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Medicine > Gastro > Flashcards

Gastro Flashcards

1
Q

whats the most common peptic ulcer

A

duodenal

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2
Q

whats the casue of peptic ulcers

A

break down of mucosa
= sterid, nsaids, aspirin
h.pylori

increase in stomach acid= stress, alcohol, caffeine, smoking, spicy foods

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3
Q

signs and symptoms of peptic ulcer

A

epigastric pain/disconfort
nasuea and vomiting

dyspepsia- heart burn, reflux, bloating, belching= indigestion
haeatemesis- cofee ground vomit
meleana
iron deficincey anemaia
gastric ulcer pain worse on eating
duodenal ulcer pain better on eating

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4
Q

fpatient has indigestion and when eat the pain worsens. what is this

A

gastric ulcer

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5
Q

what investigfations for peptic ulcer

A

endoscopy is diagnositic
rapid urease test- CLO = see if h.pylori
biopsy when there to see if cancerous not ulcer as look similar

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6
Q

management of peptic ulcer

A

like gord
ppi strong one

if got h.pylori then 7 day regime of ppi and amoxicillin and either clarithromycin or metronidazole twice daily

if allergic to pennicillin have metronidazole and clarithromycin

lifestyle adives

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7
Q

risk factrs for deeloping peptic ulcer

A

h.pylori infection
stress, alcohol, smoking
steroids
nsaids
asprin
bisphosphnates
potassium supllements
ssri
recreational drugs
zollinger ellison syndrome

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8
Q

complications of peptic ulcers

A

bleeding from ulcer- can be life threatening
perforation=> acute abdomen and peritonitits
scarring and stricture= pyloric stenosis = hard for food to empty out of stomach = upper abdo pain, nasuea and vomiting worse after eating and ditention

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9
Q

patient had a peptic ulcer then took ppi for it. they they found they got full quickly and were vomiting and abdo pain worse after eating. what is this complicartion

A

pyloric stenosis

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10
Q

whats gord

A

acid from stomach refluxes throgh lower oesopahgeal spincter and irritaes lining of oesopahgus

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11
Q

whats dyspesia

A

comples of upper gi symtoms thats typically there for at least 4 weeks
= feeling of indegestion

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12
Q

signs and symtpoms of gord/ covers dyspesia

A

heart burnacid regurgitation
retrosternal/epigastric pain bloating
nasuea and vomiting
noctunral cough
hoarse voice
asthma affected
dental erosions

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13
Q

risk factros for gord

A

obestiy tight clothing
trigger foods
smoking and alcohol coffee stress
pregnancy
drugs that lower oesphageal spincter pressure= CCB, anticholinergics, theophylline, benzodizapines, nitrates

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14
Q

pt comes with gord symptoms. what do you do

A

offer h.pylori test
if not wanting test give ppi for 4 weeks
if oesphagitis then 8 weeks
lifestyle advice

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15
Q

when would you refer a patient with gord symptoms for an endoscopy

A

restiant to treatment
pt doesnt want long term medication which is needed
firsk factors of barrets

dysphagia = red flag 2ww
weight loss
over 55= 2ww

upoer abdo pain and relfux

nasuea and vomitng
low hb
high platelet count

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16
Q

treatment for gord

A

lifestyle advice= use pillow at night eat smaller lighter meals
weight loss
decrease tea, coffee, alcholol
avoid heay melas before bed
sit up after a meal
avoid triggers

acid neutralising med when needed= gaviscon, rennie

ppi = omeprazole, lansoprazole

ranitidine= h2 r antagonist - alternative to ppi
surgery= laproscopic fundoplication= wrap fundus around lower pesopageal sphincter
h.pylori test

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17
Q

what h.pylori test are there and how does h.pylori damage stomach

A

burrows through mucosa to avoid acidic enviroment which exposes wppithelial cells to gastric acid
h.pylori produces urease which converts urea to ammonia to reduce acid envirmoment. ammonia dmaages the epithelial cells

urea breath test with carbon 13
stool antigen test

rapid urease test - done in edocscopy. get biopsy

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18
Q

how to treat gord with h.pylori present

A

triple therpay fr 7 daysppi + amoxicllin + clarithromycin or metronidazole

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19
Q

what type of bactieria is h.pylori

A

gram negative aerobic

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20
Q

whats barrets oesopahgus

A

metaplasia
squamous-> columnar
symtpoms will subside moramlly when this happens
goes from columnar with no dysplasia to low grade dysplasia to high grade dysplasia to adenocarcinoma of oesopahgus

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21
Q

treat barrets

A

like gord =

ppi or if low grade or high grade dysplasia can do ablation therpay to kill the cells and allow new ones to form= cyrotherpay/ laser therpay/ photodynamic therapy

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22
Q

casues of upper gi bleed

A

mallory weiss tear
oesopaheal varices
peptic ulcer
stomach/duodenal cancer

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23
Q

pt jaundice
low hb
high urea

A

oesophgeal varices due to liver disease

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24
Q

s and s of upper gi bleed

A

haemetemsis
coffee ground vomit
meleana
haemodynamically unstable= low bp, tachycardia
low hb
high urea
syncopy

may hae symptoms of underlying pathologu
jaundice= liver disease causing oesophageal varices
epigastric pain and dyspesisa= peptic ulcer

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25
Q

invetigations for upper gi bleed

A

glasgow blatchford score= risk of having upper gi bleed score baove 0 high risk

rockall score = pt have had endocsopy and risk of rebleed

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26
Q

management of upper gi bleed

A

abated

abcde approach irst for resus
bloods
access = 2 large bore cannula
transufse
endoscopy- within 24 hrs
drugs= stop nsaids and anticoagulants

