GI and friends Flashcards
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.
2
Q
What is inflammation of the stomach classed as
A
acute or chronic gastritis
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
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
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
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)
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
8
Q
What are other names for chemical gastritis
A
reactive, type C, bile-reflux gastritis
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
10
Q
What are ulcerations
A
localised defects passing into at least the submucosal layer due to pepsin and acid attack.
11
Q
How can you classify gastroduodenal ulcerations
A
chronic and acute
12
Q
What are the causes of acute ulcers
A
occurs with acute gastritis
ischemia
extreme hyperacidity
13
Q
Where do chronic ulcers most commonly occur
A
mucosal junctions
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.
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
16
Q
How do ulcers heal on their own
A
combination of:
the regeneration of epithelium cells
progressive fibrosis
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)
18
Q
How do we treat ulcerations
A
H2 blockers, PPI
stress relief because stress leads to more acid
enteric coated aspirin
19
Q
What does PPI raise the risk of?
A
C. diff infections
20
Q
What is GORD
A
Gastro-oesophageal reflux disease due to stomach acidic content going into oesophageal
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
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
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
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
25
How do you treat GORD
```
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
```
26
What is hematemesis
blood in vomit
27
What do we call blood in vomit
hematemesis
28
What is haemoptysis
coughing up blood
29
What can cause hematemesis
```
NSAIDS (from ulcers)
peptic ulcer disease
oesophageal varices
malignancy of stomach or oesophagus
Mallory Weiss tear
gastritis
bleeding/coagulation disorder
```
30
What are the two management plans for hematemesis based on
amount of blood loss so
1) lots of blood loss
2) not lots of blood loss
31
How do we manage hematemesis with lots of blood loss
ABC
Oxygen
Fluid replacement e.g. transfusions if needed
treat underlying condition
32
How do we manage hematemesis with not lots of blood loss
gastroscopy
PPI
fluid replacement
treat underlying cause
33
What are varices
dilated veins
34
Where are varices found
distal oesophagus
proximal stomach
isolated varices: distal stomach, large and small intestines
35
What is linked to varices occurring
the size and change of bleeding of varices is linked to the portal pressure which is linked to underlying liver disease severity
36
What can cause oesophageal varices
```
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
```
37
What can increase the risk of oesophageal variceal haemorrhage occurring
```
alcohol intake
physical exercise
increase intra-abdominal pressure
decompensation of liver disease
malnutrition
NSAIDs
Aspirin
bacterial infection
```
38
What are some common symptoms and signs of oesophageal varices
```
hematemesis
dysphagia
abdominal pain
low blood pressure
pallor
tachycardia (shock signs)
peripheral blood shut down
sepsis signs sometimes
low urine output
confusion
```
39
What investigations do you do for oesophageal varices
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
40
How do you manage oesophageal varices
```
vasoactive drug (but NOT for severe hypovolemic shock)
Antibiotic prophylaxis
endoscopic band ligation
transjugular intrahepatic portosystemic shunt
```
41
Give some examples of bowel inflammation
```
Crohn's disease
Ulcerative colitis
diverticulitis disease
ischaemic colitis
infective colitis
```
42
What do we mean by inflammatory bowel disease
Crohn's disease and Ulcerative colitis
43
What are the causes of inflammatory bowel disease
Idiopathic mostly
44
Where are inflammatory bowel disease more common
Northern Europe
| North America
45
Where can Crohn's disease affect?
Whole bowel from mouth to anus
46
Where does Crohn's disease affect most commonly
Ileum
| Colon
47
What is the pattern of Crohn's disease
skip patchy lesions
48
How much of the bowel wall does Crohn's disease affect
can affect full thickness
49
What type of inflammation is seen in Crohn's disease and what are the associated features
```
granulomatous inflammation with:
lymphocytes
strictures and fistulas
fissuring ulcers
Neuromuscular hypertrophy
```
50
What is the course of Crohn's disease
chronic
| exacerbations and remissions
51
What could be the cause of Crohn's disease and give evidence
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
52
Briefly describe the epidemiology of Crohn's disease
females> males
| starts usually at early adulthood
53
How does Crohn's disease present
```
weight loss
malaise
fever
clubbing
arthritis
diarrhoea (can be bloody, can be chronic)
mouth ulcers
anal lesions
abdominal pain
palpable mass in the abdomen
```
54
What are the possible complications of Crohn's disease
```
malabsorption
fistula formation
malignancy
obstruction
perforation
systemic amyloidosis (rare)
```
55
What are the anal lesions possible with Crohn's disease
anal tags
anal fistulas
anal fissures
56
Why could malabsorption occur in Crohn's disease
damage to bowel from disease
resectioning of bowel during surgery leading to short bowel syndrome
fistulas could lead to part of bowel being bypassed
57
Why could obstruction occur in Crohn's disease
neuromuscular hyperplasia so narrowed lumen and thick walls
| progressive fibrosis
58
Why could malignancy occur in Crohn's disease
Crohn's disease increased risk of colorectal cancer due to increased cell turnover
59
How can fistulas form in Crohn's disease
ulcers can lead to fistulas
60
Why would perforation occur in Crohn's disease
ulcers can perforation out of the bowel wall and lead to content leaking into peritoneal space and peritonitis occurring and also haemorrhage can occur
61
What investigations do you carry out for Crohn's disease
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
62
What is the management plan for Crohn's disease
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
63
Where can ulcerative colitis affect?
rectum and colon only
starts at the rectum and ascends usually but never past colon
anal transitional period and anal canal not affected
64
What are three things common in Crohn's disease but not in Ulcerative colitis
granulomas
fissures
fistulas
65
What is the pattern of the lesions in Ulcerative colitis
continuous lesions
66
How much of the thickness of the bowel is affected by ulcerative colitis
superficial mucosa
| ulcers in mucosa and submucosa but in SEVERE can perforate full thickness
67
What are the ulcers like in ulcerative colitis
irregular edges
small
shallow
bleed and produce pus
68
What is the inflammation like in ulcerative colitis
diffuse with plasma cells
69
What is the course of the disease in ulcerative colitis
chronic with exacerbations and remissions
70
Briefly describe the epidemiology of ulcerative colitis
males> females slightly
71
What is the cause of ulcerative colitis
idiopathic
link with autoimmune: immune mistaking commensal organisms as pathogens and attacking
smoking is actually a protective factor
72
What are the presentations of ulcerative colitis
```
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
```
73
Which inflammatory bowel disease would you see anal lesions
Crohn's disease
| Ulcerative colitis has normal anus
74
Which IBD would you see continuous vs patchy lesions
continuous in ulcerative colitis
| patchy in Crohn's disease
75
Which IBD would you see lesions that are superficial vs full thickness of bowel
superficial in UC
| Deep in Crohn's
76
Which IBD only shows in colon and rectum
ulcerative colitis
77
Which IBD shows all over gut: mouth to anus
Crohn's
78
Which IBD has granulomatous inflammation vs diffuse and what are the main cell present
granulomatous with lymphocytes in Crohn's
| Diffuse with plasma cells in Ulcerative colitis
79
Which IBD is slightly more common in men compared to females and vice versa?
UC male slightly more common
| Crohn's disease females slightly more common
80
What are the complications of Ulcerative colitis
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
81
What investigations do you carry out with UC
FBC
Ultrasound
stool sample to exclude infective diarrhoea
Abdominal XR to see air in colon and dilation
endoscopy
82
What is the management plan for UC
```
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
```
83
How do you use corticosteroids in UC
orally, short-term, to induce remission
84
What is a side effect of amino-salicylate
nephrotoxic so monitor
85
What is IBS
Irritable bowel syndrome
one of the major functional bowel disorders
group of symptoms with no evidence of underlying damage
chronic
86
What causes IBS
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
87
Briefly describe the epidemiology of IBS
Women 2-3 times more common than men
88
What is the common presentation of IBS
```
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
```
89
In which IBD is smoking a protective factor
ulcerative colitis
90
How do we diagnose IBS
```
History taking of symptoms
tests to exclude other causes:
blood test- Coeliac disease
endoscopy- IBD
stool sample- infective diarrhoea
```
91
What is the classification of IBS
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)
92
How do we treat IBS
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
93
Give some examples of FODMAP items
```
apples, mango
cow milk and cottage cheese
broccoli and mushrooms
custard
chickpeas
```
94
What is intestinal obstruction
blockage of the lumen of anywhere in the gut with arrest to the onward propulsion of the intestine's content
95
How can we divide the causes of causes of intestinal obstruction
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
96
What causes small bowel obstruction in adults
malignancy
Crohn's
adhesion
hernia
97
What causes small bowel obstruction in children
volvus
insussception
appendicitis
hypertrophic polyps stenosis
98
What are some rare causes of bowel obstruction
diverticulitis
radiation
gallstones
99
What causes large bowel obstruction in Caucasian adults vs Afrocaribbean adults
C: colorectal cancer
A: volvus
100
What causes large bowel obstruction in children
imperforation of anus e.g. missing anus, fistula between anus and rectum
Hirschsprung disease
101
What are the 4 options for classifying causes of obstruction regarding where they are in relation to the bowel lumen
Intraluminal (inside the lumen)
intramural (inside the wall of the bowel)
extraluminal (outside the bowel)
other
102
What are some causes of obstruction that occur in the lumen
diaphragmatic disease
tumours e.g. colorectal cancers and lymphomas
meconium ileus
gallstone ileus
103
What are some causes of obstruction that occur in the wall of the bowel
tumours e.g. colorectal cancers, gastrointestinal stromal tumours
Hirschsprung disease
Crohn's disease
Diverticulitis
104
What are some causes of obstruction that occur outside the bowel
peritoneal cancers e.g. ovarian cancer spread to cavity
volvulus
adhesion
105
What are some "other" causes of obstruction not intraluminal, intramural, extraluminal
a hernia
atresia
intussusception
106
What is diaphragmatic disease and where does it cause obstruction
intraluminal obstruction
due to lots of NSAID use and recurrent ulcerations
fibrous band/diaphragm forms in lumen
107
What is meconium ileus and where does it cause obstruction
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
108
What is gallstone ileus and where does it cause obstruction
intraluminal obstruction
gallstone causes obstruction. stone gets in from cholecyto-enteric fistula when stone in gallbladder erodes out of the gallbladder and into bowel.
109
What is Hirschsprung disease and where does it cause obstruction
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
110
What are adhesions in bowel obstructions and where does it cause obstruction
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
111
What are volvulus and where do they cause obstruction
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.
112
what is the method of obstruction in Hirschsprung disese
paralytic obstruction
113
What is the method of obstruction in volvulus
closed loop obstruction
114
What is a hernia and what type of obstruction does it cause
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
115
What is intussusception
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
116
What are the two types of intussusception
idiopathic
| eneteroenteral intussusceptions e.g. jejunojenal, jejunoileal, ileoileal
117
What is atresia
when there is absence of opening in hallow structure
118
What are two types of obstructions associated with cystic fibrosis
intussusception
| meconium ileus
119
What are the common symptoms of small bowel obstruction
```
vomiting: projectile, feculent, early sign
constipation, obstination late sign
pain
distension
tenderness
```
120
What are the common symptoms of large bowel obstruction if caused by malignancy or strictures
```
vomiting: late sign
constipation, obstination early sign
pain
tenderness
discomfort
nausea
weight loss
bloody stool
tenesmus
bloating
```
121
What are the common symptoms of large bowel obstruction if caused by volvus
sudden pain
| distenstion
122
When is distension due to obstruction largest
the more distal the obstruction the larger the distension
123
What does obstipation mean
no stool passes
124
What does tenesmus mean
hard to pass stool
125
How does small bowel obstruction cause pathology
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
126
Why does necrosis, ischaemia, perforation occur in obstruction of small bowel
dilation of bowel causes more pressure on intramural vessels so less blood flow
127
why does pain, nausea, anorexia, vomiting, electrolyte imbalance occur in obstruction of small bowel
more secretion occurs due to dilation of bowel which leads to the following
128
How does large bowel obstruction cause pathology
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
129
What are useful imagining techniques to complete with obstruction intestinal
XR
| CT
130
What would you see on an XR to indicate small, large bowel obstruction, cecum, sigmoid obstruction
larger than 3 cm small bowel- SBO
larger than 6 cm large bowel- LBO
larger than 9 cm cecum or sigmoid- obstruction
131
How would you manage obstruction intestines
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
132
What type of obstruction intestinal would you operate immediately vs watch and wait
volvus watch and wait
| hernia immediate operation
133
What is intestinal ischaemia
reduced blood flow to intestines
134
What are the three types of intestinal ischaemia
```
ischaemic colitis (large bowel)
acute and chronic mesenteric ischaemia (small bowel)
```
135
What can cause ischaemia colitis
```
thromboembolism
hypotension
hypovolaemia
obstruction
CV surgery
vasoactive drugs
```
136
How does ischaemia colitis cause pathology
- 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
137
What do we call ischaemic colitis if there is necrosis vs. if there is no necrosis
gangrenous ischaemia for necrosis
| non-gangrenous ischaemia for no necrosis
138
What are the three phases of presentation of ischaemic colitis
hyperactive phase
paralytic phase
shock phase
139
What is the presentation of the hyperactive phase of the ischaemic colitis
bloody stool
sudden pain usually in left lower quadrant
most people recover here
140
what is the presentation of paralytic phase of ischaemic colitis
no bloody stool
no abdominal sounds
pain more diffuse now
141
What is the presentation of the shock phase of ischaemic colitis
signs of septic shock
abdominal guarding
rebound tenderness
142
What phase of ischaemic colitis would you see bloody stool?
hyperactive phase
143
What phase of ischaemic colitis would you see diffuse pain
paralytic phase
144
How do you diagnose ischaemic colitis
XR- air in colon
CT- thick walled colon
Lab results: high lactate, high creatine kinase, leukocytosis, metabolic acidosis
colonoscopy: oedema, cyanosis, ulcers
145
How do we treat ischaemic colitis
anti-platelet drugs
surgery if signs of sepsis or peritonitis
supportive care: IV fluids, bowel rest
reduce the risk of atherosclerosis
146
What causes mesenteric ischaemia
arteriole embolism
arteriole thrombus
venous thrombus
147
How does mesenteric ischaemia cause pathology
```
sudden loss of blood flow to intestines
hypoxia
haemorrhagic infarction and necrosis
can perforate and release contents to peritoneal cavity
causing sepsis
```
148
What is the presentation of mesenteric ischaemia
```
periumbilical pain
nausea
vomiting
diarrhoea (bloody at later stage)
leukocytosis
fever
gangrenous intestine
```
149
How do we treat mesenteric ischaemia
acute: supportive care
| surgery if continuous or becomes chronic
150
What are the 4 features that hernias can have and what do they mean
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
151
What are the 4 main types of abdominal hernias
inguinal-most common
femoral
hiatus
incisional
152
What does hiatus hernia mean
stomach contents protrude through the diaphragm into the thoracic cavity
153
What does incisional hernia mean
abdominal contents protrude through incisional scar from surgery
usually within 3 years of surgery
154
What type of abdominal hernia is the most common
inguinal hernia
155
Where is the inguinal canal and what runs in it
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
156
What are the two types of inguinal hernias and describe them
direct: abdominal content protrude through a defect hole in the posterior wall of the inguinal canal
indirect: abdominal content protrude through the deep ring
157
What are the causes of inguinal hernia
```
anything that can cause increased intra-abdominal pressure or weakness to abdominal muscles e.g.
chronic cough
obesity
constipation
old age
heavy lifting
```
158
What are the presentations of ingional hernia
asymptomatic or symptomatic
pain esp. when coughing
change in bowel habits
burning sensation in groin
159
How do we treat inguinal hernia
surgery, same surgery for both types
| if small and asymptomatic don't do surgery
160
What key structures pass under the inguinal ligament and in what order
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
161
What is a femoral hernia
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
162
Give some examples of the job of the liver
glucose and fat metabolism
albumin, clotting factor synthesis
bilirubin, ammonium, drugs, pollutants, hormone excretion
163
What kind of tests can we do to investigate the liver
Liver function tests
imaging: abdominal CT, XR, Ultrasound
Immunological testing
liver biopsy
164
What do the liver function tests look at:
liver enzymes which are released upon liver cell death/damage
bilirubin
albumin
iron
165
What liver enzymes do we look at in LFT
aspartate amino transferase (AST)
alanine amino transferase (ALT)
Gamma-glutamyl-transferase (GGT)
Alkaline phosphatase
166
What do we look for in liver immunological testing
auto-antibodies
level of immunoglobulins and antibodies
antigens and antibodies against viruses
167
Looking at what gives an indication of the liver function
bilirubin, albumin, immunoglobulin, clotting factor levels
| not the liver enzymes
168
Describe the bilirubin pathway of getting it out via urine starting with the RBC
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
169
Describe the bilirubin pathway of getting out via stool starting with the RBC
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
170
What is jaundice in a simple term
yellow skin
171
What is the simple cause of jaundice
increase in serum bilirubin
| over 50 micromols/L
172
What are the three types of jaundice
prehepatic (unconjugated)
intrahepatic (conjugated/ cholestasis)
posthepatic (conjugated.cholestasis)
173
What is the cause of prehepatic jaundice
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
174
What is the presentation of prehepatic jaundice
```
normal urine, stool
yellow skin
enlarged spleen
no itching
due to high serum unconjugated bilirubin without changes to urobilin, stercobilin or conjugated bilirubin
```
175
What is intrahepatic jaundice caused by
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
176
What is the presentation and blood results of intrahepatic jaundice
low urobilin and low stercobilin so dark urine and pale stool
yellow skin because high serum conjugated and unconjugated bilirubin
enlarged spleen
itching possibly
177
What is the cause of posthepatic jaundice
damage to the biliary tree e.g. inflamed, obstructed, swollen e.g. from
pancreatic cancer
gallstones
cholangitis
178
What is the presentation and blood results of posthepatic jaundice
```
high serum conjugated bilirubin
Normal serum unconjugated bilirubin
yellow skin
low urobilin and stercobilin so dark urine and pale stool
itching possible
```
179
How can we treat the itching in jaundice
anti-histamines, plasmapheresis, UV light, opiate antagonist but these won't make it go away fully, only treating the cause of jaundice will.
180
What is the likely cause of dark urine, pale stool, yellow skin
conjugated jaundice
181
What is the likely cause of normal urine, normal stool, yellow skin
unconjugated jaundice
182
Does high liver enzymes suggest obstruction
no, suggests liver disease
183
what are the types of liver diseases
hepatitis: viral, alcohol, drug, immune
neoplasm
congestion
ischemia
184
what are the types of liver obstructions
gallstones
strictures: ischaemia, malignancy, inflammatory
blocked stent
185
What are the two options for endpoints of acute liver injury
liver failure
| recovery
186
What are the main causes of acute liver injury
```
viral hepatitis
alcohol high consumption
adverse drug reactions
congestion from heart failure
vascular injury (rare as has two blood supplies)
biliary tree obstruction
```
187
What is the main presentation of acute liver injury
malaise
nausea
anorexia
jaundice
188
What are some rare presentations of acute liver injury
coma, confusion- accumulate toxic metabolites which mimic neurotransmitters
liver pain
hypoglycaemia
bleeding -low clotting factors produced
189
What happens to the cells in acute liver injury
cell damage and loss via necrosis and apoptosis
| neutrophils suggest necrosis
190
How can we classify the viruses that infect the liver
the ones that infect the liver only
| the ones that infect the liver via systemic infections
191
Which viruses only infect the liver
hepatitis A, B, C, D, E, G
192
which viruses infect the liver as part of a systemic infection
```
epstein Barr virus
yellow fever
adenovirus
varicella virus
herpes virus
cytomegalovirus
```
193
What are the symptoms of viral hepatitis
malaise
fever
jaundice
upper abdominal discomfort
194
How long do viral hepatitis symptoms last
3-4 weeks then recover
| some can become chronic though
195
Which viruses are likely to cause chronic viral hepatitis
hepatitis B, C, D
196
Who often get alcohol liver injury: alcoholics or non-alcoholics
non-alcoholics more commonly
| i.e. not alcohol dependent
197
What is the spectrum of alcohol liver injury
fatty changes
acute hepatitis in Mallory hyaline due to cytoskeletal protein accumulation and neutrophil invasion
portal fibrosis
cirrhosis
198
How does alcohol cause liver injury
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
How does the liver try and deal with the alcohol liver injury
tries to compensate but eventually cannot (long period or trigger e.g. infection) so acute liver decompensation occurs
200
How do we treat alcohol liver injury
spironolactone, gastroectomy, bands on varicies
201
What is fat accumulation in the liver called
steatosis
202
what does steatosis mean
fatty accumulation in liver
203
Which zone of the liver is fibrosis most common in
zone 3
204
Why must we consider drugs with liver injury
liver involved in metabolism, coagulation, excretion of toxic substances including drugs
drug-induced liver injury could occur
205
What are the two mechanisms of action of drug-induced liver injury
hepatocellular (damage to cells like viral hepatitis)
| cholestatic (damage to bile production and excretion ability of liver)
206
What would cause you to suspect a drug-induced liver injury from the history
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
How long do most drug-induced liver injuries resolve with abstinence of the drug
3 months for 90% of cases
| 5-10% prolonged
208
What are some usual suspects of DILI
```
antibiotics
immunosuppressants
analgesics
GI, MSK, CNS drugs
multiple drug interactions
dietary supplements
```
209
What are some safe drugs for people with liver disease
paracetamol
short-acting benzodiazepine
monitor diuretics
210
What two drugs types would you definitely avoid with liver disease
ACE-i
| aminoglycosides
211
When is paracetamol dangerous for the liver
overdose
| causes paracetamol-induced liver injury
212
How do you treat a paracetamol-induced liver injury
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
What things would indicate bad prognosis and paracetamol-induced liver failure
presents late, NAC less effective >24 hours
acidosis
prothrombin>70 seconds
serum creatine>300mmols/L
214
What is N-acetyl cysteine's mechanism of action
activates glutathione transferase which converts dangerous metabolite into a stable metabolite
215
What is the main cause of biliary obstruction causing liver injury
gallstones
216
What are the symptoms of biliary obstruction causing liver injury
colicky pain
fever if there is a superimposed infection
jaundice
217
What is the mechanism of action of biliary obstruction causing liver injury
portal tract fibrosis
| secondary biliary cirrhosis via nodular regeneration
218
What is an example of a vascular injury to cause liver injury
hepatic vein occlusion
219
What can cause hepatic vein occlusion
thrombus e.g. in Budd-Chiari syndrome
venous-occlusive disease e.g. from radiation
membrane obstruction
220
How do we treat hepatic vein occlusion
anti-coagulation therapy
transjugular-intrahepatic-portosystemic shunt
liver transplant
221
What is the definition of chronic hepatitis
clinical or histological evidence of liver inflammation lasting more than 6 months
222
What are the options for what chronic hepatitis can lead to
fibrosis (and cirrhosis)
recovery (does not mean resolution necessarily)
liver failure
varices
hepatoma
(cirrhosis can also lead to the other four)
223
What do we call severe fibrosis in the liver
cirrhosis
224
What are the causes of chronic liver injury
```
autoimmune
alcohol
drugs
viral hepatitis B, C
non-fatty liver disease
metabolic: iron, copper overload, antitrypsin alpha-1 deficiency
```
225
What are the common presentations of chronic liver injury
```
malaise
anorexia
easy bruising
hematemesis
ascites
oedema
itching
hepatomegaly
```
226
What are the rare presentation of chronic liver injury
jaundice
| confusion
227
Which type of liver injury: acute or chronic would you most likely see jaundice
acute
228
What is cirrhosis
irreversible disturbance to the liver architecture in all its entirety associated with fibrosis and nodular regeneration (lobules replaced with nodules in liver)
229
What are the stages of cirrhosis with regards to histology
small nodules-> cirrhosis micronodules-> large macronodules
230
What are the complications of cirrhosis
portal hypertension, carcinoma, liver failure
231
What are the two ways that the body can deal with cirrhosis
compensatory
| decompensate
232
What occurs in cirrhosis compensation
no changes to liver function
| inactive causative agent
233
What occurs in cirrhosis decompensation
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
What can cause portal hypertension
cirrhosis, thrombus, fibrosis
235
Why does portal hypertension occur
increased hepatic resistance and increase splenic blood flow
236
What is spider naevi and what causes it
hyperoestrogenism from decompensation of liver
| small vascular lesions on skin
237
What are the complications of portal hypertension
varices
| splenomegaly
238
Why is there a risk of carcinoma from cirrhosis
cirrhosis has lots of cell turnover to create nodules so more room for errors while replicating
239
What are 3 types of primary liver tumours
hepatocellular carcinoma
cholangiocarcinoma
angiosarcoma
240
What is the main primary liver tumour
hepatocellular carcinoma
241
What increases your risk of hepatocellular carcinoma
men>women
cirrhosis
viral hepatitis B and C
haemochromotosis
242
How does hepatocellular carcinoma present
decompensation of liver disease symptoms
weight loss
ascites
abdominal pain
243
What is the treatment for hepatocellular carcinoma
liver transplant
resectioning of tumour but usually too much cirrhosis
sorafenib to prolong life
244
What metastatic tumours commonly present in the liver
breast, bowel, pancreas, lung
245
What are the main types of autoimmune liver conditions
autoimmune hepatitis
primary biliary cirrhosis
sclerosing cholangitis
246
which gender is most at risk of autoimmune liver conditions
females
247
What is the histological picture of autoimmune hepatitis
like chronic hepatitis
| lots of plasma cells and rosette style arrangement of swollen liver cells
248
What auto-antibodies are there in autoimmune hepatitis
anti-smooth muscle antigens
anti-kidney-liver microsome antigens
anti-DNA
249
What is the raised globin type in autoimmune hepatitis
lgG
250
What is the histological picture of primary biliary cirrhosis
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
What are two symptoms of primary biliary cirrhosis
itching
| fatigue can be disabling
252
How do you treat fatigue in primary cirrhosis
not a reason for transplant anymore
| treat with Modafinil
253
How do you treat the lack of bile in primary biliary cirrhosis
ursodeoxycholic acid
254
What benefit does ursodeoxycholic acid give to primary biliary cirrhosis
```
improves liver enzyme function
reduces inflammation
reduces portal pressure and so risk of varices bursting
reduces need for transplants
reduces death rate
```
255
What benefit does ursodeoxycholic acid not give to primary biliary cirrhosis
it doesn't stop the itching
| it doesn't remove or stop the fibrosis
256
What are the auto-antibodies against in primary biliary cirrhosis
anti-mitochondria
257
What is the raised immunoglobulin in primary biliary cirrhosis
IgM
258
How useful is steroid use for autoimmune hepatitis
good
259
How useful is steroid use for primary biliary cirrhosis
limited effect
260
What is sclerosing cholangitis
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
Which two autoimmune liver conditions can cause ductapenia
sclerosing cholangitis
| primary biliary cirrhosis
262
What is ductapenia
no functioning duct
263
What is the raised immunoglobulin and what is the auto-antibody in sclerosing cholangitis
varied raised immunoglobulin
anti-neutrophils
cytoplasmic
264
What are the symptoms of sclerosing cholangitis
itching
pain
rigours
jaundice
265
How do we treat sclerosing cholangitis
liver transplant
steroid little use
ursodeoxycholic acid unclear use
266
What condition is associated with sclerosing cholangitis
ulcerative colitis
267
Which autoimmune liver condition is associated with ulcerative colitis
sclerosing cholangitis
268
Describe the different types of iron overload in the liver
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
What is the genetic risk that can give you hemochromatosis
C282Y in homozygous states
| accumulation of iron
270
What can iron removal do to help iron overloaded liver
reverse fibrosis sometimes
271
What is the genetic disorder that leads to copper accumulation
Wilson's disease
272
What is Wilson's disease
an autosomal recessive condition where copper accumulates in the liver and basal ganglia because liver can't secrete copper in bile
273
What are the complications of Wilson's disease
chronic hepatitis
| cirrhosis
274
Where is anti-trypsin alpha-1 made and secreted
made in liver and immediately secreted into blood
275
What is anti-trypsin alpha-1
anti-proteolytic protein
276
What is the disposition that gives you a deficiency in alpha-1 anti-trypsin
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
What will alpha-1 anti-trypsin give you a predisposition to?
hepatic cirrhosis
| emphysema
278
What is a definition of a patient with non-alcoholic fatty liver disease
```
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
How do you treat non-alcoholic fatty liver disease
no treatment
| losing weight can help
280
What is another name for gallstones
cholelithiasis
281
What are cholelithiasis
gallstones
282
where do gallstones mostly happen and what symptoms
mostly gallbladder and asymptomatic but can happen in bile duct also and with symptoms
283
What would suggest that the gallstone was in the gallbladder
cholecystitis
no cholangitis or pancreatitis
maybe jaundice
biliary pain
284
What would suggest that the gallstone is in the bile duct
```
pancreatitis
cholangitis
no cholecytitis
biliary pain
obstruction jaundice
```
285
What are the risk factors for gallstones
female
obese
diabetes mellitus
286
What are gallstones made off and why do they occur
cholesterol 70%
bile 30%
+/- calcium
occur due to an imbalance between cholesterol and bile salts with cholesterol increasing and bile salts decreasing
287
How do you treat gallstones
in gallbladder: laparoscopic cholecystectomy and bile acid dissolution therapy
in bile duct: sphincterotomy, remove gallstone, stent
288
What are patients with liver dysfunctions at risk to
```
infections
endocrine problems
coagulopathy
malnutrition
hypoglycaemia
```
289
Why are patients with liver dysfunctions at risk to infections
impaired reticuloendothelial system
| impaired leukocyte function
290
What type of infections are patients with liver dysfunctions at risk to
```
spontaneous bacterial peritonitis
septicemia
UTI
skin infections
pneumonia
```
291
What things could trigger an exacerbation in a person with chronic liver conditions
```
GI bleeds
Cardio problems
intra-cranial problems
drugs
alcohol withdrawal
infections
low sodium
low potassium
hypoglycaemia
```
292
What is ascites
detectable abnormal or chronic fluid collection in the peritoneal cavity
293
how much fluid is there physiologically in men and women
men little or none
| females 20ml
294
What are the stages of ascites
1) detectable only after careful examination
2) easily detectable but not a lot
3) obvious but not tense ascites
4) tense ascites
295
What are some causes of ascites
```
heart failure
TB
malignancy
pancreatitis
cirrhosis (main one)
```
296
What are the three methods of getting ascites and give an example or few for them
portal hypertension- cirrhosis
non-portal hypertension- malignancy, nephrotic syndrome, heart failure
chylous ascites: trauma, abdominal surgery, radiation, congenital
297
What is the type of fluid which could be in ascitic fluid
exudate (proteins and fluid) or transudate (fluid only, no proteins)
298
How does exudate fluid enter peritoneal space in ascites
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
How does transudate fluid enter peritoneal space in ascites
imbalance between oncotic pressure and hydrostatic pressure
| pushes fluid out only
300
What are the causes of ascites with exudate fluid
```
malignancy
Infection
pancreatitis
bowel obstruction
bowel leak
```
301
What are the causes of ascites with transudate fluid
- 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
What is the clinical picture of ascites
```
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
What methods do we use for diagnosis of ascites
- 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
What do we do with the ascites tap
culture for pathogens
cytology if cancer suspect
protein count- amylase high suspect pancreatitis, SAAG, total protein count
305
What is the SAAG,
| for exudate and transudate
SAAG (serum ascites albumin gradient)
exudate <1.1g/dL low
transudate >1.1g/dL high
306
What is the total protein for exudate and transudate from ascites tap
exudate >2.5
| transude <2.5
307
What is the management plan for ascites
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
What is the major complication of ascites and why
spontaneous bacterial peritonitis
| static fluid in ascites means high potential for infection
309
What is spontaneous bacterial peritonitis
bacterial infection of the ascitic fluid in the absence of other intra-abdominal causes.
Commonly klebsiella spp. streptococci pneumonia, E. coli cause it
310
What are the symptoms of spontaneous bacterial peritonitis
If ascites occurs due to liver problem then liver decompensation commonly
commonly asymptomatic but abdominal pain, tense abdominal walls, fever also can occur
311
How do we treat spontaneous bacterial peritonitis
diagnose SBP first then treat, usually hard to find the pathogen
broad antibiotic: cephalosporin IV
drain fluid
312
What is peritonitis
Inflammation of the peritoneum which lines the peritoneal cavity. usually caused by the presence of air, pathogens, GI contents, blood
313
How can we classify peritonitis
acute/chronic
causes: primary/secondary
location: localised/generalised
314
what are primary causes of peritonitis
rare
| usually from the haematological or lymphatic spread of irritants
315
Who is most at risk of primary causes of peritonitis
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
What are secondary causes of peritonitis
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
What is localised peritonitis
local inflammation of an underlying organ before perforation
318
What are some symptoms of localised peritonitis
less rapid onset
symptoms of underlying cause
guarding local area
319
What is generalised peritonitis
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
What are some symptoms of generalised peritonitis
quick onset
guarding whole area by lying completely still
quick sudden pain
321
What are the symptoms of peritonitis caused by intestinal obstruction
colicky pain central abdominal
peritonitis occurs only if the bowel is threatened
bilious vomiting
322
What are the symptoms of peritonitis caused peptic ulcers and what is the treatment
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
What is acute appendicitis
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
What are the symptoms of appendicitis
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
How do you treat appendicitis
antibiotics
bowel rest
appendectomy
326
What is ectopic pregnancy
conceptions placed in area other than uterine cavity e.g. most commonly in the fallopian tube
327
Why do you always suspect ectopic pregnancy in females of childbearing age
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
What are you worried about in peritonitis with women of child-bearing age
ectopic pregnancy
329
What are two less common causes of peritonitis that involve the immune system
autoimmune diseases e.g. lupus
| systemic infections e.g. TB
330
What is the treatment of ectopic pregnancy
call gynaecologist
blood transfusion usually
surgery
331
What are the symptoms and signs of peritonitis
```
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
Why do you get fever and chills in peritonitis
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
What are the investigations we do for peritonitis
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
How do we manage peritonitis
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
What are the complications from peritonitis
- 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
You have performed surgery for your peritonitis patient and they are not improving what are you going to suspect
peritoneal abscess
occurs esp. after surgery
collection of pus in peritoneal cavity that is guarded by inflammatory barrier
337
What factors can reduce a patients chance of survival after and before treatment for peritonitis
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
Why is septicaemia easy to occur from peritonitis
peritoneum is highly permeable
large surface area
drained by lymphatic vessels
all mean easy for pathogens to reach systemic circulation
339
What is helicobacter pylori and how does it survive
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
How does helicobacter pylori cause pathology
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
What are the symptoms of helicobacter pylori infection
epigastric pain, nausea
| can be asymptomatic often
342
How do we treat helicobacter pylori infection
omeprazole
| amoxicillin and clarithromycin
343
What is diarrhoea
3 or more loose stools per day
| "loose" can be different for different patients
344
What is a way we can classify stool
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
Who is at risk of diarrhoea
children in nursery
people working with uncooked food
people working with vulnerable people
people with unsatisfactory hygiene
346
How big is diarrhoea a cause for infant mortality
2nd leading cause of death in infants is diarrhoea due to malnutrition mainly
347
What key things do we want to ask about in history for diarrhoea
travel, animal, family history
food/water taken?
immunocompromised
348
```
What are suspecting with these cases of diarrhoea:
fresh water
well water
puppies
reptiles
flooding
Raspberries
small children
```
```
fresh-water- Aeromonas
well water- giardiasis
puppies- campylobacter
reptiles- salmonella
flooding- cryptosporidiosis
Raspberries- cycospora
small children- rotavirus, shigella
```
349
What is the most common cause of diarrhoea
viral
350
What are the three most common causes of viral diarrhoea
norovirus
rotavirus
adenovirus (less common than other two)
351
When do rotavirus outbreaks occur
developing countries: year round
| developed countries: dec to march
352
When do norovirus outbreaks occur
winter more common but year round can occur
353
Where do we worry about norovirus outbreaks
nurseries
nursing homes
hospitals
cruise ships
354
What is traveller's diarrhoea
```
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
What most commonly causes traveller's diarrhoea
bacterial- ETEC, shigella
| and others: norovirus, giardia
356
What are the two types of diarrhoea that bacteria can cause and name some examples
inflammatory- EIEC, Shigella, non-typhoid salmonella
| secretory: ETEC, EHEC, Vibrio cholera
357
When does c. diff occur
after taking lots of antibiotics usually
358
What is c.dif
clostridium difficile
gram-positive bacteria
produces a toxin: toxin A
359
Who is at risk of getting diarrhoea with c.diff
```
older patients
co-morbidities
PPI
immunocompromised
long hospital stay
antibiotics: co-amoxiclav, clindamycin, cephalosporin, ciprofloxacin
NG feeding tube
post-operative
```
360
What can be the presentation of c. diff infections
asymptomatic carriage
not severe illness responding well to withdrawal of antibiotics
severe illness with diarrhoea, fever, enteritis
361
How do you treat c. diff infections
oral vancomycin
metronidazole
rifampicin
stool transplant from healthy patient
362
What is the best way to clean to protect yourself for c.diff
soap and water
| c.diff has spores that are resistant to alcohol gel
363
How is c.diff transferred
faecal-oral route
| spores
364
What are two ways we can classify diarrhoeal illnesses
infective and non-infective causes
365
What is one of the reasons why diarrhoeal illnesses can lead to death in children
significant fluid loss
366
What protozoa can cause diarrhoea
entamoeba
giardia
cryptosporidium
367
What helminths can cause diarrhoea
Strongyloides
schistosomiasis
in general helminths don't cause diarrhoea
368
What are some symptoms of schistosomiasis infection
```
fever
cough
wheeze
diarrhoea
eosinophilia
hepatosplenomegaly
```
369
What are some symptoms from Strongyloides infection
```
cough
wheeze
eosinophilia
diarrhoea
can be asymptomatic
```
370
What are the methods of transfer of diarrhoeal illness give examples
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
What are some non-infective causes of diarrhoea
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
How do we treat diarrhoeal illnesses
zinc replacement
fluid replacement prevent dehydration
treat underlying cause
373
What are three infective biliary diseases
ascending cholangitis
acute cholecystitis
liver abscess
374
What is ascending cholangitis
bacterial infection of the biliary tree
| obstruction
375
What are the symptoms of ascending cholangitis
charcot triad
| fever, RUQ pain, jaundice
376
What investigations do we do for ascending cholangitis
bloods
ultrasound
endoscopy
377
how do we treat ascending cholangitis
IV fluids, antibiotics
remove stones if any
stenting
378
What is acute cholecystitis
infection of gallbladder
379
What are the symptoms of acute cholecystitis
fever
RUQ pain
high inflammatory markers
380
What is a complication of acute cholecystitis
reccurrent acute cholecystitis can cause pancreatitis
| esp. if obese and diabetes
381
what are the two causes of liver abscesses
bacterial infection
| amoebic infection
382
Which bacteria are most common in causing liver abscesses
E. coli
klebsiella pneumonia
streptococcus milleri
383
How can bacterial infections cause liver abscesses
```
can enter from biliary tree
haematogenous spread
infection of tumour or cyst
trauma
direct extension from gallbladder
```
384
What are the clinical features of liver abscesses
```
fever
RUQ pain
weight loss
obstructive jaundice
right shoulder pain
```
385
What is diverticular disease
outpouching of mucosal layer through hole in muscularis layer in large intestine esp. signoid
386
What is diverticulitis
when there is material in out-pouches of mucosal layer that become infected
387
What are the symptoms of diverticulitis
fever
abdominal pain
high WCC
diarrhoea/constipation
388
How do we treat diverticulitis
co-amoxiclav and percutaneous drainage
| try and treat conservatively but surgery used if complications e.g. obstruction
389
What are the benign types of oesophageal cancers
rare
leiomyoma (most common benign)
lipoma
Fibroma
390
What are the common malignant oesophageal cancers and rarer ones
adenocarcinoma, squamous cancer
| rare; sarcoma, melanoma
391
What are the symptoms of malignant tumours of the oesophageal
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
What is squamous cancer of the oesophageal
from squamous cells
| maybe procceded by dysplastic cells
393
What are the risk factors for squamous cancer of the oesophageal
```
vitamin deficiencies
tobacco
alcohol
men
repeated thermal injury
nitrosamine in food
human papillomavirus
```
394
What are the predisposing conditions to adenocarcinoma in oesophagus
gastroesophageal reflux
| barrett's oesophagus
395
What happens in gastro-oesophageal reflux to cause cancer
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
What happens in Barrett's oesophageal
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
Why do different cells grow in Barrett's oesophageal
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
How do we treat oesophageal cancers
surgery if early
| usually present late so palliative
399
what is the most common type of gastric cancers and how are they classified
adenocarcinoma
| intestinal and diffuse adencarcinoma
400
What are intestinal adenocarcinomas
those that arise usually from intestinal metaplasia
| (normal gastric cells->intestinal metaplasia ->dysplasia-> early gastric cancer -> advanced gastric cancer
401
What are diffuse adenocarcinomas
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
What do we mean by early and advanced stages of gastric cancer
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
How do gastric cancers present
```
dysphagia
nausea
indigestion
loss of appetite
weight loss
hematemesis
```
404
What are the types of tumours that grow in the large intestine
adenoma
| adenocarcinoma
405
What are the type of tumours that grow in the small intestine
lymphoma
| endocrine cell tumours
406
What are polyps and where are they most found
protuberant outgrowths
| mostly in large intestine
407
What are adenoma polyps
benign epithelial polyps
408
What is the main type of polyp in the LI
adenoma polyps
409
What polpy predispose patients to colorectal cancer
colorectal polyp
410
What is the precursor of most colorectal cancers
adenomas
411
What makes a polyp more likely to progress to become cancerous
the larger the polyp the more likely it will become cancerous
412
What are two genetic conditions that increase the risk of colorectal cancer
FAP (Familial adenomatous polyposis)
| HNPCC (hereditary non-polyps colorectal cancer)
413
What are the causes of gastric cancers
```
genetic (CDH1 germline mutation)
smoking
diet (eating smoked, processed food)
obesity
helicobacter pylori
previous gastric surgeries
```
414
Describe FAP
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
How do you treat FAP
remove all colon because too many polyps to remove individually
416
Describe HNPCC
hereditary non-polyp colorectal cancer
| loss of DNA repair proteins so leads to colorectal cancers
417
what do we have to consider with HNPCC for treatment
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
What is the most common type of large bowel cancer
colorectal cancer
419
What are the two main risk factors for colorectal cancer
genetic: FAP, HNPCC
| Diet
420
Why does diet increase risk of colorectal cancers
can affect bowel transit time, bacterial flora growth in bowel, amino acid content etc.
