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GI system > GI tract > Flashcards

GI tract Flashcards

1
Q

How is the stomach lining protected against autodigestion?

A

gastric lining is protected by:
- mucus secreted by surface epithelial and mucous neck cells
- bicarbonate secreted by epithelial cells under mucous layer
these processes are prostaglandin-dependent so using NSAIDs inhibits them and increases risk of gastritis and ulcers

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2
Q

what are the phases of regulation of gastric acid secretion and stomach emptying?

A

cephalic phase
gastric phase
intestinal phase

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3
Q

what stimulates the cephalic phase?

A

sight, smell, taste and thoughts of food activates the parasympathetic nervous system

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4
Q

what happens in the cephalic phase?

A

stimulus activates the submucosal plexus which causes the secretion of mucus from mucus cells, pepsinogen and HCl from parietal cells
Gherlin is also released from stomach when it is empty and acts on hypothalamus to stimulate appetite, gastric secretions and motility

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5
Q

16SrRNA sequencing

A

for identifying bacteria - new species

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6
Q

what stimulates the gastric phase?

A

process of food entering the stimulates stretch receptors in the stomach

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7
Q

what happens in the gastric phase?

A

stretch receptors activate the submucosal plexus, myenteric plexus and parasympathetic nervous system - vagus nerve
submucosal plexus = causes the release of mucus, pepsinogen, HCl and gastrin
myenteric plexus increases the contractions of stomach
presence of gastrin and vagus nerve causes release of histamine

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8
Q

what does histamine do?

A

stimulates the parietal cells to release more HCl

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9
Q

where is mucus produced?

A

mucous cells of stomach

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10
Q

where is pepsinogen produced?

A

chief cells of stomach

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11
Q

where is gastrin produced?

A

G cells of stomach

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12
Q

where is somatostatin produced?

A

D cells of stomach

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13
Q

where is HCl produced?

A

parietal cells of stomach

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14
Q

where is intrinsic factor produced?

A

parietal cells of stomach

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15
Q

what stimulates the intestinal phase?

A

process of chyme being in duodenum activating duodenal stretch receptors and chemoreceptors

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16
Q

what happens in the intestinal phase?

A

stretch receptors and chemoreceptors stimulate myenteric plexus and release of inhibitory hormones
myenteric plexus is inhibited by this process, reducing contraction and motility
small intestine releases secretin, somatostatin, leptin and CCK

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17
Q

secretin

A

released from S cells in response to low pH which stimulates pancreatic and bile secretions

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18
Q

somatostatin

A

released from D cells

inhibits chief cells, reducing the concentration of pepsinogen and inhibits parietal cells, reducing secretion of HCl

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19
Q

leptin

A

released by adipose tissue, acts on hypothalamus to suppress appetite and regulate adipose tissue mass

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20
Q

CCK

A

released from I cells which causes the gallbladder to contract to release bile from gallbladder and stimulates pancreatic secretions

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21
Q

stomach motility

A
  • pacemaker cells initiate weak peristaltic waves that move towards antrum and last 15-20 seconds
  • peristaltic wave reaches antrum and intensity of contraction increases, causing contents within antrum to become under higher pressure
    wave continues towards the pylorus, digging deep into the food
    wave continues to pylorus, which contracts preventing the majority of contents from entering duodenum so only a few ml of chyme enter duodenum with each mixing wave
    forces contents of antrum back up to main body of stomach - retropulsion
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22
Q

retropulsion

A

important for mixing of stomach contents

takes around 1-3 hours to empty stomach

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23
Q

what factors inhibit the stomach emptying?

A

factors that inhibit stomach motility and secretions are caused by food entering duodenum:
- duodenal distension
- irritation of duodenal mucosa
- lipids, fatty acids, proteins and CHO
- acidity - pH>3.5-4
- increase in osmolarity
myenteric reflex - stretching of stomach promotes and increases pyloric pump and inhibits pylorus tone
CCK, GIP and secretin are released to inhibit

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24
Q

GIP

A

gastric inhibitory polypeptide

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25
Q

what mediates the vomiting centre?

A

histamine - H1 and serotonin 5-HT3

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26
Q

what are the vomiting trigger zones?

A

chemoreceptor trigger zone in medulla oblongata
cortex
labyrinth - vestibular nuclei
GI receptors to nucleus tractus solitarius to vomiting centre

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27
Q

chemoreceptor trigger zone in medulla oblongata

A

mediated by dopamine - D2 and histamine - H1

triggered by chemotherapy, opioids and anaesthetics

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28
Q

cortex

A

triggered by smell, sight and anxiety

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29
Q

Labyrinth

A

vestibular nuclei
mediated by ACh M1 and histamine H1
triggered by motion and anaesthetics

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30
Q

GI receptors

A

to nucleus tractus solitarius to vomiting centre
mediated by serotonin - 5-HT3
triggered by distension and toxins

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31
Q

how does emesis occur?

A

held inspiration/ breath held which increases abdominal pressure
glottis closes preventing aspiration
duodenum contracts, blocking transit of contents in the stomach
gastro-oesophageal sphincter relaxes
abdominal wall contracts abruptly
causing gastric contents to be ejected forcefully

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32
Q

what is the function of the small intestine?

A

continued digestion and absorption of nutrients
90% of nutrient absorption occurs here
most occurs in first 1/4 of small intestine - duodenum and jejunum

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33
Q

what are the sections of the small intestine?

A

3:

  • duodenum
  • jejunum
  • ileum
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34
Q

what does the duodenum receive and from what?

A

receives secretions from the liver, gallbladder and pancreas

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35
Q

what breaks down sucrose?

A

sucrase-isomultase - brush border enzyme

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36
Q

what are the types of lipases?

A

lingual lipase
gastric lipase
pancreatic lipase
lipoprotein lipase

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37
Q

what does lipoprotein lipase do?