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27
Q

what do you look for in bloods of supexed upper gi bleed

A

fbc for hb
u and e for urea
lft for liver disease
coagulation by looking at inr, and fbc for platlets
cross matcch 2 units of blood

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28
Q

when do you transfuse a pt with upper gi bleed

A

give blood, platlemts and fresh frozen plasma if major haemorrhage
too much blood can be harmful

platelts if actve bleeding or if thrombocytopenia - less than 50
prothrombin complex concentrate if actively bleeding and on warfarin

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29
Q

what do you do if suspected oesopahgeal varices

A

give terlipressin
prophylactic broad spectrum anitbiotic

ogd to stop bleed = banding vcarices or cauterisation of vessel

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30
Q

Watery travellers diarrhoea with stomach cramps and nausea
what is cause

A

enterotoxigenic E.coli

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31
Q

how does loperamide work

A

opioid receptor agonist
Loperamide is a μ-opioid receptor agonist which does not have systemic effects as it is not absorbed through the gut

The mechanism by which loperamide works is through stimulation of μ-opioid receptors in the submucosal neural plexus of the intestinal wall. This, in turn, reduces peristalsis of the intestines decreasing gastric motility.

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32
Q

what presntation of mesenteric ischemia

A

severe abdo pain
v high lactate= 7.1
low co2
low bicarb
acidic ph

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33
Q

A markedly raised ALP suggest what

A

pathology of the bile duct
or bone issues

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34
Q

autoimmune hepatitis will show what with the lfts

A

v high alt and ast
high but not very high alp
have antimitochondrial antibody negative

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35
Q

whats primary sclerosing cholangitis

A

stiffening ad hardening of the bile ducts and inflammtion of the bile duct

intrahepatic and extrahepatic ducts become strictured and fibrotic

chronic bile obstruction leads to liver inflammation (hepatitis) leads to fibrosis leads to cirrhosis

have obstruction of the bile into the small intestine

not sure on casue- genetic/autoimmune/intestinal microbiome/ enviroment

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36
Q

patients with ulcerative colitis are strongly asociated with what condition

A

primary sclerosisng cholangitis

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37
Q

risk factors for priamry sclerosisng cholangitis

A

male
30-40
ulcerative colitits
fma hist

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38
Q

jaundice
pruritus
chroic right upper quadrant pain
fatigue
hepatigmegaly

what is this

A

primary scleorisng cholangitis
similar to priamry billirary cirrhosis(cholangitis)

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39
Q

what investigfations do for priamry sclerosing cholangitits

A

rasied ALP the most of all lfts
can have raised ast and alt later on in more severe disease too
rasied billriubin in more severe disease as strictures become more severe
pANCA, ANA, aCL antibodies may be present but not specific to disease only there to aid in treaamtnet cus can give immunosupressants if got these antibodies

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40
Q

how to diagnose primary sclerosisng cholangitits

A

MRCP- mri of liver, pancreas and bile ducts
may show bile duct strictures/lesions

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41
Q

whats primary sclerosisng cholangitis assocaitedwith and comolications

A

acute bacterial cholangitis
cholangiocarcinoa
colorectal cancer
cirrhosis and liver failure
biliary strictures
fat soluble vitamin deficiey

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42
Q

how to manage primary sclerosisng cholangitits

A

liver transplant will cure
ursodeoxycholic acid
colestryamine = prevents bile acid reabsrbed in intestine = less go into blood
monitor for cholangiocarcinoma, liver failure/cirrhosis and oesopageal varices

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43
Q

primary sclrosing chokangitis or primary biliary cirrhosis/cholangitis is associated with bile duct cancer?

A

primary sclerosisng cholangitits- cholangiocarcinoma

primary biliary cholangitis/cirrhosis is associtated with hepatocellular carcinoma

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44
Q

whats primary biliary cirhosis/cholangitits

A

autoimmune condition
immune system attacks small bile ducts in liver= canals of hering

causes obstruction of bile out = cholestasis

the back pressure leads to liver inflamammtion–> fibrosis–> cirrhosis–> liver failure

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45
Q

what will be rasied in the blood in primary biliary cholangitis/cirrhosis

A

billirubin, bile acid, cholesterol will be raised as they cant be excreted out throigh the bile duct into the small intestine so get absorbed into the blood

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46
Q

signs and symptoks of priamry biliary cholangitis/cirrhosis

A

often starts asymptomatic as it then starts to preogress

fatigue
pruritus=due to rasied bile acid in blood
jaundice= due to rasied billirubin in blood
pale greasy stools= due to less billrubin getting into the intestine so stools paler and due to les bile acids getting into small intestine so cant absrob as much fat so greasy stools
gi disturbance and abdo pain- right upper quadrant
xanthoma and xantherlasma= high cholesterol in blood
signs of cirrhosis= ascites, splenomegaly, spider naevi

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47
Q

why us cardio vascualr disease risk increased in primary biliary cirrhosos/cholangitits

A

cholesterol isnt excreted in the bile due to it being blocked so more cholesterol absorbed into the blood so get depsotis in the blood vessles

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48
Q

whats the casue of primary biliary cholangitis/cirhossis

A

anti-mitochondrial antibodies

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49
Q

how to diangose/investigations for primary biliary cholangitits/cirhosis

A

rasied alp= cholestatic pciture
other liver enzymes and billirubin may be rasied esp in later satge
anti-mitochondrial antibodies
may have antinucelar antibodies
rasied ESR
rasied IgM
liver bioppsy to diagnosie and stage

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50
Q

complicaitons of primary biliary cholangitits/cirrhosis

A

advanced liver cirrhosis
potal hypertension = top two
symptomatic pruritus
fatigue
steathorrea
distal renal tubular acidosis
hypothryoidism
osteoporosis
hepatocellular carcinoma

