Gastro Flashcards
(200 cards)
1
Q
whats the most common peptic ulcer
A
duodenal
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
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
4
Q
fpatient has indigestion and when eat the pain worsens. what is this
A
gastric ulcer
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
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
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
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
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
10
Q
whats gord
A
acid from stomach refluxes throgh lower oesopahgeal spincter and irritaes lining of oesopahgus
11
Q
whats dyspesia
A
comples of upper gi symtoms thats typically there for at least 4 weeks
= feeling of indegestion
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
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
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
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
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
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
18
Q
how to treat gord with h.pylori present
A
triple therpay fr 7 daysppi + amoxicllin + clarithromycin or metronidazole
19
Q
what type of bactieria is h.pylori
A
gram negative aerobic
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
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
22
Q
casues of upper gi bleed
A
mallory weiss tear
oesopaheal varices
peptic ulcer
stomach/duodenal cancer
23
Q
pt jaundice
low hb
high urea
A
oesophgeal varices due to liver disease
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
25
invetigations for upper gi bleed
glasgow blatchford score= risk of having upper gi bleed score baove 0 high risk
rockall score = pt have had endocsopy and risk of rebleed
26
management of upper gi bleed
abated
=
abcde approach irst for resus
bloods
access = 2 large bore cannula
transufse
endoscopy- within 24 hrs
drugs= stop nsaids and anticoagulants
27
what do you look for in bloods of supexed upper gi bleed
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
28
when do you transfuse a pt with upper gi bleed
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
29
what do you do if suspected oesopahgeal varices
give terlipressin
prophylactic broad spectrum anitbiotic
ogd to stop bleed = banding vcarices or cauterisation of vessel
30
Watery travellers diarrhoea with stomach cramps and nausea
what is cause
enterotoxigenic E.coli
31
how does loperamide work
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.
32
what presntation of mesenteric ischemia
severe abdo pain
v high lactate= 7.1
low co2
low bicarb
acidic ph
33
A markedly raised ALP suggest what
pathology of the bile duct
or bone issues
34
autoimmune hepatitis will show what with the lfts
v high alt and ast
high but not very high alp
have antimitochondrial antibody negative
35
whats primary sclerosing cholangitis
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
36
patients with ulcerative colitis are strongly asociated with what condition
primary sclerosisng cholangitis
37
risk factors for priamry sclerosisng cholangitis
male
30-40
ulcerative colitits
fma hist
38
jaundice
pruritus
chroic right upper quadrant pain
fatigue
hepatigmegaly
what is this
primary scleorisng cholangitis
similar to priamry billirary cirrhosis(cholangitis)
39
what investigfations do for priamry sclerosing cholangitits
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
40
how to diagnose primary sclerosisng cholangitits
MRCP- mri of liver, pancreas and bile ducts
may show bile duct strictures/lesions
41
whats primary sclerosisng cholangitis assocaitedwith and comolications
acute bacterial cholangitis
cholangiocarcinoa
colorectal cancer
cirrhosis and liver failure
biliary strictures
fat soluble vitamin deficiey
42
how to manage primary sclerosisng cholangitits
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
43
primary sclrosing chokangitis or primary biliary cirrhosis/cholangitis is associated with bile duct cancer?
primary sclerosisng cholangitits- cholangiocarcinoma
primary biliary cholangitis/cirrhosis is associtated with hepatocellular carcinoma
44
whats primary biliary cirhosis/cholangitits
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
45
what will be rasied in the blood in primary biliary cholangitis/cirrhosis
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
46
signs and symptoks of priamry biliary cholangitis/cirrhosis
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
47
why us cardio vascualr disease risk increased in primary biliary cirrhosos/cholangitits
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
48
whats the casue of primary biliary cholangitis/cirhossis
anti-mitochondrial antibodies
49
how to diangose/investigations for primary biliary cholangitits/cirhosis
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
50
complicaitons of primary biliary cholangitits/cirrhosis
advanced liver cirrhosis
potal hypertension = top two
symptomatic pruritus
fatigue
steathorrea
distal renal tubular acidosis
hypothryoidism
osteoporosis
hepatocellular carcinoma
51
risk factors fir pirmary biliary cholangitits/ cirrhosis
female
other autoimmune conditions- thryoid, coeliac
rheumatoid conditions- ra, sjorgrens(have dry mucous membranes too), systeic sclerosis
52
patient is
tired
right ipper quadrant pain for while
poo greasy and pale
very itchy and slightly yellow
eyes sore (dry eyes)
primary biliary cirhosis/cholangitits
53
treatment for primary biliary cholangitits/cirhosis
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
54
whats primary bilairy cholangitis associated with
anti mitochondrial antibodies
55
whtas primary sclrosing cholangitits associated with
is associated with inflammatory bowel disease, and often has P-ANCA positivity.
