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Pathology and final year > Gastro > Flashcards

Gastro Flashcards

1
Q

RFs for NAFLD

A

Obesity
diabetes
dyslipidaemia
rapid weight loss
total parentral nutrition

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2
Q

describe the progression of NAFLD

A

hepatic fat accumulation without inflammation
–> steatohepatitis,
–> fibrosis,
–>cirrhosis
–> end-stage liver disease.

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3
Q

diagnostic factors of NAFLD

A

dont drink much ETOH
RFs
deranged LFTs
truncal obesity
hepatosplenomegaly
RUQ pain

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4
Q

medications associated with hepatic steatosis

A

tamoxifen, corticosteroids, diltiazem, nifedipine, methotrexate, valproate, griseofulvin, intravenous tetracycline, amiodarone, and antiretroviral therapy for HIV.

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5
Q

AST and ALT in NAFLD

A

both elevated but usually no higher than 300IU/L

AST:ALT ratio usually <1 (which differs from alcoholic LD where ratio is >2)

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6
Q

Investigations for liver conditions

A

Bloods:
FBC- Hb for anemia
U&Es- Uraemia
LFTs + billirubin
lipids
clotting screen
serum albumin
autoimmune Ab screen
Iron studies
Hep B and C

Imaging:
Liver USS/ fibroscan
Abdo MRI

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7
Q

possible signs in a patient for liver disease

A

General:
jaundice
abdo distension
unwell looking
bruising/ petechiae
Bronzed appearance- haemochromatosis

Hands/nails:
Leukonychia and mherkles lines- hypoalbuminaemia
Asterixis- uraemia
dupyutrens contracture- chronic liver disease
clubbing- chronic stable liver disease
palmar erythema

Neck:
raised JVP- right sided heart failure secondary to hepatic congestion

face:
Conjunctival pallor- anaemia
Kayserfleisher rings- Wilsons
corneal arcus- hyperlipidaemia
yellowing of sclera- uraemia, billirubinaemia
Xanthelasma- hyperlipidaemia
angular stomatitis- anaemia

chest:
spider naevi
gynaecomastia

abdo:
Ascites
caput madusae
bruising
hepato/splenomegaly

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8
Q

differentials for NAFLD

A

alcoholic liver disease
autoimmune hepatitis
viral hepatitis

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9
Q

Management of NAFLD

A

Diet and exercise
consider pioglitazone
vitamin E
liver transplant

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10
Q

complications of cirrhosis

A

Ascites
Portal hypertension- splenomegaly, hepatopulmonary syndrome
oesophageal varices
uraemic encephalopathy
Hepatocellular carcinoma
hepatorenal syndrome

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11
Q

signs of chronic stable liver disease

A

Palmar erythema (high oestrogen)
dupyutrens contrcture
clubbing

gynaecomastia (male- failure of liver to break down oestradiol)
spider naevi

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12
Q

signs of portal hypertension

A

SAVE

Splenomegaly
Ascites
Varices
Encephalopathy

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13
Q

pressure in portal venous system

A

5-10mmHg

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14
Q

mechanism of hepatic encephalopathy

A

toxic metabolites such as ammonia/ urea not cleared by the liver
can cross BBB

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15
Q

Mechanism of oesophageal varices

A

portosystemic shunts are made to minimise portal hypertension at 3 points where the potal system meets the systemic system (oesphagus, anus and round ligament)

causes varices which are very fragile and easly rupture casuing massive upper GI bleeding

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16
Q

mechanism of caput medusae

A

round ligament (originally umbilicus at birth and closed off) rechannels blood from portal vein to abdominal veins which dilate

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17
Q

mechanism of splenomegaly in chronic liver disease

A

portal hypertension causes blood to back up into the spleen leading to congestive splenomagaly

–> anaemia, thrombocytopenia and thrombocytopenia as these cells get congested in spleen

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18
Q

mechanism of ascites

A
  1. decreased oncotic pressure from hypoalbuminaemia causes water to leak out
  2. portal hypertension leads to NO release from endothelial cells which causes vasodilation. as a result RAAS is stimulated and more water and Na are retained –> fluid overload
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19
Q

causes of portal hypertension

A

prehepatic
- obstruction
eg. portal vein thrombosis

intrahepatic
- cirrhosis
- sarcoidosis
- schistosomiosis

post hepatic
- right sided heart failure
- constrictive pericarditis
- Budd-chiari syndrome (hepatic vein obstruction eg. thrombus in PCV or a tumor)

