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BPT Clinical Exam Prep > The abdomen > Flashcards

The abdomen Flashcards

1
Q

What is the normal liver span?

A

About 12.5cm

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2
Q

What is the differential for massive hepatomegaly?

A

Metastases
Alcoholic liver disease with fatty infiltration
Myeloproliferative disease
Right heart failure
Hepatocellular carcinoma

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3
Q

What is the differential for moderate hepatomegaly?

A

The massive causes earlier in their course (mets, AFLD, myeloproliferative disease, right heart failure, HCC) AND
Metabolism associated fatty liver disease
Other haematological disorders (CML, lymphoma)
Haemochromatosis

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4
Q

What is the differential for mild hepatomegaly?

A

Early course of the massive and moderate hepatomegaly causes.
Hepatitis
Cirrhosis
Biliary obstruction
Graulomatous disorders
Hydatid disease
Amyloidosis and other infiltrative diseases
HIV
Ischaemia

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5
Q

What is the differential for a firm and irregular liver?

A

Cirrhosis
Metastatic disease
Cysts (ADPKD for e.g.)
Granulomas
Hydatid disease
Amyloid
Lipoidoses

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6
Q

What is the differnetial list for a tender liver?

A

Hepatitis
Rapid liver enlargement (e.g. right heart failure, budd-chiari syndrome)
HCC

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7
Q

What is the differential for a pulsatile liver?

A

Tricuspid regurgitation
HCC
Vascular abnormalities affecting the liver

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8
Q

What are the differentials for bilateral renal masses?

A

Polycycstic kidneys
Hydronephrosis or pyonephrosis
Hypernephroma (bilateral RCC)
Acute renal vein thrombosis
Amyloid, lymphoma or other infiltrative disease
Acromegaly
In thin patients, early diabetic nephropathy leads to mild enlargement

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9
Q

What are the possible causes of unilateral renal masses?

A

Renal cell carcinoma
Hydronephrosis or pyonephrosis
Polycystic kidneys with assymmetrical enlargement
Acute renal vein thrombosis
Solitary kidney

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10
Q

What’s a differential for right iliac fossa masses?

A

Appendiceal abscess
Carcinoma of the caecum
Crohn’s disease
Pelvic kidney
OVarian tumour or cyst
Carcinoid tumour
Amoebiasis
Psoas abscess
Ileocaecal TB

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11
Q

What’s a differential for right iliac fossa masses?

A

Appendiceal abscess
Carcinoma of the caecum
Crohn’s disease
Pelvic kidney
OVarian tumour or cyst
Carcinoid tumour
Amoebiasis
Psoas abscess
Ileocaecal TB

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12
Q

What are the possible causes of left iliac fossa masses?

A

Faeces
Carcinoma of sigmoid or descending colon
Diverticular disease
Ovarian tumour or cyst
Psoas abscess

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13
Q

What are the possible causes of upper abdominal masses?

A

Retroperitoneal lymphadenopathy
Abdominal aortic aneurysms
Carcinoma of the stomach
Pancreatic pseudocyst or tumour
Carcinoma of transverse colon

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14
Q

What are the possible causes of massive splenomegaly?

A

Chronic myeloid leukaemia
Myelofibrosis
Primary lymphoma of spleen, heairy cell leukaemia, malaria, kal-azar

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15
Q

What are the causes of moderate splenomegaly?

A

Massive causes early in their courses
Portal hypertension
Lymphoma
Leukaemia
Thalassaeia
Storage diseases (e.g. Gaucher’s disease)

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16
Q

What are the possible causes of mild splenomegaly?

A

The causes of massive and moderate splenomegaly, early in their course
Polycythaemia vera
Essential thrombocythaemia
Haemolytic anaemia
Megaloblastic anaemi9a
Infection (infectious mononucleosis, hepatitis, or infective endocarditis)
Connective tissue disease or vasculitis (RA, SLE, PAN)
Infiltration (amyloidosism, sarcoidosis)

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17
Q

What are the distinguising features on exam of a spleen?

