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gastro Flashcards

1
Q

layers of gut wall

A

mucosa - epithelium + LP
submucosa - connective tissue, nerve plexus
muscularis - sm, main nerve plexus
serosa/advendita

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2
Q

swallowing phases + oesophageal sphincters

A

oral - both upper + lower contracted

pharyngeal - both open

upper oes - upper closes behind bolus - inferior circular rings dilate

lower oes - lower sphincter closes as food goes through

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3
Q

parts of stomach + secretions

A

fundus - mucus, pepsinogen, hcl
antrum - gastrin from g-cells
cardia + pyloric - mucus

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4
Q

segmentation vs peristalsis in stomach

A

S: main - 80%, weak => mix food, enz + acid

P: minor - 20%, strong => pushes food along

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5
Q

chief cells

A

high: RER, golgi, secretory granules
secrete pepsinogen

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6
Q

parietal cells

A

high: mito, tubulo-vesicles fused with cananiculi
secrete HCl

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7
Q

g cells

A

in antrum
stimulated by distention of stomach + vagus nerve
secrete gastrin

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8
Q

phases of gastric secretion

A

cephalic - thought/sight etc = starts sec
gastric - stretch/chemo recs in antrum
intestinal - excitatory + inhibitory phase

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9
Q

omeprazole

A

blocks proton pumps (H+/K+)

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10
Q

ranitidine

A

blocks H2 receptor = x histamine cascade

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11
Q

hepatic inflow

A

hep artery = 25% = oxygenation of liver

portal vein = mixed venous blood from gut w/nutrients + waste

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12
Q

central structure in hepatic lobule

A

central vein => collects blood from hepatic sinusoids => hepatic veins

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13
Q

structure of lobules

A

rows of hepatocytes w/sinusoid facing side + cananiculi facing side

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14
Q

hepatocyte function

A

process nutrients
detoxify blood
excrete waste

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15
Q

zones of hepatic acinus

A

1 => early exposure - most O2 but also most toxins
2 => medium O2 + toxins
3 => least O2 but also least toxins

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16
Q

kuppfer cells

A

hepatic macrophages (in sinusoids)

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17
Q

hepatic sinusoidal cells

A

endothelial
fenestrated => lipids + large molecules

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18
Q

stellate cells

A

in space of disse
vitamin A stored in cytosolic droplets

activate into fibroblasts => ECM maintenance by laying down collagen

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19
Q

hepatocytes

A

synthesis: albumin, clotting factors, bile salts

drug metabolism

receive nutrients from sinusoids

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20
Q

cholangiocytes

A

line cananiculi
HCO3- + H2O secretion into bile

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21
Q

sphincter of oddi

A

regulates bile entry into duodenum
at major ampulla

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22
Q

pigments in bile

A

bilirubin (yellow)
billiverdin (green)

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23
Q

functions of bile

A

cholesterol homeostasis (bile salts)

absorption of lipids + lipid sol vits ADEK (emulsification)

excretion (cholesterol metabolites, drugs, hormones, alkaline phosphatase)

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24
Q

primary vs secondary bile secretion

A

primary => hepatocytes - salts, lipids, organic ions

secondary => cholangiocytes - alter pH/H2O, secrete: Cl-, IgA

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25
Q

how is Cl- secreted

A

CFTR

cystic fibrosis transmembrane regulator

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26
Q

bile transporters + functions

A

bile salt excretory pump => AT of bile acids to bile

MRP => 1+3 - bile salts into bile

products of familial interhepatic cholestasis gene (F1C1)

products of multidrug resistant genes: MDR - 1 => excretion of xenobiotics + cytotoxins, 3 => phosphatidyl choline

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27
Q

synthesis of bile acids

A

cholesterol + sodium/potassium salts of bile acids conjugated in liver => glycine + taurine

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28
Q

primary bile acids => secondary

A

cholic acid => deoxycholic acid
chenodeoxycholic acid => lithocholic acid

made in liver (pri) => sec in gut by bac

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29
Q

secondary bile acid excreted in stool

A

lithocholic

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30
Q

what happens to bile salts after they emulsify fats (primary)

A

95% = reabsorbed via enterohepatic circulation => portal vein (Na+/K+ ATPase)

