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Gastro Flashcards

1
Q

what is the progression of alcoholic liver disease?

A

alcohol related fatty liver –> alcoholic hepatitis –> cirrhosis

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2
Q

what questionnaires are used in alcohol dependence?

A

CAGE and AUDIT questionnaires

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3
Q

what are the complications of alcohol dependence?

A

alcoholic liver disease, cirrhosis, dependence and withdrawal, Wernicke’s, Korsakoff’s, pancreatitis, cardiomyopathy

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4
Q

what are the signs of liver disease?

A

jaundice, hepatomegaly, spider naevi, palmar erythema, asterixis, caput medusae, gynaecomastia, bruising, ascites

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5
Q

what investigations should be done for alcohol dependence and liver disease?

A

bloods - FBC shows increased MCV, LFTs - high AST, ALT and GGT, clotting and U&Es
endoscopy
CT/MRI
liver biopsy

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6
Q

what is the management of alcoholic liver disease?

A

detoxification, abstinence, nutritional support with protein and thiamine, steroids, manage complications, liver transplant

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7
Q

what is the progression of alcohol withdrawal?

A

in 6-12 hours - sweating, headache, tremor, craving, anxiety
12-24h - hallucinating
24-48h - seizures
24-72h - delirium tremens

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8
Q

what is the pathophysiology of DT?

A

GABA underfunction and glutamate overfunction - excitability due to adrenergic activity - confusion, agitation, delusions, hallucinations

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9
Q

what are the signs of DT?

A

tachycardia, HTN, tremor, hyperthermia, ataxia, arrhythmia

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10
Q

how is DT managed?

A

benzodiazepines

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11
Q

how is alcohol withdrawal managed?

A

chlordiazepoxide, diazepam, pabrinex, thiamine

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12
Q

what is liver cirrhosis?

A

chronic inflammation and damage to the liver cells resulting in scar tissue and nodules - resistance and portal HTN

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13
Q

what are the causes of cirrhosis?

A

alcoholic liver disease, hep B or C, NAFLD etc

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14
Q

what are the tests for cirrhosis?

A

bloods, enhanced liver fibrosis test for NAFLD, USS, fibroscan, endoscopy, CT, MRI, biopsy and Child Pugh score

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15
Q

what is the management for cirrhosis?

A

USS every 6m and AFP, endoscopy every 3m, high protein, low sodium diet, MELD score, liver transplant and manage complications

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16
Q

what are the complications of liver cirrhosis?

A

malnutrition (regular meals), low sodium and high protein, portal HTN and varices (propanolol, shunt, elastic band ligations, sclerosant injection, resuscitation with vasopressin analogues, vit K and FFP, ABx, endoscopy), ascites (transudative - anti-aldosterone diuretics, paracentesis, ABx, TIPS, transplantation), bacterial peritonitis, hepatorenal syndrome, hepatic encephalopathy

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17
Q

how is spontaneous bacterial peritonitis managed?

A

ascitic culture and give IV cephalosporin

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18
Q

what are some causes of hepatitis?

A

viral, autoimmune, drug, NAFLD, alcohol

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19
Q

what is the presentation of hepatitis?

A

abdominal pain, fatigue, jaundice, pruritis, fever, muscle and joint aches, nausea and vomiting, increased AST/ALT and increased bilirubin

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20
Q

what is hep A?

A

RNA virus transmitted through faecal oral route, gives nausea, vomiting, jaundice, cholestasis, pale stools, dark urine, hepatomegaly. It is self limiting in 1-3m - manage with analgesia, vaccination and notify PHE

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21
Q

what is hep B?

A

DNA virus, transmitted via direct contact and vertical transmission, self limiting or chronic
HBcAB is a previous infection and HBsAg is current
give vaccination, screen for other BBVs, refer, notify PHE, stop smoking and alcohol, education, treat complications, liver transplant if required

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22
Q

what is hep C?

A

RNA virus - direct contact
liver cirrhosis and HCC are complications
screen for antibodies and RNA
manage complications, refer, notify PHE, educate, stop drinking and smoking, antivirals for 8-12 weeks and liver transplant

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23
Q

what is hep D?

A

RNA virus - only if Hep B is also present
mild and self limiting and rare to progress
no vaccine but inform PHE

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24
Q

what is hep E?

