METSS2 Flashcards
which amino acids are glucogenic? [2]
which a.a are ketogenic? [2]
glutamine
Alanine
lysine and leucine are ketogenic
which cells regulate water contents in the gut?
what is the mechanism of this?
secretory cells of the intestinal crpyts:
- CFTR channel within these cells controls this:
a) Cl- moves from ECF via Na/K/CL2 cotransporter (as does Na & K)
b) Cl- enters lumen through CFTR channel
c) Na+ is reabsorbed via Na/K ATPase
d) negative Cl- in lumen attracts Na by paracellular pathway (through cell gaps)
e) water follows the Na into the lumen
gastric epithelial cells
- parietal cells produce HCl. But HCl is actually quite toxic. how does the body cell overcome this issue of not causing self harm via the HCl? (2)
1. HCl is only produced when food is in the stomach = get unstimualted and stimulated parietal cells:
a) unstimulated parietal cells have H+ ATPase Pumps in the cytosol
b) stimulated parietal cells have H+ ATPase Pumps on apical surface
- *2. surface mucus cells secrete mucus**
- without mucus = would directly interact with cells
- mucus works as:
a) physical barrier; gel layer
b) chemical barrier; bicarbonate
explain how diabetes disrupts gluconeogensis pathway ox
insulin doesnt work:
SO
- pyruvate dehydrogenase remains phosphorylated & therefore inactive
- = less acetyl co-A to go into krebs cycle from pyruvate
- instead fats are broken down to produce fatty acids & acetyl co-A & goes into krebs cycle instead
- means that pyruvate is available for gluconeogenesis
explain what happens to the stomach when food enters the intestines?
a) hormonal control
b) nervous control
Primarily inhibits gastric acid secretion when FOOD AND ACID ENTERS THE INTESTINES
NERVOUS CONTROL:
- *It signals the sympathetic system to stop gastric secretions**
- Inhibition of parietal and chief cells
HORMONAL CONTROL:
- *- Cholecystokinin, secretin and GIP (gastric inhibitory protein) produced by duodenum –> inhibit gastric secretions**
- Cholecystokinin and GIP released by presence of lipids and carbohydrates
- Secretin released when pH decreases (due to entrance of acidic chyme into the duodenum)
Q
PDH is regulated in two ways:
- PDH is de/-phosphorylated by which enzymes? what do they add / remove? what is their effect?
which substances control 1.?
:)
- PDH Kinases inhibit PDH by adding PO4
- PDH Phosphatases activate PDH by removing PO4
//
- *control of PDH kinases**
- PDH kinases are activated: by ATP, acetyl Co-A and NADH (last two are products of PDH) = switch off PDH.
- Pyruvate & insulin inhibits PDH Kinasese (as pyruvate wants PDH to be active to break pyruvate down) = switch on PDH.
control of PDH phosphatases
- Ca2+ ions activate PDH phosphatises - increases PDH. occurs in muscle -> eventually get more ATP production = switch on PDH
- insulin activates PDH phosphatases - actives PDH
what does Akt do in muscle?
Akt: phosphorylates and inactivates glycogen synthase kianse = activates glyocgen synthase
how is the TCA cycle controlled in response to exercise?
(3)
1.
- Ca2+ is an allosteric keeps the pyruvate deyhyrogenase complex activated.
- therefore causes **quicker conversion of pyruvate -> acetly co-A
- increases TCA to occur more**
(PDH controls the entry to the TCA, it’s activity is regulated. The enzyme is phosphorylated and dephosphorylated depending on whether it is active or inactive. The calcium is promoting essentially the active state of PDH, by influencing PDH phosphatase (this PDH phosphatase will remove phosphates from the PDC and activate it)
2:
calcium and ADP drive activity of two dehydrogenase enzymes in the TCA to maintain high ATP production
3.
Low levels of ATP/NAD pushes PDH into its active state.
what are the step changes in metabolism that undergo during starvation? (5)
- glucose starts falling; insulin goes down, glucagon up
- glycogen can keep brain alive for 2/3 days / 30 hrs
- swith to FA break down = energy for 2-3 days due to gluconeogenesis
- FA then switches to ketone bodies. (ketone bodies can go into brain - important !)
- final resource = break down proteins to release amino acids for gluconeogenesis
to put simply - insulin has what effect on PDH?
what effect does insulin have of kinases & phosphatases?
what do adrenaline and glucagon do to PDH? - why?
insulin caueses the activation of PDH & eventual production of acetyl co-A
insulin = -ve effect on kinases (which inhibit PDH)
+ve effect on phosphatases (which activate PDH)
adrenaline and glucagon: want pyruvate untouched, so it can be used to make glucose via gluconeogenesis = inhibit PDH
NADPH is a co-factor created by immune cells.