A

No palpable upper border
Notch
Moves with respiration
No resonance over splenic mass
Not ballotable
Friction rub over the spleen on auscultation

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18
Q

Where should you ausculatate on the abdomen?

A

Liver, spleen and renal area for bruits and venous hums. Then the gut for ?bowel sounds

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19
Q

What are the most common causes of a systolic bruit heard over the liver?

A

HCC
Acute alcoholic hepatitis

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20
Q

What causes a friction rub over the liver?

A

Tumour
Recent iver biopsy
Infarction
Gonococcal perihepatitis

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21
Q

What causes a friction rub over the spleen?

A

Infarction

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22
Q

What are the chest wall features of chronic liver disease?

A

In men - gynaecomastia, hair loss, spider naevi
In women - breast atrophy

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23
Q

Why do a cardiac exam if cirrhosis is suspected?

A

Restrictive pericarditis leads to cirrhosis

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24
Q

Why examine the lungs if you find ascites on an abdominal exam?

A

For pleural effusion

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25
Q

Why look at the eyes when suspecting chronic liver disease?

A

Kayser-Fleischer rings
Jaundice
Xanthelasma (common in advanced primary biliary cholangitis)
Anaemia

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26
Q

Other than the eyes, what should be looked at on the face of patients suspected to have chronic liver disease?

A

?Parotid enlargement (alcoholis)
?Angular stomatitis
?Atrophic glossitis
?Fetor hepaticus (ammonia)

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27
Q

What should be looked for in the arms of patients suspected of having chronic liver disease?

A

Spider naevi
Hepatic flap
Leukonychia - Terry’s nails are characterised by 2/3 or more leukonychia nails. Typical of cirrhosis.
Palmar erythema (increased eostrogen)
Dupuytren’s contractures (alcohol use or trauma)
Arthopathy - ?haemochromatosis

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28
Q

What are the most common neurological disease findings associated with alcoholism?

A

Peripheral neuropathy
Proximal myopathy
Cerebellar syndrome
Wernicke’s encephalopahy (which inlcudes bilateral VI nerve palsies)
Korsakoff’s psychosis

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29
Q

What should you ask to add onto the end of an abdominal exam when time runs out?

A

Rectal exam
Testicular exam including hernia exam
Urinalysis
Temperature chart

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30
Q

If you suspect acute polycystic kidney disease, how should you proceed?

A

Blood pressure
Urinalysis
Look for evidence of anaemia (conjunctival pallor, palmar crease pallor)
Look for evidence of polycythaemia (facial flushing)
Ensure to feel for nodular liver border indicating liver cysts, and splenic cysts
Look for third nerve palsy ?unruptured berry aneurysm
Lower limbs ?oedema (should be included in any abdo exam
Neck scars ?parathyroidectomy ?central venous cathetar
Fistular?

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31
Q

If a nodular liver suspicious for malignancy is felt, how should you proceed?

A

Lymph node exam: axillar, cervical, supraclavicular, inguinal, epitrochlear
Breast exam
Thorax for signs of lung malignancy

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32
Q

What does a scar hear indicate?

A

Nephrectomy scar, likley due to autosomal dominant polycystic kidney disease or malignancy

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33
Q

What are cevron/mercades benz/rooftop scars used for?

A

Liver transplant, gasstrectomy, oesophagectomy, bilateral adrenalectomy, hepatic resections, pancreatic surgery, combined liver/kidney surgery.

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34
Q

What exam findings should be looked for it is suspected the patient is a transplant recipient?

A

Cushingoid
Thin skin
Striae
Proximal myopathy
Tremor (Cyc A/Tac/MMF)
Gingival hyperplasia (cyc A)
Arthraliga (mTOR)
Acne vulgaris (which is just acne, mTOR)
Lymphadenopathy (PTLD)
Warts
Skin cancers

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35
Q

How should assess kidney graft function if asked?

A

CBE for anaemia
Renal function bloods
Calcium and phosphate
CXR for volume overload
Bicarb and pH for acidosis
Imaging if concern for calculi

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36
Q

What are the clinical findings for haemochromatosis?

