Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PACES > Abdominal > Flashcards

Abdominal Flashcards

1
Q

Causes of Chronic liver disease

A
  • Alcoholic liver disease
  • Non-alcoholic steatohepatitis
  • Viral hepatitis
  • Immune mediated:
    o PBC
    o PSC – Anti mitochondrial Ag and elevated IgM
    o Autoimmune hepatitis
  • Metabollic:
    o Haemochromatosis
    o Wilson’s disease
    o Alpha 1 anti trypsin
  • Drugs: methotrexate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Investigation approach CLD

A
  • History
    o PMH
    o Drugs
    o Alcohol
    o Travel
    o Family
  • Bloods: FBC, U&E, LFT, Coag, BBV screening, ferritin and cereuloplasmin, autoAb screen
    o Auto Ab: ANA, Anti mitochondrial Ab, Smooth muscle Ab, LKM Ab
    o Tumour markers: AFP (HCC)
  • US Abdo
  • ?CT
  • ?Biopsy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Presentation, Auto Ab and complications and management of PBC

A
  • May present with chronic liver disease
  • More commonly present with fatigue and pruritis
  • Complications: CLD and cirrhosis, link with HCC
  • Management: Ursodeoxycholic acid (relieve symptoms and improve prognosis)
    o Ultimately the only other treatment is transplant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Presentation of ADPKD

A

-Most people diagnosed through screening programme for relatives of affected patients (most people asymptomatic until 40s)
- Hypertension
-Polyuria/nocturia due to urine concentrating defect
- Signs and symptoms renal failure/seen on blood test
- Proteinuria/haematuira
- Extra-renal manifestations such as pancreatic cysts/liver cysts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Extra renal manifestations of ADPKD

A
  • HTN
  • Cysts in other organs: liver, pancreas, seminal vesicles, spleen (but these are all mostly asymptomatic)
  • Cerebral aneurysms (intracerebral haemorrhage or SAH) - if positive Fhx more likely
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Types of ADPKD and inheritance of them

A
  • Autosomal dominant
  • 2 main genetic mutations: 85% mutation on Chr 16, remaining on Chr 4, small amount have no detectable genetic mutations
  • ADPKD 1: mutation on Chr 16, more severe, progressions to ESRF in 50s
  • ADPKD 2: mutation on Chr 4, tends to be less severe, later onset, less cysts and later progression to RF
    (- Do also have infantile polycystic kidney disease which is recessive and less common and liver cysts more commonly occur in this one )
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Management of ADPKD and indications for nephrectomy

A

Management:
- Largely preventative
- Aggressive control of BP with an ACEi
- Statin to control hyperlipidaemia
- High fluid, low salt diet
- Early phases vasopressin2 receptor antagonists may be of use (slow progression of cysts and to ESRF but specific criteria to meet under NICE approval)
- Later stages RRT
Indications for nephrectomy:
- Ideally avoid it but sometimes need it
- Make space for a donor kidney (don’t always, ideally leave in place)
- Chronic pain or chronic infection
- Progression to malignancy
- Large/problematic haematuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Waffle about the side effects of immunosuppression in transplant patients?

A
  • Increased risk malignancies – especially skin
  • Steroids – thin skin, easy bruising, fat redistribution
  • Ciclosporin – gum hypertrophy, hirsuitism, HTN, tremor, diabetes
  • Tacrolimus – tremor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are some of the possible barriers to renal transplant?

A

o Donor matching – no available donor
o Malignancy
o Ongoing vasculitis
o Ongoing deep seated infection
o Severe obesity – technical ability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the 3 most common causes of end stage renal failure?

A

Hypertension
Diabetes
Glomerulonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Key management of ALD?

A
  • Alcohol cessation with MDT
  • Pabrinex
  • Alcohol withdrawal therapy with chlordiazepoxide
  • Gastroscopy to look for varices if evidence of cirrhosis
    o Only use endoscopic therapy if a history of haemorrhage
  • Chronic pancreatitis should be considered
    o Combination of faecal elastase, serum albumin, vitamin D and magnesium gives an indication
    o Pancreatic enzyme replacement with creon with a PPI will affect prognosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How do you calculate the SAAG and what are the causes of low and high?

A

o SAAG: Serum ascites albumin gradient ((serum albumin)-(ascites albumin))
>1.1g/dl = portal HTN or low albumin or Meig’s syndrome
<1.1g/dL = peritoneal carcinomatosis, TB, pancreatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What tests can you do on ascites?

A

WCC (neutrophils >250/mm cubed) indicates abx
Gram -ve stain
ZN stain
Cytology
Albumin
Lipase/amylase
Glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What type of dialysis tends to be used in ADPKD and why?

