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Abdominal > Abdominal > Flashcards

Abdominal Flashcards

1
Q

Causes of MASSIVE splenomegaly?

A

Myeloproliferative disease- CML or myelofibrosis
Chronic malaria
Glycogen storage disorders

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2
Q

Cause of non massive splenomegaly?

A

Portal hypertension
Lymphoproliferative disease (CLL, Hodkins) (should have lymphadenopathy)
Sarcoidosis
Infection- especially EBV, CMV, HIV

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3
Q

What would you send ascitic fluid for?

A

Albumin, amylase/lipase, cytology, MCS, cell count

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4
Q

Usual NILS?

A 
Autoantibodies and immunoglobulins 
Ferritin 
A1AT 
Caeruloplasmin (<45) 
Viral hepatitis screen incl EBV/CMV if acute 
AFP 
Coeliac screen 
TFTs
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5
Q

Complications of cirrhosis

A

HCC
Variceal haemorrhage
SBP
Encephalopathy

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6
Q

Signs of portal hypertension?

A 
Ascites 
Hepatosplenomegaly 
Raised JVP 
Variceal bleeding 
Distended veins in abdomen
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7
Q

Chronic management of cirrhosis?

A

Abstinence from alcohol
Salt restriction and good nutrition
Diuretics, if resistant then regular large volume paracentesis
If previous encephalopathy- laxatives and rifaximin
Propranolol and/or endoscopic therapies for varices
Liver transplantation

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8
Q

Causes of palmar erythema? (5)

A 
RA 
CLD 
Pregnancy 
Polycythaemia 
Hyperthyroidism
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9
Q

Causes of gynaecomastia? (6)

A 
Spironolactone or other drugs 
CLD 
Kleinefelters 
Physiological- puberty and senility 
Testicular tumour/orchidectomy (loss of testosterone) 
Endocrinopathy
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10
Q

Which antibody in usually identified in PBC?

A

Antimichondrial antibody with increased IgM?

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11
Q

Which antibody is usually found in PSC

A

ANA, Anti-smooth muscle antibody

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12
Q

Which antibody is typically found in AI?

A

Anti-smooth muscle, anti liver/kidney microsomal type (LKM1) and sometimes ANA

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13
Q

Treatments of PBC?

A

Ursedeoxycholic acid helps with symptoms and improves prognosis. May require transplant.

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14
Q

What should you present in a patient with CLD?

A

Presence of decompensation i.e. jaundice, ascites, encephalopathy
Clues as to aetiology
Signs of portal hypertension i.e. ascites, distended veins, hepatomegaly/splenomegaly
Evidence of treatment i.e. liver transplant scar, ascitic drain/tap sites

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15
Q

Clinical signs of haemachromatosis?

A 
Increased skin pigmentation (slate grey) 
Stigmata of chronic liver disease 
Hepatomegaly 
Evidence of venesection 
Evidence of joint replacement 
Rooftop scar- hemihepatectomy for HCC
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16
Q

Evidence of complications of haemachromatosis

A

Finger prick marks or insulin injection sites
Congestive heart failure
Arthropathy (pseudogout)

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17
Q

Describe the inheritance of haemachromatosis?

A

Autosomal recessive on chromosome 6. Affects HFE gene.

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18
Q

How do patients with haemachromatosis generally present?

A

Pruritis and fatigue
CLD
Incidental diagnosis or family screening
Usually seen earlier in men as women are protected by menstrual losses.

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19
Q

What other investigations should you consider in haemachromatosis apart from transferrin and ferritin (to screen for complications0?

A

Cardiac- ECG and echo
Endocrine- glucose and HbA1c
Liver: Liver USS and AFP (may still have cirrhosis even in the presence of normal LFTs as not inflammatory)

20
Q

Treatment of haemochromatosis?

A 
Regular venesection (1 unit/week) until iron deficient then 1 unit 3-4/year 
Alcohol avoidance 
Surveillance for HCC (200 x increased risk if cirrhotic)
21
Q

How would you screen family members for Haemachromatosis?

A 
Iron studies (ferritin and TSAT) Ferritin >200 in females, >300 in males with TFS >40% females and >50% in males 
Positive HFE gene does not guarantee heamochromatosis as has variable penetrance. 
Liver biopsy and genotyping if positive
22
Q

What clues might you get as to the aetiology of splenomegaly? (4)

A

Lymphadenopathy if haematological or infiltrative.
Stigmata of CLD in portal hypertension.
Peripheral stigmata of IE
RA hands in Feltys

23
Q

First line investigations for splenomegaly?