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51
Q

risk factors fir pirmary biliary cholangitits/ cirrhosis

A

female
other autoimmune conditions- thryoid, coeliac
rheumatoid conditions- ra, sjorgrens(have dry mucous membranes too), systeic sclerosis

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52
Q

patient is
tired
right ipper quadrant pain for while
poo greasy and pale
very itchy and slightly yellow
eyes sore (dry eyes)

A

primary biliary cirhosis/cholangitits

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53
Q

treatment for primary biliary cholangitits/cirhosis

A

ursodeoxycholic acid= decrease intestine absobion pf cholesterol

colestyramine = binds to bile acids in small intestine and prevents reabsorbtion so helps with the itching

liver tranplant at end satge

immunosupression- steroids for some

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54
Q

whats primary bilairy cholangitis associated with

A

anti mitochondrial antibodies

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55
Q

whtas primary sclrosing cholangitits associated with

A

is associated with inflammatory bowel disease, and often has P-ANCA positivity.

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56
Q

difference of primary biliary cholangitis and primary sclerosisng cholangitits

A

both thought to be autoimmune
similar in presentation
PBC= anti-mitochondrial anitbodies and affetcs the smaller intra hepatic bile ducts mainly

PSC= assocaited with IBD and some ahve pANCA posititvity and affects mainly the medicum and larger bile ducts intra and extra hepatic

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57
Q

progression of alcholicliver disease

A

alcholic related fatty liver disease(reversible if no drinking takes 2 weeks)
then
alcoholic hepaitits - inflammation of liver. mild is reversible with permeenat stop drinking also get in binge drinking
then
cirrhosis = irreversible= nodules of scar tissue

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58
Q

whats recommened alchol intake

A

14 units a week
over 3 or more days
no more than 5 units in one dat

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59
Q

complications of alcohol

A

alcholic liver disease
cirrhosis - andthe complications
pacnreatitis
alchol dependence and withdrawal
alcholic cardiomyopathy
wernicke-korsakoff encephalppathy

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60
Q

signs of liver disease

A

caput medusae
palmar erythema
gynaecomastia
bruisin- due to less clottin
asterixis
hepatomegaly
jaundice
spider naevi
ascites

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61
Q

investigations for alcholic liver disease

A

fbc= raised MCV
lft= rasied alt an ast and esp rasied gamma GT
rasied alp later on
raised billirubin in cirhsosi
low albumin- low syntheitc function of liver
increased prothrombin time (less clotting factors made)
u and e deranged in hepatorenal syndrome

us = fatty liver= increased echogenicity

fibroscan= elastiticty of liver- asses degree of cirrhosis

endocsop- asses and treat oesophgeal vcarices

mri and ct= fatty liver inflammation
hepatocellular carcinoma
hepatosplenomegaly
abnormla blood vessles
ascites
l
liver biopsy- confrim fatty liver/cirrhosis - need to do if thinking of treating for steroids

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62
Q

management of alcholic liver disease

A

stop drinking
high b vitamin and protein diet
detox regime
treat complicatios
lover tranplant - need be no drinking for 3 onths prior to referal
steroids may help short term - need get bleeding etc sorted first and no long term help

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63
Q

whats the stages of alhol withdrawal and what happens

A

6-12hrs= tremor, sweating, anxiety, craving, headche

12-24hrs= hallucinations

24-48hrs= seizures

48-72hrs= delerium tremens

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64
Q

why does alchol withdrawal and the symptos happen in delerium tremens

A

alcohol is gaba = so body produces less gaba and increases glutamate to respond to try balance
when abruptly stop have exessive glutamate thats not regulated and have excessive adrenergic activity

tremor
hallucinations and delusions
acute confusion
tachycardia
hypertension
hyperthermia
ataxia= diff coordinating movements
arrythmia
severe agitiation

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65
Q

how do you manage alchol withrawal

A

chloradiazepoxide - librium
= benzodiazapine
give orally and reducing regime for 5-7 days
less common use diazapam

also give iv high dose vitamin B = pabrinex
then give orally dose of thiamine to prevent and treat wernickes korsakoff syndrome

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66
Q

whats wernicke korsakoff syndrome

A

think patient alcholic. confusion eye muslces and ataxia going mad
think wernickes encephalopathy

due to b1 deficicney as less absorbed in gut with alchol and also poor diet

first have wernicke encephalopahty= medical emergency
confusion
ataxia
oculomotro disturbanes

then get korsakoff syndrome = mosttly irreversible
memory impairment- anterograde and retrograde
behavioural changes
need institutional care

prevet and treat with thiamine and stop alchol

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67
Q

causes of hepatitis

A

alcholic hepatitis
non alcoholic fatty liver disease
autoimmune heaptitis
viral hepaitits
drug indices hepatits= paracetamol overdose

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68
Q

presentation of hepatitis

A

can be asymtpomatic/non-specific
nasuea and vomiting
jaundice
abdo pain
fever in viral
fatigue
muslce and joint aches
pruritus- itching
rasied alt and ast more than alp
rasied billirubin

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69
Q

what viral hepatitis is dna and what is rna

A

hepatitis b is dna
rest are rna

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70
Q

whats most common viral hepaitits

A

hepatitis a
relatively low in uk compared to rest of world

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71
Q

what hepaitits viral is transmited foecal-oral and what is blood and bodily fluids

A

a and E are foeco oral route = contaminted water/food

B,C,D are blood and bodily fluids

B can be transmited vertical transmission via pregancy and delvery to baby

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72
Q

s and of hepaitits A

A

n and v
jaundice
anorexia
can casue cholestatis= pale stools and dark urine
moderate hepatomegaly

