Abdominal Clinical Examination

Question 1

Laparoscopy Scars

Answer 1

Inguinal hernia repair
Pyloromyotomy for pyloric stenosis
Appendicectomy
Cholecystectomy
Fundoplication
Total or partial nephrectomy

Question 2

Laparotomy Scars

Answer 2

Laparotomy and colostomy incision - Assoc w T21 for Hirschprung’s. If no colostomy, possible duodenal or intestinal atresia
If CF likely, meconium ileus repair
If ex-prem, NEC
If thoracolumbar or laparoscopy scars as well - possible renal transplant

Kasai for biliary atresia
Malrotation
Intussuception
Tumour removal

Question 3

Below R subcostal margin (Kocher’s)

Answer 3

After cholecystectomy & gallstone removal
Assoc w SCD & hereditary spherocytosis

Question 4

Transverse upper abdominal incision

Answer 4

CDH repair (L>R)

Question 5

Upper abdominal midline incision

Answer 5

Nissan’s fundoplication
Severe GORD - assoc w neurodevelopmental problems
Now usually laparoscopic

Question 6

Small right upper transverse incision

Answer 6

Ramstedt’s pyloromyotomy (M>F)
Hypertrophic pyloric stenosis

Question 7

RIF scar

Answer 7

Appendectomy

Question 8

Lateral thoracolumbar incision

Answer 8

Nephrectomy

Question 9

Subumbilical/peri-umbilical scar

Answer 9

Gastroschisis or exomphalos
Umbilical hernia repair

Question 10

Hepatomegaly

Answer 10

R hypochondrium
Cannot get above it
Moves w respiration
Dull to percussion

Question 11

Splenomegaly

Answer 11

L hypochondrium
Cannot get above it
Moves with respiration
Dull to percussion
Has a notch

Question 12

Weight gain in 1st year of life

Answer 12

200g/week 1st 3 mo
150g/week 2nd 3 mo
100g/week 3rd 3 mo
50g/week 4th 3mo

Question 13

Genetic/Endocrine/Oncological causes of Obesity

Answer 13

T21
Kleinfelter
Prader-Willi
Lawrence Moon Biedl

GH deficiency
Hypothyroidism
Cushing Syndrome
Polycystic ovarian syndrome

Pituitary tumour

Hence baseline investigations are: TFT, fasting glucose, lipid profile, insulin levels, LFT

Question 14

Genetic/Endocrine/Oncological causes of Obesity

Answer 14

T21
Kleinfelter
Prader-Willi
Lawrence Moon Biedl

GH deficiency
Hypothyroidism
Cushing Syndrome
Polycystic ovarian syndrome

Pituitary tumour

Hence baseline investigations are: TFT, fasting glucose, lipid profile, insulin levels, LFT

Question 15

CF Gastrointestinal

Answer 15

Pancreatic
Insufficiency in 85% of patients
Impaired glucose tolerance in 10% of 2nd decade

Intestinal
DIOS
Atresia
Meconium ileus
Rectal prolapse
Chronic strictures 2ry to pancreatic supplements

Hepatobilliary
Common bile duct obstruction
Cholelithasis
Cholestasis in infancy -> Obstructive jaundice
Fatty liver
Gall bladder abnormalities

Jaundice, ascites and portal hypertension

Question 16

Crohn’s:

-Pathology
-PC
-Signs
-Tx

Answer 16

Transmural and skip lesions. Granulomatous mucosa with deep ulcers = cobblestone appearance

PC: Abdo pain, diarrhoea and weight loss. Systemic: lethargy and fever.
Sign: Pallor of anaemia. Extr intestinal: uveitis, arthritis, erythema nodosum, pyoderma gangrenosum, erythema multiforme
Growth failure - delayed bone maturation and sexual development

Tx: Chronic Relapsing
Corticosteroids - initially and for relapses
Immunosuppression: azathioprine
Elemental diet for 8 weeks then controlled reintroduction = remission in 80% of cases
Anti-inflammatories: Oral 5-ASA derivatives or enemas
Anti-TNF
Antibiotics
Surgery if persistent symptoms despite medial tx, intolerable SE of medications. Abscesses that are unresponsive or toxic mega-colon

