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MD > Gastrointestinal > Flashcards

Gastrointestinal Flashcards

1
Q

How to WBC find their way to the gut tissue?

A

a4b7 hunts down MADCAM in gut

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2
Q

What are the two main causes of cirrhosis?

A

Hepatitis infection and alcohol abuse.

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3
Q

What could cause pain in the left iliac fossa?

A

Colon issues, IBD, Inguinal hernias, Kidney stones

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4
Q

How often do the small and large bowels have episodes of peristalsis?

A

Small Int - every 3 mins
Large Int - every 15-30 minutes.

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5
Q

A key history question for gall stones?

A

Does the pain get worse after eating

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6
Q

Which liver enzymes come from where?

A

GGT and ALP from biliary tree
AST and ALT from hepatocytes

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7
Q

How do squamous cell carcinomas impact bone?

A

Paraneoplastic syndrome due to PTHrP - parathyroid hormone related protein

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8
Q

What does high transferrin typically indicate?

A

Body is searching for iron - iron deficiency.

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9
Q

Explain dysphagia in terms of liquids and solids.

A

If have difficulty with solids only = obstruction like cancer.
If have difficulty with both liquids and solids = neuro or muscular issue like spasms.

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10
Q

Mnemonic for absorption of key blood factors?

A

Dude Is Just Feeling Ill Bro
Duodenum - iron
Jujenum - Folate
Ileum - B12

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11
Q

Where does most water get reabsorbed in the gut?

A

Small intestine

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12
Q

Where are carbs digested?

A

Starts in mouth with amylase, more amylase in duodenum, brush border begins at jujunum which releases all the small sugar enzymes like maltase - absorbed here for portal system.

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13
Q

Where are proteins absorbed in the small intestine?

A

All 3 levels (all of small int)

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14
Q

How and where do fats gets digested and absorbed?

A

Start in mouth with chewing and a small amount of lipases, gastric lipases in stomach, in duodenum get bile salts to emulsify fats and get pancreatic lipases - fats mostly absorbed in the ileum.

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15
Q

What symptom will poor bile reabsorption result in?

A

Diarrhoea - bile salts irritate the intestines, if they make it to the colon they will cause increased motility. The bile salts will drag water with them.

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16
Q

Why can maldigestion cause bloating?

A

If absorption is bad, too many nutrients will reach bacteria in the colon, they will make gasses out of them due to fermentation.

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17
Q

Which protein carries conjugated bilirubin?

A

Albumin

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18
Q

How can bilirubin exit as urine?

A

It can either be made into urobilinogen in the gut OR if bile is building up it can enter the blood from the liver and enter the kidney - that’s no good.

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19
Q

What happens if bilirubin from the liver is blocked due to a post-hepatic cause?

A

Bilirubin will go backwards and into the blood

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20
Q

What could cause pre-hepatic jaundice?

A

All caused by unconjugated bilirubin - leads to CNS issues.
Could be due to:
-haemolysis
-crap liver
- albumin competition
- low albumin

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21
Q

Will urine bilirubin be elevated in a pre-hepatic cause?

A

NO - just builds up.
Bilirubin in the urine is always conjugated, so must be hepatic or post-hepatic cause.

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22
Q

What type of bilirubin issue (hepatic, pre or post) would cause regular brown stools with urine full of bilirubin?

A

Hepatic only.
Bilirubin can still get to gut, so not a post-hepatic.
Bilirubin present in urine so can’t be pre-hepatic.

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23
Q

List the functions of a liver.

A
  • blood glucose
  • stores vitamins
  • makes bile
    -makes complement
    -makes albumin
  • makes coagulation factors
  • detoxification
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24
Q

Describe the transmission of each type of Hepatitis

A

Ass and Eating - A and E are fecal-oral
The rest are body fluids. C is Chronic, B is acute or chronic, D is dependant on B.

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25
Q

What does steatorrhea indicate?

A

fatty stools are likely due to poor absorption or not enough bile to allow for absorption.

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26
Q

How would post-hepatic issues present on history?

A

urine - low urobilinogen or urobilin (may be pale)
poo - pale due to no stercobilinogen
also would have steatorrhea and vitamin deficiency (ADEK)

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27
Q

Is unconjugated or conjugated bilirubin a bigger risk?

