Abdomen Flashcards
Extra abdominal manifestations IBD
Clubbing
Uveitis
Arthropathy / sacroilitis
Pyoderma gangrenosum / erythema nodosum
Oedema (hypoalbuminaemia)
Stoma rif
Ileostomy
Stoma lif
Colostomy
Crohns vs UC
Mouth to anus vs colon
CD characterised by skip lesions
Transmural vs mucosal
Granulomas vs crypt abscesses
Fat malabsorption deficiency in CD
Perianal disease in CD
Bilateral ballotable masses in the flanks Dx
Autosomal dominant adult polycystic kidney disease
What to comment on when suspected diagnosis is polycystic kindey disease
- Any evidence of renal failure
- Volume status
- Any evidence of RRT
Common presentation of polycystic kidney disease
Familial screening
HTN
Signs and symptoms of renal failure
Blood tests
Proteinuria/haematuria
Extrarenal manifestations - cysts in liver/pancreas
Inheritance of PKD
Autosomal dominant
80% mutation in PKD1 on Ch16 - Type 1
Type 2 - mutation in PKD2 on Ch4 - less severe, later onset, less cysts, later progression to renal failure
Infantile PKD which is autosomal recessive
Small number have no detectable abnormality
Management of PKD
- Management of HTN - with ACEi
- Management of hyperlipidaemia
- High fluid, low salt diet
- Use vasopressin receptor antagonists early in disease (vaptans)
- As disease progresses, may require RRT / transplant
Extrarenal manifestations of PKD
HTN
Cysts in liver / pancreas / seminal vesicles
Risk of cerebral aneurysms -> intracerebral / subarachnoid haemorrhage
Colonic diverticulae
Indication for nephrectomy in PKD
In general, nephrectomy should be avoided
- Make room for renal transplant
- Progression to renal cell carcinoma
- Chronic pain
- Chronic infection
- Significant haematuria
How to confirm kidney on palpation?
- Can palpate above
- Ballotable
- Moves with deep respiration
Causes of chronic liver disease
In UK
1) Alcoholic liver disease
2) Non-alcoholic fatty liver disease
3) Autoimmine - AI hepatitis / PBC / PSC
4) Haemochromatosis
5) Wilsons Disease
6) a1 antitrypsin deficiency
7) Hereditarty haemorrhagic telengectasisa
8) Medications related
Globally
1) Viral hepatitis
Initial Ix CLD
1) Full Hx - particularly symptoms, drugs, family, EtOH, travel - and examination of other systems
2) Bloods - FBC, U&Es, LFTs, coagulation, Hepatitis screen, ferritin, caerulopalsmin, auto-antibody screen
3) Liver USS, possibly CT
4) Consider referral to hepatology ?biopsy
Auto-antibodies in CLD
ANA
AMA (PBC)
Anti-smooth muscle antibody (AI hepatitis)
Anti-LKM (anti-liver-kidney-microsomal Ab)
Liver tumour markers
AFP (marker of HCC)
Elevated AMA & IgM levels
Most likely diagnosis is primary biliary cholangitis
Presentation of PBC
Commonest symtpom is generalised fatuigue & pruritus, or can present with CLD
Complications of PBC
CLD
Malignancy (HCC)
Treatment of PBC
Ursodeoxycholic acid - improves symptoms and prognosis
Only other treatment is liver transplantation
Signs of portal hypertension
Caput medusae
Splenomegaly
How to present CLD
1) Hepatomegamly
2) Peripheral signs
3) Any evidence of portal hypertension
4) Any evidence of decompensation
5) Any clues as to aetiology - E.g. tattoos / xanthalasma
Commonest causes of ESRF
1) HTN
2) DM
3) Glomerularnephritides
4) ADPKD
When should a patient be worked up for a renal transplant
While approaching ESRF, but before need for dialysis
Transplantation has better prognosis if performed before the initiation of dialysis
ESRF definition
eGFR <15ml/min
Contrainidcations to renal transplantation
1) Lack of appropriate donor
2) Malignancy
3) Ongoing infection / vasculitis
4) Very high/low BMI
5) Conditions or lifestyles where poor compliance to medications / clinic - E.g. Mental health disorders
