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Flashcards in GASTROENTEROLOGY Deck (81)
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1
Q

What is HELLP

A

Haemolysis + hypertension
Elevated liver enzymes
low plateletes

Hepatic manifestation of pre-eclampsia

  • Thrombocytopenia occurs due to microangiopathic haemolytic anaemia in liver sinusoids due to HTN
  • This gives rise to biliary congestion
  • Blockade also causes focal hepatic ischaemia and necrosis
2
Q

What is Ischaemic Collitis

A

Ischaemia and necrosis caused by a stenosis or compelte occulsion of flow through the SMA / IMA

Can be chronic or acute

Chronic may present non specifically:
Chronic abdominal pain
weight loss
loose stool
non specific dieficiencies - b12 / folate / fat soluble vitamins
misdagnosed as coeliac / ibs / ibd / anorexia

Acute may present:
peritonitis
deranged LFTs secondary to ischaemia
alongside AAA rupture or AA dissection or Thoracic aorta dissection
shock
bloody diarrhoea
absolute constipation
no bowel sounds
Gas+++ AXR
CTAP
bowel wall gas
bowel wall oedema
biliary air
hepatic necrosis 
perforation
Causes: vitamin C
vascular
-Aortic dissection
-Post AAA repair
-Cardic emobolism / septic embolism
-atherosclerotic disease
-factor V leiden
-antiphospholipid
-paradoxical embolism via ASD / VSD

infective:
Water shed from hypovolaemia
TNF-a septic storm

Trauma:
volvulus
interssusseption

autoimmune:
antiphospholipid

metabolic:
Sickle cell

Iatrogenic / drug induced
HIT - heparin induced thrombocytopenia type 2 - IgG mediated platelet depletion and converse hypoercoagulable state
adhesional obstruction

neoplastic:
direct pressure
embolism

Congenital:
MEC ileus
bowel atresia
malrotation - lads bands
interssusspetion
3
Q

How does PBC present

A

Primary Biliary Cirrhosis
Anti mitochondrial Abs - 90%

AI condition targetting intrahepatic bile ducts ONLY
more common in women especially following pregnancy
presentation 40

4 stages of inflammation leading to cirrhosis
1 - inflammation of bile duct sinusoids
2- extension of inflammatory infiltrate towards liver lobules with increasing fibrosis of local structures
3 - fibrotic septations extend into lobules and begin partitioning liver and reorganising structure
4 - number of immune cells is now reduced. Biliary sinusoids destroyed and fribrosed with limited cellular component. regnertive nodules present

Gradula destruction of intrahepatic bile ducts leading to cholestasis, fibrosis, recurrent cholangitis and hepatic cirrhosis

Px:
• Females are most commonly affected, less
often males
• First disease manifestation following pregnancy
• Pruritus 
• fatigue, reduced performance
• xanthelasmata (subcutaneous fat
deposits in the eyelids)
Keiser fleischer rings
jaundice
associated disorders i
• Associated rheumatic disorders
Joint complaints - RA
Hashimoto thyroiditis
Sicca syndrome - Exocrine glands
• Osteoporosis
• Vitamin deficiency
• Skin changes typical for cirrhosis (see table 4)
• Hepatocellular carcinoma
4
Q

Causes of bloody diarrhoea

A
infective:
Salmonella
Shigella
Compylobacter - C.Diff
Entamoeba
E.Coli

autoimmune
Ulcerative collitis
Miced IBD

vasculitic
wegners granulomatosis and polyangitis

congenital
herediatary haemorrhagic telangiectasia
angiodysplasia

metabolic:
Variceal haemmorhage
Torrential UGIB

5
Q

Causes of watery diarrhoea

A

infective:
Cholera
Tropica Sprue - cause unclear - chronic infection?
Cryptosporidium - parasite - Nitazoxanide / praziquantel

Autoimmune
Coeliac
IBS
IgG4 AI pancreatitis

iatrogenic
Abx induced
short bowel syndrome / dumping syndrome

metabolic
Alcohol - pancreatic insufficiency - need creon
chronic pancreatitis

cancer:
Zollinger Ellison - +++ gastrin

6
Q

What is Coeliac Disease

A

Autoimmune sensitivity propogated by Il-15 and anti-ttg abs and anti-endomysial abs against the a-gliadin peptide of gluten.