A
  • Haemodialysis more likely
  • Peritoneal dialysis avoided as requires a lot of fluid in the abdomen which along with the bulk of polycystic kidneys can cause discomfort and peritoneal dialysis also increases the risk of cyst infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the poor prognostic indicators of PKD and what is the most common cause of mortality?

A
  • Poor prognostic features:
    o Declining eGFR
    o Proteinuria
    o Early symptoms onset
    o Male gender
    o eGFR correlates with increasing kidney size and cyst volume
    o Risk of HTN increases with age
     Most hypertensive by time of eSRF
    o Most die from cardiac causes
    o 10% have cerebral saccular aneursyms, with HTN sign
    o Renal cancer not common sequelae
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the causes of splenomegaly?

A

Causes of splenomegaly:
- Infiltration:
o Myeloproliferative disorder
o Lymphoproliferative disorders
o Lymphomas
o Amyloidosis
o Sarcoidosis
o Gaucher’s lipid storage disease
o Thyrotoxicosis
- Increased function – removal of defective red cells
o Spherocytosis
o Thalassemia
o Nutritional anaemias
o Early sickle cell
- Immune hyperplasia in response to infection:
o Chronic malaria
o Visceral leischmaniasis (kala-azar)
o Glandular fever
o Subacute bacterial endocarditis
o Brucellosis
o Viral hepatitis
- Disordered immune regulation
o Felty’s syndrome – RA, neutropenia and splenomegaly
o SLE
o Sarcoidosis
- Abnormal flow
o Cirrhosis
o Hepatic or portal vein obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the causes of massive splenomegaly?

A

Causes of massive splenomegaly:
- Chronic myeloid leukaemia
- Myelofibrosis
- Gaucher’s storage disease
- Chronic malaria
- Kala-azar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is hereditary spherocytosis and how is it diagnosed and managed?

A
  • Autosomal dominant condition
  • Type of congenital haemolytic anaemia
  • Diagnosed by osmotic fragility test, confirmed by flow cytometry
  • Small dark red cells with loss of central pallor
  • Increased reticulocytes
  • Splenectomy for mod to severe disease but not in mild disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

3 most common conditions requiring liver transplant?

A
  • Cirrhosis
  • Hepatocellular carcinoma
  • Fulminant liver failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the variant syndromes which can require liver transplant?

A
  • Diuretic resistant ascites
  • Intractable pruritis
  • Hepato-pulmonary syndrome
  • Chronic hepatic encephalopathy
  • Polycystic liver disease
  • Recurrent cholangitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is your waffle for work up and selection for liver transplant?

A
  • MDT approach
  • Cautions and contraindications to consider would include - IVDU, ongoing alcohol XS, significant medical or psychiatric conditions which may impact on survival
  • Need to have a projected 5y survival of 50% or more
  • For CLD need to have a UK End stage liver disease score of 49 or more
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the indications for acute transplant in paracetamol OD?

A

 pH <7.25 24h after OD and after fluid resus
 INR >6.5 or PT >100 secs
 Creatinine >300 or anuria
 Encephalopathy grade 3-4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the definition of acute liver failure?

A
  • Multisystem disorder in which severe acute liver dysfunction with encephalopathy within 8 weeks of onset of symptoms with no evidence of underlying chronic liver disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the complications post liver transplant?

A
  • In the acute phase higher risk of rejection
  • Risks also associated with immunosuppression:
    o Infection
    o Malignancy – skin and lymphoproliferative disorders
    o Metabolic syndrome commonly develops
    o Can’t have live vaccines
  • Renal issues:
    o Acute and chronic renal disease common for a multitude of reasons:
     Calcineurin inhibitors
     Diabetes
     HTN
  • Hepatobiliary complications:
    o Acute or chronic rejection
    o Biliary leak or stricture
    o Recurrence of primary liver disease may occur
     Viral hepatitis, primary biliary cirrhosis or budd chiari syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are the possible causes of ascites?

A
  • Vascular:
    o Liver disease with portal HTN
    o CCF
    o Constrictive pericarditis
    o Budd chiari
  • Low albumin
    o Nephrotic syndrome
    o Protein losing enteropathy
  • Peritoneal disease
    o Meig’s syndrome – benign ovarian tumour, pleural effusion and ascites
    o Infectious peritonitis – TB/fungal
    o Malignancy – ovarian/GI
  • Miscellaneous
    o Pancreatic leak
    o Peritoneal dialysis related ascites
    o Advanced hypothyroidism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the management of haemochromatosis?

