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first year med > GI conditions > Flashcards

GI conditions Flashcards

1
Q

where are the common locations to find squamous cell carcinoma of the mouth? How do they present?

A

floor of mouth
lateral borders of the tongue

hard, indurated ulcer with raised + rolled edges

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2
Q

what are some precursors to oesophageal adenocarcinoma?

A

oesophagitis (reversible) -> Barrett’s oesophagus (irreversible?) -> adenocarcinoma

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3
Q

what red flags indicate a 2 week endoscopy referral?

A

> 55 y/o with new onset pain / reflux with anaemia
weight loss
anaemia - could be indicated by conjunctival pallor
dysphagia + odynophobia
GI bleed - melaena or coffee ground vomiting
worsening GI pain with N+V, low Hb + raised PLT count

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4
Q

what is gastropathy?

A

epithelial cell damage and regeneration without inflammation

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5
Q

what is gastroparesis? what is it’s treatment?

A

partial paralysis of the stomach - delayed gastric emptying

treatment = remove cause + correct nutritional deficiencies
–> may requite pro-motility agents / gastric pacemaker

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6
Q

what is functional dyspepsia and what are it’s investigations?

A

dyspepsia symptoms but no structural abnormality for explanation

investigations = H. pylori excluded via stool antigen test

    • young (<50) need no further investigations
  • – older or red flag symptoms require endoscopy
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7
Q

does eating worsen or improve pain from duodenal ulcers?

A

eating improve pain of duodenal

** eating worsens pain when gastric ulcer

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8
Q

what are the investigations for peptic ulcers?

A

<55 - typical symptoms + positive for H. pylori = start eradication therapy + no further investigations required

older or red flags - endoscopic diagnosis (rapid urease test (CLO) + exclusion of cancer

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9
Q

management of peptic ulcers?

A

high dose protein pump inhibitors - omeprazole
if H. pylori - eradication therapy
–> amoxicillin (metronidazole if allergic) + clarithromycin

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10
Q

what is the histological change in barretts oesophagus?

A

metaplasia of the lower oesophagus from squamous to columnar epithelium

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11
Q

what is the management of barretts oesophagus?

A

PPI - omeprazole

if dysplastic = ablation treatment - photodynamic, laser or cryotherapy
–. destroys epithelium so replaced by normal cells (prevents progression to cancer) - don’t use if no dysplasia

monitored for dysplasia

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12
Q

what is achlasia and what can cause it?

A

impaired peristalsis (ring of muscles don’t open properly) + failure of LOS to relax

causes-
nerve damage to oesophagus
viral infection
autoimmune condition

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13
Q

what are signs + symptoms of achlasia?

A

gradually worsening symptoms (few years) until impossible to swallow

dysphagia
bringing up undigested food
chocking/coughing
spontaneous chest pain - due to oesophageal spasm
gradual weight loss
chest infections

lower oesophageal pressure elevated in >50%

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14
Q

what are the investigations for achlasia?

A

CXR - dilated oesophagus, fluid level behind heart, absent fundal gas shadow

manometry - small plastic tube, measures pressure at various points

barium swallow - lack of peristalsis, ‘bird’s beak’ due to failure of sphincter relaxation

endoscopy - passes with little resistance

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15
Q

what is the treatment for achlasia?

A

all palliative
nitrates / pifedipine - relax muscles, side effects = headaches
balloon dilation - often need repeated, may cause rupture
botox injections - needs repeated
Heller’s myotomy = surgery (permanent)

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16
Q

what is Heller’s myotomy? when would it be carried out?

A

surgery where muscle fibres are cut to make swallowing easier
permanent fix
can cause reflux + heartburn

used for achlasia treatment

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17
Q

how would you discover an oesophageal diverticulum?

A

barium swallow

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18
Q

what type of bacteria is helicobacter pylori? how does it effect the GI tract?

