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GI Flashcards

1
Q

Risk of which cancer increases following renal transplantation?

A

squamous cell carcinoma of the skin

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2
Q

What organism causes peritonitis secondary to peritoneal dialysis?

A

Staphylococcus epidermis

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3
Q

What is Henoch-Schonlein purpura?

A

IgA mediated small vessel vasculitis
Seen in children following an infection

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4
Q

What are the H causes of acute pancreatitis in GET SMASHED?

A

hypertriglyceridemia
Hyperchylomicronaemia
Hypercalcaemia
Hypothermia

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5
Q

What are features of Granulomatosis with polyangiitis/Wegener’s granulomatosis?

A

Upper respiratory tract: epistaxis, sinusitis, nasal crusting
Lower respiratory tract: dyspnoea, haemoptysis
Rapidly progressing glomerulonephritis
Saddle-shape nose deformity
Others: vasculitis, rash, eye involvement, cranial nerve lesions

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6
Q

What are the features of hyperacute rejection of a transplant?

A

Due to pre-existing antibodies against ABO or HLA antigens
An example of a type II hypersensitivity reaction
Leads to widespread thrombosis of graft vessels -> ischaemia and necrosis of the transplanted organ
No treatment is possible and the graft is removed

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7
Q

What are the features of acute graft failure?

A

occurs before 6 months
usually due to mismatched HLA - cell-mediated (cytotoxic T cells)
usually asymptomatic and is picked up by a rising creatinine, pyuria (pus in urine) and proteinuria
Other causes include CMV infection
May be reversible with steroids and immunosuppressants

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8
Q

What is given as prophylaxis for hepatic encephalopathy?

A

lactulose first-line with the addition of rifaximin

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9
Q

What is the most common renal malignancy?

A

renal cell carcinoma - an adenocarcinoma of the renal cortex

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10
Q

What is Budd-Chiari syndrome?

A

hepatic vein thrombosis - seen in the context of underlying haematological disease

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11
Q

What are the causes of Budd-Chiari syndrome?

A

polycythaemia rubra vera
thrombophilia
pregnancy
COCP

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12
Q

What are the features of Budd-Chiari syndrome?

A

abo pain - sudden onset, severe
ascites
tender hepatomegaly

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13
Q

What is the initial investigation if you suspect Budd Chiari syndrome?

A

ultrasound with Doppler flow studies

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14
Q

What is used to treat acute episodes of alcoholic hepatitis?

A

steroids e.g. prednisolone

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15
Q

What is the management for RCC?

A

for confined disease - partial or total nephrectomy - patients with a T1 tumour < 7cm in size are typically offered a partial nephrectomy

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16
Q

What are the features of primary sclerosing cholangitis?

A

cholestasis: jaundice, pruritus, raised bilirubin + ALP
right upper quadrant pain
fatigue

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17
Q

what is primary sclerosing cholangitis?

A

biliary disease of unknown aetiology characterised by inflammation and fibrosis of intra and extra-hepatic bile ducts

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18
Q

what is typically seen on x-ray in sigmoid volvulus?

A

large bowel obstruction: large, dilated loops of colon, often with air-fluid levels
coffee bean sign

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19
Q

What are the complications of laparoscopy?

A

general risks of anaesthetic
vasovagal reaction e.g. bradycardia in response to abdo distention
- extra-peritoneal gas insufflation - surgical emphysema
- injury to GI tract
- injury to blood vessels e.g. common iliacs, deep inferior epigastric artery

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20
Q

What feature is most suggestive of Wilson’s disease?

A

serum caeruloplasmin is decreased

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21
Q

What are the investigation findings in alcoholic hepatitis?

A

gamma-GT is characteristically elevated
Ratio of AST:ALT is normally >2, a ratio >3 is strongly suggestive of acute alcoholic hepatitis

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22
Q

What is acute intermittent porphyria?

A
  • deficiency of one of the enzymes needed to synthesize haem
  • build up can cause acute attacks of severe abdominal pain, with vomiting, hypertension, tachycardia
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23
Q

How does acute intermittent porphyria present?

A

abdo: abdo pain, vomiting
neurological: motor neuropathy
psychiatric: depression
hypertension and tachycardia common

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24
Q

What is small bowel bacterial overgrowth syndrome?

A

disorder characterized by excessive amounts of bacteria in the small bowel resulting in GI symptoms

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25
Q

what are risk factors for small bowel bacterial overgrowth syndrome and how does it present?

