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Year 6 Medicine > Gastro > Flashcards

Gastro Flashcards

1
Q

Complications of Crohn’s?

A

small bowel cancer
colorectal cancer
osteoporosis

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2
Q

Indications for surgery in Crohn’s?

A

around 80% of patients with Crohn’s disease will eventually have surgery
stricturing terminal ileal disease → ileocaecal resection
segmental small bowel resections
stricturoplasty
perianal fistulae
perianal abscess
acute GI bleed

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3
Q

what is the M rule for PBC?

A

IgM
anti-Mitochondrial antibodies, M2 subtype
Middle aged females

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4
Q

Clinical features of PBC?

A

early: may be asymptomatic (e.g. raised ALP on routine LFTs) or fatigue, pruritus
cholestatic jaundice
hyperpigmentation, especially over pressure points
around 10% of patients have right upper quadrant pain
xanthelasmas, xanthomata
also: clubbing, hepatosplenomegaly
late: may progress to liver failure

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5
Q

Mx of PBC?

A
  • first-line: ursodeoxycholic acid
    slows disease progression and improves symptoms
  • pruritus: cholestyramine
  • fat-soluble vitamin supplementation
  • add prednisolone if associated autoimmune disease
  • liver transplantation
    e.g. if bilirubin > 100 (PBC is a major indication)
    recurrence in graft can occur but is not usually a problem
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6
Q

Complications of PBC?

A

cirrhosis → portal hypertension → ascites, variceal haemorrhage
osteomalacia and osteoporosis
significantly increased risk of hepatocellular carcinoma (20-fold increased risk)

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7
Q

Ix/ diagnosis of PBC?

A

Bloods:
cholestatic liver biochemistry (raised GGT/ALP, normal transaminases)

immunology:
anti-mitochondrial antibodies (AMA) M2 subtype are present in 98% of patients and are highly specific
Anti-SMA in 30% of patients
raised serum IgM

imaging:
required before diagnosis to exclude an extrahepatic biliary obstruction (typically a right upper quadrant ultrasound or magnetic resonance cholangiopancreatography (MRCP)

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8
Q

What is PBC?

A

Bile ducts damaged by a chronic inflammatory process causing progressive cholestasis

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9
Q

which conditions are associated with PBC?

A

Sjogren’s syndrome (seen in up to 80% of patients)
rheumatoid arthritis
systemic sclerosis
thyroid disease

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10
Q

Alcoholic ketoacidosis biochemistry?

A 
Metabolic ketoacidosis with normal or low glucose: 
Metabolic acidosis
Elevated anion gap
Elevated serum ketone levels
Normal or low glucose concentration
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11
Q

Mx alcoholic ketoacidosis?

A

infusion of saline and thiamine

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12
Q

What is the most common cause of hepatocellular carcinoma?

A

Chronic hepatitis B is the most common cause of HCC worldwide
chronic hepatitis C is the most common cause in Europe.

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13
Q

What are the main risk factors for HCC?

A 
liver cirrhosis, for example secondary to:
hepatitis B & C
alcohol
haemochromatosis
primary biliary cirrhosis
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14
Q

Management HCC?

A 
early disease: surgical resection
liver transplantation
radiofrequency ablation
transarterial chemoembolisation
sorafenib: a multikinase inhibitor
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15
Q

Who is screened for HCC?

A

patients liver cirrhosis secondary to hepatitis B & C or haemochromatosis
men with liver cirrhosis secondary to alcohol

+ AFP screening as raised in HCC

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16
Q

What is the management of a variceal bleed?

A

ABC: patients should ideally be resuscitated prior to endoscopy
correct clotting: FFP, vitamin K
vasoactive agents: terlipressin
prophylactic IV antibiotics: quinolone
both terlipressin and antibiotics should be given before endoscopy in patients with suspected variceal haemorrhage
endoscopy: endoscopic variceal band ligation
Sengstaken-Blakemore tube if uncontrolled haemorrhage
Transjugular Intrahepatic Portosystemic Shunt (TIPSS) if above measures fail

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17
Q

Variceal bleed prophylaxis?

A

propranolol: reduced rebleeding and mortality compared to placebo
endoscopic variceal band ligation (EVL) - should be performed at two-weekly intervals until all varices have been eradicated
Proton pump inhibitor cover

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18
Q

what is seen on barium enema of UC?

A

loss of haustrations
superficial ulceration, ‘pseudopolyps’
long standing disease: colon is narrow and short -‘drainpipe colon’

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19
Q

what is the most most common organism found on ascitic fluid culture in SBP?

A

E.coli

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20
Q

What are the features of SBP?

A

Ascites
abdominal pain
fever

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21
Q

How do you diagnose SBP?

A

USS to confirm ascites
paracentesis: neutrophil count > 250 cells/ul
MCS: the most common organism found on ascitic fluid culture is E. coli

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22
Q

what is the management of SBP?

A

Piptazobactam or cefotaxime

prophylaxis: ciprofloxacin + propanolol

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23
Q

when should antibiotic prophylaxis be given to patients with ascites?

A

Antibiotic prophylaxis should be given to patients with ascites if:
patients who have had an episode of SBP
patients with fluid protein <15 g/l and either Child-Pugh score of at least 9 or hepatorenal syndrome
NICE recommend: ‘Offer prophylactic oral ciprofloxacin or norfloxacin for people with cirrhosis and ascites with an ascitic protein of 15 g/litre or less until the ascites has resolved’

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24
Q

What vaccine should those with coeliac disease get annually?

A

pneumococcal due to hyposplenism

Coeliac UK recommends that everyone with coeliac disease is vaccinated against pneumococcal infection and has a booster every 5 years
Currrent guidelines suggest giving the influenza vaccine on an individual basis

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25
Q

what are the risk factors for Barrett’s oesophagus?

A

gastro-oesophageal reflux disease (GORD) is the single strongest risk factor
male gender (7:1 ratio)
smoking
central obesity

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26
Q

What is Barrett’s oesophagus?

A

Barrett’s refers to the metaplasia of the lower oesophageal mucosa, with the usual squamous epithelium being replaced by columnar epithelium.

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27
Q

What are the three conditions causing ischemia to the lower GI tract?

A

acute mesenteric ischaemia
chronic mesenteric ischaemia
ischaemic colitis

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28
Q

What are the risk factors for bowel ischaemia?

A

increasing age
atrial fibrillation - particularly for mesenteric ischaemia
other causes of emboli: endocarditis, malignancy
cardiovascular disease risk factors: smoking, hypertension, diabetes
cocaine: ischaemic colitis is sometimes seen in young patients following cocaine use

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29
Q

What are the features of ischaemic bowel?

A 
abdominal pain
 physical exam findings
rectal bleeding
diarrhoea
fever
bloods typically show an elevated white blood cell count associated with a lactic acidosis
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30
Q

What is the management of acute mesenteric ischaemia?