5% = converted to secondary in colon

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31
Q

what does GB do to bile

A

stores - concentrates + acidifies

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32
Q

free/indirect bilirubin

A

insoluble
unconjugated
yellow
associated to albumin

from: Hb breakdown. catabolism of other haem-proteins, inneffective erythropoiesis

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33
Q

how does indirect BR become direct

A

dissociates from albumin in liver + enters hepatocytes

BR + 2x UDP-glucoronate => BR diglucoronide

=> cannaniculi => GIT

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34
Q

fates of BR

A

excreted - faeces (lithocholic acid)
enterohepatic circulation
systemic circulation + excreted by kidneys

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35
Q

BR in faeces

A

BR
urobillionogen
stercobillinogen
stercobillin (brown)

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36
Q

prehepatic jaundice

A

increased production of BR

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37
Q

intrahepatic jaundice

A

decreased uptake (BR remains in blood)

decreased conjugation (remains insoluble)

decreased secretion (x into cannaniuli)

decreased outflow (cholestasis - small bile ducts become obstructed)

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38
Q

investigations in pancreas/GB

A

MRCP - magnetic resonance cholangic pancreatography
CT
angiography

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39
Q

pancreatic divisum

A

major + minor pancreatic ducts not fused => large amount of bile cant fit through minor

frequent acute pancreatitis

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40
Q

acinar vs duct/centroacinar secretions

A

acinar => low volume, viscous, enzyme rich PJ

d/ca => high volume, watery, HCO3- rich

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41
Q

functions of HCO3-

A

protects duo from acid damage
optimal pH for enzymes
washes low volume acinar secretion out of panc => duo

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42
Q

why does HCO3- secretion plateau after increasing pH by a little

A

other alkaline secretions also help neutralise

bile/brunners gland secretions

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43
Q

prevention of autodigestion by enzymes in pancreas

A

proteases secreted as inactive zymogens
trypsin inactivator in pancreas = trypsin not activated

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44
Q

enterokinase

A

in duo

trypsinogen => trypsin

t converts all other proteases into active forms

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45
Q

why lipases don’t cause auto-digestion even though in active forms

A

need bile salts + colipases to be effective => none in pancreas

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46
Q

control of PJ secretions

A

acini => vagus + cck (I cells in duo in response to FA + AA - inhibited by trypsin as enz not req once EK activatied)

duct => secretin (S-cells in response to drop in pH)

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47
Q

Main blood supply of small bowel

A

Superior mesenteric artery

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48
Q

Plicae circulares

A

Increase SA

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49
Q

Cells in small bowel - villi + crypts

A

Vili- enterocytes, goblet cells, enteroendocrine

Crypts of luberkhun - paneth + stem

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50
Q

What coats microvili of vili of enterocytes

A

Glycocalyx
Rich carb layer
Protection + allows absorption
Traps water + mucus in ‘unstirred layer’

51
Q

How abundance of goblet cells change along bowel

A

Increase dis tally along length of bowel

52
Q

Enteroendocrine cells

A

Columnar
Hormone secreting

Influence gut motility

53
Q

Paneth cells

A

Base of crypt
Large acidophilus granules - antibacterial enzymes, glycoprotein + zinc

engulf some bad + protozoa

54
Q

Why enterocytes have rapid turnover

A

Must replace surface epithelium lost at to of villus

First line of defence against pathogens

55
Q

Brunners glands

A

In duodenum
Submucosal coiled tubular mucus glands
Secrete alkaline fluid

Open into base of crypt

56
Q

Jejunum vs duodenum

A

J- wider/thicker walls, redder, more plicae, mesentery above + left of aorta
(1-2 arterial arcuates w/long terminal vessels)

D- thinner, less plicae, mesentery below + right of aorta (3-4 arterial arcades w/short terminal vessels)

57
Q

Segmentation

A

Stationary contraction if circular muscles at intervals

Mix food

58
Q

Peristalsis

A

Sequential contractions of adjacent rings
Waves => propels food to colon

59
Q

Migrating motor complex

A

Cycles of SM contractions
Stomach => SB => colon

Next wave = from duo

Prevents colonic bacteria migrating back up into GI tract

60
Q

Carb digestion

A

Salivary + pancreatic amylase

Require Cl- for optimum activity
Make simple carbs to be absorbed at brush border