Because of pathophysiology there must be an initial insult to small bowel to allow antigen exposure to vasculature / resident MALT unless this occurs via random sampling by DCs.

Presentation:
abdominal pain - sporadic to gluten containing foods
malabsorption - b12 / folate / fat sol vit a/d/e
wartery diarrhoea
bloating
FTT

Dermatitis herpetiformis is specific for coeliac
- 1cm to widespread vesicular painful and pruritic rash

histology:
flattened villi
shallow crypts
inflammatory infiltrates

treatment
Avoidance rye / wheat / cereals containing gluten
Dapsone for Dermatitis herpetiformis
SULFAPYRIDINE for DH if non responsive - needs monitorinf due to risk of agranulocytosis

7
Q

What is the pathophysiology of recurrent hydrothorax in cirrhotic liver disease?

A

Recurrent ascites from raised portal pressures
Typically also causes a right hydrothorax
microdefects in diaphragm allow communication

Lights criteria = transudative - sterile
i.e. normal glucose
pleural protein / serum protein <0.5
Pleural LDH  < 2/3 serum LDH
pH >7.35
MCS negative
normal CT

Management:
1. Drain if symptomatic
2. TIPS - transjugular intrahepatic portosystemic shunt
60-80% have improvement
3. Chemical pleurodesis - better in malignancy
4. liver transplant

8
Q

What is PPI induced colitis

A

Long term use of PPI is associated with lymphocytic collitis

Withdrawal of ppi usually is curative

Dx:
Colonoscopy and biopsy

9
Q

How does CMV collitis present

A

Diagnosis:
Colonscopy + biopsy

Biopsy:
Nuclear inclusion bodies
intracytoplasmic inclusion bodies

10
Q

Who is at risk of CMV collitis

A
Immunosupressed:
ANTI TNFa infliximab / adalimumab / gadalimumab
ANTI INTEGRIN A1B4 vedalizumab
HIV
MTX  / azathioprine

Congenital CMV

11
Q

How is CMV collitis managed

A

Suppotive only

IV ganciclovir + oral maintenance if immunosupressed

12
Q

What antibodies are present in PSC and what is it assoicated with

A

inflammation of bile ducts and sinusoids leading to CLD / fibrosis and cirrhosis via biliary obstruction and inflammation

Abs:
P-ANCA
ANA
and Anti-smooth muscle

Associated with IBD
UC > CD

13
Q

What anitbodies are present in PBC

A

Anti-mitochondrial abs

14
Q

What are the key differences between PBC and PSC

A

PSC – PRIMARY SCLEROSING CHOLANGITIS
PBC – PRIMARY BILIARY CHOLANGITIS

SEX AGE SMOKING
PSC
60%men
40s
non smokers
PSC
90% women
Typically post partum ?trigger
smokers
>45

DISEASE SITE:
PSC
Larger Bile ducts inside and outside the liver
Small duct PSC (10-15% of patients) only the small ducts inside the liver are affected

PBC
Small bile ducts inside the liver only

ANTIBODY PROFILE
PSC
limited
anti-smooth muscle
ANA
P-ANCA +Ve

PBC
Anti-mitochondrial
ANA

DIAGNOSED BY
PSC
MRCP
liver biopsy

PBC
Raised ALP
AMA
diagnostic liver biopsy.

MALIGNANCY RISK:
PSC
increased risk of HCC and colon cancer

PBC
No increased risk

RESPONSE TO URSODEOXYCHOLIC ACID(UDCA)
PSC
Improves liver blood tests in some patients
not conclusively proven to slow disease progression

PBC
Associated with improved prognosis in those individuals who respond well to UDCA

IBD ASSOCIATION
PSC
80% of patients have IBD – mostly UC

PBC
IBD not common
RA / hashimotos and SJORGENS and coeliac are more common

BOTH PRESENT THE SAME:
Itching, fatigue, abdominal pain, cholangitis flares Itching, fatigue, dry eyes and mouth, abdominal pain

PSC
FIBROSIS OF MEDIUM AND LARGE BILE DUCTS INSIDE AND OUTSIDE LIVER
DIAGNOSIS VIA MRCP
MEN AND WOMEN IN 40s most commonly
ASSOCIATED UC

INCREASED RISK OF COLON AND HCC

NO CURE - SLOW PROGRESSION ONLY
BLOODS IMPROVED BY URSODEOXYCHOLIC ACID but no change to prognosis

PBC
SMALL INTRAHEPATIC BILE DUCTS ONLY
MAINLY WOMEN 90% WHO SMOKE AND OVER 45
ASSOCIATED RA . HASHIMOTOS . SICCA

DIAGNOSIS VIA BLOODS AND AMA

RESPONSE TO UDCA CORROLATES TO SURVIVAL AND LOWER RISK OF TRANSPLANT

NO ASSOC WITH CANCER or IBD

15
Q

What is Truelove and Witts Criteria and what is it used for

A
Used to grade severity of UC presentation
6 areas 
-Frequency
-Blood
-Pyrexia
-Pulse
-Anaemia
-ESR

Summary
1-4 stools +/- blood + no fever + normal ESR/CRP
>4 stools + minimal fever / tachycardia
>6 bloody stools with systemic disturbance and ESR>30

Frequency
1-4 stools more than normal
>4 stools more than normal
>6 stools more than normal

Blood
<50% blood
>50% blood
All blood

Pyrexia
no fever
no fever
>38

Pulse
no tachy
no tachy
>tachy

Anaemia
no anaemia
no anaemia
anaemia

ESR
normal ESR
<30
>30

16
Q

What is measured prior to starting azathioprine / mercaptopurine therapy?

A

TPMT activity
THIOPURINE METHYL TRANSERASE - changes azathioprine to mercaptopurine

nb xanthine oxidase breaks down mercaptopurine

Low activity = increased risk of BM suppression and toxicity with normal dose of azathioprine or mercaptopurine (toxic compounds hang around longer)

Beware allopurinol - xanthane ox inhibtor - will prevent breakdown of mercaptopurine extending half life and potential toxicity.

Can be used therapeutically to deliver a tiny dose of purine antagonist.

LFT and FBC monitored at 2/4/8/12 weeks
3 monthly thereafter
MMP and TGN levels done at 4 weeks then 12-16 weeks or 4 weeks after dose alteration
ration important as shows appropriate breakdown to avoid toxicity of purine metabolites

17
Q

What is the best management for fistulating crohns

A

Primary intervention would be IV hydrocortisone 400mg per day as for UC

Infliximab / adalimumab have the best evidence for fistulating crohns

Fistulas tend to improve within the first 2-3 weeks in 2/3 patients

Need immunoscreen prior:
HBV HCV TB quantiferon / mantoux HAV HEV CMV EBV TPMT

Treatment ladder:
1-IV hydrocort or pred (esp maintenance) +XRay +stool culture
2-elemental diet - mixed evidence
3-rectal and oral enemas of mesalazine - 5’ASA
4-Azathioprine - need TPMT level - steroid sparing agent
Mercaptopurine
5-MTX if intolerant to thiopurines or TPMT low
6-Infliximab
7-adalimumab
8-vedalizumab
9-colectomy

18
Q

What is Gardener’s Syndrome

A

Aut Dominant inheritance
COLONIC ADENOMAS
OSTEOMAS
SOFT TISSUE TUMOURS.

Mx:
surveillance colonoscopy
Pancolectomy once polyps appear

Multiple adenomatous polyps throughout large bowel
LESS THAN FAP
INCREASING RISK OF COLONIC CANCER YEAR ON YEAR

7% AT 21
50% AT 39
90% AT 45

19
Q

What is carcinoid syndrome

A

Carcinoid tumours secrete serotonin - NEUROENDO
Detected by urinary collection of 5’hydroxyindoleacetic acid

85% CARCINOID:
FLUSHING
DIARRHOEA
NEW MURMUR / CARDIAC INOVLEMENT
-RIGHT VALVULAR STENOSIS

DETECTION:
URINARY ANALYSIS OF SEROTONIN METABOLITE AS ABOVE
IMAGING WITH PENTREOTIDE

can be tumours anywhere
COLORECTAL
BRONCHIAL

20
Q

How does acute porphyria present

A

Abdominal pain 85-95%
Vomiting 50-90%
Paresis - 40%
Neurological symptoms - seizures 10-30%

  1. Urine changes colour on standing - due to uro-porphobilinogen
  2. uro porphobilinogen >300
  3. photolytic rash

Mx:
avoid triggers
sunlight / alcohol / anti-epileptics / metoclopramide
blood letting in PCT as iron inhibits UROD - UROPORPHYNOGEN DECARBOXYLASE
CHLOROQUINES in PCT
HAEM arginate - replenishes haem and reduces synth
Dextrose - inhibits haem synth and reduces porphyrins

21
Q

What is the MOA of haem arginate

A

Replenishes haem store - reduces synthetic drive that causes build up of porphyria

22
Q

What is oesophagial cancer associated with?

A

Dermatomyositis
same as bronchial cancer

male
smoker
barretts
achalasia
coeliac
tylosis pylori - AD keratosis of hands and feet
23
Q

How Is UC Graded - 2 systems

A
TRUELOVE AND WITTS
Frequency 1-4 / 4-6  / >6
blood <50% / >50% / just blood
pyrexia no/ no/ yes
tachycardia no/ no /  yes
anaemia no/ no/ yes
ESR no / <30 / >30
MAYO SCORE - 4 areas = x/12
Frequency
-1-2 stools > than normal
-3-4 stools >than normal
->4 stools than normal per day

Rectal Bleeding

  • blood present <50% time
  • blood present >50% time
  • passing blood alone

Endoscopic Findings
physician’s global assessment - systemic features

GLobal assessment
pyrexia / tachycardia / BP (HD stability)

Not a diagnostic tool
good for assessment

Remission is often defined as a total score of 2 or less with all individual categories ≤1.
Most clinical trials define mucosal healing as an endoscopic score of 0 or 1

24
Q

How is UC managed

A
  1. Score presentation (MAYO / TW) + Xray
  2. Stool culture + screen TB HAV HEV HBV HCV CMV EBV
  3. Start IV hydrocort - review after 72 hours
  4. Oral pentasa / rectal pentasa 2.4g / mesalazine
    - left sided tisease mainly rectal preps
  5. Endoscopy to assess + biopsy
  6. Ciclosporin / tacrolimus for steroid resistant disease
  7. infliximab
  8. colectomy

In states of remission can be weaned onto azathioprine or mercaptopurine - may need maintenacne infliximab if this fails

25
Q

Differential for raised isolated ALT

A

Viral hepatitis

Blood transfusion - think HCV or HBV
e.g. haemophiliac

26
Q

What is Achalasia

A

Failure of LOS relaxation 1/1000 PEOPLE

manometry = failure of peristalsis in distal oesophagus
Endoscopy = normal or LOS fails to relax on swallow

intermittent symptoms
hallitosis from residual food
aspiration due to recurrent nocturnal aspiration

27
Q

How is an acute variceal bleed managed

A
  1. Resus - activate major haemorrhage protocol
    2 fluids and blood products
  2. urgent variceal banding and commence terlipressin

TERLIPRESSIN / SOMATOSTATIN / OCTREOTIDE
good evidence to support reduced re-bleeding rate and early complications

Sclerotherpay is superior to balloon tamponade but not to banding

28
Q

How is PBC treated

A
Remember PBC
90% female with ANTI MITOCHONDRIAL ABS
>45
smokers
post pregnancy trigger
intrahepatic biliary only
NO CANCER
NO IBD
RA / hashimotos + sjorgrens +coeliac

UDCA
Response to UDCA predicts better outcome
failed response add in budesonide / pred
Colestyramine for pruritis (binds bile salts for excretion)

Osteoporosis
Bisphosphonates and exercise
Vit D

Liver transplant
Once jaundiced survival is <2 years

29
Q

How is PSC treated

A
Remember PSC
Intra or extrahepatic biliary
Associated with anti-smooth muscle PR3 - anca (P-ANCA) and ANA
60% men
non smokers
ASSOC IBD and HCC / COLON

no cure - same as PBC

Treatment
UDCA
bisphosphonates and vit D and diet + oestrogens
Liver transplant

30
Q

What does Barium swallow show in Achalasia?

what other differentials are raised

A

Birds beak appearance caused by barium hold up caused by impaired peristalsis and failure of LOS relaxation

Diffs:
Oesophagial Ca - pseudo achalasia
Compressive bronchial cancer

manometry gold standard
progress to endoscopy to visualise

31
Q

What would achalasia look like on manometry

A

Raised resting LOS pressure

non propagated lower oesophagial body contractions

32
Q

How do you monitor for lithium toxicity?

A

raised GGT

raised lithium levels

33
Q

How is ALD monitored

A

AST: ALT ratio

ALD = AST x2 : ALD i.e. ratio >2
abdo USS
Na
recurrent ascites
HCV/HBV status
ALC liason nurse
34
Q

What is Peutz Jeghers syndrome

A

Autosomal dominant condition more common in Ashkenazi Jews

MUTATION IN serine threonine kinase 11

Significant risk of malignant tranformation

almost 50% with PJ develop cancer and die by age 57
STOMACH / COLON / PANC / BREAST

  • macular oral pigmentation crossing vermillion border
    (mucocutaenous melanocytic macules)
  • hamartomatous polyps

Mx:
yearly mammography / uss
endoscopy yearly
abdo uss

35
Q

What is Plummer Vinson Syndrome

A

Triad:
Iron def
Oesophagial webs + Dysphagia
Angular chelitis

RF for SCC of oesophagus

36
Q

What is Tropical Sprue

A

Diagnosis of exclusion for state of malabsorption on returning from abroad

Typically thought to be due to floral imbalance
Common caribbean and far east

small intestinal malabsorption due to infection
See villous atrophy
crypt hypertrophy
megaloblastic / macrocytic anaemia due to folate and b12
fat malabsorption

Rx: abx for 6/12
Tetracyclin
ampicillins
b12 and folate replacement

37
Q

What is Pellagra

A

Deficiency of niacin or tryptophan (precursor)
A) Primary deficiency
B) Secondary
- malabsorption state e.g. tropical sprue / coeliac
-consumptive state - carcinoid tumours use native tryptophan and convert this to serotonin. This prevents production of niacin and thus pellagra

diarrhoea dementia dermatitis death
confusion / inattention / memory loss / thick skin

Substrate for serotonin production

deficiency = dementia

replace with nicotinic acid

38
Q

How can boehaaves present?

A

Spontaneous oesophagial rupture secondary to vomiting

  • Epigastric pain radiating to back
  • dyspnoea
  • pleural effusion
  • empyema
  • surgical emphysema of neck
39
Q

What are side effects of ileal resection

A
SBS
-chronic malabsorption of  b12 / folate
(IF binds b12 for absorption ileum)
- macrocytic anaemia
- Dermatitis (no linoleic acid absorption)
-chronic diarrhoea + dehydration
-dumping syndrome
-weight loss
- bile salt malabsorption - fatty stools
Abnormal 14C glycolate test (also seen in bacterial overgrowth and H.Pylori) - can also be done with 13C
Rx:
Parenteral nutrition
loperamide
codeine
teduglutide = GLP-2 agonist which slows gastric transit and after 6 months reduces TPN top up requirments by 20-100%
40
Q

What is Zollinger Ellison syndrome

A

Heightened Gastrin production - GASTRINOMA

  1. FASTING GASTRIN LEVEL ON 3 SEP DAYS
    -release is pulsatile
    3 normal = gastrinoma unlikely
  2. secretin stimulation test
  3. basal acid output

Treatment:
Excision
ocreotide
IFN / chemo

41
Q

What are the extra GI manifestations of CD

A
  1. PSC (anti smooth muscle / malignancy / UDCA / >men)
  2. seronegative spondyloathropathy or RA like
  3. Uveitis or episcleritis
  4. PYODERMA GANGRENOSUM (failed wound healing / stoma ulcers / new ulcers - TOPICAL TAC / oral/ IV pred or inflix or tac)
  5. Gall stones- Bile acid malabsorption and Bact overgrow
  6. erythema nodosum
42
Q

What mutation is the most common in the HFE gene

A

C282Y

43
Q

What is the treatment for NASH

A

weight loss

44
Q

What causes MALT lymphoma?

A

B cell lymphoma associated with H.Pylori infection.

Urease 13/14 breath test
drink radio-labelled compound
detect radio-isotope in expired breath only if h.pylori present

treat anyway due to incidence of fa;se negative

Treatment:
1 H.Pylori eradication = remission in 75% of cases

if not - chemo and resect

45
Q

What is Whipple’s disease?

Whiipples = coeliac+ mulitsystem + wobbly and fatal

A

Rare multi system disorder caused by T.Whippelei.

  • cardiac / pericarditis / endocard / conduction defects
  • Diarrhoea
  • weight loss
  • cerebellar ataxia / seizures / CN lesions
  • pleurisy / fibrosis
  • pigmentation
  • fatty stool
  • lymphadenopathy

Diag:
histology
Acid Schiff positive mcrophages in small intestine mucosa
flattened villi - Coeliac / tropical sprue

Treat abx
30% relapse

46
Q

What are the sequelae of entamoeba hystolica infection?

A
Fever
abdominal pain
weight loss
malabsorption
watery diarrhoea

liver abscess - usually single right lobe
mutliple left sided abscesses also possible

Rx:
trophozoite is susceptible to metronidazole
10 day course

47
Q

When should diarrhoea be treated with antibiotics?

A

Conditions:
Pyrexia
>6 stools per day without improvement after 72 hours or worsening symptoms
HD compromise

no history of IBD

48
Q

What medications are used in liver transplant?

A
Immunosuppressive therapy options
following liver transplantation
• Cortisone preparations (e. g. prednisolone or
prednisone)
• Cyclosporin A
• Tacrolimus
• Azathioprine
• Mycophenolate Mofetil
• Combination of the above medications
49
Q

What are the sequelae of C. Diff

A

PSEUDOMEMBRANOUS COLLITIS

Yellow plaques on flexi-sigmoidoscopy

Mort in elderly = 10%

Rx:
Vancomycin - oral = 0 absorption so good for gut treatment
Metronidazole

Cholestyramine may be useful to reduce diarrhoea

50
Q

How does fatty liver of pregnancy present?

A

Late onset in gestation

DIC
raised wcc
Raised ALT
Nausea and vomiting
low albumin
prolonged PT indicating abnormal synthetic function
encephalopathy if enters decoompensated liver disease

May need ITU admission
May also require FFP / cryo precipitate

protein restriction to reduce ammonia
laxatives

51
Q

Intrahepatic cholestasis of pregnancy

A

Bile acid transporter defect
Last trimester

Prutiris
jaundice
prolonged PT due to vit K deficiency

52
Q

Selective B12 deficiency with normal folate

A
B12 is coupled to IF for absorption in TI
Therefore 
a) ileal disease
Crohns
ileal resection
TB

b) Pernicious anaemia

c) b12 excess utilisation with little to absorb
bacterial overgrowth
diverticula 
fistulae
radiation enteritis
systemic sclerosis
53
Q

How does Haemochromatosis present and how is it managed?

A

Iron storage disoder leading to iron overload and deposition in organs causing systemic dysfunction and CLD.

  • weakness
  • fatigue
  • bronze diabetes
  • impotence
  • depression
  • Cardiomyopathy
  • Signs of CLD

Most common mutation
C282Y = HFE mutation

Diagnosis

1) transferrin saturation >55%
2) genotyping
3) biopsy if remains unclear

RX:
Weekly venesection until transferrin <16%
Aim ferritin <50%
Desferoxamine iron chelation

54
Q

What are the causes of acute pancreatitis and how is it graded?

A

Glasgow criteria for pancreatitis:
PANCREAS - >3 = severe

Pa02 <8
Age >55
Neutrophils >15
Calcium <2 (norm 2.25-2.5 mmol/l)
Renal Urea >16
Enzymes - LDH>600 or ASt>2000
Albumin <32
Sugar >10

Causes: I GET SMASHED

IDIOPATHIC

GALL STONES
ETOH
TRAUMA or Mechanical - sphincter of Odi dysfunction

STEROIDS
MUMPS
AUTO IMMUNE IGG4
SCORPION STINGS
HEREDITARY and hypercalcaemia and hypertrigyceridaemia - CF / PRIMARY CILIARY DYSK / AIH
ERCP
DIURETICS - THIAZIDE / THIAZIDE LIKE / LOOPS

55
Q

What is a sensitive marker for measuring lithium toxicity?

A

GGT

56
Q

What LFT ratio is common in ALD?

A

AST:ALT
2:1

57
Q

OGD confirms low grade dysplasia - next step?

A

6 monthly OGDs

Oral omeprazole 40mg OD or equiv

58
Q

How is bacterial overgrowth syndrome managed?
How might it present?
What is it associated with?

A

Associations:
SBS post small bowel
- crohns
- obstruction / mechanical / ischaemic /
Dumping syndrome in Ziehl Niehsson gastrinoma
Systemic sclerosis

Wartery diarrhoea
malabsorption
Fatty vitamin dieficiency - prolonged INR / steatthorhoea / offensive stool / b12 def - mixed motor and sensory neurop / folate def = macrocytic anaemia / iron def anaemia (normocytic or micro) / bile salt malaborption

Test:
Increased hydrogen on H breath test

59
Q

Acute management of UGIB?

A
A BLATCHFORD AT PRESENTATION
ROCKALL POST ENDOSCOPY
1. Massive transfusion protocol + /- sengstaken tube
2.PLT transfusion only if
 - PLT<50
 - active bleeding
3. FFP if PT is x1.5
4. Reverse Warfarin with PTC / berryplex
5. Prep endoscopy
60
Q

What is the blatchford score used for?

A

Stratify patients based on risk of mortality into intervention tiers

  • Hb
  • urea
  • BP
  • M/F
  • HR>100
  • meleana?
  • syncope?
  • liver disease?
  • HF?

0 = likely no need for intervention
>0 = itervention
higher scores corrolate with mortality

61
Q

Management of Variceal bleed?

A
A BLATCHFORD AT PRESENTATION
ROCKALL POST ENDOSCOPY
1. Massive transfusion protocol + /- sengstaken tube
2.PLT transfusion only if
 - PLT<50
 - active bleeding
3. FFP if PT is x1.5
4. Reverse Warfarin with PTC / berryplex
5. IV Terlipressin for 5 days
6. Neomycin or rifaximin
5. Prep endoscopy

Oesophageal varices
- band ligation

  • Transjugular intrahepatic portosystemic shunts (TIPS)

Gastric varices

  • endoscopic injection of N-butyl-2-cyanoacrylate
  • TIPS ifnot controlled by N-butyl-2-cyanoacrylate.
62
Q

What is the evidence behind PPI use in UGIB?

A

Reduces rebleed risk by 50% and surgical intervention by 40% - meta-analysis of 21 RCTs

H2 inhibitors (ranitidine) are less effective

Note for PPI post stabilisation!

63
Q

HCV is associated with what renal problem?

A

Can be associated with a mixed cryoglobulinaemia
can present at ay time

Associated with systemic vasculitis and purpuric presentation

This may result in nephritic presentation

Treatment is focused on the reduction of systemic viraemia which is though to drive the process

Note there may be crossover in HIV

HIV associated nephropathy is an FSGS pattern and associated with heavy heavy proteinurea

64
Q

GORD management

A
History
sodium alginate
lansoprazole
omeprazole
-both associated with lymphocytic colitis and hyponatraemia
-omeprazole can also interfere with cyt p450
OGD
h.pylori eradication
65
Q

What is pyoderma gangrenosum associated with?

A

Crohns
treat with topical tac
oral pred
iv hydrocort if widespread

66
Q

How can SBS be managed?

A
Parenteral nutrition
Creon
loperamide
codeine
teduglutide = GLP-2 agonist which slows gastric transit and after 6 months reduces TPN top up requirments by 20-100%
67
Q

How can NASH be managed?

A
diet
weight loss
Liraglutide
- reduces hepatic steatosis
- aids weight loss
-stabilises glycaemia
TIPS / banding / terlipressin
68
Q

Evidence of decompensated CLD

A

Ascites
Asterixis
Altered GCS

69
Q

Causes hepatomegally x3

A

Alcohol related liver disease
Congestive cardiac failure
Metastases

Plus
Infection
Auto immune (PSC PBC AIH)
Infiltrative (amyloid CML)

70
Q

Cirrhosis investigation

A
Liver screen
HAV HBV HCV CMV EBV HIV
A1 ANTI TRYPSIN
AFP
Ferritin if >500 HFE AND IN 30s
Caeruloplasmin and Copper
AIH - antimitochondrial 

Plus

INR AND ALB for synthetic function
LFTs
Liver biopsy
Liver USS with Dopplers
ERCP (PSC brushings )
71
Q

Malignancy Ix

A
CXR AND CT
PET
LIVER BIOPSY
MDT
RESECTION 
RFA
72
Q

Complications of Cirrhosis

A
Hepatic Encephalopathy
G1 disorientated
G2 Confused 
G3 fluctuant GCS cannkt fimmow commands 
G4 Flat and depressed GCS and death
SBP 
Wcc >250 on tap
Variceal haemorrhage
73
Q

Child Pugh score

A
Prognostic indicator of mortality 1 year
Encephalopathy
Ascites
Inr and albumin
Br

<6 100%survival 1 year
7-9 81% survive 1 year
10-15 45% survive 1 year

74
Q

Treatment ascites

A
Drain
Pleurex (palliative)
Abstinence
Low salt and nitrogen diet
Spironolactone
Transplant
75
Q

Causes splenomegally

A

Massive >8cm
Myelofibrosis or myeloproloferative (P rubra vera) and CML CLL or Non hodgkins or hairy cell lymphoma
Malaria and Leishmaniasis

Moderate >4cm
Myelofibrosis or proliferative 
Haemolysis
Chronic Infectious hepatitis or EBV
Gaucher amyloid sarcoid TV

Minor Tip
ITP / AIHA /Haemolysis
Portal HTN
Infection acute Hav hev hbv hcv ebv htlv

Myeloproliferative or lymphoproliferative
CML / MYELOFIBROSIS
Infectious 
Malaria/ TB/ Leishmaniasis
Haemolysis
B THAL / ITP /Autoimmune /sickle cell
Infiltrative
Gaucher / amyloid/ sarcoid
76
Q

Splenomegally screen

A
FBC
- raised wcc
- raised plt
- raised rbc / rdw
Calcium and ACE
LFTS
BNP
Viral screen
ABDO USS
FILM
nuclear inclusions / blasts - myeloprololif
Smear +ve old small wcc - CLL
Tear drop poikilocytosis high basophil and eosonophil myeloproliferative

Hb electrophoresis

SPECIAL
JAK 2 for Polycythaemia rubra vera
BCR ABL for CML
Protein elec and IGs for MGUS SMG MM
MPL for myelofibrosis
Malaria screen thick and thin film trophozoites
77
Q

Reasons for liver transplant

A
CIRRHOTIC LIVER DISEASE
-ALD NAFLD SARCOID AMYLOID
Acute liver failure
-PCT OD and Viral hep plus PBC PSC
HCC
-HFE / viral hep / etc
78
Q

Causes Gum Hypertrophy

A
Ciclosporin Nifedipine Phenytoin
Scurvy
AML
Pregnancy
Familial
79
Q

Transplant skin signs

A
Bcc and Melanoma X 10
Scc X 100
Acitinic keratosis
Viral warts 
Cellulitis
80
Q

Transplant side effects

A
Immunosuppression
-PCP / CMV / viral hep or TB
Side effects
-Tac tremor and HTN
Ciclosporin gumnhypertrophy and nephro tox
-Chronic Rejection
Minor HLA incompatibility
Recurrence of original disease 
Skin malignancy
Other malignancy or lymphoma
81
Q

Liver transplant causes

A

CIRRHOSIS
ALF
HCC