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PACES > Abdomen > Flashcards

Abdomen Flashcards

1
Q

Extra abdominal manifestations IBD

A

Clubbing
Uveitis
Arthropathy / sacroilitis
Pyoderma gangrenosum / erythema nodosum
Oedema (hypoalbuminaemia)

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2
Q

Stoma rif

A

Ileostomy

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3
Q

Stoma lif

A

Colostomy

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4
Q

Crohns vs UC

A

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

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5
Q

Bilateral ballotable masses in the flanks Dx

A

Autosomal dominant adult polycystic kidney disease

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6
Q

What to comment on when suspected diagnosis is polycystic kindey disease

A
  1. Any evidence of renal failure
  2. Volume status
  3. Any evidence of RRT
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7
Q

Common presentation of polycystic kidney disease

A

Familial screening
HTN
Signs and symptoms of renal failure
Blood tests
Proteinuria/haematuria
Extrarenal manifestations - cysts in liver/pancreas

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8
Q

Inheritance of PKD

A

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

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9
Q

Management of PKD

A
  1. Management of HTN - with ACEi
  2. Management of hyperlipidaemia
  3. High fluid, low salt diet
  4. Use vasopressin receptor antagonists early in disease (vaptans)
  5. As disease progresses, may require RRT / transplant
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10
Q

Extrarenal manifestations of PKD

A

HTN
Cysts in liver / pancreas / seminal vesicles
Risk of cerebral aneurysms -> intracerebral / subarachnoid haemorrhage
Colonic diverticulae

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11
Q

Indication for nephrectomy in PKD

A

In general, nephrectomy should be avoided

  1. Make room for renal transplant
  2. Progression to renal cell carcinoma
  3. Chronic pain
  4. Chronic infection
  5. Significant haematuria
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12
Q

How to confirm kidney on palpation?

A
  1. Can palpate above
  2. Ballotable
  3. Moves with deep respiration
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13
Q

Causes of chronic liver disease

A

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

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14
Q

Initial Ix CLD

A

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

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15
Q

Auto-antibodies in CLD

A

ANA
AMA (PBC)
Anti-smooth muscle antibody (AI hepatitis)
Anti-LKM (anti-liver-kidney-microsomal Ab)

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16
Q

Liver tumour markers

A

AFP (marker of HCC)

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17
Q

Elevated AMA & IgM levels

A

Most likely diagnosis is primary biliary cholangitis

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18
Q

Presentation of PBC

A

Commonest symtpom is generalised fatuigue & pruritus, or can present with CLD

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19
Q

Complications of PBC

A

CLD
Malignancy (HCC)

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20
Q

Treatment of PBC

A

Ursodeoxycholic acid - improves symptoms and prognosis

Only other treatment is liver transplantation

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21
Q

Signs of portal hypertension

A

Caput medusae
Splenomegaly

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22
Q

How to present CLD

A

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

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23
Q

Commonest causes of ESRF

A

1) HTN
2) DM
3) Glomerularnephritides
4) ADPKD

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24
Q

When should a patient be worked up for a renal transplant

A

While approaching ESRF, but before need for dialysis

Transplantation has better prognosis if performed before the initiation of dialysis

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25
Q

ESRF definition

A

eGFR <15ml/min

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26
Q

Contrainidcations to renal transplantation

A

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

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27
Q

Complications of long-term immunosuppression

A

Infection & malignancy, particularly skin

Many drugs can be used
Steroids - skin thinning, bruising, cushingoid appeareance
Ciclosporin - gingival hyperplasia, hirsutism
Tacrolimus - tremor

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28
Q

Things to present in context of previous transplant

A
  1. Functioning transplant
  2. Evidence of side-effects from immunosuppression
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29
Q

To complete abdominal examination

A

To palpate external hernial orrifices & palpate for inguinal lymph nodes, examine external genitalia and DRE

Observations
Urinalysis

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30
Q

Importance of ascitic tap in ascites

A

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

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31
Q

Check synthetic function of liver

A

INR, albumin, glucose (expect to be raised due to insulin resistance)