A

Bronzing
Arthopathy - esp degenerative arthritis of the MCP joints of the index and middle fingers
Testicular atrophy (due to iron deposition in the pituatary gland)
Dilated cardiomyopathy
Glycosuria (resulting from diabetes mellitus)

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37
Q

What is Felty’s syndreome?

A

Rheumatoid arthritis manifestation that includes arthopathy, splenomegaly and neutropoenia. Autoantibodies to histones and other components of neutrophil NETs cause neutrophil sequestration to the spleen - leading to neutropoenia and splenomegaly.

38
Q

If haematological malignancy is suspected, what should be looked for in the mouth?

A

Ulcers, enlarged lymphatic tissue (tonsils and adenoids), atrophic glossitis, angular stomatitis, gum hypertrophy.

39
Q

What is the differential for combined hepatosplenomegaly?

A

Chronic liver disease with portal hypertension
Haematological disease (myeloproliferative disease, lymphoma, leukaemia, pernicious anaemia, sickle cell anaemia)
Infection (viral hepatitis, mononucleosis)
Infilitration (sarcoid/amyloidosis)
Connective tissues disease (SLE)
Acromegaly
Thyrotoxicosis

40
Q

What is the proceed if haematological malignancy is suspected from the abdominal exam?

A

Inguinal nodes
Femoral chain
Spring pelvis
Hands and nails
Epitrochlear nodes
Sit up
Go to back
Head and neck nodes
Press on spine and shoulders
Come to front
Axillary nodes
Press sternum
Ask to examine fundi

41
Q

What are the differentials for lymphadenopathy?

A

Lymphoma
Leukaemia
Mets
Infection
Connective tissue disease
Infilitrations
Phenytoin (pseudolymphoma)

42
Q

At what concentration of bilirubin is jaundice normally evident?

A

> 40micromols/L (twice the ULN)

43
Q

What is Zieve’s syndrome?

A

Binge drinking syndrome - Coombs-negative haemolysis, cholestatic jaundice, transietn hyperlipidaemia. The mechanism is likely related to lipid accumulation in RBC membranes due to increased blood ethanol concentration.

44
Q

What is the underlying deficiency that is likely associated with leukonychia?

A

Hypoalbuminaemia

45
Q

Which way does blood flow into collatertal abdominal wall veins in portal hypertension?

A

Away from the umbilicus. Helpful to differentiate from IVC obstruction if you test a vein below the umbilicus - IVC obstruction will fill upwards fast, portal hypertension will flow downwards fast.

46
Q

What does blood flow upwards when milking abdominal wall collateral vessels indicate?

A

Inferior vena cava obstruction

47
Q

Where is a venous hum from portal hypertension best heard?

A

The epigastrium

48
Q

What is Budd-Chiari syndrome?

A

Occlusion, regardless of the mechanis, of the liver outflow. Recall that liver outflow is via the right, middle and left hepatic veins into the inferior vena cava.

49
Q

How might you detect Budd-Chiari syndrome clinically?

A

Absence of hepatojugular reflux

50
Q

Differential diagnosis in cirrhosis?

A

Viral (B, C)
Autoimmune (PBC, PSC, Autoimmune Hepatitis)
Metabolic (MAFLD, Haemachromatosis, alpha 1 antitrypsin deficiency, Wilson’s disease, CF)
Grugs (MTX, isoniazid, amiodarone, phenytoin)

51
Q

What are the consequences of portal hypertension?

A

Varicies
Ascites
Splenomegaly
Thrombocytopoenia

52
Q

What are the consequences of liver dysfunction?

A

Coagulopathy
Encephaloptahy
Jaundice
Hypoalbuminaemia

53
Q

What are the causes of decompensation of liver disease?

A

Infection
SBP
Hypokalaemia (reduces amonia clearance)
GI bleeding
Sedative
HCC

54
Q

What is primary biliary cholangitis (formerly primary biliary cirrhosis)?

