:L Flashcards
during fetal develop, the foregut, midgut and hindgut develop from what?
foregut: perotineum develops from ventral mesogastrium & dorsal mesogastrium:
i) the liver develops within the ventral mesogastrium. it exapnds
ii) dorsal mesogastrium: spleen develops in it,
get shift from
midgut & hindgut develop from dorsal mesogastrium
the dorsal mesogastrium forms connections between which structures? [2]
dorsal mesogastrium forms connections between:
stomach & spleen [1]
spleen and posterior ab. wall [1]
which three strucutres do you find in the free border of the lesser omentum?
- bile duct
- hepatic artery proper
- hepatic portal vein
which arteries do u find in the greater omentum?
= gastroepiploic arteries
where do u find the potential spaces in body? [2]
- *subphrenic recesses:**
- divided into L&R by falciform ligament
- *subhepatic recesses:**
- lesser sac on L
- hepatorenal recesss / pouch of morrison on the R
Q
whats the difference between primary or secondary strucutres?
give e.g.s
primary retroperitoneal srtuctures:
develop along posterior peritoneal wall & stay !
-great vessesl
- kidneys
- ureter
- lower rectum / anal canal
secondary retriperitoneal structures:
develop intrapetrioneally but move retro
- pancreas
- distal parts of duo
- upper rectum
what is v general overview of role of:
chylmicron
VLDL
IDL
LDL
HDL
- *chylomicron**: fat transport from GI tract –> rest of body
- *very low density lipo:** (similar to chylomicrons) fat transport -> rest of body. VLDL produced in the liver
- *intermediate DL**: left over chylomicrons –> become either LDL or VLDL
LDL: deliver cholesterol to cells
HDL; pick up excess cholesterol and send back to liver
what is the function of lipoprotein lipase?
what activates lipoprotein lipase?
where is lipoprotein lipase most active:
a) during periods of starvation?
b) after a meal
lipoprotein lipase: breaks down fats from inside lipoproteins and carries them into the cells
activated by: Apo C2
where is lipoprotein lipase most active:
a) during periods of starvation: muscle (where FA being used for energy in TCA)
b) after a meal: adipose cells (to form fat)
what is the function of low density liporpotein?
where AND how made? (which enzyme)
low density lipoprotein:
- function: deliver cholesterol to peripheral cells of the body
- produced @: liver
- formed by: remains of VLDLS after distribiting most of triglycerides. causes them to be more dense = IDLS. hepatic TAG ligase converts IDL to cholesterol rich LDL, having only Apo B100
what is familial hypercholeserolemia ? caused by mutation of which 3 genes?
- autosomal dom disease. mutation of one of three genes:
i) LDLR - receptor for receptor mediated endocytosis
ii) PCSK9: kinase that controls recyclingof LDLRs
iii) APOB: gene for ApoB which binds to LDL
= causes increased levels of cicrulating blood LDL bc not taken up into cells. increases chance of CHD.
causes heart attacks even in children
how can ur body create cholesterol? (which enzyme)
how does high cholesterol induce negative feedback of cholesetol production? (3)
- acetyl co-A –> cholesterol (via enzyme HMG-coA reductase)
high cholesterol induces negative feedback of cholesetol production
- *- reduces expression of HMG co-A reductase
- reduced gene expression of LDL (which brings the cholesterol)
- XS stored as cholesterol esters**
explain how having high LDLs leads to the formation of plaque formation & atherosclerosis
- high LDLs stay in blood system become damaged due to ROSs
- damaged LDLs get taken up by macrophages
- but bc there isnt anything really to kill - theyre just cholesterol: macrophages become foam cells (filled with chol)
- foam cells stick to walls of capillaries - fatty streaks -> fatty plaques -> atherosclerosis
explain mech. of HDLs reducing body cholesterol
- reverse transport pathway:
i) ApoA1 released by liver -> goes around body and picks up cholesterols from other cells through ABCA1 / G1 receptors
ii) changes the cholesterol -> cholesterol esters
iii) goes back to liver
iv) HDL transfers XS cholesterol ester to liver by binding to scavenger receptors (SR-B1)
explain the two ways statins reduce blood chol levels
- statins block the activity of HMG-Co A reductase. so less cholesterol is made [1]
causes more LDL receptors to be made & take in MORE LDLs -> reducing blood LDLs [1]
which lipoprotein carries fats from the liver to peripheral cells?