Complications of long-term immunosuppression
Infection & malignancy, particularly skin
Many drugs can be used
Steroids - skin thinning, bruising, cushingoid appeareance
Ciclosporin - gingival hyperplasia, hirsutism
Tacrolimus - tremor
Things to present in context of previous transplant
- Functioning transplant
- Evidence of side-effects from immunosuppression
To complete abdominal examination
To palpate external hernial orrifices & palpate for inguinal lymph nodes, examine external genitalia and DRE
Observations
Urinalysis
Importance of ascitic tap in ascites
Albumin:protein ratio - can indicate underlying cause
High protein - systemic cause - liver cirrhosis / cardiac failure
Low protein - malignancy / pancreatitis / Tb
Amylase level ?pancreatitis
Cytology ?malignancy
MCS ?infection
Check synthetic function of liver
INR, albumin, glucose (expect to be raised due to insulin resistance)
Causes of hepatomegaly
3Cs 4Is
Cirrhosis (alcoholic)
Carcinoma
Congestion
Infection - viral hepatitis
Immune - AI hepatitis / PBC / PSC
Infiltrative - Amyloid / myeloproliferative
Iron - Haemochromatotis
AST:ALT ratio > 2:1
Characterisitc of alcoholic liver diease
AST:ALT ratio > 50:1
Ischaemic hepatitis
How to determine extent of liver fibrosis
Fibroscan
Test for pancreatic exocrine function
fecal elastase
Why is PD less likely in polycystic kidney disease
Combination of enlarged kidneys and large peritoneal volumes can be uncomfortable for patients
Also increases the risk of cyst infections -> complications
How is PKD diagnosis most commonly made?
Via screening, in those with a family history of PKD
Natural Hx of PKD
Most asympomatic until 4th decade
Poor prognostic features in PKD
Declining eGFR
Proteinuria
Early onset of symptoms
Male gender
Risk of HTN in PKD
Increases with age
Almost all have HTN when develop ESRF
Test for malaria
3x thick & thin blood films
Spot Test
As per local microbiology guidelines
Ix for isolated splenomegaly
Bloods:
FBC, Blood film, Renal, U&Es, LFTs, INR, AI screen, HIV
Abdominal USS
If concerned about malignancy, perform CT CAP
If concerned about haematological malignancy, consider bone marrow aspiration and trephine biopsy
Causes of massive splenomegaly
Myelofibrosis
Chronic Myeloid leukaemia
Infectious - chronic malaria & visceral leishmaniasis (Kala Azar)
Clinical signs to comment on when find splenomegaly
?clinical anaemia
?hepatomegaly / jaundice
?lymphadenopathy
?euthyroid
Cause of splenomegaly
INFILTRATIVE
- Myeloproliferative
- Lymphoproliferative
- Lymphomas
- Amlyoidosis
- Sarcoidosis
- Gaucher’s lipid storage disease
- Thyrotoxicosis
INCREASED FUNCTION
- Increased removal of defective RBCs, hereditary spherocytosis, thalassaemia, nutritional anaemias, early sickle cell
IMMUNE HYPERPLASIA
In response to bacterial, fungal, parasitic or viral infection
- Chronic malaria
- Visceral leishmaniasis
- Subacute bacterial endocarditis
- Infectious mononucleosis
- Brucellosis
DISORDERED IMMUNE REGULATION
- RA
- Felty’s syndrome
- SLE
- Sarcoidosis
DISORDERED FLOW - portal HTN or vascular obstruction
Spenomegaly in Ashkenazi Jewish
Possible Gauchers disease
Genetics and diagnositic test in hereditary spherocytosis
Autosomal dominant
Osmotic fragility test
Can be confirmed via flow cytometry
Complications of immunosuppression
Infections - bacteria, viral, fungal, mycobacterail or posarisitic
Malignancies - particularly skin
Nephrotoxitiy & HTN
Tremor (tacrolimus)
Jaundice in liver transplant
?graft dysfunction
Causes for liver transplantation
Cirrhosis
- EtOH / NAFLD / AI / Chronic viral hepatitis
Acute liver failure - paracetamol overdose / HCC
How to determine who would benefit most from a liver transplant?