Question 17

Short and pale - IDA
Thin with reduced SC fat, poor muscle bulk and wasting
Abdominal distension
Dermatitis herpetiformis - itchy, blistering rash
Apthous stomatitis
Hx: chronic diarrhoea and poor weight gain
Nauseas, constipation, anorexia, flatulence, irritable

Answer 17

Malabsorption syndrome
- Most likely Coeliac
- CMPA (non-IgE form)
-CF
- Immunodeficiency
(Giardiasis, Soya intolerance, AI diseases)
- inflammatory bowel disease
- post surgical

Question 18

Coeliac disease:
- Haplotypes
- Associations
- Tx

Answer 18

Gluten-sensitive enteropathy - wheat, rye and barley
HLA DQ2 or DQ8
Assoc w Turner’s, T21, AI thyroid or liver and T1DM
Risk of rickets and osteomalacia
Dermatitis herpetiformis - itchy, blistering rash

Symptomatic Dx: on 2g of gluten for 6/52. TTG-IgA = if >10x UL = likely villous atrophy -> antiEMA Ab + and HLA + = can avoid biopsy.
But if <10x UL or other tests negative -> duodenal biopsy

Asymptomatic raised TTG and HLA + -> biopsy.

Biopsy: sub-total villous atrophy, crypt hyperplasia, intra-epithelial lymphocytes

TX: gluten free for life
If not, increased risk for SI lymphoma, short stature, OP, IDA, delayed puberty

Gluten challenge is not routinely recommended

Question 19

Constipation
-Signs
-Causes
-Tx

Answer 19

O/E: full abdomen, palpable mass in LLQ that indents and is hard
Check for spina bifida - saddle sensation
Further ix: perianal region - overflow soiling and risk of fissure

Causes:
Hirschprung’s
Thyroid disease
Meconium ileus
Spina Bifida

Poor diet, low fluid intake, psychosocial problems
Osmotic: macrogol, lactulose. Stimulant: senna

Question 20

Umbilical hernia

Answer 20

Almost never obstructs - usually resolves by 2 years
Surgery considered by 4-5yrs
Assoc hypothyroidism, MPS, Beckwith Wiedermann, T18, T13, connective tissue diseases

Question 21

Ascites

-Signs
-DDx

Answer 21

Bulging of flanks
Umbilical protrusion
Scrotal swelling
Fluid thrill
Shifting dullness

DDx:
Cirrhosis
Congestive HF
Nephrotic syndrome
Protein losing enteropathy

Question 22

GSD 3
Cori’s
- Inheritance
- Pathology
- Signs
- Sequlae

Answer 22

Autosomal recessive
Enzyme deficiency of liver and muscle - deficiency in glycogen debranching enzymes.
Layman: “buildup of glycogen in certain organs and tissues – especially in the liver and muscles.”

Signs:
Hepatomegaly
Myopathy
Developmental delay

Risk: cardiomyopathy and cirrhosis

Question 23

GSD IV Andersen’s
- Inheritance
- Pathology
- Signs
- Sequlae

Answer 23

Autosomal recessive
Absence of the glycogen branching enzyme, which is critical in the production of glycogen.
Abnormal glycogen molecules accumulate in cells; most severely in cardiac and muscle cells

Signs:
Hepatomegaly, Ascites & portal hypertension

Fatal perinatal neuromuscular type
* Excess fluid builds up around and in the body of the fetus
* Decreased fetal movement, stiff joints, low muscle tone and muscle wasting
* Do not survive past the newborn stage

Congenital muscular type
* Early infancy: Dilated cardiomyopathy
* Only survive a few months

Progressive hepatic type
* Infants: FTT, hepatomegaly and irreversible cirrhosis
* High BP in hepatic portal vein and ascites
* Die of liver failure in early childhood

Non-progressive hepatic type
* Liver disease is not so severe, rarely develop cirrhosis
* Muscle weakness and hypotonia
* Survive into adulthood

Childhood neuromuscular type
* Late childhood: myopathy and dilated cardiomyopathy
* Varies: some have severe cardiomyopathy and die in early adulthood

Question 24

Gaucher’s
- Inheritance
- Pathology
- Signs
- Sequlae

Answer 24

Autosomal recessive
Glucocerebrosidase deficicency - > lipid (glucocerebroside) accumulation

Signs:
- Portal hypertension and cirrhosis
- Painless hepatomegaly and splenomegaly
- Easy bruising: Hypersplenism & pancytopenia
- Arthalgia
Risk: splenic rupture.