A

urgent surgery is usually required

poor prognosis, especially if surgery delayed

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31
Q

What causes acute mesenteric ischaemia?

A

embolism resulting in occlusion of an artery which supplies the small bowel

classically history of af

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32
Q

What is chronic mesenteric ischaemia?

A

Colickly, intermittent abdominal pain occurs
‘intestinal angina’
non specific

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33
Q

What is the management of ischaemic colitis?

A
  • usually supportive
  • surgery may be required in a minority of cases if conservative measures fail. Indications would include generalised peritonitis, perforation or ongoing haemorrhage
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34
Q

What investigations are done for ischaemic colitis?

A

Investigations

‘thumbprinting’ may be seen on abdominal x-ray due to mucosal oedema/haemorrhage

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35
Q

Where is ischaemic colitis most likely to occur?

A

‘watershed’ areas such as the splenic flexure that are located at the borders of the territory supplied by the superior and inferior mesenteric arteries.

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36
Q

What is ischaemic colitis?

A

Ischaemic colitis describes an acute but transient compromise in the blood flow to the large bowel. This may lead to inflammation, ulceration and haemorrhage.

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37
Q

What are some adverse effects of metoclopramide?

A

extrapyramidal effects: oculogyric crisis. This is particularly a problem in children and young adults
hyperprolactinaemia
tardive dyskinesia
parkinsonism

should also be avoided in bowel obstruction due to prokinesis

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38
Q

what are the complications of coeliac disease?

A

anaemia: iron, folate and vitamin B12 deficiency (folate deficiency is more common than vitamin B12 deficiency in coeliac disease)
hyposplenism
osteoporosis, osteomalacia
lactose intolerance
enteropathy-associated T-cell lymphoma of small intestine
subfertility, unfavourable pregnancy outcomes
rare: oesophageal cancer, other malignancies

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39
Q

what is seen on duodenal biopsy in coeliac?

A

complete atrophy of the villi with flat mucosa
marked crypt hyperplasia
Intraepithelial lymphocytosis
Dense mixed inflammatory infiltrate in the lamina propria.

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40
Q

coeliac associated conditions?

A 
Autoimmune thyroid disease
Dermatitis herpetiformis
Irritable bowel syndrome
Type 1 diabetes
First-degree relatives (parents, siblings or children) with coeliac disease
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41
Q

S/S coeliac?

A

Chronic or intermittent diarrhoea
Failure to thrive or faltering growth (in children)
Persistent or unexplained gastrointestinal symptoms including nausea and vomiting
Prolonged fatigue (‘tired all the time’)
Recurrent abdominal pain, cramping or distension
Sudden or unexpected weight loss
Unexplained iron-deficiency anaemia, or other unspecified anaemia

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42
Q

What does a high SAAG indicate?

A

A high SAAG (>11g/L)
portal hypertension and the ascitic fluid is a transudate. liver cirrhosis/failure/mets -> most common
right heart failure, pericarditis
hepatic failure
venous occlusion (e.g. Budd Chiari syndrome)
alcoholic hepatitis
myxoedema

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43
Q

What does a low SAAG indicate?

A 
A low SAAG (<11g/L)
ascitic fluid is an exudate. 
malignancy
infection
pancreatitis
nephrotic syndrome
bowel obstruction
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44
Q

what is the management of ascites?

A 
reduce dietary sodium
fluid restriction if sodium <125
spironolactone
drainage if tense ascites
paracentesis
prophylactic ciprofloxacin
TIPS
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45
Q

What is the Child pugh score for?

A

Child–Pugh score is used to assess the prognosis of chronic liver disease, mainly cirrhosis

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46
Q

What is the triad of liver failure?

A

encephalopathy, jaundice and coagulopathy

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47
Q

What are some causes of acute liver failure?

A

paracetamol overdose
alcohol
viral hepatitis (usually A or B)
acute fatty liver of pregnancy

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48
Q

what are some features of acute liver failure?

A 
jaundice
coagulopathy: raised prothrombin time
hypoalbuminaemia
hepatic encephalopathy
renal failure is common ('hepatorenal syndrome')
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49
Q

What is the best way to assess ‘synthetic liver function’?

A

PT

albumin level

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50
Q

What is type 1 hepatorenal syndrome?

A

Type 1 is a rapid onset hepatorenal syndrome (less than two weeks). This typically occurs following an acute event such as an upper GI bleed

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51
Q

What is type 2 hepatorenal syndrome?

A

Type 2 is a more gradual decline in renal function and is generally associated with refractory ascites

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52
Q

What is the pathophysiology behind hepatorenal syndrome?

A

vasoactive mediators cause splanchnic vasodilation which in turn reduces the systemic vascular resistance. This results in ‘underfilling’ of the kidneys.

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53
Q

What are the features of type 1 hepatorenal syndrome?

A

Rapidly progressive
Doubling of serum creatinine to > 221 µmol/L or a halving of the creatinine clearance to less than 20 ml/min over a period of less than 2 weeks
Very poor prognosis

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54
Q

What are the features of type 2 hepatorenal syndrome?

A

Slowly progressive

Prognosis poor, but patients may live for longer

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55
Q

What is the management of hepatorenal syndrome?

A

vasopressin analogues, for example terlipressin, have a growing evidence base supporting their use. They work by causing vasoconstriction of the splanchnic circulation
volume expansion with 20% albumin
transjugular intrahepatic portosystemic shunt

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56
Q

What is the most common type of pancreatic cancer?

A

adenocarcinoma at the head of the pancreas (80%)

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57
Q

What are the associations with pancreatitis?

A 
increasing age
smoking
diabetes
chronic pancreatitis (alcohol does not appear an independent risk factor though)
hereditary non-polyposis colorectal carcinoma
multiple endocrine neoplasia
BRCA2 gene
KRAS gene mutation
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58
Q

What are the investigations for pancreatic cancer?

A

ultrasound has a sensitivity of around 60-90%
high-resolution CT scanning is the investigation of choice
imaging may demonstrate the ‘double duct’ sign - the presence of simultaneous dilatation of the common bile and pancreatic ducts

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59
Q

What is courvoisiers law?

A

in the presence of painless obstructive jaundice, a palpable gallbladder is unlikely to be due to gallstones

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60
Q

What is the management of pancreatic cancer?

A

less than 20% are suitable for surgery at diagnosis
a Whipple’s resection (pancreaticoduodenectomy) is performed for resectable lesions in the head of pancreas. Side-effects of a Whipple’s include dumping syndrome and peptic ulcer disease
adjuvant chemotherapy is usually given following surgery
ERCP with stenting is often used for palliation

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61
Q

How do you calculate units in a drink?

A

multiply the number of millilitres by the ABV and divide by 1,000. For example:

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62
Q

what are some features of hepatic encephalopathy?