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73
Q

treatment for hep a

A

resolves by self 1-3 months
basci analgeisa
vaccination available

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74
Q

whats the screening test for hepatitis B

A

HBcAb = for previous infection
HBsAg = for activie infection

of these are positigve then test for HBeAg and viral load= HBV DNA

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75
Q

HBcAb with IgM that high means what

A

active infection and acute

igm means active infection
high tire means acute
low titre means chronic

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76
Q

HBcAb with IgG mwans what

A

past infection if the HBsAg is negative

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77
Q

HBeAg means what

A

acute phase of infection- replicating
the more there is the more infectious person is

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78
Q

if HbeAg is negativ but HbeAb is positive means what

A

had replication phase byt mow stopped and les snfectious

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79
Q

whats usedin the hepb vaccine

A

HbsAg
so if have HbSAb then could have infection but could also have ust had vaccine
vacicne ge tin three doses and test fir the antibody to see if reacted to the antigen to see if vaccin worked

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80
Q

management of hep b

A

notify to public health
stop smoking and alcohol
screen using fibroscan for cirrhosis ad us for hepatocellular carcinoma
screen for other blood born viruses - hep c and hiv and other std
give antivirals
liver transplant

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81
Q

how many are chronic in hepatisi c

A

3 in 4 become chronic
no vaccine

82
Q

complications of hep c

A

cirrhosis
hepatocellular carcinoa

83
Q

test for hep c

A

screen usig hep C antibody
diangose by hep C RNA to confrim diagnosis

84
Q

manangemnt of hep c

A

same as hep b but use direct actig antivirals for 8-12 weeks

85
Q

whats hep d

A

needs hep b
worsens hep b
rna
v low rates in uk

86
Q

whats hep e

A

mild illnrd
foecal oral route
rare progression to chronic hepatitis
no vaccination

87
Q

whats autoimmune hepaitis

A

rare cause of chronic hepatitis
two types

88
Q

whats type 1 autoimmune hepaitits and autoantibodies associate

A

t1 is more in adults
women 40-50
before or after menopause
fatigue and liver disease features
less acute than type 2

anti nuclear antibodies - ANA
anti smooth muscle antibodies - anti actin.
anti soluble liver antigen- anti SLA/LP

89
Q

patient has anti actin antibodies. what autoimmune hepatitis is this

A

type 1
more common in adults

90
Q

whats type 2 hepaitis and autoanitbodies associated

A

more acute than t1
in childnre
teenaage/ early 20s
acute hepaitis
with riaseed alt and ast and jaundice
rasied IgG

anti liver kidney microsomes 1 = anti LKM1
anti liver cytososol antigen 1 = anti LC1

91
Q

diagnose and treat autoimmune hepatitis

A

biopsy for confimation of diangosis
treat with high dose steroids- prednisolone then once in remiision stay in remiision on immunosupressants- azathioprine = life long

liver trnaplan t- cxan recur though in transplant

92
Q

wjats alpha 1 antitrypsin deficicey

A

autosomal recessive
chromosome 14
deficicnt = its a protease inhibitoor

neutrophils produce elastase that digests connective tissue

so have too much connective tissue digestion

93
Q

what does alpha one antitrypsin deficincy casue

A

pulmonary basal emphysema affter 30yrs old
liver cirrhosis after 50 yrs old - dont always get this

94
Q

how to diagnose alpha one antitrypsin deficicny

A

screening test of choice= low serum alpha one antityrpsin

liver biopsy= liver cirrhosis
acid schiff positive staining globules in hepatocytes= stains the breakdown products of the proteases

genetic testing = A1AT
high resolution ct thorax for pulmonary emphydema

95
Q

when to suspect alph one antitrypsin deficiny

A

copd in young patient
progressive severe copd in any pt
cirrhosis in over 50 youngish ?

96
Q

what can a person with alpha one antitrypsin deficiny present with

A

hepatitis
liver cirrhosis and fibrosis, liver fialure
breathing issues - copd
jaundice etc
deranged lft

97
Q

managemet of alpha one antitrypsin deficicny

A

stop smoking!!! makes it much worse
symtpom management
organ transplant
monitor for compications - hepatocellular carcinoma= increased risk due to cirrosis of liver

98
Q

whats non alcoholic fatty liver disease

A

fat gets depositied in the liver cells which interfers with the functioning of the liver

can progress as get inflammation- hepattis and the liver heals but scar forms so get fibrosis and then lots fibrosis then join together to form nodules of healthy liver surrounded by fatty fibrosed lvier=cirrhosis

nafld–> non alcholic steatohepatitis–> fibrosis–> cirrhosis

99
Q

what risk factors are there for non alcoholic fatty liver disease

A

same as rf for cv and diabetes
obestity
smoking
high blood pressure
poor diet and low activity
high cholesterol
type 2 diabetes
middle age onwards

100
Q

investigations for non alcholic fatty liver disease

A

so if get abnormla lfts then do a non invasive liver screen:
us of liver
hep b and c serology
autoantibodies- see if casue is autoimmune hepatitis, PBC, PSC= ana, smooth muscle antibodies, antimitochondrial antibodies,, antibodies LKM1

immunoglobulins- autoimmune hepatitis, PBC

caerculoplasmin- wilsons disease
alpha 1 antitrypsin
ferritin and transferrin sats - hereditary haemochromatotisis

101
Q

what investigations do you do once investigated abnormal lfts

A

frist line- ELF blood test for assesing fibrosis
measure HA, PIIINP, TIMP-1

NAFLD fibrosis score = second line for fibrosis assesment - helpful to tule out
not helpfulto say how severe fibrosisi is

fibroscan = do if elf/nadld indicates fibrosisi

liver ultrasound will confrim diagnosis of fatty liver - doesnt give severity, function or fibrosis