56
difference of primary biliary cholangitis and primary sclerosisng cholangitits
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
57
progression of alcholicliver disease
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
58
whats recommened alchol intake
14 units a week
over 3 or more days
no more than 5 units in one dat
59
complications of alcohol
alcholic liver disease
cirrhosis - andthe complications
pacnreatitis
alchol dependence and withdrawal
alcholic cardiomyopathy
wernicke-korsakoff encephalppathy
60
signs of liver disease
caput medusae
palmar erythema
gynaecomastia
bruisin- due to less clottin
asterixis
hepatomegaly
jaundice
spider naevi
ascites
61
investigations for alcholic liver disease
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
62
management of alcholic liver disease
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
63
whats the stages of alhol withdrawal and what happens
6-12hrs= tremor, sweating, anxiety, craving, headche
12-24hrs= hallucinations
24-48hrs= seizures
48-72hrs= delerium tremens
64
why does alchol withdrawal and the symptos happen in delerium tremens
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
65
how do you manage alchol withrawal
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
66
whats wernicke korsakoff syndrome
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
67
causes of hepatitis
alcholic hepatitis
non alcoholic fatty liver disease
autoimmune heaptitis
viral hepaitits
drug indices hepatits= paracetamol overdose
68
presentation of hepatitis
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
69
what viral hepatitis is dna and what is rna
hepatitis b is dna
rest are rna
70
whats most common viral hepaitits
hepatitis a
relatively low in uk compared to rest of world
71
what hepaitits viral is transmited foecal-oral and what is blood and bodily fluids
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
72
s and of hepaitits A
n and v
jaundice
anorexia
can casue cholestatis= pale stools and dark urine
moderate hepatomegaly
73
treatment for hep a
resolves by self 1-3 months
basci analgeisa
vaccination available
74
whats the screening test for hepatitis B
HBcAb = for previous infection
HBsAg = for activie infection
of these are positigve then test for HBeAg and viral load= HBV DNA
75
HBcAb with IgM that high means what
active infection and acute
igm means active infection
high tire means acute
low titre means chronic
76
HBcAb with IgG mwans what
past infection if the HBsAg is negative
77
HBeAg means what
acute phase of infection- replicating
the more there is the more infectious person is
78
if HbeAg is negativ but HbeAb is positive means what
had replication phase byt mow stopped and les snfectious
79
whats usedin the hepb vaccine
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
80
management of hep b
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
81
how many are chronic in hepatisi c
3 in 4 become chronic
no vaccine
82
complications of hep c
cirrhosis
hepatocellular carcinoa
83
test for hep c
screen usig hep C antibody
diangose by hep C RNA to confrim diagnosis
84
manangemnt of hep c
same as hep b but use direct actig antivirals for 8-12 weeks
85
whats hep d
needs hep b
worsens hep b
rna
v low rates in uk
86
whats hep e
mild illnrd
foecal oral route
rare progression to chronic hepatitis
no vaccination
87
whats autoimmune hepaitis
rare cause of chronic hepatitis
two types
88
whats type 1 autoimmune hepaitits and autoantibodies associate
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
patient has anti actin antibodies. what autoimmune hepatitis is this
type 1
more common in adults
90
whats type 2 hepaitis and autoanitbodies associated
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
diagnose and treat autoimmune hepatitis
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
wjats alpha 1 antitrypsin deficicey
autosomal recessive
chromosome 14
deficicnt = its a protease inhibitoor
neutrophils produce elastase that digests connective tissue
so have too much connective tissue digestion
93
what does alpha one antitrypsin deficincy casue
pulmonary basal emphysema affter 30yrs old
liver cirrhosis after 50 yrs old - dont always get this
94
how to diagnose alpha one antitrypsin deficicny
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
when to suspect alph one antitrypsin deficiny
copd in young patient
progressive severe copd in any pt
cirrhosis in over 50 youngish ?
