therapy for a severe exacerbation of UC. The use of IV ciclosporin should be considered if no improvement in the first 3 days.
64
When would you consider surgery in an acute flare of UC?
Toxic dilatation of the colon >5.5cm. Following 3 days of intensive treatment in patients with >8 stools/day or CRP >45. Cases of UC that have failed to respond to treatment after 10 days.
65
What is sclerosing cholangitis?
Inflammation of bile ducts, leading to scarring and biliary obstruction. Untreated causes CLD and liver failure.
66
When would you start a Crohn's disease patient on anti-TNF therapy?
Infliximab is indicated in steroid refractory and fistulating disease - must fulfill all 3 criteria: 1. Severe active CD 2. Disease refractory to steroids and steroid-sparing agents / intolerant to these drugs 3. Surgery is inappropriate (diffuse disease / short bowel)
67
Alternative explanation for midline scar that is not IBD?
SPK: simultaneous kidney pancreas transplant.
68
What is the genetic basis of PKD?
ADPKD: affects adults, chromosome 16 in PKD 1, chromosome 4 in PKD 2. Autosomal recessive: more severe liver involvement than ADPKD.
69
List some other manifestations of ADPKD
Cystic disease: liver, spleen, pancreas Berry aneurysm Pain / haematuria Renal cell carcinoma Valvular disease: mitral and aortic HTN with LV hypertrophy GI: colonic diverticulum, herniae
70
What are the indications for nephrectomy in ADPKD?
Reccurent infections, chronic pain, recurrent haematuria, GI pressure symptoms (early satiety), size / creating space for transplant
71
List some other renal cystic disorders.
Unilateral: benign cysts, RCC, PKD Bilateral: bilateral RCC, amyloidosis, VHL syndrome, tuberous sclerosis
72
What are the most common causes for a renal transplant?
Diabetes mellitus Glomerulonephritis ADPKD Hypertension
73
What investigations would you request in a patient with a renal transplant admitted with a rise in serum creatinine?
Bloods: renal function, FBC, bone profile, LFTs, CRP if signs of infection + blood cultures / virology (CMV, BK virus PCR), immunosuppressive levels (check for toxicity) Urine: (check for haematuria, proteinuria, leucocytes and nitrites), urine microscopy, culture and sensitivity, virology for BK virus Imaging: USS of the transplanted kidney with Dopplers of the vessels: to assess for obstruction, renal perfusion, possible RAS and renal vein thrombosis Transplant biopsy: if no other cause found, can biopsy the transplanted kidney
74
What are the signs of a failing transplant?
Progressively declining renal function Proteinuria Fluid overload Tenderness over transplant graft Fibrosis / atrophy / vascular changes in tx kidney biopsy
75
What do you know about the manifestations of Alport's syndrome?
AS is a genetic disease in which there is defective type 4 collagen. 3 main types: X-linked (most common), AD and AR. Manifestations: - Kidney failure (50% require transplant by age 25y) - Ears: sensorineural hearing loss - Eyes: anterior lenticonus leads to slow progressive visual loss
76
How do you manage transplant rejection?
Immunosuppression Dialysis re-initiation Allograft nephrectomy Re-transplantation
77
What are the causes of hepatomegaly?
Cirrhosis (alcoholic) Carcinoma (secondaries) CCF PLUS Infective (HBV and HCV) Immune (PSC, PBC and AI hepatitis) Infiltrative (myeloproliferative disorders and amyloid)
78
What investigations should be performed if you suspect liver cirrhosis?
Bloods: autoantibodies and immunoglobulins, hepatitis B and C serology, ferritin, caeruloplasmin, A1AT levels, alpha fetoprotein. INR and albumin to test liver synthetic function. Imaging: ERCP (PSC) Other: liver biopsy
79
What are some of the complications of liver cirrhosis?
Variceal haemorrhage due to portal hypertension Hepatic encephalopathy SBP
80
What scoring system is used to classify liver cirrhosis?
Child-Pugh classification of cirrhosis Prognostic score based on bilirubin / albumin / INR / ascites / encephalopathy A - score of 5-6, 100% 1-year survival B - score of 7-9, 81% 1-year survival C - score of 10-15, 45% 1-year survival
81
What are the causes of ascites?
