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GI Flashcards

1
Q

Define GORD

A

Reflux of gastric contents into oesophagus or beyond -> symptoms due to loss of lower oesophogeal sphinchter tone, delayed and impaired gastric emptying.
commonest cause of oesophagitis

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2
Q

Typical GORD presentation

A

Heartburn post meals, not usually exertional, worse after lying down/bend over/night
Sour taste in mouth

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3
Q

Rf for GORD

A
  1. Obesity
  2. Hiatus hernia
  3. FH
  4. Older age
  5. Drugs: nitrates, calcium channel blockers, alpha- and beta-adrenergic agonists, theophylline, and anticholinergics
  6. Other: stress, asthma, NSAIDs etc!
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4
Q

How is GORD diagnosed

A

Clinical

- trial PPI with px

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5
Q

Define eosinophilic oesophagitis

A

infilitration of oesophageal epithelium with eosinophils => immune mediated oesophageal dysfunction

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6
Q

Presentation of eosinophilic oesophagitis

A
  1. Long term dysphagia
  2. Food avoidance and behaviour modification
    +
  3. heartburn, chest discomfort
  4. N+V
  5. Acid regurg
  6. Abdo pain
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7
Q

RF of eosinophilic oesophagitis

A
  1. FH
  2. kids. young
  3. Men
  4. White
  5. Atopic diseases
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8
Q

What is Barrett’s oesophagus

A

COLUMNAR METAPLASIA = Normal squamous cell epithelium lining oesophagus is replaced with columnar
INTESTINAL METAPLASIA = develop glands too
Changes are usually secondary to chronic GORD
Biggest concern -> oesophageal/barrets adenocarcinoma

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9
Q

Hepatitis A

  • Cause
  • Timescale
  • Route transmission
  • Diagnosis
  • Complications
  • Prevention
A

pretty chill average 1 month incubation
RNA virus
Time: Only acute not chronic carrier
Route: Faecal-oral = close contact, contaminated food/water
Diagnosis: HAV-IgM for recent and IgG for ever
CAN -> fulminant, cholestatic/relapsing hep but NOT Chronic or HCC
Prevention: vaccine

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10
Q

Who gets hep A`

A

Large communities , children resevoir
-> travelers
+ gay men
+ IVDU

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11
Q

Hepatitis E

  • Cause
  • Timescale
  • Route transmission
  • Diagnosis
  • Complications
  • Prevention
A

Cause: 4 genotypes
Timescale: acute only, v similar to hep A
Route: faecal-oral BUT very little person to person (vs A)
Diagnosis: igM and igG
Complications: chronic + HCC (vsA)
Prevent: no vaccine, water clean

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12
Q

Hepatitis B

  • Cause
  • Timescale
  • Route transmission
  • Diagnosis
  • Complications
  • Prevent
A

Cause DNA virus
Time: acute and chronic carriers
Route: vertical, close contact, sexual and blood: health workers, IVDA, sex workers and gay
Diagnosis: many blood tests inc HBV DNA in serum and HBsAg
Complications: chronic asymptomatic, active, cirrhosis, HCC
Prevent: vaccine

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13
Q

Hepatitis D

  • Cause
  • Timescale
  • Route transmission
  • Diagnosis
  • Complications
  • Prevent
A

CAN ONLY GET WITH HEP B and it works harder, limited tx options, quite uncommon
Timescale: coinfect with hep B= severe acute or superinfect= chronic HDV but may present as acute hep
Route: skin + Sex
Diagnosis: Abs
Complications:cirrhosis, failure, HCC
Prevent: no vaccine, avoidance

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14
Q

Hepatitis C

  • Cause
  • Timescale
  • Route transmission
  • Diagnosis
  • Complications
  • Prevent
A 
Cause: RNA virus
Timescale: acute or chronic carriers
Route: BLOOD tissue donor, skin, sex,  (mother - baby)less than hep b
Diagnosis: anti hcv
Complications: cirrhosis, HCC
Prevent- no vaccine 
Aim to eradicate 2030
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15
Q

Treatments of hepatitis

A
  1. Interferon = chronic hep b
  2. Ribavirin= hep A
  3. Direct antivirals ending -vir = entecavir, tenofovir for hep B suppress progression to liver disease. Hep C too.
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16
Q

