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year 1 flash cards > GI clinical sessions > Flashcards

GI clinical sessions Flashcards

1
Q

what are the main functions of the liver

A
  • cholesterol metabolism
  • drug metabolism
  • carbohydrate metabolism
  • -FA metabolism
  • NH3 metabolism
  • protein synthesis
  • bile formation
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2
Q

what are the 4 clinical problems we can get with the liver

A

acute hepatitis
chronic liver disease
extrahepatic billary obstruction
fatty liver disease

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3
Q

what is Hep A? how is it spread? how does it affect the liver

A

RNA virus
spread via the faecal-oral route
- causes hepatocyte necrosis and inflammation as it replicates in hepatocytes

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4
Q

what are the symptoms of hep A

A 
jaundice 
dark urine (bilirubin metabolism is altered)
pale stools 
malaise 
anorexia 
nausea 
abdominal pain
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5
Q

what are the clinical features of hep A

A

jaundice
hepatomegaly
splenomegaly
rash

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6
Q

what are the consequences of hep A

A

can cause relapsing hepatitis or cholestatic hepatitis (prolonged phase of jaundice) which can be recovered from

or acute liver disease which can lead to death if no liver transplant (v rare)

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7
Q

can people be asymptomatic with hepA

A

yes- for most people lines normally short and no treatment is required

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8
Q

what is chronic liver disease

A

a permeant and progressive pathological change throughput the liver (associated with repeat liver injury)

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9
Q

how does chronic liver disease effect the structure of the liver

A

changes the lobular architecture - portal tracts separated from portal viens

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10
Q

what can chronic liver disease lead to

A

fibrosis and cirrhosis

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11
Q

what are the causes of cirrhosis

A 
alchohol 
fatty liver disease 
hep C and B
primary billary cirrhosis 
auto immune liver disease
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12
Q

what are the morphological changes in cirrhosis

A
  • hepatocytes damaged and function poorly
  • sinusoidal/canalicular pathways disturbed
  • disrupted intrahepatic biliary drainage
  • disturbed vascular perfusion
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13
Q

what are the clinical effects of cirrhosis

A
  • jaundice
  • ascites
  • encephalopathy (abnormal brian function)
  • portal hypotension
  • splenomegaly
  • renal failure
  • heptocelluar carcinoma
  • bleeding tendency
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14
Q

how can portal hypertension cause renal failure

A

increased pressure in portal vein openes up channels in liver that are normally not needed leading to the liver becoming differ and the sinusoidal channels disrupted = blood flow in liver is disrupted and flows around the liver = urea and waste not removed

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15
Q

what are the symptoms of liver disease

A 
jaundice 
anemia 
heptomegaly
splenomegaly 
thin: muscle wasting 
liver palms 
clubbing 
dilated periumbical viens 
spider nevai
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16
Q

what are spider nevi

A

spider like marking on the skin

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17
Q

what characteristic is associated with portal hypertension

A

distended abdomen - larger than pregnancy

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18
Q

what are liver palms ? why do they happen

A

dilated hands- sex steroid hormones not verbalised and accumulate

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19
Q

what is billary obstruction ? what are the main causes ?

A

obstruction of the extraheptic billary system leading to decreased excretion of bile

commonly due to gallstones or pancreatic cancer

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20
Q

what is billary obstruction also known as

A

obstructive jaundice

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21
Q

what are the clinical effects of biliary obstruction

A
  • jaundice
  • dark urine
  • pale stools
  • itching
  • steatorrhoea
  • weight loss
  • vit déficiences (lipid soluble ones:AKED)
  • pain
  • disturbed lipid metabolism
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22
Q

what can cause fatty liver disease

A 
lots of things:
alchohol 
drugs 
diabetes 
obesity
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23
Q

what is the metabolic syndrome? what is it also known as

A

also known as the deadly quartet :

  • abdominal obesity
  • hypertension
  • diabetes mellitus
  • dyslipidaemia
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24
Q

what is the 2 immunological cells in the liver and what are they involved in

A

kupfer cells- bacterial degradation

pit cells –> liver NK cells

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25
Q

what are the 3 most common causes of liver disease in the UK

A

viral hepatitis
alchohol consumption
Non alcoholic fatty liver disease : NAFLD)

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26
Q

what is viral hepatitis

A

liver inflammation

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27
Q

what is the least serious type of Hepatitis

A

Hep A

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28
Q

do people normally become chronically affected with hep A

A

no usually resolves within a few weeks

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29
Q

which type of hepatitis mainly causes chronic liver disease

A

Hep B
(usually no acute hepatitis but can remain chronically affected for their lifetimes )
Hep C

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30
Q

what are the symptoms of Hep B

A

similar to Hep A but fever more common

also many include:
raises, pain and polyarhritjs

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31
Q

what is polyarthritis

A

swelling of the joints

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32
Q

do individuals recover form hep B

A

yes usually full revcovery made, however 1-5% patients remain chronically affected

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33
Q

what can chronic infection of Hep B lead to

A

cirrhosis and liver cancer (hepatocellular carcinoma- HCC)

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34
Q

do symptoms start early for Hep B

A

no usually patients dont know they have been effected in the early stages

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35
Q

what does the treatment of Hep B involve

A

48 week course of Pegylated interferon injection administered weekly

or oral antiviral agens - Tenofovir to supress levels of virus

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36
Q

what kind of infection does Hep C involve (acute or chronic?)