96
what can a person with alpha one antitrypsin deficiny present with
hepatitis
liver cirrhosis and fibrosis, liver fialure
breathing issues - copd
jaundice etc
deranged lft
97
managemet of alpha one antitrypsin deficicny
stop smoking!!! makes it much worse
symtpom management
organ transplant
monitor for compications - hepatocellular carcinoma= increased risk due to cirrosis of liver
98
whats non alcoholic fatty liver disease
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
what risk factors are there for non alcoholic fatty liver disease
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
investigations for non alcholic fatty liver disease
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
what investigations do you do once investigated abnormal lfts
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
how to manage non-alcoholic fatty liver
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
whats the types of liver cancer
hepatocellular carcinoma - 80%
cholangiocarcinoma
can get metasisis from anywhere in body
104
risk factors for liver cancer
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
presentation of hepatocellular carcinoma
often asymptomatic until late
abdo pain
weight loss
nause and vomiting
jaundice
pruritus
anorexia
106
presentation of cholangiocarcinom
pailess jaundice like pancreatic cancer
107
investigations for liver cancer
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
what does alpha fetoprotein mean
tumour marker for hepatocellular carcinoma
109
wht does CA19-9 mean
tumour marker for cholangiocarcinoma
110
treatment for hepatocellular caricnom
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
treatment for cholangiocarcinoma
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
what are two benign tumours o the live
haemangioma
focal nodular hyperplasia
113
what haemangioma
benign coimmon tumour of liver
found incidentally often
asymptomatic
no potential to become cancerous
no monitoring or treatment needed
114
whats focal nodular hyperplasia
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
focal nodular hyperplasia can be related to what hormone
oestrogen
116
whats type tranplants of liver can have
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
en do you do liver trasnplant
actue liver failure - top of wiaitng list= paracetamol over dose/ acute viral hepatitis
chronic liver failure- wait standard time around 5 months
118
when is a liver tranplant unsuitable
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
what incsion is made for liver tranplant
rooftop
/ mercedes benz
lower costal margin
120
what post tranplantation care is there for liver tranplant
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
pt had liver transplant
whats signs need tolook out for transnplant rejection
jaundice
fever
fatigue
abnormla LFTs
122
whats liver cirrhosis
chronic inflammation and damage to liver cells
increased resistance through liver
portal hypertension
123
causes of liver cirrhosis
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
signs of cirrhosis
jaundice
asterixis - in decompensated liver disease
caput medusae
spider naevi
gynaemastia
palmar erythema
brusing
ascites
hepatomegaly
splenomegaly
125
what ivestigations do you do for liver cirrhosis
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
whats the general management of cirrhosis
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
who is at risk of developing cirrhosis - what condtions
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
complications of cirrhosis
portal hypertension and oesophageal varices and bleed
hepatorenal syndrome
malnutrition and muscle wasting
ascites spontaneous bacterial peritonitits
hepatic encephalopathy
hepatocellular carcinoma
129
whats the portal vein made of
splenic vein and superior mesenteric vein
130
where can you get vcarices from portal hypertension
oesophagela
rectum
umbilical= caput medusae
ileoceacal junction
131
how do you treat stable varices caused by portal ht
propanolol
elastic band ligation
i jection of sclerosant
tips
132
treatment of bleeding oseophageal varices
fluid ressusitation
vasopressin= terlipressin
vit k and fresh frozen plasma if got deragned clotting
broad spectrum antibiotics
urgent endoscopy = sclerolant, sengstaken, blackmore tube
133
how do you manage patient with muscle wasting amd malnuturtion due to liver cirrhosis
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
what type of fluid is ascites in liver cirrhosis
transudative low protein content
135
how to treat ascited in liver cirrhosis
low sodium diet
diuretcis- potassium sparing aldosterone antagonsit ones = spirinolactone
paracentesis
tips
prophylactic antibitoics to help prevent sponatoeus bacterial peritonitis
tips
lvier transplant
136
spontaneous bacterial peritonitits and presentation
10% pt with ascites get it
asymtpotmatic
fever
abdo pain
high crp, wbc and creatine
metabolic acidosis ileus- dec movement of intestine
hypotension
137
what the most common organsim casuing spontaneous bacterial peritonitits
e coli
klebsiella penumonaie
gram postive cocci- ostaphy and strep
138
treatment for spontaneous bacterial peritonitis
ascititc culture
iv cephlasporin = cefotaxime
139
wjats hepatorenal syndrome
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
cause of coeliac disease
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
presentation of coeliac disease
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
what genetic associations are there with coeliac disease
HLA DQ2- 90%
HLA-DQ8
143
WHAT ASSOCIATIONS ARE THERE WITH COELIAC DISEASE-when to suspect coeliac disease
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
a patient is newly diagnosed with type 1 diabetes
what should you test for as well
coeliac disease = test all new cases of t1dm for coeliac as associated
145
what autoantibodies are there in coeliac disease
anti TTG= tissue transglutaminase antibodies
endomysial antibodies EMAs
deaminated gliadin peptides antibodies - anti DGPs
146
when may you get false negative for coeliac
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
how do you diagnose coeliac disease