A

Autoimmune disease targeting the interlobular bile duct. Natural history is the development of cirrhosis, however ursodeoxycholic acid has led to normal life expectancy.

55
Q

What is the epidemiology of primary biliary cholangitis?

A

Typically woman between the age of 30 and 65

56
Q

What are the typical exam findings in patients with primary biliary cholangitis?

A

Hyperpigmentation - melanin deposits (unclear mechanism)
Xantholasma/xanthomata
Xerosis
Scratch marks from puritis
Fungal infections of the feet or nails
Jaundice is a very late findings

57
Q

What are the classical laboratory findings in patients with primary biliary cholangitis?

A

Elevate ALP
Positive AMA (antimitochondial antibodies) in almost all patients
Positive ANA in about 70% of patients
– multiple nuclear dots pattern (ENA Sp100)
– rim-like membranous pattern (ENA gp210, nucleoporin p62 or lamin B receptor)
– sometimes SSA or DS-DNA abs
Hyperlipidaemia
Increased serum IgM

58
Q

What are the other diseases associated with primary biliary cholangitis?

A

Sjogren’s - most common
Autoimmune thyroid disease
Inflammatory arthropathies

59
Q

What is the classic epidemiology of people with primary sclerosing cholangitis?

A

Mostly men in around the 40s.

60
Q

What are the classic laboratory findings for patients with primary sclerosing cholangitis?

A

Atypical perineuclear ANCA (P-ANCA) positive
Increased IgM (40-50%)
Increased IgG (~30%)
Raised ALP/GGT/Bilirubin
Absent AMA

61
Q

What is the most important disease association with primary sclerosing cholangitis?

A

Up to 90% of patients with PSC have ulcerative colitis. However, only 5% of patients with UC have PSC.

62
Q

What are the most common causes of ascites?

A

Cirrhosis
Malignancy
Heart failure
TB
Pancreatitis

63
Q

What investigations should be done if ascites is found?

A

Diagnostic abdominocentesis
- alabumin and total protein for SAAG
- PMN count for ?SBP
- MCS
- cytology ?malignancy
Abdo US
- hepatic vein and portal vein doppler
- hepatomegaly character
- ?splenomegaly
Bloods
- LFTs, coags, FBC (esp. platelets)

64
Q

What is SAAG?

A

Serum ascites albumin gradient
= Serum albumin - ascitic fluid albumin

SA-AG > 11g/L suggests as a transudate
SA-AG <11g/L suggests exudate

65
Q

What are the hepatic manifestations of sickle cell disease?

A

Gall stone disease due to chronic haemolysis with pigment stones
Sickle hepatic crisis - due to sickle thrombosis causing sinusoidal obstruction. Presents with right upper quadrant pain, jaundice, tender hepatomegaly.
Intrahepatic cholestasis - due to cickle thrombosis in susoids, causing hepatocyte swelling and intrahepatic biliary obstruction.
Associated liver diseases - iron overload due to transfusions, viral hepatitis from blood transfusions.

66
Q

What is the most likely cause of massive splenomegaly in the absence hepatomegaly or lymphadenopathy or RA signs suggest?

A

Myeloproliferative disease (e.g. CML/myeloproliferative disease). With hepatomegaly suggests portal hypertension. With lymphadenopathy suggests lymphoproliferative disease. With RA suggests Felty’s disease.

67
Q

What’s the cause of hepatomegaly in haematological malignancy?

A

Extramedullary haematopoiesis.

68
Q

What is the classic gene mutation associated with chronic myeloid leukaemia?

A

BCR-ABL translocation (Philidelphia chromosome) in ~95% of cases.

69
Q

How is haemochromatosis inherited?

A

HFE gene - autosomal recessive.

70
Q

What type of heart failure to patients with haemochromotosis get?

A

Restrictive or dilated cardiomyopathy.
Can see it on cMRI.

71
Q

What needs to be treated in patients with primary biliary cholangitis?

