Week 3 Flashcards

(373 cards)

1
Q

Where is cholesterol synthesised?

A

In the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Is the liver an endocrine organ?

A

Yes eg produces hormones like angiotensin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Where is the main detoxification unit in the body?

A

The liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Where does urea production happen?

A

In the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is urea

A

Urea nitrogen is a waste product, it develops when your body breaks down the protein in the foods you eat. Travels from liver to the kidneys

We like urea, indicates kidney function.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Where can insulin and hormones be broken down?

A

The liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

When does jaundice occur?

A

Excess bilirubin in the bloodstream

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

6 common causes of jaundice as

A

1) liver conditions eg cirrhosis, hepatitis, alcoholic liver disease

2) haemolytic anemia = body destroys red blood cells quickly

3) bile duct obstruction eg due to hall stones of pancreatic cancer

4) medications

5) infections of the liver eg hepatitis

6) newborn jaundice (immature liver)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What’s phototherapy got to do with jaundice?

A

Phototherapy May be used to help the body break down bilirubin more effectively

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Use the mnemonic LIVER BMN to remember the causes of jaundice

A

Liver conditions
Infections
Viral hepatitis
Excessive haemolysis
Red blood cell conditions
Bile duct obstruction
New born jaundice

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

So we know that bilirubin is conjugated by hepatocytes in the liver, after leaving the spleen. Why is it conjugated?

A

To make it water soluble. Goes to bile / intestines, and then Either back to blood stream (Pee) or modified by gut bacteria (bm)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Mnemonic for function of liver =
VIP SLIM-PR

(The liver is a vip, so is slim shady???? idek at this point lol)

A

Vitamin and mineral storage
Immune system support
Protein synthesis
Storage of glycogen and lipids
Lipid metabolism
Iron storage
Metabolism of carbs (regulate blood sugar levels)
Processing and detox of drugs and toxins
Regulation of blood clotting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How does the liver regulate blood sugar levels?

A

Metabolism of carbs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Think about why the liver might obviously be an immune organ?

A

Because it’s the first port of entry from the gut!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Zinc is stored throughout the body, but what organ plays a role in regulating zinc levels?

A

Liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Zinc deficiency can lead to weight loss, t or f

A

T

Zinc plays a role in metabolism, so low zinc = inefficient use of nutrients. Also zinc deficiency can lead to weakened immune system = illness leads to weight loss.
Chronic inflammation can lead to catabolic state = weight loss

Also zinc is needed for digestion.

Zinc deficiency can lead to loss of appetite

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What happens when the liver stops working

A

Jaundice
Ascites (fluid in abdomen)
Variceal bleeding (mainly from oesophagus)
Hepatic encephalopathy (confusion due to toxin build up)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What’s the 3 way classification of jaundice

A

Pre hepatic
Hepatic
Post hepatic

All to do with bilirubin remember

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

History of anemia eg dyspnoea, fatigue, chest pain, is what classification of jaundice?

A

Pre hepatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

If bilirubin is conjugated and can come out in the urine, then it’s either which two classifications of jaundice?

A

Hepatic or post-hepatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Risk factors for liver disease like drug intake and also, decompensation like ascites, variceal bleed, encephalopathy is what classification of jaundice

A

Hepatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Abdominal pain, pale stools and high coloured urine suggests what type of jaundice?

A

Post hepatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

A palpable hall bladder suggests what

A

Post hepatic jaundice, as obstruction below level of cystic duct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What’s the most important test to figure out where the jaundice is coming from?