102
Q

how to manage non-alcoholic fatty liver

A

weight loss
exercis e
stop smoking
control diabetes, bp, cholesterol
avoid alcohol
refer pt with fibrosis to liver specialsit - treat with vitamin E / pioglitazone (diabetes)

103
Q

whats the types of liver cancer

A

hepatocellular carcinoma - 80%
cholangiocarcinoma

can get metasisis from anywhere in body

104
Q

risk factors for liver cancer

A

hepatocellular carcinoma=
liver cirrhosis due to:
hep b/c
non alcholic fatty liver disease
alcholol
other chronic liver idsease
- pt with liver cirrhosis get screened for HCC

cholangiocarcinoma=
associated with primary sclerosisng cholangitits
presents over 50 unless with PSC

105
Q

presentation of hepatocellular carcinoma

A

often asymptomatic until late
abdo pain
weight loss
nause and vomiting
jaundice
pruritus
anorexia

106
Q

presentation of cholangiocarcinom

A

pailess jaundice like pancreatic cancer

107
Q

investigations for liver cancer

A

alpha fetoprotein - tumour marker for HCC
CA19-9 = tumour marker for cholagniocarcinoma
liver us= identify tumours
mri/ct= staging and diagnosis
ERCP- biopsy and brushings to diagose cholagiocarcinoma

108
Q

what does alpha fetoprotein mean

A

tumour marker for hepatocellular carcinoma

109
Q

wht does CA19-9 mean

A

tumour marker for cholangiocarcinoma

110
Q

treatment for hepatocellular caricnom

A

bad prognosis unless caught early
resection if early on= curative
liver tranplant if early on and isolate= curative
kinase inhibitors = sorafenib, regorafenib, lenvatinib - can extend life by months
reistant to chemo/radiotherpay

111
Q

treatment for cholangiocarcinoma

A

poor prognosis unless caught early
resection if caught early- curative
ercp= put stnet in where cancer is compressing bile duct= help improve symtpoms
resistant to chemo and radiotherpay

112
Q

what are two benign tumours o the live

A

haemangioma
focal nodular hyperplasia

113
Q

what haemangioma

A

benign coimmon tumour of liver
found incidentally often
asymptomatic
no potential to become cancerous
no monitoring or treatment needed

114
Q

whats focal nodular hyperplasia

A

benign tumour of liver
no potential to become cancerous
often no symptoms
no treastment or monitoring needed
can be related to oestrogen- more common in women and thpse on cocp

115
Q

focal nodular hyperplasia can be related to what hormone

A

oestrogen

116
Q

whats type tranplants of liver can have

A

orthotopic tranplant= straight from dead pt

living dononr trasnplant= give some to pt and both regerate and beconme fully functioning livers

split donation= half a dead pt liver and give to two pts and both will regernate

117
Q

en do you do liver trasnplant

A

actue liver failure - top of wiaitng list= paracetamol over dose/ acute viral hepatitis

chronic liver failure- wait standard time around 5 months

118
Q

when is a liver tranplant unsuitable

A

end stage HIV
excessive weight loss and malnutrtion
significant co morbiditits- sevre heart disease/ kindey disease
active hepaittis b / c infection or other infection
actuve alcohol use- need be abstinant for 6 months

119
Q

what incsion is made for liver tranplant

A

rooftop
/ mercedes benz
lower costal margin

120
Q

what post tranplantation care is there for liver tranplant

A

no alcholol or smoking
treat oppurtunistic infections
immunosupressants life long- steroids, azathioprine, tacrolimus
monitor for disease recurrence= hepatitis, primary bilialr cholangitits
monitor for cancer- increased risk due to immunosupressants
monitor for transplant rejection

121
Q

pt had liver transplant
whats signs need tolook out for transnplant rejection

A

jaundice
fever
fatigue
abnormla LFTs

122
Q

whats liver cirrhosis

A

chronic inflammation and damage to liver cells
increased resistance through liver
portal hypertension

123
Q

causes of liver cirrhosis

A

non alcholic fatty liver disease
alcholic liver disease hepatitis b
hepaitits c
others that are reversible causes :
primary biliary cholangitis
haemachromatosis
alpha 1 anti tryspin deficicnecy cystic fibrosis
autoimmune hepatitis
drugs:
amiodarone
methotraxate
sodium valporate

124
Q

signs of cirrhosis

A

jaundice
asterixis - in decompensated liver disease
caput medusae
spider naevi
gynaemastia
palmar erythema
brusing
ascites
hepatomegaly
splenomegaly

125
Q

what ivestigations do you do for liver cirrhosis

A

bloods - alt, ast a, alp and billirubin deranged in decompensated cirrhosis

low albumin
ELF test to asses for fibrosis in nafld
incerased prothrombin time
hyponatraemia- fluid retention
urea and creatine deraged in hepatorenal syndrome
alpha fetoprotein - marker for hepatocellular carcinoma - check every 6 months for pt with cirrhosis
ultra sound = odularity of surface, corkscrew appreance of hepatic artery due to increased flow and to compensate for low portal vein flow , enlarged portal vein with low flow ,ascited, splenomegaly

fibroscan = asses defree of cirhosis

endoscopy- asses for oesophageal varices

ct/mri - see if cancer
liver biopsy- confrim diagnosis of cirrhosis

126
Q

whats the general management of cirrhosis

A

minotir every 6 months for alpha fetoprotein and us to screen for hepatoceullular carcinoma endoscopy every 3 years in paitehtns without known varices
high protein, low sodium diet
MELD score every 6 months
consider liver transplant