Type I: Poor olfaction and cognition
Type II: Convulsions, hypertonia, poor suck, intellectual disability
Type III: Myoclonus, convulsions, ocular muscle apraxia

Dx: Genetic
Alt: High ALP, ACE and immunoglobulin

OP: 75% of patients develop visible bony abnormalities due to the accumulated glucosylceramide.
Yellowish-brown skin pigmentation

Tx : enzyme replacement (life long)

Question 25

GSD1 Von Gierke’s
- Inheritance
- Pathology
- Signs
- Sequlae
- Tx

Answer 25

Autosomal recessive
Reduced glucose 6 phosphatase activity

Signs
In 1st 6 mo:
Low blood sugar (chronic hypoglycemia), due to impairment of glycogen breakdown (glycogenolysis) causing insufficient fasting blood glucose (leads to lactic acidosis on fasting and hyperlipidaemia)

O/E:
Short & Doll like face
Asymptomatic hepatomegaly (deposition of glycogen and fat), large kidneys
Plt dysfunction, delayed puberty
Risk: renal calculi and hepatic adenoma
+- Neutropaenia

Tx: Continuous feeds
If neutropaenia: Filgrastim

Question 26

Portal Hypertension

Answer 26

Faltering growth and reduced muscle bulk
Splenomegaly - low plt, hb and wcc
Caput medusae
Venous hum above the umbilicus
Haemorrhoids
Ascites

Cirrhosis
Portal vein obstruction - can be congenital defect/sepsis
CHF
Hepatic vein outflow obstruction (Budd Chiari)

Question 27

CHF

Answer 27

Auto Rec
Large hard liver with good liver function
75% have polycystic kidneys

Assoc with ciliopathies that affect the kidneys, called hepatorenal fibrocystic diseases (FCD), include polycystic kidney disease (PKD), nephronophthisis (NPHP) chronic tubulointerstitial disease.

Typically hepatomegaly, portal hypertension and fiber-like hepatic connective tissue (hepatic fibrosis).

Question 28

Hepatomegaly

Answer 28

Glycogen or storage disorders
RS HF

Less examinable:
Infection: Hepatitis A B; EBV
Neoplasm: Primary liver tumours. Secondary liver tumours -lymphoma, leukaemia, neuroblastoma. Esp LARGE: leukaemia
Vascular: Hepatic Vein Thrombosis
Inflammatory: AI hepatitis, alpha 1 antitrypsin deficicency
Trauma:
Endocrine:
Degenerative: Esp LARGE: Congestive cardiac failure
Metabolic: Esp LARGE = Storage disorder - CF, Malnutrition, TPN; Gaucher’s, Niemann Pick’s, GSD
Wilson’s.
Drugs:
Congenital: Congenital hepatic fibrosis

Question 29

Splenomegaly

Answer 29

Portal hypertension (if no liver disease or hepatomegaly - portal vein obstruction is likely diagnosis). If large liver but no cirrhosis - likely congenital hepatic fibrosis)
Infection incl Glandular fever
Hereditary spherocytosis
Sickle Cell Disease
ITP
Myeloproliferative disease

Less examinable:
Infection: Septicaemia, Mononucleosis, Malaria
Neoplasm: Leukaemia, Hodgson’s
Vascular: Hereditary Spherocytosis, SCA, Thalassaemia
Inflammatory: JIA, SLE
Trauma:
Endocrine
Degenerative: Portal hypertension, Cirrhosis, Heart failure
Metabolic: Gaucher’s
Drugs:
Congenital:

Hyperplasia of reticuloendothelial system
Excessive stimulations by antigens
Excessive destruction of blood cells
Neoplasia
Disorders of splenic flow - portal HTN
Infiltration of the spleen

Question 30

Case: pale and well grown. Caput medusae. Full but not distended abdomen. Large spleen to 6cm below costal margin. Ascites present.