A

Ultrasound

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Most important screening test for liver
Prothrombin time
26
What enzyme is raised (liver screening test) of alcohol abuse?
Gamma GT
27
As diagnostic procedures, MRCP and ERCP, which is the therapeutic option (perhaps with radiation)?
ERCP (more invasive)
28
What’s important for the definitive diagnosis of certain conditions eg autoimmune hepatitis?
Liver biopsy
29
What are varices? (Which can occur in the digestive tract due to portal hypertension)
Enlarged and fragile blood vessels
30
Portal hypertension can lead to ascities, what is this
Abdominal fluid accumulation
31
What’s hepatic encephalopathy
Brain dysfunction due to liver disease
32
How might congestive heart failure cause portal hypertension?
Affects right side of heart, can lead to increased pressure in the portal vein due to blood backing up in the liver
33
How might liver cirrhosis lead to portal hypertension?
Portal vein thrombosis
34
What is the most common cause of portal hypertension?
Cirrhosis Leads to distortion of liver architecture, making it difficult for blood to flow through the liver, leading to increased pressure in the portal vein
35
Risk factors (2) non alcoholic fatty liver disease?
Obesity Diabetes
36
Biggest drug to cause cirrhosis?
Methotrexate
37
For cirrhosis, what’s a compensated version? (Investigations)
When it’s only picked up on liver function test, so no like hepatic encephalopathy, or ascites or variceal bleeding…
38
What’s happens in ascites?
Gradual sodium retention Water retention Renal vasoconstriction
39
Ascites, apart from liver cirrhosis, can also be caused by what:
Heart failure, kidney disease, cancer
40
What does a high SAAG (serum albumin ascites gradient) of ascites fluid suggest?
Portal hypertension We basically do a SAAG to find out if the ascites is due to portal hypertension or not
41
How is the SAAG test for ascites patients calculated, as in the gradient?
albumin concentration of the blood serum - Albumin concentration of the ascital fluid -
42
Why would a high SAAG in ascites fluid suggest portal hypertension?
Increased portal hypertension = albumin leaks out of vessels into peritoneal cavity.
43
Why would you treat ascites with diuretics?
Promotes removal of excess salt and water from the body, therefore symptom relief. (E.g. pressure of diaphragm) = prevents risk of hernia, symptom relief etc.
44
What are aquaretics?
Medications that promote the secretion of excess water from the body without significantly affecting the excretion of sodium and potassium
45
Difference between aquaretics and diuretics?
Aquaretics is only targeting water retention
46
Link between ascites and hepatorenal syndrome?
Ascites often precedes the development of hepatorenal syndrome , as circulatory changes and worsening liver function = development of hepatorenal syndrome
47
What is hepatorenal syndrome?
Sudden development of kidney dysfunction specifically alongside liver dysfunction or cirrhosis.
48
Why would we expand blood volume with albumin in hepatorenal syndrome due to portal vein hypertension?
1) portal hypertension = vasodilation of the splenic vasculature 2) so the body feels the the blood volume effect is less 3) RAAS kicks in, adrenaline released. To raise blood pressure 4) increased vasoconstriction, so less renal blood flow I.e. hypovolemia So must expand blood volume with albumin
49
How does portal hypertension cause variceal haemorrhage?
It can cause alternative blood routes
50
How do you treat variceal haemorrhage of the esophageal?
Endoscopic band ligation
51
What drug do you give for oesophageal variceal haemorrhage? To reduce pressure in the veins
Terlipressin
52
Why might ammonia build up in the brain in liver disease, causing hepatic encephalopathy?
Toxins from the gut are converted (especially in the colon) into ammonia, by bacteria. Liver can’t handle this ammonia, so escapes to the brain.
53
What are the risk factors for hepatocellular carcinoma?
Liver disease e.g. cirrhosis Also hepatitis b and c
54
Hepatocellular carcinoma might present as either decompensated liver disease? Or compensated?
Decompensated
55
Why might propranolol be prescribed to patients with cirrhosis and esophageal varices?
Prophylactic/preventative, lower risk of bleeding. It slows down heart rate
56
Which viral hepatitis is self limiting?
A and e Others chronic
57
Which vital hepatitis strains are enteric?
Only a and e actually
58
Meaning of hepatitis
Inflammation of the liver
59
Which hepatitis (viral) strains can be prevented through vaccination?
A and B
60
Which viral hepatitis has asymptomatic children?
A
61
Which is the most common drug to induce liver injury?
Paracetamol
62
Which drug treats paracetamol overdose?
N-acetylcysteine
63
For screening for hepatitis B, we test for: HBcAb, HBsAg, and HBeAg. Which is for previous infection, active infection, or acute phase of infection showing how infectious
HBcAb = previous infection HBsAg = active infection HBeAg = infectivity / acute phase To remember, think C = I can ‘see’ the past clearly, think s is like an active snake, and e for me, how infectious am I
64
Who do we treat for HBV?
Just those with high viral loads
65
Hepatitis E- has it got a vaccine?
No
66
Oral contraceptives can affect the hepatic system how?
Cholestasis
67
What’s cholestasis?
Slowing or stalling of bile flow through your biliary system. Bilirubin accumulates in blood rather than going out in urine.
68
Non alcoholic fatty liver disease is the umbrella term for what three things
Simple steatosis Non alcoholic steatohepatitis Fibrosis and cirrhosis
69
What’s non alcoholic steatohepatitis?
Accumulation of fat, therefore causing inflammation
70
Fatty liver causes steatohepatitis, = inflammation. What might this lead to if it’s chronic
Fibrosis and cirrhosis
71
Fibrosis Vs cirrhosis, what’s the difference?
Cirrhosis is irreversible
72
How is fatty liver disease diagnosed?
Through ultrasound
73
How do we diagnose fatty liver disease?
Through ultrasound and also liver biopsy
74
What does Fib-4 score?
How advanced the fibrosis is
75
Biggest three autoimmune liver diseases?
1) autoimmune hepatitis 2) primary biliary Cholangitis 3) primary sclerosing Cholangitis
76
For autoimmune hepatitis, is it male or female dominant d
Female
77
T or f, autoimmune hepatitis is high IgG?
True
78
What does autoimmune hepatitis respond well to?