127
Q

who is at risk of developing cirrhosis - what condtions

A

hepatitis b and c
heavy alchol misuse
alcholic liver disease
nafld with fibrosis on elf test

for these do a fibroscan every 2 years to asses for cirrhosis

128
Q

complications of cirrhosis

A

portal hypertension and oesophageal varices and bleed
hepatorenal syndrome
malnutrition and muscle wasting
ascites spontaneous bacterial peritonitits
hepatic encephalopathy
hepatocellular carcinoma

129
Q

whats the portal vein made of

A

splenic vein and superior mesenteric vein

130
Q

where can you get vcarices from portal hypertension

A

oesophagela
rectum
umbilical= caput medusae
ileoceacal junction

131
Q

how do you treat stable varices caused by portal ht

A

propanolol
elastic band ligation
i jection of sclerosant
tips

132
Q

treatment of bleeding oseophageal varices

A

fluid ressusitation
vasopressin= terlipressin
vit k and fresh frozen plasma if got deragned clotting
broad spectrum antibiotics
urgent endoscopy = sclerolant, sengstaken, blackmore tube

133
Q

how do you manage patient with muscle wasting amd malnuturtion due to liver cirrhosis

A

due to glycogen not being able to be stored and released properly from the liver so use the energy from the muscles so gwe wasting
les sprotein is also produced by the liver

treat;
regular meals
high protein
low sodium diet (minimise fluid retention )
high calrorie if needed
avoid alcholol

134
Q

what type of fluid is ascites in liver cirrhosis

A

transudative low protein content

135
Q

how to treat ascited in liver cirrhosis

A

low sodium diet
diuretcis- potassium sparing aldosterone antagonsit ones = spirinolactone
paracentesis
tips
prophylactic antibitoics to help prevent sponatoeus bacterial peritonitis
tips
lvier transplant

136
Q

spontaneous bacterial peritonitits and presentation

A

10% pt with ascites get it
asymtpotmatic
fever
abdo pain
high crp, wbc and creatine
metabolic acidosis ileus- dec movement of intestine
hypotension

137
Q

what the most common organsim casuing spontaneous bacterial peritonitits

A

e coli
klebsiella penumonaie
gram postive cocci- ostaphy and strep

138
Q

treatment for spontaneous bacterial peritonitis

A

ascititc culture
iv cephlasporin = cefotaxime

139
Q

wjats hepatorenal syndrome

A

fatal in week
portal ht dilates the portal blood vessles so they stretch. so have loss of volume circulation in kideys so get hypotesion in kidneys
raas is activated so get renal vasoconstriction and low circulating volume so no blood to kidneys so have decreased kidey fucntion

140
Q

cause of coeliac disease

A

autoimmune reaction to gluten
auto antibodies created that target epithelial cells of small intestine
inflammation efects aminly the jejunum first

causes atrophy of villi and so get malabsorbtion and symptoms

141
Q

presentation of coeliac disease

A

diarrhoea
fatgiue
weight loss
failure to thrive in children
can be asymtpomaitc
mouth ulcers
anaemia secondary to iron, b12, folate deficincy
dermatitis herpetiformis = itchy blistering rashes esp on abdomen

can present neuro rarely =

peripheral neuropahty
cerebellar ataxia
epilepsy

142
Q

what genetic associations are there with coeliac disease

A

HLA DQ2- 90%
HLA-DQ8

143
Q

WHAT ASSOCIATIONS ARE THERE WITH COELIAC DISEASE-when to suspect coeliac disease

A

gi unexplained symptoms
ibs
faltered growth/pubertu
prlonged fatigue
persistant/recurrent mouth ulcers
anaemia
type 1 diabetes !
autoimmune thryoid disease
autoimmune hepatitis
primary biliary cholangitis
selctive IgA deficiency

144
Q

a patient is newly diagnosed with type 1 diabetes
what should you test for as well

A

coeliac disease = test all new cases of t1dm for coeliac as associated

145
Q

what autoantibodies are there in coeliac disease

A

anti TTG= tissue transglutaminase antibodies

endomysial antibodies EMAs
deaminated gliadin peptides antibodies - anti DGPs

146
Q

when may you get false negative for coeliac

A

if the patient has a total low IgA= anti TTG and anti EMA are IgA then they may be low but actually it becasue they have low iga total

147
Q

how do you diagnose coeliac disease

A

test while on a gluten diet
first check for total IgA levlels to exclude IgA deficicnecy

then cehck for rasied anti TTG antibodies frist choice
can check for raised endomysial antibodies
endocscopy and intestinal biopsy = crypt hypertrophy, villous atrophy

148
Q

if pt has low total IgA what can you test for

A

the IgG version of anti TTG and anti EMA / endoscopic biopsy instead

149
Q

what will endoscopy and biospy shpw for coeliac disease

A

crypt hypertrophy
villous atrophy

150
Q

treatment for coeliac disease

A

life long gluten free diet

151
Q

whats anti TTG

A

tissue transglutaminase antibodies

152
Q

risk factors of IBS

A

female
younger adults
stress, anxiety, depression
post infection
deit- alcohol, spoicy foods, caffeine, fatty food, proccessed food
antibiotics

153
Q

whats ibs

A

fucntional bowel disordere
abdnomral functioning of a normal bowel
no identifiable organic disease unerlyinh

154
Q

s and s of ibs

A

diarrhoea
constipation
bloating
abdo pain
fluctuating bowel habit
worse after eating improved by opening bowels
straining, urgency, incomplete evacuation
mucus with stools

155
Q

what investigfations do for ibs

A

diangosed by exclusion
normal fbc, crp and esr
faecal calprotectin negative
negative coeliac serology - negative anti ttg
cancer not suspected/ryuled out

criteria=
abdo pain/discomfort and thats releived on bowel opening or asscoaite dwith change in bowel habit
and 2 of …
abrnomal stool passage(straining, urgency, incomplete evacuation)
bloating
symptoms worse after eating
mucus with stool