Glucose + glactose = secondary AT via SGLT1 co-transporter

Fructose = fac diff via GLUT5

Exit of products via GLUT 2 from basolateral to interstitium

61
Q

protein digestion

A

pepsin in stomach => breakdown => inactivated in high pH of duo

pancreatic proteases secreted as precursors into duo => activated by trypsin => form single aas + oligopeptides

single aas => direct absorption into brush border by aa transporters

multi aas (oligopeptides) => brush border progressively hydrolyses w/surface peptidases => mono

some oligos directly absorbed via H+/oligopeptide co-transporter PepT1

multis = digested in cyto => aas by tri/dipeptidases

62
Q

part 1 of lipid digestion (outside cell)

A

bile salts + pancreatic lipase secretion

emulsification by BS = increased SA for digestion

enz hydrolysis of ester linkages => lipase + colipase complex => stops bile salts displacing lipase in fat droplet

lipase action => FA + MG

solubilisation of lipolytic products in bile salt micelles

63
Q

part 2 of lipid digestion (in cell)

A

FA + MG = leave micelle + enter enterocyte

FA + MG re-synthesise Tg via monoglycerate activation (main) + phosphatidic acid pathway

CMs = lipoprotein particles (transport Tgs) made as emulsion in golgi

CM leave by exocytosis => lacteal => away from bowel

64
Q

main functions of large bowel

A

reabsorption of electrolytes & water
elimination of undigested food & waste

65
Q

parts of colon

A

ascending => caecum to hepatic flexure
transverse => hepatic flexure to splenic flexure
descending => splenic flexure to sigmoid colon

sigmoid => rectum => anus

66
Q

taeniae coli

A

3 longitudinal bands of smooth muscle around colon

between = thin

shorter than intestine => haustra

67
Q

haustra

A

pouches
individually contract
formed by taenia coli

68
Q

appendices epiploicae

A

fatty tags on the peritoneum
unknown function

69
Q

secondary lymphoid tissue in gut

A

peyers patches

70
Q

blood supply to colon

A

asc + proximal trans = middle colic artery (branch of the superior mesenteric artery)

distal trans + desc = inferior mesenteric artery

due to embryological division between mid + hindgut

region between = sensitive to ischaemia (blood supply not extensive)

71
Q

how is rectum distinguished

A

transverse rectal folds in submucosa
no taenia coli in muscularis externa

72
Q

anal canal musculature

A

internal (circular muscle) anal sphincter

external (striated muscle) anal sphincters

73
Q

similarities between LB & SB

A

enterocytes + goblet cells
many crypts w/stem cells

74
Q

how LB different to SB

A

no vili
crypts = mainly goblet cells as opposed to stem/paneth cells in SB

75
Q

Mucus in LB

A

facilitates passage of increasingly solid colonic contents + covers bacteria & particulate matter

release stimulated by ACh in PNS + ENS

76
Q

circular muscle in LB

A

segmentally thickened

77
Q

contractions in proximal colon

A

anti-propulsive patterns
retain chyme and allows time for colon to absorb water & electrolytes

78
Q

contractions in transverse + distal colon

A

haustral contractions (localised segmental contractions of circular muscle) = back and forth mixing

short propulsive movements every 30 mins → increase in frequency following a meal

79
Q

mass movement in colon

A

1-3 times/day (like peristaltic wave)

stimulated by food in stomach

propel contents 1/3-3/4 of length of large intestine in few seconds

increased by fibre rich foods

80
Q

ANS control of LB

A

PNS: asc + most of transverse = vagus nerve
SNS: lower thoracic and upper lumbar spinal cord

81
Q

defecation reflex

A

mass movement fills rectum with faeces
controlled by sacral spinal cord (reflex + voluntary)

sudden distention in rectum walls => pressure receptors send signals via myenteric plexus

peristaltic wave in desc, sigmoid + rectum => internal + anal sphincter = relax

external = voluntary => control when you want to go

82
Q

importance of social part of rectum - last few cm

A

distinguish solid, liquid, gas
important in knowing what can be passed appropriately in what circumstance