Steroids (A lot of inflammation, lots of like lymphocytes, plasma cells, other inflammatory cells)
79
What immunoglobulin is raised in primary biliary cholangitis?
IgM elevated
80
What specifically is inflamed in primary biliary cholangitis? (Think biliary)
Predominantly bile ducts that are involved And therefore blockage of bike within the liver causing cholestasis
81
Is primary sclerosis cholangitis male or female predominant?
Make
82
What is primary sclerosis cholangitis
Stricturing of the bile ducts
83
Primary sclerosis cholangitis patients present with what?
Recurrent cholangitis and jaundice
84
Would active extrahepatic malignancy be a contraindication for liver transplant?
Yes
85
What score is used to decide who gets prioritised for liver transplantation?
UKELD score
86
What is steatosis?
Fatty liver
87
What is steatohepatitis? (3)
Fatty liver with inflammation, Neutrophil infiltration and fibrosis/cirrhosis (build up of scar tissue)
88
Initial physical findings of liver disease?
Majority no physical findings
89
Signs of chronic liver disease?
Spider naevi Loss of axillary and pubic hair Ascites Encephalopathy Red hands I.e. palmar erythema Moobs on men I.e gynecomastia Jaundice Muscle wasting
90
Why does spider naevi occur in liver disease?
Well spider naevi are abnormal capillaries near the skin’s surface But liver disease can lead to increased pressure in the blood vessels that supply the liver (portal hypertension) = capillaries dilate
91
How might spider naevi be formed in liver disease apart from due to portal hypertension?
Accumulation of toxins in the blood stream affects blood vessels Also affected by hormonal imbalances (liver involved in metabolising hormones)
92
What stage finding is jaundice for liver disease?
Late
93
What would an ultrasound show in liver disease? (Think about what happens to the liver)
Fatty liver
94
What blood tests for liver diseases that’s suggestive of alcohol?
Aspartate amino transferase (AAT) > alanine amino transferase (ALT) If AAT is more than twice the ALT, then it’s alcohol
95
When alcohol affects the liver, we see thrombocytopenia, what is this
Low platelets This can affect your bone marrow
96
Really severe hepatic encephalopathy leads to what
A coma
97
Hepatic encephalopathy presents late stage liver disease patients with underlying *what*
Infection So we screen for that
98
Why might constipation cause hepatic encephalopathy?
Bowel can’t clear toxins eg ammonia, which can cross blood brain barrier
99
Why would internal GI bleed lead to hepatic encephalopathy?
Blood into bowel, has lots of proteins, this gets broken down and this releases ammonia
100
Treatment of hepatic encephalopathy?
Bowel clear out Antibiotics- everyone, even if infection isn’t immediately obvious Airway support- because depressed conscious level
101
Hepatic encephalopathy- conscious level too depressed for medications?
Give medications through nasogastric tube into the stomach
102
Ascites will often present endstage liver disease. Ie spontaneous bacterial peritonitis. What’s the complication here that could occur?
Excess fluid could get infected, so abdominal pain
103
Spontaneous bacterial peritonitis, signs? Of the liver (Think: it’s an infection. What complication could be infected, what might you see in a normal infection?)
Abdominal pain because ascites is infected Fever, rigors Renal impairment as kidneys infected Signs of sepsis, tachycardia, temperature
104
How do we diagnose spontaneous bacterial peritonitis?
Tap some fluid from the abdomen, send away for protein levels and glucose levels And culture to see which bacteria
105
Proteins in spontaneous bacterial peritonitis is high or low?
Low
106
Someone looks like they have spontaneous bacterial peritonitis. We need to make sure that it isn’t actually caused by what
Surgical causes, so we do a CT scan
107
Treatment for bacterial peritonitis?
High dose broad spectrum antibiotics, usually given intravenously
108
Why do we give albumin intravenously when ascites?
Because it creates oncotic pressure 1) so helps retain fluid within the blood vessels and prevent it from leaking. 2) Also draws fluid back into the bloodstream I.e. reduce volume of ascitic fluid and increase vascular volume.
109
Why might ascites occur in liver cirrhosis?
Albumin production by liver reduced. Oncotic pressure lost and fluid leaks
110
Where is albumin primarily synthesised
The liver
111
What’s delirium tremens?
Medical emergency of alcohol withdrawal. Psychosis? Heart arrhythmias, severe dehydration, seizures etc Tremors Agitation Profuse sweating and fever Tachycardia and high blood pressure
112
Treatment for delirium tremens
Benzodiazepines
113
Purpose of benzodiazepines for delirium tremens
They enhance the effects of neurotransmitter GABA, to calm the individual Helps agitation, tremors, hallucinations, calm central nervous system. They also prevent seizures
114
For alcoholic hepatitis, treatment?
Mainly supportive Treat infections (common) And Treat encephalopathy Acid reducing meds M
115
How to diagnose alcoholic hepatitis?
Raised bilirubin Alcohol history Exclude other causes
116
There is inflammation in alcoholic hepatitis, so why wouldn’t we use steroids or prednisone?
It increases the risk of GI bleeding (Possibly use in very very severe alcoholic hepatitis)
117
What percentage of patients with alcoholic hepatitis are malnourished?
100% = there’s an awful lot of death If they remain malnourished, only 15% will survive two years
118
Korsakoff’s encephalopathy will occur after being malnourished (alcoholic hepatitis-please fact check this) What vitamin do you need to replenish to do that?
Thiamine Vitamin B Otherwise permanent brain damage
119
Why would you pass a nasogastric tube into someone with alcoholic hepatitis?
They have high energy requirements that they can’t meet, malnourished
120
Prognosis for alcoholic hepatitis is linked to what
Alcohol cessation
121
Is there treatment for non alcoholic fatty liver disease?
No just lifestyle
122
Non alcoholic fatty liver disease can progress to what
Non-alcoholic steatohepatitis and cirrhosis
123
Difference between primary sclerosis cholangitis and primary biliary cholangitis?
Bile ducts: sclerosing = inside AND outside the liver, Vs biliary which is only small bile ducts in the liver Sclerosing is associated with increased risk of bile duct cancer and colon cancer- not for biliary though