Answer 30

Portal Hypertension
Possible secondary to pre-hepatic portal vein obstruction

Question 31

Hepatosplenomegaly

Answer 31

Infection: EBV
Chronic: Cystic fibrosis -> portal HTN
Haem: Thalasaemia
Portal HTN
Storage: MPS – Gaucher’s
Congenital: Hepatic fibrosis
Infiltrative: Lymphoma/Leukaemia

Question 32

Portal Hypertension

Answer 32

Faltering growth and reduced muscle bulk
Splenomegaly - low plt, hb and wcc
Caput medusae
Venous hum above the umbilicus
Haemorrhoids
Ascites

Prehepatic:
Portal vein obstruction - can be congenital defect/sepsis

Intrahepatic
Neoplastic
Infection: Schistosmoiasis, hepatitis
Congenital: CHF, Biliary atresia
Metabolic: A1 antitrypsin deficiency
Cirrhosis

Hepatic congestion
Hepatic vein outflow obstruction (Budd Chiari)
RHF
Constrictive pericardiits

Question 33

Cirrhosis (usually small liver)

Answer 33

Congenital:
- Biliary: Biliary atresia (+- Kasai -> liver disease); Choledochal cysts; CHF; CF; Schlerosing cholangitis
- Genetic: alpha 1 AT deficicency; Wilson; GSD
Infection: Hep B & C; CMV
Vascular: Budd-Chiari and heart failure
Inflammatory: Autoimmune liver disease
Metabolic: Gaucher’s
Drugs: Alcohol

Tx: protein and essential fatty acid, trace elements and vitamins
Ascites: restrict salt +- diuretics
Emergency:
- Alimentary bleeding - crossmatch. Variceal ligation, portosystemic shunt, sclerotherapy
-Bacterial peritonitis - antibiotic
- Hepatic encephalopathy - ammonia accumulation, reduced protein intake, antibiotics, lactulose

Question 34

Kasai scar
Palpable liver
Portal HTN
Chronic liver disease

Answer 34

Extrahepatic Biliary atresia

NN presentation of cholestasis
Portoenterostomy (before 3 mo)
Post op - high risk cholecystitis and IV abx
Liver transplant

Question 35

Alagille syndrome
- Pathology
- Signs
- Sequalae
- Tx

Answer 35

Autosomal dominant

Liver signs:
Jaundice, pruritus, pale stools (acholia), hepatomegaly, splenomegaly & xanthomas

Reduced fat absorption: FTT
“Butterfly vertebrae”
Facies: broad, prominent forehead, deep-set eyes, and a small pointed chin

Dx:
Liver biopsy: too few bile ducts (bile duct paucity) or the complete absence of bile ducts (biliary atresia).
Genetics

Tx: supportive - liver treatments/transplants
Improve bile excretion from the liver, reduce pain caused by the disease, and help improve nutritional deficiencies

Question 36

Alpha 1 Antitrypsin

Answer 36

Auto rec
Cholestasis in infancy
Cirrhosis in childhood
Shortness of breath following mild activity, reduced ability to exercise, and wheezing. Other signs and symptoms can include unintentional weight loss, recurring respiratory infections, and fatigue
Increased risk - hepatocellular carcinoma

(TRIVIA: alpha-1 antitrypsin, which protects the body from a powerful enzyme called neutrophil elastase. Neutrophil elastase is released from white blood cells to fight infection, but it can attack normal tissues (especially the lungs) if not tightly controlled by alpha-1 antitrypsin.)