A

confusion, altered GCS
asterix: ‘liver flap’, arrhythmic negative myoclonus with a frequency of 3-5 Hz
constructional apraxia: inability to draw a 5-pointed star
triphasic slow waves on EEG
raised ammonia level

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63
Q

what is the grading of hepatic encephalopathy?

A

Grade I: Irritability
Grade II: Confusion, inappropriate behaviour
Grade III: Incoherent, restless
Grade IV: Coma

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64
Q

What may precipitate hepatic encephalopathy?

A 
infection e.g. spontaneous bacterial peritonitis
GI bleed
post transjugular intrahepatic portosystemic shunt
constipation
drugs: sedatives, diuretics
hypokalaemia
renal failure
increased dietary protein (uncommon)
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65
Q

What is the management of hepatic encephalopathy?

A

treat any underlying precipitating cause
NICE recommend lactulose first-line + rifaximin for the secondary prophylaxis of hepatic encephalopathy
embolisation of portosystemic shunts
liver transplantation in selected patients

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66
Q

How is the severity of flares in UC assessed?

A

Mild: <4 stools/day little blood
Moderate: 4-6 s/d, varying blood
Severe: >6 bloody stools, systemic upset

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67
Q

Which criteria may be used to assess severity of IBD

A

True-Love and Witt’s

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68
Q

what are the investigations for IBD?

A 
bloods: FBC, U&E, CRP, LFTs, pANCA
stool cultures, scope, colonoscopy
faecal calprotectin
barium or gastrograffin enema
acute - CTAP

C-reactive protein correlates well with disease activity IN Crohn’s

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69
Q

Extra-intestinal manifestations of IBD?

A 
A PIE SAC
aphthous ulcer [CD>UC]
pyoderma gangrenosum
eye - iritis, uveitis, episcleritis [CD>CD]
erythema nodosum 
sclerosis cholangitis [UC]
arthritis
clubbing [CD>UC]
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70
Q

What are the symptoms of Crohn’s?

A 
non bloody diarrhoea
RIF mass
gallstones
anal fissures
perianal skin tags
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71
Q

what is the pattern of inflammation in Crohn’s

A

skip lesions
rose thorn ulcers
cobblestoning
string sign of Kantor (narrow ileum stricture)

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72
Q

What are the symptoms of UC?

A

bloody diarrhoea + mucous diarrhoea
LIF pain
nocturnal incontinence
tenesmus

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73
Q

what is the pattern of inflammation in UC?

A 
Continuous lead pipe
pseudo polyps
thumb printing 
PSC
CRC risk higher in UC
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74
Q

How does Crohn’s affect the gut layer?

A

transmural (goblet,granulomas)

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75
Q

How does UC affect the gut later?

A

mucosa and submucosa (goblet cells, crypt abscess)

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76
Q

How do you induce remission in Crohn’s

A

Pharmacological:
mild: oral prednisolone 300 mg
severe: IV hydrocortisone - no improvement after 5 days -> IV infliximab.
Distal ileal, ileo-caecal, R sided colonic -> oral budesonide

Nutritional:
Whole protein modular diet for 6-8w

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77
Q

How do you maintain remission in Crohn’s?

A

STOP SMOKING

1: DMARDs (azathioprine, mercaptopurine)
2: vaccines (no live - pneumococcal, influenza)

alternative: aminosalicylates, anti-TNF abs in infliximab

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78
Q

What needs to be checked before starting a patient on azathioprine/6MP?

A

TPMT levels

use methotrexate instead if low

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79
Q

what is the management of UC?

A

1: distal colitis: topical aminosalicylates (4w) -> oral +/- topical
extensive colitis past splenic flexure: topical + oral aminosalicylates
2: topical -> oral beclomethasone
3: oral tacrolimus
4: biologics (infliximab, adalimumab)
5: surgery

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80
Q

what is the management of severe UC?

A

Fulminant: IV steroids +/- ciclosporin/infliximab (if not improvement in 72h then colectomy)
Non fulminant: topical aminosalicylates + oral + oral corticosteroid

after severe or >=2 exacerbations in past year -> oral azathioprine or 6MP

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81
Q

what surgery is used in UC?

A
  • emergency: Hartmann’s proctosigmoidectomy + end ileostomy + later ileal pouch anal anastomosis (IPAA)
  • proctocolectomy + IPAA
  • panproctocolectomy + end ileostomy
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82
Q

What surgery is used in Crohn’s?

A

proctectomy (not that useful)

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83
Q

What is the classic presentation of IBS?

A

young female, anxious, stressed and may have depression, pain , bloating, diarrhoea/constipation

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84
Q

How is IBS diagnosed?

A

Diagnosis of exclusion based on ROME III criteria

  • improvement with defecation
  • change in stool frequency
  • change in stool form/appearance/consistency
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85
Q

What is the management of IBS?

A

1: Diet and lifestyle
2nd: meds

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86
Q

What causes haemorrhoids?

A

displacement of anal cushions via gravity, straining and increased anal tone

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87
Q

What are the types of haemorrhoids?

A

1: in rectum after defecation
2: prolapse through anus at defecation, spontaneous reduction
3: prolapse through anus at defecation, manual reduction
4: persistently prolapsed

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88
Q

What are the investigations for haemorrhoids?

A

abdo exam
DRE
proctoscopy, sigmoidoscopy

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89
Q

what is the management of haemorrhoids?

A

1: increased fluids/fibre, stool softener, topical analgesics, steroids
2: rubber band ligation, sclerotherapy, electrotherapy, infraredcoagulation
3: haemorrhoidectomy, haemorrhoidopexy, HALF

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90
Q

What is the treatment for botulinum gastroenteritis?

A

anti-toxin

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91
Q

What is the treatment for c.diff

A

metronidazole

vancomycin

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92
Q

what is the treatment for listeria ?

A

amoxicillin

ampicillin

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93
Q

What is the treatment for salmonella typhi/paratyphi?

A

ceftriaxone initially

switch to cipro if sensitive

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94
Q

What is the treatment for vibrio parahaemolyticus?

A

doxycycline

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95
Q

What is the treatment for vibrio vulnificus?

A

doxycycline

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96
Q

What is the treatment for severe campylobacter jejune?

A

SL

treat if severe-> clarithromycin or cipro

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97
Q

What is the treatment for entamoeba histolytic?

A

metronidazole

paromomycin

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98
Q

What is the treatment for giardiasis lamblia?

A

metronidazole

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99
Q

What is the treatment for cryptosporidium parvum?

A

paromomycin

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100
Q

What is coeliac?

A

autoimmunity to gliadin (in gluten, wheat, barley and rye) -> shorter villi and flat mucosa

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101
Q

what genetic associations does coeliac have?

A

HLA DQ2 and DQ8

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102
Q

S/S of coeliac?