A

breaks down chylomicrons into free fatty acids in blood vessels and lymphatic vessels

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38
Q

Lipoproteins

A

involved in transport of lipids:

  • chylomicrons
  • very low density lipoproteins
  • intermediate density lipoproteins
  • low density lipoproteins
  • high density lipoproteins
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39
Q

chylomicrons

A

transports dietary triglycerides to peripheral tissues

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40
Q

very low density lipoproteins

A

transports endogenous to peripheral tissues

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41
Q

low density lipoproteins

A

transports cholesterol to peripheral tissues and can cause atherosclerosis

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42
Q

high density lipoproteins

A

transports cholesterol from peripheral tissues to liver

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43
Q

what is the function of the pancreas?

A

involved with secreting substances for digestion

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44
Q

what exocrine substances does the pancreas secrete?

A 
bicarbonate 
enzymes in response to secretin and CCK:
- trypsin
- chromotrypsin
- carboxypeptidase
lipase
- amylase
- ribonuclease
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45
Q

bicarbonate

A

released by ductular cells to provide optimum pH for enzyme activity

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46
Q

trypsin

A

released by acinar cells

activated by enteropeptidase

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47
Q

chromotrypsin

A

released by acinar cells

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48
Q

carboxypeptidase

A

breaks down proteins and released by acinar cells

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49
Q

what cells produce lipase, ribonuclease, deoxyribonuclease and amylase

A

acinar cells of pancreas

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50
Q

ribonuclease and deoxyribonuclease

A

break down nucleic acids

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51
Q

endocrine pancreas

A 
secretes:
insulin
somatostatin
glucagon
pancreatic polypeptide
ghrelin
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52
Q

insulin

A

beta cells

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53
Q

somatostatin

A

D cells

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54
Q

glucagon

A

Alpha cells

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55
Q

pancreatic polypeptide

A

F cells

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56
Q

what is bile made up of?

A

bile salts, lecithin - phospholipids, bicarbonate ions and cholesterol

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57
Q

how much bile is produced daily?

A

3-4g

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58
Q

what does the liver and gallbladder secrete?

A

bile
cholesterol
bile pigments - including metabolic end products
trace metals

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59
Q

what are the main functions of the liver?

A 
carbohydrate, amino acid and lipid metabolism 
drug/ toxin metabolism
synthesis of proteins - albumin and coagulation factors 
synthesis and secretion of bile 
storage of vitamins and minerals 
immune regulation
glycogenolysis and glyconeogenesis
involved in metabolism of LDL and HDL
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60
Q

role of liver in clotting cascade

A

makes clotting factors

vitamin K dependent factors - 10,9,7,2

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61
Q

bilirubin metabolism

A

RBCs broken down into free haemoglobin in kidneys
free heamoglobin is broken down at liver, kidneys and bone marrow into haem and globin
globin broken down into amino acids and recycled
haem is broken down into biliverdin and iron
iron is recycled
biliverdin converted to unconjugated bilirubin > conjugated bilirubin in liver
bilirubin secreted into bile and into duodenum via biliary tree
bilirubin reabsorbed from GI tract and enters enterohepatic circulation back to liver, it is filterd from kidneys into urobilin and some bilirubin remains in GI tract
forms sterocobilin - faeces

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62
Q

liver role in drug metabolism

A

principle site of drug metabolism:
•Drugs (orally taken) are absorbed in the gut and pass to the liver via the portal vein.
•The drugs undergo ‘first pass metabolism’ before entering the systemic circulation.
-Cytochrome P450 enzymes are abundant in the liver, they are involved in drug metabolism. Such reactions include oxidation, hydrolysis and hydroxylation.

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63
Q

role of liver in vitamins and minerals

A

stores vitamin B12, A, D in large amounts
stores vitamin K and folate in small amounts
stores minerals like iron and copper

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64
Q

parts of the large intestine

A 
cecum
ascending colon
transverse colon
haustra
descending colon
sigmoid colon
rectum
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65
Q

functions of the large intestine

A

reabsorption of water and some nutrients

•Storage and compaction of faecal material prior to defacation

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66
Q

defecation reflex

A

the mass movement of faeces, which has been caused by the stretch of the rectum which causes the internal anal sphincter to relax and the rectum and sigmoid colon to contract. If the external anal sphincter is relaxed, defecation occurs.

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67
Q

what are the functions of the gut microbiome?

A
  • Metabolise, digest, ferment CHOs and lipids which aid absorption.
  • Synthesis vitamins such as vitamin B and vitamin K.
  • Protect the gut from pathogens and are involved with developing the immune system.
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68
Q

main cause of stomach ulcers

A

helicobacter pylori

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69
Q

what is the microbiome?

A

all the microorganisms in an environment

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70
Q

what is the microbiota?

A

microorganisms themselves in a microbiome

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71
Q

what is species richness?

A

how many species

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72
Q

what is species eveness

A

measure of evenness

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73
Q

how can microbiome affect change of developing health conditions?

A
  • C-section leads to increased asthma and obesity (diff microbes break down sugars, gut handling of sugar and appetite) (diff microbiome).
  • Bacteria can affect immunity.
  • Autism.
  • Cancer.
  • Bacterial vaginosis.
  • Liver disease.
  • MS.
  • Depression/stress.
  • Rheumatoid arthritis.
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74
Q

what factors affect the microbiome?

A
  • Diet.
  • Antibiotics.
  • Animals.
  • Human genetics.
  • Sleep deprivation.
  • Stress.
  • Occupation.
  • Local environment.
  • Physical interaction.
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75
Q

what are the functions of the liver?

A 
metabolism of drugs
produces bile
glycogen storage
synthesis of clotting factors
deamination of amino acids
production of proteins, such as albumin
storage of vitamins and minerals 
carbohydrate, amino acid and lipid metabolism
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76
Q

what makes up the liver?

A

liver lobules

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77
Q

liver lobules

A

make up liver segments
6 acinus make up one lobule
contain portal triad

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78
Q

what makes up the portal triad?

A

hepatic artery
hepatic portal vein
bile duct

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79
Q

how many acinus zones are there?