Question 37

Liver transplantation

Answer 37

Indications:
End stage disease - death in 18 months
Unacceptable quality of life
Growth or neurodevelopmental impairment secondary to disease
Fulminant liver failure: <2 years or INR >4
Life threatening complications of liver disease (bleeding varices, gross encephalopathy, severe ascites)

Rejection up to 50%
Sepsis high cause of mortality
Biliary leak in 20%

90% 2 year survival. 80% 5 year survival

Question 38

Chronic Abdominal Pain
Red flags

Answer 38

Red flags:
Very young
Well localised and far from umbilicus
Vomiting - esp bilious
Unexplained fever
Change in bowel habit - exp diarrhoea/blood
Nocturnal waking w pain
Weight loss/ Poor growth
Fam hx of IBD or Coeliac

Question 39

Chronic Abdominal Pain
Investigations

Answer 39

FBC, inflammatory marker, LFT, coeliac, stool culture, Urine MCS
+- USS
Symptom diary - w dietary/social triggers

If reassuring - functional abdominal pain - (Theory: abnormal bowel reactivity to physiological and psychologically stressful stimuli)

Recurrent Abdominal Pain = abdominal pain >2 in 3 months.
1) Functional dyspepsia - related to food
2) IBS - loose stools and constipation
3) Abdominal migraine - pallor, nauseas +- vomiting w fam hx of migraine
4) Functional abdo pain
- Simple analgesia
- Consider CAMHS or pain team input
- Healthy eating and plenty of fluids
- Regular exercise

Question 40

Clubbing Differential

Answer 40

Cardiac
Congenital heart disease with cyanosis
Infective endocarditis
AV malformations

Endocrine
Acromegaly
Hyperthryoidism
Hyperparthryoidism

Gastrointestinal
Achalasia
Celiac disease
Cirrhosis
Crohn’s disease
Tropical sprue
Ulcerative colitis

Infectious disease
Tuberculosis

Pulmonary
Cystic fibrosis
Interstitial lung disease – particularly bronchiectesis, but this is a large differential diagnosis itself.
Abscess and empyema
Lung cancer – primary and metastatic
Sarcoidosis

Other
Hypertrophic osteopathy – primary and secondary
Malignancy
Palmoplantar keratoderma
Pregnancy
Pseudoclubbing

Question 41

Renal Mass - most likely?

Answer 41

Polycystic renal disease most likely is ADPKD
PKD1, 2 or 3. Grossly dilated nephrons -> compression of surrounding parenchyma -> ischaemia

S: Abdo pain - stretching of cysts, haemorrhage or rupture
Haematuria and proteinuria
Rec UTI
HTN
Renal failure

Mx
USS screening of 1st degree relatives
Supportive mx: ACE inhibitor for hypertension

Question 42

ARPKD

Answer 42

Less common 1:40000. PKHD1 on Chr 6
Cysts in collecting ducts of nephrons
Can present as NN w renal masses and respiratory distress
Congenital hepatic fibrosis in all pt +- Portal HTN
Systemic hypertension

Question 43

RF for Wilm’s tumour

Answer 43

Beckwith-Wiedermann
Hemihypertrophy
Aniridia
DRASH syndrome

Question 44

Wilms’ Tumour (nephroblastoma)

Answer 44

1:10000 before 15y

• Painless, palpable abdominal mass
• Appetite loss
• Abdominal pain
• Fever
• N&V
• Haematuria in 20%
• HTN
• Varicoele

Metastasis usually to the lung - hematogenous metastases (lung, liver, bone, or brain)
5-year survival approximately 90%

Question 45

Nephrotic syndrome

Answer 45

Nephrosis
* Oedema
* Pallor
* Tachypnoea and SOB
* Pleural effusions and ascites
* Peripheral oedema
* HTN

Assess circulating volume with BP and HR; JVP; Core-peripheries temp difference; CRT

Complications
* HTN
* ARF or Chronic RF
* Infection
* Thrombosis
* Malnutrition
* Hyperlipidaemia

Mx
HAS for severe symptomatic oedema after discussion with renal team
Steroid therapy Prednisolone 60mg/m2 for 4/52, then halve for 4/52
Consider cyclophosphamide

Referral for biopsy
* Steroid resistant
* <12 mo or >12y
* Haematuria
* HTN not 2ry to circulatory problems
* Renal impairment
* Low complement