A

pathogneumonic = dermatitis herpetiformis (pruritic papulovesicular elbow/knee rash)
watery, grey, frothy stool
IDA >folate def >B12 def

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103
Q

where is iron absorbed?

A

duodenum

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104
Q

where is folate absorbed?

A

jejunum

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105
Q

where is b12 absorbed?

A

ileum

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106
Q

what are the investigations for coeliac?

A

IgA TTG
If IgA deficient - do IgGDGP
IgA EMA is helpful but less sensitive

FBC, BLOOD SMEAR (iron def, vit b12/folate def, vit D def,)

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107
Q

What is seen on blood smear in coeliac?

A

target cells

howell Jolly bodies

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108
Q

How is diagnosis of coeliac confirmed?

A

OGD + duodenal biopsy

very young children: EMA and HLA DQ2/DQ8 testing

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109
Q

What is seen on duodenal biopsy in coeliac?

A

villous atrophy, crypt hyperplasia, increased IELs

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110
Q

What is the management of coeliac?

A

MDT
remove all wheat, rye and barley for life
dietician referral - annual 6-12m review
education
warn of non adherence: micronutrient deficiency, osteoporosis, EATL, hyposplenism.

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111
Q

what is the gold standard investigation for oesophageal cancer?

A

endoscopy + biopsy

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112
Q

What is the most common type of oesophageal cancer?

A

adenocarcinoma

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113
Q

what are the features of oesophageal cancer?

A

dysphagia: the most common presenting symptom
anorexia and weight loss
vomiting
other possible features include: odynophagia, hoarseness, melaena, cough

RF: Barrett’s oesophagus, GORD, excessive smoking or alcohol use

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114
Q

how is oesophageal cancer diagnosed?

A

Upper GI endoscopy with biopsy is used for diagnosis
Endoscopic ultrasound is the preferred method for locoregional staging
CT scanning of the chest, abdomen and pelvis is used for initial staging
FDG-PET CT may be used for detecting occult metastases if metastases are not seen on the initial staging CT scans.
Laparoscopy is sometimes performed to detect occult peritoneal disease

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115
Q

what is the management of oesophageal cancer?

A

Operable disease is best managed by surgical resection - the most common procedure is an Ivor-Lewis type oesophagectomy
The biggest surgical challenge is that of anastomotic leak, with an intrathoracic anastomosis resulting in mediastinitis
In addition to surgical resection many patients will be treated with adjuvant chemotherapy

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116
Q

what investigations can be used for appendicitis?

A 
Mostly diagnosed clinically
CT abdo/USS
Urinalysis: mildly elevated leukocytes
DRE: right sided pain
bloods: increased inflammatory markers, increased WCC
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117
Q

what score can be used to grade appendicitis?

A

Alvarado score

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118
Q

What are the S/S of appendicitis?

A

Rovsings sign
Cope’s sign
Psoas sign - retrocaecael appendix
Rebound tenderness

N&V
loose stools
anorexia
mild pyrexia

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119
Q

What is the management of acute appendicitis?

A

IV abx alone are successful in majority but expect recurrence within 12m
laparoscopic appendicectomy
perforation -> abdominal lavage
appendix mass -> broad spectrum abx and interval appendicectomy

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120
Q

What is Admirands triangle?

A

conditions for crystallised cholesterol and gallstones

  • low lecithin
  • low bile salts
  • high cholesterol
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121
Q

What is acute cholecystitis?

A

inflammation of gallbladder often due to stone impaction in hartmann’s pouch

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122
Q

What is the sequelae of acute cholecystitis?

A
  1. resolution and recurrence
  2. gangrene and rarely perforation
  3. chronic cholecystitis
  4. empyema
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123
Q

what is the presentation of acute cholecystitis?

A

RUQ pain - may radiate to scapula and epigastrium
fever
vomiting

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124
Q

what blood results are seen in acute cholecystitis?

A

ALT/AST normal
BR normal
amylase slightly high
ALP slightly high

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125
Q

what is seen on examination of acute cholecystitis?

A 
local peritoneum in RUQ
tachycardia and shallow breathing
\+/- jaundice
Murphy's sign +ve
Boas sign +ve
126
Q

what investigations are done for acute cholecystitis?

A

Urine: bilirubin, urobilinogen
Bloods: FBC (raised WCC), U&E (dehydration), amylase, LFT, G&S, clotting CRP
Imaging: AXR, erect CXR, US, hIDA cholescintigraphy, MRCP if dilated ducts

127
Q

what are the symptoms of chronic cholecystitis?

A 
flatulent dyspepsia
vague upper abdominal discomfort
bloating, distension
nausea, 
flatulence
128
Q

Ix for chronic cholecystitis?

A

AXR: porcelain gallbladder (chronic calcification)
US: stones, fibrotic, shrunken gallbladder
MRCP

129
Q

Management of chronic cholecystitis?

A

Medical: bile salts
Surgical: elective cholescystectomy
ERCP first if US shows dilated ducts and stones

130
Q

Management of acute cholecystitis?

A

C: NBM, fluids resuscitation
analgesia

M: Abx: cefuroxime and metronidazole (80-90% settle over 24-48h)

S: elective Surgery at 6-12 weeks when inflammation settled
if <72h may perform lap whole in acute phase

131
Q

What are the complications of chronic cholecystitis?

A

cholangiocarcinoma

132
Q

What is the Mirizzi syndrome?

A

large stone in gall bladder obstructs common hepatic duct

obstructive jaundice

133
Q

complications of laparoscopic cholecystectomy?

A

diarrhoea - give cholestyramine
Vitamin malabsorption (A,D,E,K) - Can cause bleeding though reduced vit K
Jaundice - ligation fo CBD/CHD, sepsis, CBD stone

134
Q

What are the risk factors for biliary colic?

A

female, fat, forties. fair

135
Q

What symptoms are seen in ascending cholangitis?

A

Charcots triad
fever>RUQ pain > jaundice

Reynolds pentad
+ hypotension
+confusion

136
Q

What % of gallstones are radio-opaque

137
Q

What is seen on ultrasound of gallstones?

A

acoustic shadow
dilated ducts >6mm
Inflamed GB wall

138
Q

Management of ascending cholangitis?

A 
C: fluids, antiemetics, analgesia
M:IV cef and met
S: Surgical referral 
ERCP
open or lap stone removal +/- tube drain
139
Q

What are the RFs for cholangiocarcinoma?

A 
GB disease
polyps
infection
porcelain GB
PSC
obesity
smoking
140
Q

What are the S/S of cholangiocarcinoma?

A

asymptomatic
RUQ, anorexia, n&v, malaise, WL, palpable GB
obstructive jaundice

141
Q

What are the investigations for cholangiocarcinoma?

A 
LFTs (abnormal
CA-19, CEA
USS
CT abdo 
ERCP (gold standard for staging)
MR (staging)
142
Q

Management for cholangiocarcinoma?