chylomicron
very low density lipo
intermediate DL
LDL
HDL
which lipoprotein carries fats from the liver to peripheral cells?
chylomicron
very low density lipo
intermediate DL
LDL
HDL
name two differences in the structure of HDLs & LDLs [2]
name two differences in the structure of HDLs & LDLs [2]
- Low-density lipoproteins contain **B-100 proteins
- HDL particles contain mostlyA-I and A-II proteins. high protein content, low fat cotent**
sources of endogenous reactive species? [3]
endogenous sources: mito, peroxisomes, ER
which micronutrient is important in imprinting home to the gut mucosa from peyers patches?
how does it occur (2)
vitmain A: precursor for retinoic acid !
- gut dendritic cells use retinoic acid to inform the niave T cells
- causes niave T cells to change transcription to express CCR9 & a4B& to do gut honing
which population are micronutrients most important in?
WHY? (3)
most important in paediatric population: (body growth & development; energy supply; healthy infants have 3x energy per kg body weights than adults)
which vitamins can be stored? how? where?
- *fat soluble: A D E K -**> can be stored in liver (but can be toxic in XS)
- absorbed with fats (readily absorb in micelles & chylomicrons)
why is commensal bacteria gut overgrowth clinically significant regarding vitamins?
commensal bacteria: providers AND consumers of B vitamins & vitamin K.
overgrowth: likely to have B12 deficiency & high B9
what are the clinical features of deficiences in
vitamin A
vitamin D
vitamin E
vitamin K
(fat soluble vitamins)
vitamin A: eyes -> xeropthalmia (Xerophthalmia refers to the spectrum of ocular disease caused by severe Vitamin A deficiency (VAD))
vitamin D: rickets (in adults = osteomalacia)
vitamin E: peripheral neuropathy
vitamin K: coagulopathy
what are the clinical features of deficiences in
- vit c
- B1
- B2
- B3
- B4
- B6
- B12
- folate?
- vit c: scurvy
- B1: beri beri
- B2: angular stomatitis
- B3: pellagra
- B4: anemia
- B6: anemia
- B12: anemia (but also lots of neurological disorders)
- folate: anemia
what is the biological activity of vitamin D? [3]
biological activity:
- *i) increases gut Ca2+ absorption
ii) increases bone calcification
iii) increases reabsorbtion of calcium**
iron metabolism:
- absorbed where in GI?
- function in the body? (2)
- stored where (2) and as what (1)?
iron metabolism:
- absorbed where in GI: duodenum (and proximal jejunum)
- function in the body: oxygen transport with Hb (1) myoglobin function in skeletal muscle
- stored: liver (1) & macrophages (1) as ferratin (1)
what two important things does niacin (B3) create? [2] roles?
- forms: NAD & NADP -> imporant hydrogen acceptors. when reduced forms: hydrogen donors
* if the diet is deficinet in niacin (B3), cells can manufacture it from WHAT? *
trpytophan
what are vegans likely to be deficient in? (2)
vitamin D: (oily fish, dairy products) vitamin B12 (meat and dairy food)
the spleen is the site of ? (2)
is it intraperitoneal / retroperiotneal? why is the answer clincally significant?
lymphocyte proliferation (1) rbc filtration, destruction and storage (1)
spleen is intraperitoneal. able to move around. means that during blunt trauma to peritoneum, can be torn away from the splenic artery and cause internal bleeding
A: coeliac trunk
B: splenic artery
C: hepatic artery proper
D: gastroduodenal
describe the branches of the SMA (6)
- inferior pancreaticoduedenal artery
- jejnunal and ileal branches
3 middle colic artery
- right colic artery
- ileocolic artery -> appendicular artery
describe pathway of common hepatic artery –> hepatic artery proper —> ?? :)
common hepatic artery: branches into
- gastroduodenal artery, which branches to give right gastroepiploic artery - which anastamoses with left gastroepiploic artery.
