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Year 1 NME > GIT Revision > Flashcards

GIT Revision Flashcards

1
Q

Looking for leukonychia in the hands on a GIT examination should be included. What is leukonychia?

A
  • white lines or dots appear on your finger or toenails
  • sign of liver disease
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2
Q

Looking for koilonychia in the hands on a GIT examination should be included. What is koilonychia?

A
  • finger nails appear scooped up like a spoon
  • common in iron deficiency
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3
Q

Looking for dupuytren’s contractures in the hands on a GIT examination should be included. What is dupuytren’s contractures?

A
  • 1 or more fingers bend in towards your palm
  • may be due to excessive alcohol
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4
Q

What is a stoma and what are the 2 types of stomas?

A
  • an opening of the abdomen
  • colostomy and ileostomy
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5
Q

Of the 9 areas of palpation on the abdomen, what are the top 3 from left to right?

A
  • left hypochondriac
  • epigastric
  • left hypochondriac
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6
Q

Of the 9 areas of palpation on the abdomen, what are the middle 3 from left to right?

A
  • left lumber
  • umbilicus
  • right lumbar
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7
Q

Of the 9 areas of palpation on the abdomen, what are the lower 3 from left to right?

A
  • left inguinal
  • hypogastric
  • right inguinal
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8
Q

In the gastrointestinal examination we need to be able to look for an acute abdomen, what are the 3 things we need to look for?

A

1 - guarding

2 - rigidity

3 - rebound tenderness (pain when removing the hand)

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9
Q

What is splenomegaly and hepatomegaly?

A
  • enlerged spleen and liver
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10
Q

In a normal healthy patient where would we expect to find the liver when feeling and percussing?

A
  • upper border is 5th rib
  • lower border is 10th rib
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11
Q

There are 2 signs of GIT disorders in the legs, one is called pyoderma gangrenosum, what is this?

A
  • inflammatory skin disorder
  • causes small, red bumps or blisters (papules or nodules) that eventually erode to form swollen open sores (ulcerations)
  • can be caused by crohns disease
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12
Q

There are 2 signs of GIT disorders in the legs, one is called erythema nodosum, what is this?

A
  • painful red nodules (or lesions) that most often develop on the arms or lower legs
  • common in ulcerative colitis
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13
Q

How do we calculate BMI?

A
  • weight (kg) / height (m)2
  • me as an example: 80kg/1.86m2 = BMI of 23kgm2
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14
Q

According to NICE what are the cut offs for the different categories of BMI?

A
  • healthy weight = BMI of 18.5-24.9 kg/m2
  • overweight = BMI of 25-29.9 kg/m2
  • obesity l = BMI of 30-34.9 kg/m2
  • obesity ll = BMI of 35-39.9 kg/m2
  • obesity lll = BMI of 40 kg/m2
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15
Q

What is the Malnutrition Universal Screening Tool (MUST) score used for?

A
  • to determine if a patient is malnourished
  • score of _>_2 means patients need treating
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16
Q

In order to create a Malnutrition Universal Screening Tool (MUST) score what is needed from the patient?

A
  • BMI
  • any unplanned weight loss (last 3-6 months)
  • if patient is acutely ill
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17
Q

In order to create a Malnutrition Universal Screening Tool (MUST) score the patients BMI is needed, however, what can also be used to estimate BMI if normal BMI cannot be calculated?

A
  • mid upper arm circumference
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18
Q

What is coeliac disease?

A
  • autoimmune condition
  • immune system attacks its own tissue when gluten is eaten
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19
Q

How common is coeliac disease?

A
  • affects 1% of the population
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20
Q

What are the 3 main dietery components that commonly trigger coeliac disease?

A
  • wheat, barley, rye and contaminated oats
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21
Q

Does coeliac disease affect the whole bowel?

A
  • no
  • small intestines only
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22
Q

What are the most common symptoms of coeliac disease?

A
  • anaemia (B12, folate or iron)
  • abdominal symptoms
  • dermatitis herpetiformis (itchy blisters and raised red skin lesions)
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23
Q

To help diagnose patients with coeliac disease, you can screen them for antibodies. What antibodies can be screened for?

A
  • anti tissue transglutaminase (TTG)
  • anti-gliadin (main protein in gluten that causes the problem)
  • anti-endomysial (connective tissue around smooth muscle in GIT)
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24
Q

When taking a biopsy from a patient with coeliac disease, which is the gold standard for diagnosis, what would we expect to see on biopsy?