MDT approach
Use UK end-stage liver disease model to predict mortality - used in transplant planning
Ix for suspected haemochromatosis
Bloods - FBC, iron studies (ferritin + transferritin saturation - both to be raised)
To confirm diagnosis - genetic testing of HFE gene
Scar for liver transplant
Inverted J scar (Makukchi incision)
Definition of acute liver failure
Multi-system disorder
Severe acute impairment of liver function with encephalopathy within 8 weeks of symptom onset with no recognised underlying chronic liver disease
Variant syndromes that might result in liver transplantation
Diuretic-resistant ascites
Chronic hepatic encephalopathy
Chronic, intractable pruritus
Polycystic liver disease
Recurrent cholangitis
Contraindications to liver transplant
IVDU
EtOH excess
Significant medical / psychiatric co-morbidities - if likely to affect post-transplant survivability
Prior malignancy would be strongly considered - particularly if recurrence if high
Scores for predicting prognosis in alcoholic hepatitis
Maddrey’s score
Glasgow alcoholic hepatitis score
Survival prognosis required for liver transplant
> 50% survival at 5 years
Urgency of liver transplantation
Elective
Urgent
Super-urgent
Complications of liver transplantion
Acute rejection
Infection secondary to immunosuppression
Malignancy secondary to immunsuppresion
Development of metabolic syndrome - HTN, BM, hyperlipidaemia, obesity
Patient with fever and ascites - What to be concerned about? How to Ix?
Spontanoues bacterial peritonitis
Ascitic tap, look at corrected neutrophil count (neutrophils >250 concerning)
Start broad spectrum abx
Ix in patient with cirrhosis and ascites
Take full Hx and complete examination
Bloods - FBC, Coagulation, Glucose, Albumin, Renal, LFTs, AFP, viral screen, AI screen, ferritin, caeruloplasmin
Perform liver USS / Fibroscan
Consider OGD ?variceal disease / portal hypertensive gastropathy / GAVE
Ascitic tap - serum ascites albumin gradient >1.1 is consistent with liver cirrhosis
Conditions associated with SAAG > 1.1g/L
Liver cirrhosis (portal HTN)
CCF
Budd Chiari syndrome
Nephrotic syndrome
Meig’s syndrome (Females)
Conditions associated with SAAG <1.1g/L
Malignancy
TB
Pancreatitis
Trauma
How do you perform liver biopsy in context of ascites?
Via transjugular route
Causes of ascites?
Most commonly secondary to portal HTN secondary to cirrhosis.
Causes subdivided into:
- Vascular
- Low albumin
- Peritoneal disease
- Miscellaneous
Vascular causes of ascites:
Portal HTN
Budd-Chiari
Congestive cardiac failure
Constrictive pericarditis
Low albumin causes of ascites
Nephrotic syndrome
Protein-losing enteropathy
Peritoneal causes of ascites
Meig’s Syndrome (pleural effusion, ascites, benign ovarian tumour)
Infectious peritonitis - TB / Fungal
Malignancy - Gastrointestinal / ovarian
Investigation for query SBP?