A

3 zones, relative to the portal tract and have different metabolic functions

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80
Q

what are the acinus

A

zone 1
zone 2
zone 3

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81
Q

acinus zone 1

A

closest to oxygenated blood supply, nutrients and toxins

these cells are more metabolically active

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82
Q

acinus zone 3

A

furthers from the portal tracts and closest to the central vein
deal with hypoxia and have lower concentration of nutrients and toxins

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83
Q

liver cells

A

hepatocytes, carry out the major functions of the liver

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84
Q

what are the different types of liver cells?

A

sinusoidal epithelial cells
kupffer cells
stellate cells

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85
Q

sinusoidal epithelial cells

A

line sinuses between hepatocytes

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86
Q

kupffer cells

A

macrophages
remove bacteria from blood
remove haemoglobin from the blood

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87
Q

stellate cells

A

store vitamin A

produce collagen and extracellular matrix

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88
Q

flow of bile through the liver

A

bile synthesised by hepatocytes
secreted into bile canaliculi
canaliculi merge and drain into bile ductile and then larger ducts
bile goes from right and left hepatic duct
enters common hepatic duct and joins with cystic duct to form the common bile duct which enters the duodenum

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89
Q

fatty acids as an alternative fuel

A

used by heart and skeletal muscle

converted by beta oxidation to acetyl coenzyme A and used by krebs cycle

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90
Q

ketone bodies

A

produced from fatty acids in liver

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91
Q

starvation

A

lack of fuel rather than a water/ electrolyte deprivation

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92
Q

responses to starvation

A

production of more glucose by glycogenolysis and gluconeogenesis
or other sources:
- lactate
- amino acids - ketone bodies which can then be used by the brain to maintain consciousness without glucose
glycerol and fatty acids

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93
Q

what hormones regulate starvation?

A

glucagon
cortisol
adrenaline

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94
Q

what are the main sources of glycogen?

A

fat
muscle
liver

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95
Q

body’s response to high glucose

A

insulin released from beta cells in islets of langerhands in pancreas

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96
Q

what does insulin do?

A

glycogenesis
lipogenesis
protein synthesis
anabolism

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97
Q

use of ketone bodies

A

used mostly by brain tissues as they can cross the BBB and then be converted back to acetyl coenzyme A and enter krebs cycle

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98
Q

what are the 4 quadrants of the abdomen?

A

right and left upper quadrants

right and left lower quadrants

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99
Q

what are the 9 sections of the abdomen?

A 
right and left hypochondrium
epigastric
right and left flank/ lumbar 
umbilical
right and left groin/ inguinal 
pubic
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100
Q

what does glucagon do?

A

released from alpha cells
causes glycogenolysis - only occurs fully in liver as muscles lack glucose-6-phosphatase
only occurs for 24 hours

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101
Q

what does adrenaline do?

A

lipolysis

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102
Q

what does cortisol do?

A

gluconeogenesis in liver using:

  • lactate
  • amino acids
  • triglycerides
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103
Q

liver function tests

A 
ALT - alanine aminotransferase 
AST - aspartame aminotransferase 
Alk P - alkaline phosphatase 
Gamma-GT - gamma glutamyltransferase 
albumin
bilirubin
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104
Q

ALT liver function test

A

liver cell damage

could indicate cardiac or skeletal damage

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105
Q

AST liver function test

A

liver cell damage

could indicate cardiac or skeletal damage

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106
Q

AST>ALT

A

cirrhosis

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107
Q

Alk P

A

biliary tree blockage

may be due to bone disease or from placenta

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108
Q

Gamma-GT

A

biliary tree blockage, may be due to chronic drug exposure - alcohol or anticonvulsants

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109
Q

albumin

A

impaired synthetic function

may be decreased in malnutrition, sepsis or major trauma

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110
Q

bilirubin

A

disturbance of bilirubin handling

may be from myoglobin break down - muscle damage

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111
Q

grouping of liver function tests

A

liver injury - ALT, AST, Alk P and Gamma-GT
liver synthesis - albumin
liver excretion - bilirubin

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112
Q

cori cycle

A

lactate created by anaerobic respiration is transported from muscles to liver
converted to pyruvate
which is converted to glucose - requiring ATP
glucose can then be used by other tissues

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113
Q

lipolysis

A

triglycerides are broken down into fatty acids, used directly, broken down further to form ketone bodies
glycerol used in gluconeogenesis

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114
Q

chronic liver disease - blood tests

A

liver function tests
hepatitis B and C screen
fasting glucose, cholesterol and triglyceride
autoimmune liver screen
immunoglobulins
ferritin, transferrin saturation and iron studies
alpha 1 trypsin
TSH
anti-TTG - coeliac screen
caeruloplasma/ serum copper screen in young

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115
Q

autoimmune liver screen

A

ANA
SMA
LKMA
AMA

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116
Q

immunoglobulins in chronic liver disease testing

A

IgG
IgM
IgA

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117
Q

chronic liver disease imaging

A

liver ultrasound
liver CT triple phase
fibroscan

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118
Q

liver ultrasound

A

texture
focal lesions, assess portal vein for thrombus
flow rate - portal hypertensions
splenomegaly

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119
Q

liver CT triple phase

A

looks for liver masses

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120
Q

fibroscan

A

measures stiffness of liver

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121
Q

diagnosis of chronic liver disease

A

blood tests
imaging
liver biopsy

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122
Q

liver biopsy

A

used to determine cause of cirrhosis/ degree of liver damage if uncertain
conducted by percutaneous methods or transjugular methods

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123
Q

how to manage chronic liver disease acutely

A

treat cause of decompensation - alcohol, infection or bleed
ascitic tap if ascites present to rule out spontaneous bacterial peritonitis
diuretics
ascitic drain
check INR - vitamin K >1.4
UGI endoscopy if bleeding/ varices
give banding/ beta blockers
lactulose / enemas to prevent encephalopathy
if acute kidney injury give terlipressin