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20
Q

Management of decompensated liver disease

A

beta blockers may help portal HPTN

Rifaximin- targets GIT bacteria which will reduce ammonia production

lactulose- improvs ammonia clearance

Ascitic tap for WCC and MC&S to rule out SBP- if previously had give prophylactic ciprofloxacin

Ascites- 20% human albumin solution and diuretics (spironolactone/ frusemide) and drain

OGD to look for varices- band ligation if necessary

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21
Q

signs of decompensated liver disease

A

Ascites
Jaundice
asterixis
encephalopathy
portal hypertension

22
Q

Main investigations for pt with suspected liver disease

A

bloods:
FBC- may have anaemia, thrombocytopenia
CRP
U&Es- uraemia
LFTs
Renal function + Cr- hepatorenal syndrome
clotting profile- synthetic marker of liver function
serum albumin

serum hepatitis virology
Immunoglobulins- aSM, amitochondrial, aANCA
caeruloplasmin and Cu- wilsons
Iron studies- haemochromatosis

23
Q

extra hepatic manifestations of haemochromatosis

A

arthritis
secondary T2DM and insulin resistance
infertility

24
Q

secondary causes of diabetes mellitus

A

cystic fibrosis
pancreatitis
pancreatic cancer
haemochromatosis
phaochromocytoma
cushings

25
Q

markers of synthetic liver function

A

albumin
clotting
platelets (liver makes thrombopoetin)

26
Q

causes of acute liver failure

A

Hep A&E
paracetamol OD
TB antibiotics
some tropical infections

27
Q

criteria for hepato-renal syndrome

A
  1. Chronic liver disease or acute liver disease with LIVER FAILURE.
  2. Poor GFR
  3. Absence of volume depletion
  4. no nephrotoxic drugs.
    6 Absence of shock
  5. No evidence of kidney disease (ie proteinuria or haematuria) / Ultrasound shows no obstruction.
  6. No improvement in creatinine after withdrawing diruetics or using 1.5 litre of fluid to replete.
28
Q

types of hepato-renal syndrome

A

Type 1 is rapidly progessing over 2 weeks. Where as type 2 is more slowly progessing and sometimes a cause can be found such as SBP.

29
Q

what are the 2 types of autoimmune hepatitis

A

Type 1: This is the most common type of autoimmune hepatitis. This type patients have ANTI-SMOOTH MUSCLE ANTIBODIES and ANTI-NUCLEAR antibodies.

Type 2: this is rarer, and seen mainly in children, with anti-liver/kidney microsomal type 1 antibodies.

30
Q

emphysema plus cirrhosis

A

alpha 1 antitrypsin deficiency

31
Q

causes of ascites

A

3C’s and an N

Cirrhosis
Cardiac failure
Cancer
Nephrotic synrome

32
Q

what is the SAAG and what are different types/ casues

A

serum ascites albumin gradient
serum albumin- ascites albumin

exudative- SAAG <1.1g/dL
casues (MINP): malignancy, infection (eg.TB), nephrotic syndrome, and pancreatitis

transudative- SAAG >1.1g/dL
Casues: Alcoholic hepatitis, Budd-chiari syndrome, cirrhosis, Kwashiorkor malnutrition

Another way of differentiating between an exudate and a transudate is to assess the ascitic fluid’s lactate dehydrogenase (LDH) level:

LDH <225 U/L = transudate
LDH > 225U/ L = exudate

33
Q

causes of chronic liver failure

A

hep B, C and D
alcoholic liver disease
Metabolic associated steatohepatitis/ NAFLD

rare:
Wilsons
Haemochromatosis
Autoimmune hepatitis
alpha1 antitrypsin deficiency

34
Q

complications of cirrhosis

A

hepatocellular carcinoma

portal hypertension- rupture of oesophageal varices

ascites and spontaneous bacterial peritonitis

clotting dysfunction and bleeding

uraemic encephalopathy- confusion, reduced GCS, seizure

35
Q

what is creon

A

tablet of exogenous pancreatic enzymes

36
Q

causes of pancreatitis

A

Idiopathic
Gall stones
ERCP
Trauma
Steroids
Malignancy, mumps
Autoimmune
Scorpion venom
Hhypercalcamia, hypertriglyceride
Ethanol
Drugs (sulfonamides, azathioprine, NSAIDs, diuretics)