Name 2 functions of NADPH
- as a reducing agent (like NADH)
- to generate ROS: immune cells use NADPH oxidase to reduce O2 to free radical and the H202. H202 then used to kill engulfed pathogens = respiratory burst
what covers the rectus abodminis?
rectus sheath
what does tissue transglutaminase (tTG) do to gliadin in CD patients? [1]
removes amide group / deamination
Name the cells bordering the lumen [1]
paneth cell
what region of the GI tract is this? [1]
how can you tell? [1]
duodenum [1]
brunners glands [1]
label A-E
A = **enterocyte brush border** B = **lacteal** C = **goblet cell** D = **immune cells (lymphocytes)** E = **lamina propria**
name this region of the intestine [1]
how can you tell [1]
jejunum
plicae circularis
Plicae circulares are out foldings of both the mucosa and submucosa. Projecting from these folds are numerous villi that are outfoldings of the mucosa.
label A-H of the lymph node
A = afferent lymphatic, B =subcapsular sinus, C = cortex, D = medullary cords, E = medulla, F = efferent lymphatic, G = hilus, H = secondary follicles
label A-H of the lymph node
A = afferent lymphatic, B =subcapsular sinus, C = cortex, D = medullary cords, E = medulla, F = efferent lymphatic, G = hilus, H = secondary follicles
name this region of the intestine [1]
how can you tell [1]
jejunum
plicae circularis
Plicae circulares are out foldings of both the mucosa and submucosa. Projecting from these folds are numerous villi that are outfoldings of the mucosa.
what is the squamocolumnar junction? - chang
squamocolumnar junction
- abrupt change in the mucosa from stratified squamous to columnar cells (and glands)
- Oesophagus joins at an acute angle
- only the mucosa changes, the underlying layers stay the same !!
(oespahus -> stomach?)
what is the squamocolumnar junction? - chang
squamocolumnar junction
- abrupt change in the mucosa from stratified squamous to columnar cells (and glands)
- Oesophagus joins at an acute angle
- only the mucosa changes, the underlying layers stay the same !!
(oespahus -> stomach?)
label A-E
A = **enterocyte brush border** B = **lacteal** C = **goblet cell** D = **immune cells (lymphocytes)** E = **lamina propria**
what region of the GI tract is this? [1]
how can you tell? [1]
duodenum [1]
brunners glands [1]
Name the cells bordering the lumen [1]
paneth cell
when is insulin / glucagon released?
what do insulin and glucacon to do: & how?
a) glycogen synthase
b) glycogen phosphorylase
* key - learn this *
insulin: released after meal. insulin works via protein phosphatase (removes Ps):
- *- activates glycogen synthase - by removing P
- inhibits glycogen phosphorylase - by removing P**
glucagon & adrenaline: released between meals / when fasting: works via cAMP, protein kinase A and phosphorylase kinase: adds P
- *- inhibits glycogen synthase - adds P
- activates glycogen phosphorylase - adds P**
what does a lack of cAMP doe regarding glucose release? [1]
lack of cAMP causes glucagon and adrenaline effects to be stopped (and less glucose released)
what does a lack of cAMP doe regarding glucose release? [1]
lack of cAMP causes glucagon and adrenaline effects to be stopped (and less glucose released)
how do u tell histoligcally if you have significant oesophagitis? (2)
how do u tell histoligcally if you have barret oesph? (1)
how do u tell histoligcally if you have CD? (3)
significant oesophagitis: eosinophils in squamous mucosa & neutrophils
barret oesophagus: complication of chronic gastro reflux disease (GERD). characterised by change of squamous mucosa in oesph to simple columnar epithelim
CD: atrophy of villi (1), hyperplasia of intestinal crypts, more lymphocytes
IgA anti-gliadin, anti-tTG and anti-endomysial* (EMAs) are produced by which immune cell? [1]
B cells
which inflammatory cytokines are associated with CD?
IFN-γ
TNF-a
IL-1
IL-6
which inflammatory cytokines are associated with CD?
IFN-γ
TNF-a
IL-1
IL-6
which inflammatory cytokines are associated with CD?
IFN-γ
TNF-a
IL-1
IL-6
which inflammatory cytokines are associated with CD?