A

usually asymptomatic acute infection and 70-80% develop chronic infection , remaining asymptotic

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37
Q

when is Hep C usually diagnosed

A

when patients present with chronic liver disease years after original infection

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38
Q

how is Hep C usually transmitted

A

usually by blood to blood products (therefore in drug users)

also common in patents with haemophilia

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39
Q

does Hep B or C carry a better chance of cure

A

Hep C - successful treatment prevent progression of liver disease

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40
Q

which Hep is the commost common in the UK

A

Hep E

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41
Q

how can Hep E be transmitted

A

via faecal-oral route or consumption of raw undercooked pork or shellfish

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42
Q

which individuals are most at risk of Hep E

A

those with underlying liver diseases or alcohol-related liver disease

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43
Q

what is the treatment for Hep E

A

normally resolves on own

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44
Q

what is alcoholic liver disease

A

inflammation (alcoholic hepatitis) and fatty acid accumulation (accumulation of triglycerides) in heptocytes

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45
Q

what are the long term effects of alcoholic liver disease

A

fibrosis or cirrhosis

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46
Q

why do we get fatty acid accumulation in alcoholic liver disease

A

decrease in fatty acid metabolism and increase in fatty acid synthesis

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47
Q

what are the risk factors for non alcoholic fatty liver disease (NAFLD)

A

hypertension
obesity
insulin resistance
type 2 diabetes

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48
Q

how does NAFLD affect the liver

A

fat accumulation can be associated with inflammation which may lead to fibrosis or cirrohsis

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49
Q

are patients with NAFLD usually asymptomatic or not?

A

usually asymptomatic until complications of liver disease and cirrhosis present (jaundice, ascites, bleeding, HCC)

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50
Q

in most. cases what does inflammation of the liver usually lead to ?

A

fibrosis and cirrhosis

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51
Q

describe the structural changes to the liver of cirrhotic patients on a cellular level

A
  • micro nodular aperence (due to the regeneration )
  • thick bands of collagen (scar tissue)
  • cells swollen ( with fat droplets)
  • mallory body (cytoplasms with denatures keratin)
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52
Q

what are inherited conditions that cause liver cirrhosis

A
  • galactosaemic
  • glycogen storage diseases
  • Wilsons disease
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53
Q

how can immune mediated damage effect the liver

A

primary billary cirrhosis

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54
Q

how can bile duct damage effect the liver

A

bile accumulates and damages the liver and tissues = secondary billary cirrhosis

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55
Q

what is the difference between hepatitis and cirrhosis of the liver? are they reversible?

A

hepatitis = inflammation - reversible

cirrhosis = scarring = irreversible

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56
Q

what do you normally test for in a liver function test

A 
albumin 
total bilirubin 
alkaline phosphatase 
alkaline transaminase 
aspartate transaminase 
y-glutamyl transferase
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57
Q

in liver disease are albumin levels high or low? what does this normally cause

A

low levels

can result in oedema and ascites

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58
Q

in liver disease are bilirubin levels high or low? what is this due to?

A

high

due to damage in the liver or bile duct blockage

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59
Q

high levels of billirbun causes…

A

jaundice

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60
Q

are levels of alkaline phosphatase in liver disease usually high or low ? why

A

high as released when cells are destroyed- from damaged bile ducts

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61
Q

are levels of alanine and aspartate transaminase in liver disease usually high or low ? why

A

high due to liver damage - enzymes are released when hepatocytes damaged

usually used to show ongoing liver damage

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62
Q

what does y-glutamyl transferase indicate in a LFT

A

induced by alcohol so can indicate early liver dysfunction

NOTE- not specific can be raised from drugs

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63
Q

other than a liver function test what other tests could you carry on on patients suspected for liver damage

A

imaging of the liver : ultrasound or biopsy

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64
Q

why might oesophageal varicies lead to the vommiting of blood

A

blood flow through varices - can burst - patient can bleed to death

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65
Q

why would oesophageal varicies develop

A

fibrosis of the liver can disrupt the portal vein increasing resistance so blood flow through other vessles in the oesophagus

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66
Q

why might someone with liver disease have itchy skin

A

accumulation of bile salts in skin = irritation

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67
Q

why might someone with liver disease have steatorrhoea

A

due to pancreatitis which occurs with increased alcohol use = lipase not released = fat not broken down

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68
Q

why might someone with liver disease have more bruising and bleeding

A

lack of synthesis of clotting factors and Vit K

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69
Q

why might heavy drinkers be hypoglycemic.

A

liver damage = less hepatocytes = cant store glucose as well or carry out gluconeogensis

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70
Q

Why are patients with liver disease always given an i.v. injection of thiamine (vitamin B1) before
administration of glucose

A

because B1 is a cofactor for pyruvate dehydrogenase involved to allow pyruvate to enter the Krebs

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71
Q

how can lack of B1 lead to WKS

A

without B1 pyruvate turn to lactate leading to lactic acidosis and neurological damage =WKS

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72
Q

Why should alcohol be consumed with caution when taking other drugs?

