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PACES > Station 1: Abdo > Flashcards

Station 1: Abdo Flashcards

1
Q

Surgical scars in the abdomen?

A

Rooftop: upper GI e.g. gastrectomy, pancreas
Mercedes-Benz: liver transplant
Kocher’s: right subcostal incision e.g open cholecystectomy
Midline: emergency e.g laparotomy when diagnosis is not clear
Paramedian: general abdo surgery e.g. colectomy
Gridiron/Lanz: open appendicectomy
Loin: open renal procedures
Rutherford-Morrison: renal transplant
Pfannenstiel: gynae and obstetric surgery
Groin: hernia, varicose vein stripping, vascular surgery
RIF stoma: loop or end ileostomies
LIF stoma: loop or end colostomies

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2
Q

Common nail changes and causes?

A

Clubbing:
- Cirrhosis
- Coeliac disease
- Crohn’s/ulcerative colitis

Leuconychia:
- Hypoalbuminaemia (malabsorption, malnutrition, protein-losing enteropathy)
- Idiopathic
- Familial
- Arsenic or heavy metal poisoning

Koilonychia:
- Chronic iron deficiency
- Idiopathic
- Familial
- Poor peripheral circulation

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3
Q

Things to look for in the face, lips, tongue?

A

Face
- Anaemia: malabsorption, IBD, CKD
- Jaundice: pre-hepatic will have absence of other features of chronic liver disease
- Microstomia

Lips/tongue
- Oral ulcers: IBD, SLE
- Telangiectasia on lips and tongue: Osler Weber Rendu or systemic sclerosis
- Buccal hyperpigmentation: Addison’s disease
- Pigmented macules on lips: Peutz-Jeghers syndrome
- Macroglossia: acromegaly, amyloidosis
- Glossitis: iron deficiency
- Gum hypertrophy: ciclosporin in transplanted patients

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4
Q

To complete examination - ascites/hepatomegaly (without signs of chronic liver disease)?

A
  • Check urinalysis
  • Check JVP
  • Examine other systems for possible primary tumours
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5
Q

To complete examination - renal abdomen?

A
  • Measure BP
  • Check urinalysis
  • Auscultate heart for pericardial rub
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6
Q

Causes of spider naevi?

A

Excess oestrogens, located in the distribution of SVC
- Chronic liver disease
- Pregnancy
- Oral contraceptive pills
- Thyrotoxicosis

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7
Q

Causes of gynaecomastia?

A

Relative deficiency in androgens and excess in oestrogens
- Chronic liver disease
- Chronic renal disease
- Thyrotoxicosis
- Testicular atrophy, tumour, cystectomy
- Klinefelter syndrome
- Drugs: spironolactone

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8
Q

Causes of acanthosis nigricans?

A
  • Insulin-resistant type 2 DM
  • Hypo or hyperthyroidism
  • Acromegaly
  • Cushing’s disease
  • Paraneoplastic
  • Obesity: idiopathic or familial
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9
Q

How to differentiate renal from liver/splenic masses?

A

Renal: ballotable, able to palpate above, resonant percussion note, no movement with respiration

Liver/spleen: not ballotable, not able to palpate above, dull percussion note, movement with respiration

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10
Q

Differential diagnosis for single and bilateral palpable kidney?

A

Single kidney:
- Hydronephrosis
- RCC
- PKD
- Congenital anomalies e.g. horseshoe kidney

Bilateral kidney:
- Bilateral hydronephrosis
- Bilateral RCC (occurs in VHL)
- Bilateral renal cysts -> causes: PKD, VHL, tuberous sclerosis, Trisomy 13 (Patau), Trisomy 18 (Edward), Trisomy 21 (Down)
- Amyloidosis

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11
Q

ADPKD - clinical signs and important negatives?

A

Signs:
- Hepatomegaly with irregular liver edge (cyst)
- Splenomegaly (cyst)
- Distended abdomen with fullness in flanks
- Flank masses, possible to palpate above, overlying resonant percussion note

Important negatives:
- Anaemia
- Stigmata of chronic liver disease
- Volume status (raised JVP/peripheral oedema)
- Uraemia
- Encephalopathy (asterixis)
- RRT

Other features:
Measure blood pressure
Examine CVS (MV prolapse, AR) and neuro systems (old stroke, ruptured Berry aneurysm)

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12
Q

ADPKD - extra renal manifestations?