Perform ascitic up and look for corrected neutrophil count of more than 250
Send for my microscopy, culture and sensitivity
Commence broad spectrum antibiotic
How do you assess synthetic liver function
Check coagulation profile, including INR
Check albumin
Check glucose and HB A1c
Malignant complication of cirrhosis
Hepatocellular carcinoma
Send alpha fetoprotein
Investigations to carry out and first presentation of cirrhosis
Bloods including FBC, liver function test, coagulation, renal profile, and AFP
Liver imaging - liver ultrasound and fibroscan
OGD, looking for oesophageal varices and GAVE
If diagnosis is unclear, consider tissue biopsy
Presentation with arthralgia, raised HbA1c and fatigue - ?diagnosis
Think hereditary haemochromatosis
Clinical signs to look for with herdiatary haemochromatosis
Joint swelling
Venesection marks in ACFs
Evidence of raised HbA1c ?signs of diabetes
Inheritance of herdiatary haemochromatosis
Autosomal recessive
Mutation of HFE gene
Located on Ch 6
Typical presentation of herediatary haemochromatosis
Screening in patients with first degree relatives with condition
Diagnosed in those found to have raised ferritin
Those with severe disease may present with arthralgia, sexual dysfunction, cardiomyopathy, diabetes, bronzed pigmentation
Screening in haemochromatosis
In patients with first-degree relatives with condition
Ferritin
Females >200
Males >300
Transferritin saturation
Females >40%
Males >50%
Then can consider HFE genotyping - but due to incomplete penetrance not everyone with mutation will have phenotypic disease
Complications of haemochromatosis and screening of these
T1 Diabetes - monitor HbA1c
Cirrhosis - serial liver USS
HCC - monitor AFP
Baseline echocardiogram to look for cardiomyopathy
Plain radiographs of joints ?chondrocalcinosis
Liver biopsy in haemochromatosis
Not needed for diagnosis
Can be used to assess severity
Treatment of haemochromatosis
Regular venesection until ferritin and transferrin saturation has been brought down to an acceptable level (20-30ug/l and <50%)
Following this monitor ferritin and transferrin saturation to guide maintenance venesection
Rest of treatment is to address complications e.g. diabetes and cardiomyopathy
Haemochromatosis - joints most susceptible to swelling? what do you see on a radiograph?
MCPs
Chondrocalcinosis on XR
Organs affected by iron overload in HH?
Liver
Pancreas
Heart
Ant. pituitary
Testicles
HH - associated with calcium pyrophosphate deposition
Pseudogout
chondrocalcinosis
Chronic arthropathy
Other systems to examin after abdomen in HH?
Joints
Cardiovascular
Lifestyle changes in HH?
Abstain from EtOH
Much more likely to get liver damage with EtOH use
Inheritance of hereditary spherocytosis
Autosomal dominant
Typically, due to a defective one of five genes encoding RBC proteins
Most common defect on Ch 8
Triad of symptoms/signs associated with hereditary spherocytosis
& other typical presentations
Fatigue
Jaundice
Splenomegaly
Via familial screening
Neonatal jaundice
Complications associated with hereditary spherocytosis
Aplastic crisis secondary to infection
Anaemia requiring RBC transfusion
Pigment gallstones requiring cholecystectomy
How to establish a diagnosis of hereditary spheocytosis
Bloods including looking at reticulocyte count and blood film to look for spherocytes
Haemolysis screen, including LDH and haptoglobin
Split bilirubin - expect high unconjugated bilirubin
EMA binding test (expect it to be reduced) or osmotic fragility test
Coombs test can be used to rule out AI haemolysis
Why is splenectomy virtually curative in hereditary spherocytosis?
Most of the haemolysis occurs in the spleen, in the presence of spherocytosis, therefore, splenectomy, reduces overall rate of haemolysis
Treatment of herditary spheocytosis
Give folic acid, particularly in pregnancy
Treat complications e.g. anaemia
May require splenectomy, need up to date vaccinations, inc. meningococcal, pneumococcal & influenza
Require prophylactic antibiotics for encapsulated organisms
Three Most common differentials for splenomegaly.
CML
Myelofibrosis
Malaria
Weight loss in normal abdo exam diffenterials
Inflammatory bowel disease
AI - Coeliac
Thyroid function
Infective causes
Ix coeliac disease
Bloods - FBC, haematinics, renal and liver function, anti-TTG, TFTs
OGD while on gluten diet - d2 biopsy looking for subtotal villous atrophy
Mx coeliac disease
Avoidance of gluten
Wheat, rye, barley
Ensure patient is educated
Refer to dietician
Types of kidney transplant
Cadaver - DBD vs DCD
Live kidney transplant
Can have combined pancreas and renal transplant in severe diabetes related ESRF
Drainage of transplanted pancreas
Traditionally into bladder, but can result in frequent uti and reflux pancreatitis.