A

gram negative aerobic bacteria

forces way into gastric mucosa to avoid acidic environment - breaks created exposes epithelial cells to acid
produces ammonia to neutralise acid - also damages epithelial cells

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19
Q

what investigations are carried out for H. pylori infections?

A

urea breath test
stool antigen test - no antibiotics or H2 antagonists for 4 weeks
rapid urease test (CLO test) - done during endoscopy, (stomach mucosa biopsy + urea -> if present urease enzymes produce ammonia -> pH test alkaline)

offered to anyone with dyspepsia - 2 weeks PPI free before testing

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20
Q

what is the treatment for H. pylori?

A

triple therapy for 7 days

- omeprazole + amoxicillin (metronidazole if allergic) + clarithromycin

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21
Q

how do you test for giardia and amoeba?

A

stool microscopy

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22
Q

how do you test for salmonella, campylobacter, shigella?

A

stool culture - salmonella, campylobacter, shigella

blood cultures - salmonella

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23
Q

how do you test for C. Diff?

A

stool toxin

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24
Q

describe staph aureus in association with gastroenteritis

A

gram positive coccus
fast incubation - 1hr of eating milk, meat, fish (preformed toxin)
acts on vomiting centre in brain
goes yellow on blood agar - beta haemolysis

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25
Q

list some causes of upper GI haemorrhages

A

oesophageal varices
mallory-weiss tear - tear of mucous membrane at oesophagogastric junction
peptic ulcers
peptic cancers

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26
Q

what scoring is used in upper GI bleeds?

A

glasgow-blatchford score - risk of having upper GI bleed

rockall score - post endoscopy for risk of rebleed / overall mortality

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27
Q

how is variceal bleeding treated?

A

terlipressin - vasoconstrictor (not for ischaemic HD)
+ prophylactic broad spectrum antibiotics at presentation (before endoscopy)

band ligation
injections of sclerosant

TIPS if both fail

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28
Q

why does urea rise in upper GI bleeds?

A

blood in GI tract gets broken down by the acid and digestive enzymes
–> one of the breakdown products is urea + this urea is then absorbed in the intestines

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29
Q

list the management of upper GI bleeds? (ABATED)

A

ABCDE resuscitation
Bloods - test for Hb, coagulation, urea, liver disease
Access - 2 large bore canula (for fluids + blood)
Transfuse
Endoscopy - ASAP, within 24hrs is stable
Drugs - stops coagulants + NSAIDs

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30
Q

transfusion treatment is based on the individual presentation, what are the different types of transfusion that would be given for an upper GI bleed?

A

massive haemorrhage = blood, platelets + clotting factors (fresh frozen plasma)

active bleeding + thrombocytopenia (platelets <50) = platelets

actively bleeding warfarin patients = prothrombin complex concentrate

** transfusing more blood than necessary is harmful **

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31
Q

what is the pathogenesis of appendicitis?

A

obstruction of the lumen -> lumen fills with mucus -> increased intraluminal pressure -> reduced blood flow to the appendix -> inflammation + ischaemia -> perforation -> peritonitis

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32
Q

what are causes of appendicitis?

A

obstructed lumen by faecolith (hard stoney mass of faeces)
bacterial
viral
parasites

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33
Q

signs + symptoms of appendicitis?

A

central pain that migrates to right iliac fossa - worsens when laughs, goes over bumps
anorexia
no bowel movements that day

mild pyrexia + tachycardia
tender, localised pain in RIF
pressing left causes pain on right
pain on flexing hip + internally rotating causes pain

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34
Q

signs of malabsorption?

A

diarrhoea - fat, globules, offensive
easy bruising
spooning of nails

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35
Q

symptoms of small bowel obstruction?