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124
Q

terlipressin

A

human albumin solution

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125
Q

long term management of chronic liver disease

A
  • treat underlying cause of liver disease and liver biopsy if unsure
  • alcohol cessation
  • lactulose and rifaximin to excrete ammonia
  • nutrition
  • diuretics
  • beta blockers if varices
  • liver transplant
  • prophylaxis for spontaneous bacterial peritonitis
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126
Q

causes of jaundice

A

pre-hepatic haemolysis
hepatic
post-hepatic

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127
Q

pre-hepatic haemolysis

A

when RBCs are broken down in kidney

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128
Q

hepatic

A

hepatocytes impairment when the liver cannot convert unconjugated bilirubin into conjugated bilirubin

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129
Q

post-hepatic

A

biliary stasis - when the bilirubin cannot get into GI tract via biliary tree and goes into blood instead

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130
Q

causes of liver disease

A

alcohol
obesity
hepatitis B and C

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131
Q

risk factors of liver disease

A

alcohol
blood transfusions - hepatitis
high BMI

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132
Q

signs and symptoms of liver disease

A

Ascites - fluid in the abdomen and increased oedema.
•Anaemia.
•Haemotemesis.
•Itchy.
•Confusion.
•Chest - gynaecomastia and spider naevae.
•Hands - palmar erythema, leukonychia (white nails) and clubbing.
•Abdomen - hepatomegaly. Splenomegaly and caput medusae (bobbly looking swollen veins).
•Legs - oedema.
•Eyes/skin - jaundiced, loss of hair and bruising.

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133
Q

HELLP syndrome

A

severe variant of advanced pre-eclampsia with 3 features

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134
Q

3 features of HELLP syndrome

A

haemolysis
elevated liver enzymes
low platelet count

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135
Q

signs and symptoms of HELLP syndrome

A 
Raised blood pressure.
•Oedema.
•Proteinuria.
•Headache.
•Epigastric pain.
•Poor fetal growth.
•Massively raised AST and ALT.
•Raised mixed bilirubin.
•Lowered haemoglobin.
•Lowered platelets.
•Raised creatinine.
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136
Q

treatment for HELLP syndrome

A
  • Magnesium to prevent maternal seizures.

* Blood or platelet transfusion depending on severity.

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137
Q

mortality in HELLP syndrome

A

high
up to 30% for mother
up to 60% for baby

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138
Q

hereditary spherocytosis with haemolysis

A

t is an inherited condition (autosomal dominant) where red cell wall proteins are abnormal, resulting in an inability to adjust their shape to pass through capillaries.

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139
Q

signs and symptoms of hereditary spherocytosis with haemolysis

A
  • LUQ pain (spleen).
  • Mild anaemia.
  • Jaundice.
  • Splenomegaly (Use to fragile red cells being destroyed by the spleen).
  • Raised unconjugated bilirubin.
  • Lowered haemoglobin.
  • Raised reticulocytes
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140
Q

treatment for hereditary spherocytosis

A

transfusion

splenectomy

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141
Q

alcohol cirrhosis with GI bleed cause

A

excessive alcohol consumption

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142
Q

signs and symptoms of alcohol cirrhosis with GI bleed

A
  • History of vomiting blood.
  • Increased heart rate.
  • Decreased blood pressure.
  • Ascites.
  • Massively raised Gamma-GT.
  • AST > ALT.
  • Decreased haemoglobin
  • Raised INR.
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143
Q

management of alcohol cirrhosis with GI bleed

A

Fluid resuscitation so give fluids.
•Then correct coagulopathy and endoscopy to try to band or sclerose any Varices.
•Restrict sodium and give diuretics to manage ascites.
•If drastic, abdominal paracentesis may be required, portal vein decompression or liver transplant.
•Abstinence from alcohol is essential.

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144
Q

What are the signs and symptoms of a carcinoma of the head of the pancreas?

A 
Patient age.
•Weight loss.
•Abdominal pain.
•Palpable gallbladder.
•Deep jaundice.
•Dark urine due to bilirubin being majorly conjugated so urine is dark.
•Light faeces as pigments do not reach the intestine.
•Raised ALT
•Raised Gamma-GT.
•Raised conjugated bilirubin.
•Raised INR.
•Dilated biliary system.

Anatomy of

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145
Q

who is chronic hep C common in?

A

homeless and poor people

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146
Q

what are the signs and symptoms of chronic hep C?

A

AST > ALT.
•Raised gamma-GT.
•Anti-HCV positive.
-Can lead to cirrhosis (20-30%) or hepatocellular carcinoma (up to 4%).

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147
Q

causes of chronic hep C

A

blood to blood contact

usually from needle sharing

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148
Q

what is the management of chronic hep C?

A

antivirals

abstinence from alcohol

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149
Q

what is gilbert’s syndrome?

A

It is an inherited (autosomal recessive) condition where UDP-glucuronosyltransferase is defective (Involved in the glucuronidation pathway).

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150
Q

what are the signs and symptoms of gilbert’s syndrome?

A

few and may be unnoticed for years

  • mild jaundice
  • exacerbated by illness, fasting or extreme exercise
  • raised unconjugated bilirubin
  • enzymes normal
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151
Q

what is the daily protein allowance?

A

50g

152
Q

what is primary biliary cirrhosis

A

It is an auto-immune condition which leads to inflammation and fibrosis of the small intra-hepatic biliary ducts
diagnosis is primary sclerosing cholangitis where biliary obstruction is exta-hepatic

153
Q

what are the signs and symptoms of primary biliary cirrhosis

A
  • Dark urine.
  • Splenomegaly.
  • Raised ALP.
  • Raised Gamma-GT.
  • Raised mixed bilirubin.
  • AMA positive.
  • Biliary dilatation is intrahepatic.
154
Q

what are some complications of primary biliary cirrhosis?

A

portal hypertension
splenomegaly
oesophageal varices
vomiting large volumes of blood

155
Q

who is at risk of primary biliary cirrhosis?

A

Female (90%) and usually 40-60.