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32
Q

Causes of hepatomegaly
3Cs 4Is

A

Cirrhosis (alcoholic)
Carcinoma
Congestion

Infection - viral hepatitis
Immune - AI hepatitis / PBC / PSC
Infiltrative - Amyloid / myeloproliferative
Iron - Haemochromatotis

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33
Q

AST:ALT ratio > 2:1

A

Characterisitc of alcoholic liver diease

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34
Q

AST:ALT ratio > 50:1

A

Ischaemic hepatitis

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35
Q

How to determine extent of liver fibrosis

A

Fibroscan

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36
Q

Test for pancreatic exocrine function

A

fecal elastase

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37
Q

Why is PD less likely in polycystic kidney disease

A

Combination of enlarged kidneys and large peritoneal volumes can be uncomfortable for patients

Also increases the risk of cyst infections -> complications

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38
Q

How is PKD diagnosis most commonly made?

A

Via screening, in those with a family history of PKD

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39
Q

Natural Hx of PKD

A

Most asympomatic until 4th decade

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40
Q

Poor prognostic features in PKD

A

Declining eGFR
Proteinuria
Early onset of symptoms
Male gender

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41
Q

Risk of HTN in PKD

A

Increases with age
Almost all have HTN when develop ESRF

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42
Q

Test for malaria

A

3x thick & thin blood films
Spot Test
As per local microbiology guidelines

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43
Q

Ix for isolated splenomegaly

A

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

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44
Q

Causes of massive splenomegaly

A

Myelofibrosis
Chronic Myeloid leukaemia
Infectious - chronic malaria & visceral leishmaniasis (Kala Azar)

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45
Q

Clinical signs to comment on when find splenomegaly

A

?clinical anaemia
?hepatomegaly / jaundice
?lymphadenopathy
?euthyroid

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46
Q

Cause of splenomegaly

A

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

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47
Q

Spenomegaly in Ashkenazi Jewish

A

Possible Gauchers disease

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48
Q

Genetics and diagnositic test in hereditary spherocytosis

A

Autosomal dominant
Osmotic fragility test
Can be confirmed via flow cytometry

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49
Q

Complications of immunosuppression

A

Infections - bacteria, viral, fungal, mycobacterail or posarisitic

Malignancies - particularly skin

Nephrotoxitiy & HTN

Tremor (tacrolimus)

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50
Q

Jaundice in liver transplant

A

?graft dysfunction

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51
Q

Causes for liver transplantation

A

Cirrhosis
- EtOH / NAFLD / AI / Chronic viral hepatitis

Acute liver failure - paracetamol overdose / HCC

52
Q

How to determine who would benefit most from a liver transplant?

A

MDT approach

Use UK end-stage liver disease model to predict mortality - used in transplant planning

53
Q

Ix for suspected haemochromatosis

A

Bloods - FBC, iron studies (ferritin + transferritin saturation - both to be raised)

To confirm diagnosis - genetic testing of HFE gene

54
Q

Scar for liver transplant

A

Inverted J scar (Makukchi incision)

55
Q

Definition of acute liver failure

A

Multi-system disorder

Severe acute impairment of liver function with encephalopathy within 8 weeks of symptom onset with no recognised underlying chronic liver disease

56
Q

Variant syndromes that might result in liver transplantation

A

Diuretic-resistant ascites
Chronic hepatic encephalopathy
Chronic, intractable pruritus
Polycystic liver disease
Recurrent cholangitis

57
Q

Contraindications to liver transplant

A

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

58
Q

Scores for predicting prognosis in alcoholic hepatitis

A

Maddrey’s score
Glasgow alcoholic hepatitis score

59
Q

Survival prognosis required for liver transplant

A

> 50% survival at 5 years

60
Q

Urgency of liver transplantation

A

Elective
Urgent
Super-urgent

61
Q

Complications of liver transplantion

A

Acute rejection

Infection secondary to immunosuppression

Malignancy secondary to immunsuppresion

Development of metabolic syndrome - HTN, BM, hyperlipidaemia, obesity

62
Q

Patient with fever and ascites - What to be concerned about? How to Ix?