- right gastric artery (goes to less curvature of stomach). anastamoes with left gastric artery
after these two: becomes the hepatic artery proper; branches into:
- right hepatic artery –> cystic artery (gall bladder)
- left hepatic artery
A: jenunal
B: superior mesentric
C ileocolic
what are the 3 branches of the IMA?
what connects the SMA & IMA?
inferior mesenteric artery branches:
- left colic artery
- sigmoidal artery
- superior rectal artery
- SMA & IMA connected by marginal artery
rectal blood supply:
rectum gets supply from which 3 main arteries? where do each of these come from?
- superior rectal artery: from SMA
- middle rectal artery: internal iliac artery
- inferior rectal artery: from pudendal artery
which veins dont go to liver & directly drain into IVC? (4)
- gonadal vein
- renal vein
- internal iliac vein
- external iliac vein
what are the 3 locations of the ganglia where splachnic nerves (sympathetic NS) synapse?
(ie for foregut ? midgut? hindhut?)
if innervating the:
foregut -> coelaic ganglia
midgut -> superior mesenteric ganglia
hindut -> inferior mesenteric ganglia
explain the Para and sympathetic nerve supply to the gut. what do they normally do
(motor component (Parasymp and Sym) of autonomic:)
sympathetic nerves effect (T1-L2)
- pass through sympathetic trunk & synapse in the abdomen = splachnic nerves
- inhibits digestion
parasym nerves (CN III, VII, IX, X & s2-s4)
- vagus nerve runs up to 2/3 transvers colon. after which sacral nerves take over and supply the hindgut: pelvic splachnic nerves
- salivation
- stimulates digestion
- colon motility
- urinatin / defecation
A: left colic
B: sigmoidal
C: superior rectal
what is transamination?
how does it occur?
where does it occur mostly?
what is the enyzme used for it
transamination: transfer of an amino group. new amino acids can be made by using the carbon skeleton of other amino acids and transferreing a new side chain on it
mechanism:
- keto acid / group (a.a but instead of the NH2, is replaced by C double bonded O) swaps with the amine of another amino acid
- requires an intermediary: pyridoxal phosphate (from vitamin B6)
location: liver
Enzyme: tranaminase
what are glucogenic and ketogenic amino acids?
- *glutogenic**: can be converted to glucose by gluconeogenesis or enter the TCA
- can either be transaminated to oxaloacetate or pyruvate (or other intermediates that will form oxaloacetate):
- e.g. alanine or glutamate
ketogenic: can be converted to ketone bodies, these can feed into the TCA cycle, mostly via A-CoA or acetoacetyl-CoA.
1how is ammonia produced?
how is ammonia excreted from body ? why is it excreted?
- occurs as a reult of amino acids underoing deamination reactions (reactions where you lose amine groups): when amino acids are converted to other molecules, but there arent other molecules to pick up with NH4+ (which is toxic).
- remove the NH4+ via the urea cycle:
the conversion of the glutamine (a.a) to glutmate and then a-ketoglutarate generates WHAT?
why might this conversion occur?
why is lots of NH4+ produced?
generates free ammonia (as NH4+)
- a-ketoglutarate is needed for TCA cycle for energy.
- Glutamine has 2 amino groups, glutmate has 1, a-keto glutarate has 0 - so each step removes/adds an amino group so the metabolism of glutamine releases a lot of ammonium.
what is glutamine used for? (4)
Source of fuel during fasting - especially in muscles and immune cells.
Used for gluconeogenesis, esp. in kidney.
Produces ammonia, which can act as buffer for unwanted protons.
Glutamine has anti-inflammatory properties in the gut.
Overall: fuel, building block, needed for metabolites: a-ketoglutarate and glutamate.
MoA of urea cycle:
a) what is the rate determining step?
b) what are the two amino groups required? for it
c) what is the key regulating enzyme?
Rate controlling step:
o HCO3- + NH4+ –> carbamoyl phosphate (via enzyme carbamoyl phosphate synthase 1)
o Requires 2 ATP.
o Controlled allosterically by glutamate metabolite: N-acetyl glutamate - this is formed in an excess of glutamate, so drives urea cycle.
b) the two amino groups required from: aspartate (1) & ammonia (1)
essentially is a shuttle reaction of NH4 into from aspartate and ammonia into urea
what does the addition of ApoC2 and ApoE by HDLs do to chylomicrons? [2]
- ApoC2 added: allows chylomicrons to give its triglycerides to peripheral cells
- ApoE added: allows chylomicron remenant to be taken up by the liver to deliver FA & cholesterol
