GI Flashcards

1
Q

role of brunners glands

A

in duodenum, produce alkaline mucus to neutralise chyme

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2
Q

order of small intestine

A

duodenum, jejunum, ileum

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3
Q

acronym for retroperitoneal organs

A

SADPUCKER

surpaadrenal glands
aorta
duodenum (lower1/3)
pancreas
ureter
colon (ascending and descending)
kidney
eosophagus
rectum

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4
Q

describe s and ps innervation gut

A

s- T5-L2. pre sympathetic splanchnic nerves synapse with Sm, Im, and pelvic splanchnic nerves.

ps- vagus to transverse colon and then pelvic beow. release ACh, Gip and VIP

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5
Q

describe the endocrine, paracrine and neurocrine gut hormones

A

endocrine- gastrin
paracrine- somatostatin
neurocrine- GIP

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6
Q

role gastrin

A

released from g cells in antrum of stomach in response to stretch, vagus or H+. increases partietal cell action

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7
Q

role CCK

A

released from I cells in response to increased FA, AA and H+. this causes increased bile and enzyme release

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8
Q

role secretin

A

released when H+ levels from s cells are high to increase HCO3- release from pancreas

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9
Q

role GIP

A

increases insulin and decreases glucose.

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10
Q

role somatostatin

A

inhibits G cells, stimulated by low pH

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11
Q

what do crypts contain

A

enteroendocrine cells that secrete hormones, paneth cells which produce antibacs to protect stem cells, and stem cells

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12
Q

what are the 2 plexus and where are they lo0cated

A

myenteric (motility) in Muscularis mucosa.
submucosal (blood flow) in submucosa

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13
Q

innervation abdo msucles

A

anterior rami T7-T12, Io and Ta have L1 also

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14
Q

compare above and below arcuate line

A

above- RA enclosed by EO, TA and IO
below- EO, TA, IO anterior to RA

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15
Q

boundaries inguinal canal

A

floor- inguinal and lacunar ligament
anterior- external oblique
roof- inferior oblique and transversus abdomonis
posterior- transversalis fascia and conjoint tendon

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16
Q

compare indirect and direct inguinal hernia

A

direct- medial
indiret- lateral

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17
Q

boundaries hesselbachs triangle

A

L- inferior epigastric vessels
M- rectus abdomonis
I- inguinal ligament

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18
Q

boundaries femoral canal

A

M- lacunar ligament
L- femoral vein
A- inguinal ligament
P- pectineal ligament

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19
Q

common incisional sites for hernias

A

midline, paramedian, gridion

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20
Q

what forms greater and lesser omenta

A

greater- dorsal
lesser- ventral

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21
Q

what contains liver and spleen

A

liver- ventral
spleen- dorsal

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22
Q

what membranes form from ventral mesentry and dorsal mesentry

A

ventral- lesser omentum and falciform ligament
dorsal- splenorenal and gastrosplenic

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23
Q

describe abnormalities of midgut rotation

A

one clockwise rotation- small intestine in front of TC
one rotation anticlockwise- LHS colon

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24
Q

what does the cloaca develop into

A

urogenital sinus and anorectal space

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25
Q

what is the producteum

A

ectoderm covering anal depression

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26
Q

what is gastrochesis

A

failure of abdominal wall to form

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27
Q

what is the 2 rule for merkels diverticulum

A

under 2s, 2 foot proximal to ileocecal valve, 2%, 2:1 ratio male to female

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28
Q

describe the pharyngeal phase of swallowing

A

pharyngeal constrictors push food back, soft pallets seals off the nasopharynx, epiglottis elevates and seals off larynx, vocal cords adduct, opening of UOS

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29
Q

describe the role of ductal cells and how this varies at high/low flow speeds

A

ductal cells add HCO3- and K+, and remove Cl- and Na+. this makes solution hypotonic.

slow flow speeds- more contact- more modification- more hypotonic

high flow speeds- less contact- less modification- less hypotonic

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30
Q

describe the resting and active phases of parietal cells

A

resting- K+ impermeable. tubulovesicles not associated with apical membrane.
active- tubulovesicles in contact with apical membrane

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31
Q

what 3 things stimulate parietal cells

A

gastric, histamine, ach

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32
Q

describe muscles stomach outside to inside

A

oblique, circular, longitudinal

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33
Q

blood supply to stomach

A

lesser curve- R/L gastric
greater curve- gastroepiploic
neck- short gastric

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34
Q

4 causes GORD

A

LOS weakness, slow gastric emptying, pregnancy, obestiy

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35
Q

symptoms of immune gastritis

A

anorexia, glossitis, anaemia (due to no b12 as no intrinsic factor)

