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Phase 2a Introductory Clinical Science > GI and friends > Flashcards

GI and friends Flashcards

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1
Q

What is the underlying cause of gastritis or ulcerations

A

dysfunction between the balance of acid produced from cells and the mucin buffer layer of the cells.

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2
Q

What is inflammation of the stomach classed as

A

acute or chronic gastritis

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3
Q

What can cause acute gastritis

A

excessive alcohol intake
certain medication e.g. NSAID, Aspirin
eating or drinking corrosive substances
ischemia due to severe stress on the body e.g. shock, trauma, burns

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4
Q

How does gastritis occur

A

exposure of the mucosa to noxious substances/situations leading to loss of surface epithelium cells
less mucin produced
more damage from acid

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5
Q

What does the body do to try and heal the damage from acute gastritis

A

vasodilation
lamina proper consolidation
neutrophil polymorph response
hyperplasia of pit lining epithelium cells

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6
Q

What can cause chronic gastritis

A

helicobacter pylori
long-term excessive alcohol
long-term NSAID use
chemical gastritis due to alkali duodenum substances refluxing into the stomach
autoimmune gastritis when antibodies attack parietal cells (leads to pernicious anaemia also)

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7
Q

What is the pathogenesis of reactive gastritis

A

alkali substances from duodenum reflux back into the stomach
loss of surface epithelium
loss of mucus layer
more damage from acid

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8
Q

What are other names for chemical gastritis

A

reactive, type C, bile-reflux gastritis

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9
Q

What does the body do to try and repair from reactive gastritis

A

hyperplasia of pit lining epithelium
lamina proper oedema
vasodilation
no significant inflammatory cell infiltration

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10
Q

What are ulcerations

A

localised defects passing into at least the submucosal layer due to pepsin and acid attack.

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11
Q

How can you classify gastroduodenal ulcerations

A

chronic and acute

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12
Q

What are the causes of acute ulcers

A

occurs with acute gastritis
ischemia
extreme hyperacidity

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13
Q

Where do chronic ulcers most commonly occur

A

mucosal junctions

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14
Q

Why does severe stress to the body cause ischaemia in the stomach

A

the blood flow to less important organs e.g. stomach reduces so that more blood can go to brain and heart etc.

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15
Q

What do ulcers look like

A

clear-cut edge
the base of ulcer has necrosis tissue and neutrophil polymorph exudate which is overlaying:
inflamed granulation tissue which is merged with mature fibrous tissue

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16
Q

How do ulcers heal on their own

A

combination of:
the regeneration of epithelium cells
progressive fibrosis

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17
Q

What are the possible immediate complications from ulcers

A

perforation- ulcer creates a hole in stomach/duodenum so contents leak into peritoneal space leading to peritonitis
penetration-ulcer penetrates into adjacent structures e.g. liver
haemorrhage- ulcer can penetrate into vessels and cause bleeding (shows in vomit if stomach ulcer and in faeces if duodenum or below ulcer)

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18
Q

How do we treat ulcerations

A

H2 blockers, PPI
stress relief because stress leads to more acid
enteric coated aspirin

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19
Q

What does PPI raise the risk of?

A

C. diff infections

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20
Q

What is GORD

A

Gastro-oesophageal reflux disease due to stomach acidic content going into oesophageal

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21
Q

What can cause GORD

A

high alcohol
smoking
certain foods e.g. chocolate, caffeine, fats
obesity
dysfunction of the lower oesophageal sphincter
a hiatus hernia

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22
Q

Why do certain foods cause GORD

A

they can slow the gastric emptying time

they can reduce the contractility of the lower oesophageal sphincter

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23
Q

What are the symptoms of GORD

A

salivation a lot due to acid in oesophageal
chocking at night due to the acid irritating larynx
regurgitation of food/acid into mouth esp. while lying flat
dyspepsia (heartburn)- spasm of lower sphincter
dysphagia

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24
Q

How do we diagnose GORD

A

clinically only possible esp. with under 45s
with the help of also:
barium swallow -see reflux
24hr luminal pH monitoring
endoscopy to see the level of inflammation
biopsy to see the histological level of inflammation

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25
Q

How do you treat GORD

A 
treat symptoms
raise head while sleeping
don't eat late night meals
don't wear tight clothes
lose weight
stop smoking
reduce alcohol
PPI
antacids
pro-kinetic agents increase the gastric emptying time
surgery if all else fails
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26
Q

What is hematemesis

A

blood in vomit

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27
Q

What do we call blood in vomit

A

hematemesis

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28
Q

What is haemoptysis

A

coughing up blood

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29
Q

What can cause hematemesis

A 
NSAIDS (from ulcers)
peptic ulcer disease
oesophageal varices
malignancy of stomach or oesophagus
Mallory Weiss tear
gastritis
bleeding/coagulation disorder
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30
Q

What are the two management plans for hematemesis based on

A

amount of blood loss so

1) lots of blood loss
2) not lots of blood loss

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31
Q

How do we manage hematemesis with lots of blood loss

A

ABC
Oxygen
Fluid replacement e.g. transfusions if needed
treat underlying condition

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32
Q

How do we manage hematemesis with not lots of blood loss

A

gastroscopy
PPI
fluid replacement
treat underlying cause

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33
Q

What are varices

A

dilated veins

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34
Q

Where are varices found

A

distal oesophagus
proximal stomach
isolated varices: distal stomach, large and small intestines

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35
Q

What is linked to varices occurring

A

the size and change of bleeding of varices is linked to the portal pressure which is linked to underlying liver disease severity

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36
Q

What can cause oesophageal varices

A 
portal vein thrombosis
portal vein obstruction (stenosis)
increase portal vein flow e.g. from fistula
compression e.g. from tumour
increased splenic blood flow
Budd-Chiari syndrome
acute hepatitis esp. alcoholic
cirrhosis
idiopathic portal hypertension
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37
Q

What can increase the risk of oesophageal variceal haemorrhage occurring

A 
alcohol intake
physical exercise
increase intra-abdominal pressure
decompensation of liver disease
malnutrition
NSAIDs
Aspirin
bacterial infection
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38
Q

What are some common symptoms and signs of oesophageal varices

A 
hematemesis
dysphagia
abdominal pain
low blood pressure
pallor
tachycardia (shock signs)
peripheral blood shut down
sepsis signs sometimes
low urine output
confusion
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39
Q

What investigations do you do for oesophageal varices

A

endoscopy
FBC (low haemoglobin, low platelets, high WBC)
check clotting ability
check LFT
Renal function
CXR (for infection signs)
Ascitic tap if suspecting bacterial peritonitis

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40
Q

How do you manage oesophageal varices

A 
vasoactive drug (but NOT for severe hypovolemic shock)
Antibiotic prophylaxis
endoscopic band ligation
transjugular intrahepatic portosystemic shunt
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41
Q

Give some examples of bowel inflammation

A 
Crohn's disease
Ulcerative colitis
diverticulitis disease
ischaemic colitis
infective colitis
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42
Q

What do we mean by inflammatory bowel disease

A

Crohn’s disease and Ulcerative colitis

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43
Q

What are the causes of inflammatory bowel disease

A

Idiopathic mostly

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44
Q

Where are inflammatory bowel disease more common

A

Northern Europe

North America

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45
Q

Where can Crohn’s disease affect?

A

Whole bowel from mouth to anus

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46
Q

Where does Crohn’s disease affect most commonly

A

Ileum

Colon

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47
Q

What is the pattern of Crohn’s disease

A

skip patchy lesions

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48
Q

How much of the bowel wall does Crohn’s disease affect

A

can affect full thickness

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49
Q

What type of inflammation is seen in Crohn’s disease and what are the associated features

A 
granulomatous inflammation with:
lymphocytes
strictures and fistulas
fissuring ulcers
Neuromuscular hypertrophy
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50
Q

What is the course of Crohn’s disease

A

chronic

exacerbations and remissions

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51
Q

What could be the cause of Crohn’s disease and give evidence

A

multifactorial
genetics- family history
Western diet, social life- more common in the West
immune-related- auto-antibodies, previous infection triggering abnormal immune system
Smoking- more severe problems in smokers

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52
Q

Briefly describe the epidemiology of Crohn’s disease

A

females> males

starts usually at early adulthood

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53
Q

How does Crohn’s disease present

A 
weight loss
malaise
fever
clubbing
arthritis
diarrhoea (can be bloody, can be chronic)
mouth ulcers
anal lesions
abdominal pain
palpable mass in the abdomen
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54
Q

What are the possible complications of Crohn’s disease

A 
malabsorption
fistula formation
malignancy
obstruction
perforation
systemic amyloidosis (rare)
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55
Q

What are the anal lesions possible with Crohn’s disease

A

anal tags
anal fistulas
anal fissures

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56
Q

Why could malabsorption occur in Crohn’s disease

A

damage to bowel from disease
resectioning of bowel during surgery leading to short bowel syndrome
fistulas could lead to part of bowel being bypassed

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57
Q

Why could obstruction occur in Crohn’s disease

A

neuromuscular hyperplasia so narrowed lumen and thick walls

progressive fibrosis

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58
Q

Why could malignancy occur in Crohn’s disease

A

Crohn’s disease increased risk of colorectal cancer due to increased cell turnover

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59
Q

How can fistulas form in Crohn’s disease

A

ulcers can lead to fistulas

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60
Q

Why would perforation occur in Crohn’s disease

A

ulcers can perforation out of the bowel wall and lead to content leaking into peritoneal space and peritonitis occurring and also haemorrhage can occur

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61
Q

What investigations do you carry out for Crohn’s disease

A

barium swallow- see mucous changes, strictures, fistulas
CT- see a patchy pattern of lesions
Colonoscopy- view and biopsy to see inflammation type
Stool sample- exclude infective diarrhoea

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62
Q

What is the management plan for Crohn’s disease

A

The aim is to induce and maintain remission:
corticosteroids
immunosuppressant drugs e.g. ciclosporin, anti-TNF alpha antibodies
pain relief
conservative surgery so not to get small bowel syndrome
manage diet: low fat, treat vitamin deficiencies
stop smoking

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63
Q

Where can ulcerative colitis affect?