A

Resectable-> cholecystectomy (+/- debunking)

Non resectable -> chemoradiotherapy +/-stenting

143
Q

What is acute gallstone ileus?

A

large stone >2.5 cm erodes from GB -> duodenum

may impact in distal ileum -> obstruction

144
Q

What are the signs of gallstone ileus?

A

riglers triad:
pneumobilia
small bowel obstruction
gallstones RLQ

145
Q

Mx of gallstone ileus?

A

stone removal via enterotomy

146
Q

What is PSC?

A

a biliary disease characterised by inflammation and fibrosis of intra and extra hepatic bile ducts

147
Q

What are the associations with PSC?

A

UC (80% with PSC have UC)
Crohn’s
HIV

148
Q

What are the S/S OF PSC?

A 
pruritis
obstructive jaundice
splenomegaly
raised ALP
Steatorrhoea

p-ANCA, male, 40-60, iBD

149
Q

what are the investigations for PSC?

A

Diagnostic: MRCP (preferred) > ERCP ‘beaded appearance from biliary strictures
p-ANCA
anti-SMA
Biopsy of bile duct (fibrous, obliterative cholangitis often described as onion skin)

150
Q

What is the management of PSC?

A

Observation (surveillance colonoscopy, DEXA) -> LIVER TRANSPLANT

151
Q

What are the complications of psc?

A

cholangiocarcinoma (10%), colorectal cancer, hepatic osteoporosis/osteopenia

152
Q

What are the associations with autoimmune hepatitis?

A

AI disorders, hypergammaglobulinaemia, HLAB8, HLA DR3

153
Q

What are the 3 types of autoimmune hepatitis and their associations?

A

T1: ANA or Anti SMA - affects adults and children
T2: Anti-LKM 1,2,3 affects children only
T3: Anti-soluble liver antigen (anti-SLA and anti-LP), affects middle aged adults

154
Q

What are the signs and symptoms of autoimmune hepatitis?

A

amenorrhoea (common)

chronic liver disease OR acute hepatitis

155
Q

What are the investigations for autoimmune hepatitis?

A

antibodies: ANA,SMA,LKM1
raised IgG
biopsy: inflammation extending beyond limiting plate - ‘piecemeal necrosis’, bridging necrosis

156
Q

What is the mx for autoimmune hepatitis?

A

steroids +/- azathioprine

liver transplantation

157
Q

What are the features of Wernicke’s ?

A 
COAT
Confusion
ophthalmoplegia
ataxia
thiamine deficiency
158
Q

What are the features of korsakoffs?

A 
RACK
retrograde amnesia
anterograde amnesia
confabulation
korsakoff psychosis
159
Q

What are the S/s of chronic stable liver disease?

A

palmar erythema
dupuytrens
clubbing
eyes: kayser Fleischer (wilsons), corneal arcus
gynaecomastia, axillary hair loss, spider naevi

160
Q

what are some S/S of acute decompensation?

A

portal hypertension [SAVE]

  • Splenomegaly
  • Ascites
  • Varices
  • Encephalopathy

Failed synthetic function
Failed clotting factor and albumin
Failed clearance bilirubin
Failed clearance of ammonia -> encephalopathy -> asterixis

161
Q

What are the investigations for suspected liver disease?

A 
Bloods: FBC, U&E, CRP, clotting, AFP, iron studies, hepatitis serology, autoantibodies, caeruloplasmin
USS abdomen (+/ fibroscan +/-biopsy)
Endoscopy (OGD, colonoscopy)
162
Q

what is the management of hepatic encephalopathy?

A

lactulose

rifaximin

163
Q

what is the management of weirnickes?

A

thiamine, Mg2+, folic acid

164
Q

what’s the management of decompensation liver disease?

A

lactulose, diuretic, TIPPS

165
Q

What may cause liver decompensation?

A 
CONSTIPATION
SBP
GI bleed
Renal failure
Hypokalaemia
166
Q

What is the management of ascites?

A

Diet - restrict ETOH and fluids (if Na<125; <1.5L a day), low Na, daily weight
Diuretics - spironolactone + furosemide
SBP prophylaxis - ciprofloxacin + propanolol

if ascites and protein of <= 15g/L start prophylaxis immediately

167
Q

what is the cause of SBP?

A

E.coli> Klebsiella >strep

168
Q

Ix Sbp?

A 
USS - confirm ascites
ascitic tap (PMN >250mm^3 +MC&S)
169
Q

Mx SBP?

A

Piptazobactam or cefotaxime

170
Q

What is the prophylaxis for SBP?

A

Ciprofloxacin + propanolol

171
Q

What is haemochromatosis?

A

AR disorder of iron absorption and metabolism results in iron accumulation

172
Q

What is the gene for haemochromatosis

A

AR HFE gene on both copies Chr 6

173
Q

What are the investigations for haemochromatosis?

A

Iron studies - TF saturation >55% M, >50% F
- Ferritin raised
- Iron raised
- TIBC reduced
Liver biopsy - Perl stain
XR - chonedrocalcinosis (calcium inarticulate cartilage)

174
Q

What is the management of haemochromatosis?

A
  1. venesection (TF kept <50%)

2. Desferrioxamine

175
Q

What is NAFLD?

A

Key hepatic manifestation of metabolic syndrome

liver disease not caused by alcohol

176
Q

steatosis vs steatohepatitis?

A

steatosis is fatty liver

steatohepatitis is inflamed fatty liver

177
Q

What are some associated factors wth NAFLD?

A

Obesity
T2DM
hyperlipidaemia
sudden weight loss or starvation

178
Q

What are the investigation for NAFLD?

A
  1. LFTs (ALT>AST), lipids, cholesterol
  2. USS (increased echogenicity)
  3. Enhanced liver fibrosis (ELF) panel OR a fibroscan
  4. liver biopsy
179
Q

What does an ELF panel consist of ?

A

hyaluronic acid
procollagen III
tissue inhibitor of metalloproteinase 1

180
Q

What is a fibroscan?

A

liver stiffness measurement

181
Q

who is fibroscan offered to?

A

HCV infection
ETOH related liver disease
Men >50 u/week ETOH
Women >35u/week ETOH

182
Q

Mx NAFLD?

A

Lifestyle changes and WL
monitoring
ongoing research into gastric banding/insulin sensitising drugs

183
Q

What are some causes of pancreatitis?

A 
I GET SMASHED
Idiopathic
Gallstones
Ethanol
Trauma
Steroids
Mumps
Autoimmune
Scorpion venom
Hyperlipidaemia
ERCP
Drugs
184
Q

what are some S/S pancreatitis?

A

severe epigastric pain radiates through to back
N&V
Cullens/Grey-Turner’s sign
Rare: ischaemic retinopathy

185
Q

What are some investigations for pancreatitis?