-Usually high cholesterol is seen and may lead to nodular xanthomas.

156
Q

what is the treatment for primary biliary cirrhosis?

A

little treatment available

liver transplants as last resort

157
Q

vitamin A

A

retinol

158
Q

sources of vitamin A

A 
dairy
egg
fish
liver
vegetables
159
Q

signs and symptoms of vitamin A deficiency

A

xerophthalmia - dryness of conjunctiva and cornea and inflammation
night blindness
keratomalacia
follicular hyperkeratosis - keratin build up around hair follicles

160
Q

calories in carbohydrates

A

4kcal/ g

161
Q

calories in fat

A

9kcal/g

162
Q

calories in protein

A

4kcal/ g

163
Q

vitamin D

A

cholecalciferol

164
Q

sources of vitamin D

A

fish

egg

165
Q

signs of vitamin D deficiency

A

rickets

osteomalacia

166
Q

what are macronutrients?

A

larger energy yielding nutrients - carbohydrates, proteins and lipids
non-energy nutrient = fibre, helps with digestion

167
Q

what are micronutrients?

A

smaller non-energy yielding nutrients such as vitamins and minerals

168
Q

basal metabolic rate

A

rate at which body expends energy for maintenance activities

169
Q

how is basal metabolic rate calculated for women?

A

•BMR for Women = 65.51 + (9.6 x weight [kg]) + (1.8 x height [cm]) - (4.7 x age [years]).

170
Q

how is basal metabolic rate calculated for men?

A

•BMR for Men = 66.47 + (13.7 x weight [kg]) + (5 x height [cm]) - (6.8 x age [years]).

171
Q

what is EER?

A

estimated energy requirement
the average dietary energy intake that will maintain energy balance in a healthy person of a given age, gender, height and physical activity level

172
Q

vitamin B6

A

pyridoxine

173
Q

sources of vitamin B6

A

meat

grains

174
Q

signs of vitamin B6 deficiency

A

polyneuropathy

175
Q

vitamin B9

A

folate

176
Q

source of vitamin B9

A

vegetables

177
Q

signs of vitamin B9 deficiency

A

megaloblastic anaemia

178
Q

vitamin C

A

ascorbate

179
Q

sources of vitamin C

A

fresh fruit

180
Q

signs of vitamin C deficiency

A

scurvy

181
Q

daily carbohydrate allowance

A

260g

182
Q

signs of sodium/ salt deficiency

A

fatigue
nausea
cramps

183
Q

what are the sections of the oesophagus?

A 
cervical 
upper thoracic
middle thoracic 
lower thoracic 
abdominal
184
Q

sources of calcium

A

dairy
vegetables
cereals

185
Q

signs of deficiency of calcium

A

problems with bones/ teeth

clotting

186
Q

daily fat allowance

A

<70g

saturates <20g

187
Q

what are the parts of the stomach?

A

fundus
body
antrum
pylorus

188
Q

peritoneal ligaments

A

falciform ligament
lesser omentum
greater omentum

189
Q

sources of iron

A

meat
cereal
veg

190
Q

signs of iron deficiency

A

microcytic anaemia

191
Q

lesser omentum

A

made up of hepatogastric and hepatoduodenal ligaments

192
Q

vitamin E

A

tocopherol

193
Q

source of vitamin E

A

vegetables

194
Q

vitamin K

A

quinone

195
Q

source of vitamin K

A

vegetables

196
Q

signs of vitamin K deficiency

A

coagulation defects

neurological defects

197
Q

source of fluoride

A

fluoridated water

198
Q

sign of fluoride deficiency

A

tooth decay

199
Q

vitamin B1

A

thaimin

200
Q

sources of vitamin B1

A

cereals and nuts

201
Q

signs of vitamin B1 deficiency

A

beriberi

wernicke-korsakoff syndrome

202
Q

vitamin B2

A

riboflavin

203
Q

sources if vitamin B2

A

liver

dairy

204
Q

signs of vitamin B2 deficiency

A

angular stomatitis

205
Q

vitamin B3

A

niacin

206
Q

sources of vitamin B3

A

liver and meat

207
Q

signs of vitamin B3 deficiency

A

pellagra

208
Q

vitamin B12

A

cobalamin

209
Q

difference between jejunum and ileum structure

A

jejunum has longer vasa recta and fewer arterial arcades

ileum has shorter vasa recta and more arterial arcades

210
Q

sources of vitamin B12

A

meat
fish
eggs

211
Q

signs of vitamin B12 deficiency

A

megaloblastic anaemia

neurological deficiencies

212
Q

rectus sheath

A

contains rectus abdominis

213
Q

what connects part of rectus abdominis?

A

tendinous intersections

214
Q

what are the tendinous intersections made of?

A

aponeurosis of transverse abdominis

internal and external oblique muscles

215
Q

sources of potassium

A

fruit
veg
dairy

216
Q

signs of potassium deficiency

A

confusion
weakness
heart failure

217
Q

sources of phosphorus

A

dairy
meat
fish
eggs

218
Q

anterior lobes of liver

A

right posterior
right anterior
left medial
left lateral

219
Q

arterial blood supply of GI tract

A

foregut - coeliac trunk via common hepatic, left gastric and splenic arteries
midgut - superior mesenteric artery
hindgut - inferior mesenteric artery

220
Q

magnesium sources

A

cereals
fruits
vegetables

221
Q

signs of magnesium deficiency

A

cardiovascular problems
bone problems
nerve problems

222
Q

venous drainage of GI tract

A 
hepatic portal vein 
inferior vena cava 
foregut - splenic vein 
midgut - superior mesenteric vein
hindgut - inferior mesenteric vein
223
Q

posterior lobes of liver

A

left lateral
left medial
right anterior
right posterior

224
Q

innervation of GI tract

A

autonomic

225
Q

sympathetic innervation of GI tract

A 
abdominopelvic splanchnic nerves
lower thoracic splanchnic nerves 
greater splanchnic - T5-T9/10
lesser splanchnic - T10-11
lumbar splanchnic - L1-2/3
226
Q

parasympathetic innervation of GI tract

A

vagus nerve

pelvic splanchnic nerves -S2-4

227
Q

sources of zinc

A

dairy
egg
fish
cereal

228
Q

signs of zinc deficiency

A

delayed puberty

impaired growth

229
Q

vestibule of mouth

A

space between teeth and the lips and cheeks

230
Q

what is located in the vestibule?