A

Spontanoues bacterial peritonitis

Ascitic tap, look at corrected neutrophil count (neutrophils >250 concerning)

Start broad spectrum abx

63
Q

Ix in patient with cirrhosis and ascites

A

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

64
Q

Conditions associated with SAAG > 1.1g/L

A

Liver cirrhosis (portal HTN)
CCF
Budd Chiari syndrome
Nephrotic syndrome
Meig’s syndrome (Females)

65
Q

Conditions associated with SAAG <1.1g/L

A

Malignancy
TB
Pancreatitis
Trauma

66
Q

How do you perform liver biopsy in context of ascites?

A

Via transjugular route

67
Q

Causes of ascites?

A

Most commonly secondary to portal HTN secondary to cirrhosis.

Causes subdivided into:
- Vascular
- Low albumin
- Peritoneal disease
- Miscellaneous

68
Q

Vascular causes of ascites:

A

Portal HTN
Budd-Chiari
Congestive cardiac failure
Constrictive pericarditis

69
Q

Low albumin causes of ascites

A

Nephrotic syndrome
Protein-losing enteropathy

70
Q

Peritoneal causes of ascites

A

Meig’s Syndrome (pleural effusion, ascites, benign ovarian tumour)
Infectious peritonitis - TB / Fungal
Malignancy - Gastrointestinal / ovarian

71
Q

Investigation for query SBP?

A

Perform ascitic up and look for corrected neutrophil count of more than 250

Send for my microscopy, culture and sensitivity

Commence broad spectrum antibiotic

72
Q

How do you assess synthetic liver function

A

Check coagulation profile, including INR

Check albumin
Check glucose and HB A1c

73
Q

Malignant complication of cirrhosis

A

Hepatocellular carcinoma
Send alpha fetoprotein

74
Q

Investigations to carry out and first presentation of cirrhosis

A

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

75
Q

Presentation with arthralgia, raised HbA1c and fatigue - ?diagnosis

A

Think hereditary haemochromatosis

76
Q

Clinical signs to look for with herdiatary haemochromatosis

A

Joint swelling
Venesection marks in ACFs
Evidence of raised HbA1c ?signs of diabetes

77
Q

Inheritance of herdiatary haemochromatosis

A

Autosomal recessive
Mutation of HFE gene
Located on Ch 6

78
Q

Typical presentation of herediatary haemochromatosis

A

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

79
Q

Screening in haemochromatosis

A

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

80
Q

Complications of haemochromatosis and screening of these

A

T1 Diabetes - monitor HbA1c
Cirrhosis - serial liver USS
HCC - monitor AFP
Baseline echocardiogram to look for cardiomyopathy
Plain radiographs of joints ?chondrocalcinosis

81
Q

Liver biopsy in haemochromatosis

A

Not needed for diagnosis
Can be used to assess severity

82
Q

Treatment of haemochromatosis

A

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

83
Q

Haemochromatosis - joints most susceptible to swelling? what do you see on a radiograph?

A

MCPs
Chondrocalcinosis on XR

84
Q

Organs affected by iron overload in HH?

A

Liver
Pancreas
Heart
Ant. pituitary
Testicles

85
Q

HH - associated with calcium pyrophosphate deposition

A

Pseudogout
chondrocalcinosis
Chronic arthropathy

86
Q

Other systems to examin after abdomen in HH?

A

Joints
Cardiovascular

87
Q

Lifestyle changes in HH?

A

Abstain from EtOH
Much more likely to get liver damage with EtOH use

88
Q

Inheritance of hereditary spherocytosis

A

Autosomal dominant
Typically, due to a defective one of five genes encoding RBC proteins
Most common defect on Ch 8

89
Q

Triad of symptoms/signs associated with hereditary spherocytosis

& other typical presentations

A

Fatigue
Jaundice
Splenomegaly

Via familial screening
Neonatal jaundice

90
Q

Complications associated with hereditary spherocytosis

A

Aplastic crisis secondary to infection
Anaemia requiring RBC transfusion
Pigment gallstones requiring cholecystectomy

90
Q

How to establish a diagnosis of hereditary spheocytosis

A

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

91
Q

Why is splenectomy virtually curative in hereditary spherocytosis?

A

Most of the haemolysis occurs in the spleen, in the presence of spherocytosis, therefore, splenectomy, reduces overall rate of haemolysis

91
Q

Treatment of herditary spheocytosis

A

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

92
Q

Three Most common differentials for splenomegaly.

