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Regulation of Body Functions > GI problems > Flashcards

GI problems Flashcards

1
Q

Crohns disease

A
  • Any part of GI tract
  • Discontinuous inflammation- Skip lesions!, may spare rectum
  • Deep ulcers, cobblestone appearance
  • Transmural inflammation
  • Granulomas may form
  • -Made worse by smoking
  • Different behaviours due to transmural nature: fistulising, strictures (abdo pain distension, vomiting,bowels not opening), perianal (abcess, fistula, fissure, ca occur in isolation)

most common is ascending colon and terminal ileum, ileo-caecal valve

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2
Q

Ulcerative Colitis

A 
Colon only
Continuous inflammation, starts at rectum
Shallow ulcers
Mucosal inflammation
Smoking is protective
Inflammatory

Colectomy is curative

Complications is toxic megacolon: parlytic bowel, air is trapped and dilate- perforation

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3
Q

Extra intestinal manifestations of IBD

A
  • Liver and bile ducts: Primary cholganing scleritis in Crohns
  • UVEITIS
  • Sore joints
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4
Q

Treatments of IBD

A

5-ASA’s (salazines)- maintenance due to anti-inflammatory properties
Steroids for flares
Immunsuppression: azathioprine
Anti-TNF: infliximab, adalimumab `

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5
Q

Causes of upper GI bleeding

A
  • Peptic ulcers ( H.Pylori (stool antigen test (-ve when reslved), serology), medications (NSAIDs)
  • Varices: Liver disease, varices: larger bleeding, haematemesis
  • Stomach Cancer: iron deficiency, mild bleeding
  • Oesophageal cancer: Dysphagia
  • Oesophagitis: GORD, some haematemesis
  • Angiodysplasia
  • Mallory Weiss tear: retching, recurrent
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6
Q

Lower GI bleeding

A
  • Angiodysplasia
  • Diverticula
  • Carcinoma
  • Meckel’s diverticulum
  • Anal fissure/haemorrhoids
  • Rectal ulcer
  • UC/Crohns
  • Polyps
  • Ischaemic colitis: inflammatory response and bleeding, older people
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7
Q

Coeliac serology

note gluten insensitivity, AI

Treat w gluten free diet, oats is okay, no gliadin (small numbers of people can not tolerate, be careful of cross contamination)

A

First test used to confirm coeliac, needs to be done while consuming gluten. If restricted before test, falsely negative
-TTG IgA Ab preffered
-Can do DGP
Can be falsely negative in IgA deficiency, NB common with coeliacs

NB most coelaic people have HLA-DQ2 or HLA-DQ8, +Ve is not indicative, as 50% of gen population have, -ve rules out

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8
Q

Coeliac duodenal biopsy finding

A
  • Intra-epithelial lymphocytosis
  • Crypt hyperplasia
  • Villous blunting (most diagnostic)

proximal duodenum

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9
Q

Coeliac associations

A 
Dermatitis herpertiformis- 100%*
1st degree relative with, should test*
Type 1 diabetes- strong*
AI-Thyroid disease (Graves?)
Osteoporosis
Infertility/recurrent miscarriage
Unexplained neurological
Unexplained liver disease
Addisons
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10
Q

Terminology, Gallstones

A

Biliary Colic: RUQ pain associated with inflammation of gall bladder or common bile duct
Cholelithiasis: Gall stones, uncomplicated
Cholecystitis: Inflammation of gall bladder
Choledocholithiasis: Stone in bile duct
Cholangitis: Choledocholithiasis + inflammation (fever, rigors etc)

80% cholesterol stones, others are pigmented

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11
Q

Common causes of elevated GGT and ALP

A

Stones, biliary disease (PSC, Primary biliary Cirrhosis), drugs, tumour

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12
Q

Significance of pain and jaundice

A

Biliary colic would suggest gall stones, must confirm

Painless jaundice has list of differentials

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13
Q

Choledocholithiasis

A

Typically secondary stones, from GB
Rarely stones form inside, pigmented

GB removal will likely treat, however ca still be complicated by pigment stones

Typically a negative Murphys sign, but jaundice

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14
Q

Cholangitis

A

Charcots triad, of
fever
Pain (suggestive of biliary colic)
Jaundice

Complication of choledocholithiasis, bacteria enter from duodenum

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15
Q

MRCP vs ERCP

A

MRCP: if not seen on US, do this. Accurate visualisation of biliary tree. ADV: noninvasive, DISADV: non-therapeutic