A

intermittent pain - colicky (trapped wind, central, cramping
absolute constipation - no farts or stool
vomiting - feeling better after it
burping
abdominal distension

high pitched bowel sounds

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36
Q

list some extra-gastrointestinal manifestations of IBD

A

eyes - uveitis, conjunctivitis

joints - arthritis, inflammatory back pain

skin - erythema nodosum, pyoderma gangrenosum

liver + biliary tree - sclerosing cholangitis, chronic hepatitis cirrhosis, gallstones

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37
Q

list characteristics of crohn’s disease

A 
No blood or mucus
Entire GI 
Skip lesions
Terminal ileum most affected
Transmural inflammation
Smoking is a risk factor

non-caseating granuloma
cobble stoning

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38
Q

what is the management for inducing and maintaining remission in crohn’s?

A

inducing -
first line = steroids (oral prednisolone, IV hydrocortisone)
if not enough add immunosuppressant (azathioprine, meracaptopurine)

maintaining -
patient specific, may not require medication
first line = azathioprine or mercaptopurine

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39
Q

list characteristics of ulcerative colitis

A 
Continuous inflammation
Limited to colon + rectum
Only superficial mucosa affected
Smoking is protective
Excrete blood and mucus
Use aminosalicylates
Primary sclerosing cholangitis (PSC)

lack of goblet cells
pseudopolyps

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40
Q

what is PSC?

A

primary sclerosing cholangitis = disease that causes scarring of bile duct - obstruction out of liver to intestines

–> leads to hepatitis, fibrosis + cirrhosis

associated with UC

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41
Q

what is the management for inducing remission of ulcerative colitis?

A

mild + moderate -
first line = aminosalicylate (mesalazine oral or rectal)
second line = corticosteriods (prednisolone)

severe -
first line = IV corticosteroids (IV hydrocortisone)
second line = IV ciclosporin (immunosuppressant )

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42
Q

what is the management for maintaining remission of ulcerative colitis?

A

aminosalicylate - mesalazine oral or rectal

azathioprine (immunosuppressant)

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43
Q

list immunosuppressants given for IBD

A 
azathioprine
mercaptopurine
methotrexate
infliximab
adalimumab
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44
Q

what surgical interventions can be done in UC?

A

proctocolectomy = removal of colon + rectum (UC only effects colon + rectum)

patient is either left with an ileostomy or a ileo-anal anastomosis (‘J-pouch’)
–> ileum is folded back on itself + functions like a rectum

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45
Q

what is required for the diagnosis of IBS?

A

Abdominal pain/discomfort ( ? 3 days a week for 3 months ? )
o Relived on opening bowels OR
o Associated with a change in bowel habit (stool form + frequency)

AND 2 of:
o	Abnormal stool passage – in complete emptying
o	Bloating
o	Worse symptoms after eating
o	PR mucus
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46
Q

should you recommend a high or low FODMAP diet in IBS?

A

LOW

avoid - wheat, rye, garlic, onions, milk, yogurt, calorie sweeteners, agave

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47
Q

what genes are associated with coeliac disease?

A

HLA-DQ2

HLA-DQ8

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48
Q

what antibodies are tested for in coeliac disease?

A

anti-tissue transglutaminase (anti-TTG)

anti-endomysial (anti-EMA)

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49
Q

what histological features are associated with coeliac disease?

A

villous atrophy - causes malabsorption

crypt hyertrophy/hyperplasia

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50
Q

symptoms of coeliac disease

A

dermatitis herpetiformis - itchy skin vesicular rash typically on abdomen
failure to thrive
weight loss
iron deficiency anaemia - due to malabsorption
mouth ulcers

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51
Q

investigations for coeliac disease

A

must be on gluten diet for 6 weeks prior to testing

raised anti-TTG, anti-EMA
–> total IgA first to exclude IgA deficiency (prevents false negative)

endoscopy + biopsy - villous atrophy + crypt hypertrophy/hyperplasia

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52
Q

biliary colic symptoms

A

gallstones in cystic duct

sudden onset of constant colicky pain in epigastrium or RUQ
–> may radiate to back

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53
Q

what is murphys sign and what is it a sign of?

A

murphys sign = inspiratory arrest upon palpation of RUQ

commonly seen in acute cholecystitis (inflammation of gall bladder)

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54
Q

symptoms of acute (ascending) cholangitis

A

bacterial infection / inflammation of biliary tree

charcot’s triad = RUQ pain, fever, jaundice
septic/unwell -> hypotension, confusion

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55
Q

pathophysio of pre-hepatic (haemolytic) jaundice

A

excess haemolysis > leads to increase bilirubin (end product of haem breakdown) > accumulation of UNconjugated bilirubin > jaundice

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56
Q

what would the LFTs of pre-hepatic (haemolytic) jaundice look like?

A 
raised total bilirubin
normal conjugated bilirubin levels
raised unconjugated bilirubin 
normal urine/stool colour
normal ALP, ALT/AST
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57
Q

pathophysio of intra-hepatic (hepatocellular) jaundice

A

dysfunction of hepatic cells - liver cannot conjugate bilirubin
can lead to cirrhosis -> compresses the intrahepatic portions of biliary tree to cause a degree of obstruction

leads to both unconjugated + conjugated bilirubin in the blood = “mixed picture” LFTs

58
Q

what would the LFTs of intra-hepatic (hepatocellular) jaundice look like?

A 
raised total bilirubin
raised conjugated 
raised unconjugated
dark urine/pale stool
raised ALP, ALT/AST - AST/ALT more prominent than ALP (due to liver damage)
59
Q

what are the true liver function tests - those which reflect synthetic function of the liver?

A

albumin
prothrombin time
bilirubin

60
Q

what do raised AST/ALT (transaminases) indicate?

A

hepatocellular injury

61
Q

what does a raised ALP (alkaline phosphatase) indicate?

A

obstruction

62
Q

what causes post-hepatic jaundice (cholestatic)?

A

obstruction of biliary drainage –> flow of bile is backed up to liver + overspills it’s constituents into the blood

63
Q

what would the LFTs of post-hepatic (cholestatic) jaundice look like?

A 
raised total
raised conjugated
normal unconjugated
dark urine/pale stool
raised ALP, AST/ALT - (ALP more)
64
Q

pathophysio of diverticular diasease

A

thickening of muscle layer due to high intraluminal pressures
–> pouches of mucosa extrude through muscular wall through weakened area near blood vessels to form diverticula

65
Q

clinical features + complications of diverticular disease

A

most asymptomatic
intermittent left iliac fossa pain
erratic bowel habit

pericolic abscess
perforation (peridiverticulitis)
haemorrhage
fistula
stricture
66
Q

what causes diverticulitis?

A

when faees obstruct the neck of the diverticulum -> accumulates bacteria causing inflammation

alters gut motility, increases luminal pressure, disordered colonic microenvironment

67
Q

clinical features of diverticulitis

A

LIF pain/tenderness
fever, tachycardia
constipation
left side guarding + rigidity

similar to appendicitis but on left

68
Q

management of diverticulitis

A

mild = antibiotics - ciprofloxacin + metronidazole

severe = IV fluids, IV antibiotics + bowel rest

69
Q

clinical features of ischaemic colitis

A

sudden onset abdominal pain
passage of bright red blood PR, with or without diarrhoea
distended tender abdomen

AXR - * thumb-printing at splenic flexure *
sigmoidoscopy + biopsy - epithelial cell apoptosis + lamina propria fibrosis

CT to exclude perforation

70
Q

symptoms + signs of intestinal obstruction

A 
intermittent pain - colicky, central, cramping
absolute constipation - no farts/stool
burping
abdominal distension + tenderness
bowel sounds - high pitched
fever, tachycardia

**small only - vomiting + feeling better after it

71
Q

complications of parental nutrition

A

sepsis
SVC thrombosis
line fracture, leakage, migration
psycho-social

72
Q

what type of bacteria is yersinia? how is it commonly spread + how do patients present?

A

gram neg bacillus
raw pork

commonly children -> watery/bloody diarrhoea, abdo pain, fever, lymphadenopathy

adults can present similar to appendicitis

73
Q

what is hartmanns procedure?

A

removal of rectosigmoid colon + creation of colostomy - rectal stump sutured closed

usually done in emergency - acute obstruction, tumour, significant diverticular disease

–> colostomy may be permanent or reversed at a later date

74
Q

risk factors for colorectal cancer

A

family history of bowel cancer -
familial adenomatous polypois (FAP) - polyps throughout bowel
hereditary nonpolyposis colorectal cancer (HNPCC) = Lynch syndrome

biggest risk factor = red + processed meat consumption

IBD
increased age
sedentary lifestyle, obesity (red meat, low fibre), smoking, alcohol

75
Q

presentation of colorectal cancer

A

unexplained weight loss
change in bowel habits - looser + more frequent
rectal bleeding
unexplained abdominal pain
iron deficiency anaemia - microcytic anaemia with low ferritin –> fatigue, pale eyelids
abdominal / rectal mass

–> may present with obstruction (tumour blocking bowel) - vomiting, abdo pain, absolute constipation

76
Q

what method is used for bowel screening in scotland? at what age is this done and how often is it carried out?

A

faecal immunochemical test (FIT) - human haemoglobin in stool

50-72 y/o in scotland home FIT test every 2 years - if positive = colonoscopy

if risk factors (FAP, HNPCC, IBD) - regular colonoscopy to check

77
Q

what test can be carried in a GP for those who have suspected colorectal cancer but don’t meet the 2-week referral colonoscopy?

A

faecal immunochemical test (FIT)

78
Q

how are colorectal cancers staged?

A

staging CT - CT thorax, abdomen, pelvis (CT TAP)

MRI for rectal cancers

79
Q

what are the surgical resection options for colorectal cancer?

A

right hemicolectomy - caecum, ascending, proximal transverse
left hemicolectomy - distal transverse, descending
sigmoid colectomy
anterior resection - sigmoid + upper rectum
–> increase urgency + frequency of bowel movements, faecal incontinence, difficulty controlling flatulence

abdomino-perineal resection (APR) - rectum + anus
–> permanent colostomy

80
Q

what is involved in the follow up post colorectal cancer?

A

CT TAP

serum carcinoembryonic antigen (CEA) - tumour marker blood test
–> predicting relapse

81
Q

what criteria is used to diagnose IBS?

A

Rome IV

82
Q

what are FODMAPs?

A

a collection of short-chain carbohydrates (sugars) that are not properly absorbed in the gut

A low FODMAP diet is considered a second line dietary intervention for individuals with medically
diagnosed IBS. It should only be trialled under the supervision of a dietitian

83
Q

list some non-GI symptoms of coeliac disease

A

recurrent mouth ulcers
prolonged fatigue
anaemia
neurological symptoms

84
Q

what is the pathophysio of achlasia?

A

Degenerative loss of ganglia from Auerbach’s plexus

85
Q

pathophysio of cirrhosis

A

Hepatic stellate cells found in the space of Disse are activated and transformed into myofibroblasts under the influence of cytokines

–> these activated cells synthesise collagen leading to fibrosis

86
Q

pathophysio of primary biliary cirrhosis

A

immune system attacks small bile ducts within the liver
first part affected = intralobar ducts (canal of Hering)
causes obstruction of bile (cholestasis)

–> eventually obstruction leads to fibrosis, cirrhosis + liver failure

bile acids, bilirubin + cholesterol overflow into blood as not being excreted

87
Q

clinical features of primary biliary cirrhosis

A 
fatigue
pruritus
GI disturbance + abdo pain
jaundice
pale stools
steatorrhoea
xanthoma 
signs of cirrhosis - ascites, splenomegaly, spider naevi
88
Q

primary biliary cirrhosis investigations

A

most specific = anti-mitochondrial antibodies

LFTs - ALP raised (obstructive)

blood tests - ESR + IgM raised

liver biopsy = diagnosing + staging disease

89
Q

primary biliary cirrhosis treatment

A

ursodeoxycholic acid - reduces intestinal absorption of cholesterol

obeticholic acid ?

colestryamine - binds to bile acids to prevent absorption in the gut –> helps with pruritus

consider immunosuppression
liver transplant @ end stage liver disease

90
Q

signs of liver cirrhosis

A

jaundice
hepatomegaly - can shrink in severe
splenomegaly - due to portal hypertension
spider naevi
palmar erythema - due to hyperdynamic circulation
gynaecomastia + testicular atrophy in males - due to endocrine dysfunction
bruising
ascites - cirrhosis causes transudative (low protein)
caput medusae - bulging veins around umbilicus
asterixis - ‘flapping tremor’

91
Q

what scoring is used in liver cirrhosis?

A

Child-pugh - indicates severity + prognosis

MELD score - gives percentage estimated 3 month mortality

    • helps guide transplant referral
    • used every 6 months in patients with compensated cirrhosis
92
Q

extra-GI manifestations of IBD

A

eyes - uveitis, conjunctivitis

joints - arthritis, inflammatory back pain

skin - erythema nodosum, pyoderma gangrenosum

mouth ulcers, anaemia

93
Q

pathophysio of acute pancreatitis

A

epithelial injury to pancreatic duct - bile reflux, duct obstruction due to stone damage to sphincter of Oddi

–> loss of protective barrier allows autodigestion of pancreatic acini (cells that produce digestive enzymes)

  • -> release of lytic pancreatic enzymes:
      • proteases - tissue destruction + haemorrhage
      • lipases - intra + peripancreatic fat necrosis
94
Q

most common causes of acute pancreatitsis

A

alcohol
gallstones
post-ERCP

95
Q

what is elevated serum amylase a common sign of?

A

acute/chronic pancreatitis

96
Q

list characteristics of the 2 main types of inherited colorectal carcinoma

A 
HNPCC -
late onset - right sided tumours
autosomal dominant
inflammatory response (crohns like)
defect in DNA mismatch repair
mutation in MLH-1, MLH-2, PMS-1 or MSH-6 
FAP - 
early onset - throughout colon
autosomal dominant 
defect in tumour suppression
mutation in FAP gene
97
Q

why can bowel obstructions causes hypovolaemia + shock?

A

no fluid is absorbed in colon due to obstruction –> fluid loss into GI tract + reduced fluid in intravascular space = hypovolaemia

== ‘third-spacing’

98
Q

causes of bowel obstruction

A

adhesions - small bowel
hernias - small bowel
malignancy - large bowel

volvulus - large bowel
diverticular disease
strictures
intussusception - bowel slides into adjacent part (young kids 6months - 2yrs)

99
Q

signs of peritonitis

A

guarding - tensing abdo muscles when palpated

rigidity - involuntary persistent tightness

rebound tenderness - rapidly releasing pressure on abdomen creates worse pain than pressure itself

coughing test
percussion tenderness

100
Q

signs + symptoms of haemorrhoids

A

constipation + straining
sore/itchy anus
feeling a lump around or inside anus

painless, bright red bleeding –> after opening bowels, NOT mixed with the stool

101
Q

what are the 3 main complications of hernias?

A

incarceration - when irreducible, can lead to obstruction + strangulation

obstruction - when causes blockage in passage of faeces, absolute constipation

strangulation - irreducible AND base of hernia becomes tight cutting off blood supply (ischaemic/gangrenous tissue) = surgical emergency

102
Q

how can you distinguish between direct + indirect inguinal hernias?

A

when pressure applied

indirect - hernia reduced to deep inguinal ring (mid way from ASIS to pubic tubercle) + remains reduced

direct = irreducible

103
Q

what is the difference between direct + indirect inguinal herniation?