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36
Q

how is h pylori adapted to survive

A

produces urea which forms ammonium. raises local pH

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37
Q

symptoms PUD

A

epigastric/back pain, night pain, bleeding, early satiety, weight loss

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38
Q

causes of non alcoholic fatty liver disease

A

diabetes, metabolic syndrome, obestiy

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39
Q

willsons disease

A

deposition of copper in liver due to reduced biliary secretion

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40
Q

3 signs of portal hypertension

A

splenomegaly, jaundice, ascites

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41
Q

3 portosystemic anastomoses

A

porto systemic
umbilical- veins of ligamentum teres, epigastric
rectal- superior rectal, m/I rectal
oesophogeal- left gastric, azygous

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42
Q

hepatorenal syndrome

A

portal hypertension

arterial vasodilation

kidney recieves as reduced circulatory volume

RAAS activates

renal artery vasoconstriction and so reduced kidney functon

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43
Q

biliary colic

A

CCK causes contraction of gall bladder around compared stone in cystic duct. RUQ pain

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44
Q

acute cholecystitis

A

infection of compacted gall stone in cystic duct. caused by e coli. RUQ and inflammation

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45
Q

acute cholangitis

A

infection of biliary tree. chariots triad- pain, inflammation, jaundice

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46
Q

what are ALT and ALP specific go

A

ALT- liver (hepatocyte)
ALP- biliary tree

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47
Q

gross pathology chrons disease

A

Hyperaemia

  • Cobblestone Appearance
  • Discrete superficial ulcers & deep ulcers
  • Fistulae (bowel – bowel, bladder, vagina, skin)
  • Mucosal Oedema
  • Transmural inflammation
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48
Q

gross pathology UC

A
  • Chronic inflammatory infiltrate of lamina propria
  • Crypt abscesses
  • Crypt distortion
  • Goblet cells
  • Pseudopolyps
  • Loss of haustra
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49
Q

what forms bile

A

Bile acid-dependent: bile acids and pigments

  • Bile-acid independent: alkaline solution
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50
Q

2 primary bile acid

A
  • Cholic acid
  • Chenodeoxycolic acid
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51
Q

2 amino acids that bind to bile

A

glycine, taurine

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52
Q

what zymogens does pancreas produce

A

trypsin, elastase, chymotrypsin

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53
Q

what damages zone 1/3 of liver

A

1- toxins
3- ischameia

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54
Q

where is b12 absorbed

A

terminal ileum. bound to intrinsic factor

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55
Q

how is
glucose
galactose
fructose
amino acids
di/tripeptides absorbed

A

glucose/galactose- SGLT-1 with Na+
fructose- GLUT5
amino acids- co transport with Na
di/tripeptides- peptide transporter with H+

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56
Q

3 effects of coeliac disease

A

crypt hypertrophy, loss microvilli, lymphocytes in epithelium

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57
Q

diagnosis coeliac

A

serum IgA, upper gi endoscopy

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58
Q

effects and causes of b12 deficency

A
  • not enough in diet, chrons causing terminal ileum inflammation, lack IF
  • megaloblastic anaemia, neurological problems
59
Q

X-ray signs chrons vs uc

A

chrons- sign of kantour
uc- lead pipe colon

60
Q

describe difference types of pain felt in appendicitis

A

normal- poorly localised umbillical

retrocaecal/pelvic- suprapubic/rectal/vaginal

61
Q

what is diverticulosis vs diverticulitis

A

diverticulosis- presence of diverticula
diverticulitis- infection and inflammation of diverticula

62
Q

red flag symptoms duodenal cancer

A

Anaemia
Loss weight
Anorexia
Recent and progressive
Malena

63
Q

left sided colon cancer

A

• Left sided colon cancer
◦ Descending
◦ Lumen is narrower and contents more solid so more bowel obstruction
◦ Tenesmus
◦ Early change in bowel habit
◦ More obvious PR bleeding
◦ Less advanced disease at presentation
◦ Stenosing growth.
‣ Causes apple core sign.

64
Q

right sided colon cancer

A

• Right sided colon cancer
◦ Ascending
◦ Less likely to have bowel obstruction as the lumen is bigger and contents are more liquid
◦ Less likely to have change in bowel habit early on
◦ More advanced disease at presentation.
◦ Fungating growths. On stalk with ball. Grow out into lumen of bowel.