ERCP: diagnostic and therapeutic way of curing choledocholithiasis. ADV: therapeutic. DISADV: risk of complications

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16
Q

PBC vs PSC

A 
PBC:
-Effects intra-hepatic bile ducts, no way to visage
- Need biopsy
-Associated with AMA (anti-mitochondrial antibody) Diagnosis
PSC:
-Intra and extra hepatic bile ducts
-Diffuse stricturing on imaging
-Associated with IBD
-Diagnosed by biopsy or imaging
17
Q

PBC presentation

A

Gradually increasing LFT’s
fatigue, pruritus, steatorrhea, fatigue
Long term cirrhosis

Associated with dyslipidaemia (high), ostopenia/osteoporosis

18
Q

PSC presentation

A

Diffuse strictures in bile ducts
No antibody seen, maybe triggered by bacterial infection
Often seen with IBD, UC (If PSC, UC, if UC, not necessarily PSC)
Similar presentation to PBC (gradually increase in LFT’s(cholestasis)), pruritus, fatigue, steatorrhea
Can get jaundice, cirrhosis
Can get recurrent infections
PSC is likely going to need liver transplantation, maybe need stent, ERCP in large ducts

19
Q

Tumours causing obstructive jaundice

A

Head of pancreas cancer

Cholangiocarcinoma

20
Q

Signs of chronic liver disease

A 
Jaundice
Palmar erythema (redness on outer edges)
Spider naevi (chest/upper back)
Ascites (portal hypertension)
Caput medusae
21
Q

Basic break down of the LFT’s

A

GGT up alone: steatosis
ALP + GGT: Cholestasis
AST/ALT: hepatocellular pattern

22
Q

Causes of steatosis

A

Alcohol

NAFLD: From metabolic syndrome, diabetes, dyslipidaemia, HT, increased BMI. Typically increased ALT

23
Q

Most common causes of hepatitis

A

Viral; alcoholic; non-alcholic; auto-immune; ischaemic; haemochromatosis; drugs (bear in mind, also over the counter stuff. New drugs or long standing)

24
Q

Alcoholic liver disease

A

Alcohol exposure over time can lead to steatosis, and abstinence can restore a normal liver
Severe exposure can cause a hepatitis, and abstinence can lead to steatosis
Steatotic livers continually exposed can cause hepatitis, and together can make liver cirrhosis

25
Q

rehash on hepatitis risk factors and transmission

A

A: faecal oral, travel. Acute (also E)
B: Parenteral, sexual transmission, vertical transfusion. D comes with B
C: blood borne, IVDU

26
Q

Read Char’s notes on AI hepatitis, ishchaemic and haemochromatosis

A

-

27
Q

Handy hints reading LFT’s

A
  • If AST/ALT are in thousands, either viral; ischaemia; paracetamol
  • If in the hundreds, not so helpful
  • If AST > 2 x ALT suggestive of alcoholic hepatitis (AST/ALT ratio reversed)
28
Q

Hepb transmission

A

Perinatal (Asia)
Horizontal transmission
Sexual
Parenteral (IVDU/transfusion)

29
Q

4 Phases of chronic Hep B

A

1) Child, HepB high in blood, body does not act against virus as immature
2) Body tries to clear virus, ALT goes up, HepB load drops, treatment considered. In 20s/30s. Most at risk, inflammation. Can last years
3) Body controls the virus, ALT lowers.
4) Virus never leaves, but stays suppressed. Can last years, and can reactivate and rise in virus, recurrent inflammation and liver damage

30
Q

Encephalopathy stages

A

Confusion- drowsiness- coma

Can be incoordinated, tremor, asterixis, ataxia

31
Q

Liver functions

A
  • Removes toxins
  • Metabolises nutrients from foods to produce energy
  • helps fight infection by removing bacteria
  • Prevents nutrient shortage by storage (vitamins, minerals, sugar)
  • Produces most proteins needed by body
  • Produces bile to digest and absorb fat and fat soluble vitamins
32
Q

Hepatorenal disease

A

Can occur with ascites (cirrhosis, portal hypertension) associated with a loss of renal function due to RAAS activation

33
Q

Tumour marker for HCC

A

AFP

Regulation of Body Functions (31 decks)

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