A

risk factors:
- neonates with congenital GI abnormalities
- scleroderma
- diabetes mellitus

features:
- chronic diarrhoea
- bloating, flatulence,
- abdo pain

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26
Q

hhow is small bowel bacterial overgrowth syndrome diagnosed?

A
  • hydrogen breath test
  • small bowel aspiration and culture
  • clinicians may sometimes give a course of abx as a diagnostic trial
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27
Q

how do you calculate an anion gap?

A

(sodium + potassium) - (bicarb + chloride)

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28
Q

what is a normal anion gap?

A

8-14 mmol/l

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29
Q

what are causes of a normal anion gap metabolic acidosis?

A
  • GI bicarb loss: diarrhoea, fistula
  • renal tubular acidosis
  • drugs: acetazolamide
  • addison’s
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30
Q

What are causes of a raised anion gap metabolic acidosis?

A
  • lactate: shock, hypoxia
  • ketones: dka, alcohol
  • urate: renal failure
  • acid poisoning: salicylates, methanol
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31
Q

what complications are associated with coeliac disease?

A
  • anaemia: iron/folate/b12
  • hyposplenism
  • osteoporosis/osteomalacia
  • lactose intolerance
  • enteropathy associated t-cell lymphoma
  • subfertility
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32
Q

What is a Hartmann’s procedure and what does it involve/when is it indicated?

A

resection of the rectosigmoid colon
when there is perforation of the rectosigmoid bowel, and subsequent peritonitis - can be due to colon cancer, diverticulitis, trauma etc…
An end colostomy is formed which is brought out onto the left side of the abdomen and sewn flush with the skin, and a rectal stump is sewn

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33
Q

What is membranous glomerulonephritis?

A

commonest type of glomerulonephritis in adults and is the third most common cause of end-stage renal failure - presents with nephrotic syndrome or proteinuria

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34
Q

What is seen on renal biopsy in membranous glomerulonephritis?

A

basement membrane is thickened with subepithelial electron dense deposits - “spike and dome” appearance

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35
Q

what is the management of membranous glomerulonephritis?

A

all patients should receive and ACE inhibitor or ARB

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36
Q

What is the prognosis for membranous glomerulonephritis?

A

rule of thirds:
- 1/3 = spontaneous remission
- 1/3 = remain proteinuric
- 1/3 = develop ESRF

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37
Q

what are the causes of membranous glomerulonephritis?

A

idiopathic: due to anti-phospholipase A2
infections: hep B, malaria, syphilis
malignancy: prostate, lung, lymphoma, leukaemia
drugs: gold, penillamine, NSAIDS
autoimmune disease: SLE, thyroiditis, rheumatoid

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38
Q

What is the management of ascites?

A

reducing dietary sodium
fluid restriction is sometimes recommended if sodium is < 125 mmol/L
aldosterone antagonists e.g. spironolactone
drainage if tense ascites

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39
Q

In what surgeries is there definite chance of transfusion and how much should be given?

A

cross match 4-6 units in:
- total gastrectomy
- oophorectomy
- oesophagectomy
- elective AAA repair
- cystectomy
- hepatectomy

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40
Q

In what surgeries is there likely chance of transfusion and how much should be given?

A

cross-match 2 units in:
- salpingectomy for ruptured ectopic
- total hip replacement

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41
Q

what is acute mesenteric ischaemia?

A

severe and life threatening surgical emergency due to sudden onset intestinal hypoperfusion
The most common site of occlusion is the superior mesenteric artery

42
Q

what is the presentation of acute mesenteric ischaemia?

A

sudden severe abdominal pain and guarding, - pain is out of proportion to the physical exam
nausea and vomiting
signs of shock
metabolic acidosis on abg
PR bleeding is occasionally seen in advanced ischaemia

43
Q

what are the risk factors for acute mesenteric ischaemia?

A

AF or other causes of emboli such as infective endocarditis or aortic aneurysm
Atherosclerosis - suspect if history of ischaemic heart disease or peripheral vascular disease
Any cause of coagulopathy

44
Q

how is acute mesenteric ischaemia diagnosed?

A

ct angio

45
Q

What is Fitz Hugh Curtis syndrome?

A

peri-hepatitis that causes inflammation of the liver capsule, resulting in adhesions
It is a post infectious syndrome caused by:
- N. gonorrhoeae
- Chlamydia trachomatis

46
Q

What are the features of acute tubular necrosis?

A

features of AKI: raised urea, creatinine, potassium
muddy brown casts in the urine

47
Q

What is primary biliary cholangitis?

A

autoimmune condition causing scarring and inflammation of the bile ducts, eventually leading to liver cirrhosis
approx. 25% of patients are women younger than 40, and about 10% of pts are men

48
Q

What are the clinical features of PBC?