156
Q

management for ibs

A

reassure
health and exercise advice :
adequate fluid intake
regular small meals
avoid triggers
redcue proccessed food
redcue caffeine, alcohol
low fodmap diet = low in short chain carbs that small intestine absorbs poorly
trial probiotics for 4 weeks

first line= loperamide for diarrhoea
laxatives for constipation - avoid lactulose as can cause bloating and make it worse- linaclotide use if not repsponding to fisrt line laxatives
antispasmodics- for cramps- hyoscine butylbromide= buscopan

2nd line=
tricylic anti d - amitryptilline 5-10mg at night help with pain

3rd line = ssri ant d
cbt to help cope

157
Q

signs and symptoms of crohns disease

A

nests
no blood or mucus - less common in stool
entrie gi tract
skip lesions
termial iluem most affected and transmural inflmmation
smoking is a risk facotr - dont set the nest on fire
stricutres
fistulas

diarhoea
arhtirits
mouthulcers
abdo pain
weight loss
passing blood may occur pyoderma gangrenosum urgency
erythema nodosum

158
Q

management of crohns in erson having a flare

A

induce remission- steroids = oral prednisolone/ iv hydrocortisone
if not wokring then add in immunosupressants =
azathioprine
mercaptopurine
methotrexate
infliximab
adalimumab

159
Q

mangagement of crohsn to maitnain remission

A

may not need if well
azathioprine/ mercaptopurine= 1st line
methotrexate
infliximab
adalimumab

surgery id affecting only the distal ileum - resect

can do surgery to treat stricutres/ fistulas

160
Q

s and s of ulcerative colitits

A

close up
continuous inflammation
limted to colon and rectum
only superfical mucosa afected
smoking protective
excrete blood and mucus
use aminosalicylates
primary scleorisisng cholangititis! - ascoaited with

uveitis
colorectal cancer

esp lower quadrant abdo pain
diraahoea
arthritis weight loss
erythema nodosum
urgency

161
Q

uveitits and erythema nodosum and bowel issues asccoitated with what illness

A

ulcerative colitits

162
Q

bowel issues and erythema nodosum

A

ibd

163
Q

lung issues and erythema nodusm

A

sarcoidosis

164
Q

which ibd assocaited with colorectal cancer and eye issues

A

ulcerative colitits

165
Q

ulcerative colitis is associated with what that can casue jaundice and pruritus

A

primary sclerosisng cholangitis

166
Q

on colonoscopy see what in ukcerative colitits

A

pseudopolyps
neutrophils migrate thorgh walls of glands to form crypt absess
depletion of goblet cells and mucin from gland epithelium

167
Q

when would you do a flexi sigmoioscopy in ulcerative colitis/ crohsn

A

if the illnes bad as dont want to perforate

168
Q

barium enema in ulcerative colitis show what

A

loss of haustrations
pseudopolypts
in long standing disease the colon is short and narrow= drain pipe colon

169
Q

management of ulcerative colitis inducing remission

A

mild to moderate- aminosalicylate= mesalazine oral/rectal
2nd line= cortiosteroids eg. prednisolone

severe disease= iv cortiocsetorids - hydrocortisone
2nd lie= iv ciclosporin

170
Q

management in matintaining remission in ulcerative colitis

A

aminosalicylate- mesalazine oral / rectal
azathiorprine
metcaptopurine

surgery- remove colon and rectum= panproitocolectomy

permeenant ileostomy or j puch = ileo-anal anastamoses

171
Q

testing for IBD

A

faecal calprotectin = screening test
routine bloods for - anemia, thyroid, infection, kidney and liver function

endoscopy- with biospy for diagnosis
us,ct,mri to look for complications - strictures, fistulas, absess

172
Q

screening test for ibd

A

faecal calprotectin

173
Q

diangosis for ibd

A

colonoscopy with biopsy

174
Q

features of autoimmune hepatitis

A

Autoimmune hepatitis is condition of unknown aetiology which is most commonly seen in young females. Recognised associations include other autoimmune disorders, hypergammaglobulinaemia and HLA B8, DR3. Three types of autoimmune hepatitis have been characterised according to the types of circulating antibodies present

Type I
Anti-nuclear antibodies (ANA) and/or anti-smooth muscle antibodies (SMA)
Affects both adults and children

type 2
Anti-liver/kidney microsomal type 1 antibodies (LKM1)
Affects children only

type 3
Soluble liver-kidney antigen
Affects adults in middle-age

Features
may present with signs of chronic liver disease
acute hepatitis: fever, jaundice etc (only 25% present in this way)
amenorrhoea (common)
ANA/SMA/LKM1 antibodies, raised IgG levels
liver biopsy: inflammation extending beyond limiting plate ‘piecemeal necrosis’, bridging necrosis

Management
steroids, other immunosuppressants e.g. azathioprine
liver transplantation

175
Q

villous atrophy, raised intra-epithelial lymphocytes, and crypt hyperplasia

is what

A

coeliac disease

176
Q

dyspepsia
elevateed platelts
some nasuea
60 yrs old
what do

A

refer for upper gastrointestinal endoscopy. This patient has some alarm features for possible upper gastrointestinal malignancy, i.e. dyspepsia with associated nausea and elevated platelet count. Thrombocytosis can occur in the context of malignancy as a reaction to inflammation and therefore is included as a criterion in the NICE guidelines for suspected cancer referrals. These guidelines recommend consideration of non-urgent direct access upper gastrointestinal endoscopy for patients aged 55 or over who have dyspepsia with raised platelet count or nausea/vomiting.