A

competition between alchohol and drugs for cytochrome P450 enzymes and so slower clearance of both substances = increasing side effects from both

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73
Q

what drugs should not be taken with alcohol

A

antihistamines
NSAIDS
antibiotics
antidepressants

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74
Q

why might heavy drinkers beed increased dosage of prescribed drugs

A

because high levels of CYP450 enzymes always present so you have increased metabolism of drugs

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75
Q

what drugs can decrease withdrawal symptoms of alcohol

A

chlordiazepoxide
chlorometriozole
diazepam

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76
Q

what does disulphiram do

A

inhibits the action of aldehyde dehydrogenase making person feel ill to drink

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77
Q

what treatments are given to patients with severely damaged livers

A 
diruretics - oedema 
antibiotics - infections 
b blockers -portal hypertension 
clotting agents - internal bleeds 
liver transplant if v sevre
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78
Q

what does ‘dys’ and what does ‘pepsis’ mean in latin

A 
dys = bad
pepsis = digestion

= dyspepsia = indigestion

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79
Q

what are the 4 different types of dyspepsia

A
  • dyspepsia with alarm symptoms (with red flag features)
  • uncomplicated/ simple dyspepsia (dyspepsia without ‘red flag’ features)
  • uninvestigated dyspepsia (dyspepsia presenting to physician for the first time)
  • functional (‘non-ulcer’)
    dyspepsia (have symptoms of dyspepsia but no evidence on endoscopy)
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80
Q

what are alarm features for dyspepsia

A
  • weigh loss
  • dysphagia : difficultly swallowing
  • odynophagia : pain when swallowing
  • haematemesis : vomiting blood
  • melaena : dark poo, upper GI bleeding
  • palpable epigastric mass
  • family history of gastric cancer
  • over 45-55 years
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81
Q

what are potential causes of dyspepsia

A
  • gastro-oesophageal reflex
  • peptic ulcer
  • gastric cancer
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82
Q

which type of dyspepsia is most common ? why

A

functional dyspepsia due to a normal endoscopy

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83
Q

why would you perform a urgent GI endoscopy

A

if a patient presents with alarm symptoms

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84
Q

what is GI endoscopy poor in predicting

A

GI cancer

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85
Q

what are the strategies for managing dyspepsia

A
  • endoscopy
  • test for H.pylori
  • empirical PPI (proton pump inhibitors)
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86
Q

what is the problem with endoscopy

A

v expensive on NHS , not cost effective

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87
Q

symptoms and signs of peptic ulcer?

A

epigastric pain

  • epigastric tenderness
  • nausea
  • anorexia
  • weight loss
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88
Q

in a peptic ulcer when does the epigastric pain present ? how can it be relieved

A
  • after eating

- antacids, eating, drinking milk

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89
Q

what are the causes of peptic ulcers

A

*H.pylori *
non-steroidals/NSAIDS: aspirin, ibuprofen
Zollinger-ellison syndromes
Crohn’s disease

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90
Q

what is Zollinger-Elison syndrome

A

too much gastric acid production due to tumour cells in pancreas

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91
Q

what does H.pylori cause

A

gastric and duodenal ulcers

gastric cancer

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92
Q

how does H.pylori create an environment to enable to it survive

A

bacterium produces urease —> converts urea to NH3 anf H20 —> cloud of ammonia neutralises gastric acid pH in stomach = damages gastric linning (gastritis) and causes ulceration = it can survive

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93
Q

what methods can we use to diagnose for H.Pylori

A
  • carbon urea breathe test
  • H.Pylori serology (blood test)
  • H.pylori stool antigen

invasive: done at time of endoscopy
- rapid urease test
- histological examinations of biopsy

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94
Q

what would you tyts for in a H.Pylori serology (blood test)

A

IgG - once have H.Pylori will always have the antibodies present

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95
Q

how do we treat patients with H.Pylori (ie. gastric ulcer/cancer, functional dyspepsia)

A 
PPI- proton pump inhibitor 
and 2 ANTIBIOTICS: 
-amoxicillin
-clarithromycin
-metronidazole
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96
Q

what are the complications of peptic ulcers

A
  • perforation (GI contents leak into peritoneal cavity:peritinitis )
  • haemorrhage - bleeding (haemteasis, maleana)
  • gastric outlet obstruction (pyloric stenosis)
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97
Q

how does gastric outlet obstruction (pyloric stenosis) presents

A
  • persistant abdominal pain and discomfort

- massive somtach (food and build builds up)

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98
Q

how would you treat perforation or pyloric stenosis

A

surgery

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99
Q

how would you treat a bleeding ulcer

A

coagulation of bleeding point with adrenaline injections

if not work- heat probe

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100
Q

what are the symptoms and signs of a bleeding peptic ulcer

A
  • haematemesis
  • coffe-ground vomiting
  • melaena
  • rectal bleeding
  • tachycardia
  • hypotension
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101
Q

how does a peptic ulcer develop in the stomach/duodenum

A

break in the epithelial cells which penetrates to the muscularis mucosa

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102
Q

what is the difference between epigastric pain in stomach and duodenual ulcers

A

epigastric pain/ upper abdomen pain is worse at night in duodenal ulcers

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103
Q

what are the consequences of peritonitis caused by perforation of ulcers

A

sevre abdominal pain
shock
collapse

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104
Q

what kind of bacteria is H.Pylori

A

gram negative

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105
Q

what are the 2 strains of H.Pylori and how do they differ

A

CagA and VacA

  • Cag A infects the epithelial cells, altering cell replication and leading to apoptosis
  • VacA increases permeability of host cells and prevents stomal immune response so increases the ease of infection
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106
Q

how does H.pylori cause ulceration

A

causes infection and inflammation by increasing gastrin release and inhibiting somatostatin release

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107
Q

which blood group is at an increased risk of duodenal ulceration

A

blood group O

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108
Q

how do NSAIDS work

A

inhibit COX enzyme responsible for converting arachidonic acid into wide range of substances including prostaglandins

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109
Q

how might aspirin cause ulcers

A

inhibits prostoglands = more activation of parietal cells= increase gastric acid secretion

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110
Q

how many COX isoenzymes do we have

A

COX 1 (expressed all the time on gastric mucosa, kidneys, endothelial cells, platlets) and 2(expressed only in response to inflammation on monocytes and macrophages)

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111
Q

which COX isoenzyme is responsible for an inflammatory response and which is responsible for effects on gastric mucosa

A

COX 1 =effects on gastric mucosa

COX2 = inflammatory response

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112
Q

why might COX 2 specific NSAIDS be preferable to ibuprofen? what are the side effects of this?

A

more specific to inflammatory prostoglands not gastric mucosa prostoglands

however can increase clotting and constriction of capillaries leading to additional heart disease

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113
Q

why might aspirin promote haemorrhage from peptic ulcers

A

inhibits thromboxin formation = inhibiting blood clotting

114
Q

what does a proton pump inhibitor inhibit

A

K+/H+ ATPase

115
Q

other than PPI what other anti-ulcer drug can be used ? how do they work

A

H2 antagonists - prevent the binding of histamine one the H2 receptor = decrease acid release

116
Q

why might someone with a haemorrhaged gastric ulcer become breathless and have a raised pulse but low BP

A

due to anaemia from blood loss

117
Q

what abnormalities might someone with a haemorrhaged gastric ulcer have in their blood test

A

low Hb

high levels of urea (digestion of large amounts of RBC\

118
Q

Does perforation or ulceration go through more layers

A

perforation

119
Q

what is malabsorption

A

defective mucosal uptake and transport of adequately digested protein, fat, carbs, nutrients

120
Q

disturbances to what 3 normal digestive functions leads to malabsorption

A
  • intraluminal digestion (pancreatic enzyme secretion and emulsification by bile salts)
  • terminal digestion (enzymatic hydrolysis in brush border of small intestine)
  • trans-epithelial transport (nutrients, fluid and electrolytes transported across the epithelium)
121
Q

why is absorption of electrolytes and nutrients paticulllary sodium important absorption ?

A

because all the water that is absorbed is absorbed via osmosis

122
Q

what can a disturbance in electrolyte absorption lead to?

A

osmotic diarrhoea

123
Q

what protein does cholera effect and how can it lead to watery diarrhoea

A

activates CFTR chloride channel and leads to large amounts of Na+, Cl-, and HCO3- secretion into lumen meaning water follows = watery diarrhoea

124
Q

what 2 molecules are hydrolysed by brush border enzymes

A

starches: a-dextrins

peptides

125
Q

what is lactose intolerance

A

defences in brush border enzymes (eg.lactase) = can lead to failure to breakdown disaccharides (eg.lactose) into glucose and galactose

126
Q

how can lactose intolerance cause diarrhoea

A

disaccharides are not digested and remain in the gut so increases osmotic potential = draws more fluid into gut = diarrhoea

127
Q

what is steatorrhea

A

presence of excess fat in faeces

128
Q

what are the charcteriscts of steatorrhea

A
  • stools may float in pan- hard to flush
  • oil apprentice
  • foul smelling
129
Q

in what diseases do we see steatorrhoea

A

cholestatic liver disease
pancreatitis
coeliac disease

130
Q

what is cholestatic liver disease

A

inadequate flow of bile

131
Q

if fat absorption is impaired which vitamins will we see deficiencies in

A

A K E D

132
Q

what is calcium absorption greatly reduced by

A

vit D deficiency

133
Q

what can calcium malabosoprtion lead to

A

osteoporosis - reduced bone density

134
Q

what are the causes for osteoporosis

A 
anorexia 
smoking 
alcoholism 
malabsorption 
steroid therapy 
vit D or calcium defiancey
135
Q

what is osteomalacia

A

normal amount of bone but the mineral content is low (poor quality- dense but soft)

136
Q

what disease can lead to osteomalacia

A

ricks (if it happens during the period of bone growth)

137
Q

what are the causes pf osteomalacia

A
  • vit D deficiency

- malabsorption (coeliac, intestinal resection, cholestasis), renal disease

138
Q

levels of which minerals does osteomalacia effect

A
  • mildly decreased: calcium and phosphate

- increased: alkaline phosphate and parathyroid hormone

139
Q

where is lit A mainly absorbed

A

small intestine

140
Q

what can vitamin A deficiency cause

A

Xerophthalmia - eye problems

141
Q

where is vitamin B12 absorption

A

small intestine

142
Q

what can deficiencies in vitamin B12 lead to

A

angular stomatis (raw cuts around the mouth)

cheilitis (inflammation of the lips)

143
Q

what is vitamin B1 also known as

A

thiamine

144
Q

where is vitamin B1 absorbed

A

small intestine

145
Q

what can deficiencies in vitamin B1 lead to

A

Beriberi and WKS

146
Q

where is vitamin B6 absorbed

A

small intestine

147
Q

what can deficiencies in vitamin B6 lead to

A

polyneuropathy

148
Q

where is vitamin B12 absorbed

A

terminal ileum

149
Q

what can deficiencies in vitamin B12 lead to

A

anemia
large RBC/macrocytic anemia
SCDC- degeneration of the spinal chord

150
Q

where is vitamin C absorbed ? defines?