A

Supplementation of fat soluble vitamins (ADEK)
Treatment of associated osteoporosis
Treatment of hypercholesterolaemia
Treatment of liver disease with ursodeoxycholic acid
Treatment of pruritis with cholestyramine, rifampicin or naltrexone.
Treatment of fatigue
Transplantation consideration

72
Q

If a renal transplant is located, what should be commented on when describing graft function?

A

Mental status
Asterixis
Exrcoriation marks
Tachypnoea
Pericardial rub
Pallor

73
Q

Where will a tunnelled venous catheter be?

A

Subclavicular region - go into the subclavian vein

74
Q

What is the ideal PTH in chronic kidney disease?

A

2-9x the ULN.

75
Q

What are the indications for renal replacement therapy?

A

Pericarditis
Pleuritis
Volume overload refractory to diuretics
Hypertension refractory antihypertensives
Refractory hyperkalaemia
Refractory acidosis
Encephalopathy or decline in mental status due to uraemia
Removal of toxins

76
Q

What is the definition of nephrotic syndrome?

A

> 3.5g proteinuria per 24hrs

77
Q

What are the causes of nephrotic syndrome?

A

Minimal change disease
Focal segmental glomerulosclerosis
Membranous glomerulonephritis
Membranoproliferative glomerulnephritis
(myeloma, hep c or b, cryoglobulinaemia, SLE, Sjogren’s, RA, C3G, DDD, post-infectious)

77
Q

What are the causes of nephrotic syndrome?

A

Minimal change disease
Focal segmental glomerulosclerosis
Membranous glomerulonephritis
Membranoproliferative glomerulnephritis
(myeloma, hep c or b, cryoglobulinaemia, SLE, Sjogren’s, RA, C3G, DDD, post-infectious)

78
Q

What is the antibody associated with 80% or primary membraneous nephropathy cases?

A

Anti-M-type phospholipase A2 receptor.

79
Q

What are the complications of nephrotic syndrome?

A

Oedema
Hypertension
Hypercholesterolaemia
Thrombosis
Infection

80
Q

How is haemoglobin impacted in autosomal dominant polycystic kidney diseaes?

A

Early, the kidneys produce more erythropoeitin, and patients become polycythaemic
At times, cysts can rupture, leading to blood loss and reudction in haemoglobin.
At later stages, when renal function fails, EPO production reduces and patietns require darbapoeitin.

81
Q

What percentage of patients with polycystic kidney disease also have hepatic cysts?

A

~70%

82
Q

What are the subtypes of ADPKD?

A

ADPKD1 - 90% or cases - chromosome 16 - more severe.
ADPKD2 - 10% of cases - chromosome 4 - less severe.

83
Q

What does flink pain indicate in a patient with ADPKD?

A

Cyst torsion, haemorrhage or infection.
Renal calculi

84
Q

What needs to be considered when treating cyst infection?

A

Cyst penetration requires abx that a lipophilic. Fluroquinolones are a good choice.

85
Q

What are the causes of right upper quadrant mass?

A

Liver
Right kidney
Riedel’s lobe of liver (normal variant that is lateral to the gall bladder)
Gall bladder (moves with respiration)
Colon

86
Q

What are the causes of a left upper quadrant mass?

A

Spleen
Left kidney
Colon
Pancreas
Stomach

87
Q

What are the causes of a right lower quadrant mass?

A

Colon
Small instestine
Appendix
Pelvic mass

88
Q

What are the causes of a left lower quadrant mass?

A

Sigmoid colon - diverticular disease or lesion
Pelvic mass

89
Q

What are the autosomal dominant hereditary conditions that pre-dispose patiente to colorectal cancer?

A

Hereditary nonpolyposis colorectal cancer (aka HNPCC aka Lynch Syndrome)
Familial adenomatous polyposis (FAP)
Peutz-Jeghers Syndrome

90
Q

What are the most common types of small bowel cancers?

A

Neuroendocrine tumour
Lymphoma
Adnenocarcinoma
GIST

BPT Clinical Exam Prep (8 decks)

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