A
  • Hypertension
  • Polycythaemia
  • Cerebral aneurysm
  • Common cyst: liver, spleen, pancreas
  • Other cysts: uterus, ovaries, testes, lungs, thyroid, bladder
  • CVS: MV prolapse, AR
  • Diverticular disease
  • Aortic aneurysm
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13
Q

ADPKD - principles of management?

A
  1. Treatment of acute pain:
    - Differentiate cause - infection, haemorrhage, ruptured cyst
    - Treat accordingly: abx, nephrectomy
  2. Manage hypertension
  3. Treat anaemia
  4. Phosphate binders if high PO4
  5. Vit D if hyperPTH
  6. Early specialist referral for RRT
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14
Q

ADPKD - indication for nephrectomy?

A
  • Pain: possible cause infected cyst, haemorrhagic cyst, nephrolithiasis, diverticulitis, AAA, strangulated hernia
  • Recurrent infections
  • Ruptured cyst
  • Traumatic injury
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15
Q

ADPKD - what do you know about the genetics, and when would you recommend screening?

A
  • Typically autosomal dominant -> a variety of genetic defects have been described
  • 90% ADPKD1, mapped to chromosome 16
  • The rest ADPKD2, mapped to chromosome 4, milder phenotype
  • Some arise from spontaneous mutation
  • ARPKD is rare, presents in infancy and is associated with severe liver and renal disease

Screening: USG kidneys
Cysts develop with ageing, screen in those with FHx after age 20yo

Criteria for diagnosis:
- 15-39yo: > 3 cysts unilateral or bilateral
- 40-59yo: > 2 cysts unilateral
- 60yo: > 4 cysts unilateral

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16
Q

Renal abdomen - approach to presentation?

A
  1. Current mode of RRT
  2. Previous mode of RRT
  3. Adequacy of RRT (uraemia, encephalopathy, volume status)
  4. Complications of renal disease e.g. anaemia, parathyroidectomy, uncontrolled HTN, CVS disease
  5. Complications of immunosuppressant therapy
  6. Possible aetiology of renal disease
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17
Q

Renal abdomen - clinical features and important negatives?

A

HD
- Presence of catheter + catheter-site infection (important -ve)
- Presence of fistula, functioning vs non-functioning
- Chest/neck scars from previous vascular access sites
- Volume status: JVP, peripheral oedema
- Encephalopathy: asterixis
- Uraemia
- Anaemia
- Iliac fossa mass/scar: transplant
- Complications of immunosuppressants
- Possible cause

PD
- Presence of peritoneal dialysis catheter + catheter-site infection (important -ve)
- Laparotomy scar - may indicate prev surgery for peritonitis
- Flank dullness that shifts with rotation of the patient - consistent with dialysis fluid within peritoneal cavity
- Abdominal wall hernia (important -ve)
- Others same as above

Transplant
- Remember to say ‘ESRF with a renal transplant’
- Scar in RIF
- Overlying smooth, firm, non-tender mass, dull percussion note, no bruit
- Euvolaemic + no signs of active RRT (no catheter or functioning fistula) -> functioning transplant

Complete exam (based on aetiology):
- Fundoscopy: HTN, DM
- Urine dipstick for proteinuria/haematuria/glycosuria: HTN, DM, GN
- CVS/neuro exam: PKD

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18
Q

Renal abdomen - signs of the aetiology of native kidney disease?

A
  • DM: pinprick marks at fingertips indicating frequent glucose testing, lipodystrophy indicating subcutaneous insulin use
  • HTN: ask for BP
  • PKD: large ballotable kidneys, nephrectomy scars
  • Alport’s syndrome / aminoglycoside induced nephrotoxicity + ototoxicity: hearing aids
  • GN type 2: facial lipodystrophy
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19
Q

Renal abdomen - signs of immunosuppressive therapy?

A
  • Ciclosporin: HTN, gum hypertrophy
  • Tacrolimus: DM, tremor
  • Steroids: purpura, Cushingoid features
  • AZA: skin warts
  • Increased skin pigmentation and premature ageing
  • Skin malignancies (BCC/SCC)
  • Surgical scars or radiation burns suggestive of treatment of other malignancies e.g. lymphoma
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20
Q

Renal abdomen - major causes of chronic renal disease?

A
  • DM
  • HTN
  • Chronic GN
  • PKD
  • Other causes: obstructive uropathy, analgesic nephropathy
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21
Q

Renal abdomen - principle of management of chronic renal disease?