A

USS abdomen to confirm splenomegaly then
Full panel of blood tests including FBC with blood film. If infection suspected then thick and thin films and viral serology.
If haematological pathology suspected then consider bone marrow aspirate, lymph node biopsy, CT thorax and abdomen.

24
Q

Indications for splenectomy?

A

Trauma

Haematological (ITP and hereditary spherocytosis)

25
Q

What investigations would you do in a patient with enlarged kidney?

A 
USS kidney ?cysts, hydronephrosis +/- biopsy 
Bloods incl UEs 
Urine cytology
CT KUB if RCC suspected 
Genetic studies in ADKPD
26
Q

Describe the genetics of PKD?

A

Progressive replacement of normal kidney tissues with systs. 85% ADPKD chromosome 16, 15% ADPKD2 (less severe) chromosome 4

27
Q

How does ADPKD present?

A

Incidental or family screen.
Recurrent bleeding or UTI.
Hypertension.
Abdo pain.

28
Q

What associations are there with ADPKD?

A

Hepatic cysts and hepatomegaly
Intracranial berry aneurysms
Mitral valve prolapse

29
Q

What are the top three causes of liver transplant?

A

Cirrhosis
Acute hepatic failure (Hep A and B and paracetamol OD)
HCC

30
Q

What would expect the SAAG to be in portal hypertension?

31
Q

In a patient with low SAAG <1.1, what might be the cause?

A

Malignancy
Infection (TB)
Pancreatitis

32
Q

Take me through the causes of splenomegaly?

A
  1. Infiltration
    - Myeloproliferative disorder- myelofibrosis or CML
    - Lymphoproliferative disorders- lymphoma or CLL
    - Amyloidosis
    - Sarcoidosis
    - Gauchers (glycogen storage disease common in Ashkenazi Jews)
    - Hyperthyroidism
  2. Increased function (breaking down defective RBC)
    - Early sickle cell
    - Thalassaemia
    - Hereditory spherocytosis
    - Haemolytic anaemia
  3. Immune hyperplasia
    - Viral- EBV/HIV
    - Bacterial- subacute IE
    - Fungal
    - Parasites- chronic malaria, visceral leishmaniasis
    - RA via Feltys
  4. Impaired flow
    - Portal Hypertension
33
Q

What are important negatives to include in a patient presenting with Splenomegaly? (5)

A 
Lymphadenopathy 
Signs of CLD/hepatomegaly 
Thyrotoxicosis 
Anaemia 
RA
34
Q

Would you use a liver biopsy in hereditary haemachromatosis?

A

Not required for diagnosis but may be used for severity.

35
Q

Where would you commonly see the arthropathy associated with hereditary haemachromatosis?

A

Metacarpophalyngeal joints. Chondrocalcinosis on XR.

36
Q

What should you describe if you see a stoma? (5)

A 
Location
Contents 
Health of stoma 
Parastomal herniation (ask to cough) 
Surgical scars
37
Q

Standard treatments for non severe UC?

How would you escalate (OP treatments)?

A

Mesalazine (5-ASA) oral and enema preparations
If more than 2 flares requiring steroids then…
Escalate to azathioprine or biologics i.e. infliximab

38
Q

Most common causes of pancreatitis?

A 
Gallstones 
Alcohol 
ERCP 
Drugs (steroids, immunosupressants)
Hypertrigleridaemia
39
Q

Complications of chronic pancreatitis?

A

Pseudocyst- usually best drained endoscopic approach (AXIOS stent)
Diabetes
Failure to secrete pancreatic enzymes causing malabsorption (don’t show clinical signs until 90% of the function is lost)
PV thrombus
Stricturing

40
Q

Management of chronic pancreatitis?

A

Avoid triggers- alcohol and smoking

CREON (always give with PPI to avoid it being broken down in the stomach)

41
Q

How would you screen for malabsorption in chronic pancreatitis?

A
  • FBC, UES, LFTS (particularly albumin), Vit D, Mg (very helpful!)
  • Low faecal elastase
42
Q

What is included in the Child Pugh score?

A

Jaundice, albumin, INR, ascites and encephalopathy

43
Q

Other features of alcoholism (except liver disease)

A

Polyneuropathy, korsakoffs, cerebellum signs

44
Q

Which diabetic complications are not removed by a combined kidney and pancreas transplant?

A

Diabetic retinopathy

45
Q

What else would you want to examine/investigate in a patient with haemachromatosis?

A

CVS and joints
ECG ?cardiomyopathy
CBG and urine dip ?glycosuria

46
Q

Is liver disease and heart disease reversible with venesection in haemachromatosis?

A

There is potential for small improvements

Abdominal (1 decks)

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