Now more commonly into small bowel.
Best treatment for T1DM related ESRF
Combined pancreas and kidney transplant
Effect of pancreatic transplant on diabetes complications.
If done alongside renal transplant, would prevent diabetic nephropathy
Would expect neuropathy to be static or improved
Effects on retinopathy remain unclear
Complications of pancreatic transplant
Acute rejection
Graft thrombosis
Graft pancreatitis
Infection
Alternative to pancreatic transplant
Islet cell transplantstion
To complete abdo exam
Examine external genitalia, hernial orifices & perorm DRE
Urinalysis
Multiple scars in flanks
Think about regular ascitic drainage
How to assess for hepatic encephalopathy?
Assess for constructional apraxia - ask to draw a clock and a start
Mortaloity risk score in Cirrhosis
Child-Pugh - Bili / albumin / INR / encephalopathy / ascites
Treatment of ascites
Stepwise approach:
- Fluid restriction
- Trial of diuresis - spironolactone
- Consider drainage - albumin cover for every 2L ascites drained
- If refractory to drainage, consider TIPS
- Liver transplant is definitive management
Complication of TIPS
5-10% risk of encephalopathy
Can result in coagulopathy
Causes of gynaecomastia
Caused by excessive of oestogrens, lack of androgens
CLD
MRAs / digoxin
Testicular atrophy or tumour
Genetic conditions - Klinefelters
Facial sign of EtOH CLD
Parotid swelling
What is caput medusae
Late sign of portal hypertension, due to shunting via peri-umbilical veins
Complications of Cirrhosis
Variceal haemorrhage
Ascites +/- infection
HCC
Hepato-renal syndrome
Hepato-pulmonary syndrome
Medical management of varices
Non-selective B blocker
Carvedilol
Causes of pancreatitis
Gallstones
Ethanol
Trauma
Steroids
Mumps
Autoimmune
Scorpion sting
Hyper - calcaemia/triglyceridaemia
ERCP
Drugs - azathioprine
Cancer
Genetic causes of pancreatitis
CF
Hereditary pancreatitis - mutations in SPINK1 & PRSS1 (autosomal dominant)
Complications of pancreatitis
Acute
- Multisystems inflammatory response syndrome
- Resulting in respiratory failure -> death
Chronic - result in exocrine and endocrine function
- Chronic pancreatitis - pancreatic insufficiency, pain, diabetes
- Splenic vein thrombosis
- Formation of pseudocysts - obstruction to local sturctures
- T3DM
- Pancreatic duct or duodenal stricturing
- Pancreatic cancer
How are pancreatic pseudocysts drained?
Via endoscopy - US-guided approach - place axios stent (typically 6 weeks after acute presentation)
Typical presentation of chronic pancreatitis
Pain - variable - radiation to back - can be associated with food - gnawing pain
Management of chronic pancreatitis
- Avoid causes of pancreatic inflammation - eliminating smoking and alcohol
- Analgesia as required
- Pancreatic insufficiency (steatorrhoea - loose greasy pale stool, hypoalbuminaemia, hypomagnesaemia fecal elastase) -> creon
- PPI (reduce acid breakdown of creon in stomach)
- Ensure healthy balanced diet
What should you offer to do in patients with stoma
Digital examination of stoma
How would you Ix pt with ?IBD
Bloods - inflammatory markers, FBC, haematinics, CEA, renal, liver
Stool MCS
AXR ?megacolon
OGD / Colonoscopy + biopsies
Why are ileostomies spouted?
To prevent skin irritation due to bile acid contents
Emergency indications for surgery in IBD
Toxic Megacolon
Haemorrhage
Perforation
What can be formed in emergency surgery for UC
Mucus fistula
Medical therapy in UC
Mild to moderate disease - 5aminisalicylcic acids - Mesalazine - oral or rectal enema
May need oral steorids in those who do not respond - recommend in mod-severe disease
5ASAs are mainstay of maintenance therapy
In those with >2 flare or requiring steroids, teatment can be escalated to Azathioprine or biologics E.g. Infliximab