A 
superior labial frenulum 
inferior labial frenulum 
opening of parotid gland 
buccinator muscle
pads of fat in babies
231
Q

superior labial frenulum

A

connects upper lips to vestibule

232
Q

inferior labial frenulim

A

connects posterior part of the tongue to the bottom of the mouth cavity

233
Q

sources of copper

A

shellfish
cereal
nuts

234
Q

signs of copper deficiency

A

impaired growth
mental retardation
bone lesions
brittle hair

235
Q

incisor teeth to cricopharyngeal junction

A

15cm

236
Q

cricopharyngeal junction to lower oesophageal sphincter

A

25cm

237
Q

sources of iodine

A

seafood

milk

238
Q

signs of iodine deficiency

A

hypothyroidism

239
Q

what medications lead to C difficile

A

clindamycin
ciprofloxacin
co-amoxiclav
cephalosporins

240
Q

what causes the symptoms of C difficile

A

toxins released by C difficile bacteria
toxin A - enterotoxin
Toxin B - cytotoxin
cause chloride permeability and tissue necrosis

241
Q

microbiology of C difficile

A

gram positive bacillus which is spore forming

obligate anaerobe

242
Q

sources of selenium

A 
cereal
meat
fish
dairy
egg
243
Q

signs of selenium deficiency

A

heart disease

244
Q

signs of C difficile infection

A 
occur after taking antibiotics
Yellow and runny stools (blood is rare).
•Abdominal pain.
•Fever.
•Albumin under 25.
•Lactate above 2.4
•WCC above 15.
•Temperature 38.5.
•CRP above 200.
•Toxic mega colon - surgery may be needed. The cause is myenteric plexus damage and muscular injury which causes segmental paralysis.
•Pseudomembranes containing neutrophils, debris and fibrin thrombus
245
Q

drug contraindications with C difficile

A

ramipril - other antihypertensives
omeprazole
salbutamol inhaler

246
Q

diagnosis for C difficile

A

•C Diff toxin vs antigen:
-Antigen detects presence of C diff.
-Toxin detects presence of acute C diff toxic infection.
-If antigen positive, toxin negative then may do PCR.
-If PCR negative - no C diff infection.
-If PCR positive may have C diff - isolate and consider treatment.
•AXR for toxic mega colon and CXR to chest for perforation of toxic mega colon.

247
Q

treatment for C difficile infection

A 
isolation 
PPE
IV rehydration 
oral metronidazole first then vancomycin 
faecal transplant if needed
248
Q

what makes up the GI system

A 
GI tract
accessory organs:
- teeth
- tongue
- salivary
- pancreas
- liver
- gallbladder
249
Q

where is norovirus common in?

A

hospitals
care homes
schools
elderly are at risk

250
Q

signs of norovirus

A

diarrhoea

vomiting

251
Q

management of norovirus

A

isolate to prevent further spread
hydrate with fluids
confirm causative organism and notify public health england

252
Q

how long does norovirus take to resolve?

A

1-3 days

253
Q

Bacillus cereus

A

common in rice dishes that have been improperly refrigerated

entertoxins survive reheating

254
Q

what are the signs of bacillus cereus?

A

diarrhoea
vomiting
self-limiting and resolves within 1-2 days

255
Q

listeria incubation period

A

3 days to 10 weeks

256
Q

signs and symptoms of listeria

A

meningitis
sepsis
fever

257
Q

sources of listeria

A

soft cheeses
unpasteurised milk
ready to eat deli meats

258
Q

what are located on the anterior 2/3 of the tongue?

A

medial sulcus

vallate papilla

259
Q

what are located on posterior 1/3 of tongue

A

lingual tonsil

260
Q

what are the abdominal planes?

A
  • Transpyloric plane (L1).
  • Transumbilical plane.
  • Midclavicular line.
  • Median plane.
  • Subcostal plane.
  • Transtubercular plane.
261
Q

signs of cholera

A

rice-water diarrhoea

262
Q

effects of vomiting

A

hypokalaemia
alkalosis
dehydration

263
Q

when is vomiting treated with drugs?

A

when the cause is known only

264
Q

what are the types of drugs used to treat vomiting?

A

D2 dopamine antagonist.
•H1 histamine antagonist.
•Muscarinic ACh antagonist.
•5-HT3 antagonists.

265
Q

when are D2 dopamine antagonists used?

A

post-operative nausea and vomiting

266
Q

H1 histamine antagonists

A

used to treat most nausea and vomiting

e.g. clyclizine

267
Q

what are the tissue layers of the anterolateral abdominal wall?

A 
skin
subcutaneous tissue layers
external oblique muscle and aponeurosis 
transversus abdominis muscle and aponeurosis
extraperitoneal fat
parietal peritoneum
268
Q

what are the subcutaneous tissue layers of the anterolateral abdominal wall?