A
  • Regular venesection – weekly or fortnightly until ferritin 20-30 and transferrin saturation <50%
  • Then maintenance venesection
  • Abstinence from alcohol
  • Manage complications
    o DM
    o Cardiomyopathy
    o Liver cirrhosis
27
Q

How may haemochromatosis present?

A

Presentation
- Screening of affected relatives
- Asymptomatic with raised ferritin
- Typical triad of arthralgia, lethargy sexual dysfunction
- Arthralgia
o Typically in MCPJs
o Squaring of joints
o Differentiated from OA on XR by presence of chondrocalcinosis
- Sexual dysfunction
o Testicular and anterior pituitary iron deposition
- Lethargy
- Late features:
o T1 Diabetes
o Cardiomyopathy
o Liver cirrhosis
o Bronze pigmentation to skin

28
Q

What is involved in the screening tests for haemochromatosis?

A
  • Undertaken in patients with affected first degree relative
  • Ferritin >200 females, >300 males
  • Also transferrin saturation >40% females >50% males
  • Then confirm with HFE gene defect screen – but there is variable penetrance so not everyone with defect will have phenotype of the disease
29
Q

What is the inheritance of haemochromatosis?

A
  • Autosomal recessive
  • Usually HFE gene on Chr 6 short arm
30
Q

What bedside tests would you perform after haemochromatosis diagnosis?

A

o ECG – AF and other arrythmias
o Urinalysis – glucosuria
- Initial bloods
o FBC ?polycythaemia
o LFTs – but because iron deposition is not inflammatory cirrhosis can still occur with normal transaminases
o INR – liver synthetic function
o Fasting glucose/HbA1c
o AFP – HCC suspected or patient at risk

31
Q

What blood tests findings in haemochromatosis would prompt referral to hepatology for assessment of fibrosis?

A
  • If ferritin >1000 and any with raised transaminases need to refer to hepatology for fibrosis assessment and exclusion of cirrhosis
32
Q

What imaging may be done in a patient diagnosed with haemochromatosis?

A
  • Echo ?dialted cardiomyopathy
  • Plain films of joints - ?chrondrocalcinosis/squaring of MCPs
  • If have cirrhosis then need 6 monthly US and AFP
  • Elastography used to assess those that need a biopsy which can assess severity of fibrosis
33
Q

How is ADPKD investigated if suspected and as diagnosis of ADPKD made?

A

Imaging
- If no Fhx need 10 or more cysts on each kidney
- If +ve Fhx then number of cysts depends on age
In equivocal cases can use genetic testing

34
Q

What would be the differentials for loin pain in ADPKD?

A
  1. Cyst rupture
  2. Cysts haemorrhage
  3. Renal stones
  4. Infection
  5. Cyst enlargement causing renal capsule pain
35
Q

How does hereditary spherocytosis present?

A
  • Variable age may be asymptomatic for years, most have mild to mod haemolysis
  • Classic triad: anaemia, jaundice and splenomegaly
  • Neonatal jaundice
  • Later in adults anaemia/lethargy/gall stones
  • May be screening of relatives
  • Tend to get more haemolysis in infections/pregnancy, esp. infectious mononucleosis where you get a transient splenomegaly
36
Q

What is the inheritance pattern and pathophysiology of hereditary spherocytosis?

A
  • Autosomal dominant
  • Caused by a defect in one of 5 genes encoding for proteins in the red bloods cell membrane
  • Most common defect on Chr 8
  • Gene defects in RBC produce abnormal red cells which are spherocyte shaped rather than bi-concave
  • Abnormal red cells have a shortened lifespan and undergo haemolysis – mainly in spleen, this is basically why it eliminates haemolysis and anaemia
37
Q

What are the investigations in hereditary spherocytosis?

A
  • FBC – reticulocyte count and MCH
  • Haemolysis screen – high LDH, low or absent haptoglobin, high unconjugated bilirubin
  • Blood film – spherocytes and haemolysis
  • Coombs test – to exclude immune mediated haemolysis
  • EMA binding test – dye which binds to red cell membrane proteins, reduced fluorescence detected by flow cytometry
  • If EMA not available can do osmotic fragility test which tests resistance to haemolysis – less sensitive and specific
37
Q

What are the complications of hereditary spherocytosis?

A
  • Aplastic crises – due to infection
  • Anaemia – blood transfusion
  • Pigment gall stones – might be presenting problems, ½ have gallstones
38
Q

What is the management of hereditary spherocytosis?

A
  • No therapy to target faulty membrane protein
  • All have folic acid as increased requirment with increased red cell production– esp if pregnant
  • Treat complications
  • Anaemia – serial blood transfusions
  • Cholecystectomy for gallstones
  • Mod-severe get splenectomy (vaccinations, esp meningococcal, pneumococcal and influenza, and prophylactic antibiotics)
39
Q

Investigations in coeliac disease?