How does hepatitis B cause liver damage

A

Not via infection/replication

Liver damage is immune mediated: inflammation -> scarring -> cirrhosis

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17
Q

What is NAFLD/NASH

A

Range of severity but defined as histological steatosis of liver in individuals without alcohol xs

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18
Q

Pathophysiology of NAFLD

A

Obesity, metabolic syndrome -> insulin resistance -> circulating carbs/fats ->lipogenesis and lysis -> free FA in liver
free FA -> reactive ox species -> inflammation -> fibrosis -> cirrhosis
NB main cause of mortality is CV effect

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19
Q

Treatment of NAFLD

A

Lifestyle modification
Target metabolic syndrome
Treat end stage cirrhosis

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20
Q

Investigations to identify fibrosis

A 
Raised AST:ALT ratio
Raised AST: platelet (splenomegaly secondary to cirrhosis)
FIB-4 estm severity criteria
NAFLD fibrosis score
IMAGING: 
fibroscan
follow up w biopsy = gold
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21
Q

Alcohol metabolism

A

Relies on NAD not being saturated otherwise get toxic acetaldehyde build up
Overstimulating pathway -> met change = ketogenesis + FA production -> steatosis w impaired oxidation -> inflammation -> fibrosis + cirrhosis

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22
Q

What is alcoholic hepatitis

A 
Clinical syndrome characterised by:
Jaundice
Enlarged, painful liver
Ascites
Very sick px
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23
Q

Treatment of alcoholic liver disease

A
  1. stop drinking
  2. manage complications of portal hypertension
  3. Manage nutrition and sometimes use steroids
  4. Liver transplant
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24
Q