A

extreme fatigue, itching, dry skin, dry eyes, jaundice

49
Q

What are patients with PBC at higher risk of developing?

A

hepatocellular carcinoma, prognosis is poor

50
Q

How is PBC investigated?

A

abnormal LFTs
positive anti-mitochondrial antibodies in >90% of individuals
abdominal ultrasound
liver biopsy - inflammation and scarring

51
Q

What are the clinical features of nephrotic syndrome?

A

proteinuria
oedema
hypalbuminaemia
hyperlipidaemia
lipiduria

52
Q

What is the prophylaxis of variceal haemorrhage?

A

propranolol - reduced rebleeding and mortality
endoscopic variceal band ligation - should be performed at two-weekly intervals until all varices have been eradicated

53
Q

what is the presentation of renal stones/urolithiasis?

A

severe, intermittent loin pain which can radiate to the groin
patient is often restless
haematuria - either macroscopic or microscopic although a negative dipstick would not exclude a renal stone
nausea and vomiting is common
2ndary infection of a stone may cause fever or signs of sepsis

54
Q

How does acute liver failure present?

A

jaundice
coagulopathy: raised prothrombin time
hypalbuminaemia
hepatic encephalopathy
renal failure is common -> hepatorenal syndrome

55
Q

What investigation should be performed in a pt with a severe flare of UC?

A

sigmoidoscopy with biopsy
colonoscopy should be avoided due to risk of perforation

56
Q

What are the features of an ileostomy?

A

located in RIF
spouted appearance
liquid output

57
Q

What are the features of a colostomy?

A

location varies but more likely on the left side of the abdomen
flushed to the skin
produces solid contents

58
Q

what are the features of ADPKD?

A

hypertension
recurrent UTIs
flank pain
haematuria
palpable kidneys
renal impairment
renal stones
hepatomegaly
berry aneurysms

59
Q

how can you classify severity of UC?

A

mild: < 4 stools/day, only small amount of blood
Moderate: 4-6 stools/day, varying amounts of blood, no systemic upset
- severe: >6 stools per day + features of systemic upset - pyrexia, tachycardia, anaemia, raised inflammatory markers

60
Q

what can be given to patients with ADPKD to reduce the rate of CKD progression?

A

tolvaptan

61
Q

What medications are used to induce remission of Chron’s?

A
  • glucocorticoids: oral/topical/IV are generally used to induce remission, budesonide is an alternative in a subgroup of patients
  • 5-ASA drugs e.g. mesalazine are used 2nd line to glucocorticoids but are not as effective
  • azathioprine or mercaptopurine may be used as an add-on medication to induce remission but is not used as monotherapy - methotrexate is an alternative to azathioprine
  • infliximab is useful in refractory disease and fistulating Chron’s - patients typically continue on azathioprine and methotrexate
  • metronidazole is used for isolated peri-anal disease
62
Q

How do you maintain remission of Chron’s?

A

as above, stopping smoking is a priority - smoking makes Chron’s worse, but may help UC
azathioprine or mercaptopurine is used first-line to induce remission

63
Q

what are the stages of AKI?

A

Stage 1: increase in creatinine by 1.5-1.9/increase in creatinine by >26.5/reduction in urine output to < 0.5ml/kg/hr for > 6 hours
Stage 2: increase in creatinine to 2-2.9 times baseline or reduction in urine output to <0.5ml/kg/hr for >12hrs
Stage 3: increase in creatinine to >3 times baseline or reduction in urine output to 0.3ml/kg/hr for > 24 hours or the initiation of kidney replacement therapy or in patients less than 18y/o, a decrease in eGFR to < 35ml/min

64
Q

How common is bowel cancer in the UK?

A

4th most common, behind breast, prostate and lung

65
Q

what are the risk factors for colorectal cancer?

A

family history
familial anenomatous polyposis
hnpcc/lynch syndrome
ibd
increased age
diet high in red and processed meat and low in fibre
obesity and sedentary lifestyle
smoking
alcohol

66
Q

what is FAP?

A

familial adenomatous polyposis is an autosomal dominant condition involving malfunctioning of the tumour suppressor genes called adenomatous polyposis coli - results in many polyps developing along the large intestine - these polyps have the potential to become cancerous usually before the age of 40 - patients have their entire large intestine removed prophylactically to prevent the development of bowel cancer (panproctocolectomy)

67
Q

what is the 2 week wait criteria for bowel cancer?