A

proximal ileum

scurvy

151
Q

where is vitamin D absorbed? defines can lead to?

A

small intestine/skin

osteomalacia

152
Q

where is vitamin E absorbed? defines can lead to?

A

small intestine

bleeding disorders

153
Q

where is vitamin K absorbed? defines can lead to?

A

small intestine

bleeding disorders

154
Q

how does vitamin B12 get absorbed

A

forms a complex with intrinsic factor in the stomach, facilitating its absorption —> absorbed in the terminal ileum

155
Q

what diseases can lead to B12 defiency

A
  • gastric mucosal atrophy

- terminal ideal disease

156
Q

what does B12/folate control

A

the normal proliferation of cells - necessary for efficient thymidilate synthesis and production of DNA

157
Q

where do we get our iron intake from

A

diet

158
Q

where does iron normally get absorbed

A

duodenum

159
Q

why might we get iron loss

A

bleeding

160
Q

what is coeliac disease

A

inflammatory condition of the small intestinal mucosa produced by an autoimmune reaction to ingestion of gluten

161
Q

how does coeliac disease effect the structure of the small intestine mucosa

A

villous atrophy - flat and blunted
intestinal inflammation
intraepithelial lymphocytosis

162
Q

what is the clinical presentation of coeliac disease in infants

A

impaired growth
diarrhoea
vomiting
abdominal distension

163
Q

what is the clinical presentation of coeliac disease in older children

A 
anaemia 
short stature 
pubertal delay 
rickets 
recurrent abdominal pain 
behavioural disturbance
164
Q

what is the clinical presentation of coeliac disease in adults

A

chronic anemia, diarrhoea, abdominal pian, bloating, nutritenial deficiencies, reduced fertility, osteoporosis, osteomalacia, abnormal Liver function tests

165
Q

what can intestinal inflammation in coeliac disease lead to

A

intestinal transit = things move into gut v quickly

166
Q

what does intestinal transit lead to

A

-decreased macronutrient absorption
-negative/calorie protein balance
= diarrhoea and weight loss

167
Q

what can villous atrophy lead to

A

reduced surface area for absorption = decreased absorption of osmotically active substances = diarrhoea

168
Q

what specific nutrient defences can occur in coeliac disease and what can they lead to

A
  • iron/ folate –> anaemia
  • calcium –> osteomalacia
  • fat soluble vitamins AKED –> clotting disorders
169
Q

how would you diagnose a patient for coeliac disease

A
  • clinical history
  • serological tests (for anti-tissue trnasglutaminase antibodies)
  • duodenal biopsy via upper GI endoscopy
170
Q

what is the management for coeliac disease

A
  • gluten free diet
  • replace nutritional deficneies (iron, calcium, folate, vit D)
  • monitor bone density
  • repeat small intestinal biopsy
171
Q

is coeliac disease more common in men or women

A

women

172
Q

what is parasthesia? why is it caused? what disease is it linked to

A

tingling in hands- caused by malabsorption of calcium

seen in coeliac disease

173
Q

what is pancreatic insufficiency

A

reduced delivery of pancreatic enzymes to duodenum

174
Q

in what diseases can we get pancreatic insufficiency

A

CF (reduced HCO3- and pancreatic fluid secretion ad blockage of ductus with mucous)

Chronic pancreatitis

175
Q

what is chronic pancreatitis

A

irreversible glandular destruction and alteration of anatomy/ function due to chronic inflammation

176
Q

what are the clinical features of chronic pancreatitis

A
  • epigastric pain- often radiating towards the back - food or alcohol may exacerbate the pain
  • wright los
177
Q

what are the causes of chronic pancreatitis

A 
alchohol 
familial
 congenital 
autoimmune 
genetic
178
Q

what other disease is closely linked with chronic pancreatitis? why?

A

diabetes due to endocrine insufficiency

179
Q

what investigations would you carry out for suspected chronic pancreatitis

A
  • facael elastase-1 (produced by pancreas and passed into stool largley unaltered)
  • abdominal X-ray
  • ultrasound/CT
180
Q

how do you manage chronic pancreatitis

A
  • remove precipitant (eg.alchohol)
  • pain control
  • treat diabetes
  • pancreatic enzyme supplemts (lipase, protease, amylase)
  • vitamin supplements
181
Q

what is cholestatic liver disease

A

impairment of bile formation of flow

182
Q

what are the consequences of cholestatic liver disease

A

steatorrhoea

fat vitamin malabsorption

183
Q

what is primary sclerosis cholangitis - PSC? what does it lead to

A

inflammatory/ fibrotic process affecting intra/extrahepatic bile ducts - type of cholestatic liver disease

leads to bile duct strictures (narrows bile ducts)

184
Q

what is primary sclerosis cholangitis most commonly associated with

A

IBD

185
Q

how does cholestatic liver disease (and PSC) present

A
  • pruritus : itching as bile salts in skin
  • fatigue
  • jaundice
186
Q

what does cholestatic liver disease (and PSC) lead to

A

cirrhosis and liver failure as bile can cause liver inflammation

187
Q

what is the treatment for cholestatic liver disease (and PSC)

A

liver transplant

188
Q

what is small bowel bacterial overgrowth to ? what is it normally seen with? how is it treated

A

bacteria degonjugate bile salts and metabolise B12

seen with structural abnormality (eg. Crohn’s)

rotating course of antibiotics

189
Q

where are NA+/K+ ATPase normally found

A

all cells - distributed evenly on cell surface or clustered in membrane domains in basolateral membrane

190
Q

how is Na rapidly excreted out of a cell? why is this importnant

A

sodium pumps - pumps it into intercellular spaces between adjacent enterocytes
establishes a high osmotic potential

191
Q

how is sodium trnaprted into the cell

A

down its conc gradient alongside glucose and amino acids

or H+/Na+ antiport pump

192
Q

how do chloride ions enter the cell

A

antiport Exchange with bicarbonate ions

193
Q

how do we treat someone who is severely dehydrated form sevre diarrhoea

A

oral rehydration solutions containing water salts and glucose

194
Q

why do oral rehydration solutions not only contain water

A

because the glucose and salts (Na and Cl) creates the osmotic gradient which is more negative allowing water to follow

195
Q

what are the 2 processes which establish an osmotic gradient

A
  • increase in luminal osmotic pressure from influx and digestion of foodstuffs
  • crypt cells actively secreting electrolytes via their ion channels
196
Q

what ion channel do crypt cells contain

A

CFTR

197
Q

what 2 cells are villi mainly covered in

A

enterocytes and goblet cells

198
Q

what cells are the crypts of leubrikun covered in

A

younger cells and stem cells (give rise to younger enterocytes which make their way up the villi as they mature)

199
Q

highlight the process of water secretion across crypt cells

A

1- Na/K+ pump pumps sodium from cells = establishes Na gradient
2- symporter on basolateral surface transports Na, Cl, K into cell = secondary active transport via Na
3- CFTR activated from cAMP lead to Cl secretion
4- accumulation of Cl in crypt draws Na+ acrosss via tight junctions = secretion of NaCl
5- accumulation of NaCl creates transepithelial osmotic gradient drawing water across

200
Q

what are the 3 main reasons we get malabsorption

A
  • impaired digestion (pancreatic insifficnecy-CF, chronic pancreatisis)
  • lack of bile
  • lack of intestinal enzymes (lactose intolerance)
201
Q

what are the 4 differnt types of diarrhoea

A
  • osmotic: stuff in GI tract that cant be absorbed
  • secretory : excess secretions into GI overwhelms ability to reabsorb fluid
  • inflammatory : prevents absorption
  • abnormal motility : chyme moving too rapidly through GI tract so absorption cant take place fully
202
Q

why might we get bloating and flatulence from sugar

A

sugar is fermented by bacteria in large intestine producing acidic stools and gas

203
Q

what are symptoms of lactose intolerance in a child

A

failure to gain weight

204
Q

what are symptoms of lactose intolerance in an adult

A
  • audible bowel sounds
  • abdominal bloating
  • flautulence
  • nausea
  • urge to defecate
  • diarrhoea
  • abdominal cramps
205
Q

how do we diagnose for lactose intolerance

A
  • eating dose of lactose and monitoring what happens in the 20-30 mins and whether the glucose levels go up (they shouldn’t)
  • biopsy of small intestine to rule out coeliac disease
206
Q

what is the treatment for lactose intolerance

A

avoid foods containing lactose

calcium suplements

207
Q

what secretions are reduced in CF and why

A

pancreatic fluid and HCO3- due to blockage of ducts with mucous = preventing delivery from pancreas to duodenum (leading to steatorrhea)

208
Q

what is meconium ileus

A

most common cause of CF in babies - disability of baby to pass first poop/meconium as pooop too thick and stickyyyyyyyy that it blocks the ileus

209
Q

why do we get diarrhoea in adults with CF? what kind of diaoreha is this

A

osmotic diarrhoea

thickened mucus blocks the pancreatic duct = lack od digestive enzymes = poor digestion of food = increase osmotic potential of gut lumen

210
Q

what are the 3 phases to cholera infection ? which phase can be/is fatal

A
  • evacuation phase –> profuse watery ‘rice water’ diarrhoea and sometimes vomittin
  • collapse phase –> caused by dehydration and decreased blood volume - can be fatal
  • recovery phase - if you survive
211
Q

why is it a selective advantage against cholera if you are a carrier of CFTR mutation gene

A

have half the number of CFTR channels so if you get cholera you lose less water - might survive

212
Q

what would you check in a blood test for anemia in coeliac disease

A

components of erhypoeisis:
ferritin
folic acid
B12

213
Q

what are the 3 components of the innate immune system

A
  • toxic/ inhibitory substances
  • complaint system
  • cells which make up out in=immune system
214
Q

give examples of toxic/inhibitory substances of the innate immune system

A

CRP- C reative protein (enhances phagocytosis)
deffensins in skin and gut
enzymes (lysozymes in tears)

215
Q

what are the cellular components of the innate immune system

A
  • phagocytes: neutrophils, monocytes, dendritic cells, eosinophils
  • NK cells
  • mast cells and eosinophils (release mediators- eg.histamine)
216
Q

are T cells or B cells long lived

A

T cells are long lived most produced before puberty

B cells are short lived

217
Q

where are B and T cells produced and matured

A

B cells are produced and matured in the bone marrow \

T cells are produced in the bone marrow and matured in the thymus

218
Q

a region on which chromosome codes for MHC

A

region on chromosome 6

219
Q

what are the antigens that MHC present called ? what is the significance of these antigens

A

Human leukocyte antigens : HLAs

HLAs are polymorphic and so its hard to find 2 individuals with matching HLAs so imunosupressents given in transplant

220
Q

briefly describe humoral immunity

A

B cells trigged by matching antigen –> B cell engulfs and digests antigen —> displays antigen via MHC molecule –> attracts T-cell —> T cell releases cytokines —> helps B cell mature and multiply into plasma cells —> released into blood —> antigen antibody complexes formed —> removed via complement cascade

221
Q

what are the 3 types of T helper cells ? describe their function

A
  • Th1 –> promote inflammation, stimulator phagocytosis- responses to microbial pathogens
  • Th2–> promote antibody production - specially IgE (involved in parasite and allergic reactions)
  • Th17 –> roles in intestinal lamina propia
222
Q

what are T helper cells also known as

A

CD4+ T lymphocytes

223
Q

what are the 3 components of the mucosal immune system

A

GALT
intraepithelial lymphocytes
lamina propria lymphocytes

224
Q

what are the components of GALT (gastric associated lymphocytic tissue)

A
  • tonsils
  • adenoids
  • Peyers patches
  • appendix
225
Q

what are intraepithelial lymphocytes and where are they found

A

intersperse amongst epithelial tissues - contain mainly CD8+ T cells

226
Q

what do lamina propia lymphocytes contain

A

CD4+ T cells, B lymphocytes, mast cells

227
Q

what are the 3 IBD (inflammatory bowel diseases)

A

ulcerative colitus

Crohn’s disease

228
Q

what is IBD

A

chronic relapsing and remitting inflammatory disorders of the intestines

229
Q

what I the aeiotology if IBD

A

remains mainly unknown

230
Q

what is the cure for IBD

A

no real medical cure

231
Q

what is thought to be the trigger for the inflammorty response in IBD

A

inappropriate response to stimuli in genetically susceptible individuals

232
Q

what are trigger stimuli in IBD

A

genes, environment, gut microbiome

233
Q

where is Cronhs disease and where is ulcerative colitis located in the gut

A

Crohn’s –> anywhere in GI

ulcerative collitus –> colon/rectum

234
Q

what is the disease distribution in crohns disease

A

full wall thickness

patchy ‘cobblestone’ appearance —> spaces with active inflation and normal intestinal cells in between

235
Q

what is the disease distribution in ulcerative collitus disease

A

only effects the mucosa

continuous areas of inflammation

236
Q

what are the histological findings in Crohns disease

A
  • transmural inflamamtion (entire wall of intestine inflamed)
  • granulomas –> spherical areas formed during chronic inflammation, if not degradable foreign matter or presence of pathogens present (absence of necrosis)
237
Q

what are the histological findings in ulcerative collitus

A

mucosa and submucosal inflammation
crypt abcesses
gland destruction
lack of goblet cells

238
Q

what are the complications associated with Crohns disease

A
  • fistulas (abnormal connection between the GI tract and the outside to other organs in the abdominal cavity) - leads to perforation and abcess formation
239
Q

what are the complications associated with ulcerative collitus

A

colonic dilation

toxic megacolon

240
Q

which IBD does smoking improve disease course

A

ulcerative collitus

241
Q

which IBD may surgery be a possible cure

A

ulcerative collitus as an remove part of colon or rectum

242
Q

what are the symptoms of IBD

A
  • diarrhoea
  • rectal bleeding
  • production of mucous in. stools
  • faecal urgency
  • incontinence (need to pee immediately)
  • abdominal and perianal pain
  • weight loss
  • fatigue and lethargy
  • mouth ulcers
243
Q

what are mouth ulcers called

A

aphthous stomatitis

244
Q

what are the signs of IBD

A
  • abdominal tenderness
  • mass on palpitation
  • anaemia (caused by malabsorption )
  • fistulae
  • perianal abcess
245
Q

what are dermatological extra intestinal manifestations of IBD?

A 
erythema nodusum (painful fleshy bumps on skin)
pyoderma gangrenosum (necrotic ulcer on legs)
aphthous stomatitis (mouth ulcers)
246
Q

what are musculoskeletal extra intestinal manifestations of IBD?

A

inflammation resulting in:

  • peripheral arhtitius
  • sacroileitis (inflation of sacroiliac joint)
  • ankylosing spondylitis (arthritis in spine)
  • osteoporosis
247
Q

what are vascular extra intestinal manifestations of IBD?