Complications of cirrhosis

A
  1. Portal hypertension
    - varisces + haem
    - ascites + SBP + HRS
  2. Liver failure
    - encephalopathy
    - jaundice
  3. HCC
    NB also more permeable gut -> sepsis
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25
Causes of ascites
1. Portal hypertension eg secondary to cirrhosis 2. Malignancy 3. Infection eg tb 4. Nephrotic syndrome 5. HF
26
Management of ascites
1. Salt control 2. Diuretics (can -> hyponatraemia, renal failure, enceph) 3. Paracentesis (+ fluid replace, albumin) 4. Definitive = liver transplant or TIPS NB prophylactic abx considered esp prev SBP
27
Blood supply to gut
Celiac trunk: foregut (oes->D1/2) SMA: midgut (D3-> prox 2/3 of transverse) IMA: hindgut (distal 1/3 of transvere -> anal canal)
28
Signs of upper GI haemmorhage
1. Haematemesis- red, emesis to inc coffee ground 2. Malaena - black tar stool 3. Collapse/anameic 4. Abdo pain
29
Causes of upper GI bleed
1. Gastric erosions/ ulcer 2. Duodenal ulcer NB PERFORATED ULCER PRESENT W PAIN NOT HAEM 3. Varices 4. Mallory weiss syndrome 5. Oesophagitis secondary to gord 6. Rarer causes inc cancer
30
Mallory Weiss Tear
Tear of gastro-eosophageal junction History of forecful vomiting = superficial tears NB these are not full thickness tears = Boerhaaves v diff pres
31
Management of upper GI bleed
``` Airways- NBM Breathing - Oxygen C- 2 x large cannula, IV fluids G+S, CM. May need to transfuse FFP, beriplex vit k etc Reassess Endoscopy PPI is only post endoscopy NB RESUS IS SAME FOR LOWER GI will just have colonscopy/angiography/surgery ```
32
Rockhall scoring system
Identify patients risk of adverse outcome post upper GI bleed therefore whether to discharge NB to decide if endscopy is urgent - blatchford score
33
Management of varisces
``` same resus protocol + ABX Terlipressin to reduce portal pressure even BEFORE endoscopy THEN OGD + band ligation if fail balloon tamponade, rescue tipss ```
34
6 causes of cirrhosis
``` 3 acquired: 1. AFLD 2. NAFLD 3. Hepatitis AND 3 AI: 1. AIH 2. PBC 3. PSC ```
35
What is autoimmune hepatitis
chronic inflammatory liver disease of unknown aetiolofy that leads to T cell mediated destruction of hepatocytes involving B+plasma cells
36
Diagnosis of AIH
No single test | Abnormal LFT - always screen for igG and autoantibodies
37
Treatment of AIH
Immunosuppresion(IS) - induced with high dose steroids - maintain with azathioprine(IS)and maybe low dose steroids
38
What is fulminant hepatitis
Can develop from hepatitis Rapid acute liver failure = decreased synthetic function and rapid onset encephalopathy -
39
What is primary biliary cholangitis
Autoimmune destruction of INTRA hepatic bile ducts by T cells Most common autoimmune liver disease but still rare
40
Morbidity and mortality of PBC
UNMET CLINICAL NEED - no cure, re-transplantation 1. constant fatugue 2. intense itch PBC can be managed with oxicolic acid
41
What is primary sclerosing cholangitis
Autoimmune destruction of EXTRA hepatic bile ducts Men with UC> crohns Gold standard diagnosis MRCP
42
Extra hepatic manifestations of PSC when assd with IBD
Pyoderma gangrenosum Erythema nodosum Episcleritis
43
PSC treatment
None, same as PBC (oxycolic acid) NB treat the IBD and recurring cholangitis IT IS THE MOST LIKELY ONE OF THREE AID TO RECUR POST TRANSPLANT
44
Define fistula
Abnormal connection between two epithelial lined viscera
45
Causes of PR bleed
FATTHUD 1. Haemorrhoids (H) 2. Anal fissure (F) 3. IBD (U) + other colitis 4. colorectal cancer (T) 5. Diverticulitis (D) 6. Telangectasia (A)
46
Haemorrhoids presentation
Pain/less rectal bleeding - bright red on tissue paper/loo - pruritis - tenesmus - peri/anal mass
47
Anal fissure presentation
Severe pain on defecation - passing glass, can be burning Fresh blood on stool or papers - anal spasm - sentinel pile
48
Haemorrhoids define
tear/protrusion of enlarged anal cushions (3,7,11)
49
Anal fissure define
Split of skin of distal anal canal due to repeated hard stool
50
Define UC
Inflammatory bowel disease involving the mucosal layer of rectum and variable lengths of colon but continuous in nature. Multifactorial disease, aetiology ? smoking protective
51
Presentation of UC
``` Bloody diarrhoea Abdo pain Rectal bleeding Arthritis/spondylarthropathy Malnutrition NB can get weight loss,fever, constipation etc ```
52
Diagnosing UC
1. Stool sample - negative c diff culture - WBC - elevated faecal calprotectin = Inflam 2. FBC 3. LFT to check for PSC 4. ESR/CRP 5. Imaging: x ray (TOXIC MEG), flex signoidoscopy, colonoscopy = BIOPSY
53
Management of UC
Severe: IV steroid, IV IS cyclosporin or surgery toxic meg/failing Mild: 5-ASA IS like drugs eg mesalazine, oral and rectal steroids Maintain: 5 ASA, no steroids
54
Define crohns
Granulomatous transmural inflammation of GIT anywhere from mouth ->anus, skip lesion. Most common at terminal ileum. Transmural -> fibrosis, fistulas, perforations
55
Crohns presentation
Same as UC | + bowel obstruction(bloat,distend,vomit, constipation, pain)
56
Management of varices
1. A to E including fluid resus, may give packed RBC transfusion, will give prophylactic abx 2. Vasoconstriction drug PRE endoscopy+ endoscopic variceal ligation Terlopressin, Vasopression or Octreotide 3. If this fails = TIPS rescue OR balloon tamponade 4. beta blockers as secondary prophylaxis
57
Management of uc
1. mild = mesalazine 2. moderate = prednisolone induction + mesalazine 3. severe - hospital, rescue ciclosporin or infliximab (TB) then maintain azathioprine or infliximab + surgery
58
Manage Crohns
1. smoking cessation, nutrition 2. mild oral steroids(budesonide) 3. worse - steroids + immunomodulator (methotrexate, azathioprine) 4. even worse + biologic infliximab (TB) severe - admit hospital + surgery
59
Complications of UC
1. colorectal cancer 2. toxic megacolon -> bowel perforation -> IAS 3. PSC
60
Complications of Crohns
1. anaemia, malnutrition 2. Colorectal cancer 3. Toxic megacolon 4. Small bowel obstruction 5. abscesses

CC2 (8 decks)

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