A

Unconjugated - affects CNS

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28
Q

What pathology can GORD lead to?

A

It causes basal cell hyperplasia which becomes Barrett’s Esophagus - squamous to columnar metaplasia. SALMON MUCOSA.

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29
Q

What autoimmune conditions often clump with coeliac?

A

T1D and Thyroid diseases.

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30
Q

What are the 3 coeliac histo findings?

A
  • Villous atrophy
  • Crypt hyperplasia
  • Intra-epithelial lymphocytes
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31
Q

What are the 2 antibodies screened for in coeliac?

A

Tissue transglutaminase IgA and deaminated gliadin IgG.

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32
Q

Compare Crohn’s to UC.

A

Chrons - ass to mouth, skip lesions, cobblestone appearance, transmural, cause fistulae, steatorrhea.

UC - Just colon and rectum, polyps, just the submucosa, typically associated with blood.

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33
Q

Complications of IBD?

A

Chrons - fistulas, cancer, vitamin deficiency
UC - vitamin deficiency, cancer, toxic megacolon

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34
Q

How does the cephalic phase impact stomach acid?

A

Cephalic phase, thinking about eating, will cause Ach release to increase acid and will also inhibit somatostatin which itself inhibits acid production.

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35
Q

What chemicals does the duodenum produce to aid in digestion?

A

CCK - stimulates pancreas to release lipases
Secretin - for pancreatic bicarbonate
Somatostatin - inhibit acid

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36
Q

What are the gut divisions? What arteries supply them?

A

Foregut - mouth to duodenal papilla. Coeliac trunk.
Midgut - duodenal papilla to 2/3 of transverse colon. Superior Mesenteric.
Hindgut - the rest. Inferior mesenteric.

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37
Q

Which IBD can cause granulomas?

A

Chrons

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38
Q

Fowl smelling stools typically means what parasite for MD1?

A

Giardia

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39
Q

Which hepatitis is incurable?

A

Chronic HBV

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40
Q

Why can liver failure cause esophageal varices?

A

Due to portosystemic anastamoses - blood will divert past the portal system if it is under huge pressure, which can lead to blood buildup and even rupture in key areas like the lower esophagus.

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41
Q

Name 3 causes of hematemesis.

A
  1. Burst varice (liver damage)
  2. Peptic ulcer
  3. Cancer
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42
Q

What are the 5 sites of portosystemic anastamoses?

A

Lower esophagus (gastroesophageal junction), umbilicus, anal canal, retroperitoneal, bare area of liver.

“varices of the Gut, Butt and Caput”

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43
Q

What causes leuchonychia?

A

Low albumin

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44
Q

Which liver enzymes are alcohol related?

A

GGT and AST - Giant Gin and Tonic, A Shot Thanks

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45
Q

What conditions can be suggested best on the ratio of which two liver enzymes?

A

If AST is more than ALT - think alcohol
If ALT is more than AST - think viral (hepatitis)

46
Q

Describe the rectus sheath and which muscles form it

A

Formed by the external and internal obliques and the transversus abdominus. The middle line of the abs is the linea alba.

47
Q

How does the rectus sheath change as it goes down?

A

rectus sheath is posteriorly deficient in the bottom 1/4 of the abdomen - only covers anterior. This means the rectus abdominus directly touches the transversalis fascia in that area.

48
Q

What level is the transpyloric plane?

A

L1

49
Q

What are the folds of the stomach called?

A

Rugae

50
Q

Mnemonic for retroperitoneal structures?

A

ugh, kim possible caught doing ron.
Ureters, kidneys, pancreas, colon (except transverse), duodenum (most), rectum.

51
Q

Where do the hepatic veins empty?

A

directly in IVC

52
Q

Describe the ducts of the billiary system

A

The left and right hepatic ducts join to form the common hepatic which meets the cystic duct (connect gallbladder) to form the common bile duct.

53
Q

Where are Paneth cells and what do they do?

A

Small intestine, they make antimicrobials.

54
Q

What are some histology giveaways to workout where you are in the small intestine?