A
  1. Treatment of reversible causes:
    - Diagnosis of treatable glomerular disease
    - Cessation of nephrotoxic drugs
    - Exclusion of obstructive uropathy or renovascular disease
  2. Slowing disease progression
    - Obtaining optimal control of HTN and DM
    - Treatment of cardiovascular risk factors - aspirin, lipid lowering therapy, smoking cessation
  3. Treatment of complications of chronic renal disease
    - Volume overload: diuretics and dietary Na restrictions
    - Anaemia: due to reduced EPO production and concomitant IDA (treat iron supplements/IV iron therapy + possible EPO injections)
    - Hyperkalaemia: dietary K restrictions
    - Metabolic acidosis: oral sodium bicarbonate
    - HyperPTH: oral phosphate binders, limit development of renal osteodystrophy
    - Renal osteodystrophy: treat hyperPTH, vit D analogues in hypercalcaemia to prevent 2ndry hyperPTH
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22
Q

Renal abdomen - indication for RRT?

A

Preparation for RRT should begin when GFR < 30ml/min (stage 4)

Indications for acute HD:
- Volume overload refractory to diuretics
- Refractory hyperkalaemia
- Refractory metabolic acidosis
- Symptomatic uraemia: pericarditis, bleeding, encephalopathy
- Removal of toxins

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23
Q

Renal abdomen - name some of the associated opportunistic infections with renal transplant?

A
  • CMV
  • PCP
  • EBV
  • BK virus -> causes ureteric stricture and interstitial nephritis
  • JC virus -> causes PML
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24
Q

Renal abdomen - indications for transplant nephrectomy?

A
  • Primary non-function
  • Acute rejection refractory to treatment
  • Recurrent UTI
  • Malignant tumours
  • Transplant rupture
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25
Q

Chronic liver disease - clinical findings?

A
  • Undernourishment
  • Peripheral stigmata: clubbing, leuconychia, palmar erythema, Dupuytren’s contractures (alcohol)
  • Altered sex hormone metabolism: spider naevi, gynaecomastia, loss of body hair
  • Petechiae, ecchymoses
  • Jaundice
  • Anaemia -> important negative: blood loss from portal gastropathy, alcohol excess causing bone marrow suppression and poor nutrition
  • Parotid enlargement (alcohol)
  • Caput medusae (portal hypertension)
  • Hepatomegaly -> if present note irregular liver edge (malignancy)
  • Splenomegaly (portal hypertension)
  • Ascites (portal hypertension or hypoalbuminaemia)
  • Peripheral oedema (hypoalbuminaemia)
  • Scar: liver biopsy or liver transplant
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26
Q

Chronic liver disease - signs of portal hypertension?

A
  • Splenomegaly
  • Caput medusae (umbilical vein recanalization due to portal HTN or IVC obstruction)*
  • Ascites
  • Oesophageal varices on endoscopy

*To differentiate:
- Portal HTN: flow away from umbilicus towards legs
- IVC obstruction: flow towards umbilicus towards head

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27
Q

Chronic liver disease - specific signs to suggest underlying cause?

A

Rare but if present:
- Alcohol: parotid enlargement, Dupuytren’s contractures, cerebellar syndrome, peripheral neuropathy
- Chronic viral hepatitis: tattoos, IV use
- PBC: hyperpigmentation, xanthelasma, xanthomata, excoriation marks
- Haemochromatosis: bronze pigmentation, arthropathy, glucose testing skin pricks
- Wilson’s disease: Kayser-Fleischer rings (on slit lamp), akinetic-rigid syndrome
- a1 antitrypsin deficiency: lower zone emphysema
- CCF: raised JVP, S3

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28
Q

Chronic liver disease - causes of cirrhosis?

A
  1. Alcoholic liver disease
  2. Chronic viral hepatitis
  3. Non-alcoholic steatohepatitis
  4. Autoimmune: PBC, PSC, autoimmune hepatitis
  5. Metabolic: haemochromatosis, Wilson’s disease, a1 antitrypsin deficiency
  6. Drugs: amiodarone, methotrexate, isoniazid, phenytoin
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29
Q

Chronic liver disease - complications?

A
  • Portal hypertension
  • Upper GI bleeding: variceal bleed, gastric ulcers
  • Ascites
  • Spontaneous bacterial peritonitis
  • Hepatic encephalopathy
  • Hepatorenal syndrome
  • Hepatopulmonary syndrome
  • Hepatocellular carcinoma
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30
Q

Chronic liver disease - precipitating factors for decompensation?