A
  • flattened villi in small intestines
  • hyperplasia of crypts
  • raised lymphocytes
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25
Q

What is the most effective treatment for coeliac disease?

A
  • gluten free diet
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26
Q

Do patients with ceoliac disease, do they have blood in their stool?

A
  • no
  • diarrhoea
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27
Q

Ulcerative colitis (UC) if an inflammatory bowel disease. Does UC affect the whole GIT?

A
  • no specific to colon
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28
Q

Ulcerative colitis (UC) if an inflammatory bowel disease. How does UC present when we look at tissue biopsies from the colon? Is the inflammatuion continous or is it patchy?

A
  • continous inflammation with no gaps
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29
Q

Ulcerative colitis (UC) if an inflammatory bowel disease. How does UC present when we look at tissue biopsies from the colon? Does the inflammatuion affect all 4 layers of the GIT or just the top layers?

A
  • only affects the mucosa
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30
Q

Ulcerative colitis (UC) if an inflammatory bowel disease. Is smoking a risk factor for UC?

A
  • no
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31
Q

Ulcerative colitis (UC) if an inflammatory bowel disease. It generally begins in the rectum and works its way through the colon. What % of patients require surgery?

A
  • 20-30%
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32
Q

Chrohns disease (CD) is an inflammatory bowel disease. Does CD affect the whole GIT?

A
  • it can affect anywhere in the GIT
  • mouth to anus
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33
Q

Chrons disease (CD) if an inflammatory bowel disease. How does CD present when we look at tissue biopsies from the colon? Is the inflammatuion continous or is it patchy?

A
  • inflammation is patchy
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34
Q

Chrons disease (CD) if an inflammatory bowel disease. In addition to patchy inflammed areas, CD can cause other changes in the tissue, such as?

A
  • fistulas = abnormal connection between 2 hollow tubes
  • stricture = abnormal narrowing of GIT
  • abscesses = collection of pus (inflammation, immune and dead cells)
  • perianal disease = inflammed anal tissue
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35
Q

Crohns disease (CD) is an inflammatory bowel disease. How does DC present when we look at tissue biopsies from the colon? Does the inflammatuion affect all 4 layers of the GIT or just the top layers?

A
  • transmural
  • affects all 4 layers
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36
Q

In crohns disease are granulomas present?

A
  • yes
  • but non necrotising
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37
Q

In crohns disease associated with smoking?

A
  • yes
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38
Q

What % of patients with crohns disease require surgery?

A
  • 50%
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39
Q

In ulcerative colitis (UC) patients are at risk of perforation in an acute flair up of UC. Why is perforation in UC patients a medical emergancy?

A
  • perforation is where mucosa is damaged and gas enters GIT wall
  • this can expand and eventually rupture
  • very dangerous
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40
Q

In ulcerative colitis (UC) patients are at risk of perforation in an acute flair up of UC. Perforation is where mucosa is damaged and gas enters the GIT wall, which can expand and eventually rupture. If a patient presents with this, how must they be treated?

A
  • IV hydrocortisone
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41
Q

When treating chronic ulcerative colitis (UC) what is the order of treatments from: thiopurines, mesalazines and biologics?

A

1st = mesalazines

2nd = thiopurines

3rd = biologics

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42
Q

When treating chronic crohns disease what is the first treatment from thiopurines and biologics?

A

1st - thiopurines

2nd - biologics

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43
Q

What is Primary sclerosing cholangitis (PSC)?

A
  • a chronic liver disease (suggested to be autoimmune)
  • characterized by a progressive course of cholestasis )blockage of bile)
  • causes inflammation and fibrosis of the intrahepatic and extrahepatic bile ducts
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44
Q

Why is Primary sclerosing cholangitis (PSC) important to consider in inflammatory bowel diseases?

A
  • 80-90% of patients with PSC also have ulcerative colitis (UC)
  • 5% of patients with UC have PSC
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45
Q

When doing an abdominal examination the acronym SOCRATES can be useful, what does it stand for?

A
  • S = site of pain
  • O = onset (when did it start)
  • C = character (sharp/dull)
  • R = radiates (e.g. loin to groin)
  • A = associated symptoms
  • T = time
  • E = excentuate/relieve
  • S = severity
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46
Q

Where are the 3 main areas of the abdomen we should consider?

A

1 - foregut

2 - midgut

3 - hindgut

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47
Q

When talking to a patient about diarrhoea, what chart should we use?

A
  • bristol stool chart
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48
Q

When talking to a patient about diarrhoea, what should we ask about that might be present in the stool?

A
  • blood
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49
Q

When talking to a patient about diarrhoea in addition to discussing the bristol stool chart and asking about the prescence of blood, what should we ask about?

A
  • timings
  • morning (IBS)
  • evening
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50
Q

When a patient presents with diarrhoea what would be the most common differentials?

A
  • infection
  • IBS
  • IBD (ulcerative colitis and crohns)
  • coeliac disease
  • colorectal cancer
  • neuroendocrine tumour
  • diverticulitis
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51
Q

If a patients presents with rectal bleeding, what should we ask the patient?

A
  • colour
  • mixed in with stool or on toilet paper
  • if on toilet paper indicated rectal bleed (haemorrhoids)
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52
Q

When a patient presents with rectal bleeding what would be the most common differentials?

A
  • colorectal cancer
  • haemorrhoids
  • ischaemic colitis
  • diverticulitis
  • IBD
53
Q

When a patient presents with rectal bleeding what needs to be ruled out?

A
  • upper GIT bleeding
54
Q

If a patient presents with GIT symptoms what are the 2 main red flags?

A
  • rectal bleeding
  • weight loss
55
Q

What causes cystic fibrosis?

A
  • mutation of cystic fibrosis transmembrane conductance regulator
  • CFTR
56
Q

What does autosomal recessive mean?

A
  • mutation affecting the non-sex chromosomes
  • recessive means you need a mutated gene from mum and dad
57
Q

What does autosomal dominant mean?

A
  • mutation affecting the non-sex chromosomes
  • dominant means you need only one mutated gene from a parent
58
Q

Cystic fibrosis can cause thick and sticky scretions in the GIT due to a mutation of the cystic fibrosis transmembrane conducatance tregulator (CTFR). Cl- does not get secreted, meaning H2O is not drawn into the secretions such as mucus. What can this cause in the GIT, especially in babies?

A
  • blockage of the ducts in the pancreas
  • Distal Intestinal Obstructive Syndrome (DIOS)
59
Q

Cystic fibrosis can cause thick and sticky scretions in the GIT due to a mutation of the cystic fibrosis transmembrane conducatance tregulator (CTFR). Cl- does not get secreted, meaning H2O is not drawn into the secretions such as mucus. This can this cause Distal Intestinal Obstructive Syndrome (DIOS). How can this be treated?

A
  • rehydrate
  • laxatives
60
Q

Cystic fibrosis can cause thick and sticky scretions in the GIT due to a mutation of the cystic fibrosis transmembrane conducatance tregulator (CTFR). Cl- does not get secreted, meaning H2O is not drawn into the secretions such as mucus. This can cause blockage of the pancreatic ducts, what can this then lead to?

A
  • acute pancreatitis
  • acute can then cause chronic pancreatitis
61
Q

In addition to affecting the lungs, pancreas and GIT, what other organs can be affected in cystic fibrosis?

A
  • oesophagus (gastro oesophageal reflux disease (GORD))
  • liver
  • gall bladder
  • biule ducts
62
Q

In patients with cystic fibrosis the GIT can be affected. What are cystic fibrosis patients at an increased risk of, which needs to be screened?

A
  • colorectal cancer
  • screened >40 years old using colonoscopy or qFIT
63
Q

What is refeeding syndrome?

A
  • malnourished patient begins refeeding
  • the additional food causes spikes in insulin
  • insulin makes cells absorb K+, Mg2+ and phosphate, decreasing already low levels in the blood
  • cardiac, pulmonary and neurological symptoms can all occur and be fatal
64
Q

When considering enteral feeding, what are the 3 potential approaches that can be used?

A
  • oral feeding
  • naso-gastric feeding
  • naso-jejunem feeding
65
Q

There are 3 approaches to enteral feeding which are oral feeding, naso-gastric feeding and naso-jejunem feeding. These are temporary, what are the 2 alternatives that can be used for enteral feeding?

A
  • percutaneous endoscopic gastrostomy (PEG), camera is fed down throat to collect tube
  • radiologically inserted gastrostomy (RIG), tube is inserted using radiological methods
66
Q

What are the 2 cells in the islets of langerhands in the pancreas that secrete insulin and glucagon?

A
  • alpha cells = glucagon
  • beta cells = insulin
67
Q

What is the range of blood glucose that should be maintained?

A
  • 3.5 - 8mmol/L
68
Q

What is the blood glucose in hypoglycaemia?

A
  • <3.5mmol/L
69
Q

In the fed and fasted state what would we expect to see in terms of the insulin and glucagon ratios?

A
  • fed = high insulin:glucagon ratio
  • fasted = low insulin:glucagon ratio
70
Q

In all patients with diabetes, what % is type 1 and type 2?

A
  • type 1 = 10%
  • type 2 = 90%
71
Q

What is the general phenotype of patients with type 1 and type 2 diabetes?

A
  • type 1 = thin, genetic cause, onset young age
  • type 2 = obese, lifestyle, insulin resistance
72
Q

What is insulinoma?

A
  • a small tumor in the pancreas
  • produces excessive amounts of insulin causing hypoglycaemia
73
Q

What are the symptoms of hypoglycaemia?

A
  • sweating
  • anxiety
  • palpatations
  • loss of cognitive function
74
Q

If a patient has hypoglycaemia, how can they be treated?

A
  • sugary drink
  • hypostop gel
  • dextrose via a drip
  • intramuscular glucagon
75
Q

What are the 4 types of blood measures that can be used to diagnose patients with diabetes?

A
  • random blood glucose
  • OGTT
  • fasting glucose

HBA1c

76
Q

In patients with diabetes, what are some of the non-metabolic problems that can occur in patients?

A
  • retinopathy (eye damage)
  • neuropathy (nerve damage)
  • nephropathy (kidney damage)
  • atherosclerosis (small blood vessel damage)
77
Q

How can we distinguish between if a patient has acute or chronic liver disease?

A
  • medical hisotry
78
Q

What is hepatocellular and cholestatic disease?

A
  • hepatocellular disease related to inside the liver
  • cholestatic disease relates to the bile ducts
79
Q

If a patient is suspected of having liver disease, and the platelet count comes back low, does this suggest acute or chronic liver disease?

A
  • portal hypertension forces blood back into spleen
  • spleen destroys platelets
  • caused by chronic liver disease
80
Q

When trying to determine if a patient has hepatocellular of cholestatic disease, what can we determine in the liver enzymes?

A
  • hepatocellular = raised ALT and AST
  • cholestatic = raised ALP and GGT
81
Q

In patients with liver failure, what may they present with?

A
  • encepalopathy
  • jaundice
  • hypoalbuminaemia
  • hypoglycaemia
  • renal failure
82
Q

What is portal hypertension?

A
  • increased resistance to portal blood flow through the liver
  • most common cause is liver cirrhosis
83
Q

Portal hypertension, which is an increase in pressure in the portal vein, with the most common cause being liver cirrhosis. What else can this then go on to cause in the organs supplying the portal vein?

A
  • build up of pressure
  • ascites (fluid in abdomen)
  • splenomegaly
  • varices
84
Q

Jaundice can be caused by liver damage. The start of this process is due to the death of all RBCs. What happens to the RBCs and in the macrophages?

A
  • macrophage engulf old RBCs and break RBCs into heme and globin
  • heme breakdown forms iron and protoporphyrin
  • protoporphyrin is converted into un-conjugated biliruben (UCB)
85
Q

Jaundice can be caused by liver damage. The start of this process is due to the death of all RBCs, where macrophage engulf old RBCs and break RBCs into heme and globin. The heme is then broken down to form iron and protoporphyrin. Protoporphyrin is converted into un-conjugated biliruben (UCB). UCB is lipid soluble so cannot freely move in plasma. What does it have to bind with to makes its way to the liver?

A
  • albumin
86
Q

Jaundice can be caused by liver damage. The start of this process is due to the death of all RBCs, where macrophage engulf old RBCs and break RBCs into heme and globin. The heme is then broken down to form iron and protoporphyrin. Protoporphyrin is converted into un-conjugated biliruben (UCB). UCB is lipid soluble so cannot freely move in plasma, therefore it binds to albumin and makes its way to the liver. What then happens to UCB in the liver?

A
  • UCB is converted to conjugated bile (CB)
  • uridine glucuronyl transferase (UGT) does this in hepatocytes
  • CB is now water soluble
87
Q

Once conjugated biliruben (BC) has been created in the hepatocytes, where does it go?

A
  • enters the bile cannaliculi and travels to the gall bladder
  • stored in the gall bladder as bile
88
Q

The conjugated bile that is present in the gall bladder as bile can be secreted in bile for what?

A
  • bile is secreted into GIT to aid fat digestion
89
Q

Once conjugated biliruben (CB) is in the GIT as a component of bile, what happesn to CB in the GIT?

A
  • converted into urobilinogen by microbes in the GIT
90
Q

Once conjugated biliruben (CB) is in the GIT as a component of bile, it is converted into urobilinogen (UBG) by microbes in the GIT. What 2 things can then happen to UBG?

A

1 - can be reduced to stercobilin and excreted, making stool brown

2 - UBG can be reabsrobed

91
Q

Some urobilinogen (UBG) can be reabsorbed by the enterohepatic circulation, where it enters the plasma as urobilin. What then happens to this urobilin?

A
  • some is sent to kidneys for excretion, making urine yellow
  • most is sent to the liver
92
Q

Jaundice can be pre-hepatic, hepatic or post hepatic. If the hepatocytes or biles ducts are damaged, meaning the cause would be hepatic would the jaundice be caused by conjugated or unconjugated biliruben?

A
  • conjugated biliruben
93
Q

Jaundice can be pre-hepatic, hepatic or post hepatic. If there is problems getting the unconjugated biliruben to the liver, does this mean that the cause is pre-hepatic, hepatic or post hepatic?

A
  • pre hepatic
94
Q

What is Gilbert’s syndrome (GS)?

A
  • a condition in which you have higher than normal amounts of bilirubin in your blood
95
Q

What is the cause of Gilbert’s syndrome (GS)?

A
  • mutation causing low levels of uridine glucuronyl transferase (UGT)
  • so biliruben is not congugated
96
Q

There are 5 different types of viral hepatitis, A, B, C, D and E. Which of these are acute and which are chronic?

A
  • acute = A and E
  • chronic = B, C and D (start acute and become chronic)
97
Q

There are 5 different types of viral hepatitis, A, B, C, D and E. Hepatitis D cannot exist alone, which other viral hepatitis does it need?

A
  • B
  • B is bad, but B and D togther is even worse
98
Q

What % of patients with hepatitis B will serocovert (get rid of the infection) and what is the clinical sign patients have this?

A
  • 95% serocovert
  • patients present with jaundice
99
Q

Most people with hepatitis B acquire the virus in what way?

A
  • born with it
  • congenital
100
Q

Chronic hepatitis can be subdivided into 4 phases, what are these?

A

1 = immuno tolerent (high viral load but normal LFTs)

2 - immuno active (high viral load and LFTs and e antigen positive )

3 - inactive (low viral load and normal LFTs)

4 - immune active (low viral load, high LFTs and e antigen negative)

101
Q

Which of the 5 viral hepatitis can increase the risk of hepatocellular cancer?

A
  • B and C
  • most dangerous of the 5
102
Q

In patients with acute viral hepatitis, how can we expect to see their ALTs?

A
  • >1000s
  • helps distinguish betwen other hepatitis disease
103
Q

If the liver becomes inflammed what are the stages it progresses through?

A
  • steatosis
  • steatohepatitis
  • fibrosis
  • cirrhosis
104
Q

Othr than a biopsy, what are 2 ways liver fibrosis can be diagnosed?

A
  • FIB-4 score (need age, AST, ALT, platelets)
  • fibrosis scan
105
Q

What is the recommended limit for alcohol consumption?

A
  • 14 units
106
Q

Which group of patients are most likely to consume excessive alcohol?

A
  • 55-64 year olds
  • deprived areas and linked with crime and violence
  • males tne dot drink more than females
107
Q

Does alcoholic liver disease follow the same process as NAFLD?

A
  • yes
108
Q

What are some clinical presentations of chronic excessive alcohol?

A
  • dupuytren’s contracture
  • enlarged parotid gland
109
Q

What can we measure in the blood to determine if someone drinks excessive alcohol chronically?

A
  • raised MVC
  • raised AST is higher than ALT
  • increased IgA
110
Q

What is CAGE questrionnaire in alcoholic liver disease?

A
  • C = have you felt the need to Cut down uoutr alcohol
  • A = have you become Annoyed by someone criticising your alcohol
  • G = do you feel Guilty about your drinking
  • E = have you had an Eye opening moment
111
Q

HITS is an acronym used to describe someone with alcoholic withdrawal, what does HITS stand for?

A
  • H = Hallucinations
  • I = Insomnia
  • T = Tremen (confusion)
  • S = Shakes
112
Q

CIWA and SADQ are 2 regimes used in alcoholic withdrawal. What are they used for?

A
  • to determine the degree of treatment a patient with withdrawal may need
113
Q

The Wernicke Korsakoff syndrome is caused by Vitamin B1 (thiamine) deficiency. Alcohol can severely deplete thiamine levels. What is Wernicke encephalopathy is the acute reverisble stage of the syndrome, what is it?

A
  • neurological disorder caused by alcohol
114
Q

The Wernicke Korsakoff syndrome is caused by Vitamin B1 (thiamine) deficiency. Alcohol can severely deplete thiamine levels. What is Korsakoff syndrome is the chronic irreverisble stage of the syndrome, what is it?

A
  • severe memory dysfunction
  • psychosis
115
Q

Once we have finished auscultation of the abdomen, we would then examine the legs. We may see pyoderma gangrenosum, what is this and what may cause this?

A
  • inflammatory skin disease
  • painful pustules or nodules become ulcers that grow
  • common in crohns disease
116
Q

What is the classification of the lower GIT?

A
  • inferior to the suspensory muscle of the duodenum
  • ligament of Treitz
117
Q

Gastric cancer is one of the main diseases that can be caused by Helicobacter pylori (H. pylori). What are the 2 most common types of cancer caused by H. pylori?

A
  • adenocarcinoma (starts in mucus-producing glandular cells)
  • mucosa-associated lymphoid tissue (MALT) lymphoma (92-98% cases), can also cause non-hodgkins lymphoma
118
Q

A hiatal hernia is probably the second most common condition of the upper GIT. What is a hiatal hernia?

A
  • hiatal refers to the hiatus opening in diaphragm
  • stomach push through the diaphragm and into the oesophagus
120
Q

There are 2 types of hiatal hernias, a sliding hernia is the most common, accouting for 85-95% if hiatal hernias. What is a sliding hernia?

A
  • gastrooesophageal junction (GOJ) is mobile
  • GOJ slides into oesophagus and part of stomach follows through the oesophageal hiatus
  • diaphragmatic sphincter is lost
  • negative thoracic pressure pulls gastric contents into the oesophagus causing reflux
121
Q

There are 2 types of hiatal hernias, what are these called?

A

1 - sliding

2 - rolling

122
Q

What is a rolling hiatal hernia that accounts for between 5-15% of hiatal hernias?

A
  • gastrooesophageal junction (GOJ) remains fixed in its normal position below the diaphragm
  • part of the stomach pushes up and roles through the hiatus in the diaphragm next to the oesophagus
124
Q

In a sliding hiatus hernia the gastrooesophageal junction (GOJ) (which is where the oesophagus and stomach meet) is mobile and slides through the diaphragm sphincter and part of the stomach follows into the oesophagus. What are the most common symptoms of this?

A
  • mostly asymptomatic
  • reflux/dyspepsia (indigestion)
  • regurgitation or vomiting
  • dysphagia (swallowing difficulties)
126
Q

What symptoms does a rolling hiatal hernia that accounts for between 5-15% of hiatal hernia present with?

A
  • often asymptomatic
  • chronic non specific symptoms/signs
  • abdominal pain, early satiety, anaemia, dysphagia
  • risk of strangulation (1%) causing a surgical emergency
127
Q

Patients can present with ulcers in an acute or chronic manner. In acute symptoms, what are the 3 key symptoms?

A

1 - haematemesis (vomiting fresh blood)

2 - coffee-ground” vomiting

3 - melaena (dark sticky stool)

128
Q

In addition to the symptoms patients experience, clinicians can look for physical signs of coeliac disease. What are the most common?

A
  • anaemia causing glossitis (B12 and iron deficiency)
  • mouth ulcers
  • rash called dermatitis herpetiformis (skin rash similiar to herpes)
129
Q

What is the adenoma-carcinoma sequence?

A
  • stepwise progression from normal bowel mucosa to bowel cancer
  • can take years
  • hyperplasia, dysplasia, adenoma/polyp, carcinoma in situ to invasive carcinoma
131
Q

What is Familial Adenomatous Polyposis (FAP)?

A
  • autosomal dominant inherited disease
  • causes adenomatous polyposis coli (APC) mutation (tumour supressor)
  • results in uncontrolled cell growth and polyp formation
132
Q

What causes Lynch syndrome?

A
  • mutations in the DNA mismatch repair genes
  • screens repairs, erroneous insertions, deletions, and mis-incorporation of bases that can arise during DNA replication and recombination
  • can also repair DNA damage
133
Q

What is the Amsterdam criteria?

A
  • diagnostic criteria used by doctors
  • helps identify families who are likely to have Lynch syndrome

Year 1 NME (61 decks)

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