A

Duodenum - submucosal glands i.e a layer of glands UNDERNEATH another layer of glandular tissue.

Ileum - Peyer’s patches

55
Q

Mince meat Histology is located where?

A

Liver

56
Q

CCK is made by which cells and what does it do to the brain?

A

CCK is made by enteroendocrine cells and sends saiety signals to the brain.

57
Q

Which cells make pepsinogen?

A

Chief cells of stomach

58
Q

CCK causes release of which 3 molecules from the pancreas? What other organ does it target?

A

Amylase, lipases, trypsinogen (all 3 biomacromolecule types).
Gallbladder.

59
Q

Which enzymes does trypsin activate?

A

Other peptidases like chymotrypsin and carboxypeptidase as well as colipase which will then go on to activate pancreatic lipases.

60
Q

What molecule carries triglycerides from the gut?

A

Chylomicron

61
Q

Where are bile acids resorbed?

A

Ileum

62
Q

Which two systems innervate the esophagus?

A

The Vagal nerve and the enteric nervous system.

63
Q

What level does the iliac artery bifurcation occur?

A

L4

64
Q

Describe the course of the Coeliac trunk.

A

Starts at L1.
Splits into 3 - the left gastric artery to do the stomach and esophagus, the common hepatic and the splenic artery.

NOTE ALL THE ORGANS IN THIS SYSTEM ARE ALL BY THE COELIAC TRUNK. So just think hard and you’ll be able to work out where they arise from.

65
Q

Which arteries supply the stomach and where do they come from?

A

lesser curve of stomach = left gastric
fundus = short gastric artery of splenic
the greater curve is done by the right and left epiploic arteries - which come off the hepatic and splenic respectively.

66
Q

Where does the superior mesenteric start and what does it supply?

A

L1 as with the coeliac trunk. Supplies the bottom 1/3 of the duodenum, some of the pancreas and the gut all the way to 1/3 of the way down the transverse colon.

67
Q

What are the two exocrine cell types of the pancreas and what do they make?

A

Acinar cells - enzymes
ductal cells - carbonate

68
Q

Mallory Denk bodies are a sign of what?

A

Liver Damage

69
Q

What is the main liver cancer I need to know?

A

Hepatocellular carcinoma

70
Q

Name a factor predisposing someone to gallbladder cancer.

A

Chronic cholecystitis

71
Q

Does pancreatitis cause steatorrhea?

A

yes - no good lipases = fat doesnt get absorbed.

72
Q

What 2 molecules do gastric chief cells make?

A

pepsinogen and gastric lipases.

73
Q

If you see sawtooth histology, what are you thinking?

A

Hyperplastic polyps of the colon.

74
Q

Iron anaemia in old men is a red flag for what?

A

GIT cancer

75
Q

name the benign polyp dysplastic condition?

A

Adenoma

76
Q

Treatment for diarrhoea?

A

Typically just fluids, dont usually give antibiotics for diarrhoea unless it’s serious like Salmonella.

77
Q

Name two molecules that inhibit stomach acid secretion?

A

Somatostatin and prostoglandin

78
Q

Describe the stomach acid production pathway and which cells are involved.

A

G cells make gastrin, which binds go CCK receptor on ECL cells which make histamine which binds to H2 on parietal cells which make acid.
parasympathetic can use Ach to activate any of these levels.
Somatostatin can inhibit any of these levels.

79
Q

Name 3 drug classes for stopping stomach acid.

A
  1. Antacids eg. aluminium
  2. H2 histamine receptor antagonist
  3. Proton Pump Inhibitors - best one because they will block all acids. eg. Omeprazole
80
Q

What 3 classes of drugs would be used for the lower GIT?

A

Motility Stimulation - anti dopamine (dopamine stops gut movement).
Anti-motility - opioids
Anti-spasmodics - anticholinergic M3.

81
Q

How can alcohol consumption impact Warfarin efficacy?

A

All to do with enzyme CYP2E1 which helps liver deal with alcohol.
Chronic alcohol use will cause too much of the enzyme to be made, so it will metabolise warfarin easily and warfarin will be less effective.
Binge drinking will cause competition over the enzyme so warfarin will not be broken down as fast and it will be overeffective.