A
  • FBC and haematinics
  • WCC – any sign of infection
  • Baseline renal and liver function
  • Anti TTG Ab test, screen for other auto-immune conditions such as thyroid conditions so do a TSH
  • If TTG is borderline – check if on gluten diet or not (if not then might be low)
  • Endoscopy and biopsy from D2 looking for subtotal or total villous atrophy
40
Q

Management of coeliac disease?

A
  • Avoidance of gluten – wheat, rye and barley
  • May need dietician
41
Q

Aim of a combined kidney pancreas transplant and indications?

A
  • Effective for selected pts with poorly controlled diabetes and related ESRF
  • Typically received by T1 diabetics but increasingly being offered to T2 diabetics who are insulin dependent and meet certain criteria
  • Decision for transplant made by combo of MDT outcome and pt choice
  • Improved quality of life: free of dialysis, insulin therapy
  • Reduces some diabetic complications: prevents recurrence of diabetic nephropathy, diabetic neuropathy is static or improves, effect on retinopathy not yet clear
42
Q

Types of renal transplant and combined kidney pancreas transplant? Comparison of outcomes generally?

A
  • Live or deceased doner
  • Live: related or altruistic
  • Cadaveric: can be donated after circulatory death or neurological death
  • A combined pancreas kidney transplant will be from a deceased donor after neurological death or live donor kidney and a separate deceased donor pancreas
  • For isolated renal transplant live kidney has better results that deceased donor kidney (donor and recipient can be bought together in same hospital reducing handling time of organ and warm and cold ischaemic time hopefully leading to better graft function)
  • Combined cadaveric kidney and pancreas transplant has improved 10y survival for compared to a cadaveric kidney alone
  • Outcome from an isolated liver donor kidney is equal to a deceased donor combined kidney pancreas transplant up to 10y but outcomes from a combined transplant are superior beyond that
43
Q

Isolated pancreas transplant types and indications?

A
  • Isolated deceased donor pancreatic transplant or islet cell transplantation for T1DM or the latter for patients with chronic pancreatitis requiring total pancreatectomy
  • For islet cell transplantation:
    o In T1DM at least 500,000 cadaveric islets infused into portal vein
    o Chronic pancreatitis get infusion of own cells– no immunosuppression needed
  • Pancreas transplant versus islet cell transplantation:
    o No RCTs comparing
    o Higher rate insulin independence from pancreas transplantation but higher morbidity related to surgery
  • 3-5y follow up 60% have almost normoglycaemia
44
Q

Complications of pancreatic transplant?

A
  • Acute rejection of isolated transplanted pancreas is common in 60-80% and can occur within days
  • Intensive immunosuppression then needed
  • Less rejection of combined kidney pancreas transplant – pancreas rejection lags behind kidney rejection which can be easily monitored by blood tests
  • Technical graft failure in 5-7%, primarily graft thrombosis
  • Graft pancreatitis
  • Infection
45
Q

Placement of pancreatic transplant anatomically and monitoring?

A
  • Pancreas placed in pelvis usually still attached to duodenal portions and attached to SB or bladder
  • If attached bladder can do urinary lipase monitoring for allograft transplant rejection but can get complications of frequent UTIs and reflux pancreatitis
  • Native pancreas remains in situ
46
Q

How is ascites managed (not investigated)?

A
  • Initially treated with fluid restriction and diuresis
  • Can be drained if uncomfortable or causing respiratory distress or CV compromise
  • Ascitic drain – HAS with every 2-2.5L drained
  • Refractory to drainage – TIPS or liver transplant
  • Problems with TIPS in this:
    o Coagulopathy
    o 5-10% become encephalopathic following this
47
Q

In addition to liver cirrhosis what are some of the other complications of alcohol excess?

A
  • Dilated cardiomyopathy
  • HTN
  • Pancreatitis
  • UGI cancer
  • Peptic ulceration
  • Cerebellar atrophy
  • Polyneuropathy
  • Wernickes encephalopathy
  • Korsakoffs sydnrome
48
Q

What are the grades of hepatic encephalopathy and how would you assess for them?

A
  • Assess for asterixis
  • Assess for constructional dyspraxia by asking to draw a 5 pointed star
  • Grades:
    o 1 = alterations in behaviour, mild confusion, disordered sleep
    o 2 = lethargy, asterixis, moderate confusion
    o 3 = somnolent but rousable
    o 4 = coma
49
Q

What prognostic scoring systems can be used in liver cirrhosis?

