Abdominal Clinical Examination Flashcards
Laparoscopy Scars
Inguinal hernia repair
Pyloromyotomy for pyloric stenosis
Appendicectomy
Cholecystectomy
Fundoplication
Total or partial nephrectomy
Laparotomy Scars
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
Below R subcostal margin (Kocher’s)
After cholecystectomy & gallstone removal
Assoc w SCD & hereditary spherocytosis
Transverse upper abdominal incision
CDH repair (L>R)
Upper abdominal midline incision
Nissan’s fundoplication
Severe GORD - assoc w neurodevelopmental problems
Now usually laparoscopic
Small right upper transverse incision
Ramstedt’s pyloromyotomy (M>F)
Hypertrophic pyloric stenosis
RIF scar
Appendectomy
Lateral thoracolumbar incision
Nephrectomy
Subumbilical/peri-umbilical scar
Gastroschisis or exomphalos
Umbilical hernia repair
Hepatomegaly
R hypochondrium
Cannot get above it
Moves w respiration
Dull to percussion
Splenomegaly
L hypochondrium
Cannot get above it
Moves with respiration
Dull to percussion
Has a notch
Weight gain in 1st year of life
200g/week 1st 3 mo
150g/week 2nd 3 mo
100g/week 3rd 3 mo
50g/week 4th 3mo
Genetic/Endocrine/Oncological causes of Obesity
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
Genetic/Endocrine/Oncological causes of Obesity
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
CF Gastrointestinal
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
Crohn’s:
-Pathology
-PC
-Signs
-Tx
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
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
Malabsorption syndrome
- Most likely Coeliac
- CMPA (non-IgE form)
-CF
- Immunodeficiency
(Giardiasis, Soya intolerance, AI diseases)
- inflammatory bowel disease
- post surgical
Coeliac disease:
- Haplotypes
- Associations
- Tx
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
Constipation
-Signs
-Causes
-Tx
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
Umbilical hernia
Almost never obstructs - usually resolves by 2 years
Surgery considered by 4-5yrs
Assoc hypothyroidism, MPS, Beckwith Wiedermann, T18, T13, connective tissue diseases
Ascites
-Signs
-DDx
Bulging of flanks
Umbilical protrusion
Scrotal swelling
Fluid thrill
Shifting dullness
DDx:
Cirrhosis
Congestive HF
Nephrotic syndrome
Protein losing enteropathy
GSD 3
Cori’s
- Inheritance
- Pathology
- Signs
- Sequlae
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
GSD IV Andersen’s
- Inheritance
- Pathology
- Signs
- Sequlae
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
Gaucher’s
- Inheritance
- Pathology
- Signs
- Sequlae
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)
GSD1 Von Gierke’s
- Inheritance
- Pathology
- Signs
- Sequlae
- Tx
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
Portal Hypertension
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)
CHF
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).
Hepatomegaly
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
Splenomegaly
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
Case: pale and well grown. Caput medusae. Full but not distended abdomen. Large spleen to 6cm below costal margin. Ascites present.
Portal Hypertension
Possible secondary to pre-hepatic portal vein obstruction
Hepatosplenomegaly
Infection: EBV
Chronic: Cystic fibrosis -> portal HTN
Haem: Thalasaemia
Portal HTN
Storage: MPS – Gaucher’s
Congenital: Hepatic fibrosis
Infiltrative: Lymphoma/Leukaemia
Portal Hypertension
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
Cirrhosis (usually small liver)
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
Kasai scar
Palpable liver
Portal HTN
Chronic liver disease
Extrahepatic Biliary atresia
NN presentation of cholestasis
Portoenterostomy (before 3 mo)
Post op - high risk cholecystitis and IV abx
Liver transplant
Alagille syndrome
- Pathology
- Signs
- Sequalae
- Tx
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
Alpha 1 Antitrypsin
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.)
Liver transplantation
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
Chronic Abdominal Pain
Red flags
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
Chronic Abdominal Pain
Investigations
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
Clubbing Differential
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
Renal Mass - most likely?
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
ARPKD
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
RF for Wilm’s tumour
Beckwith-Wiedermann
Hemihypertrophy
Aniridia
DRASH syndrome
Wilms’ Tumour (nephroblastoma)
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%
Nephrotic syndrome
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
Chronic Kidney Disease
Short, nutritonal impairment, pallor
PD catheter or fistula
Chronic Kidney Disease
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
Renal transplant
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
Case: slim and shirt. Pale. Scars from cannula, catheter in RLQ with no bag attached.
CKD w PD
BP and urine dip
Case: 15 y thin, bilateral ballotable loin masses - can’t get above, resonant to percussion, do not move w respiration . Normal BP, otherwise well
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
Case: 2 y, large. Transverse ear lobe creases and macroglossia. Scar around umbilicus and loin scar on right. No organomegalt. No hemihypertrophy
Beckwith Wiedemann
(Exopthalos and Nephrectomy scars (Wilm’s)
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.
Transplanted kidney
BP and urine dip
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.
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
RF for Wilm’s tumour
Beckwith-Wiedermann
Hemihypertrophy
Aniridia
DRASH syndrome