A

The liver can decompensate as a result of ongoing liver injury.
Clinically will present as ascites, encephalopathy, hepatorenal syndrome, hepatopulmonary syndrome.

Causes:
- Continuous alcohol intake
- Untreated chronic active viral hepatitis
- Infections
- Large salt intake
- Hypokalaemia, hyponatraemia
- GI bleeding
- Dehydration
- Constipation

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31
Q

Chronic liver disease - grade the severity of encephalopathy?

A

Graded according to West Haven criteria.
Describes the reversible neurological dysfunction or coma due to liver disease.

Grade 0: usually normal, mild memory problems
Grade 1: reversed sleep pattern, impaired mental tasks such as addition
Grade 2: lethargy, disorientation, personality change, impaired mental tasks such as subtraction
Grade 3: gross confusion and disorientation, somnolence
Grade 4: comatose

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32
Q

Chronic liver disease - grade the severity of cirrhosis?

A

Child-Pugh score
- Most commonly used
- Grades severity of cirrhosis based on clinical and biochemical parameters
- Ascites, encephalopathy, albumin, bilirubin, INR
- Grade A (score 5-6): 100% 1 year survival
- Grade B (score 7-9): 80% 1 year survival
- Grade C (score > 10): 50% 1 year survival

MELD (Model for End-Stage Liver Disease) score
- Stratifies severity of liver disease, to prioritise for transplant
- Predicts 3-month survival in: after TIPS, cirrhotic patients undergoing non-transplant surgery, acute alcoholic hepatitis, acute variceal haemorrhage
- Scores between 6-40
- Dialysis, creatinine, sodium, bilirubin, INR

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33
Q

Chronic liver disease - what is hepatorenal syndrome?

A
  • Acute progressive kidney failure in decompensated cirrhosis
  • Due to inadequate hepatic breakdown of vasoactive substances, which lead to renal vasoconstriction
  • The kidneys attempt to conserve maximum salt and water, which produces highly concentrated urine with low sodium
  • Diagnosis of exclusion: after sepsis, obstruction, nephrotoxic drugs are excluded

Terlipressin:
- Synthetic vasopressin analogue
- Vasoconstriction in splanchnic circulation -> decreased portal blood inflow and portal HTN
- Circulation redistributed from splanchnic to systemic circulation -> improves renal perfusion

34
Q

Chronic liver disease - principles of management in cirrhosis?

A
  1. Treating underlying cause - alcohol abstinence, antiviral therapy, immunosuppression in autoimmune causes
  2. Surveillance for hepatoma or HCC - 6 monthly USG and AFP
  3. Surveillance for oesophageal varices - endoscopy, if present primary prophylaxis with beta-blockers
  4. Liver transplant
35
Q

Chronic liver disease - how do you manage ascites?

A
  1. No added salt diet (90mmol or 5.2g salt/day)
  2. Spironolactone 100-400mg/day as tolerated without excessive hyperkalaemia
  3. Frusemide 40-160mg/day
  4. Therapeutic abdominal paracentesis if all measures fail or persistent symptoms
  5. TIPS procedure may relieve portal HTN but carries high risk for encephalopathy
  6. Liver transplant is curative
36
Q

Ascites - causes and associated signs?

A

Causes:
- Liver cirrhosis with portal hypertension
- Malignancy e.g. GI, liver, ovarian, peritoneal mesothelioma (in the absence of stigmata of CLD)
- Congestive cardiac failure
- Nephrotic syndrome
- Tuberculous peritonitis
- Budd-Chiari syndrome, portal vein thrombosis
- Myxoedema
- Ovarian disease

Associated signs:
- Malnutrition or cachexia
- Lymphadenopathy
- Anaemia
- Stigmata of chronic liver disease
- Raised JVP, S3, peripheral oedema
- Abdominal scars or recent paracentesis
- Abdominal distension and umbilical eversion

37
Q

Ascites - initial investigations to determine cause?

A
  1. Abdominal paracentesis
    - Serum ascites albumin gradient (SAAG)
    - Transudate > 11g/L: portal HTN, CCF, hepatic/portal vein thrombosis, myxoedema
    - Exudate < 11g/L: malignancy, TB, pancreatitis
    - Cell count, gram stain and culture, cytology
  2. Abdomen ultrasound
    - Abdominal masses, splenomegaly
    - Hepatic and portal vein doppler to look for thrombosis
  3. Blood tests
    - FBC, LFT, clotting profile, RP, electrolytes
38
Q

Ascites - how to distinguish between transudative and exudative ascites?