75% Minimal change disease
Others: Focal segmental glomerulosclerosis, mesangiocapillary glomerulonephritis, membranous nephropathy

Signs of Steroid toxicity

Question 46

Chronic Kidney Disease

Answer 46

Short, nutritonal impairment, pallor
PD catheter or fistula

Question 47

Chronic Kidney Disease

Answer 47

Persisting renal injury
GFR < 90ml/min/1.73 m^2 for over 3 month
S1: GFR >90 but eveidnce of bilateral injury
S5: GFR< 15

Commonest diff:
Congenital abnormalities of renal tract
Renal cystic disease
Nephrotic syndrome
Glomerulonephritis

Puberty is delayed - proportion of RRT
Mx:
* Prevent proteinuria with ACE inhibitors and monitor early morning P:C ratio, U&E and Creatinine
* Control HTN - salt reduction, anti-hypertensives: ACE inhibitor
* Intercurrent illness: maintain hydration, no nephrotoxics - re NSAIDS or using renal doses
* If polyuric from a tubular defect = sodium and bicarb supplmeentation
* If glomerular = retention of salt and water = lower intake Dietician
* Prevention of bone disease: reduced phosphate, vitamin D supplements
* Monitor growth: may need supplementation/gastrostomy. ?GH
* Correct anaemia: EPO and iron supplements
* Imms + influenza (live vaccines before transplant

Question 48

Renal transplant

Answer 48

Nephrectomy scars
Kidney in iliac fossa - superficial and palpable
Loin scars or laproscopic scars- post nephrectomy (risk of sepsis if ongoing reflux)

Complications
* SE immuosupression - infection risk
* Rejection of transplanted kidney
* Dehydration with intercurrent illness - risk of AKI, lower threshold for IV fluids and IV steroids
* Obstruction: USS of kidney, renal pevis measurements pre and post micturation

Management
* Live vaccines contraindicated (nasal influenza, oral polio, MMR, varicella)
* Prophylaxis with cotrimoxazole and valganciclovir post transplant
* Varicella exposure - vaccinate pre-transplant. If non immune post transplant for varicella IG for contact and aciclovir for tx
* Avoid nephrotoxics
* Clinic rv of weight, BP, U&E, creatinine

Question 49

Case: slim and shirt. Pale. Scars from cannula, catheter in RLQ with no bag attached.

Answer 49

CKD w PD
BP and urine dip

Question 50

Case: 15 y thin, bilateral ballotable loin masses - can’t get above, resonant to percussion, do not move w respiration . Normal BP, otherwise well

Answer 50

Most likely ADPKD as bilateral and well

DDx
Hydronephrosis
Cyst
Multicystic dysplastic kidney
Wilms’
Neuroblastoma
Unilateral renal agenesis - hypertrophy of other kidney
Renal vein thrombosis
Storage disorder
Beckwith Wiedermann
Sepsis

Question 51

Case: 2 y, large. Transverse ear lobe creases and macroglossia. Scar around umbilicus and loin scar on right. No organomegalt. No hemihypertrophy

Answer 51

Beckwith Wiedemann
(Exopthalos and Nephrectomy scars (Wilm’s)

Question 52

Case: 6y, short. Scar in RIF and scars bilaterally of both loins. Non tender abdomen with mass in RIF. Can get above and below, dull to percussion.

Answer 52

Transplanted kidney

BP and urine dip

Question 53

Case: 4y M small. Pale and oedematous w swollen abdomen. Bilateral ankle and leg welling. Well perfused and hydrated.
Oedema obstructing JVP. HS normal. No resp distress, chest clear no effusions. Shifting dullness present.

Answer 53

Nephrotic syndrome
Urine dip for protein (early am P:C ratio >200)
Hypoalbuminaemia in oedematous child

If Abdo pain - peritonitis or splanchnic vasoconstriction due to intravascuar depletion. Assess volume and consider sepsis, then treat
Urinary electrolytes helpful

Question 54

RF for Wilm’s tumour

Answer 54

Beckwith-Wiedermann
Hemihypertrophy
Aniridia
DRASH syndrome