A

indirect = herniates through inguinal canal

  • reducible
  • lateral to epigastric artery
  • lies within spermatic cord (layers of abdo wall)

direct = herniates through hesselbach’s triangle

  • irreducible
  • medial to inferior epigastric artery
  • lies parallel to spermatic cord
104
Q

what do LFTs look like in hepatitis?

A

high AST/ALT

less of a rise in ALP

105
Q

which strains of hepatitis are self-limiting (no increased risk of hepatocellular carcinoma)?

A

A + E

106
Q

how is hep A spread?

A

faecal oral - poor hand hygiene, in foreign markets touching lots of food

107
Q

how do you diagnose hep A?

A

presence of hep A IgM

IgG will be detectable for life

108
Q

treatment for hep A?

A

supportive, avoid alcohol

109
Q

how is hep B spread?

A

3 B’s
Blood
Babies - pregnant mother to child (vertical transmission)
Body fluid - sex hehe

incubation = 1-6months
endemic - recent travel?

110
Q

HBsAg –> negative
HBcAb –> positive
HBsAb –> positive

what do these hep B serology results indicate?

A

resolved HBV infection

HBcAb IgG

111
Q

HBsAg –> negative
HBcAb –> negative
HBsAb –> positive

what do these hep B serology results indicate?

A

vaccinated

112
Q

HBsAg –> positive
HBcAb –> positive
HBsAb –> negative

what do these hep B serology results indicate?

A

active infection

if HBcAb IgM present - acute

113
Q

what does the presence of HBeAg in serology results imply?

A

implies high infectivity

e antigen = marker of viral replication

114
Q

management of HBV

A

antivirals:
first line = interferon alfa
tenofovir - reduces viral replication

notify public health

115
Q

how is hep C spread? symptoms?

A

blood + bodily fluids

most asymptomatic - release when they get chronic symptoms

116
Q

when does a hep C infection become chronic?

A

presence of HCV RNA > 6months

hep C = commonest hep to develop hepatocellular carcinoma (via cirrhosis)

117
Q

diagnosis of hep C

A

HCV-PCR test - if positive -> HCV RNA

chronic if HVC > 6 months
–> liver biopsy to assess damage

118
Q

treatment of hep C

A

curable

protease inhibitors for 8-12 weeks
daclatasvir + sofosbuvir
sofosbuvir + simeprevir

–> always 2+ drugs (reduces resistance)

no vaccine available

119
Q

which viral hepatitis exacerbates HBV

A

hep D
–> requires hep B to function

diagnosis = HDV RNA PCR on blood

120
Q

characteristics of hep E

A

similar to hep A
self-limiting mostly
faecal-oral spread
zoonotic spread - pigs

diagnosis = blood for HEV IgM

121
Q

causes and risk factors of haemolytic uraemic syndrome

A

causes - E coli 0157, shigella –> shiga/shiga-like toxin (verotoxin)

risk factors = NSAIDS, anti-motility agents (loperamide), antibiotics

122
Q

HUS signs + symptoms

A 
petechiae (red spots on skin)
oliguria (low urine volume)
fever 
bloody diarrhoea
high WBC, low platelets

(acute renal failure, thrombocytopenia, haemolytic anaemia)

123
Q

PSC symptoms

A 
jaundice
* CHRONIC * RUQ pain
pruritus 
fatigue
hepatomegaly
124
Q

PSC investigations

A

gold = MRCP - bile duct lesions/strictures

LFT - cholestatic picture (raised ALPs)

125
Q

PSC treatment

A

ursodeoxycholic acid - slows disease progression
colestyramine - helps pruritus, binds to bile acids preventing absorption

ERCP - stent strictures
liver transplant = curative

126
Q

sudden onset colicky pain in RUQ, radiates to back, worst postprandially (after meals)

A

biliary colic - gallstones

127
Q

investigations for cholecystitis

A

USS - gallstones + thickening of gall bladder wall

2nd line (if diagnosis unclear) = cholescintigraphy (HIDA scan)

128
Q

management of ascending cholangitis

A

fluids + IV antibiotics (broad spectrum)

ERCP - drain bile ducts, ?stent idk

129
Q

what is a TIPS procedure?