A

over 40 with abdo pain and unexplained weight loss
over 50 with unexplained rectal bleeding
over 60 with a change in bowel habit or iron deficiency anaemia
under 50 with rectal bleeding and abdo pain or change in bowel habit or weight loss or iron-deficiency anaemia

68
Q

what is the bowel cancer screening programme?

A

people aged 60-74 are sent a home FIT test to do every 2 years - if the result comes back positive they are sent for a colonoscopy

69
Q

what is the Dukes classification?

A

system previously used for bowel cancer, has now been replaced by TNM classing
Dukes A - confined to mucosa and part of muscle of bowel wall
Dukes B - extending through muscle of bowel wall
Dukes C - lymph node involvement
Dukes D - metastatic disease - liver, lungs, brain

70
Q

what marker can be used to test for recurrence of bowel cancer?

A

CEA

71
Q

what is the acute treatment of variceal haemorrhage?

A
  • A-E
  • correct clotting
  • vasoactive agents: terlipressin
  • prophylactic IV antibiotics - shown to reduce mortality in patients with liver cirrhosis - both terlipressin and abx should be given before endoscopy in patients with suspected variceal haemorrhage
  • endoscopy: endoscopic variceal band ligation
  • sengstaken-blakemore tube if uncontrolled haemorrhage
72
Q

how do you diagnose spontaneous bacterial peritonitis?

A

paracentesis: neutrophil count > 250 cells/ul

73
Q

what should be done in management of DKA once blood glucose < 14mmol/l?

A

an infusion of 10% dextrose should be started at 125mls/hr in addition to saline regime

74
Q

what is the difference between post-strep and IgA nephritis?

A

post-strep - after 1-2 weeks after URTI3
igA - 1-2 days after URTI

75
Q

when should patients with a suspected upper GI bleed have an endoscopy?

A

within 24 hours of admission

76
Q

how can you manage acute intermittent porphyria?

A

avoiding triggers
for acute attacks: IV haematin/haem arginate, IV glucose

77
Q

what are the features of nephritic syndrome?

A

there are no set criteria but there are usually the following features:
- haematuria - blood in the urine - can be microscopic or macroscopic
- oliguria - reduced urine output
- proteinuria - protein in the urine - less than 3g/24 hours
- fluid retention

78
Q

what are the criteria for nephrotic syndrome?

A

for nephrotic syndrome, a patient must fulfil the following criteria:
- peripheral oedema
- proteinuria - more than 3g/24 hours
- serum albumin less than 25g/l
- hypercholesterolaemia

79
Q

what can nephrotic syndrome predispose a patient to?

A

can predispose patients to thrombosis, hypertension and high cholesterol

80
Q

what is the most common cause of nephrotic syndome?

A

children - minimal change disease
adults - focal segmental glomerulosclerosis

81
Q

How does hepatitis present?

A

abdo pain
fatigue
pruritus
muscle and joint aches
nausea and vomiting
jaundice
fever

82
Q

what might you see on bloods in a pt with hepatitis?

A

derangement of lfts - high transaminases - AST/ALT with proportionately less of a rise in ALP
bilirubin can also rise as a result of inflammation of the liver cells - high bilirubin causes jaundice

83
Q

what is the most common viral hepatitis and how is it spread?

A

Hep A - most common worldwide but rare in the UK
RNA virus
transmitted via faecal oral route usually by contaminated water or food
presents with nausea, vomiting, anorexia, jaundice
Can cause cholestasis
resolves without treatment in around 1-3 months
Management is with basic analgesia
vaccination is available to reduce chance of developing infection
it is a notifiable disease and public health need to be notified of all cases

84
Q

What is Hep C and how does it present and how can it be tested for?

A

RNA virus
spread by blood and body fluids No vaccine is available and it is now curable with direct acting antiviral meds
1 in 4 will fight off the virus and make a full recovery
3 in 4 develop chronic infection
complications include liver cirrhosis and hepatocellular carcinoma
hep C antibody is the screening test
Hep C RNA testing is used to confirm diagnosis of Hep C, calculate viral load and assess for individual genotype

85
Q

How is Hep C managed?

A

there should be a low threshold for screening
you should screen for other blood borne viruses e.g. hep A and B and HIV and other sexually transmitted diseases
refer to gastro, hepatology, or infectious disease for specialist management
stop smoking and alcohol
education about reducing transmission and informing potential at risk contacts
testing for complications: Fibro Scan for cirrhosis, ultrasound for hepatocellular carcinoma
antiviral treatment with direct acting antivirals - tailored to the specific viral genotype - they successfully cure the infection in over 90% of patients - typically taken for 8 - 12weeks
liver transplantation may be required for end-stage renal disease

86
Q

What is Hep D and how does it survive?

