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CC2 > GI > Flashcards

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
Q

Causes of ascites

A
  1. Portal hypertension eg secondary to cirrhosis
  2. Malignancy
  3. Infection eg tb
  4. Nephrotic syndrome
  5. HF
26
Q

Management of ascites

A
  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
Q

Blood supply to gut

A

Celiac trunk: foregut (oes->D1/2)
SMA: midgut (D3-> prox 2/3 of transverse)
IMA: hindgut (distal 1/3 of transvere -> anal canal)

28
Q

Signs of upper GI haemmorhage

A
  1. Haematemesis- red, emesis to inc coffee ground
  2. Malaena - black tar stool
  3. Collapse/anameic
  4. Abdo pain
29
Q

Causes of upper GI bleed

A
  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
Q

Mallory Weiss Tear

A

Tear of gastro-eosophageal junction
History of forecful vomiting = superficial tears
NB these are not full thickness tears = Boerhaaves v diff pres

31
Q

Management of upper GI bleed

A 
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
Q

Rockhall scoring system

A

Identify patients risk of adverse outcome post upper GI bleed therefore whether to discharge
NB to decide if endscopy is urgent - blatchford score

33
Q

Management of varisces

A 
same resus protocol
\+ 
ABX
Terlipressin to reduce portal pressure even BEFORE endoscopy
THEN OGD
 \+ band ligation
if fail balloon tamponade, rescue tipss
34
Q

6 causes of cirrhosis

A 
3 acquired: 
1. AFLD
2. NAFLD
3. Hepatitis
AND 3 AI: 
1. AIH
2. PBC
3. PSC
35
Q

What is autoimmune hepatitis

A

chronic inflammatory liver disease of unknown aetiolofy that leads to T cell mediated destruction of hepatocytes involving B+plasma cells

36
Q

Diagnosis of AIH

A

No single test

Abnormal LFT - always screen for igG and autoantibodies

37
Q

Treatment of AIH

A

Immunosuppresion(IS)

  • induced with high dose steroids
  • maintain with azathioprine(IS)and maybe low dose steroids
38
Q

What is fulminant hepatitis

A

Can develop from hepatitis
Rapid acute liver failure = decreased synthetic function and rapid onset encephalopathy
-

39
Q

What is primary biliary cholangitis

A

Autoimmune destruction of INTRA hepatic bile ducts by T cells
Most common autoimmune liver disease but still rare

40
Q

Morbidity and mortality of PBC

A

UNMET CLINICAL NEED - no cure, re-transplantation
1. constant fatugue
2. intense itch
PBC can be managed with oxicolic acid

41
Q

What is primary sclerosing cholangitis

A

Autoimmune destruction of EXTRA hepatic bile ducts
Men with UC> crohns
Gold standard diagnosis MRCP

42
Q

Extra hepatic manifestations of PSC when assd with IBD

A

Pyoderma gangrenosum
Erythema nodosum
Episcleritis

43
Q

PSC treatment

A

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
Q

Define fistula

A

Abnormal connection between two epithelial lined viscera

45
Q

Causes of PR bleed

A

FATTHUD

  1. Haemorrhoids (H)
  2. Anal fissure (F)
  3. IBD (U) + other colitis
  4. colorectal cancer (T)
  5. Diverticulitis (D)
  6. Telangectasia (A)
46
Q

Haemorrhoids presentation

A

Pain/less rectal bleeding

  • bright red on tissue paper/loo
  • pruritis
  • tenesmus
  • peri/anal mass
47
Q

Anal fissure presentation

A

Severe pain on defecation - passing glass, can be burning
Fresh blood on stool or papers
- anal spasm
- sentinel pile

48
Q

Haemorrhoids define

A

tear/protrusion of enlarged anal cushions (3,7,11)

49
Q

Anal fissure define

A

Split of skin of distal anal canal due to repeated hard stool

50
Q

Define UC

A

Inflammatory bowel disease involving the mucosal layer of rectum and variable lengths of colon but continuous in nature.
Multifactorial disease, aetiology ? smoking protective

51
Q

Presentation of UC

A 
Bloody diarrhoea
Abdo pain 
Rectal bleeding
Arthritis/spondylarthropathy
Malnutrition
NB can get weight loss,fever, constipation etc
52
Q

Diagnosing UC

A
  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
Q

Management of UC

A

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
Q

Define crohns

A

Granulomatous transmural inflammation of GIT anywhere from mouth ->anus, skip lesion.
Most common at terminal ileum.
Transmural -> fibrosis, fistulas, perforations

55
Q

Crohns presentation

A

Same as UC

+ bowel obstruction(bloat,distend,vomit, constipation, pain)

56
Q

Management of varices

A
  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
Q

Management of uc

A
  1. mild = mesalazine
  2. moderate = prednisolone induction + mesalazine
  3. severe - hospital, rescue ciclosporin or infliximab (TB) then maintain azathioprine or infliximab

+ surgery

58
Q

Manage Crohns

A
  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
Q

Complications of UC

A
  1. colorectal cancer
  2. toxic megacolon -> bowel perforation -> IAS
  3. PSC
60
Q

Complications of Crohns

A
  1. anaemia, malnutrition
  2. Colorectal cancer
  3. Toxic megacolon
  4. Small bowel obstruction
  5. abscesses

CC2 (8 decks)

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