A

RNA virus, faecal oral route
mild, self limiting, rare progression, no vaccine
notifiable

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25
what is autoimmune hepatitis?
T1 - adults - fatigue and liver disease symptoms - ANA and anti-actin, antiSLA and LP T2 - young - high AST, ALT and jaundice - antiLKMI or LCI liver biopsy, prednisolone, azathioprine, transplant
26
what is the pathophysiology of PSC?
intra and extrahepatic ducts become strictured and fibrosed - obstruction of bile flow out - inflammation, fibrosis and cirrhosis
27
what is the presentation of PSC?
jaundice, hepatomegaly, deranged LFTs, chronic RUQ pain, p-ANCA, ANA, aCL
28
how is PSC diagnosed?
MRCP - see lesions and strictures
29
what are the complications of PSC?
acute bacterial cholangitis, cholangiocarcinoma, cirrhosis, CRC, liver failure, fat soluble vitamin deficiencies, biliary strictures
30
what is the management of PSC?
liver transplant, ERCP for stenting and dilating, colestyramine, monitor complications
31
what happens in PBC?
immune system attacks bile ducts resulting in cholestasis, fibrosis, cirrhosis and LF
32
what is the presentation of PBC?
fatigue, pruritus, GI disturbance, abdo pain, jaundice, pale stools, xanthoma, xanthelasma, liver failure signs, cirrhosis
33
what is associated with PBC?
middle aged women, other autoimmune conditions and rheumatoid conditions
34
what is the diagnosis of PBC?
LFTs (increased ALP and bilirubin later), autoantibodies (anti-mitochondrial, ANA), increased ESR and IgM, liver biopsy
35
what is the management for PBC?
ursodeoxycholic acid to reduce cholesterol absorption, colestyramine, liver transplant and immunosupression
36
what is the progression of PBC?
advanced LD and portal HTN resulting in fatigue, steatorrhoea, pruritus, distal renal tubular acidosis, HCC, hypothyroidism
37
what is NAFLD?
forms part of metabolic syndrome - increased risk of MI and stroke - fat deposits in liver cells so decreased function, hepatitis and cirrhosis
38
what are the staged of NAFLD?
NAFLD, NASH, fibrosis, cirrhosis
39
what are the autoantibodies in NAFLD?
ANA, SMA, AMA, LKM-1
40
what are the risk factors for NAFLD?
obesity, poor diet, low activity, T2DM, increased cholesterol, middle age, smoking, HTN
41
what are the investigations for NAFLD?
LFTs, USS, hep B and C serology, autoantibodies, caeruloplasmin, alpha 1 AT, ferritin and transferrin saturation, enhanced liver fibrosis test (7.7+), NAFLD fibrosis score, fibroscan
42
what is the management of NAFLD?
weight loss, exercise, stop smoking, control diabetes, BP, cholesterol, avoid alcohol, ?vit A/pioglitazone
43
what is Wilson's disease?
excessive accumulation of copper in body and tissues due to mutation in protein on C13 - AR inheritance
44
what are the features of Wilsons?
hepatic problems - cirrhosis and hepatitis, neuro - dysarthria, dystonia, parkinsonism, psychiatric - depression and psychosis, KF rings, haemolytic anaemia, renal tubular damage, acidosis and osteopenia
45
how is Wilsons diagnosed and treated?
serum caeruloplasmin decrease, liver biopsy, 24h urinary copper assay and MRI brain (non specific changes) copper chelation with penicilliname or trientene
46
what is haemochromatosis?
iron storage disorder - increased total body iron and tissue iron - HFR gene of C6 is mutated and usually AR inheritance
47
what is the presentation of haemochromatosis?
chronic tiredness, joint pain, pigmentation, hair loss, erectile dysfunction, amenorrhoea, cognitive sx
48
what is the diagnosis and treatment of haemochromatosis?
serum ferritin increase, transferrin saturation increase, genetic testing, liver biopsy with Peri's stain, CT abdomen, MRI - manage with venesection, monitor serum ferritin, avoid alcohol, genetic counselling, monitor and treat complications
49
what are the complications of haemochromatosis?
T1DM, cirrhosis, iron deposits in pituitary and gonads, cardiomyopathy, HCC, hypothyroidism, chondrocalcinosis, pseudogout
50
what is alpha 1 antitrypsin deficiency?
abnormality in gene for protease inhibitors, elastase secreted by neutrophils - digests connective tissue and is usually inhibited by A1AT - AR inheritance
51
what are the complications of A1AT deficiency?
liver- mutant A1AT gets trapped in liver, accumulates, causes damage - cirrhosis and HCC lungs - A1AT deficiency - excess protease, attack CT - bronchiectasis and emphysema (COPD)
52
how is A1AT deficiency diagnosed?
serum A1AT decrease, liver biopsy - cirrhosis, CT thorax and genetic testing
53
what is the management of A1AT deficiency?
stop smoking, symptomatic, organ transplant, monitor for complications
54
what is the pathophysiology of GORD?
stomach acid refluxes and irritates the oesophageal lining due to it being squamous cells not columnar - metaplasia of these is Barrett's (pre-malignant to adenocarcinoma)
55
what is the presentation of GORD?
dyspepsia, heart burn, acid regurgitation, retrosternal and epigastric pain, bloating, nocturnal cough, hoarse voice
56
what are the red flags for GORD?