83
Q

synthesis functions of intestinal flora

A

synthesise + excrete vitamins
e.g. Vitamin K (needed to carboxylate clotting problems)

stimulate the development of certain tissues

break down fibre

produce short chain FAs

84
Q

immune role of gut flora

A

prevent colonisation by pathogens by competing for attachment sites or for essential nutrients

antagonise other bacteria by producing substances which inhibit or kill non-indigenous species

stimulate production of cross-reactive antibodies

85
Q

normal flora

A

bacteroids => most, G-ive, anaerobic, non-spore forming (implicated in initiation colitis + colon cancer)

bifidobacteria => G+ive, non-sporeforming, lactic acid, friendly, prevent colonization

86
Q

why do multicellular organisms have circulatory systems

A

bring individual cells within diffusion range

87
Q

Osmosis

A

diffusion of H2O from a hypotonic (high water conc.) to hypertonic medium (low water conc.)

88
Q

carrier vs channel proteins

A

carrier => bind solute - conformational change to transport

channel => aqueous pores that allow specific molecules across

(channel: voltage/ligand/mechanically gated)

89
Q

primary vs secondary active transport

A

P: uses ATP to power the transport

S: derives energy from the concentration gradient of another substance that is actively transported

90
Q

GLUT-2

A

high-capacity, low-affinity
facilitative transporter

91
Q

standing gradient osmosis

A

reabsorption of water against the osmotic gradient at the colon

92
Q

how is water generally absorbed

A

1 - Na+ driven => absorbed into enterocytes => intercellular spaces by Na+/K+ ATPase

2 - other electrolytes (Cl-, K+, HCO3-) => intercellular spaces

osmotic gradient formed => H2O from lumen => distends intercellular spaces => increased HP => ions + H2O across BM to capillaries

93
Q

calcium absorption

A

direct paracellular

transcellular:
fac diff via TRPV6 on ApM
binds Calbindin-D
transported through cytosol to BL-M

PMCA = Ca2+ ATPase = pumps out against conc grad
NCXI = Na+/Ca2+ exchanger = against conc grad

94
Q

PMCA vs NCXI

A

PMCA: high affinity for Ca2+ (low capacity) to maintain low intracellular concentrations

NCXI: low affinity, high capacity (requires larger concentrations to be effective)

95
Q

Importance of calbindin

A

transports Ca2+ across cell whilst maintaining a low intracellular Ca2+ conc. → Ca2+ cannot act as an intracellular signal

96
Q

how vitamin D helps calcium absorption

A

enhances transport through cytosol

increases calbindin levels

increases Ca2+ ATPase in membrane → increases rate of extrusion across baso

97
Q

Haem oxygenase

A

librates Fe2+ from erythrocytes

98
Q

iron absorption (haem)

A

heme transporter HCP1 via receptor mediated endocytosis

stored as mucosal ferritin/into blood via ferroportin 1

99
Q

iron absorption (non-haem)

A

3+ reduced to 2+ via duodenal cytochrome B
absorbed via DMT1
stored as mucosal ferritin/out via ferroportin 1

100
Q

what happens to iron after leaving enterocyte

A

hephaestin oxidises to 3+ => transported in blood bound to plasma transferrin

when reached liver => too much = hepcidin released => inhibits ferroportin

101
Q

what is mucosal ferritin + what is its function

A

globular protein complex
Fe2+ is oxidised to Fe3+ → crystallises within protein shell

formed by iron + apoferritin in cyto (irreversible)

made only in excess => helps stop absorption of too much iron as not available for transport into plasma

lost in intestinal lumen → excreted in faeces

102
Q

how is vitamin K taken up into enterocytes

A

active transport

103
Q

vitamin B12 absorption

A

B12 + R-protein Haptocorrin in saliva (prevent acid breakdown)

Haptocorrin digested past duo → free vitamin B12

B12 + IF

B12/IF => cubilin receptor on ileal brush border → taken up in distal ileum

broken inside the epithelial cells

B12 attaches to protein transcobalamin II (TCII) => crosses BM to blood

B12/TCII readily presented to liver => TCII receptors = uptake

proteolysis breaks down TCII => stores B12 forever

104
Q

Impaired vitamin B12 absorption

A

delays maturation of red blood cells → pernicious anaemia

105
Q

SNS control of stomach + colon (preganglionic => postganglionic)