A

Through the measurement of SAAG (serum-ascites albumin gradient):
> 11g/L indicates transudate
< 11g/L indicates exudate

39
Q

Ascites - what is the pathophysiology of ascites in cirrhotic liver disease?

A
  1. Cirrhosis is associated with systemic and splanchnic vasodilation
    - Reduced effective circulating volume
    - Activation of RAAS leading to renal vasoconstriction and water/salt retention
  2. Portal hypertension
    - Disruption of portal blood flow
  3. Hypoalbuminaemia
40
Q

Hepatomegaly - general causes?
Tender hepatomegaly causes?

A

General causes (top 3 commonest):
- CCF
- Malignancy: gastric, colon, HCC
- Lymphoproliferative disease: CLL, lymphoma
- Cirrhosis: alcohol, NASH, PBC
- Infections: malaria, HBV, HCV, EBV, CMV, toxoplasmosis, hydatid disease, amoebic abscess
- Infiltration: sarcoidosis, amyloidosis
- Vascular liver disease: Budd-Chiari syndrome, sickle cell

Tender hepatomegaly:
- Malignancy
- CCF
- Vascular liver disease: Budd-Chiari syndrome, sickle cell
- Alcoholic liver disease
- Chronic viral hepatitis

41
Q

Hepatomegaly - causes and clinical manifestations of Budd-Chiari syndrome?

A
  • Hepatic vein thrombosis
  • Caused by myeloproliferative disorders or thrombophilias
  • Abdominal pain, jaundice, hepatomegaly, encephalopathy
  • Diagnosis via doppler ultrasound hepatic vein
  • Treatment with anticoagulation and medical treatment of ascites
  • Thrombolysis, angioplasty, liver transplant considered in liver failure or encephalopathy
42
Q

Hepatomegaly - hepatic manifestations of sickle cell anaemia?

A
  • Cholelithiasis from pigment stones due to chronic haemolysis
  • Tender hepatomegaly due to sickle cell crisis
  • Cirrhosis from iron overload due to recurrent transfusions
  • Viral hepatitis contracted through recurrent transfusions
43
Q

Acute alcoholic hepatitis:
Histological features?
Scoring systems?
Management?

A

Histological features:
- Hepatic steatosis: fat accumulation in liver cells
- Acute inflammation and hepatocyte necrosis
- Hepatic cirrhosis

Scoring systems:
1. Maddrey’s discriminant function test
- Predicts prognosis and indication for steroid therapy
- 4.6 x PT + bilirubin
- Score > 32 carries 50% mortality rate + indicates steroid therapy

  1. Model for End stage Liver Disease (MELD)
    - Predicts 3-month survival and prioritise for liver transplant
    - Score between 6-40
    - Creatinine, dialysis Hx, bilirubin, INR

Management:
- Abstinence from alcohol
- Adequate nutrition
- Treatment of any infections
- Prednisolone 40mg for Maddrey’s score > 32
- Liver biopsy may be indicated to confirm diagnosis

44
Q

Splenomegaly - features and clinical signs?

A

The patient has splenomegaly / hepatosplenomegaly with anaemia / lymphadenopathy / RA.
In the absence of stigmata of chronic liver disease and portal hypertension, the most likely cause is myeloproliferative / lymphoproliferative disease / Felty’s syndrome.

Features:
- Asymptomatic, abdominal mass
- Fatigue
- Fever or febrile illness
- B symptoms: fever, drenching night sweats, weight loss
- Anaemia, thrombocytopaenia
- Pancreatitis

Clinical signs:
- Important negatives: anaemia, jaundice, lymphadenopathy, CLD, rheumatological disease
- Malnourished
- Excoriation marks: myelo/lymphoproliferative disease
- Splenomegaly: may be mild, moves with respiration, cannot get above, dull percussion note, not ballotable
- Traube’s space dull: between 6th rib and lower costal margin at mid axillary line
- Hepatomegaly
- Ascites: portal hypertension, not found in myelo/lymphoproliferative disease
- Hepatic encephalopathy
- Thalassaemia features: young, short stature, loss of body hair, hypogonadism, frontal bossing, maxillary overgrowth

45
Q

Splenomegaly - causes?