A

campers fascia - loose superficial fatty fascial layer

scarpa’s fascia - deep membranous fascial layer

269
Q

muscarinic ACh antagonist

A

used for motion sickness

e.g. hyoscine

270
Q

5-HT3 antagonist

A

used for post operative nausea and vomiting

e.g. ondansetron

271
Q

treatment for acid reflux

A

proton pump inhibitors

272
Q

PPIs

A

used to treat gastric/ duodenal ulcers
dyspepsia
GORD
e.g. omeprazole

273
Q

surface anatomy of the stomach

A

left hypochondrion
epigastric region
umbilical region sometimes

274
Q

H2 antagonists

A

used to treat gastric/ duodenal ulcers, dyspepsia, GORD
only used when PPIs dont work
e.g. ranitidine

275
Q

synthetic prostaglandin

A

used to treat gastric/ duodenal ulcers and NSAID associated ulcers
e.g. misoprostol

276
Q

internal surface of the anterolateral abdominal wall

A

5 umbilical peritoneal folds
3 peritoneal fossae
falciform ligament

277
Q

umbilical peritoneal folds

A

median umbilical fold
2 medial umbilical folds
2 lateral umbilical folds

278
Q

peritoneal fossae

A

supravesicle fossae
lateral inguinal fossa
medial inguinal fossae - site of the direct inguinal hernia

279
Q

antacids

A

used to treat ulcer dyspepsia and GORD

e.g. aluminium hydorxide

280
Q

nerve supply of anterolateral abdominal wall

A

cutaneous branches of the lower thoracic spinal nerve (T7-T11).
•Subcostal nerve from T12.
•Terminal branches of the anterior ramus of the lumbar spinal nerve (L1):
-Iliohypogastric nerve.
-Ilio-inguinal nerves.

281
Q

what is H pylori?

A

gram negative bacteria living in stomach

present in 15% of people but does not cause problems in most

282
Q

what does H pylori do?

A

causes stomach ulcers

283
Q

what antibiotics are used to kill H pylori?

A

clarithromycin

metronidazole

284
Q

how is GI motility decreased?

A

increasing smooth muscle tone
suppression of peristalsis
raised sphincter tone
reduced sensitivity to rectal distension

285
Q

causes of constipation

A
  • Dehydration.
  • Diet (low fibre).
  • Opioids.
  • IBS.
  • Laxative abuse.
  • Pregnancy.
  • Anorectal Disease such as fissures or haemorrhoids.
  • Parkinson’s.
  • Nerve damage.
286
Q

what are mesenteries?

A

double layers of peritoneum that enclose organs and connect them to either the anterior or posterior abdominal walls

287
Q

what are the mesenteries ?

A

Greater omentum
Lesser omentum
•Falciform ligament

288
Q

greater omentum

A

connects the stomach to the transverse colon.

289
Q

lesser omentum

A

connects the stomach and part of the duodenum to the liver.

290
Q

falciform ligament

A

connects the liver to the anterior abdominal wall.

291
Q

how to treat constipation?

A

bulk forming laxatives
osmotic laxatives
stimulant laxatives
faecal softeners

292
Q

bulk forming laxatives

A

increase in faecal mass

e.g. bran/ isphagula husk

293
Q

osmotic laxatives

A

to increase fluid in large bowel

e.g. lactulose - often given to children

294
Q

stimulant laxatives

A

increases intestinal motility

e.g. senna

295
Q

faecal softeners

A

to lubricate and soften

e.g. arachis - peanut oil

296
Q

bowel cleansing solutions

A

picolax

297
Q

what does picolax contain?

A

sodium picosulphate - stimulant

magnesium citrate - osmotic

298
Q

what is the peritoneal cavity divided into?

A

omental burse - lesser sac

299
Q

what connects the lesser and greater sac?

A

omental foramen of winslow by hepatoduodenal ligament of lesser omentum

300
Q

what is found in the omental foramen of winslow?

A 
anteriorly - portal triad:
- bile duct
- hepatic artery
- portal vein
posteriorly - inferior vena cava
inferiorly - 1st part of duodenum
superiorly - caudate lobe of liver
301
Q

treatment of diarrhoes

A

anti-motility drugs
bulking agents
symptomatic treatments

302
Q

anti-motility drugs

A

opioids - loperamide

303
Q

bulking agents

A

ispaghula

304
Q

anterior part of hard palate

A

maxilla bone

305
Q

posterior part of hard palate

A

palatine bone

306
Q

symptomatic treatment of diarrhoes

A

correction of fluid and electrolyte loss

e.g. diarolyte

307
Q

ileum

A

longer segment - distal 3/5 of small intestine

located mostly in right lower quadrant

308
Q

jejunum

A

proximal 2/5 part of the small intestine

located in the left upper quadrant of the infracolic compartment of the abdominal cavity

309
Q

what pathogens cause foodbourne diseases?

A 
norovirus
rotavirus
adenovirus
campylobacter
E.coli
salmonella
shigella
310
Q

neurovascular bundle

A

medial to lateral
artery, nerve, vein
nerve used for local anaesthetic
vein used for administering oral drugs

311
Q

borders of the jejunum and ileum

A

mesenteric

anti-mesenteric

312
Q

mesenteric border

A

concave margin of a small bowel loop, facing towards the axis of the root of the mesentery

313
Q

anti-mesenteric border

A

the convex margin of a small bowel loop, facing away from the axis of the root of the mesentery

314
Q

distinguishing between the borders of the jejunum and ileum?

A

important for diagnosis
diverticulosis = occurs at the mesenteric border
meckel’s diverticulum = occurs at anti-mesenteric border

315
Q

where is the oesophagus located?

A

C6-T10

316
Q

how long is the oesophagus?

A

25cm

317
Q

where does the oesophagus go through the diaphragm?

A

T10

318
Q

what does the mesentery connect?

A

connects intestines to posterior abdominal wall

319
Q

what are the variations of the appendix position?

A 
retro-colic
retro-caecal
sub-caecal
pelvic
retro-ileal
pre-ileal
320
Q

where is the appendix located?

A

McBurney’s point which is retro-colic or retro-caecal

321
Q

what is the peritoneum?

A

smooth thin serous membrane which lines the walls of the abdominal cavity and covers most of the viscera

322
Q

what are the layers of the peritoneum?

A

parietal layer

visceral layer

323
Q

parietal layer of peritoneum

A

lines the inner surface of the walls of the abdominal cavity

324
Q

visceral layer of peritoneum

A

covers most of the abdominal viscera

325
Q

what is the peritoneal cavity?