A

stomach: thoracic nerves (T6-9) => coeliac ganglion

SB: => superior mesenteric ganglion

colon: lumbar nerves (L2-5) => inferior mesenteric & pelvic ganglion

106
Q

PNS supply of stomach, small intestine and proximal colon

A

vagus nerve

with preganglionic neurons originating in dorsal vagal complex within brainstem from sacral spinal cord

107
Q

ENS

A

2nd brain

interacts with ANS

neurones in GI walls => myenteric/auerbach’s (muscularis) + submucosa/meissners plexuses

108
Q

function of myenteric plexus vs submucosal

A

myenteric => main control of GI movements - tone, velocity of contraction, intensity of contraction

submucosal => control for GI secretion, local blood flow, epithelial and endocrine cell function (senses local env)

109
Q

peristaltic reflex

A

food enters gut lumen
intestinal smooth muscle stretches
stimulates sensory neurones in myenteric plexus & chemicals in food stimulate sensory neurones in submucosal plexus
inhibitory/excitatory NT → smooth muscle contracts behind the food bolus and relaxes in front of it
food bolus is pushed forward along GI tract

110
Q

SNS + PNS on enteric nervous system

A

SNS = inhibitory effect - reduces peristalsis, absorption, secretion and blood flow

PNS = excitatory effect - increases peristalsis, absorption, secretion and blood flow to gut → promotes digestion

111
Q

Hirschsprung’s Disease

A

congenital absence of myenteric and submucosal ganglia

most common cause of neonatal bowel obstruction

112
Q

Gastrin (secretion, release, function, inhibition)

A

synthesised in gastric antrum + upper small intestine

stimulated by: aas + peptides in stomach lumen, gastric distension and vagus nerve

stimulates gastric acid secretion by parietal cells in stomach
trophic effects on SB, colon + stomach mucosa

inhibited when pH of stomach falls below pH 3

113
Q

Secretin (secretion, release, function)

A

secreted by S cells of the upper duodenum and jejunum

stimulus = presence of acid in duo (pH below 4.5)

stimulates pancreatic HCO3 secretion (potentiated by CCK) + biliary secretion of bicarbonate and fluid
inhibit gastrin secretion
trophic effect on the exocrine pancreas

114
Q

CCK (secretion, release, function)

A

secreted by I cells in small intestine

stimulated by fat and peptides in the upper small intestine

stimulates pancreatic enzyme release, gallbladder contraction + relaxation of sphincter of Oddi
delays gastric emptying, decreases food intake and meal size
Trophic effects on the exocrine pancreas and gallbladder

115
Q

Glucose-dependent Insulinotropic Peptide/Gastric Inhibitory Polypeptide (GIP)
(secretion, release, function)

A

secreted by mucosal K cells (predominant in duodenum and jejunum)

released following ingestion of a mixed meal

response to all 3 macronutrient types (glucose, amino acid, fatty acids)

stimulates insulin secretion

116
Q

Motilin

A

increases gastrointestinal motility

117
Q

Somatostatin

A

made in endocrine D cells of gastric + duo mucosa, pancreas

universal inhibitor (endo Cyanide)

released in response to a mixed meal

118
Q

Glucagon-like peptide-1 (GLP-1)

A

produced in the small intestine and secreted from L cells

stimulated by the presence ofhexose and fat

induces satiety
increases sensitivity of pancreatic beta-cells to glucose

119
Q

Pancreatic polypeptide

A

secreted by PP cells in the pancreas

stimulated by fat

120
Q

Peptide YY

A

secreted from L cells found throughout mucosa of terminal ileum, colon and rectum => post prandially

reduces intestinal motility, gallbladder contraction and pancreatic exocrine secretion

121
Q

Neurocrines + 3 examples

A

molecules secreted by postganglionic non-cholinergic neurons of the enteric nervous system

vasoactive intestinal peptide (VIP)
gastrin release peptide (GRP)
enkephalins

122
Q

Vasoactive intestinal peptide (VIP

A

relaxation of gut smooth muscle

123
Q

Gastrin releasing peptide (GRP)

A

induces gastrin release

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