A

Commonest cause for isolated splenomegaly worldwide:
- Chronic malaria
- Visceral leishmaniasis (kala-azar)
- Schistosomiasis
- Lymphoproliferative disease

Generally:
- Liver cirrhosis with portal hypertension
- Myeloproliferative disease: CML, myelofibrosis, PRV (massive splenomegaly)
- Lymphoproliferative disease: CLL, lymphoma (+ lymphadenopathy and hepatomegaly)
- Thalassaemia or chronic haemolytic anaemia
- Infections: chronic malaria, above, EBV, CMV, HIV, IE
- Autoimmune: RA, SLE
- Infiltrative: amyloidosis, sarcoidosis
- Portal vein or splenic vein thrombosis

46
Q

Splenomegaly - characteristic chromosomal abnormality in CML?

A
  • Philadelphia chromosome: translocation 9:22
  • Cytogenetic study from bone marrow and peripheral blood to detect translocation 9:22
  • Molecular study to detect BCR-ABL gene -> for diagnosis and monitoring disease activity
47
Q

Splenomegaly - what is Felty’s syndrome?

A
  • Seropositive RA + splenomegaly + neutropaenia
  • Rare < 1%
  • Cause unknown
  • Complications: recurrent infections, hypersplenism (anaemia, thrombocytopaenia), cutaneous ulcerations
48
Q

Hepatosplenomegaly - features and clinical signs?

A

Features:
- Asymptomatic, abdominal mass
- Fatigue
- Fever or febrile illness
- B symptoms: fever, drenching night sweats, weight loss
- Anaemia, thrombocytopaenia
- Parkinsonism: tremors, falls, dysarthria

Clinical signs:
- Important negatives: anaemia, jaundice, lymphadenopathy, CLD
- Hepatosplenomegaly
- Ascites: portal hypertension, not found in myelo/lymphoproliferative disease
- Hepatic encephalopathy
- Xanthelasma, xanthomata, pigmentation, excoriation marks: PBC
- Parkinsonism, Kayser-Fleischer rings: Wilson’s disease
- Arthropathy: Haemochromatosis

49
Q

Hepatosplenomegaly - causes?

A
  • Liver cirrhosis with portal hypertension
  • Myeloproliferative or lymphoproliferative diseases
  • Infections: chronic malaria, visceral leishmaniasis (kala-azar), schistosomiasis
  • PBC
  • Haemochromatosis
  • Wilson’s disease
50
Q

Haemochromatosis - features and clinical findings?

A

Disease of iron accumulation, takes years to manifest!
Peak incidence in middle-age, more common in men.

Features:
- Early -> fatigue, arthralgia, gonadal dysfunction
- Later -> dark skin, type 1 DM, progressive liver disease
- Heart failure
- Hypothyroidism

Clinical findings:
- Bronze pigmentation
- Stigmata of chronic liver disease
- Hepatomegaly or liver mass
- Ascites -> from CCF or HCC
- CCF -> raised JVP, S3, peripheral oedema
- Small testes

51
Q

Haemochromatosis - complications?

A
  • Type 1 DM
  • Anterior hypopituitarism e.g. gonadal dysfunction, hypothyroidism
  • Cardiomyopathy - restrictive or dilated
  • Liver cirrhosis
  • Hepatocellular carcinoma
  • Arthropathy
52
Q

Haemochromatosis - investigations?

A

Confirm iron overload:
- Iron studies, ferritin, transferrin saturation > 45%
- Liver biopsy may be considered if abnormal LFTs

Confirm haemochromatosis:
- Genetic testing for HFE gene mutation

Others:
- HbA1c
- ECHO to assess LV function, cMRI to detect myocardial iron deposition
- AFP and 6 monthly USG surveillance for HCC

53
Q

Haemochromatosis - treatment?

A
  • MDT approach given the multiorgan involvement e.g. cardio, endocrine, primary physicians, dietician
  • Avoid iron supplement
  • Avoid or abstain altogether from alcohol -> may accelerate liver cirrhosis
  • Phlebotomy to maintain TSAT < 50% -> improves DM, fatigue, skin pigmentation BUT NOT hypogonadism and cirrhosis
  • Iron chelation therapy e.g. desferrioxamine
  • Liver transplant in advanced cirrhosis or HCC
54
Q

Haemochromatosis - genetics?

A
  • Autosomal recessive
  • C282Y (HFE gene) and H63D mutations in 90% cases, which affects iron metabolism
  • Other mutations may be responsible esp in non-Caucasian populations
55
Q

PBC - features and clinical findings?

A

Middle-age, more common in women.

Features:
- Asymptomatic, abnormal LFTs or high cholesterol
- Excessive fatigue
- Intense itching
- RUQ pain

Clinical findings:
- Jaundice
- Xanthelasma, xanthomata
- Excoriation marks
- Hepatosplenomegaly
- Chronic liver disease
- Other autoimmune disease features: RA, SLE, scleroderma, Grave’s, Sjogren’s

56
Q

PBC - investigations?

A
  • Anti-mitochondrial antibody (AMA)
  • Cholestatic picture: raised ALP, bilirubin, GGT, maybe ALT
  • USG, ERCP or MRCP: exclude extra-hepatic cholestasis
  • Liver biopsy usually not needed if evidence of cholestasis and positive AMA
57
Q

PBC - treatment?

A
  • Avoid alcohol
  • Fat-soluble vitamin supplementation: ADEK
  • Ursodeoxycholic acid: reduce cholestasis and improve LFT
  • Cholestyramine: reduce circulating bile acids and improve pruritus
  • Liver transplant: abnormal LFTs, refractory pruritus or fatigue, encephalopathy, recurrent infections
58
Q

Wilson’s disease - clinical manifestations?

A

Copper accumulation, presents in 2nd decade of life.

  • CNS: Parkinsonism, dystonia, choreoathetosis, ataxia
  • Ophthal: Kayser-Fleischer rings
  • Cardio: cardiomyopathy
  • Liver: cirrhosis, hepatitis
  • Renal: RTA, nephrocalcinosis
  • MSK: chondrocalcinosis, arthropathy
  • Psychiatric: personality change, emotional lability, intellectual impairment, psychosis
  • Haematological: haemolytic anaemia (rare)
59
Q

Wilson’s disease - genetic basis?

A
  • 7B mutation gene
  • Copper accumulation in liver, with eventual spill-over into blood and urine
60
Q

Wilson’s disease - biochemical features and limitations of these tests?

A
  • High urine copper and low serum caeruloplasmin (copper-containing enzyme)
  • Both are acute phase reactants
  • Levels should be interpreted in the context of patient’s clinical condition
61
Q

Abdominal mass - features, approach and clinical signs?

A

The patient has a LUQ mass, most likely gastric or colonic in origin. The presence of cachexia and lymphadenopathy raises the suspicion of malignancy.
The patient has a RLQ mass, most likely colonic in origin. The presence of clubbing, oral ulceration and abdominal tenderness suggests an inflammatory mass due to Crohn’s disease.

Features:
- Asymptomatic, incidental abdominal mass
- Non-specific symptoms: lethargy, weight loss
- IBD symptoms

Approach:
- Location, size, consistency, regular/irregular border, mobility, tender
- Ballotable? Can get above?
- Pulsatile?
- Percussion note
- Auscultation: bruit or bowel sounds

Clinical signs:
- Important negatives: anaemia, jaundice, lymphadenopathy, CLD
- Cachexia
- IBD: clubbing, oral ulcers, Cushingoid features from steroid therapy
- Hepatosplenomegaly: lymphoma or malignancy
- Ascites: malignancy

62
Q

Abdominal mass - cause of epigastric mass?

A
  • Malignancy: gastric or pancreatic
  • Abdominal aortic aneurysm
  • Lymphoma
  • Caudate lobe of liver
63
Q

Abdominal mass - cause of RUQ mass?

A
  • Malignancy: colonic, gastric, hepatic
  • Hepatomegaly
  • Gallbladder
  • Kidney
64
Q

Abdominal mass - cause of LUQ mass?

A
  • Malignancy: colonic, gastric, pancreatic
  • Pancreatic mass
  • Splenomegaly
  • Kidney
65
Q

Abdominal mass - cause of RLQ mass?

A
  • Crohn’s disease
  • Malignancy: caecal Ca, ileal lymphoma or carcinoid
  • Ileocecal mass: TB, abscess, appendicular mass
  • Ovarian tumour
  • Renal transplant
66
Q

Abdominal mass - cause of LLQ mass?

A
  • Diverticular mass/abscess
  • Malignancy: sigmoid Ca
  • Ovarian tumour
  • Renal transplant
67
Q

Abdominal mass - inherited conditions predisposing to colorectal cancer?

A
  • Hereditary non-polyposis colorectal Ca (HNPCC)
  • Familial adenomatous polyposis (FAP)
  • Peutz-Jeghers syndrome

All autosomal dominant inheritance

68
Q

Abdominal mass - common small intestinal tumours?