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
if pt has low total IgA what can you test for
the IgG version of anti TTG and anti EMA / endoscopic biopsy instead
149
what will endoscopy and biospy shpw for coeliac disease
crypt hypertrophy
villous atrophy
150
treatment for coeliac disease
life long gluten free diet
151
whats anti TTG
tissue transglutaminase antibodies
152
risk factors of IBS
female
younger adults
stress, anxiety, depression
post infection
deit- alcohol, spoicy foods, caffeine, fatty food, proccessed food
antibiotics
153
whats ibs
fucntional bowel disordere
abdnomral functioning of a normal bowel
no identifiable organic disease unerlyinh
154
s and s of ibs
diarrhoea
constipation
bloating
abdo pain
fluctuating bowel habit
worse after eating improved by opening bowels
straining, urgency, incomplete evacuation
mucus with stools
155
what investigfations do for ibs
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
management for ibs
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
signs and symptoms of crohns disease
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
management of crohns in erson having a flare
induce remission- steroids = oral prednisolone/ iv hydrocortisone
if not wokring then add in immunosupressants =
azathioprine
mercaptopurine
methotrexate
infliximab
adalimumab
159
mangagement of crohsn to maitnain remission
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
s and s of ulcerative colitits
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
uveitits and erythema nodosum and bowel issues asccoitated with what illness
ulcerative colitits
162
bowel issues and erythema nodosum
ibd
163
lung issues and erythema nodusm
sarcoidosis
164
which ibd assocaited with colorectal cancer and eye issues
ulcerative colitits
165
ulcerative colitis is associated with what that can casue jaundice and pruritus
primary sclerosisng cholangitis
166
on colonoscopy see what in ukcerative colitits
pseudopolyps
neutrophils migrate thorgh walls of glands to form crypt absess
depletion of goblet cells and mucin from gland epithelium
167
when would you do a flexi sigmoioscopy in ulcerative colitis/ crohsn
if the illnes bad as dont want to perforate
168
barium enema in ulcerative colitis show what
loss of haustrations
pseudopolypts
in long standing disease the colon is short and narrow= drain pipe colon
169
management of ulcerative colitis inducing remission
mild to moderate- aminosalicylate= mesalazine oral/rectal
2nd line= cortiosteroids eg. prednisolone
severe disease= iv cortiocsetorids - hydrocortisone
2nd lie= iv ciclosporin
170
management in matintaining remission in ulcerative colitis
aminosalicylate- mesalazine oral / rectal
azathiorprine
metcaptopurine
surgery- remove colon and rectum= panproitocolectomy
permeenant ileostomy or j puch = ileo-anal anastamoses
171
testing for IBD
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
screening test for ibd
faecal calprotectin
173
diangosis for ibd
colonoscopy with biopsy
174
features of autoimmune hepatitis
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
villous atrophy, raised intra-epithelial lymphocytes, and crypt hyperplasia
is what
coeliac disease
176
dyspepsia
elevateed platelts
some nasuea
60 yrs old
what do
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
Metabolic ketoacidosis with normal or low glucose: think what casue
alcohol- alcoholic ketoacidosis
178
adverse affects PPI
hyponatraemia, hypomagnasaemia
osteoporosis → increased risk of fractures
microscopic colitis
increased risk of C. difficile infections
179
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?
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
whats alcoholic hepatitis know in presentation and investigations
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
how do you calcuate alchol units
volume drinking (ml) x percentage (abv)
and then / 1000 = units
Alcohol units = volume (ml) * ABV / 1,000
182
how can you measure acute liver failure
prothrombin time
has a shorter half life than albumin so can see more acute issue
183
autoimmune hepatitis charactieristics of investigation
anti smooth muscle antiboides
raised IgG
anti nuclear antibodies
184
treatment of ascities
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
high urea
iron anemia
upper gi bleed
the high urea differenciates beteen upper/lower gi bleed= upper cus its like high protein meal blood in stimach
186
charcot's cholangitis triad: fever, jaundice and right upper quadrant pain
ascending cholangitis
187
crohns and previous abdominal surgery
risk facotrs for
caecal volvulus
188
whats abdo xray look like in caecal volvulus
large dilated loop of bowel centrally
189
what drug can casue cholestasis
co-amoxiclav
190
what drug should you not prescirbe with methotraxate
co-trimaxoazole=
shouldt prescibe trimethoprim if pt on methotraxate as both reduce folate and so casue casue penia of all cells and sepsis
191
wilsons disease
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
features of wilsons disease
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
investigations wilsons disease
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
managment wilsons disease
copper chelation:
peniallamine = frist line
trentine hydrochloride
other:
zinc salts- inhibit cu absobrtion in GI
liver transplantation
195
haemachormatosis
iron overload - iron storage disorder
autosomal recessive
HFE gene on Chr 6
usually mutation in C282Y most common
196
presentation haemachromatosis
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
investigations haemachoromatosis
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
reasons for high ferritin in blood
haemachromatosis
infection- ferritin is an acute phase reactant
chronic alcholol consumption
NAFLD
hepatitic C
cancer
199
treament haemachromatoss
venesection - regulary remove blood to remove excess iron and intially do weekly
monitor serum ferrtin and montiro and treat complciations
200
compliation hameachomatosis
cardiomyopahty
chondrocalcinosis- arthtis
hypochonadoptrophic hyppogonadism
testicualr atroph
dec fertiliy
hepatocellular carcinoma
diabetis T1DM
liver cirhosis
hypothyrodism