Cirrhosis (80%) Carcinoma (HCC) CCF
82
How do you treat ascites in a cirrhotic patient?
Abstinence from alcohol Salt restriction Diuretics (aim 1kg weight loss/day) Liver transplantation
83
What are some causes of palmar erythema?
Cirrhosis Hyperthyroidism RA Pregnancy Polycythaemia (things that cause a hyperdynamic circulatory system)
84
What are some causes of gynaecomastia?
Physiological: puberty and senility Kleinfelter's syndrome Cirrhosis Drugs: digoxin and spironolactone Testicular tumour Hyper/hypothyroidism and Addison's
85
What are the relevant autoantibodies in PBC, PSC and AI hepatitis?
PBC: anti-mitochondrial antibody (M2 subtype) PSC: ANA, anti-smooth muscle AI hepatitis: anti-smooth muscle, anti-liver kidney microsomal type 1 (LKM1) and sometimes ANA
86
What is the inheritance pattern of haemochromatosis?
Autosomal recessive on chromosome 6 HFE gene mutation Homozygous prevalence 1:3000 Males affected earlier than females (menstrual loss is protective)
87
What investigations would you perform in a patient with haemochromatosis?
Bedside: ECG, blood glucose Bloods: Ferritin (increased), transferrin saturation (increased), genotyping, AFP Imaging: echo, CXR, liver USS Other: liver biopsy
88
Treatment of haemochromatosis?
Regular venesection (1 unit/week until iron deficient, then 1 unit 3-4 x per year) Avoid alcohol Surveillance for HCC
89
What is the expected prognosis for a patient with haemochromatosis?
200 x increased risk of HCC if cirrhotic. Reduced life expectancy if cirrhotic. Normal life expectancy without cirrhosis and with effective treatment.
90
Causes of massive splenomegaly?
Massive (>8cm): MMM Malaria / visceral leishmaniasis (kala-azar) CML Myelofibrosis
91
What are the indications for splenectomy?
Rupture (trauma) Haematological (ITP and hereditary spherocytosis)
92
What is included in the work-up for splenectomy?
Vaccination (ideally 2/52 before to protect against encapsulated bacteria): pneumococcus, meningococcus, haemophilus influenzae Lifelong prophylactic penicillin Medic alert bracelet
93
List some causes of unilateral renal enlargement.
Polycystic kidney disease Renal cell carcinoma Simple renal cysts Hydronephrosis due to ureteric obstruction
94
List some causes of bilateral renal enlargement.
Polycystic kidney disease Bilateral renal cell carcinoma Bilateral hydronephrosis Tuberous sclerosis (renal angiomyolipomata and cysts) Amyloidosis
95
How do patients with ADPKD usually present initially?
Hypertension Recurrent UTIs Abdominal pain (bleeding into cyst and infection) Haematuria
96
What extra-renal complications are associated with ADPKD?
Hepatic cysts and hepatomegaly Intracranial Berry aneurysms Mitral valve prolapse
97
What are the top three indications for liver transplantation?
Cirrhosis Acute hepatic failure (hepatitis A and B, paracetamol IOT) HCC
98
What are the success rates of liver transplantation?
80% 1-year survival 70% 5-year survival
99
ESRD differential diagnosis
Polycystic kidney disease Diabetes Systemic sclerosis Rheumatoid arthritis / other CTD (SLE) Amyloidosis Other organ transplantation (calcineurin inhibitor toxicity) Tuberous sclerosis
100
What are the top three causes of renal transplantation?
Diabetic nephropathy Glomerulonephritis ADPKD
101
What problems can occur following renal transplantation?
Rejection: acute or chronic Infection secondary to immunosuppression (CMV / pneumocystis carinii) Increased risk of malignancy (skin / lymphoproliferative) Immunosuppressant drug side effects / toxicity (ciclosporin) Recurrence of original disease Chronic graft dysfunction
102
What are the success rates of renal transplantation?
90% 1-year graft survival 50% 10-year graft survival (better with live-related donor grafts)

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