37
Q

Management of GORD

A

supportive
- smaller meals
- dont eat 2hrs before bed
- avoid citrusy foods

medical
- gavisocn
- PPIs

surgical
- fundoplication

38
Q

what is the montreal classification of crohns

A

A- age of onset
L- disease location
B- disease behaviour

A1: ≤16 years
A2: 17-40 years
A3: > 40 years

L1: terminal ileum
L2 : colon
L3: ileocolon
L4: upper gastrointestinal

B1: Inflammatory
B2: stricturing
B3: penetrating

39
Q

what is the montreal classification of UC

A

extent

E1: ulcerative proctitis; involvement limited to rectum (rectosigmoid junction)

E2: left sided ulcerative colitis: involvement limited to portion of colorectum distal to splenic flexure

E3: extensive ulcerative colitis: involvement extends proximal to splenic flexure

severity

S0: ulcerative colitis in clinical remission; no symptoms of UC

S1: mild UC ≤ 4 bloody stools daily, lack of fever, pulse <90 bpm, haemoglobin >105g/L, ESR < 30mm/hr

S2: moderate ulcerative colitis: > 4-5 stools daily but with minimal signs of systemic toxicity

S3: severe ulcerative colitis: ≥ 6 bloody stools daily, pulse > 90 bpm, temperatures > 37.5°C, haemoglobin < 105 g/L, ESR > 30 mm/hr

40
Q

eosinophilia plus iron deficiency anaemia

A

think parasitic infection such as giardia or strongoloides

41
Q

what would you give if someone with Cdiff diarrhoea was not responding to vancomycin?

A

oral fidaxomicin

if fulament colitis suspected then refer to surgery

42
Q

drugs that cause liver cirrhosis

A

Amiodarone
methotrexate
methyldopa

43
Q

Drugs that cause cholestasis

A

clauvulanic acid
penicillins
oestrogens
erythromycin
chlorpromazine

44
Q

Infective causes of bloody diarrhoea

A

E.coli
Salmonella
shigella
campylobacter

45
Q

causes of dysphagia

A

obstructive:
- oesophageal/ gastric carcinoma
- oesophageal web
- oesophageal strictures
- external compression: goitre, thymoma, lung cancer

motility issue:
- achalasia
- stroke
- MG
- systemic sclerosis
- MND
- parkinsons

46
Q

scoring systems used in upper GI bleed

A

Glasgow-Blachford score- calculated before a procedure to determine whether a patient will need to be admitted for medical intervention

AIMS65 -
used to calculate the risk of in-hospital mortality in patients with an upper GI bleed

Rockall score-
used after GI endoscopy to determine the percentage risk of rebleeding and mortality in patients with upper GI bleeding

47
Q

differentials for dysphagia

A

Painful to swallow:
- tonsilitis
- oesphagitis

Mechanical/ obstruction
- oesophageal cancer
- oesphageal web
- oesophageal stricture
- external compression (thymoma, goitre, lung Ca)
- pharyngeal puch

Motility disorder
- achalasia
- stroke
- bulbar/pseudobulbar palsy

48
Q

Ix for non neuro casues of dysphagia

A

REFERRAL UNDER 2WW to exclue oesphageal Ca

OGD
Barium swallow
manometry

49
Q

Differentials for dyspepsia

A

GORD
Gastric/ duodenal ulcer
- NSAIDs, steroids, H.pylori
Upper GI Ca
Achalasia
oesophagitis (think HIV with candida)
Functional

50
Q

redflag features with new dyspepsia

A

ALARM

Anaemia
Loss of weight
Anorexia +/- abdo pain
Recent symptoms
Meleana/ haematemesis

51
Q

features of a pancreatic pseudocyst

A

Pseudocysts can be asymptomatic or present with signs of biliary obstruction (abdominal pain, jaundice) or gastric outlet obstruction (post-prandial vomiting) due to mass effect of an enlarging pseudocyst on adjacent structures. There is also the risk of secondary infection

Pathology and final year (21 decks)

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