A

CML
Myelofibrosis
Malaria

93
Q

Weight loss in normal abdo exam diffenterials

A

Inflammatory bowel disease
AI - Coeliac
Thyroid function
Infective causes

94
Q

Ix coeliac disease

A

Bloods - FBC, haematinics, renal and liver function, anti-TTG, TFTs

OGD while on gluten diet - d2 biopsy looking for subtotal villous atrophy

95
Q

Mx coeliac disease

A

Avoidance of gluten
Wheat, rye, barley
Ensure patient is educated
Refer to dietician

96
Q

Types of kidney transplant

A

Cadaver - DBD vs DCD
Live kidney transplant

Can have combined pancreas and renal transplant in severe diabetes related ESRF

97
Q

Drainage of transplanted pancreas

A

Traditionally into bladder, but can result in frequent uti and reflux pancreatitis.

Now more commonly into small bowel.

98
Q

Best treatment for T1DM related ESRF

A

Combined pancreas and kidney transplant

99
Q

Effect of pancreatic transplant on diabetes complications.

A

If done alongside renal transplant, would prevent diabetic nephropathy

Would expect neuropathy to be static or improved

Effects on retinopathy remain unclear

100
Q

Complications of pancreatic transplant

A

Acute rejection
Graft thrombosis
Graft pancreatitis
Infection

101
Q

Alternative to pancreatic transplant

A

Islet cell transplantstion

102
Q

To complete abdo exam

A

Examine external genitalia, hernial orifices & perorm DRE

Urinalysis

103
Q

Multiple scars in flanks

A

Think about regular ascitic drainage

104
Q

How to assess for hepatic encephalopathy?

A

Assess for constructional apraxia - ask to draw a clock and a start

105
Q

Mortaloity risk score in Cirrhosis

A

Child-Pugh - Bili / albumin / INR / encephalopathy / ascites

106
Q

Treatment of ascites

A

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

107
Q

Complication of TIPS

A

5-10% risk of encephalopathy
Can result in coagulopathy

108
Q

Causes of gynaecomastia

A

Caused by excessive of oestogrens, lack of androgens

CLD
MRAs / digoxin
Testicular atrophy or tumour
Genetic conditions - Klinefelters

109
Q

Facial sign of EtOH CLD

A

Parotid swelling

110
Q

What is caput medusae

A

Late sign of portal hypertension, due to shunting via peri-umbilical veins

111
Q

Complications of Cirrhosis

A

Variceal haemorrhage
Ascites +/- infection
HCC
Hepato-renal syndrome
Hepato-pulmonary syndrome

112
Q

Medical management of varices

A

Non-selective B blocker
Carvedilol

113
Q

Causes of pancreatitis

A

Gallstones
Ethanol
Trauma

Steroids
Mumps
Autoimmune
Scorpion sting
Hyper - calcaemia/triglyceridaemia
ERCP
Drugs - azathioprine

Cancer

114
Q

Genetic causes of pancreatitis

A

CF
Hereditary pancreatitis - mutations in SPINK1 & PRSS1 (autosomal dominant)

115
Q

Complications of pancreatitis

A

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

116
Q

How are pancreatic pseudocysts drained?

A

Via endoscopy - US-guided approach - place axios stent (typically 6 weeks after acute presentation)

117
Q

Typical presentation of chronic pancreatitis

A

Pain - variable - radiation to back - can be associated with food - gnawing pain

118
Q

Management of chronic pancreatitis

A
  • 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
119
Q

What should you offer to do in patients with stoma

A

Digital examination of stoma

120
Q

How would you Ix pt with ?IBD

A

Bloods - inflammatory markers, FBC, haematinics, CEA, renal, liver

Stool MCS

AXR ?megacolon

OGD / Colonoscopy + biopsies

121
Q

Why are ileostomies spouted?

A

To prevent skin irritation due to bile acid contents

122
Q

Emergency indications for surgery in IBD

A

Toxic Megacolon
Haemorrhage
Perforation

123
Q

What can be formed in emergency surgery for UC

A

Mucus fistula

124
Q

Medical therapy in UC

A

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

PACES (6 decks)

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