65
Q

cause of primary and secondary peritonitis

A

primary- ascites

secondary
non bacterial
-ectopic pregnancy
-blood

bacterial

  • peptic ulcer
  • diverticulitis
  • appendicitis
66
Q

symptoms acute mesenteric ischemia

A

left sided pain (blood supply to splenic flexure ,most fragile), abdominal pain disproportionate to findings, nausea

67
Q

symptoms collapsed AAA

A

cardiovascular collapse, pulsatile abdominal mass, abdominal or back pain

68
Q

3 SCFA produced by microbiota

A

propinoate- satiety
butyrate- energy source colonocytes
acetate- cholesterol

69
Q

compare type of diarrhoea caused by bacteria

A

bloody- shigella, campylobacter

watery- ETEC, salmonella

70
Q

which bacteria can cause haemolytic uraemia syndrome

A

shigella, campylobacter

71
Q

which virus under 5s

A

rotavirus

72
Q

which parasite persistent diarrhoea

A

giardia

73
Q

mechanism cyrptospiridium

A

Cl- secretion and malabsorption cause watery diarrhoea

74
Q

mechanism emtamoeba

A
  • cyst injested, spreads to liver and mucosa
  • causes bloody diarrhoea and inflammation
75
Q

predominant cell type in stomach

A

surface mucus cell

76
Q

describe the components of the lower oesophageal sphincter mechanism

A
  • acute angle of entry stomach
  • smooth muscle of the LOS
  • right crus of diaphragm forms a sling around the lower oesophagus which tightens when intraabdominal pressure rises.
  • smooth muscle elements of the LOS contract when pressure in the stomach rises
77
Q

which receptor does gastrin bind to in parietal cell

A

CCK receptor

78
Q

When the parietal cell is in its resting phase, what cytosolic structures contain the proton pumps?

A

tubulovesicles

79
Q

What region of the stomach has the greatest density of G cells?

A

antrum

80
Q

What is different about the muscularis propria in the stomach compared with the rest of the gut tube?

A

Has an additional layer of obliquely orientated muscle

81
Q

CT landmarks
T12
L1
L3
L4

A

T12- aorta and coeliac trunk
L1- SMA, transpyloric plane
L3- IMA
L4- iliac crest, bifurcation of abdominal aorta

82
Q

which mutation

  • lung cancer
  • FAP
  • breast
  • colon
A

lung- ALK
FAP- APC
breast- BRACA1
colon- KRAS

83
Q

which tumour marker colon cancer

A

carcinoembryonic antigen

84
Q

layers to reach CSF

A

skin, fat, supraspinous ligament, interspinous. ligamentum flavum, extradural fat, dura mater, arachnoid mater, subarachnoid space

85
Q

where are bile salts reabsorbed

A

terminal ileum

86
Q

painless scrotal lump?

A

indirect inguinal hernia

87
Q

risk factor UTI

A

diabetes mellitus

88
Q

first line antibiotic simple uti

A

nitrofurantoin

89
Q

first line antibiotic complicated uti

A

co-amoxiclav

90
Q

where do
-jugulo-omohyoid
-jugulo-digastric
-submandibular
-pre-auricular
-occipital
drain

A
  • jugulo-omohyoid posterior tongue
  • jugulo-digastric tonsils
  • submandibular cheek/nose
  • pre-auricular cheek/eyelid
  • occipital occipital scalp
91
Q

which ACEi causes dry cough

A

ramipril

92
Q

high defect causes higher pressure in arms than legs

A

corarction aorta

93
Q

resting potential

  • neurones
  • skeletal muscle
  • cardiac
  • smooth muscle
  • SAN
A
  • neurones -70
  • skeletal muscle -90
  • cardiac -80
  • smooth muscle -50
  • SANc -60
94
Q

where to insert needle decomppression

A

2nd ICS, mid clavicular line above 3rd rib

95
Q

side effects rifampicin

A

peripheral neuropathy

96
Q

side effects ethambutol

A

colour blindness, loss visual acuity, headaches

97
Q

essential amino acids

A

: histidine, isoleucine, leucine, lysine, methionine, phenylalanine, threonine, tryptophan, and valine.

98
Q

risk factors pre eclampsie

A

twin pregnancy,History of preeclampsia. A personal or family history of preeclampsia significantly raises your risk of preeclampsia.
Chronic hypertension. …
First pregnancy. …
New paternity. …
Age. …
Race. …
Obesity. …
Multiple pregnancy.

99
Q

compare omphalocoele vs gastrochises

A

omphalocoele- persistance of physiological herniation. peritoneal covering
gastrochises- failure of abdominal wall to form

100
Q

3 types of mesoderm

A

paraxial- somites
lateral plate- splanchnic and somatic
intermediate- kidneys/gonad

101
Q

what forms the viscera

A

splanchopleuric mesoderm formed of splanchnic mesoderm and endoderm.