A
  • Most common is Child-Pugh combines:
    o Presence of ascites
    o Presence of encephalopathy
    o INR, bilirubin and albumin levels
  • MELD score exists
50
Q

In addition to chronic liver disease what are some of the other causes of gynaecomastia?

A
  • Relative deficiency of androgen or excess of oestrogens, happens physiologically during puberty or end of male reproductive life span
  • Testicular atrophy
  • Aldosterone excess
  • Drugs such as spironolactone or digoxin
51
Q

Causes of pancreatitis?

A

Common causes:
- Alcohol
- Gall stones
Other:
- Trauma
- ERCP
- Drug related – steroids or azathioprine
- Smoking
- Hypertriglyceridaemia
- Hypercalcaemia
- Auto-immune pancreatitis IDD4
Genetics:
- CF
- Mutations in PRSS1 gene (most common cause of hereditary, AD inheritance)
- SPINK1 is another gene mutation which can cause it

52
Q

Blood tests for hereditary pancreatitis in young people with no other clear cause?

A
  • Testing for PRSS1 mutation
  • CFTR
  • Testing for SPINK1
53
Q

What are the complications of pancreatitis?

A
  • Development of chronic pancreatitis and its own complications
    o Type 3 diabetes
    o Pancreatic ductal structuring – painful and insufficiency (can do ERCP stenting or sometimes Whipple’s procedure)
    o Compressive biliary obstruction – stent or surgical bypass
    o Duodenal stricturing
    o Increased risk of pancreatic malignancy
  • Portal vein thrombosis
  • Splenic vein thrombosis
  • Pseudocysts after acute inflammatory event – compressive effects, duodenal, biliary or pancreatic compression
    o Drain with endoscopic approach using EUS
    o Axios stent might be used – tends to be performed 6/52 after presentation of pancreatitis (as many will resolve within 6/52)
54
Q

Management of chronic pancreatitis?

A
  • Mainstay of treatment avoiding things which cause flares – no smoking or alcohol
  • Treat cause, analgesia, treat associated low vit D, treat exocrine insufficiency with creon and PPI
55
Q

How do we assess for exocrine insufficiency in chronic pancreatitis?

A
  • Assessment for insufficiency:
    o Ask about symptoms of diarrhoea and weight loss
    o BMI
    o FBC, albumin, Mg and Vit D
    o Faecal elastase – only low in mod to severe insufficiency so normal test doesn’t exclude
    o Breath test does exist but not yet widely available
    o Mg levels are most helpful in insufficiency
56
Q

How is pancreatic insufficiency in chronic pancreatitis treated?

A

o 75-125,000U before or during meals, 50-75000 units between snacks (mainly get 25000 capsules)
o Concomitant use PPI essential to prevent acid breakdown of creon in stomach
o Healthy balanced diet not low fat

57
Q

Difference between complicated and uncomplicated UTI?

A
  • Uncomplicated:
    o Women with no structural abnormality to the urinary tract system
  • Complicated:
    o Male
    o Patients with structural abnormalities to the urinary tract
58
Q

Difference between ileostomy and colostomy?

A

Ileostomy - tends to be RIF, spouted and liquid contents
Colostomy - tends to be LIF, flush to skin and more solid contents

59
Q

Investigation of a patient with IBD?

A
  • U&E, Mg, Adj Ca – electrolytes, imbalance and also renal function
  • Vitamin levels such as B12 and folate to look for evidence of malabsorption
  • Albumin – nutritional status
  • LFTs – related biliary disease,
  • Inflammatory markers – disease flare
  • Stool cultures
  • AXR – bowel dilatation or toxic megacolon
  • Endoscopy to get biopsy of large bowel (CD versus UC)
60
Q

Waffle for the difference between CD and UC?

A
  • UC – affects predominantly large bowel and rectum and only affects the mucosa. Can get lead piping fibrosis not seen in CD.
  • CD – any part of GIT and get perianal disease (fistulas) and causes transmural inflammation. Can get formation of fistulas.
61
Q

Indications for surgery in IBD?

A
  • Elective:
    o Manage chronic active symptoms despite max medical Rx
    o Structures and fistulas
  • Emergency:
    o Tosic megacolon
    o Haemorrhage
    o Perforation
62
Q

Medical therapy used in UC?

A
  • Aminosalicylates can be used for both inducing and maintaining remission
  • Oral steroids can be used in the acute phase to induce remission but not as maintenance
  • For patients with acute severe UC IV steroids (IV hydrocortisone 100mg QDS) is used
  • For patients who do not maintain remission with aminosalicylates can use other drugs such as azathioprine or biologic therapy

PACES (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions