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(SG) Phase 2A lectures > liver/GI > Flashcards

liver/GI Flashcards

1
Q

list 4 functions of the liver

A

glucose/fat metabolism
detoxification and excretion
protein synthesis
defence against infection

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2
Q

what does the liver detoxify/excrete

A

bilirubin
ammonia
drugs/hormones/pollutants

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3
Q

which proteins does the liver synthesise?

A

albumin

clotting factors

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4
Q

define hepatitis

A

inflamed liver

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5
Q

what is 1 of the major consequences of chronic liver disease?

A

susceptibiliy to infection

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6
Q

how does blood flow into the liver?

A

via the portal vein and hepatic artery

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7
Q

how is the normal liver arranged?

A

in a regular way - acinar/lobular models

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8
Q

where does the portal vein and hepatic artery lie

A

together, with a small bile duct in the portal tract (each of the corners of hexagon model)

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9
Q

blood flows into a system of WHAT that bathe liver cells?

A

sinusoids

arranged in plates, before exiting via hepatic (central) vein

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10
Q

what is the hepatic vein aka

A

central vein

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11
Q

what is the central vein aka

A

hepatic vein

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12
Q

liver cells within the lobule can be divided into which zones? why is this significant?

A

zones 1-3

receive progressively less oxygenated blood

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13
Q

what are the 2 types of liver injury?

A

acute and chronic

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14
Q

what are the 2 outcomes of acute liver injury?

A

liver failure or recovery

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15
Q

what are the 3 outcomes of chronic liver injury?

A

liver failure

recovery

cirrhosis

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16
Q

what are some causes of acute liver injury?

A 
viral (A, B, EBV)
drug
alcohol
vascular
obstruction
congestion
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17
Q

what are some causes of chronic liver injury?

A

alcohol
viral (B, C)
autoimmune
metabolic (iron, copper)

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18
Q

what may acute liver injury result in?

A

damage and loss of cells

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19
Q

chronic damage eventually leads to what?

A

fibrosis

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20
Q

what is the severest form of fibrosis termed?

A

cirrhosis

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21
Q

how does acute liver injury usually present?

A 
malaise
nausea
anorexia
jaundice
rarer: confusion, bleeding, liver pain, hypoglycaemia
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22
Q

how does chronic liver injury usually present?

A 
ascites
oedema
varices
malaise
anorexia
wasting
easy bruising
itching
hepatomegaly
abnormal LFTs
rarer: jaundice, confusion
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23
Q

define cirrhosis

A

scarring and disorganisation of liver structure

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24
Q

what do LFTs look @

A

serum bilirubin
albumin
prothrombin time

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25
Q

do serum liver enzymes give indication of liver function?

A

no

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26
Q

do LFTs give indication of liver function?

A

some

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27
Q

define jaundice

A

raised serum bilirubin

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28
Q

what are the 2 types of jaundice?

A

unconjugated (pre-hepatic)

conjugated (cholestatic) [includes hepatic and post hepatic]

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29
Q

what is cholestasis?

A

decrease in bile flow due to impaired secretion by hepatocytes/obstruction of bile flow through bile ducts)

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30
Q

is liver disease hepatic or post hepatic?

A

hepatic

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31
Q

is bile duct obstruction hepatic or post hepatic?

A

post hepatic

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32
Q

what does cholestatic jaundice include?

A

hepatic and post-hepatic

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33
Q

what is urine in pre-hepatic jaundice like?

A

normal

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34
Q

what are stools in pre-hepatic jaundice like?

A

normal

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35
Q

what are LFTs in pre-hepatic jaundice like ?

A

normal

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36
Q

what is urine in cholestatic (hepatic/post hepatic) jaundice like?

A

dark

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37
Q

what are stools in cholestatic (hepatic/post hepatic) jaundice like?

A

may be pale

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38
Q

do u get itching in cholestatic (hepatic/post hepatic) jaundice?

A

maybe

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39
Q

what are LFTs in cholestatic (hepatic/post hepatic) jaundice like?

A

abnormal

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40
Q

if there’s dark urine, pale stools and itching … what don’t they have?

A

pre-hepatic jaundice

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41
Q

why may u have biliary pain?

A

due to gallstones

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42
Q

why may u have rigorss?

A

bile duct stone(s)

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43
Q

which history is V important w the liver?

A

drug/herbs! idiosyncratic reaction is important sis

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44
Q

what should u look at when looking at social history in someone w/ liver issues?

A

alcohol !
potential hepatitis contact (sex, IVDU, travel, certain foods)
family Hx rarely helpful

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45
Q

what is a rigor?

A

sudden feeling of cold w/ shivering, accompanied by temp rise often w copious sweating

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46
Q

what tests will be done for jaundice ?

A

liver enzymes
biliary obstruction
further imaging

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47
Q

what can sickle cell cause?

A

jaundice

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48
Q

why can sickle cell cause jaundice?

A

bc sickle cells do not live as long as normal RBC they die faster than the liver can filter them out.

bilirubin from these broken down cells builds up in the system

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49
Q

where do most gallstones form

A

in the gallbladder

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50
Q

what are gallstones usually made up of?

A

80% cholesterol
30% pigment
± calcium

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51
Q

what are the 2 main types of gallstones?

A

cholesterol (usually yellow-green)

pigment (darker and made of bilirubin)

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52
Q

if u have gallstones in the gallbladder, do get biliary pains and cholecystitis (inflammation of gallbladder)?

A

yes

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53
Q

define cholecystitis

A

inflammation of the gallbladder

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54
Q

if u have gallstones in the gallbladder, will u get obstructive jaundice?

A

maybe!

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55
Q

if u have jaundice in the gallbladder, will u get cholangitis/pancreatitis?

A

no

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56
Q

define cholangitis

A

inflammation of the bile duct

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57
Q

what is the difference btwn cholecystitis and cholangitis

A 
cholecystitis = inflammation of gallbladder
cholangitis = inflammation of bile duct
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58
Q

if u have gallstones in the bile duct, will u get biliary pain?

A

yes

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59
Q

if u have gallstones in the bile duct, will u get cholecystitis (inflammation of gallbladder)?

A

no

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60
Q

if u have gallstones in the bile duct, will u have obstructive jaundice/pancreatitis/cholangitis (inflammation of bile duct)

A

yes

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61
Q

is fat intolerance/indigestion and upset bowel associated with gallstones presentation?

A

no

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62
Q

what is cholecystectomy ?

A

removal of gallbladder

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63
Q

90% of ppl w obstruction have what ?

A

dilated bile ducts

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64
Q

what is ALT?

A

alanine aminotransferase

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65
Q

why might there be low levels of ALT in the blood ?

A

expected/normal

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66
Q

why might there be high levels of ALT in the blood ?

A

liver disease ! v high levels (more than 10x usually due to acute hepatitis, sometimes viral infection

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67
Q

what is the commonest reason for drug withdrawal from formulary?

A

jaundice

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68
Q

what is DILI?

A

drug induced liver injury

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69
Q

what are the types of DILI

A

hepatocellular

cholestatic

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70
Q

when looking at DILI, what is important?

A

not what drugs they are taking

but what they started RECENTLY

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71
Q

what are the most common drugs for DILI?

A

ABs

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72
Q

what do cyp450 enzymes do

A

metabolise potentially toxic compounds incl drugs, bilirubin

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73
Q

what is the most common cause of acute liver failure?

A

paracetamol

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74
Q

how is paracetamol OD managed

A

N acetyl cysteine (NAC)

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75
Q

is liver damage detectable after a paracetamol OD?

A

not usually until at least 18h after

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76
Q

what are some causes of ascites ?

A

chronic liver disease

neoplasia

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77
Q

what is the pathogenesis of ascites like ?

A

systemic vasodilation can lead TO portal hypertension (also incr intrahepatic resistance n low serum albumin can contribute )

this can also result in secretion of RA, NA and ADH thus fluid retention

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78
Q

how can ascites be managed?

A

]diuretics

fluid n salt restriction

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79
Q

fat accumulation within hepatocytes is termed WHAT?

A

steasosis

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80
Q

what can a fatty liver result in ?

A

alcohol hepatitis

cirrhosis

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81
Q

what is the main cause of liver death in the UK

A

ALD (alcohol liver disease)

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82
Q

what are some causes of portal hypertension

A

cirrhosis
fibrosis
portal vein thrombosis

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83
Q

what happens w portal hypertension?

A

increased hepatic resistanc/splanchnic blood flow can lead to varices and splenomegaly

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84
Q

what is the commonest serious infection in cirrhosis

A

spontaneous bacterial peritonitis

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85
Q

why are liver patients vulnerable to infection?

A

bc they have:

  • impaired reticula-endothelial dysfunction
  • reduced opsonic activity
  • leucocyte function
  • permeable gut wall
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86
Q

end stage liver disease is represented by what?

A

cirrhosis

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87
Q

what is the safest analgesic to prescribe to someone w/ liver disease?

A

paracetamol

bc sensitive to opiates
NSAIDs cause renal failure

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88
Q

autoimmune hepatitis requires what for diagnosis?

A

liver biopsy

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89
Q

do antihistamines help w cholestatic (bile ducts) itch?

A

they are little help

cholestyramine (cholesterol lowering, also anti-diarrhoea)

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90
Q

what are some risk factors for NAFL (non alcohol fatty liver)

A

obesity
diabete
hyperlipidaemia

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91
Q

what is the commonest cause of mildly elevated LFTs?

A

NAFL

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92
Q

why do liver patients get ascites?

A

high BP in the veins that bring blood to the liver (portal hypertension), which is usually due to cirrhosis.

In people with a liver disorder, ascitic fluid leaks from the surface of the liver and intestine and accumulates within the abdomen. a combo of factors is responsible:

they include the following:

  • portal hypertension
  • fluid retention by the kidneys
  • alterations in various hormones and chemicals that regulate body fluids
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93
Q

acute hepatitis is when?

A

less than 6m

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94
Q

chronic hepatitis is when?

A

over 6m

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95
Q

describe a common acute hepatitis patient

A 
can be asymptomatic
general malaise (tiredness, discomfort)
myalgia (muscle pain)
upset GI
abdo pain
± jaundice (pale stools, dark urine)
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96
Q

what are characteristic features of jaundice stool/urine sample

A

pale stools

dark urine

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97
Q

what are the 2 causes of acute hep

A

infectious (viral vs non viral)

non-infectious

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98
Q

list some viral infectious causes of acute hep

A

hep A, B etc

herpes viruses

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99
Q

list some non viral infectious causes of acute hep

A

spirochaetes
mycobacteria
parasites
bacteria

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100
Q

list some non-infectious causes of acute hep

A 
alcohol
NAFL
drugs
toxins/poisoning
pregnancy
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101
Q

describe a common chronic hep patient

A

can be asymptomatic/non specific symptoms
± signs of chronic liver disease (clubbing, dupuytren’s contracture, spider naevi etc)
LFTs can be ormal
compensated - jaundice, ascites, low albumin etc

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102
Q

what are some common signs of chronic liver disease

A

clubbing
dupuytren’s contracture
spider naevi

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103
Q

what are oesophageal varices

A

v dilated submucosal veins in lower third of oesophagus

most often a cause of portal hypertension, commonly bc of cirrhosis. strong tendency to develop bleeding

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104
Q

what are the 2 types of chronic hep causes?

A

infectious n non-infectious

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105
Q

list some infectious causes of chronic hep

A

hepatitis B ± D
hep C
hep E

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106
Q

what are some non-infectious causes of chronic hep?

A 
alcohol
NAFL
drugs
toxins
autoimmune
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107
Q

how can hep A be transmitted?

A

faeco-oral !!!!!
ingesting contaminated food/water
person-to-person contact

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108
Q

what are some risk factors of hep A

A

travel
household
sexual contact (MSM)
IVDU

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109
Q

how are the different hep’s linked by transmissions? any trends?

A

A & E: faecal-oral route (travel, foooood)

B & C: via blood (childbirth, IVDU, sex)

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110
Q

does hep A develop to chronic?

A

nope

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111
Q

does hep E develop to chronic?

A

nah

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112
Q

does Hep C develop to chronic?

A

usually !

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113
Q

does hep B develop to chronic?

A

in around 20%, but the younger u are the higher the risk

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114
Q

what is hep A aka

A

HAV

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115
Q

how can hep A be managed

A

supportive
monitor LFT
manage close contacts
primary prevention vaccinations

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116
Q

risk of chronic infection in Hep E is only to who?

A

immunosuppressed patients

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117
Q

how can hep E be managed

A

if acute: supportive

if chronic: reverse immunosuppression

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118
Q

what is hep E aka

A

HEV

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119
Q

what is hep B aka

A

HBV

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120
Q

how is hep B acquired

A

blooooododddd

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121
Q

what is Hep C aka

A

HCV

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122
Q

what can hep c result in

A

cirrhosis

linked to liver cancer (hepatocellular carcinoma)

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123
Q

how can u prevent Hep C

A

no vaccine
previous infection doesn’t confer immunity either :/
BUT
u can screen blood products n have universal precautions when handling bodily fluids :)
also have lifestyle modification eg needle exchanges

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124
Q

helicobacter pylori is involved in the pathogenesis of what?

A

peptic ulcer disease

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125
Q

bacterial infection is a frequent cause of what ?

A

diarrhoea

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126
Q

clostridium difficile infection results when ?

A

broad spectrum antimicrobials allow this bacteria to overgrow in the gut :@

can result in diarrhoea in susceptible host patients (particularly elderly n immunocompromised)

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127
Q

what kills most swallowed pathogens

A

gastric acid

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128
Q

when are u classed as having diarrhoea

A

3+ loose/liquid stools in 24h

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129
Q

what are some infection causes of diarrhoea

A

intraluminal infection

systemic infections eg sepsis, malaria DON’T FORGET BITCH

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130
Q

what are some non-infective causes of diarrhoea

A 
cancer
chemical eg poisoning, side effects
IBD
malabsorption
endocrine eg T4
radiation
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131
Q

with intraluminal infection, WHAT is key?

A

history taking !

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132
Q

how does onset of diarrhoea differ?

A

acute onset: viral/bacterial

chronic: parasites/non-infectious

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133
Q

how do the characteristics of diarrhoea stool differ?

A

floating: fat? malabsorption?

blood/mucus: inflammation? cancer?

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134
Q

how does food history impact diarrhoea

A 
takeaways: food poisoning
BBQs: campylobacter
rice: bacillus cereus
poultry: salmonella
shellfish: norovirus
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135
Q

what else can influence diarrhoea?

A

hobbies, fresh wateR/? swimming?
animals?
medications

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136
Q

what are some stool tests for diarrhoea

A

microscopy
culture
toxin detection
ova, cysts and parasites esp if been abroad

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137
Q

where is watery diarrhoea located

A

proximal small bowel

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138
Q

where is bloody, mucoid diarrhoea located

A

colon

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139
Q

watery diarrhoea: inflamm or non?

A

non-inflammatory

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140
Q

bloody/mucoid diarrhoea: inflamm or non?

A

inflamatory

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141
Q

in the UK, what are 50-70% of diarrhoea cases caused by?

A

viruses

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142
Q

traveller’s diarrhoea occurs when?

A

within 2w of arrival in new country

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143
Q

what is travellers diarrhoea like?

A

3+ unformed stool per day PLUS 1 of following:

  • abdo pain
  • cramps
  • nausea
  • vomiting
144
Q

what can cause cholera?

A

contaminated food/water

145
Q

what are some consequences of cholera

A

vomiting

profuse watery “rice water” diarrhoea

146
Q

what are the red flags 4 diarrhoea? /:

A 
dehydration
electrolyte imbalance
renal failure
immunocompromise
severe abdo pain
cancer risk factors
147
Q

what are some cancer risk factors …

A 
over 50
chronic diarrhoea
weight loss
blood in stool
FHx cancer
148
Q

how can diarrhoea be treated ?

A

fluids
electrolyte monitoring n replacement eg ORS
decrease K/Mg/phosphate, increase Na
antiemetics

149
Q

what do antiemetics do ?

A

prevent nausea and vomiting

150
Q

what is a common precursor of gastritis and peptic ulcers

A

helicobacter pylori infection

151
Q

what is helicobacter pylori infection a risk factor for

A

gastric carcinoma

152
Q

where does helicobacter pylori live

A

mucus layer overlying gastric mucosa

153
Q

how can helicobacter pylori infection be diagnosed

A

stool antigen test
breath test
blood test for antibodies

154
Q

what is Charcot’s triad?

A

for cholangitis

  1. jaundice
  2. RUQ pain
  3. fever
155
Q

what are the 4F’s of gallstone risk factors

A

fair
female
fat
fertile

156
Q

what is enteric fever

157
Q

what happens in typhoid/enteric fever

A 
high fever
relative bradycardia
headache n myalgia
rose spots
constipation/green diarrhoea
158
Q

clostridium difficile is linked w what?

A

antibiotic use

159
Q

where is hep A mainly found (geographically)?

160
Q

where is hep B found geographically ?

A

asia and china

161
Q

where is hep E found geographically

A

south east Asia, India, central america

162
Q

what is the non-medical term for steatosis

A

fatty liver

163
Q

what is HbF

164
Q

when does HbF change to HbA (foetal to adult)?

A

HbF is nearly completely replaced by HbA by approx 6m postnatally, except in a few thalassemia cases in which there may be a delay in cessation of HbF production until 3–5 yrs of age

165
Q

men and women are advised not to drink regularly more than how many units of alcohol a week?

166
Q

what is a UK unit?

A

8g/10ml of pure alcohol

167
Q

how do u calculate the number of units?

A

strength of drink (% ABV) x amt of liquid in ml …. dividedd by 1000

eg
1 bottle of wine = (13.5% x 750ml)/1000 = 10 units

168
Q

what’s the diff in binge drinking btwn men and women?

A

men >8 units

women >6 units

169
Q

what are some acute effects of excessive alcohol

A 
accidents/injury
coma and death (from rest depression)
aspiration pneumonia
oesophagitits
pancreatitis
cardiac arrhythmias
cerebrovascular accidents
170
Q

what are some chronic effects of excess alcohol intake

A 
pancreatitis
CNS toxicity
liver damage
hypertension
cardiomyopathy
osteoporosis
CHD
skin disorders
171
Q

what is tremulousness ?

A

several distinct but not mutually exclusive clinical alcohol withdrawal syndromes caused by alcohol withdrawal eg shakes

172
Q

what else can u get w alcohol withdrawal?

A

shakes
seizures
hallucinations
delirium

173
Q

what is foetal alcohol syndrome ?

A

pre and post natal growth retardation bc of drinking pregnant mother

174
Q

what are some signs of FAS

A
  • CNS abnormalities (mental retardation, irritability, incoordination, hyperactivity
  • craniofacial abnormalities (smaller head, distinctive facial features eg small eyes, thin upper lip)
  • congenital defects of eyes, ears, mouth etc
175
Q

what are some psychosocial impacts of f excessive alcohol consumption

A
  • disturbances in interpersonal relationships eg violence, - depression
  • work problems
  • criminality
  • social disintegration, poverty
  • driving offences
176
Q

how does NICE guidance prevent harmful drinking ?

A

making alcohol less affordable
import allowances
limit exposure to esp children, young ppl

177
Q

what are some examples of health promotion against alcohol ? (primary prevention)

A

“know your limits” binge drinking campaign
drink aware - alcohol labelling
“THINK!” alcohol driving campaign
restriction on alcohol advertising

178
Q

what is the diff btwn primary n secondary prevention again

A

primary - health promotion

secondary - screening n intervention

179
Q

what is secondary prevention of alcoholism ?

A
  • ask abt it routinely as a doc
  • think of it as an explanation for presenting symptom
  • think of it as an explanation for presenting symptom
  • detect problem drinking
180
Q

what are some screening questions n tools for alcoholism ?

A 
clinical interview
FAST (fast alcohol screening test)
CAGE questions
in ED
as part of routine exam

in patients who are:

  • pregnant/trying to conceive
  • likely to drink heavily (smokers, adolescents)
  • have health problems that may be linked
  • experiencing chronic illness not responding to treatment
181
Q

what is alcohol dependence?

A

set of behavioural, cog and psych responses that can develop after repeated substance abuse

182
Q

“determine where, in the past 12m, your patient has…” (complete_

A
  • shown tolerance
  • shown signs of withdrawal
  • not been able to stick to drinking limits
  • spent a lot of time drinking
  • spent less time on other matters
  • kept drinking despite issues

yes to 3+ = alcohol dependence

183
Q

“determine where, in the past 12m, your patient’s drinking has repeatedly caused/contributed to…” (complete)

A
  • role failure
  • risk of bodily harm
  • run-ins with the law
  • relationship trouble

yes to 1+ = alcohol abuse (proceed to assess for dependence symptoms)

184
Q

how can alcohol dependence be treated?

A

pharmacologically and psychosocially

185
Q

what are some medications for alcohol dependence ?

A

campral (thought to stabilize chemical signaling in the brain that would otherwise be disrupted by alcohol withdrawal)

antabuse (produces an acute sensitivity to ethanol so effects of hangover occurs immediately after alcohol is consumed)

selincro (opioid antagonist)

186
Q

what are some psychosocial ways to tackle alcohol dependence?

A

therapy - cog and behavioural

social support - 1 on 1 or group therapy

187
Q

what is FRAMES

A

a summary of motivational interviewing

188
Q

discuss FRAMES interviewing

A

Feedback abt the risk of personal harm/impairment

stress personal Responsibility for making change

Advice to cut down/strop dirnking

provide a Menu of alt strategies for changing drinking patterns

Empathetic interviewing style

Self-efficacy: intuitive style which lead es patient enhanced in feeling able to cope w goals they’ve agreed to

189
Q

what is the 4-tier framework for alcohol/drug misusers?

A
  1. non-substance misuse specific services
  2. open access drug/alcohol services
  3. specialist community-based services
  4. specialist in-patient services
190
Q

what is substance misuse?

A

recurrent substance use resulting in failure to fulfil major role obligations such as work, school or home life

191
Q

what is dependence?

A

a state in which an organism functions normally only in the presence of a drug

manifests as physical disturbance when drug is withdrawn

192
Q

what is tolerance?

A

a state in which an organism no longer responds to a drug

a higher dose is required to achieve the same effect

193
Q

what is alcohol

A

a depressant

194
Q

what are the 3 ways in which intestines can be obstructed ?

A
  • if s/t is in the lumen
  • if s/t is in the wall
  • if s/t is pressing outside of the bowel
195
Q

what is a lymphoma?

A

malignant tumour of lymphoid cells

196
Q

what are the 2 types of tumours ?

A

carcinoma and lymphoma

197
Q

tumours on which side of the colon are more likely to cause obstruction due to hard faeces?

198
Q

what is Crohn’s disease?

A

inflammatory disease of the bowel (anywhere frogmouth to anus)
particularly affects terminal ileum - causes deep fissuring ulceration - fibrosis in btwn mucosa

199
Q

what does Crohn’s disease particularly affect?

A

terminal ileum

200
Q

what is diverticulitis?

A

small outpourings of mucosa - causes increased pressure within colon
associated with low fibre diet

201
Q

how does Crohn’s present ?

A

crampy right iliac fossa pain and non-bloody diarrhoea

fever, malaise n weight loss also common

202
Q

does diverticulitis tend to affect younger or older ppl?

203
Q

what are some inflammatory types of obstruction of bowel wall?

A

crohn’s

diverticulitis

204
Q

what is a neural cause of bowel wall obstruction?

A

hirschprung’s disease

205
Q

what is hirschprung’s disease?

A

a congenital GI cond

no ganglion cells (which coordinate cell contraction to move faeces) in lower section of colon

206
Q

how does hirschprung’s disease present?

A

intestinal obstruction n failure to pass meconium 24h after birth

207
Q

what is meconium?

A

baby’s 1st faeces- sticky, thick, and dark green and is typically passed in the womb during early pregnancy and again in the 1st few days after birth

208
Q

what are types of extraluminal obstruction?

A

adhesions
volvulus
tumour

209
Q

what is a volvulus?

A

when a loop of intestine twists around itself and the mesentery that supports it- resulting in a bowel obstruction.

210
Q

what are some symptoms of volvulus?

A

abdominal pain/bloating, vomiting, constipation & bloody stool.

recurrent abdo pain as it may twist n untwist

211
Q

what is gallstone ileum?

A

gallstone doesn’t go down common bile duct

gallbladder inflates, sticks to outside of small bowel

212
Q

what is intramural obstruction

A

within the walls

213
Q

what is mucosa like in Crohn’s?

A

“cobblestone”
fibrosis in btwn bits
can cause intestinal obstruction

214
Q

why may ovarian cancer be an issue ?

A

as the ovary is floating at the end of Fallopian tubes - can be a problem as cancer may spread to peritoneum

215
Q

what are the 3 wall layers of intestines (deep to superficial)

A

serosa
muscularis
submucosa
mucosa

216
Q

any foregut symptoms affect which region?

A

epigastric region

217
Q

any midgut symptoms affect which region?

218
Q

any hind gut symptoms affect which region?

A

suprapubic

219
Q

define distensibility

A

ability to stretch n expand

220
Q

what is gastric motility?

A

defined by the movements of the digestive system, and the transit of the contents within it.

when nerves or muscles in any portion of the digestive tract do not function with their normal strength and coordination, pt develops symptoms related to motility problems.

221
Q

which part of intestine absorbs water?

222
Q

where does the gut run from/to?

A

mouth to anus

223
Q

what is intestinal obstruction?

A

blockage to lumen of the gut

commonly refers to blockage of intra-abdominal parts of intestine

224
Q

how can u classify obstruction?

A

according to:

  • site
  • extent (partial/complete)
  • mechanism (mechanical/true, paralytic/pseudo obstruction)
  • pathology
225
Q

what is SBO?

A

small bowel obstruction

226
Q

what happens in small bowel obstruction?

A 
incr. secretions
more dilation
decreased absorption
mucosal wall oedema
increased pressure
intramural vessels compressed
ischaemia
perforation
227
Q

what can untreated obstruction lead to ?

A

ischaemia
necrosis - then sepsis
perfoation

228
Q

what happens in large bowel obstruction?

A

similar to SBO

colon proximal to obhstruction dilates
incr colonic pressure decreases mesenteric blood flow
mucosal oedema
transudation of fluid/electrolytes
arterial blood supply compromised
mucosal ulceration
necrosis
perforation
bacterial translocation - sepsis
229
Q

list some common causes of SBO

A

adhesions
hernias
intussusception
volvulus

230
Q

list some common causes of LBO

A

tumours
sigmoid volvulus
diverticular strictures

231
Q

how does SBO vs LBO presentation differ

A

both have acute colicky abdo pain, abdo pain and distension BUT

SBO: early vomiting onset, later constipation onset
LBO: early onset of constipation, later vomiting onset

232
Q

what happens in LBO if ileocaecal valve is competent?

A

caecum is usual site of perforation

233
Q

what happens in LBO if ileocaecal valve in incompetent?

A

faeculent vomiting

234
Q

what is the majority of intestinal obstruction?

235
Q

adhesive obstruction is usually secondary to what?

A

previous abdo surgery

236
Q

define hernia

A

abnormal protrusion of viscera through normal or abnormal defects of body cavity

237
Q

how do hernias usually present

A

as a lump or pain

238
Q

name some common hernia locations

A

umbilical
inguinal
femoral

239
Q

what is intussusception?

A

process in which a segment of intestine invaginates into the adjoining intestinal lumen, causing bowel obstruction.

when 1 intestine slips inside other intestine

240
Q

what is severe/complete constipation?

A

obstipation

241
Q

define adenoma

A

benign tumour of glandular tissue - has the potential to develop into cancer

242
Q

diff btwn resection and excision?

A

resection - cutting all of a body part

excision - cutting part of a body part

243
Q

how many types of stool are there in the Bristol stool chart?

244
Q

which stool type (BSC) is rabbit dropping like ?

A

type 1 - severe constipation

245
Q

which stool type (BSC) is like a bunch of grapes?

A

type 2 - mild constipation

246
Q

which stool type (BSC) is like corn on the cob?

A

type 3 - normal

247
Q

which stool type (BSC) is like a sausage/snake?

A

type 4 - normal

248
Q

which stool type (BSC) is like chicken nuggets?

A

type 5 - lacking fibre

249
Q

which stool type (BSC) is like porridge?

A

type 6 - mild diarrhoea

250
Q

which stool type (BSC) is like gravy?

A

type 7 - severe diarrhoea

251
Q

what are some non-infective causes of diarrhoea?

A

neoplasm - hormonal
inflammatory - radiation
irritable bowel - chemical
aatomical

252
Q

what are some infective causes of diarrhoea?

A

non-bloody

bloody (dysentery)

253
Q

what is dysentery?

A

infection of the intestines that causes diarrhoea containing blood or mucus.

other symptoms include: painful stomach cramps. nausea or vomiting, a fever of 38C

254
Q

what are some direct routes of diarrhoea transmission?

A

STIs, faeco-oral route

255
Q

what are some indirect routes of diarrhoea transmission?

A

vector-borne (malaria, dengue)

vehicle-borne (hep B)

256
Q

what are vector borne diseases?

A

caused by parasites, viruses and bacteria that are transmitted by mosquitoes, sandflies, triatomine bugs, blackflies, ticks, tsetse flies, mites, snails and lice etc

257
Q

what are vehicle borne diseases?

A

when an inanimate object becomes contaminated with disease

258
Q

what are the 3 types of transmission?

A

direct
indirect
airborne

259
Q

what is an airborne route of diarrhoea transmission?

A

resp route

eg TB

260
Q

list some diarrhoea diseases

A

dysentery
typhoid
hepatitis
cholera

261
Q

what is the major cause of winter vomiting?

262
Q

what happens w norovirus?

A

mainly causes vomiting
may cause: diarrhoea, nausea, cramps, headache, fever, chills, myalgia

lasts 1-3d

263
Q

what is gastroenteritis?

A

infectious diarrhoea (stomach flu)

264
Q

what is clostridium difficile (c diff)

A

bacteria that can infect the bowel and cause diarrhoea.

infection most commonly affects people who have recently been treated with (broad spectrum) ABs. can spread easily to others.

265
Q

how is c diff spread?

A

faeco-oral route directly

or through spores in the environment

266
Q

how can c diff infection be prevented?

A

spores are highly resistant to chemicals so alcohol hand rubs don’t destroy them

hand washing (soap/water) will remove them

267
Q

what does enteric mean?

A

occurring in/to do with the intestines

268
Q

how is c diff investigated?

A

stool samples

can culture

269
Q

why is diarrhoea an important PH issue?

A

2nd leading cause of death among children under. globally

kills more young children than AIDS, malaria and measles combined :(

270
Q

what is the WHO-UNICEF diarrhoea treatment package?

A

fluid replacement to prevent dehydration

zinc treatment

271
Q

what are the 5 moments for hand hygiene?

A 
before patient contact
before an aseptic task
after body fluid exposure risk
after patient contact
after contact with patient surroundings
272
Q

what are notifiable diseases?

A

diseases, conditions and infections listed as notifiable under PH regulations 1988

legal obligation for any doc that suspects a case to inform proper officer

don’t have to wait for a lab combo

273
Q

why are they notifiable diseases?

A
  • stuff that makes u very scared eg cholera, plague, rabies
  • stuff that is quite nasty eg TB, leprosy, malaria
  • vaccine preventable diseases eg diphtheria, MMR, whooping cough
  • diseases that need specific control measures eg scarlet fever, food poisoning
274
Q

how are communities protected from infectious diseases?

A
  • investigate
  • identify and protect vulnerable persons
  • exclude high risk persons from high risk settings
  • educate, inform, raise awareness
  • co-ordinate multi-agency responses
275
Q

what are the 5 types of immunoglobulins?

276
Q

what are the 2 types of active immunity?

A

cell-mediated

antibody-mediated

277
Q

what is passive immunity?

A

protection provided from transfer of antibodies from immune individuals - most commonly cross-placental transfer

278
Q

what are vaccines made from?

A 
inactivated
attenuated live organisms
secreted prods
constituents of cell walls/subunits
recombinant components
279
Q

what is the diff btwn primary and secondary vaccine failure?

A

primary - person doesn’t develop immunity from vaccine

secondary - initially responds but protection wanes over time

280
Q

define sequela

A

a condition which is the consequence of a previous disease or injury

281
Q

all cases of suspected meningitis are notifiable and must eye notified without delay

A

regardless of cause

282
Q

what is contact tracing for meningitis?

A

any person having close contact w/ a case in past 7d (kissing, sleeping with, spending night, spending >8H in same room)

283
Q

what is the incubation period?

A

time from exposure to onset of symptoms (includes latent period and infectious period)

284
Q

what happens w mucosal ischaemia?

A 
less blood to the stomach
so cells have less supply
so cells not producing mucin
so acid can attack cells
they die
285
Q

what is increased acid caused by?

A

caused by stress
helicobacter bugs increase acid secretion
aspirin n other drugs - NSAIDs

286
Q

which drugs get rid of acid?

A

proton pump inhibitors

287
Q

where does helicobacter pylori live? does it like acid?

A

in the stomach ad no

288
Q

what does helicobacter pylori do

A

produces chemicals that induce inflammation and ilceration

289
Q

where does peptic ulceration most commonly happen?

A

in the 1st part of the duodenum

290
Q

what are the signs of malabsorption?

A
  • can see patients weight loss but not eat enough food
  • not absorbing fat properly
  • ppl anaemic w/o explanation
  • lymphocytes in gut to fight off bugs which has been ingested
  • insufficient intake
  • defective intraluminal digestion
291
Q

what is Crohn’s disease in simple terms?

A

inflammatory disease in the bowel - typically in the terminal ileum

292
Q

what are the complications of Crohn’s?

A

mostly to the bowel (malabsorption, obstruction, perforation, fistula etc)

293
Q

where does ulcerative colitis affect?

A

the colon only

294
Q

define metaplasia

A

change in differentiation of a cell from 1 fully differentiated type to a different fully differentiated type

295
Q

what is the biggest cause of metaplasia?

296
Q

what is a risk factor for oesophageal squamous cancer risk factor?

297
Q

what is a risk factor for adenocarcinoma?

298
Q

what is the diff btwn early n late gastric cancer?

A

as log as it doesn’t go out the submucosa into the muscular wall, even if it goes to lymph nodes - it’s earlyyyy

if it goes through the muscular wall - it’s late gastric cancer

299
Q

define peritonitis

A

inflammation of the peritoneum

300
Q

define peritonism

A

tensing of muscles to prevent movement of peritoneum

301
Q

what causes inflammation?

A 
inflamed organ
air
pus
faeces
luminal contents 
blood
302
Q

what are some common causes of peritonitis?

A

cholecystitis (gall bladder inflammation)
pancreatitis
appendicitis
diverticulitis

303
Q

define diverticulitis

A

inflammation of a diverticulum, especially in the colon, causing pain and disturbance of bowel function

304
Q

why do ppl die of peritonitis?

A 
sepsis
multi-organ failure
CV events
resp complications (pneumonia, pul. embolus)
surgical complications
poor physiological reserve/frailty
305
Q

what is the iff btwn laparotomy n laparoscopy?

A

laparotomy ie big cut

laparoscopy ie key hole

306
Q

how do u treat someone w/ peritonitis?

A
  • surgery
  • treat problem (patch hole, remove organ/cause)
  • wash out infection
307
Q

what is the aftercare for peritonitis like?

A
  • intensive care
  • kidney support
  • physio/early mobilisation
  • nutrition support
308
Q

define ascites (dictionary def)

A

“effusion and accumulation of serous fluid in the abdomen cavity”

effusion = pouring out
exudate (actively) or transudate (passively)

309
Q

define ascites (clinical def)

A

detectable collection of fluid in the peritoneal cavity

chronic accumulation of fluid within the peritoneal cavity

310
Q

what are some synonyms for ascites?

A

abdominal dropsy
peritoneal dropsy
hydrops abdomini

??lol TF

311
Q

how much fluid do healthy men normally have in their peritoneal cavity

312
Q

how much fluid do healthy women normally have in their peritoneal cavity

A

up to 20ml

313
Q

how can ascites be classified?

A

into 4 categories (S1-S4)

S1 - MILD - detectable only after careful exam/US scan
S2 - easily detectable but of relatively small volume
S3 - MODERATE - obvious, not tense ascites
S4 - LARGE - tense ascites

314
Q

how can ascites be classified?

A

portal hypertension vs non-portal hypertension

315
Q

what is ascites ?due? to portal hypertension?

A
  • a state of Na water imbalance

- interplay of various neurohormonal agents - R, A, SNS, NO

316
Q

what is ascites ?due? to non-portal hypertension

A
  • malignancy
  • cardiac failure
  • syndrome
317
Q

what is exudate ?

what is transudate ?

A

actively

passively

318
Q

what is the history of ascites like ?

A

relating to liver disease

  • LT heavy alcohol consumption
  • infection
  • non-alcoholic steatohepatitis (cirrhosis)
319
Q

what is NASH? (non-alcoholic steatohepatitis)

A

advanced form of NAFLD (non-alcoholic fatty liver disease)

320
Q

what are the clinical symptoms of ascites?

A
  • abdominal distension (clothes tighter, maybe weight gain)
  • nausea, loss of appetite
  • constipation
  • cachexia, weight loss
  • associated symptoms of underlying cause
321
Q

define cachexia

A

weakness and wasting of the body due to severe chronic illness

322
Q

if there’s malignancy with ascites, what do u get?

A

pain/discomfort

323
Q

if there’s no malignancy with ascites, is it painful?

324
Q

what are some clinical presentations of ascites?

A

jaundice

  • abdo distension
  • puddle sign
  • shifting dullness
  • flanks fullness
  • fluid thrill
325
Q

what investigations do u for ascites?

A

naked eye assessment
chemistry (proteins, amylase)
microscopy (cytology, organisms)
culture

326
Q

what biochem do u do for ascites?

A

serum ascites album gradient (SAAG)

S Alb

327
Q

what treatment is there for ascites?

A

treatment of underlying cause
adjuncts
- 95% portal hypertension
- shunts

328
Q

what is the gallbladder for

A

storage n conc of bile

329
Q

where does the gallbladder empty into

A

2nd part of duodenum

330
Q
  • look @ enterohepatic circulation *
331
Q

what is the most common biliary problem seen, esp in west

A

gallstones !

332
Q

list 3 risk factors for gallstones

A

raised cholesterol

oestrogen exposure ? (contraceptive pill?)

haemolytic anaemia (pigment gallstones, esp for hereditary ones but not many)

333
Q

what are the 5 f’s for gallstones

A

female forty fertile fat fair

334
Q

how do gallstones present (7 :/)

A

mucocoele (big sterile fluid collection around stone, kinda like an abscess)

biliary colic

cholecystitis (gallbladder inflammation)

choledocholithiasis (bile duct stone)

cholangiitis (bile vessel inflammation)

pancreatitis

gallstone ileus

335
Q

what is general diagnostic approach for gallstones?

A

sick or not? if not causing issues, no reason as to why it should be removed

bloods : FBC,

LFT (elevated liver enzymes suggest inflammation

elevated bilirubin suggests blockage of biliary system

U&E (biliary system problems can cause renal failure)

PT

USS abdomen

336
Q

is gallbladder foregut/midgut/hindgut?

A

foregut - epigastric/RUQ (probs localised) pain

337
Q

what does colicky pain feel like?

A

“grabbing and squeezing insides”

338
Q

what is surface marking of gallbladder?

A

midclavicular line, underneath bottom rib

339
Q

what is cholecystitis/biliary colic pain like (4)

A

RUQ/epigastric
colicky
radiating to shoulder tip
typically LFTs normal

340
Q

what is treatment for biliary colic/cholecystitis (3)

A

analgesia!!!

ABs if infection (coamoxiclav, 3-5d)

laparoscopic cholecystectomy

341
Q

biliary colic for 3+ days ….. ?

A

cholecystitis

biliary colic usually in response to food and doesn’t last long

342
Q

what is Murphy’s sign

A

clinical sign for cholecystitis

343
Q

what does choledocholithiasis mean

A

bile duct stone

344
Q

what does cholangiitis mean

A

inflammation of the bile duct system that is usually related to a bacterial infection

345
Q

bile in the bowel does what?

A

colours faeces - PALE stool

346
Q

with choledocholithiasis/cholangitis, what do u also get

A

also fever and rigors

347
Q

why might u get rigors? (3)

A

lobar pneumonia
pyelonephritis
choledocholithiasis/cholangiitits

348
Q

what is the treatment for bile duct stones/inflammation of bile duct system (choledocholithiasis/cholangitis)

A

ABs
IV fluids
correct clotting

MRI to confirm diagnosis
ERCP to drain
cholecystectomy w/ duct exploration

349
Q

what is the ampulla of vater

A

opening to biliary system

350
Q

galllllstone ?exam reference ??????

351
Q

what are the 2 major causes of pancreatitis?

A

gallstones and alcohol

352
Q

symptoms of acute pancreatitis?

A

pain
nausea
vomiting
relieved sitting forward (bc pancreas sits on spine, so taking pressure off as leaning forward)

SUDDEN ONSET

353
Q

signs of acute pancreatitis?

A

epigastric tenderness

bruising signs - Cullens = central/umbilicus and Turners = flanks

354
Q

diagnosis tests for acute pancreatic?

A

amylase/lipase if >3x upper limit of normal - HAVE pancreatitis

CT if unwell

355
Q
  • treatment for acute pancreatitis *
A

1st line - analgesia

2nd line - fluid management - remember chat w Marcus about leaking blood vessels n low BP but no fluid left in vessels ……. )

356
Q

complications for acute pancreatitis?

A

ARDS (acute resp distress syndrome)

renal failure

hepatic failure

357
Q

how do u predict severity of acute pancreatitis

A

PANCREAS mnemonic

glasgow coma score?

(SG) Phase 2A lectures (14 decks)

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