dysphagia, age>55, weight loss, upper abdo pain and reflux, N+V, treatment resistance, decreased Hb, increased platelets
57
what is the diagnosis for H Pylori?
urea breath test, stool antigen test, rapid urease test eradication therapy = 2xABx and PPI for 7 days
58
what is the management of GORD?
lifestyle, acid neutralisation with rennie or gaviscon, PPI, ranitidine, laparoscopic fundoplication
59
how is Barrett's treated?
PPI, photodynamic therapy, laser or cryotherapy
60
what is the most common liver cancer?
HCC
61
what are the risk factors for liver cancer?
viral hep B and C, alcohol, NAFLD, CLD, PSC
62
what is the presentation of liver cancer?
weight loss, abdo pain, anorexia, N+V, jaundice, pruritus
63
what are the investigations for liver cancer?
AFP (HCC), Ca19.9 (chca), USS, CT, MRI, ERCP
64
what is the management for HCC and CHCa?
HCC - poor prognosis, resection and kinase inhibitors CHCa - poor prognosis - resection and ERCP stent
65
what is IBD?
UC and Crohn's inflammation of walls of GIT with periods of exacerbation and remission
66
what is the presentation and characteristics of IBD?
diarrhoea, abdo pain, passing blood, weight loss UC - continuous, colon and rectum, superficial mucosa, smoking protective, excrete blood and mucus Crohns - no blood or mucus, entire GIT with skin lesions, terminal ileum is worst, transmural, smoking is RF
67
how do you test for IBD?
bloods - anaemia, infection, thyroid, kidney, liver, CRP, faecal calprotectin endoscopy USS, MRI, CT
68
what is the management for Crohn's?
induction - steroids (IV hydrocortisone or oral pred) maintenance - azathioprine, mercaptopurine, methotrexate, infliximab surgery- resection
69
what is the management of UC?
induction - mild or moderate - corticosteroid or aminosalicylate severe - IV corticosteroid or ciclosporin maintenance - aminosalicylate, azathioprine, mercaptopurine surgery - panproctocolectomy, ileostomy
70
what is a peptic ulcer?
ulceration of the mucosa of the stomach or duodenum more commonly breakdown of the protective layer and increased stomach acid from drugs, H Pylori, stress, alcohol, smoking, caffeine, spicy foods
71
what is the presentation of peptic ulcers?
epigastric pain worse with eating if gastric or better if duodenum, N+V, coffee ground vomit and haematemesis, melana, iron deficiency anaemia, bleeding
72
what is the management and some complications of peptic ulcer?
endoscopy and rapid urease test, biopsy, PPI and monitor bleeding, perforation, acute abdomen, peritonitis, scarring, strictures, pyloric stenosis
73
what is an upper GI bleed?
bleeding from the oesophagus, stomach or duodenum from varices, MW tears, ulcers, cancers etc
74
what is the presentation of a GI bleed?
haematemesis, coffee ground vomit, haemodynamic instability, epigastric pain, dyspepsia, jaundice
75
what are the scores used in upper GI bleed?
Rockall score if had an endoscopy - risk of rebleeding and mortality Glasgow Blatchford score - risk of having a bleed
76
what is the management of upper GI bleed?
A-E bleeds - FBC, U&Es, INR, LFTs, XM access with 2 large bore cannula transfuse - FFP, and prothrombin if on warfarin endoscopy and stop drugs such as NSAIDs and anticoagulants OGD - banding and cauterisation terlipressin and prophylactic ABx if OV
77
what is IBS?
functional bowel disorder - abnormal functioning in otherwise normal bowel
78
what is the presentation of IBS?
diarrhoea, constipation, fluctuation of bowel movements, abdo pain, bloating, worse after eating, improved by bowel movements
79
what is the criteria for IBS?
normal FBC, ESR, CRP, negative faecal calprotectin, negative coeliac screen, r/o cancer abdo pain relieved by bowel movement and associated with change in habit plus two of PR mucus, bloating, worse after eating, abnormal habits
80
how is IBS managed?
fluids, regular small meals, decreased processed foods, alcohol and caffeine, probiotics, loperamide, laxatives, antispasmodics, amitriptyline, SSRIs, CBT
81
what is coeliac disease?
exposure to gluten causes autoimmune reaction - inflammation with autoantibodies, that target epithelial cells (antiTTG and EMA)
82
what are the biopsy results for coeliac?
crypt cell hypertrophy and villous atrophy
83
what is the presentation of coeliac?
FTT, weight loss, diarrhoea, fatigue, mouth ulcers, anaemia, dermatitis herpetiformis, peripheral neurology, cerebellar ataxia, epilepsy
84
what genes are associated with coeliac?
HLA-DQ2 and 8
85
how is coeliac diagnosed?
whilst on gluten diet total IgA to r/o deficiency antiTTG and antiEMA biopsy
86
what are the complications and associations of coeliac disease?
complications - vitamin deficiency, anaemia, osteoporosis, ulcerative jejunitis, EATL of intestine, NHL, small bowel adenocarcinoma associations - T1DM, thyroid disease, autoimmune hepatitis, PBC, PSC
87
what is the management of coeliac?
life long gluten free diet, treat complications and monitor autoantibodies

Finals (16 decks)

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