A

rectum and colon only
starts at the rectum and ascends usually but never past colon
anal transitional period and anal canal not affected

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64
Q

What are three things common in Crohn’s disease but not in Ulcerative colitis

A

granulomas
fissures
fistulas

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65
Q

What is the pattern of the lesions in Ulcerative colitis

A

continuous lesions

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66
Q

How much of the thickness of the bowel is affected by ulcerative colitis

A

superficial mucosa

ulcers in mucosa and submucosa but in SEVERE can perforate full thickness

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67
Q

What are the ulcers like in ulcerative colitis

A

irregular edges
small
shallow
bleed and produce pus

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68
Q

What is the inflammation like in ulcerative colitis

A

diffuse with plasma cells

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69
Q

What is the course of the disease in ulcerative colitis

A

chronic with exacerbations and remissions

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70
Q

Briefly describe the epidemiology of ulcerative colitis

A

males> females slightly

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71
Q

What is the cause of ulcerative colitis

A

idiopathic
link with autoimmune: immune mistaking commensal organisms as pathogens and attacking
smoking is actually a protective factor

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72
Q

What are the presentations of ulcerative colitis

A 
bloody stool +/- mucus
abdominal tenderness, distension, discomfort, palpable mass
malaise
weight loss
urgency and frequency of stool passing
tenesmus
\+/- blood in rectum
fever and tachycardia during acute attack
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73
Q

Which inflammatory bowel disease would you see anal lesions

A

Crohn’s disease

Ulcerative colitis has normal anus

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74
Q

Which IBD would you see continuous vs patchy lesions

A

continuous in ulcerative colitis

patchy in Crohn’s disease

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75
Q

Which IBD would you see lesions that are superficial vs full thickness of bowel

A

superficial in UC

Deep in Crohn’s

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76
Q

Which IBD only shows in colon and rectum

A

ulcerative colitis

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77
Q

Which IBD shows all over gut: mouth to anus

A

Crohn’s

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78
Q

Which IBD has granulomatous inflammation vs diffuse and what are the main cell present

A

granulomatous with lymphocytes in Crohn’s

Diffuse with plasma cells in Ulcerative colitis

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79
Q

Which IBD is slightly more common in men compared to females and vice versa?

A

UC male slightly more common

Crohn’s disease females slightly more common

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80
Q

What are the complications of Ulcerative colitis

A

liver- fatty changes, chronic peri-cholangitis, sclerosing cholangitis
eyes-iritis, uveitis
skin- erythoma nodules, pyoderma gangrenosum (sterile dermal abscesses)
colon- blood loss, colorectal cancer, dilation
joints-arthritis, ankylosing spondylitis

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81
Q

What investigations do you carry out with UC

A

FBC
Ultrasound
stool sample to exclude infective diarrhoea
Abdominal XR to see air in colon and dilation
endoscopy

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82
Q

What is the management plan for UC

A 
aim: induce and maintain remission 
corticosteroids
amino-salicylate
immunosuppressant drugs e.g. ciclosporins, anti-TNF alpha antibodies
pain relief
vitamin deficiency treat
surgery last resort: remove all colon
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83
Q

How do you use corticosteroids in UC

A

orally, short-term, to induce remission

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84
Q

What is a side effect of amino-salicylate

A

nephrotoxic so monitor

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85
Q

What is IBS

A

Irritable bowel syndrome
one of the major functional bowel disorders
group of symptoms with no evidence of underlying damage
chronic

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86
Q

What causes IBS

A

exact cause unknown could be to do with:
family history- genetics
stress
food passing too fast or too slow in the gut
nerves overly sensitive
depression, anxiety, chronic fatigue are common among people with IBS

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87
Q

Briefly describe the epidemiology of IBS

A

Women 2-3 times more common than men

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88
Q

What is the common presentation of IBS

A 
stomach pain/cramps esp. after eating worse, and better after passing stool
belching and flatulence 
a backache
fatigue
incontinence
urinary problems
mucus passing from rectum
diarrhoea
constipation
bloating
nausea
no blood loss or weight gain
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89
Q

In which IBD is smoking a protective factor

A

ulcerative colitis

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90
Q

How do we diagnose IBS

A 
History taking of symptoms
tests to exclude other causes:
blood test- Coeliac disease
endoscopy- IBD
stool sample- infective diarrhoea
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91
Q

What is the classification of IBS

A

IBS with diarrhoea common (IBS-D)
IBS with constipation common (IBS-C)
IBS with both constipation and diarrhoea common (IBS-M)
IBS with neither constipation or diarrhoea common (IBS-U)

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92
Q

How do we treat IBS

A

diet: small, frequent meals. high fluid intake, avoid caffeine, alcohol, fizzy drinks, IBSD avoid insoluble fibres and eat 3 portions of fruit per day, Wind and bloating increase soluble fibres,
avoid FODMAP items
pharmacology: pain and bloating: antispasmodics e.g. mebeverine
diarrhoea antimotility e.g. loperamide
constipation laxatives e.g. mavicol
Exercise and psychological support e.g. CBT

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93
Q

Give some examples of FODMAP items

A 
apples, mango
cow milk and cottage cheese
broccoli and mushrooms
custard
chickpeas
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94
Q

What is intestinal obstruction

A

blockage of the lumen of anywhere in the gut with arrest to the onward propulsion of the intestine’s content

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95
Q

How can we divide the causes of causes of intestinal obstruction

A

according to where in the bowels they are e.g. small and large bowels
according to the patient age
according to where they are in regards to lumen

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96
Q

What causes small bowel obstruction in adults

A

malignancy
Crohn’s
adhesion
hernia

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97
Q

What causes small bowel obstruction in children

A

volvus
insussception
appendicitis
hypertrophic polyps stenosis

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98
Q

What are some rare causes of bowel obstruction

A

diverticulitis
radiation
gallstones

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99
Q

What causes large bowel obstruction in Caucasian adults vs Afrocaribbean adults

A

C: colorectal cancer
A: volvus

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100
Q

What causes large bowel obstruction in children

A

imperforation of anus e.g. missing anus, fistula between anus and rectum
Hirschsprung disease

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101
Q

What are the 4 options for classifying causes of obstruction regarding where they are in relation to the bowel lumen

A

Intraluminal (inside the lumen)
intramural (inside the wall of the bowel)
extraluminal (outside the bowel)
other

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102
Q

What are some causes of obstruction that occur in the lumen

A

diaphragmatic disease
tumours e.g. colorectal cancers and lymphomas
meconium ileus
gallstone ileus

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103
Q

What are some causes of obstruction that occur in the wall of the bowel

A

tumours e.g. colorectal cancers, gastrointestinal stromal tumours
Hirschsprung disease
Crohn’s disease
Diverticulitis

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104
Q

What are some causes of obstruction that occur outside the bowel

A

peritoneal cancers e.g. ovarian cancer spread to cavity
volvulus
adhesion

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105
Q

What are some “other” causes of obstruction not intraluminal, intramural, extraluminal

A

a hernia
atresia
intussusception

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106
Q

What is diaphragmatic disease and where does it cause obstruction

A

intraluminal obstruction
due to lots of NSAID use and recurrent ulcerations
fibrous band/diaphragm forms in lumen

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107
Q

What is meconium ileus and where does it cause obstruction

A

intraluminal obstruction
meconium is gree first faeces of newborn
here it is thicker and stickier so causes obstruction in ileum most commonly
associated with cystic fibrosis

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108
Q

What is gallstone ileus and where does it cause obstruction

A

intraluminal obstruction
gallstone causes obstruction. stone gets in from cholecyto-enteric fistula when stone in gallbladder erodes out of the gallbladder and into bowel.

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109
Q

What is Hirschsprung disease and where does it cause obstruction

A

developmental neural problem
parts of bowel wall (intramural i.e.) don’t have ganglion cells so don’t contract so faeces remains in normal segment of bowel before the abnormal section
treatment: resectioning

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110
Q

What are adhesions in bowel obstructions and where does it cause obstruction

A

extraluminal
two sections of bowel are connected/adhered via a fibrous band that pulls the bowel to abnormal position and causes obstruction
post surgery common
treatment: cut the fibrous bands

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111
Q

What are volvulus and where do they cause obstruction

A

extraluminal
twist of segment of bowel around its axis so needs a mesenteric attachment
most common in the colon at caecum or sigmoid where they turn 360 around their mesenteric attachment
causes impaired blood flow colonic so ischaemia, necrosis and perforation of bowel can occur.

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112
Q

what is the method of obstruction in Hirschsprung disese

A

paralytic obstruction

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113
Q

What is the method of obstruction in volvulus

A

closed loop obstruction

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114
Q

What is a hernia and what type of obstruction does it cause

A

abnormal protrusion of a viscus through an abnormal or normal body cavity
some are more likely to strangulate (cause blood loss)
some are more likely to obstruct
occur in small bowel obstruction

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115
Q

What is intussusception

A

when parts of the intestine telescope into one another
caused by an imbalance in longitudinal force on intestine walls
part that is invaginating is intussusceptum
part that is receiving is intussuscipien

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116
Q

What are the two types of intussusception

A

idiopathic

eneteroenteral intussusceptions e.g. jejunojenal, jejunoileal, ileoileal

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117
Q

What is atresia

A

when there is absence of opening in hallow structure

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118
Q

What are two types of obstructions associated with cystic fibrosis

A

intussusception

meconium ileus

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119
Q

What are the common symptoms of small bowel obstruction

A 
vomiting: projectile, feculent, early sign
constipation, obstination late sign
pain
distension
tenderness
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120
Q

What are the common symptoms of large bowel obstruction if caused by malignancy or strictures

A 
vomiting: late sign
constipation, obstination early sign
pain
tenderness
discomfort
nausea
weight loss
bloody stool
tenesmus
bloating
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121
Q

What are the common symptoms of large bowel obstruction if caused by volvus

A

sudden pain

distenstion

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122
Q

When is distension due to obstruction largest

A

the more distal the obstruction the larger the distension

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123
Q

What does obstipation mean

A

no stool passes

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124
Q

What does tenesmus mean

A

hard to pass stool

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125
Q

How does small bowel obstruction cause pathology

A

dilation of proximal bowel to obstruction -causes the following:
mucous wall oedema causing more distension and less absorption
more secretion so anorexia, pain, vomiting, nausea, fluid and electrolyte imbalance
air trapped
more pressure on intramural vessels so less blood flow: ischaemia, necrosis, perforation

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126
Q

Why does necrosis, ischaemia, perforation occur in obstruction of small bowel

A

dilation of bowel causes more pressure on intramural vessels so less blood flow

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127
Q

why does pain, nausea, anorexia, vomiting, electrolyte imbalance occur in obstruction of small bowel

A

more secretion occurs due to dilation of bowel which leads to the following

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128
Q

How does large bowel obstruction cause pathology

A

distension of proximal colon to obstruction
translocation of bacteria
feculent vomiting
pressure on mesenteric vessels so less blood flow so ulcers, necrosis, perforation
If volvus: fluid and electrolyte imbalance and pressure leading to ischaemia etc.
mucosal wall oedema

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129
Q

What are useful imagining techniques to complete with obstruction intestinal

A

XR

CT

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130
Q

What would you see on an XR to indicate small, large bowel obstruction, cecum, sigmoid obstruction

A

larger than 3 cm small bowel- SBO
larger than 6 cm large bowel- LBO
larger than 9 cm cecum or sigmoid- obstruction

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131
Q

How would you manage obstruction intestines

A

pain relief not oral
nil by mouth
fluid resuscitation
NG tube to decompress pressure proximal to the obstruction
treat conservatively, operate, watch and wait all options

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132
Q

What type of obstruction intestinal would you operate immediately vs watch and wait

A

volvus watch and wait

hernia immediate operation

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133
Q

What is intestinal ischaemia

A

reduced blood flow to intestines

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134
Q

What are the three types of intestinal ischaemia

A 
ischaemic colitis (large bowel)
acute and chronic mesenteric ischaemia (small bowel)
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135
Q

What can cause ischaemia colitis

A 
thromboembolism
hypotension
hypovolaemia
obstruction
CV surgery
vasoactive drugs
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136
Q

How does ischaemia colitis cause pathology

A
  • drop in blood flow via superior and/or inferior mesenteric artery
  • hypoxia and tissue damage
  • mucosal layer inflammation and bleeding and sometimes necrosis
  • mucosal layer disruption and perforation of bowel
  • bacteria and toxins released
  • sepsi
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137
Q

What do we call ischaemic colitis if there is necrosis vs. if there is no necrosis

A

gangrenous ischaemia for necrosis

non-gangrenous ischaemia for no necrosis

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138
Q

What are the three phases of presentation of ischaemic colitis

A

hyperactive phase
paralytic phase
shock phase

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139
Q

What is the presentation of the hyperactive phase of the ischaemic colitis

A

bloody stool
sudden pain usually in left lower quadrant
most people recover here

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140
Q

what is the presentation of paralytic phase of ischaemic colitis

A

no bloody stool
no abdominal sounds
pain more diffuse now

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141
Q

What is the presentation of the shock phase of ischaemic colitis

A

signs of septic shock
abdominal guarding
rebound tenderness

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142
Q

What phase of ischaemic colitis would you see bloody stool?

A

hyperactive phase

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143
Q

What phase of ischaemic colitis would you see diffuse pain

A

paralytic phase

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144
Q

How do you diagnose ischaemic colitis

A

XR- air in colon
CT- thick walled colon
Lab results: high lactate, high creatine kinase, leukocytosis, metabolic acidosis
colonoscopy: oedema, cyanosis, ulcers

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145
Q

How do we treat ischaemic colitis

A

anti-platelet drugs
surgery if signs of sepsis or peritonitis
supportive care: IV fluids, bowel rest
reduce the risk of atherosclerosis

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146
Q

What causes mesenteric ischaemia

A

arteriole embolism
arteriole thrombus
venous thrombus

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147
Q

How does mesenteric ischaemia cause pathology

A 
sudden loss of blood flow to intestines
hypoxia
haemorrhagic infarction and necrosis
can perforate and release contents to peritoneal cavity
causing sepsis
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148
Q

What is the presentation of mesenteric ischaemia

A 
periumbilical pain
nausea
vomiting
diarrhoea (bloody at later stage)
leukocytosis
fever
gangrenous intestine
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149
Q

How do we treat mesenteric ischaemia

A

acute: supportive care

surgery if continuous or becomes chronic

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150
Q

What are the 4 features that hernias can have and what do they mean

A

irreducible- hernia cannot be pushed back to where its meant to be
incarcerated- contents of hernia stuck inside it because of adhesion
obstructive
strangulation- blood loss to contents of hernia

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151
Q

What are the 4 main types of abdominal hernias

A

inguinal-most common
femoral
hiatus
incisional

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152
Q

What does hiatus hernia mean

A

stomach contents protrude through the diaphragm into the thoracic cavity

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153
Q

What does incisional hernia mean

A

abdominal contents protrude through incisional scar from surgery
usually within 3 years of surgery

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154
Q

What type of abdominal hernia is the most common

A

inguinal hernia

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155
Q

Where is the inguinal canal and what runs in it

A

inguinal canal is on top of the medial part of the inguinal ligament
inguinal ligament is from the superior iliac crest to the pubic tubercle
the inguinal canal has a deep ring (close to abdominal cavity) and a superficial ring which is close to the pubis
the cavity has the genitofemoral nerve and the spermatic cord/round ligament (men/women) in it

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156
Q

What are the two types of inguinal hernias and describe them

A

direct: abdominal content protrude through a defect hole in the posterior wall of the inguinal canal
indirect: abdominal content protrude through the deep ring

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157
Q

What are the causes of inguinal hernia

A 
anything that can cause increased intra-abdominal pressure or weakness to abdominal muscles e.g.
chronic cough
obesity
constipation
old age
heavy lifting
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158
Q

What are the presentations of ingional hernia

A

asymptomatic or symptomatic
pain esp. when coughing
change in bowel habits
burning sensation in groin

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159
Q

How do we treat inguinal hernia

A

surgery, same surgery for both types

if small and asymptomatic don’t do surgery

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160
Q

What key structures pass under the inguinal ligament and in what order

A

NAVEL
Nerve, Artery, Vein, Empty space, Lymph node
with N being most lateral and L being most medial
the artery, vein and empty space are covered in a sheath

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161
Q

What is a femoral hernia

A

abdominal content protrude into the empty space found in the sheath (contains artery, vein and empty space) that runs under the inguinal ligament
tight space so hernia here is at risk of strangulation and obstruction

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162
Q

Give some examples of the job of the liver

A

glucose and fat metabolism
albumin, clotting factor synthesis
bilirubin, ammonium, drugs, pollutants, hormone excretion

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163
Q

What kind of tests can we do to investigate the liver

A

Liver function tests
imaging: abdominal CT, XR, Ultrasound
Immunological testing
liver biopsy

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164
Q

What do the liver function tests look at:

A

liver enzymes which are released upon liver cell death/damage
bilirubin
albumin
iron

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165
Q

What liver enzymes do we look at in LFT

A

aspartate amino transferase (AST)
alanine amino transferase (ALT)
Gamma-glutamyl-transferase (GGT)
Alkaline phosphatase

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166
Q

What do we look for in liver immunological testing

A

auto-antibodies
level of immunoglobulins and antibodies
antigens and antibodies against viruses

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167
Q

Looking at what gives an indication of the liver function

A

bilirubin, albumin, immunoglobulin, clotting factor levels

not the liver enzymes

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168
Q

Describe the bilirubin pathway of getting it out via urine starting with the RBC

A

RBC in macrophage- breaks haemoglobin into haem and globin.
Haem broken into FE2+ and bilirubin which travels in blood attached to albumin to the liver
In the liver, bilirubin becomes conjugated bilirubin
Conjugated bilirubin is excreted out the liver in bile into the intestine
Some of it is reabsorbed into the blood and carried to kidneys where it leaves as urobilinogen
which is converted to urobilin (yellow) giving urine its colour

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169
Q

Describe the bilirubin pathway of getting out via stool starting with the RBC

A

RBC in macrophage- breaks haemoglobin into haem and globin
Haem broken into FE2+ and bilirubin which travels in blood to liver attached to albumin
in liver bilirubin becomes conjugated bilirubin and is excreted into the intestines
in large intestine it becomes stercobilinogen and that becomes stercobilin (which is brown) giving faeces its colour

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170
Q

What is jaundice in a simple term

A

yellow skin

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171
Q

What is the simple cause of jaundice

A

increase in serum bilirubin

over 50 micromols/L

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172
Q

What are the three types of jaundice

A

prehepatic (unconjugated)
intrahepatic (conjugated/ cholestasis)
posthepatic (conjugated.cholestasis)

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173
Q

What is the cause of prehepatic jaundice

A

increased breakdown of RBC leading to increased serum unconjugated bilirubin e.g.
malaria
sickle cell anaemia
thalassemia
physiological jaundice of newborn when their foetal RBC are broken down

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174
Q

What is the presentation of prehepatic jaundice

A 
normal urine, stool
yellow skin
enlarged spleen
no itching
due to high serum unconjugated bilirubin without changes to urobilin, stercobilin or conjugated bilirubin
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175
Q

What is intrahepatic jaundice caused by

A

hepatocellular inflammation, swelling leads to cells being unable to take in bilirubin properly, to convert it to conjugated bilirubin and to excrete bilirubin.
Caused by things such as viral, alcohol hepatitis, drugs, cirrhosis

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176
Q

What is the presentation and blood results of intrahepatic jaundice

A

low urobilin and low stercobilin so dark urine and pale stool
yellow skin because high serum conjugated and unconjugated bilirubin
enlarged spleen
itching possibly

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177
Q

What is the cause of posthepatic jaundice

A

damage to the biliary tree e.g. inflamed, obstructed, swollen e.g. from
pancreatic cancer
gallstones
cholangitis

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178
Q

What is the presentation and blood results of posthepatic jaundice

A 
high serum conjugated bilirubin
Normal serum unconjugated bilirubin
yellow skin
low urobilin and stercobilin so dark urine and pale stool
itching possible
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179
Q

How can we treat the itching in jaundice

A

anti-histamines, plasmapheresis, UV light, opiate antagonist but these won’t make it go away fully, only treating the cause of jaundice will.

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180
Q

What is the likely cause of dark urine, pale stool, yellow skin

A

conjugated jaundice

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181
Q

What is the likely cause of normal urine, normal stool, yellow skin

A

unconjugated jaundice

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182
Q

Does high liver enzymes suggest obstruction

A

no, suggests liver disease

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183
Q

what are the types of liver diseases

A

hepatitis: viral, alcohol, drug, immune
neoplasm
congestion
ischemia

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184
Q

what are the types of liver obstructions

A

gallstones
strictures: ischaemia, malignancy, inflammatory
blocked stent

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185
Q

What are the two options for endpoints of acute liver injury

A

liver failure

recovery

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186
Q

What are the main causes of acute liver injury

A 
viral hepatitis
alcohol high consumption
adverse drug reactions
congestion from heart failure
vascular injury (rare as has two blood supplies)
biliary tree obstruction
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187
Q

What is the main presentation of acute liver injury

A

malaise
nausea
anorexia
jaundice

188
Q

What are some rare presentations of acute liver injury

A

coma, confusion- accumulate toxic metabolites which mimic neurotransmitters
liver pain
hypoglycaemia
bleeding -low clotting factors produced

189
Q

What happens to the cells in acute liver injury

A

cell damage and loss via necrosis and apoptosis

neutrophils suggest necrosis

190
Q

How can we classify the viruses that infect the liver

A

the ones that infect the liver only

the ones that infect the liver via systemic infections

191
Q

Which viruses only infect the liver

A

hepatitis A, B, C, D, E, G

192
Q

which viruses infect the liver as part of a systemic infection

A 
epstein Barr virus
yellow fever
adenovirus
varicella virus
herpes virus
cytomegalovirus
193
Q

What are the symptoms of viral hepatitis

A

malaise
fever
jaundice
upper abdominal discomfort

194
Q

How long do viral hepatitis symptoms last

A

3-4 weeks then recover

some can become chronic though

195
Q

Which viruses are likely to cause chronic viral hepatitis

A

hepatitis B, C, D

196
Q

Who often get alcohol liver injury: alcoholics or non-alcoholics

A

non-alcoholics more commonly

i.e. not alcohol dependent

197
Q

What is the spectrum of alcohol liver injury

A

fatty changes
acute hepatitis in Mallory hyaline due to cytoskeletal protein accumulation and neutrophil invasion
portal fibrosis
cirrhosis

198
Q

How does alcohol cause liver injury

A
  1. alcohol metabolism takes energy from fat metabolism so fat accumulation, once alcohol stopped, fat reduces
  2. alcohol metabolite: acetaldehyde binds to liver proteins and causes injury to hepatocytes
  3. alcohol stimulates collagen synthesis leading to fibrosis and cirrhosis.
199
Q

How does the liver try and deal with the alcohol liver injury

A

tries to compensate but eventually cannot (long period or trigger e.g. infection) so acute liver decompensation occurs

200
Q

How do we treat alcohol liver injury

A

spironolactone, gastroectomy, bands on varicies

201
Q

What is fat accumulation in the liver called

A

steatosis

202
Q

what does steatosis mean

A

fatty accumulation in liver

203
Q

Which zone of the liver is fibrosis most common in

A

zone 3

204
Q

Why must we consider drugs with liver injury

A

liver involved in metabolism, coagulation, excretion of toxic substances including drugs
drug-induced liver injury could occur

205
Q

What are the two mechanisms of action of drug-induced liver injury

A

hepatocellular (damage to cells like viral hepatitis)

cholestatic (damage to bile production and excretion ability of liver)

206
Q

What would cause you to suspect a drug-induced liver injury from the history

A

occurs 1-12 weeks after a new drug has been started

earlier is rare and maybe if rechallenging immunity e.g. retaking drug after you stopped due to side effects first time)

207
Q

How long do most drug-induced liver injuries resolve with abstinence of the drug

A

3 months for 90% of cases

5-10% prolonged

208
Q

What are some usual suspects of DILI

A 
antibiotics
immunosuppressants
analgesics
GI, MSK, CNS drugs
multiple drug interactions
dietary supplements
209
Q

What are some safe drugs for people with liver disease

A

paracetamol
short-acting benzodiazepine
monitor diuretics

210
Q

What two drugs types would you definitely avoid with liver disease

A

ACE-i

aminoglycosides

211
Q

When is paracetamol dangerous for the liver

A

overdose

causes paracetamol-induced liver injury

212
Q

How do you treat a paracetamol-induced liver injury

A

N-acetyl cysteine drug
supportive care for damage done: coagulation defects, renal failure, fluid-electrolyte and acid-base balance, hypoglycaemia
if failure, bad prognosis consider an emergency liver transplant if available

213
Q

What things would indicate bad prognosis and paracetamol-induced liver failure

A

presents late, NAC less effective >24 hours
acidosis
prothrombin>70 seconds
serum creatine>300mmols/L

214
Q

What is N-acetyl cysteine’s mechanism of action

A

activates glutathione transferase which converts dangerous metabolite into a stable metabolite

215
Q

What is the main cause of biliary obstruction causing liver injury

A

gallstones

216
Q

What are the symptoms of biliary obstruction causing liver injury

A

colicky pain
fever if there is a superimposed infection
jaundice

217
Q

What is the mechanism of action of biliary obstruction causing liver injury

A

portal tract fibrosis

secondary biliary cirrhosis via nodular regeneration

218
Q

What is an example of a vascular injury to cause liver injury

A

hepatic vein occlusion

219
Q

What can cause hepatic vein occlusion

A

thrombus e.g. in Budd-Chiari syndrome
venous-occlusive disease e.g. from radiation
membrane obstruction

220
Q

How do we treat hepatic vein occlusion

A

anti-coagulation therapy
transjugular-intrahepatic-portosystemic shunt
liver transplant

221
Q

What is the definition of chronic hepatitis

A

clinical or histological evidence of liver inflammation lasting more than 6 months

222
Q

What are the options for what chronic hepatitis can lead to

A

fibrosis (and cirrhosis)
recovery (does not mean resolution necessarily)
liver failure
varices
hepatoma
(cirrhosis can also lead to the other four)

223
Q

What do we call severe fibrosis in the liver

A

cirrhosis

224
Q

What are the causes of chronic liver injury

A 
autoimmune
alcohol
drugs
viral hepatitis B, C
non-fatty liver disease
metabolic: iron, copper overload, antitrypsin alpha-1 deficiency
225
Q

What are the common presentations of chronic liver injury

A 
malaise
anorexia
easy bruising
hematemesis
ascites
oedema
itching
hepatomegaly
226
Q

What are the rare presentation of chronic liver injury

A

jaundice

confusion

227
Q

Which type of liver injury: acute or chronic would you most likely see jaundice

A

acute

228
Q

What is cirrhosis

A

irreversible disturbance to the liver architecture in all its entirety associated with fibrosis and nodular regeneration (lobules replaced with nodules in liver)

229
Q

What are the stages of cirrhosis with regards to histology

A

small nodules-> cirrhosis micronodules-> large macronodules

230
Q

What are the complications of cirrhosis

A

portal hypertension, carcinoma, liver failure

231
Q

What are the two ways that the body can deal with cirrhosis

A

compensatory

decompensate

232
Q

What occurs in cirrhosis compensation

A

no changes to liver function

inactive causative agent

233
Q

What occurs in cirrhosis decompensation

A

liver failure which can cause:

  • low albumin so low oncotic pressure so oedema
  • low clotting factors
  • less excretion of toxic substances which can:
  • -mimic neurotransmitters causing coma
  • -act as hormones so high oestrogen and androgen (high oestrogen leading to spider naevi)
234
Q

What can cause portal hypertension

A

cirrhosis, thrombus, fibrosis

235
Q

Why does portal hypertension occur

A

increased hepatic resistance and increase splenic blood flow

236
Q

What is spider naevi and what causes it

A

hyperoestrogenism from decompensation of liver

small vascular lesions on skin

237
Q

What are the complications of portal hypertension

A

varices

splenomegaly

238
Q

Why is there a risk of carcinoma from cirrhosis

A

cirrhosis has lots of cell turnover to create nodules so more room for errors while replicating

239
Q

What are 3 types of primary liver tumours

A

hepatocellular carcinoma
cholangiocarcinoma
angiosarcoma

240
Q

What is the main primary liver tumour

A

hepatocellular carcinoma

241
Q

What increases your risk of hepatocellular carcinoma

A

men>women
cirrhosis
viral hepatitis B and C
haemochromotosis

242
Q

How does hepatocellular carcinoma present

A

decompensation of liver disease symptoms
weight loss
ascites
abdominal pain

243
Q

What is the treatment for hepatocellular carcinoma

A

liver transplant
resectioning of tumour but usually too much cirrhosis
sorafenib to prolong life

244
Q

What metastatic tumours commonly present in the liver

A

breast, bowel, pancreas, lung

245
Q

What are the main types of autoimmune liver conditions

A

autoimmune hepatitis
primary biliary cirrhosis
sclerosing cholangitis

246
Q

which gender is most at risk of autoimmune liver conditions

A

females

247
Q

What is the histological picture of autoimmune hepatitis

A

like chronic hepatitis

lots of plasma cells and rosette style arrangement of swollen liver cells

248
Q

What auto-antibodies are there in autoimmune hepatitis

A

anti-smooth muscle antigens
anti-kidney-liver microsome antigens
anti-DNA

249
Q

What is the raised globin type in autoimmune hepatitis

A

lgG

250
Q

What is the histological picture of primary biliary cirrhosis

A

spectrum from 1-5 but patchy so can see lots of stages in one go

1) autoimmune destruction of bile ducts esp. small intrahepatic ducts, lots of lymphocytes and granulomas
2) proliferation of bile ducts
3) portal fibrosis causes architectural destruction
4) cirrhosis
5) copper overload because of ion not leaving because no functioning bile duct (ductapenia)

251
Q

What are two symptoms of primary biliary cirrhosis

A

itching

fatigue can be disabling

252
Q

How do you treat fatigue in primary cirrhosis

A

not a reason for transplant anymore

treat with Modafinil

253
Q

How do you treat the lack of bile in primary biliary cirrhosis

A

ursodeoxycholic acid

254
Q

What benefit does ursodeoxycholic acid give to primary biliary cirrhosis

A 
improves liver enzyme function
reduces inflammation
reduces portal pressure and so risk of varices bursting
reduces need for transplants
reduces death rate
255
Q

What benefit does ursodeoxycholic acid not give to primary biliary cirrhosis

A

it doesn’t stop the itching

it doesn’t remove or stop the fibrosis

256
Q

What are the auto-antibodies against in primary biliary cirrhosis

A

anti-mitochondria

257
Q

What is the raised immunoglobulin in primary biliary cirrhosis

A

IgM

258
Q

How useful is steroid use for autoimmune hepatitis

A

good

259
Q

How useful is steroid use for primary biliary cirrhosis

A

limited effect

260
Q

What is sclerosing cholangitis

A

chronic inflammation cells around ducts i.e. inflammation of bile ducts extra- and intra-hepatic
this becomes fibrosis
obstruction of bile ducts by strictures occurs
ductopenia occurs
gallstones+/-

261
Q

Which two autoimmune liver conditions can cause ductapenia

A

sclerosing cholangitis

primary biliary cirrhosis

262
Q

What is ductapenia

A

no functioning duct

263
Q

What is the raised immunoglobulin and what is the auto-antibody in sclerosing cholangitis

A

varied raised immunoglobulin
anti-neutrophils
cytoplasmic

264
Q

What are the symptoms of sclerosing cholangitis

A

itching
pain
rigours
jaundice

265
Q

How do we treat sclerosing cholangitis

A

liver transplant
steroid little use
ursodeoxycholic acid unclear use

266
Q

What condition is associated with sclerosing cholangitis

A

ulcerative colitis

267
Q

Which autoimmune liver condition is associated with ulcerative colitis

A

sclerosing cholangitis

268
Q

Describe the different types of iron overload in the liver

A

hemosiderin is the form iron is deposited in
hemosiderosis is when there is iron overload in the liver but no architectural disruptions
hemochromatosis is when there is iron overload with increased risk of cirrhosis

269
Q

What is the genetic risk that can give you hemochromatosis

A

C282Y in homozygous states

accumulation of iron

270
Q

What can iron removal do to help iron overloaded liver

A

reverse fibrosis sometimes

271
Q

What is the genetic disorder that leads to copper accumulation

A

Wilson’s disease

272
Q

What is Wilson’s disease

A

an autosomal recessive condition where copper accumulates in the liver and basal ganglia because liver can’t secrete copper in bile

273
Q

What are the complications of Wilson’s disease

A

chronic hepatitis

cirrhosis

274
Q

Where is anti-trypsin alpha-1 made and secreted

A

made in liver and immediately secreted into blood

275
Q

What is anti-trypsin alpha-1

A

anti-proteolytic protein

276
Q

What is the disposition that gives you a deficiency in alpha-1 anti-trypsin

A

having two, homozygous, of the abnormal phenotype means alpha-1 anti-trypsin cannot leave the liver to the blood easily so accumulates in the liver

277
Q

What will alpha-1 anti-trypsin give you a predisposition to?

A

hepatic cirrhosis

emphysema

278
Q

What is a definition of a patient with non-alcoholic fatty liver disease

A 
patient with 3 of the following:
-central obesity
-type 2 diabetes mellitus
-hypertriglyceridemia
-low HDL cholesterol
-high blood pressure
on liver biopsy find fat and inflammation
279
Q

How do you treat non-alcoholic fatty liver disease

A

no treatment

losing weight can help

280
Q

What is another name for gallstones

A

cholelithiasis

281
Q

What are cholelithiasis

A

gallstones

282
Q

where do gallstones mostly happen and what symptoms

A

mostly gallbladder and asymptomatic but can happen in bile duct also and with symptoms

283
Q

What would suggest that the gallstone was in the gallbladder

A

cholecystitis
no cholangitis or pancreatitis

maybe jaundice
biliary pain

284
Q

What would suggest that the gallstone is in the bile duct

A 
pancreatitis
cholangitis
no cholecytitis
biliary pain
obstruction jaundice
285
Q

What are the risk factors for gallstones

A

female
obese
diabetes mellitus

286
Q

What are gallstones made off and why do they occur

A

cholesterol 70%
bile 30%
+/- calcium
occur due to an imbalance between cholesterol and bile salts with cholesterol increasing and bile salts decreasing

287
Q

How do you treat gallstones

A

in gallbladder: laparoscopic cholecystectomy and bile acid dissolution therapy
in bile duct: sphincterotomy, remove gallstone, stent

288
Q

What are patients with liver dysfunctions at risk to

A 
infections
endocrine problems
coagulopathy
malnutrition
hypoglycaemia
289
Q

Why are patients with liver dysfunctions at risk to infections

A

impaired reticuloendothelial system

impaired leukocyte function

290
Q

What type of infections are patients with liver dysfunctions at risk to

A 
spontaneous bacterial peritonitis
septicemia
UTI
skin infections
pneumonia
291
Q

What things could trigger an exacerbation in a person with chronic liver conditions

A 
GI bleeds
Cardio problems
intra-cranial problems
drugs
alcohol withdrawal
infections
low sodium
low potassium
hypoglycaemia
292
Q

What is ascites

A

detectable abnormal or chronic fluid collection in the peritoneal cavity

293
Q

how much fluid is there physiologically in men and women

A

men little or none

females 20ml

294
Q

What are the stages of ascites

A

1) detectable only after careful examination
2) easily detectable but not a lot
3) obvious but not tense ascites
4) tense ascites

295
Q

What are some causes of ascites

A 
heart failure
TB
malignancy
pancreatitis
cirrhosis (main one)
296
Q

What are the three methods of getting ascites and give an example or few for them

A

portal hypertension- cirrhosis
non-portal hypertension- malignancy, nephrotic syndrome, heart failure
chylous ascites: trauma, abdominal surgery, radiation, congenital

297
Q

What is the type of fluid which could be in ascitic fluid

A

exudate (proteins and fluid) or transudate (fluid only, no proteins)

298
Q

How does exudate fluid enter peritoneal space in ascites

A

inflammation causes fluid out
inflammation causes vasodilation, low blood pressure, low blood flow so stasis of blood
inflammation increases intra-endothelial space so protein can leave

299
Q

How does transudate fluid enter peritoneal space in ascites

A

imbalance between oncotic pressure and hydrostatic pressure

pushes fluid out only

300
Q

What are the causes of ascites with exudate fluid

A 
malignancy
Infection
pancreatitis
bowel obstruction
bowel leak
301
Q

What are the causes of ascites with transudate fluid

A
  • hypoproteinemia: malnutrition, protein-losing enteropathy, malignancy, TB (reduced oncotic pressure)
  • portal hypertension (increased hydrostatic pressure)
  • cirrhosis
  • heart failure
  • liver metastasis
  • alcohol hepatitis
  • liver failure
302
Q

What is the clinical picture of ascites

A 
abdominal distension
nausea
constipation
weight gain
pain (hints malignancy vs no pain hint vice versa)
an umbilicus hernia (hints cirrhosis)
jaundice if liver problem
303
Q

What methods do we use for diagnosis of ascites

A
  • examination: round ball abdomen with skinny elsewhere, umbilicus hernia, prominent vessels
  • imaging: XR chest and abdomen (heart failure check etc), ultrasound, CT if small liquid
  • ascitic tap 20ml
  • FBC, U&E, LFT
304
Q

What do we do with the ascites tap

A

culture for pathogens
cytology if cancer suspect
protein count- amylase high suspect pancreatitis, SAAG, total protein count

305
Q

What is the SAAG,

for exudate and transudate

A

SAAG (serum ascites albumin gradient)
exudate <1.1g/dL low
transudate >1.1g/dL high

306
Q

What is the total protein for exudate and transudate from ascites tap

A

exudate >2.5

transude <2.5

307
Q

What is the management plan for ascites

A

treat underlying cause
diuretics
if diuretics don’t work/intolerant/contraindication do regular large-volume paracentesis
if over5L taken in paracentesis give human albumin solution
lose weight, avoid caffeine, salt limitation, avoid over-hydration
transjugular intrahepatic portosystemic shunt
treat spontaneous bacterial peritonitis if it occurs

308
Q

What is the major complication of ascites and why

A

spontaneous bacterial peritonitis

static fluid in ascites means high potential for infection

309
Q

What is spontaneous bacterial peritonitis

A

bacterial infection of the ascitic fluid in the absence of other intra-abdominal causes.
Commonly klebsiella spp. streptococci pneumonia, E. coli cause it

310
Q

What are the symptoms of spontaneous bacterial peritonitis

A

If ascites occurs due to liver problem then liver decompensation commonly
commonly asymptomatic but abdominal pain, tense abdominal walls, fever also can occur

311
Q

How do we treat spontaneous bacterial peritonitis

A

diagnose SBP first then treat, usually hard to find the pathogen
broad antibiotic: cephalosporin IV
drain fluid

312
Q

What is peritonitis

A

Inflammation of the peritoneum which lines the peritoneal cavity. usually caused by the presence of air, pathogens, GI contents, blood

313
Q

How can we classify peritonitis

A

acute/chronic

causes: primary/secondary
location: localised/generalised

314
Q

what are primary causes of peritonitis

A

rare

usually from the haematological or lymphatic spread of irritants

315
Q

Who is most at risk of primary causes of peritonitis

A

liver disease people with ascites and spontaneous bacterial peritonitis
females
immunocompromised patients.
Patients on peritoneal dialysis usually with staph. aureus and coagulase-negative staph

316
Q

What are secondary causes of peritonitis

A

more common
due to pathology of underlying organs with trauma or perforation e.g.
perforation of bowel, stomach and release of content e.g. from peptic ulcers, diverticular disease
ischaemia leading to perforation
surgery causing trauma and perforation
inflammation of abdominal organs such as appendicitis, pancreatitis

317
Q

What is localised peritonitis

A

local inflammation of an underlying organ before perforation

318
Q

What are some symptoms of localised peritonitis

A

less rapid onset
symptoms of underlying cause
guarding local area

319
Q

What is generalised peritonitis

A

more dangerous than localised peritonitis
Peritoneum irritated from the presence of pathogens/infections and chemical irritants e.g. from perforated organ- GI content
Inflamed peritoneum occurs and produces inflammatory exudant

320
Q

What are some symptoms of generalised peritonitis

A

quick onset
guarding whole area by lying completely still
quick sudden pain

321
Q

What are the symptoms of peritonitis caused by intestinal obstruction

A

colicky pain central abdominal
peritonitis occurs only if the bowel is threatened
bilious vomiting

322
Q

What are the symptoms of peritonitis caused peptic ulcers and what is the treatment

A

epigastric pain +/- pain in shoulder tip
surgery to close the hole and wash put abdominal cavity
give antibiotics to treat any infections
give acid suppression medication

323
Q

What is acute appendicitis

A

inflammation of the vermiform appendix caused by either:

  • blocked appendicular lumen e.g. with tumour, lymphoid tissue, solid bits of faeces
  • stasis of mucin and fluid inside so increased pressure, ischaemia, necrosis and perforation
324
Q

What are the symptoms of appendicitis

A

pain moving from umbilicus to right lower quadrat
range from very unwell to a little bit unwell
pain worse on movement
loss of appetite

325
Q

How do you treat appendicitis

A

antibiotics
bowel rest
appendectomy

326
Q

What is ectopic pregnancy

A

conceptions placed in area other than uterine cavity e.g. most commonly in the fallopian tube

327
Q

Why do you always suspect ectopic pregnancy in females of childbearing age

A

pain occurs, +/- shoulder tip pain and bleeding but can all be asymptomatic
large space so asymptomatic bleeding can drain nearly whole systemic circulation without being detected so potentially lethal

328
Q

What are you worried about in peritonitis with women of child-bearing age

A

ectopic pregnancy

329
Q

What are two less common causes of peritonitis that involve the immune system

A

autoimmune diseases e.g. lupus

systemic infections e.g. TB

330
Q

What is the treatment of ectopic pregnancy

A

call gynaecologist
blood transfusion usually
surgery

331
Q

What are the symptoms and signs of peritonitis

A 
loss of appetite
nausea
vomiting
difficulty passing urine, gas, faeces
fluid collection in abdomen
dull pain becomes suddenly severe and sharp
pain worsened by movement
abdominal tenderness
silent abdomen 
fever and chills
hypotension and hypoxia in end stage of shock
tachycardia
332
Q

Why do you get fever and chills in peritonitis

A

fever: sepsis so vasodilation and so heart rate higher to keep cardiac output good so hot and sweaty
chills: CO cannot be maintained so shunting of blood to key organs like heart and brain and not to skin and GI

333
Q

What are the investigations we do for peritonitis

A

look: patient not moving, guarding abdomen, lying completely still
physical and clinical exam: tense muscles, rigid abdomen, pain location: (near diaphragm-upper GI problem, near umbilicus- S intestine problem, near suprapubic- left colon)
ascitic fluid analysis for fluid markers
imaging: XR, Ultrasound abdomen (CT if stuck) sometimes no time for imaging and do surgery and then see the underlying cause

334
Q

How do we manage peritonitis

A

resuscitation first: ABC, O2 if needed, antibiotics if infection, fluid IV, check organ esp kidney function before surgery
treat cause: medical only for SBP and pelvic inflammatory disease
surgery for closing hole in perforated organ, removing perforated organ, wash out with antibiotics or just saline, supportive care to organs after

335
Q

What are the complications from peritonitis

A
  • difficulty breathing due to fluid pressure on diaphragm
  • septicaemia
  • fluid loss and electrolyte imbalance leading to shock or kidney failure
  • peritoneal abscess ala intra-abdominal abscess
336
Q

You have performed surgery for your peritonitis patient and they are not improving what are you going to suspect

A

peritoneal abscess
occurs esp. after surgery
collection of pus in peritoneal cavity that is guarded by inflammatory barrier

337
Q

What factors can reduce a patients chance of survival after and before treatment for peritonitis

A

old age
immunocompromised, cancer
any single organ failure before surgery e.g.
diabetes (more chance of getting infection)
anything that affects cardiac output
respiratory problems
renal failure

338
Q

Why is septicaemia easy to occur from peritonitis

A

peritoneum is highly permeable
large surface area
drained by lymphatic vessels
all mean easy for pathogens to reach systemic circulation

339
Q

What is helicobacter pylori and how does it survive

A

gram-negative bacteria causes peptic ulcers, gastroenteritis and peritonitis
survives in stomach because microaerophilic, motile and produces urease which makes ammonia to buffer acid

340
Q

How does helicobacter pylori cause pathology

A

causes inflammation due to recruiting neutrophil polymorphs
inhibits somatostatin from D cells so lots of gastrin as no inhibition so more acid so peptic ulcers
cancer risk increase due to intestinal metaplasia occurring in the stomach due to helicobacter pylori not surviving in intestines

341
Q

What are the symptoms of helicobacter pylori infection

A

epigastric pain, nausea

can be asymptomatic often

342
Q

How do we treat helicobacter pylori infection

A

omeprazole

amoxicillin and clarithromycin

343
Q

What is diarrhoea

A

3 or more loose stools per day

“loose” can be different for different patients

344
Q

What is a way we can classify stool

A

bristol stool chart

1) hard lumps
2) sausage lumpy
3) sausage cracks
4) sausage smooth
5) lumps soft, clear-cut edges
6) fluffy bits with rough edges
7) liquid stool

345
Q

Who is at risk of diarrhoea

A

children in nursery
people working with uncooked food
people working with vulnerable people
people with unsatisfactory hygiene

346
Q

How big is diarrhoea a cause for infant mortality

A

2nd leading cause of death in infants is diarrhoea due to malnutrition mainly

347
Q

What key things do we want to ask about in history for diarrhoea

A

travel, animal, family history
food/water taken?
immunocompromised

348
Q 
What are suspecting with these cases of diarrhoea:
fresh water
well water
puppies
reptiles
flooding
Raspberries
small children
A 
fresh-water- Aeromonas
well water- giardiasis
puppies- campylobacter
reptiles- salmonella
flooding- cryptosporidiosis
Raspberries- cycospora
small children- rotavirus, shigella
349
Q

What is the most common cause of diarrhoea

A

viral

350
Q

What are the three most common causes of viral diarrhoea

A

norovirus
rotavirus
adenovirus (less common than other two)

351
Q

When do rotavirus outbreaks occur

A

developing countries: year round

developed countries: dec to march

352
Q

When do norovirus outbreaks occur

A

winter more common but year round can occur

353
Q

Where do we worry about norovirus outbreaks

A

nurseries
nursing homes
hospitals
cruise ships

354
Q

What is traveller’s diarrhoea

A 
occurs within 2 weeks of coming to new country (usually within 3 days)
diarrhoea and one of the following:
abdominal pain
cramps
bloody stool
nausea
355
Q

What most commonly causes traveller’s diarrhoea

A

bacterial- ETEC, shigella

and others: norovirus, giardia

356
Q

What are the two types of diarrhoea that bacteria can cause and name some examples

A

inflammatory- EIEC, Shigella, non-typhoid salmonella

secretory: ETEC, EHEC, Vibrio cholera

357
Q

When does c. diff occur

A

after taking lots of antibiotics usually

358
Q

What is c.dif

A

clostridium difficile
gram-positive bacteria
produces a toxin: toxin A

359
Q

Who is at risk of getting diarrhoea with c.diff

A 
older patients
co-morbidities
PPI
immunocompromised
long hospital stay
antibiotics: co-amoxiclav, clindamycin, cephalosporin, ciprofloxacin
NG feeding tube
post-operative
360
Q

What can be the presentation of c. diff infections

A

asymptomatic carriage
not severe illness responding well to withdrawal of antibiotics
severe illness with diarrhoea, fever, enteritis

361
Q

How do you treat c. diff infections

A

oral vancomycin
metronidazole
rifampicin
stool transplant from healthy patient

362
Q

What is the best way to clean to protect yourself for c.diff

A

soap and water

c.diff has spores that are resistant to alcohol gel

363
Q

How is c.diff transferred

A

faecal-oral route

spores

364
Q

What are two ways we can classify diarrhoeal illnesses

A

infective and non-infective causes

365
Q

What is one of the reasons why diarrhoeal illnesses can lead to death in children

A

significant fluid loss

366
Q

What protozoa can cause diarrhoea

A

entamoeba
giardia
cryptosporidium

367
Q

What helminths can cause diarrhoea

A

Strongyloides
schistosomiasis
in general helminths don’t cause diarrhoea

368
Q

What are some symptoms of schistosomiasis infection

A 
fever
cough
wheeze
diarrhoea
eosinophilia
hepatosplenomegaly
369
Q

What are some symptoms from Strongyloides infection

A 
cough
wheeze
eosinophilia
diarrhoea
can be asymptomatic
370
Q

What are the methods of transfer of diarrhoeal illness give examples

A

direct e.g. direct route e.g. STI, faecal-oral route
indirect e.g. vector-born (malaria mosquito), vehicle-born (hep B and dirty needles)
airborne

371
Q

What are some non-infective causes of diarrhoea

A

neoplasms (alterted bowl movements for months suspect)
IBS
IBD
anatomical- short bowel syndrome so less bowel to absorb water
hormone e.g. adrenalin, serotonin increase bowel movement
radiation
chemical

372
Q

How do we treat diarrhoeal illnesses

A

zinc replacement
fluid replacement prevent dehydration
treat underlying cause

373
Q

What are three infective biliary diseases

A

ascending cholangitis
acute cholecystitis
liver abscess

374
Q

What is ascending cholangitis

A

bacterial infection of the biliary tree

obstruction

375
Q

What are the symptoms of ascending cholangitis

A

charcot triad

fever, RUQ pain, jaundice

376
Q

What investigations do we do for ascending cholangitis

A

bloods
ultrasound
endoscopy

377
Q

how do we treat ascending cholangitis

A

IV fluids, antibiotics
remove stones if any
stenting

378
Q

What is acute cholecystitis

A

infection of gallbladder

379
Q

What are the symptoms of acute cholecystitis

A

fever
RUQ pain
high inflammatory markers

380
Q

What is a complication of acute cholecystitis

A

reccurrent acute cholecystitis can cause pancreatitis

esp. if obese and diabetes

381
Q

what are the two causes of liver abscesses

A

bacterial infection

amoebic infection

382
Q

Which bacteria are most common in causing liver abscesses

A

E. coli
klebsiella pneumonia
streptococcus milleri

383
Q

How can bacterial infections cause liver abscesses

A 
can enter from biliary tree
haematogenous spread
infection of tumour or cyst
trauma
direct extension from gallbladder
384
Q

What are the clinical features of liver abscesses

A 
fever 
RUQ pain
weight loss
obstructive jaundice
right shoulder pain
385
Q

What is diverticular disease

A

outpouching of mucosal layer through hole in muscularis layer in large intestine esp. signoid

386
Q

What is diverticulitis

A

when there is material in out-pouches of mucosal layer that become infected

387
Q

What are the symptoms of diverticulitis

A

fever
abdominal pain
high WCC
diarrhoea/constipation

388
Q

How do we treat diverticulitis

A

co-amoxiclav and percutaneous drainage

try and treat conservatively but surgery used if complications e.g. obstruction

389
Q

What are the benign types of oesophageal cancers

A

rare
leiomyoma (most common benign)
lipoma
Fibroma

390
Q

What are the common malignant oesophageal cancers and rarer ones

A

adenocarcinoma, squamous cancer

rare; sarcoma, melanoma

391
Q

What are the symptoms of malignant tumours of the oesophageal

A

dysphagia (and tumour can block fully so no swallowing)
weight loss
pain
bleeding so iron deficient anaemia
resp problems because tumour invade through oesophagus into trachea or indigested food enter trachea so coughing, recurrent pneumonia
hoarse voice

392
Q

What is squamous cancer of the oesophageal

A

from squamous cells

maybe procceded by dysplastic cells

393
Q

What are the risk factors for squamous cancer of the oesophageal

A 
vitamin deficiencies
tobacco
alcohol
men
repeated thermal injury
nitrosamine in food
human papillomavirus
394
Q

What are the predisposing conditions to adenocarcinoma in oesophagus

A

gastroesophageal reflux

barrett’s oesophagus

395
Q

What happens in gastro-oesophageal reflux to cause cancer

A

acid in oesophagus
cells don’t make mucin so die
if acid stops: new squamous cells grow
if acid doesn’t stop then new cells may form with a higher chance of becoming cancerous

396
Q

What happens in Barrett’s oesophageal

A

GORD is the biggest risk factor
defined as >3cm of columnar cells at bottom of oesophagus. these cells can produce mucin so can survive in acid conditions better . if mucin is produced by the new cells its called intestinal metaplasia, if not its called columnar metaplasia.
we have to monitor this and treat as if its GORD so lower risk factors and chance lifestyle

397
Q

Why do different cells grow in Barrett’s oesophageal

A

either:

1) columnar and squamous cells from same cell line so new condition means new columnar cells are better able to survive
2) columnar cells migrate up oesophagus from stomach

398
Q

How do we treat oesophageal cancers

A

surgery if early

usually present late so palliative

399
Q

what is the most common type of gastric cancers and how are they classified

A

adenocarcinoma

intestinal and diffuse adencarcinoma

400
Q

What are intestinal adenocarcinomas

A

those that arise usually from intestinal metaplasia

(normal gastric cells->intestinal metaplasia ->dysplasia-> early gastric cancer -> advanced gastric cancer

401
Q

What are diffuse adenocarcinomas

A

made of chains of poorly connected cancer cells that are invasive with a poorly defined margin
worse prognosis than intestinal adenocarcinomas because present late often

402
Q

What do we mean by early and advanced stages of gastric cancer

A

early: cancer is only in mucosal and submucosal layers, doesn’t matter for nodes spread, for size or duration of cancer
advanced: cancer is in and beyond muscularis propria layer

403
Q

How do gastric cancers present

A 
dysphagia
nausea
indigestion
loss of appetite
weight loss
hematemesis
404
Q

What are the types of tumours that grow in the large intestine

A

adenoma

adenocarcinoma

405
Q

What are the type of tumours that grow in the small intestine

A

lymphoma

endocrine cell tumours

406
Q

What are polyps and where are they most found

A

protuberant outgrowths

mostly in large intestine

407
Q

What are adenoma polyps

A

benign epithelial polyps

408
Q

What is the main type of polyp in the LI

A

adenoma polyps

409
Q

What polpy predispose patients to colorectal cancer

A

colorectal polyp

410
Q

What is the precursor of most colorectal cancers

A

adenomas

411
Q

What makes a polyp more likely to progress to become cancerous

A

the larger the polyp the more likely it will become cancerous

412
Q

What are two genetic conditions that increase the risk of colorectal cancer

A

FAP (Familial adenomatous polyposis)

HNPCC (hereditary non-polyps colorectal cancer)

413
Q

What are the causes of gastric cancers

A 
genetic (CDH1 germline mutation)
smoking
diet (eating smoked, processed food)
obesity
helicobacter pylori
previous gastric surgeries
414
Q

Describe FAP

A

Familial adenomatous polyposis
causes lots of adenoma polyps to grow in large intestine due to dysfunction of APC protein (comes from tumour suppressor gene)
the adenoma polyps grow between 20-30 years of age and by 35 almost always are cancerous as colorectal cancer

415
Q

How do you treat FAP

A

remove all colon because too many polyps to remove individually

416
Q

Describe HNPCC

A

hereditary non-polyp colorectal cancer

loss of DNA repair proteins so leads to colorectal cancers

417
Q

what do we have to consider with HNPCC for treatment

A

some drugs chemotherapy work by inducing apoptosis in the cancer cells but without the repair proteins in HNPCC these drugs would not work so need other drugs

418
Q

What is the most common type of large bowel cancer

A

colorectal cancer

419
Q

What are the two main risk factors for colorectal cancer

A

genetic: FAP, HNPCC

Diet

420
Q

Why does diet increase risk of colorectal cancers

A

can affect bowel transit time, bacterial flora growth in bowel, amino acid content etc.

421
Q

Why does the low fibre, high fat, high protein dit increase risk of colorectal cancer

A

low fibre: increase bowel transit time so longer exposure to carcinogens
high fat: more bile salts produced so bile salts react with NDC bacteria producing carcinogens
high protein: more amino acid transfer by bacteria which produce carcinogens

422
Q

What kind of diet increases risk of colorectal cancer

A

high fat
high protein
low fibres

423
Q

what type of cancer is colorectal cancer

A

adenocarcinoma

424
Q

Where are most colorectal cancers found

A

38% in rectum and sigmoid colon

425
Q

What are the three features of colorectal cancer that are possible

A

ulcerating with bleeding
stenosing with obstruction
polypoid also with bleeding

426
Q

What ways do we assess and code the colorectal cancer

A

resectioning code

staging: Duke’s and TNM

427
Q

What is the resectioning code for colorectal cancer

A

after surgery we do a repeat biopsy to see how much of the tumour we have taken and to check that we have circumferential resection margin positive so we have excised all the tumour
R0, R1, R2

428
Q

What does R0, R1, R2 mean in the resectioning code of colorectal cancer

A

r0: tumour completely excised locally
r1: microscopic evidence of cancer cells in margin so CRM negative
r2: macroscopic evidence of cancer cells in margin so CRM positive

429
Q

How do we stage colorectal cancer

A

TNM and DUKES

430
Q

What are the possibilities with Duke’s A, Dukes B, Dukes C1, c2

A

DA: tumour in mucosal, muscularis mucosa, submucosa, muscularis propria layers
DB: tumour past muscularis propria
DC1: Tumour past muscularis propria and node involved
DC2: tumour past muscularis propria and high nodes involved

431
Q

Describe the TNM stage for colorectal cancer

A

T1N0: tumour in mucosa layer, muscularis mucosal layer, submucosa
T2N0: tumour in muscularis propria layer
T3N0: tumour past muscularis propria
T3N1: tumour past muscularis propria and nodal involvment
T3N2 tumour past muscularis propria and higher nodal involvment
T4: tumour past peritoneal lining

432
Q

What staging dukes and tnm is it for cancer that has passed muscularis propria

A

T3N0

Dukes B

433
Q

What staging dukes and TNM is it for cancer that has entered mscularis propria

A

T2N0

DA

434
Q

what are the different treatments available for colorectal cancer and when do we use them

A

NSAIDS to prevent adenoma polyps
Endoscopy resection for adenoma
surgical resection for adenocarcinoma
chemotherapy and palliative care for metastatic adenocarcinoma

435
Q

What is the most common cancer in the small intestine

A

lymphoma usually no predispose cause

shows as plaques and multiple ones

436
Q

What are the symptoms of lymphomas in the small intestine

A

abdominal pain
anaemia from bleeding
obstruction

437
Q

What is malabsorption

A

problem with small intestine not sufficiently absorbing broken down food
sometimes maldigestion is included in the definition
leads to malnutrition

438
Q

What is maldigestion

A

problem with intra-lumen
not sufficiently breaking down food
leads to malnutrition

439
Q

What can cause malabsorption

A

-problems with lack of digestive enzymes e.g. disaccharidase deficiencies e.g. lactose intolerance
-insufficient surface area e.g.g from Crohn’s, Celiac disease, extensive surface parasitisation, small intestine bypass e.g. from morbid obesity, crohn’s, infarction
-dysfunctional epithelium transport
-insufficient intra-luminal digestion e.g. from pancreas insufficiently e.g. cystic fibrosis, pancreatitis, from lack of bile salts e.g. from biliary obstruction, ilium damage (as here bile salts reabsorbed) so fat not soluble
bacterial outgrowth that eat up food
-lymphatic obstruction e.g. from lymphomas, TB that lead to protein-losing state

440
Q

What are the symptoms of malabsorption

A

diarrhoea
steatorrhoea (stinky poo, floating poo from fat)
weight losing
anaemia from the deficiency of B12 and Fe2+
fatigue

441
Q

What is celiac disease

A

gluten sensitivity enteropathy
autoimmune response to gluten
damage to enterocytes at small intestines with severe reduction in absorptive capacity

442
Q

Where is gluten found in our diet

A

wheat, barley

others

443
Q

When is celiac disease mostly picked up i.e. age groups

A

50-60 mostly
but at any age really
childhood also

444
Q

What is the pathogenesis of celiac disease

A
  • gluten partially digested but some peptides toxic (gliadin, glutenin) are resistant to digestive enzymes
  • these peptides damage tight junctions between small intestine enterocytes which gets an immune response which causes the problems
  • HLA-DQ2 takes gliadin and glutenin to T cells
  • gliadin stimulates IL-15 release which activates T cells and intra-enterocyte lymphocytes
  • death to enterocytes at severe rate so proliferative crypts can’t keep up so villous atrophy
  • crypts still trying to keep up so crypt hyperplasia
445
Q

What do the crypts and villous look like in celiac disease

A 
hyperplasia of crypts
villous atrophy (stages partial->sub-total-> total atrophy)
446
Q

How does celiac disease present

A

persistent unexplained abdominal symptoms: diarrhoea, steatorrhoea, constipation, cramps, indigestion
anaemia due to less B12, Folate, iron absorbed
weight loss
severe or persistent mouth ulcers
irritable bowel syndrome

447
Q

What conditions is celiac disease associated with

A

metabolic bone disease like osteoporosis due to less calcium and vit D absorbed
diabetes type 1
peripheral neuropathy
hyposplenism
unexplained recurrent miscarriages and infertility
down’s and turner’s syndromes

448
Q

What are the complications from celiac disease

A

increased risk of GI cancers
less risk of breast and lung cancer
lactose intolerance and bacterial outgrowth possible

449
Q

What must the patient do before we investigate celiac disease

A

6 weeks before investigations have gluten in more than one meal per day

450
Q

How do we investigate celiac disease

A

full blood count checking for ferritin levels and serology for immunoglobulins and tissue transglutaminase
endoscopy to see less folds in duodenum
duodenum biopsy an histology see villous atrophy and crypt hyperplasia
check osteoporosis risk score, check B12, Vit D, folate for anaemia, measure BMI

451
Q

How do we treat celiac disease

A

no gluten in diet strict and life-long
dietician review
treat deficiencies from malabsorption with supplements
check/monitor osteoporosis risk score
inform patient that 10% chance that first degrees relatives have celiac
pregnant women take even more folate
immunisation offer

452
Q

Name two malabsorption conditions

A

celiac, tropical sprue

453
Q

What is tropical sprue

A

similar pathology to celiac disease but less severe
unclear causes
something to do with abnormal flora bacterial

454
Q

How do we treat tropical sprue

A

gluten-free diet not really helpful

broad spectrum antibiotics better

455
Q

What is pancreatitis

A

inflammation of the pancreas, can be acute or chronic

456
Q

What is acute pancreatitis

A

ranges from mild self-limiting to severe necrotising entire organ
can become chronic or resolve and return to normal

457
Q

what can cause acute pancreatitis

A 
idiopathic
trauma
alcohol
steroids
mumps
pregnancy
autoimmune
vascular injury/insufficiency
hyperthyroidism,
hyperlipidaemia
hypercalcemia
bile reflux
gallstone obstruction of duct
458
Q

What is the pathology of acute pancreatitis

A

depends on cause
e.g. obstruction or bile reflux into duct causes epithelial cell destruction which can spread into gland causing leakage and activation of enzymes whatever the cause the release into the blood of the lytic enzymes causes further damage because of shock and the fact that tissue degradation all over body can happen

459
Q

What is the presentation of acute pancreatitis

A 
abdominal pain that can spread to back
abdominal tenderness
nausea vomiting
shock (severe), fever, tachycardia
jaundice if obstruction cause
460
Q

what is the management of acute pancreatitis

A 
IV fluids, oxygen if needed
feeding support if needed
pain killers
surgical drainage or removal of necrotising organ if needed
thromboprophylaxis
461
Q

What does chronic pancreatitis cause

A

causes irreversible damage and pancreatic insufficiency

462
Q

What causes chronic pancreatitis

A

either relapsing from lots of acute events or primarily chronic
alcohol
gallstone obstruction
cystic fibrosis

463
Q

What is the presentation of chronic pancreatitis

A 
abdominal and back pain
diabetes can occur
nausea
weight loss
diarrhoea
steatorrhea
abdominal XR shows calcified plaques on pancreas
464
Q

What is the management of chronic pancreatitis

A 
pain killers
insulin if diabetes
gallstone removal if there
stop alcohol
surgery of pancreatectomy if pain not going away
pancreatic enzyme replacement in meals
465
Q

What type of cancer is most common in pancreas

A

adenocarcinoma

466
Q

what are the risk factors of pancreatic cancer

A

smoking

diabetes mellitus

467
Q

how do we treat pancreatic cancer

A

surgery remove part of pancreas at least, dudoenum , regional lymph nodes and fix area try
lots of complications and death
very bad prognosis of treatment and cancer

Phase 2a Introductory Clinical Science (7 decks)

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