124
Itching, fatigue and abdominal pain- are these symptoms of primary biliary cholangitis, or primary sclerosing cholangitis
Both
125
What is primary biliary cholangitis?
Bile ducts in the liver become injured and inflamed and eventually destroyed. Eventually bile builds up and destroys the live r
126
Why should we be worried about gallbladder polyps?
Because they could turn into gallbladder cancer So remove if big like at least 1cm or more
127
Risk factors for gallstones? (4 Fs mnemonic)
Fat Fair Female Forty
128
Gall stones present how?
Biliary colic: Severe, colicky epigastric or right upper quadrant pain Associated with nausea and vomiting Often triggered by meals especially high fat
129
Why might patients with gall stones be advised to avoid fatty foods?
Fat entering the digestive system causes CCK secretion from the duodenum. CCK triggers contraction of the gall bladder
130
Why would hall stones lead to obstructive jaundice
If stones block the duct then it blocks where bilirubin drains (from liver through bile ducts). Raised bilirubin = jaundice Bilirubin goes from spleen to hepatocytes in the liver to be conjugated (made water soluble)
131
A raised ALP (enzyme originating from places incl. liver) alongside right upper quadrant pain and/or jaundice, is consistent with what
Biliary obstruction
132
Aminotransferases (ALT and AST)- they are enzymes produced where
Liver
133
Aminotransferases (ALT and AST)- if they are high compared to ALP level, indicates what
Problem inside the liver
134
Which screening test for gall stones?
It’s ultrasounds
135
Patients with symptoms or complications of gall stones are treated with what
Cholecystectomy = surgical removal of the gallbladdrr
136
What is the composition of gallstones?
Cholesterol mainly
137
Gall stones are usually symptomatic or not?
Asymptomatic If they’re symptomatic, then it’s bilary colic
138
What has empyema got to do with hall stones?
Could get pus in the gallbladder- and then gallbladder might perforate = surgical emergency
139
Perforated gall bladder due to stones requires what
Draining the gall bladder
140
Why would pancreatitis occur due to gall stones?
Stones could move and obstruct the pancreatic duct
141
What is cholangitis?
Inflammation of the bile duct system
142
What’s biliary atresia?
Babies born with the absence of the bile duct. Needs significant reconstruction
143
Primary sclerosing cholangitis is autoimmune, yes or no
Yes
144
How does primary sclerosing cholangitis present?
Jaundice Some pain (Blocked bile ducts remember)
145
How could a biliary-enteric fistula happen due to gallbladder?
Through inflammation, gallbladder perforated into the duodenum
146
Why would jaundice occur due to malignant tumours?
Intra or extra hepatic
147
What’s the only treatment option for cholangicarcinoma: intrahepatic
Surgery
148
Cholangio-carcinoma is classified how?
Based on where the duct is blocked eg right hepatic duct, cystic duct, common hepatic duct etc.
149
Presentation of pancreatic cancer
obstructive jaundice Weight loss Upper abdominal pain
150
What happens to bilirubin levels in pancreatic cancer?
Raises Obvs cause of obstructive jaundice
151
What’s the kausch-whipple surgery? (For pancreatic cancer)
Entails taking half/quarter of the stomach, Head of the pancreas Lower end of the bile duct Duodenum Then anastomosing all of them together
152
The pacemaker to get the stomach to empty is located where
In the pylorus
153
Obstructive jaundice- could that be treated with stenting?
Yes Don’t rlly know why
154
Definition of acute pancreatitis
An acute inflammatory process of the pancreas, with variable involvement of other organs Can be mild- uneventful recovery Or can be severe- organ failure or local complications
155
Would a cute pancreatitis ever lead to pancreatic necrosis?
Yes
156
What causes acute pancreatitis?
Alcohol Gall stones Post ERCP procedures (Other reasons too eg scorpion venom but just learn alcohol and gall stones just now)
157
How does alcohol cause acute pancreatitis?
Acetaldehyde -as an oxidation product Also direct injury
158
How would gall stones cause acute pancreatitis?
Obstructing pancreatic duct Raised pancreatic ductal pressure
159
Jaundice can occur in pancreatic cancer why?
1) obstruction of the bile duct (pancreas is located near the bile ducts, so tumour can prevent bile from flowing into the small intestine- SO IT GOES TO THE BLOODSTREAM INSTEAD. Bilirubin then accumulates in the blood 2) compression of the duodenum = pancreatic tumours. Same as before but at duodenum level, not bile duct level. 3) liver metastasis, cancer cells go to liver and impair liver’s ability to process bilirubin
160
Difference in chronic and acute pancreatitis?
Chronic = irreversible deterioration in pancreatic function Acute = rapid onset and normal function does return
161
Why would a gallstone cause inflammation in the pancreas ie pancreatitis?
Blockage and ampulla of vater = reflux of bile and pancreatic juice
162
Why does alcohol cause pancreatitis?
Alcohol is directly toxic to the pancreas
163
Causes of pancreatitis with the mnemonic ‘I get smashed’
Idiopathic Gall stones Ethanol Trauma Steriods Mumps Autoimmune Scorpion sting Hyperlipidaemia ERCP procedures Drugs
164
What’s the most important investigation. For acute pancreatitis? And why not chronic?
Amylase Can be raised 3 x upper limit in acute. May not rise at all in chronic pancreatitis
165
Which investigative thing shows level of inflammation? (Might be useful eg in acute pancreatitis!)
C-reactive protein (CRP) > level of inflammation
166
What investigation for pancreatitis to check for gallstones?
Ultrasound
167
Necrosis, abscesses and fluid collections could never be a complication of pancreatitis, why?
Trick question. It is. Assess with CT
168
What score assesses severity of pancreatitis?
Glasgow
169
‘Pancreas’ mnemonic for Glasgow scale for testing how severe pancreatitis is?
Look at zeros to finals, can’t be bothered writing it out
170
Patient with acute pancreatitis. Has hall stones. What do you do?
ERCP procedure Or Cholecystectomy
171
When would you give antibiotics for pancreatitis?
If evidence of specific infection eg necrosis or abscess in the pancreas
172
How many days to improve after acute pancreatitis?
3-7 days
173
What’s the most common cause of chronic pancreatitis?
Alcohol
174
What’s happened, very simply, in chronic pancreatitis?
Fibrosis and reduced function
175
Pseudocysts and abscesses form in which one, acute or chronic pancreatitis
Chronic pancreatitis
176
Loss of exocrine function in chronic pancreatitis means what
Lack of pancreatic enzymes secreted e.g. lipase Also no insulin = diabetes
177
Why is there steatorrhoea in chronic pancreatitis?
Because no pancreatic enzymes released- no lipase for digesting fat. So greasy stools.
178
What’s creol used for in chronic pancreatitis?
Replace lipas- pancreas can’t produce enzymes anymore.
179
How important is nutrition for acute pancreatitis patients?
Extremely
180
How to deal with post pancreatitis fluid?
Endoscopic ultrasound guided drainage
181
Why use a nasogastric tube in acute pancreatitis?
To prevent stimulating pancreatic secretions
182
Why use a stent in pancreatitis?
1) inflammation of the pancreas can lead to narrowing or blockage of the pancreatic ducts, so use stent to relive obstruction (blockage can cause digestive enzymes and bile to accumulate in the pancreas, leading to further inflammation and pain) Might keep stent there to prevent recurrence! 2) drainage of pseudocysts when in severe acute pancreatitis. (Fluid filled). Stents can create drainage path from pseudo cyst to the digestive
183
Cough, shortness of breath, fever, and poor appetite - why would this ever be acute pancreatitis?
Due to ascites In severe cases, fluid can put pressure on the diaphragm= sob Also if fluid moves from ascites into the pleural space, can cause pleural effusion = breathing difficulties and a persistent cough
184
We look at amylase for what disease?
Pancreatitis This is because: pancreas could leak digestive enzymes, into surrounding tissue and blood stream
185
What is a sphincterotomy?
Making a small cut in the papilla of vater to enlarge the opening of the bile duct and/or pancreatic duct- to either improve drainage or to remove stones in the ducts.
186
Destruction if both exocrine and endocrine cells in chronic pancreatitis leads to what
Loss of function
187
Most common cause of chronic pancreatitis?
Alcohol Then after that cystic fibrosis, maybe some congenital anatomical abnormalities
188
Why vitamin deficiency for chronic pancreatitis?
Exocrine deficiency Enhanced dietary intervention important for this group
189
Why is there pain in pancreatic cancer?
1) Pain from tumour growth/ inflammation pressing on tissues, nerves, and blood vessels. (Celiac plexus) 2) obstruction of bile duct = buildup of digestive enzymes or bile
190
Digestion happens mainly in what part of the small intestine?
Suodenum
191
Where in the small intestine does gastric acid secretion occur?
Duodenum So that’s where bicarbonate secretion occurs, and also bicarbonate from pancreatic juice and also from the bile
192
T or f, the jejunum is usually empty
True unless during a meal, chyme will be there, otherwise mostly empty
193
Where in the small intestine does the most: Nutrient absorption Digestion Occur?
Nutrient absorption occurs mainly in the jejunum Digestion mainly occurs in the duodenum
194
Main function of ileum
Absorption of sodium chloride and water
195
In the villus are mini capillaries that absorb fats, what are these called
Lacteals So days don’t go directly to the blood capillaries, they go to the lacteals
196
Goblet cells in the small intestine secrete mucus. Where are these located
On surface of villi
197
Purpose of crypts between villi of the intestine
Secrete water And contain stem cells to be used in regeneration of intestinal, epithelial cells
198
Dead epithelial cells in small intestine can be used as what
A source of nutrients because made of proteins
199
Why does chemo have lots of gastrointestinal side effects?
Because we have rapidly dividing cells in the epithelial of the GIT,
200
Brunners glands (purple) are where in the small intestine
Submucosa
201
What type of cell in the oesophagus?
Stratified squamous non-keratinised epithelium
202
What do the cells look like histologically in the liver?
Almost exclusively epithelium Cuboidal hepatocytes with sinusoids in between
203
Epithelium in the intestines is:
Simple columnar epithelial cells
204
Villus is made of epithelial cells, and in between some of the cells on the surface are what type of cell
Mucus secreting goblet cells
205
How is water secreted in intestine from the epithelial cells lining the crypts of lieberkuhn?
H20 is secreted passively/ osmotic ally as a consequence of active secretion of chloride into intestinal lumen There are sodium potassium ATPase pumps, sodium out, potassium in and therefore chloride out
206
How does secretion of water in intestines promote the mixing of nutrients with digestive enzymes?
Action of enzymes higher than if in liquid state vs solid state
207
Water in intestines is secreted by *crypts* and absorbed by **?
Villi Paracellularly through tight junctions between the cells
208
By what channel does chloride move out into lumen of intestines?
A transmembrane channel known as CFTR- cystic fibrosis transmembrane conductance regulator
209
Why is the cystic fibrosis transmembrane conductance regulator called that? (Channel critical in moving the chloride outside the crypt epithelial and therefore moving water indirectly).
Because if there are genetic changes/defect, then cystic fibrosis
210
What problem occurs in cystic fibrosis?
Problem of chloride outside the crypt epithelial and this affects the secretion of water
211
What enzyme activates the cystic fibrosis transmembrane conductance regulator?
Adenylate cyclase
212
What does adenylate cyclase do?
It will convert ATP to cyclic amp, which will activate protein kinase A, which will phosphorylated the channels and make it active
213
What are the two different types of movement in the small intestine?
Segmentation and peristalsis
214
Segmentation movement in the small intestines is most common when?
During meals
215
How does segmentation movement work?
Contraction, then relaxation. To move chyme up and down- provides mixing of contents with digestive enzymes, and brings chyme into contact with absorbing surface
216
Segmentation contractions is initiated by what?
Depolarisation of the pacemaker cells in the longitudinal muscle layer
217
What’s the intestinal basic electrical rhythm that helps initiate segmentation contractions? (Pacemaker cells in longitudinal muscle layer).
BER produces oscillations in membrane potential that reach threshold therefore contraction
218
BER decreases in what directions of the intestine?
BER decreases as move down intestine towards rectum
219
Innervation that increases contraction in segmentation?
Parasympathetic (vagus)
220
What decreases contraction of the segmentation?
Sympathetic nervous system
221
When does peristalsis occur?
Following the absorption of nutrients
222
Why does peristalsis occur?
After nutrients absorbed, peristalsis will try and get rid of unabsorbed/ non absorbed nutrients e.g. cellulose
223
Difference between segmentation and absorption?
Segmentation = digestion and absorption Peristalsis = moving chyme towards large intestine
224
Migrating motility complex is what
Term to describe pattern of peristaltic activity travelling down from small intestine, starting from gastric antrum and ending at terminal ileum (large intestine)
225
When does migrating motility complex stop? (Peristalsis)
Arrival of food in stomach = segmentation
226
How does MMC limit bacterial colonisation of small intestine?
Keep moving chyme to large intestine where it’s okay to have undigested food- if bacteria colonises small we don’t get nutrients
227
Which hormone is involved in initiation of MMC?
Motilin
228
In segmentation, there is both relaxation and contraction in lots of different areas. Whereas in peristalsis, what’s the case?
Only contraction in one area, and mainly relaxation elsewhere
229
When bolus of chyme reaches intestinal smooth muscle, does the oral side contract or relax? (Vice versa to the anal side)
Muscle on oral side of bolus contracts
230
In gastric emptying, does segmentation activity in the ileum increase or decrease?
Increase
231
Gastric emptying: segmentation activity in the ileum increases, leading to the opening of what sphincter
The ileocaecal valve The sphincter between the ileum and the colon The sphincter then reflex contracts to prevent backflux into the small intestine
232
233
Another name for the appendix?
Vermiform
234
True or false, the appendix has no lymph nodes?
It has many False
235
What do I mean when I say that the longitudinal muscle of the large intestine is incomplete? (Vs circular muscle layer)
Three bands across the large intestine known as teniae coil
236
Why is there a puckered appearance in the colon when it contracts?
Because of the teniae coli
237
What is the mucosa of the large intestine comprised of?
It is comprised of simple columnar epithelium
238
Are there Villi in the large intestine?
No
239
Are there crypts in the large intestine?
Yes! There are! Like small intestine, with epithelium stem cells at the bottom
240
Why are there lots of goblet cells in the intestine?
They form a good layer of mucus to help lubricate the large intestine to help with the movement of faeces (Or faeces will damage)
241
What’s after the rectum
Anal canal
242
The muscularis externa of the rectum: is this thicker or thinner compared to other regions of the alimentary canal?
Thicker (To hold in faeces, and then push out)
243
The muscularis externa layer of the anal canal forms what
Internal anal sphincter
244
The internal anal sphincter is involuntary, and is controlled by what nervous system?
Autonomic Obviously not somatic cuz that’s conscious stuff
245
The external anal sphincter of the anus (there are two) is what type of muscle?
Skeletal muscle
246
Whilst the rectum is simple columnar epithelium, what is the anal canal?
Stratified squamous
247
What is located in the Baso-lateral membrane of the small intestine, that creates an electrochemical gradient for sodium?
Sodium potassium ATPase pump
248
The bacteria in the colon/ large intestine helps in forming what vitamin?
Vitamin K, which is an important blood clotting factor, helps to prevent haemorrhage
249
What are the symptoms associated with constipation?
Headache Nausea Loss of appetite Abdominal distension The symptoms come from the distension of the rectum
250
What are the causes for diarrhoea?
1) pathogenic bacteria living in our colon 2) protozoans 3) viruses 4) toxins 5) stress
251
What channel is involved in the secretion of water from crypt cells?
Sodium potassium chloride channel
252
Chloride is transported outside the cell via what transporter?
CFTR
253
How might bacteria cause diarrhoea?
Affects the CFTR channel, causing more chloride into the cell and therefore more water
254
Example of bacteria causing diarrhoea?
Vibrio cholerae > cholera
255
How does the bacteria actually increase chloride eg cholera?
Entero-toxins they release work by elevating things such as cyclic AMP
256
How many litres of water secreted into colon a day with cholera Vs not?
25 litres Vs 1.5 litres
257
Why do we give sodium/glucose solution in diarrhoea eg cholera?
For rehydration. Bacteria hasn’t affected the SGLT1 translorter so glucose and sodium can still be absorbed, and this will help in the absorption of water
258
Diarrhoea washes out the toxins. Why is it bad then?
Dehydration and loss of vitamins
259
Where is the secretory mucosal type in the GI tract?
Seen only in stomach. It’s the *crypts* that secrete water in the colon
260
What score is related to AF patients for risk of bleeding?
HAS BLED
261
What are the three types of gastritis (ABC)
Autoimmune Bacterial Chemical injury
262
How does autoimmune gastritis work?
Autoantibodies to parietal cells and intrinsic factor. Atrophy of gastric epithelium Loss of specialised gastric epithelial cells (decreased acid secretion, loss of intrinsic factor)
263
Pathology of bacterial gastritis?
Bacteria found in gastric mucus and produces an acute and chronic inflammatory response therefore increased acid production
264
Gastritis definition
Inflammation of the stomach lining.
265
Acid reflux causes inflammation of what
The oesophagus
266
Which drugs may cause chemical gastritis?
NSAIDs Non- steroidal anti-inflammatory drugs
267
Peptic ulceration is an imbalance between what?
Acid secretion and mucosal barrier
268
What parts of the GI tract do peptic ulcers affect?
Oesophagus, stomach, duodenum
269
Acute Vs chronic bleeding from peptic ulcer leads to what?
Acute = haemorrhage Chronic = anaemia
270
Perforation of a peptic ulcer can lead to what
Peritonitis
271
Healing by fibrosis of a peptic ulceration could lead to what?
Obstruction
272
Gastric cancer is associated with previous infection of what
H pylori
273
What is the dual blood supply of the liver from?