A

Transjugular Intra-hepatic portosystemic Shunt (TIPS)

creation of connection between hepatic vein + portal vein + insertion of stent

–> allows blood to flow from portal to hepatic veins - relieves pressure in portal system + varices

130
Q

pathophysio of ascites

A

Increased pressure in portal system causes fluid to leak out of capillaries in liver + bowel into peritoneal cavity – low albumin = low plasma volume

–> reduces blood pressure in kidneys

Kidneys release renin in response – leads to increased aldosterone secretion (via RAAS) + reabsorption of fluid + sodium retention in kidneys

131
Q

management of ascites

A

low sodium diet
anti-aldosterone diuretics = spironolactone
paracentesis

prophylactic antibiotics against SBP if <15g/L protein
monitor U&Es

132
Q

complications of cirrhosis

A

ascites + spontaneous bacterial peritonitis (SBP)
varices
hepatorenal syndrome
hepatic encephalopathy - excess ammonia - confusion, flappy hands
hepatocellular carcinoma

133
Q

hepatic encephalopathy treatment

A

laxatives - lactuloses - promotes excretion of ammonia

antibiotics - rifaximin - reduces bacteria producing ammonia

nutritional support

134
Q

haemochromatosis

A

def = genetic iron overload disorder – deposition of iron in tissues

  • autosomal recessive
  • mutations in human haemochromatosis protein (HFE) gene on chromosome 6

diagnosis = serum ferritin, genetic testing

complications = cirrhosis, cardiomyopathy, pancreatic failure, no erections ://

treatment = venesection (weekly protocol of removing blood to decrease total iron)

135
Q

Wilson’s disease

A

Def = excessive accumulation of copper in the body + tissues
- Wilson’s disease protein on chromosome 13 –
ATP7B copper-binding protein
- autosomal recessive

clinical features
- neurological - - dysarthria (speech difficulties),
dystonia (abnormal muscle tone), Parkinson’s
–> psychiatric – depression, full psychosis
- hepatic – chronic hepatitis > cirrhosis
- kayser-fleischer rings in cornea – deposition if
copper

treatment = copper chelation drugs – penicillamine, trientene

136
Q

what is Budd-Chiari?

A

thrombosis in hepatic vein - causes acute hepatitis

jaundice, tender hepatomegaly, ascites (chronic)

diagnosis = US
treatment = anticoag, stent, treat hepatitis
137
Q

autoimmune hepatitis

A

type 1 - adults + kids (ANA/ASMA antibodies)
type 2 - kids only (LKM1 antibodies)

Ix = presence of antibodies, liver biopsy (interface hepatitis with piecemeal necrosis)

Tx = steroids induce remission, azathioprine (immunosuppressants)

138
Q

palliative treatment of hepatocellular carcinoma

A

sorafenib = kinase inhibitors - inhibit proliferation of cancer

–>can extend life by months

139
Q

scoring of pancreatitis

A

Glasgow score = used to assess severity -> 3+ = severe

One point for each (PANCREAS mnemonic)

  • P – paO2 < 60
  • A – Age > 55
  • N – neutrophils – WBC > 15
  • C – calcium < 2
  • R – uRea > 16
  • E – enzymes – LDH > 600 or AST/ALT >200
  • A – Albumin < 32
  • S – Sugar – glucose >10
140
Q

management of pancreatic cancer

A

operable -
total pancreatectomy
distal pancreatectomy
pylorus-preserving pancreaticoduodenectomy (PPPD) = modified Whipple
radical pancreaticoduodenectomy = Whipple

in operable (palliative) -
stents / bypassing biliary obstruction
palliative chemo/radio

first year med (15 decks)

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