A

vasculitis

venous thromboembolism

248
Q

what are ocular (eyes) extra intestinal manifestations of IBD?

A
  • aveitis
  • iritis
  • scleritis
249
Q

what are renal extra intestinal manifestations of IBD?

A
  • kidney stones
  • glomeruloneptitis : inflation of glomeri
  • tubulo-intestinal nephritis : inflammation of intestinal tissue surrounding tubules of kidney
250
Q

what are hepatobillary extra intestinal manifestations of IBD?

A

primary sclerosing cholargitis

251
Q

what is the first line of treatment we would use for Crohns disease

A

short term anti-inflammatory : corticosteroids

to induce remission

252
Q

what is the second line of treatment we would use for Crohns disease to maintain remission

A
  • immunosuppressants : azathioprine, 6-mecraptoparine
  • aminosaclicylates : for disease in the colon (mesalazine)
  • methotrexate: anti inflammatory and immunosuppressant
  • antibiotics
253
Q

how do aminosalicylates work

A

aspirin analogues are broken down in the colon providing aspirin directly to the colon

254
Q

how does azathioprine works as an immunosuppressant

A

converted to 6-mercaptopurine —> purine analogue incorporated in DNA –> = poor proliferation of leukocytes = suppression of immune system

255
Q

what is infliximab

A

a biological therapy of monoclonal antibodies against TNF-a

256
Q

what does infliximab contain

A

human constant region and mouse variable region = chimeric

257
Q

what does chimeric mean

A

consisting of material from 2 differnt species

258
Q

how does infliximab work

A

binds to TNF-a on surface of T cells –> indices apoptosis of inflammatory cells and reduced amount of TNF

259
Q

name 5 autoimmune diseases other than IBD

A 
diabetes 1 (organ specific)
graves (organ specific)
MS 
rheumatoid arhtitis 
systemic lupus erythematous 
coeliac disease 
myasthenia gravis
260
Q

which sex do autoimmune diseases mainly effect

A

females

261
Q

what are the diagnostic features of anorexia nervosa?

A

active maintenance of low body weight (<85% of expected weight or BMI <17)
extreme shape and weight concern

262
Q

give some physical signs of anorexia nervosa?

A 
sever weight loss
low blood pressure
constipation and bloating
hair falls out and downy hair over body
swelling in feet and hands
low body temperature
periods stop
263
Q

what was the minnesota experiment?

A

study of human starvation with 36 conscientious objectors in WWII
3 month stability phase on 3600 kcal followed by 6 month starvation phase on 1800 kcal

264
Q

what are the diagnostic features of bulimia nervosa?

A

recurrent binge eating
compensatory behaviour (vommiting, laxatives, fasting, exercise)
extreme shape and weight concern

binge 1/week for 3 months

265
Q

what are physical signs of bulimia?

A 
fatigue
stomach pain and constipation
regular changes in weight
enlarged salivary glands 
electrolyte imbalance
swelling of hands and feet
266
Q

what is the difference between binge eating disorder and bulimia nervosa?

A

binge eating disorder has no compensatory behaviour

267
Q

what do eating disorders have in common?

A

behaviour around food (restriction)
core beliefs and associated concerns
levels of distress (mood disorders?)

268
Q

what might make someone more likely to develop an eating disorder?

A 
mental health problems
family history
perfectionism
history of dieting
being part of a sport or activity with emphasis on appearance
269
Q

what are the specific risks for eating disorders?

A

body dissatisfaction (contextual, physical and developmental)

  • negative body image
  • weight preoccupation
  • dietting
270
Q

what are non-specific risks for eating disorders?

A

self-regulatory (parental physcopathology, trauma, biological predispositions)

  • low self esteem
  • affective dysregulation
  • insecure attachment
271
Q

what are the three stages of ed treatment?

A

weight management
psychological therapies
relapse prevention

272
Q

what is the most common mutation of CFTR

A

F508del

273
Q

what are the symptoms of CF

A
  • airways clogged with mucous
  • chest infections
  • persistent cough
  • pancreatic insufficiency
  • CF related diabetes
274
Q

what does cross infection refer to in CF

A

CFs cant mix as bugs in lungs are transmissible between patients and dangerous

275
Q

what is the medication used in CF

A
  • 50 different pills a day: inc pancreatic enzymes
  • physiotherapy
  • nebulisers
  • inhalers
  • insulin
  • supplement drinks
276
Q

why do people with CF have a high fat diet

A
  • pancreatic insufficiency
  • stable BMI helps fight infections
  • helps regain weight
  • malabsorption of vitamins and minerals
  • strong correlation between weight and lung function
277
Q

what is percutaneous endoscopic gastrostomy in CF

A

used for weight management = instant liquid feed fitted directly into stomach to help patients regain weight

278
Q

CF in diabetes can lead to a problem with the use of ….

A

steroids

279
Q

what are other related complications with CF

A
  • osteoporosis
  • liver disease
  • kidney disease
  • CF related arthritis
  • sinus issues (polyps)
  • infertility in males
  • bowel cancer
280
Q

how many years can a transplant extend a CFers life

A

5 years

year 1 flash cards (23 decks)

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