A

the space between the parietal and visceral peritoneal layers

326
Q

intraperitoneal

A

when the organs are covered by the visceral peritoneal layers

327
Q

retroperitoneal

A

when organs lie behind the peritoneum - e.g. kidney

328
Q

lymphatic drainage of the stomach

A

pyloric lymph nodes

drain into celiac -preaortic lymph nodes

329
Q

what is the blood supply of the rectum and anal canal

A

superior to pectinate line = inferior mesenteric artery

inferior to pectinate line = internal iliac artery

330
Q

venous drainage of rectum and anal canal

A

superior to pectinate line = portal venous system

inferior to pectinate line = caval venous system

331
Q

where is campylobacter common?

A

south-east asia

332
Q

what is the incubation period of campylobacter

A

2-5 days

333
Q

symptoms of campylobacter

A

fever
nausea
abdominal cramps
diarrhoea - can be bloody

334
Q

what foods does campylobacter come from?

A

raw and undercooked poultry
unpasteurised milk
contaminated water

335
Q

composition of gallstones

A

cholesterol in western world

pigments in rest of world

336
Q

what are the risk factors for gallstones

A 
fair
forty
fat
fertile
female
337
Q

what are the signs of gallstones?

A

biliary colic pain caused by gallstones getting stuck in the neck of the gallbladder

  • 70-80% are asymptomatic
  • 4% are symptomatic
  • pain in right upper quadrant
  • pain may be precipitated by fatty meals
338
Q

lymphatic drainage of rectum and anal canal

A

superior to pectinate line = internal iliac lymph nodes

inferior to pectinate line = superficial inguinal lymph nodes

339
Q

differences between jejunum and ileum

A

jejunum has fewer loops of arterial arcades and a longer vasa recta within its mesentery than the ileum

340
Q

nervous supply to rectum and anal canal

A

superior to pectinate line = sympathetic and parasympathetic visceral motor and sensory innervation to internal anal sphincter
inferior to pectinate line = somatic motor and sensory innervation to external anal sphincter

341
Q

what are the muscles of the tongue?

A

hyoglossus
genioglossus
styloglossus

342
Q

salmonella incubation time

A

6-72 hours

343
Q

signs and symptoms of salmonella

A 
headache
fever
abdominal cramps
diarrhoea
vomiting and nausea
344
Q

what foods does salmonella come from?

A 
undercooked poultry
raw egg desserts
mayonnaise 
sprouts 
tahini
345
Q

signs of E.coli

A

bloody stools
triad of HUS - haemolytic uraemic syndrome
acute renal failure - high creatinine
microangiopathic haemolytic anaemia - low Hb
thrombocytopaenia - low platelet count

346
Q

management of E.coli

A

fluids
replace electrolytes
monitor Hb/ platelets and potentially replace

347
Q

surface anatomy of liver

A

right hypochondrium and epigastric region

348
Q

what is acute cholecystitis

A

inflammation of the gallbladder caused by obstruction, distension, disruption of glycoprotein mucous layer and chemical injury

349
Q

what are the causes of acute cholecystitis

A

90% caused by gallstones and 10% other causes

350
Q

what are the signs of acute cholecystitis

A

right upper quadrant pain

fever

351
Q

how is acute cholecystitis diagnosed?

A

RUQ pain/ mass/ Murphy’s sign
evidence of inflammatory response - fever, white cell count and CRP
imaging - ultrasound

352
Q

management of acute cholecystitis

A 
fasting - takes strain off gallbladder 
IV fluids 
analgesics 
antibiotics 
cholecystectomy - removal of gallbladder 
percutaneous cholecystostomy
353
Q

differential diagnosis of acute cholecystitis

A

pancreatitis
appendicitis
stomach ulcers

354
Q

what does the large intestine consist of ?

A 
cecum
appendix
ascending colon
transverse colon
descending colon
sigmoid colon
rectum
anal canal
355
Q

features of the colon

A

omental appendices
teniae coli -
haustra

356
Q

omental appendices

A
  • small fatty projections
357
Q

teniae coli

A

3 longitudinal muscle bands

358
Q

haustra

A

sacculations of the wall of the colon between the teniae

359
Q

structures of the stomach bed

A 
left dome of diaphragm
spleen
left kidney
left adrenal gland
splenic artery
pancreas
transverse mesocolon
360
Q

how is diarrhoea managed?

A 
in side room
rehydration
monitor electrolytes
analgesia
antiemetics
consider loperaminde
361
Q

anterior to oesophagus

A

trachea
left bronchus
left atrium

362
Q

posterior to oesophagus

A

vertebral bodies

descending aorta

363
Q

right of oesophagus

A

right lung

364
Q

left of oesophagus

A

aortic arch

left lung

365
Q

anterior to stomach

A

liver

366
Q

left of stomach

A

spleen

367
Q

inferior to stomach

A 
greater omentum
pancreas
spleen
transverse colon
kidney 
adrenal gland
368
Q

posterior to stomach

A

pancreas

duodenum

369
Q

incubation of shigella

A

5-7 days

symptoms occur a day or two after bacteria exposure

370
Q

signs and symptoms of shigella

A

water diarrhoea - may be bloody
fever
stomach cramps

371
Q

what food does shigella come from?

A

salads and sandwiches - lots of hand contact in preparation

raw vegetables contaminated from a field

372
Q

signs and symptoms of pancreatic insufficiency

A 
loose, pale and greasy stools which float - steatorrhoea 
weight loss 
fatigue
abdominal distension 
lack of vitamins
amylase enzymes in blood
373
Q

treating pancreatic insufficiency

A

pancreatic enzyme replacement - creole

vitamin supplementation - A,D,E,K

374
Q

what is ascending cholangitis

A

infection of biliary tree

375
Q

what causes ascending cholangitis?

A

cancer of pancreas or gallbladder

obstruction in common bile duct can lead to infection - usually gram negative

376
Q

signs of ascending cholangitis

A

charcot’s triad

raynaud’s pentard

377
Q

what is charcot’s traid?

A

jaundice
fever
right upper quadrant abdominal pain

GI system (2 decks)

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