82
Q

Is Salmonella part of the microbiota?

A

it is NEVER normal flora.

83
Q

What organism is black on DHA plates?

A

Salmonella

84
Q

How to know if a gut histology villi is dysplastic?

A

it will be darker purple then the surrounding epithelium

85
Q

Explain the process that leads from alcohol consumption to portal hypertension and liver disease.

A

Alcohol turns into acetylaldehyde which turns into acetate.
if there is too much alcohol, other mechanisms like microsomes and peroxisomes will chime in to help but will produce ROS and peroxide.
This makes hepatocytes mad, and in response they release endothelin and TGF-B into the space of Disse which causes the stellate cells to stimulate fibrosis.
This will reduce the size of the sinusoid, causing hypoxia which will further harm hepatocytes.
All of this will cause portal hypertension.

86
Q

urine is dark in which type of jaundice?

A

hepatic and post-hepatic

87
Q

stools are pale in which type of jaundice?

A

post-hepatic and a little bit in hepatic

88
Q

Which test is best to check for liver function?

A

Prothrombin time.
LFTs check for damage but not function.

89
Q

What is Gilbert’s syndrome?

A

Unable to process jaundice

90
Q

How do ascites form?

A

Liver damage leads to portal hypertension. Straight away this is going to lead to fluid buildup in the abdomen but there is another piece to the puzzle.
Portal hypertension will lead to splenic vasodilation into systemic vasodilation, this will lower blood pressure chronically leading to RAAS activation and hanging onto fluid.

91
Q

List the 5 sites of portosystemic anastamoses?

A
  1. Umbilicus
  2. Bare area of liver
  3. Peptoesophageal junction
  4. Retroperitoneal structures
  5. Upper rectum
92
Q

Describe the risk smoking poses to IBD.

A

Crohns - smoking is a huge risk factor
UC - smoking is protective

93
Q

What classic histology finding is evident in liver disease?

A

Mallory Denk bodies

94
Q

What are the targets for histamine based anti-emetics?

A

CTZ in brain and ECL cells

95
Q

How will Shigella appear on DCA and MAC?

A

DCA - beige/pink
MAC - beige (non lactose fermenter)

96
Q

What is function of the abdominal mesentery?

A

To attach the viscera to the posterior abdominal wall

97
Q

What is the usual outcome of Hepatitis C?

A

Chronic infection for life

98
Q

What type of epithelium is the stomach?

A

Simple columnar

99
Q

Which cell type makes CCK?

A

I cells

100
Q

CCK is released due to presence of which biomacromolecules?

A

Protein and lipids

101
Q

Which ligament deficiency forms the epiploic foramen and what structure is posterior to the foramen?

A

Hepatoduodenal ligament, IVC is posterior.

102
Q

Small abdominal red spots that blanch on touch are typically what?

A

Spider naevi

103
Q

Which hepatitis causes ground glass cells on histo?

A

HBV

104
Q

Which molecules are released in the cephalic phase of eating?

A

Acid and pepsinogen

105
Q

What kinetic order is the removal of ethanol?

A

Zero order kinetics

106
Q

What type of epithelium is the esophagus?

A

Stratified squamous

107
Q

Which HLA types are implicated in celiac?

A

HLA DQ 2/8

108
Q

Which rib covers most of the spleen?

A

10

109
Q

Describe the molecular targets of anti-emetic drugs? Which of these drugs has no side effects?

A

-Ach
- H1
- Serotonin (5HT3) - no side effects

110
Q

What drug types are used to stop motion sickness? What are some side effects?

A

H1 antagonists - drowsy (eg. phernergan)
M1 antagonists - (bromides) - anti-cholinergic effects
D2 Dopamine antagonists - can cause gut motility (emptying)

111
Q

What 3 types of drugs are used in the upper GIT?

A
  • antacids
  • H2 antagonists
  • Proton pump inhibitors - best
112
Q

What 3 types of drugs are used in the lower GIT?

A
  • anti motility - opiods
  • motility stimulants - dopamine antagonists
  • anti spasmodics - anti cholinergic drugs

MD (17 decks)

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