177
Q

Metabolic ketoacidosis with normal or low glucose: think what casue

A

alcohol- alcoholic ketoacidosis

178
Q

adverse affects PPI

A

hyponatraemia, hypomagnasaemia
osteoporosis → increased risk of fractures
microscopic colitis
increased risk of C. difficile infections

179
Q

A 52-year-old male presents with central chest pain and vomiting. He has drunk a bottle of vodka. On examination, there is some mild crepitus in the epigastric region. What is the likely diagnosis?

A

The Mackler triad for Boerhaave syndrome: vomiting, thoracic pain, subcutaneous emphysema. It typically presents in middle aged men with a background of alcohol abuse.

180
Q

whats alcoholic hepatitis know in presentation and investigations

A

The AST/ALT ratio in alcoholic hepatitis is 2:1

Alcoholic hepatitis usually presents between the age of 40 and 50 years in those with a history of heavy alcohol use (usually >100 g/day for more than 20 years which is equal to about 3 glasses of 12% wine or 7 beers). Common presenting symptoms include right upper quadrant pain, anorexia, weight loss, jaundice, muscle wasting, and fever. AST/ALT>2 is characteristic of alcoholic hepatitis and points toward the diagnosis in this patient.

181
Q

how do you calcuate alchol units

A

volume drinking (ml) x percentage (abv)

and then / 1000 = units

Alcohol units = volume (ml) * ABV / 1,000

182
Q

how can you measure acute liver failure

A

prothrombin time
has a shorter half life than albumin so can see more acute issue

183
Q

autoimmune hepatitis charactieristics of investigation

A

anti smooth muscle antiboides
raised IgG
anti nuclear antibodies

184
Q

treatment of ascities

A

aldosterone receptor antagonist

Loop diuretics, for example, furosemide, are not typically used to treat ascites but can be used as an adjunct. Furosemide can cause hypokalemia and alkalosis. This promotes the formation of ammonia (NH3) from the ammonium ion (NH4+, which can cross the blood-brain barrier and cause hepatic encephalopathy.

185
Q

high urea
iron anemia

A

upper gi bleed

the high urea differenciates beteen upper/lower gi bleed= upper cus its like high protein meal blood in stimach

186
Q

charcot’s cholangitis triad: fever, jaundice and right upper quadrant pain

A

ascending cholangitis

187
Q

crohns and previous abdominal surgery
risk facotrs for

A

caecal volvulus

188
Q

whats abdo xray look like in caecal volvulus

A

large dilated loop of bowel centrally

189
Q

what drug can casue cholestasis

A

co-amoxiclav

190
Q

what drug should you not prescirbe with methotraxate

A

co-trimaxoazole=
shouldt prescibe trimethoprim if pt on methotraxate as both reduce folate and so casue casue penia of all cells and sepsis

191
Q

wilsons disease

A

autosomal receivvie
mutation with the wilson disease protein gene on chr 13
ATP7B = copper binding protein
copper transporting protein is needed to remove excess copper from the body via the liver and into the bile.
so cant excrete copper so ge tbuild up of excess copper in body tissues esp liver.

192
Q

features of wilsons disease

A

young- childrne to young adults (not over 40)
liver issues normally first esp in children
build up copper in liver- chronic hepatits–> cirrhosis

build up copper in CNS=
neuor= tremor, dysarthia, dystonia
in basal ganglia- parkinsonism
pschiatirc: psycosis, behavoural abnomralties, depression, cognitive impairemnt

kayser fleischer rings
haemolytic anemia
renal tubualr acidosis esp faconi syndrome

193
Q

investigations wilsons disease

A

first= low serum caeruloplasmin (protein carrys copper to be excreted) think mutation in this hence low
low total serum copper (counter inituative but cus 95% copper is carried bt caeruloplasmin)
- free (non caeruloplasmin bound) serum copper high

high 24hr urinary copper excretion

dx confirm= analsysi of ATP7B gene
liver biospy
MRI brain- double panda sign
low hb and -ve coombs test

194
Q

managment wilsons disease

A

copper chelation:
peniallamine = frist line
trentine hydrochloride

other:
zinc salts- inhibit cu absobrtion in GI
liver transplantation

195
Q

haemachormatosis

A

iron overload - iron storage disorder

autosomal recessive
HFE gene on Chr 6
usually mutation in C282Y most common

196
Q

presentation haemachromatosis

A

after 40- takes while for iron overload to become symptomatic
women present later cus menstruation leads to loss iron

chronic tiredness
joint pain
erectile dysfunction
liver cirrhosis
mood and memory disrubance
hypothyrdoisim
T1DM- in pancreas affect function
hypogonadotrophic hypogonadsim
dec fertility
cardiomyopathy
hepatocellular carcinoma
chondrocalisnosis- arhtirtis
pigemntation - bronze skin
testicular atrophy
ammehorrea
hepatomegaly

197
Q

investigations haemachoromatosis

A

serum ferrrtin
if this high look trasnferrin sats
if tranferrin sats high then haemachormatotis - more 55% men, more 50% women

look for mutaiton in HFE gene if trasnferrin and ferritin high

can do liver biopsy w/ perls stain to se iron levels but noy do so much now cus ahve genetic

MRI- can see iron level in liver

198
Q

reasons for high ferritin in blood

A

haemachromatosis
infection- ferritin is an acute phase reactant
chronic alcholol consumption
NAFLD
hepatitic C
cancer

199
Q

treament haemachromatoss

A

venesection - regulary remove blood to remove excess iron and intially do weekly

monitor serum ferrtin and montiro and treat complciations

200
Q

compliation hameachomatosis

A

cardiomyopahty
chondrocalcinosis- arthtis
hypochonadoptrophic hyppogonadism
testicualr atroph
dec fertiliy
hepatocellular carcinoma
diabetis T1DM
liver cirhosis
hypothyrodism

Medicine (11 decks)

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