A

RNA virus
can only survive in patients who also have a Hep B infection - attaches itself to the Hep B surface antigen and cannot survive without this protein - Hep D increases complications and disease severity of Hep B - no specific treatment for Hep D and it is a notifiable disease so Public Health need to be notified of all cases

87
Q

What is Hep E and how is it spread?

A

RNA virus
transmitted by the foecal oral route
very rare in the UK
Normally it produces only a mild illness, virus is cleared within a month and no treatment is required
Rarely it can progress to chronic hepatitis and liver failure, more so in patients that are immunocompromised
There is no vaccination
It is a notifiable disease and public health need to be notified of all cases

88
Q

What is autoimmune hepatitis?

A

rare cause of chronic hepatitis however associated with a genetic predisposition and triggered by environmental factors such as a viral infection that causes a T cell-mediated response against liver cells

89
Q

What is Hep B and how does it spread?

A

DNA virus
transmitted by direct contact with blood or bodily fluids such as during sexual intercourse or sharing needles - it can also be passed through sharing contaminated household products e.g. toothbrushes or contact between minor cuts or abrasion - can be passed from mother to child during pregnancy and delivery
most people fully recover from the infection within 2 months however 10% go on to become chronic Hep B carriers - in these patients the virus DNA has integrated into their own DNA and so they will continue to produce viral proteins

90
Q

What are the viral markers for Hep B?

A

surface antigen - for active infection
E antigen - marker of viral replication and implies high infectivity
core antibodies - implies past or current infection
surface antibody - implies vaccination or past or current infection
Hep B virus DNA - direct count of viral load

91
Q

what are fibroscans useful for?

A

can be used to check the elasticity of the liver by sending high frequency sound waves into the liver - helps assess the degree of cirrhosis.
NICE recommend retesting every2 years in patients at risk of cirrhosis: hep C, heavy alcohol drinkers, diagnosed alcoholic liver disease, NAFLD, chronic hep B

92
Q

what are the symptoms of haemochromatosis?

A

chronic tiredness
joint pain
pigmentation - bronze/slate-grey discolouration
hair loss
erectile dysfunction
amenorrhoea
cognitive symptoms - mood and memory disturbance

93
Q

how can haemochromatosis be diagnosed?

A

main diagnostic method is serum ferritin - this is an acute phase reactant meaning it will go up with inflammatory conditions such as infection
liver biopsy with Perl’s stain can be used to establish iron conc. in parenchymal cells however Gold standard now is genetic testing
A ct abdomen can show a non-specific increase in attenuation of the liver
MRI can give a more detailed picture of liver deposits of iron - can also be used to look at iron deposits in the heart

94
Q

what are the complications of haemochromatosis?

A

type 1 diabetes
liver cirrhosis
iron deposits in pituitary and gonads leads to endocrine and sexual problems
cardiomyopathy due to iron deposits in the heart
hepatocellular carcinoma
hypothyroidism
chondrocalcinosis/pseudogout causing arthritis

95
Q

what happens in wilsons disease?

A

there is excessive accumulation of copper in the body and tissues

96
Q

what are the features of Wilson’s disease?

A

hepatic problems - 40%
neurological problems - 50%
psychiatric problems - 10%
copper deposition in the liver leads to chronic hepatitis and eventually cirrhosis
copper deposition in the CNS can lead to neurological and psychiatric problems
psychiatric symptoms can vary from mild depression to full psychosis
Kayser-Fleischer rings are brownish circles surrounding the iris - depositis of copper in the cornea
haemolytic anaemia
renal tubular damage leading to renal tubular acidosis
osteopenia - loss of bone mineral density

97
Q

how can wilsons disease be diagnosed?

A

low serum caeruloplasmin - can be falsely normal or elevated in cancer or inflammatory conditions so not specific
liver biopsy for copper content is definitive gold standard test
also can be established if 24 hour urine copper assay is sufficiently elevated

98
Q

what investigation best demonstrates restoration of synthetic liver function?

A

prothrombin time

99
Q

what screening investigation should be done in ADPKD?

A

abdominal ultrasound

100
Q

what is the management of gastroparesis?

A

metoclopramide, domperidone or erythromycin - prokinetic agents

101
Q

what are the scores used in patients with upper gi bleed?

A

glasgow-blatchford - before endoscopy to assess patients with suspected upper gi bleed who are deemed low risk and could be managed as outpatients
rockall score - used after endoscopy to provide estimation of rebleeding risk and mortalilty

Medicine (20 decks)

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