A

serum amylase (>3x ULN, raised in 75%)
serum lipase (more sensitive and specific than amylase)
USS - gallstones
Contrast enhanced CT

186
Q

What is the prognostic score for pancreatitis?

A 
Glasgow-Imrie
PaO2 <8kpa
Age >55yo
Neutrophils >15x10^9/L
Ca <2mmol/L
Renal urea >16 mmol/L
Enzymes (LDH>600, AST/ALT>200)
ALBUMIN <32g/L
Sugar >10 mmol/L
187
Q

Management of acute pancreatitis?

A

fluids
analgesia (IV morphine, 1-2 mg STAT until comfortable)

key features:

  • maintain enteral route of feeding
  • no abx unless indicated
  • aggressive fluid resuscitation (3-6L)
  • correct cause - MRCP/ERCP
188
Q

Management of necrotising pancreatitis?

A

fluids
analgesia
ABx

189
Q

What are the complications of acute pancreatitis?

A

early:

  • Haemorrhage
  • SIRS, ARDS
  • Hyperglycaemia, hypocalcaemia

Late:
peri-pancreatic fluid collection (admit + bowel rest)
pseudocysts (observe, cystogastrostomy/aspiration)
pancreatic abscess (infected pseudocyst -> trans-gastric drainage/endoscopic drainage)
pancreatic necrosis (conservative)

190
Q

what are the S/S of chronic pancreatitis?

A
  • pain is worse 15-30 mins following a meal
  • steatorrhoea (5 and 25 years after the onset of pain)
  • DM (>20 years after symptoms begin)
191
Q

investigations of chronic pancreatitis?

A

USS (IE for gallstones)
Contrast enhanced CT
Faecal elastase (measures exocrine function)
Screening (DM and osteoporosis)

192
Q

What is the most common type of pancreatic cancer?

A

80% adenocarcinoma

193
Q

What are the types of diverticular disease?

A

Hinchey classificationL

  • diverticular sieges (umbrella term)
  • diverticulosis (asymptomatic outpouchings in the intestinal mucosa)
  • diverticulitis (infected diverticulosis)
194
Q

What is saints triad?

A

diverticular disease
diaphragmatic (hiatus) hernia
stones (cholelithiasis)

195
Q

What are the investigations for diverticular disease?

A

acute (diverticulitis) - CT abdomen

chronic (diverticular disease ) - barium enema

196
Q

What is the management of acute diverticulitis?

A

mild - PO Abx

Severe - IV Abx, drip and suck, hartmanns, primary anastomosis

197
Q

What is the management of chronic diverticular disease?

A

soluble high fibre diet

primary anastomosis

198
Q

when should your refer for 2WW OGD?

A 
dysphagia
upper abdominal mass (?stomach cancer)
age >=55yo AND weight loss AND any of
-dyspepsia
- reflux
- GORD
- upper abdominal pain
199
Q

which drugs may exacerbate GORD?

A

alpha blockers,anticholinergics, benzodiazepines, beta blockers, bisphosphonates, CCB, corticosteroids and NSAIDs, nitrates, theophyllines

200
Q

What is the management of GORD?

A

PPI 4-8w

If no response then H2R antagonist

201
Q

what is the management of dyspepsia?

A

antacids/ alginates for short term control
review meds
(test for H. pylori first)
PPI 4w

202
Q

What is the criteria for non urgent OGD referral?

A

haematemesis
age >= 55yo AND
- treatment resistant dyspepsia
- upper abdominal pain with low Hb
- N&V + reflux, WL, dyspepsia or upper abdo pain
- Raised platelets + N&V, WL, reflux, dyspepsia or upper abdo pain

203
Q

If OGD is negative what should be done next?

A

24 hour oesophageal pH monitoring

204
Q

What is the management of dyspepsia?

A
  1. review meds for possible causes + lifestyle advice
  2. trial PPI for 4w or ‘test and treat’ H.pylori
  3. the other one that has not been tried as above - wait 2w after trial PPI before H.pylori test
  4. ‘treatment resistant dyspepsia’-> Non urgent OGD
205
Q

How do you test for H.pylori?

A

carbon-13 urea breath test OR stool antigen test OR lab based serology
- no abx in last 4 weeks
- no PPI in last 2 weeks
if repeat testing need use carbon-13 urea breath test

206
Q

What is the management of H.pylori?

A

clarithromycin, amoxicillin, PPI

207
Q

Is H.pylor gram +ve or -ve?

208
Q

What are some H.pylori associations?

A

PUD (95% duodenal ulcers, 75% gastric)
gastric cancer
MALToma
atrophic gastritis

209
Q

what are the RF for gastric cancer?

A

smoking
diet
H.pylori

210
Q

Ix gastric cancer?

A

staging CT
Virchows node
sister mary jospeh nodule

211
Q

Mx gastric cancer?

A

endoscopic mucosal resection
partial gastrectomy
total gastrectomy
chemo

212
Q

Complications of GORD/dyspepsia?

A 
oesophagitis
ulcers
anaemia
benign strictures
Barrett's oesophagus
oesophageal carcinoma
213
Q

What is the management of endoscopically proven oesophagitis?

A

if severe annual review and investigate GORD/barrett

1st: PPI for 4w then 4w then double dose for 4w
2nd: add H2 antagonist

214
Q

What is the management of endoscopically negative reflux disease?

A
  1. PPI (1 month)

2. H2RA (1 month)

215
Q

Whats the surgical management of GORD?

A 
Nissen fundoplication (gold standard)
for refractory GORD or hiatus hernia
216
Q

What are the complications of Nissen fundoplication?

A

gas bloat syndrome (cant belch or vomit)

dysphagia (wrap too tight)

217
Q

Histology of barrett’s oesophagus?

A

columnar
goblet cells
brush border

218
Q

RF barrett’s oesophagus?

A

GORD
male
smoking
obesity

219
Q

Mx barrett’s oesophagus?

A

metaplasia -> endoscopic surveillance and biopsy (every 3-5y)
high dose PPI
dysplasia -> endoscopic mucosal resection, radio frequency ablation

220
Q

What is CA125 a marker for ?

A

ovarian ca

221
Q

what is CA15-3 a marker for?

222
Q

What is Ca19-9 a marker for?

A

pancreatic cancer/ mutinous epithelial ovarian cancer

223
Q

what is CEA a marker for ?

A

bowel cancer

224
Q

what is inhibin a marker for ?

A

granulose cell tumours

225
Q

what is AFP a marker for?

A

liver cancer
non-seminoma
teratoma

226
Q

What is LDH a marker for?

A

seminoma (testicular)

227
Q

What is B-hCG a marker fro?

A

choriocarcinoma

non-seminoma (testicular)

228
Q

what is MLH1/ML2 a marker for?

A

Lynch sundrome HNPCC

229
Q

What is BRCA1/2 a marker for ?