A
  • Neuroendocrine tumours
  • Gastrointestinal stromal tumours
  • Lymphoma
  • Adenocarcinoma commonly in duodenum: associated with coeliac disease, Crohn’s disease, polyposis syndromes
69
Q

IBD - features and clinical signs?

A

Features:
- Bloody diarrhoea
- Vomiting
- Abdominal pain
- Fever, weight loss
- Anaemia
- Arthritis
- Skin lesions

Clinical signs:
- Malnourished
- Cushingoid
- Clubbing
- Small and large joint arthropathies, sacroiliitis
- Uveitis
- Oral ulcers
- Pyoderma gangrenosum, erythema nodosum
- Peripheral oedema
- Laparotomy scar: hemicolectomy, colectomy
- Stoma: RIF (ileostomy), LIF (colostomy)
- RIF mass: acute exacerbation of Crohn’s disease
- Fistulating perianal ulcers

70
Q

IBD - how to differentiate between Crohn’s disease and ulcerative colitis?

A

Site and extent of inflammation

Crohn’s
- Physical: RLQ mass, perianal fistulas or ulcers
- Fat malabsorption and vit ADEK deficiency
- Site: anywhere along GI tract from mouth to anus, characterised by skip lesions
- Extent: transmural inflammation
- Histology: granuloma

Ulcerative colitis
- Site: exclusively colon
- Extent: superficial inflammation in the mucosa
- Histology: crypt abscess

71
Q

IBD - what are Truelove and Witts criteria?

A

Used to classify severity of symptoms during IBD exacerbations.
Systemic features: fever, tachycardia, anaemia.

Mild: < 4 loose stools/day, no systemic features, normal ESR
Moderate: > 4 loose stools/day, mild systemic features
Severe: > 6 loose stools/day, systemic features, ESR > 30

72
Q

IBD - treatment strategies for Crohn’s disease?

A

Principle: Induce remission then once achieved, change to maintenance therapy to prevent relapses. Treat concomitant infections.

  • 5-aminosalicylic acid e.g. mesalazine high dose 4g/day for mild disease, topical for distal disease
  • Steroid e.g. prednisolone 40mg/day or IV hydrocortisone 400mg/day for moderate-severe disease
  • Steroid-sparing agents e.g. azathioprine for maintenance
  • Infliximab or surgery for steroid refractory or fistulating disease
  • Metronidazole or ciprofloxacin for infections
  • Smoking cessation
73
Q

IBD - when do you initiate a patient with Crohn’s disease on anti-TNF therapy?

A
  • Steroid refractory disease
  • Fistulating disease

All 3 criteria:
- Severe active Crohn’s disease
- Refractory to steroids or steroid-sparing agents or intolerant to these meds
- Surgery is inappropriate: diffuse disease or short bowel

74
Q

IBD - management of acute colitis?

A

Principle: Induce remission then once achieved, change to maintenance therapy to prevent relapses. Treat concomitant infections.

  • Steroid oral or IV
  • 5-ASA oral or topical
  • Antibiotics
  • Adequate hydration + IV fluids to replenish losses
  • Close monitoring for toxic megacolon: if suspect this, high dose IV steroids to reduce inflammation + bowel decompression
  • Consider surgery if medical therapy failed
75
Q

IBD - when is ciclosporin considered in acute exacerbation of ulcerative colitis?

A
  • No improvement in the first 3 days of high-dose steroid therapy
  • Ciclosporin dose 2mg/kg/day
76
Q

IBD - when would surgery be considered?

A
  • Immediate surgical referral when there is toxic megacolon (colon > 5.5cm, caecum > 9cm)
  • Failure to respond to 3 days of intensive treatment (stools > 8x/day, raised ESR/CRP)
  • Failure to respond to 10 days of intensive treatment in ulcerative colitis exacerbations
77
Q

IBD - what is sclerosing cholangitis?

A
  • Describes chronic inflammation of the bile ducts, leading to scarring, biliary obstruction, chronic liver disease, liver failure
  • Can occur as a primary condition with an autoimmune cause (PSC) or in association with IBD particularly ulcerative colitis
  • ANA, p-ANCA, ASMA
  • Treatment: fat-soluble vitamin supplementation, biliary stenting, liver transplant
  • Screening for cholangiocarcinoma
78
Q

Nephrotic syndrome - definition and clinical features?

A
79
Q

Nephrotic syndrome - causes?

A
80
Q

Nephrotic syndrome - complications?

A

PACES (7 decks)

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