421
Why does the low fibre, high fat, high protein dit increase risk of colorectal cancer
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
What kind of diet increases risk of colorectal cancer
high fat
high protein
low fibres
423
what type of cancer is colorectal cancer
adenocarcinoma
424
Where are most colorectal cancers found
38% in rectum and sigmoid colon
425
What are the three features of colorectal cancer that are possible
ulcerating with bleeding
stenosing with obstruction
polypoid also with bleeding
426
What ways do we assess and code the colorectal cancer
resectioning code
| staging: Duke's and TNM
427
What is the resectioning code for colorectal cancer
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
What does R0, R1, R2 mean in the resectioning code of colorectal cancer
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
How do we stage colorectal cancer
TNM and DUKES
430
What are the possibilities with Duke's A, Dukes B, Dukes C1, c2
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
Describe the TNM stage for colorectal cancer
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
What staging dukes and tnm is it for cancer that has passed muscularis propria
T3N0
| Dukes B
433
What staging dukes and TNM is it for cancer that has entered mscularis propria
T2N0
| DA
434
what are the different treatments available for colorectal cancer and when do we use them
NSAIDS to prevent adenoma polyps
Endoscopy resection for adenoma
surgical resection for adenocarcinoma
chemotherapy and palliative care for metastatic adenocarcinoma
435
What is the most common cancer in the small intestine
lymphoma usually no predispose cause
| shows as plaques and multiple ones
436
What are the symptoms of lymphomas in the small intestine
abdominal pain
anaemia from bleeding
obstruction
437
What is malabsorption
problem with small intestine not sufficiently absorbing broken down food
sometimes maldigestion is included in the definition
leads to malnutrition
438
What is maldigestion
problem with intra-lumen
not sufficiently breaking down food
leads to malnutrition
439
What can cause malabsorption
-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
What are the symptoms of malabsorption
diarrhoea
steatorrhoea (stinky poo, floating poo from fat)
weight losing
anaemia from the deficiency of B12 and Fe2+
fatigue
441
What is celiac disease
gluten sensitivity enteropathy
autoimmune response to gluten
damage to enterocytes at small intestines with severe reduction in absorptive capacity
442
Where is gluten found in our diet
wheat, barley
| others
443
When is celiac disease mostly picked up i.e. age groups
50-60 mostly
but at any age really
childhood also
444
What is the pathogenesis of celiac disease
- 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
What do the crypts and villous look like in celiac disease
```
hyperplasia of crypts
villous atrophy (stages partial->sub-total-> total atrophy)
```
446
How does celiac disease present
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
What conditions is celiac disease associated with
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
What are the complications from celiac disease
increased risk of GI cancers
less risk of breast and lung cancer
lactose intolerance and bacterial outgrowth possible
449
What must the patient do before we investigate celiac disease
6 weeks before investigations have gluten in more than one meal per day
450
How do we investigate celiac disease
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
How do we treat celiac disease
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
Name two malabsorption conditions
celiac, tropical sprue
453
What is tropical sprue
similar pathology to celiac disease but less severe
unclear causes
something to do with abnormal flora bacterial
454
How do we treat tropical sprue
gluten-free diet not really helpful
| broad spectrum antibiotics better
455
What is pancreatitis
inflammation of the pancreas, can be acute or chronic
456
What is acute pancreatitis
ranges from mild self-limiting to severe necrotising entire organ
can become chronic or resolve and return to normal
457
what can cause acute pancreatitis
```
idiopathic
trauma
alcohol
steroids
mumps
pregnancy
autoimmune
vascular injury/insufficiency
hyperthyroidism,
hyperlipidaemia
hypercalcemia
bile reflux
gallstone obstruction of duct
```
458
What is the pathology of acute pancreatitis
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
What is the presentation of acute pancreatitis
```
abdominal pain that can spread to back
abdominal tenderness
nausea vomiting
shock (severe), fever, tachycardia
jaundice if obstruction cause
```
460
what is the management of acute pancreatitis
```
IV fluids, oxygen if needed
feeding support if needed
pain killers
surgical drainage or removal of necrotising organ if needed
thromboprophylaxis
```
461
What does chronic pancreatitis cause
causes irreversible damage and pancreatic insufficiency
462
What causes chronic pancreatitis
either relapsing from lots of acute events or primarily chronic
alcohol
gallstone obstruction
cystic fibrosis
463
What is the presentation of chronic pancreatitis
```
abdominal and back pain
diabetes can occur
nausea
weight loss
diarrhoea
steatorrhea
abdominal XR shows calcified plaques on pancreas
```
464
What is the management of chronic pancreatitis
```
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
What type of cancer is most common in pancreas
adenocarcinoma
466
what are the risk factors of pancreatic cancer
smoking
| diabetes mellitus
467
how do we treat pancreatic cancer
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