Hepatic artery Portal vein
274
Primary sclerosing cholangitis is associated with what disease?
Inflammatory bowel disease
275
What’s cholecystitis?
Inflammation of the gall bladder
276
3 types of cell in the small bowel?
Goblet cells Columnar absorptive cells Endocrine cells
277
The small bowel has columnar absorptive cells. What about the large bowel?
Also columnar absorptive
278
The large and small bowel peristalsis is mediated by both intrinsic (mesenteric plexus) and extrinsic (autonomic innervation) neural control. What are the two myenteric plexuses?
Meissners plexus within the submucosa Auerbach plexus between the circular and longitude muscle of the muscularis propria
279
2 main strands of inflammatory bowel disease?
Crohn’s disease Ulcerative colitis
280
What is IBD
Recurrent episodes of inflammation in the gastrointestinal tract - ulcerative colitis and Crohn’s disease. Associated with exacerbation and remission
281
Presenting features of IBD?
Diarrhoea Abdominal pain Rectal bleeding Fatigue Weight loss
282
What are the differentiating features of crohns? (IBD). This can be remembered with the ‘crows’ NESTS mnemonic.
No blood or mucus Entire GI tract is affected- mouth to anus ‘Skip lesions’ on endoscopy T - terminal ileum most affected and full Thickness Smoking is a risk factor (don’t set the nest on fire)
283
Crypts abscesses are more seen in what type of IBD?
Ulcerative colitis Not crohns
284
What are ‘skip lesions’ of crohns?
The fact that inflammation isn’t continuous Vs it is in ulcerative colitis
285
Why can fistula form in crohns?
Due to the trans mural nature of the inflammation
286
Inflammation of ulcerative colitis?
Mucosal involvement only
287
Which IBD disease is Granulomatous?
Crohns So the histological appearance of crohns is non-caseating Granulomatous inflammation
288
Site of ulcerative colitis?
Large bowel
289
Why would nail clubbing occur in crohns?
Secondary to malabsorption
290
What hepatobiliady complication could occur in Crohn’s disease?
Primary sclerosing cholangitis, hall stone disease
291
Gold standard investigation for IBD?
Colonoscopy to show evidence of inflammation, and biopsies can confirm diagnosis
292
What imaging for IBD?
MRI small bowel imaging Or Urgent CT imaging to check for bowel obstruction or bowel perforation
293
Patients in an acute flare of Crohn’s disease will require what as first line
Cortico steroid therapy
294
What is patients with a remission in Crohn’s disease, fail first line therapy of corticosteroids?
Immunosuppressive agents like mesalazine or azathioprine
295
Why would surgical management of Crohn’s disease be necessary?
For those with severe complications such as strictures or perforation Eg resection (NB these are high risk patients to operate on).
296
Two reasons crohns patients might have osteoporosis?
Secondary to: Malabsorption Long term steroid use
297
Why are crohns patients at increased risk of fall stones?
Due to reduced reabsorption of bile salts at the terminal ileum
298
Is smoking a risk factor for which IBD disease?
Crohns
299
Sever exacerbations of crohns May result in what?
Life threatening severe systemic upset, bowel perforation or even mortality.
300
Ulcerative colitis is the least common form of inflammatory bowel disease, true or false?
False Most common
301
Is the pathophysiology of ulcerative colitis understood?
Nahhhhhh
302
What are three histological changes that occur with ulcerative colitis?
Non Granulomatous inflammation of mucosa and sub-mucosa Crypt abscesses Goblet cell hyperplasia
303
How do pseudopolyps occur in ulcerative colitis?
Repeated cycles of ulceration and healing = raised areas of inflamed tissue termed pseudopolyps
304
How to diagnose IBD?
Take history Radio graphic examination In most UC patients, they are ‘perinuclear antineutrophilic cytoplasmic antibody’
305
Would the appendix ever be involved in IBD?
Yes For ulcerative colitis , can also be localised to the rectum
306
Are there any Granulomas in ulcerative colitis?
Yes
307
How might ulcerative colitis lead to cancer?
Dysplasia of epithelium
308
What happens to the mesentery in crohns?
Thickened and fibrotic
309
How is anaemia secondary to ulcerative colitis?
Ulceration Breakdown of surface Haemorrhage and bleeding Become anaemic
310
What’s toxic megacolon? (Complication of ulcerative colitis)
Inflammation deep enough for perforations, =organisms can move beyond mucosa, into the sub mucosa, then you get an infective condition = toxic megacolon where colon expands very rapidly. And can be fatal
311
Is there a gender bias in IBD?
Only in crohns- towards females
312
What happens to the serosa in Crohn’s disease?
Becomes a granular dull grey
313
What’s ischaemic enteritis?
Where blood supply to the bowel is impinged, and is insufficient, so the bowel dies off
314
What happens when there is acute occlusion if one of the three major blood vessels eg coeliac s and I mesenteric arteries?
Infarction of segments of bowel
315
5 things that happen in chronic ischaemia?
Mucosal inflammation Ulceration Sub-mucosal inflammation Fibrosis Stricture
316
Why might vasodilation happen in chronic ischaemia?
Blood vessels dilate to try and provide more blood into the area
317
Why inflammation in ischaemia (occlusion of blood vessels)
Inflammatory cells can move in and start to repair the damage
318
Why stricture in chronic ischaemia?
Fibrosis comes to heal- that leads to structure formation
319
What’s radiation colitis?
Well people get abdominal radiation for things like prostate cancer, other cancers etc Radiation may impair normal normal proliferative activity Symptoms mimic IBD
320
How is acute appendicitis a classic IBD condition?
It can be caused by acute inflammation in the mucosa of the appendix
321
What is the appendix suspended by?
The mesoappendix
322
What is the point of the appendix?
Reservoir for intestinal flora
323
Typical cause of appendicitis?
Obstruction of opening of the appendix Usually result of hardened stool Or Lymphoid hyperplasia
324
Explain migration of pain in appendicitis first stage then second stage
First stage: initial inflammation stimulates visceral afferent pain fibres which correspond to T10 dermatome, producing umbilical pain Second stage: as appendix becomes more inflamed, it irritates parietal peritoneum which activates somatic nerve fibres, to produce localised pain, felt in the right iliac fossa (McBurney’s point)
325
Why do we vomit with appendicitis?
Non specific immune response from immune system
326
The destruction of the appendix can increase Intraluminal pressure which can result in what?
Ischaemia of the mucosa, because the blood can’t get in because the pressure here is higher than outside the appendix, so it becomes inflamed and then perforates
327
How does GI tract dysplasia often present?
Formation of a polyp (adenomatous)
328
T or f, there is reduced mucin with dysplasia
True
329
Most adenocarcinoma’s of the large bowel arise from what
They develop from epithelial cells lining the colon or rectum, as an adenocarcinoma. They develop via a progression of normal mucosa to colonic adenoma as polyps, to become invasive
330
T or F, Inflammatlry bowel disease is a risk factor for what
colorectal cancer
331
Which is worse, right sided or left sided colorectal cancer?
Right sided colon cancers are more aggressive
332
Why are right sided colon cancers got a worse prognosis?
Right sided colon cancers often grow larger before noticeable symptoms, so more likely to be diagnosed at a more advanced stage.
333
Is left or right sided colorectal adenocarcinoma related to altered bowel habit?
Left. Now the stool on the left has become firmer (water at this point has mainly been absorbed) and therefore narrowing of the lumen due to lesion = altered bowel habit.
334
When does the oesophagus begin?
At the cricoid cartilage about C6
335
When does the esophagus end?
Like T11-T12, where it enters the stomach
336
Peristalsis of the oesophagus is mediated by what nerve
Vagus nerve
337
At lower oesophageal sphincter, a mucosal rosette is formed by the acute angle of what
His
338
Persistent reflux and heartburn can lead to what?
GORD Gastro-oesophageal reflux disease Which in turn can lead to long term complications
339
Possible causes of dysphagia?
Benign stricture Malignant structure (oes cancer) Extrinsic compression eg from lung cancer Eosinophilic oesophagitis
340
Hypermotility of the eosophagus example is diffuse oesophageal spasm. What appearance has this got on a barium swallow?
“Corkscrew” appearance.
341
What does achalasia result from?
Loss of relaxation from the sphincter, secondary to loss of myenteric plexus ganglion cells It’s a swallowing dusirdee
342
What plexus innervates the lower oesophageal sphincter?
The myenteric plexus (between circular/longitudinal muscles of muscularis propria)
343
Why is achalasia, a swallowing disorder, associated with chest infection?
Stasis of oesophageal food contents
344
Treatments of achalasia?
Nitrates and calcium channel blockers
345
GORD pathophysiology?
Mucosa exposed to acid-pepsin and bile Increased cell loss and regenerative activity (inflammation)
346
Complications of GORD?
Ulceration Stricture Barrett’s (glandular metaplasia) Carcinoma
347
What occurs in Barrett’s oesophagus histology
Change from squamous to mucin secreting columnar (ie gastric type)
348
How do you usually treat Barrett’s?
Endoscopic mucosal resection
349
Treatment of GORD?
Lifestyle eg obesity, smoking, diet etc Proton pump inhibitor eg omeprazole, lansoprazole
350
Biggest symptom of oesophageal cancer?
Progressive Dysphagia Anorexia Weight loss
351
What percentage of the worlds population is infected with helicobacter pylori?
50% of the world’s population
352
What clinical condition typically occurs in patients on long term or high doses of NSAIDs and aspirin?
Peptic ulcer disease As prostaglandins are suppressed, making stomach more vulnerable to irritation and damage from stomach acid
353
Acute mesenteric ischaemia refers to what condition
Where there is a sudden decrease in blood supply to the bowel, resulting in bowel ischaemia and eventual necrosis.
354
Which are the fat soluble vitamins?
A, D, E and K
355
If patients are gonna be on NSAIDs and aspirin for more than a few days, what other drugs are they prescribed?
PPI such as omeprazole to provide gastroprotection
356
How would you expect chronic pancreatitis to affect glucose levels?
Hyperglycaemia
357
Why hyperglycaemia in chronic pancreatitis?
Impact of pancreas function. Patients can develop diabetes secondary to chronic pancreatitis, as insulin producing pancreatic cells can be damaged
358
Opioids are commonly used for pain relief, or for suppression of diarrhoea. What is a common side effect
Constipation
359
How does malabsorption occur in coeliac disease?
As a consequence of autoimmune destruction of villi
360
How does coeliac disease present?
Diarrhoea, steatorrhea, weight loss, vitamin deficiency
361
In iron deficiency, liver increases production of what?
Production of transferrin in order to increase iron uptake, and maintain iron homeostasis
362
Ferritin is an iron store. So does it increase or decrease with iron deficiency?
Levels increase when there is a high amount of iron in the blood- and decreases with iron deficiency!
363
A low ferritin is a marker of what
Iron deficiency So it’s a commonly used test
364
What is choledocolithiasis?
Gall stones in the bile duct
365
What does primary biliary cholangitis affect?
The bile ducts within the liver
366
How does cholestasis occur due to primary bilary cholangitis?
As bile ducts become damaged, they are less able to transport bile, so cholestasis and therefore accumulation of bile acids in the liver and blood stream
367
Hall stones in the bile duct: does this present as painful or painless obstructive jaundice?
Painful
368
Ascending cholangitis might be a result of what obstructing the bile duct
Gall stones in the bile duct Cholangitis is an inflammation of the bile duct
369
Bilary Cholangitis is caused by a combination of what two issues?
Biliary outflow obstruction and biliary infection. Because bile is within the gallbladder for too long, and bile sits and thickens, providing an ideal growth medium for bacteria.
370
Why might biliary cholangitis lead to biliary sepsis?
Pressure due to obstruction increases. And this increases risk of bacterial translocation into the bloodstream- resulting in biliary sepsis
371
Definitive diagnosis of Crohn’s disease?
Endoscopy findings, showing mucosal inflammation, cobblestone appearance with ulcers, skip lesions
372
What can be a side effect of use of proton pump inhibitors such as omeprazole?
Increased risk of c. Diff infection
373
Which autoantibodies are characteristic for primary biliary cholangitis?
Anti mitochondrial antibodies