A

M: breast (1,2), prostate (2)
W: breast (1,2), ovarian (1>2)

230
Q

What are the S/S of anal fissure?

A

bright red rectal bleeding; 90% on posterior midline

231
Q

what is the management of acute anal fissure?

A

<6 weeks

  • dietary advice (high fluids)
  • bulk firming laxatives
  • optional: petroleum jelly, non opioid analgesia
232
Q

what is the management of chronic anal fissure?

A

1st line: topical GTN or diltiazem or nifedipine

2nd: after 8w first line: sphincterotomy, botox toxin

233
Q

What is the management of alcoholic hepatitis?

A

prednisolone (high DF)

pentoxyphylline

234
Q

Ix alcoholic hepatitis?

A

LFTs: GGT raised, AST:ALT >2
Maddrey score predicts who benefits from steroids
Child pugh score predicts prognosis of liver cirrhosis

235
Q

How to work out maddrey score?

A

predicts prognosis and who benefits from steroids
DF = 4.6 x [PT-control time] +BR
DF>= 32 -> consider liver biopsy + corticosteroids

236
Q

what is child pugh score based on?

A 
Albumin
BR
Clotting (PT)
Distension (ascites)
Encephalopathy
A= 5-6 points
B= 7-9 points
C= 10-15 points
237
Q

What causes Budd Chiari syndrome?

A

blockage of hepatic vein
polycythaemia rubra vera
thrombophilia: activated protein C resistance, antithrombin III deficiency, protein C & S deficiencies
pregnancy
combined oral contraceptive pill: accounts for around 20% of cases

238
Q

What are the RFs for Budd Chiari syndrome?

A

OCP
PRV
thrombophilia
pregnancy

239
Q

what are the types of Budd Chiari?

A

T1- thrombosis

T2 -tumour occlusion

240
Q

What are the S/S of budd chiari?

A

triad: abdominal pain, ascites, tender hepatomegaly

241
Q

Ix budd chiari?

A

abdominal USS and doppler

very sensitive

242
Q

S/S of achalasia?

A

sudden onset solid and liquid dysphagia, halitosis, heartburn, regurgitation
Dysphagia of both liquids and solids from the start
Heartburn
Regurgitation of food - may lead to cough, aspiration pneumonia etc

243
Q

Ix achalasia?

A 
LOS manometry (excessive LOS tone)
barium swallow (birds beak)
CXR
244
Q

Management achalasia?

A

heller cardiomyotomy >botulinum intra-sphincteric injection

oesophageal balloon dilatation

245
Q

What is seen in sigmoid volvulus?

A

coffee bean sign; not associated with malignancy

246
Q

Mx of sigmoid volvulus?

A

sigmoidoscopy and air insufflation

247
Q

what is seen in caecal volvulus?

A

embryo sign

associated with malignancy

248
Q

management of caecal volvulus?

A

surgery
right hemicolectomy
ileocolic anastomosis
caecostomy

249
Q

what is carcinoid syndrome?

A

usually occurs with liver metastases that release serotonin into the systemic circulation

250
Q

What are the S/S of carcinoid syndrome?

A

flushing (often earliest symptom)
diarrhoea
bronchospasm
hypotension

Cardiac - right sided valve stenosis/pulmonary stenosis (ESM)
Endocrine - acromegaly, cushings
Pellagra- dermatitis, diarrhoea, dementia (B3 deficiency)

251
Q

What are the investigations of carcinoid syndrome?

A

urinary 5-hydroxyindolacetic acid

plasma chromogranin A y

252
Q

Management of carcinoid syndrome?

A

somatostatin analogues e.g. octreotide

diarrhoea: cyproheptadinemay help

253
Q

Malnutrition definition?

A

BMI <=18.5
Unintentioanl WL >10% within the last 3-6m
BMI <20 and unintentional WL>5% within last 3-6m

254
Q

malnutrition Ix?

A

MUST screening tool

low, med or high risk

255
Q

Malnutrition mx?

A

dietician
food first approach (food ahead of supplements)
ONS (oral nutritional supplements

256
Q

What are some causes of C.diff infection?

A

ampicillin, amoxicillin, co-amoxiclav
cephalosporin
clindamycin
quinolones

257
Q

Ix c.diff

A

C.diff toxin

258
Q

How is C.diff severity classified?

A

mild: normal WCC
moderate: raised WCC (<15), 3-5 loose stools/d
severe: raised WCC OR acutely raised creatinine (>50% above BL) OR temperature >38.5 or evidence of severe colitis
life-threatening: hypotension, partial or complete ileus, toxic megacolon or CT, evidence of severe disease

259
Q

Management of C.diff?

A

mild/mod -> oral metronidazole (10-14days)
severe -> oral vancomycin (10-14days)
then try oral fidaxomicin
Life threatening/ileus -> oral vancomycin + IV metronidazole (10-14d)

260
Q

what is small bowel overgrowth?

A

excess bacteria in small bowel -> GI symptoms

261
Q

what are the RF for small bowel overgrowth?

A

neonates w congenital Gi anomalies, scleroderma, DM

262
Q

What are the S/S for small bowel overgrowth?

A

chronic diarrhoea
bloating, flatulence
abdo pain

263
Q

Ix for small bowel overgrowth?

A

hydrogen breath test
small bowel MC&S
diagnostic ABx course
folate HIGH as bacteria produce it

264
Q

Management for small bowel overgrowth?

A

Rifamixin > co-amoxiclav, metronidazole

265
Q

S/S perianal abscess?

A

pain worse on sitting, discharge, hardened perianal area

266
Q

Mx perianal abscess?

A

1: I&D under LA (packed or left open)

Abx rarely used unless systemic upset

267
Q

What are the S/S of boerhaave’s syndrome?

A

Mackler’s triad
Chestpain
SC emphysema
vomiting

268
Q

What is Zollinger Ellison syndrome?

A

Zollinger-Ellison syndrome is condition characterised by excessive levels of gastrin, usually from a gastrin secreting tumour usually of the duodenum or pancreas

269
Q

what are the associations with Zollinger ellison syndrome?

A

MEN1 (30%)

duodenal/pancreatic tumour

270
Q

Features of ZES?

A

multiple gastroduodenal ulcers
diarrhoea
malabsorption

271
Q

Diagnosis of ZES?

A

fasting gastrin levels: the single best screen test

secretin stimulation test

272
Q

Which antiemetics should be avoided in bowel obstruction?

A

metoclopramide - pro kinetic

273
Q

What is pseudomembranous coltitis and what is seen on imaging?

A

Pseudomembranous colitis refers to swelling or inflammation of the large intestine (colon) due to an overgrowth of Clostridioides difficile (C difficile) bacteria

plain film: loss of bowel wall architecture and thumb printing
CT: moderate free fluid in pelvis and peritoneum

274
Q

What is the most accurate determinant of liver failure?