102
Q

what forms the body wall and dermis

A

somatopleuric mesoderm formed of splanchnic and ectoderm

103
Q

what is the space between the viscera and body wall called and what does it form

A

intraembryonic coelum, forms abdominal and thoracic cavity

104
Q

what forms the peritoneum

A

lateral plate mesoderm. somatic forms parietal, splanchnic forms visceral

105
Q

which part of the gut has both a ventral and dorsal mesentry

A

the foregut

106
Q

what forms the greater sac

A

the area with no ventral mesentry

107
Q

what forms the lesser sac

A

the area formed by rotation of stomach

108
Q

what connects greater and lesser sac

A

epiploic foramen at the free edge of the lesser omentum

109
Q

describe development of ligaments from the dorsal and ventral mesentries

A

ventral
- falciform and lesser omentum

dorsal
-splenorenal and gastrosplenic

110
Q

what structure connects umbillicus and midgut initially

A

yolk sac

111
Q

prior to rotation of foregut what is the posterior vagal trunk called

A

Right vagal fibres

112
Q

describe 2 constituents of developing pancreas and how they rotate

A

ventral and dorsal buds. ventral rotates as stomach rotates

113
Q

sac contents and coverings of hernia

A

sac- peritoneum
contents- gut
covering- muscles

114
Q

what remnant of processus vaginalis persists as part of normal development?

A

tunica vaginalis

115
Q

Which liver marker is specific to hepatocyte damage

A

ALT

116
Q

Foregut, midgut and hindgut pain

A

Foregut- epigastric
Midgut- periumbillical
Hindgut- suprapubic

117
Q

describe saliva at rest

A

At rest, the acinar secretion is highly modified and has the following characteristics:

Low volume
Very hypotonic
Neutral or slightly acidic
Few enzymes

118
Q

describe saliva that is highly modified

A

When the production of saliva is stimulated, flow exceeds the ductal cells maximum rate of modification and so the acinar secretion is modified less:

High volume
Less hypotonic than resting saliva
Alkaline
Many enzymes

119
Q

mechanism rotavirus

A

sglt1 disruption, chloride hypersecretion, brush border enzyme dysruption

120
Q

how does salmonella cause symptoms

A
  • enter enterocyte
  • encounter macrophage iin submucosa
  • enter RES
  • lymphoid hyperplasia
  • re enter gut from liver
121
Q

how does campylobacter cause symptoms

A

releases a cytotoxin

122
Q

how does shigella cause symptoms

A
  • invades colonocyte
  • multiplies
  • forms abscess
  • kills colonocyte
123
Q

how does ETEC cause symptoms

A

hypersecretion of chloride ions

124
Q

how does norovirus cause symptoms

A

diarrhoea due to anion secretion, vomiting due to slowed gastric emptying

125
Q

common route of infection for cryptosporidium

A

bodies of water

126
Q

how does cyrptosporidum cause symptoms

A
  • oocyst ingested
  • reproduces in small intestine epithelial cells
  • causes malabsorption and chloride secrtion
127
Q

how does giardia cause symptoms

A
  • cyst ingested
  • damages small intestine cause diarrhoea
128
Q

what can giardia cause post infection

A

lactase deficiency

129
Q

symptoms entamoeba histolytica

A

diarrhoea
liver abscess

130
Q

people at risk entamoeba histolytica

A
  • tropical travel
  • institutions with poor sanitation
  • MSM
131
Q

how does entamoeba histolytica cause disease

A
  • cyst ingested
  • invade mucosa, causes inflammatory changes
  • spread to liver
132
Q

treatmetn entamoeba histolytica

A

anti protozoals and severe colitis

133
Q
A

t12

aorta, coeliac trunk

134
Q
A

1- liver

2- coeliac trunk and aorta

3- spleen

4- stomach

5- kidney

6- vena cava

135
Q
A

L1, SMA

136
Q
A

1- liver

2- kidney

3- SMA

4- IVC

5- stomach

6- kidney

7- spleen

137
Q
A

L3 - IMA

138
Q
A

1- liver

2- psoas

3- IVC

4- aota

5- colon

6- psoas

7- small intestine

8- ureter

139
Q
A
140
Q

Describe alcoholic liver disease/steatosis

A
  • fatty change (weeks). Excess fat converted to TAG, deposited in liver. NADH formed which inhibits lipid breakdown -

alcoholic hepatitis (years). Inflammation of liver. Have jaundice/RUQ pain/hepatomegaly - cirrhosis. Irreversible, end stage

141
Q

Other causes of chronic liver disease

A
  • non alcoholic fatty liver disease. Deposition of fat and inflammation Insulin resistance, metabolic syndrome If inflammation present- non alcoholic steatohepatitis.
142
Q

Antibody autoimmune hepatitis

A
  • antibody= ASMA/AMA
143
Q

PBC

A

Primary biliary cirrhosis - anti mitochondria

144
Q

PSC

A

Primary sclerosis cholangitis - UC LINK!! - anti mitochondrial -ve