A

PT as it is a measurement of the liver’s synthetic function and has a shorter half life than albumin

275
Q

Iron deficiency anaemia vs anaemia of chronic disease?

A

Iron defiency anaemia vs. anaemia of chronic disease: TIBC is high in IDA, and low/normal in anaemia of chronic disease

both microcytic anaemia

276
Q

How to treat recurrent C.diff?

A

recurrent infection occurs in around 20% of patients, increasing to 50% after their second episode
within 12 weeks of symptom resolution: oral fidaxomicin
after 12 weeks of symptom resolution: oral vancomycin OR fidaxomicin

277
Q

What is globus pharyngis?

A

Globus pharyngis (also known as globus hystericus) is the persistent sensation of having a ‘lump in the throat’, when there is none. Symptoms are often intermittent and relieved by swallowing food or drink. Swallowing of saliva is often more difficult.

278
Q

globus pharyngis associations ?

279
Q

Causes of dysphagia?

A

Extrinsic
intrinsic
oesophageal wall
neurological

280
Q

Extrinsic causes of dysphagia?

A

Mediastinal masses

Cervical spondylosis

281
Q

intrinsic causes of dysphagia?

A

Tumours
Strictures
Oesophageal web
Schatzki rings

282
Q

oesophageal wall causes of dysphagia?

A

Achalasia
Diffuse oesophageal spasm
Hypertensive lower oesophageal sphincter

283
Q

neurological causes of dysphagia?

A 
CVA
Parkinson's disease
Multiple Sclerosis
Brainstem pathology
Myasthenia Gravis
284
Q

Features of oesopahgitis?

A

There may be a history of heartburn

Odynophagia but no weight loss and systemically well

285
Q

Features of oesophageal candidiasis?

A

history of HIV or other risk factors such as steroid inhaler use

286
Q

what is a pharyngeal pouch?

A

posteromedial herniation between thyropharyngeus and cricopharyngeus muscles
Usually not seen but if large then a midline lump in the neck that gurgles on palpation

287
Q

Symptoms of pharyngeal pouch?

A

dysphagia, regurgitation, aspiration and chronic cough. Halitosis may occasionally be seen

288
Q

what are the features of gallbladder abscess?

A

prodromal illness and right upper quadrant pain
Swinging pyrexia
Patient may be systemically unwell
Generalised peritonism not present

289
Q

mx gallbladder abscess?

A

Imaging with USS +/- CT Scanning
Ideally, surgery although subtotal cholecystectomy may be needed if Calot’s triangle is hostile
In unfit patients, percutaneous drainage may be considered

290
Q

what is calots triangle?

A

Calot triangle or cystohepatic triangle is a small (potential) triangular space at the porta hepatis of surgical importance as it is dissected during cholecystectomy. Its contents, the cystic artery and cystic duct

291
Q

What are the risks of ERCP

A

Bleeding 0.9% (rises to 1.5% if sphincterotomy performed)
Duodenal perforation 0.4%
Cholangitis 1.1%
Pancreatitis 1.5%

292
Q

What is pernicious anaemia?

A

autoimmune atrophic gastritis caused by auto abs vs parietal cells or intrinsic factor

293
Q

pernicious anaemia associations?

A

AI: Thyroid disease, vitiligo, addisons, HPT,T1DAM
3X RISK GASTRIC CA
more common blood group A

294
Q

Features of pernicious anaemia?

A

anaemia
neurological (neuropathy, SCDC, neuropsychiatric)
jaundice
glossitis

295
Q

Ix pernicious anaemia?

A

FBC -> normocytosis, hyperhsegmented neuts, low WCC/plts
Vit b12/folate
Antibodies

296
Q

Mx pernicious anaemia?

A

Vit b12 replacement IM

folic acid supplementation

297
Q

Ix Pharyngeal pouch?

A

barium swallow combined with dynamic video fluoroscopy

298
Q

where does a pharyngeal pouch occur?

A

also known as Zenker’s diverticulum) is a posteromedial diverticulum through Killian’s dehiscence. Killian’s dehiscence is a triangular area in the wall of the pharynx between the thyropharyngeus and cricopharyngeus muscles.

299
Q

RF pharyngeal pouch?

A

5x more common in men

more common in older patients

300
Q

What is commonest extra-colonic malignancy of HNPCC?

A

endometrial>ovarian ca

301
Q

What is lynch syndrome?

A

an autosomal dominant condition, is the most common form of inherited colon cancer. Around 90% of patients develop cancers, often of the proximal colon, which are usually poorly differentiated and highly aggressive

302
Q

what criteria is used to aid diagnosis of lynch syndrome?

A

The Amsterdam criteria are sometimes used to aid diagnosis:
at least 3 family members with colon cancer
the cases span at least two generations
at least one case diagnosed before the age of 50 years

303
Q

What is Gardners syndrome?

A

A variant of FAP causing osteomas of the skull and mandible, retinal pigmentation, thyroid carcinoma and epidermoid cysts on the skin

304
Q

what causes FAP?

A

due to a mutation in a tumour suppressor gene called adenomatous polyposis coli gene (APC), located on chromosome 5 which causes hundreds of polyps

305
Q

How is FAP inherited

A

autosomal dominant

306
Q

What are the three types of colon cancer?

A

sporadic (95%)
hereditary non-polyposis colorectal carcinoma (HNPCC, 5%)
familial adenomatous polyposis (FAP, <1%)

307
Q

What is wilsons disease?

A

Wilson’s disease is an autosomal recessive disorder characterised by excessive copper deposition in the tissues.

308
Q

What causes Wilson disease?

A

defect in the ATP7B gene located on chromosome 13

309
Q

At what age does onset of symptoms typically happen in Wilsons disease?

310
Q

What are some S/S of wilsons?

A

liver: hepatitis, cirrhosis
neurological:
- basal ganglia degeneration: in the brain, most copper is deposited in the basal ganglia, particularly in the putamen and globus pallidus
- speech, behavioural and psychiatric problems are often the first manifestations
- also: asterixis, chorea, dementia, parkinsonism

Kayser-Fleischer rings
renal tubular acidosis (esp. Fanconi syndrome)
haemolysis
blue nails

311
Q

Ix wilsons?

A
  • slit lamp examination for Kayser-Fleischer rings
  • reduced serum caeruloplasmin
  • reduced total serum copper (counter-intuitive, but 95% of plasma copper is carried by ceruloplasmin)
  • free (non-ceruloplasmin-bound) serum copper is increased
  • increased 24hr urinary copper excretion
  • the diagnosis is confirmed by genetic analysis of the ATP7B gene
312
Q

mx wilsons?

A
  • penicillamine (chelates copper) has been the traditional first-line treatment
  • trientine hydrochloride is an alternative chelating agent
  • tetrathiomolybdate is currently under investigation

Year 6 Medicine (18 decks)

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