IFN-γ
TNF-a
IL-1
IL-6
explain how trypsin is activated (and from what?) and what it does subsequently to activation (2)
- Trypsinogen from pancreas converted to trypsin via enterokinase (a brush border enzyme)
- Trypsin then activates chymotrypsinogen to chymotrypsin and procarboxypeptidase to carboxypeptidase
Gut honing mechanism:
dendritic cells create WHAT in the gut? - what does this cause gut homing T cells to make? (2)
- dendritic cells produce retinoic acid (vitamin A) which induce gut homing T cells to express α4β7 and CCR9.
Gut honing mechanism:
dendritic cells create WHAT in the gut? - what does this cause gut homing T cells to make? (2)
- dendritic cells produce retinoic acid (vitamin A) which induce gut homing T cells to express α4β7 and CCR9.
explain how trypsin is activated (and from what?) and what it does subsequently to activation (2)
- Trypsinogen from pancreas converted to trypsin via enterokinase (a brush border enzyme)
- Trypsin then activates chymotrypsinogen to chymotrypsin and procarboxypeptidase to carboxypeptidase
which inflammatory cytokines are associated with CD?
IFN-γ
TNF-a
IL-1
IL-6
which inflammatory cytokines are associated with CD?
IFN-γ
TNF-a
IL-1
IL-6
which inflammatory cytokines are associated with CD?
IFN-γ
TNF-a
IL-1
IL-6
which inflammatory cytokines are associated with CD?
IFN-γ
TNF-a
IL-1
IL-6
IgA anti-gliadin, anti-tTG and anti-endomysial* (EMAs) are produced by which immune cell? [1]
B cells
how do u tell histoligcally if you have significant oesophagitis? (2)
how do u tell histoligcally if you have barret oesph? (1)
how do u tell histoligcally if you have CD? (3)
significant oesophagitis: eosinophils in squamous mucosa & neutrophils
barret oesophagus: complication of chronic gastro reflux disease (GERD). characterised by change of squamous mucosa in oesph to simple columnar epithelim
CD: atrophy of villi (1), hyperplasia of intestinal crypts, more lymphocytes
when is insulin / glucagon released?
what do insulin and glucacon to do: & how?
a) glycogen synthase
b) glycogen phosphorylase
* key - learn this *
insulin: released after meal. insulin works via protein phosphatase (removes Ps):
- *- activates glycogen synthase - by removing P
- inhibits glycogen phosphorylase - by removing P**
glucagon & adrenaline: released between meals / when fasting: works via cAMP, protein kinase A and phosphorylase kinase: adds P
- *- inhibits glycogen synthase - adds P
- activates glycogen phosphorylase - adds P**
describe the structure of the rectus sheath
a) above arcuate line
b) below arcuate line
- *rectus sheath:**
- surrounds rectus abdominis muscle
- made from: aponeuroses of external oblique, internal oblique and transverse abdominis
- structure:
- *a) above arcuate line**
i) external oblique aponeuroses runs anterior to rectus abdmonis & inserts into the midline: forms linea alba
ii) i_nternal oblique aponeuroses splits in half_: half goes anterior of rectus abdominis, other half goes posterior. again insets onto linea alba
iii) transversus abdominis runs posterior to rectus abdominis
iv) transversalid fascia runs posterior to rectus abdominis - *b) below arcuate line:**
i) all of aponeuroses run anterior to rectus abdominis
ii) transveralis fascia runs posterior to rectus abdominis
why is water needed in the digestive system? (4)
Hydrolysis reactions of digestion
Facilitation of absorption (brings products of digestion into close proximity to microvilli)
Facilitation of propulsion of gut contents
Combination with mucin granules to make mucus
in the production / break down of glucagon, glycogen synthase and glycogen phosphorylase are made active / inactive by the addition of what?
glycogen synthase is activated by removing P, inactivated by adding P
glycogen phosphorylase is activated by adding P, inactivated by removing b
therefore work antagonistically !
label 1-3
1: posterior belly of digastric muscle
2: mylohyoid muscle (cut)
3: geniohydoid muscle
extrinisc innervation of the GI tract:
- which nerve controls communication between gut and CNS?
- after enetering the brain stem, where does & synapse?
extrinsic innervation - vagus nerve mediates communication gut and CNS
- has central terminals that enter brain stem and synapse to neurons of nucleus tractus solitarus
name the three papillae in the tongue
which have taste buds (2)
- *- fungiform papillae**: located anteriorly
- *- filiform papillae**: loacted centrally
- *- circumvallate papillae:** located posteriorly
fungiform and circumvallate = taste buds
upper oesophageal sphincter is made from which muscle?
EOS: cricopharnyngeus muscle
for anterior 2/3 tongue:
which nerve supplies the
a) special sensory (taste)
b) general sensory (pressure etc)
c) motor sensory?
anterior 2/3 tongue:
nerve supplies the
a) special sensory (taste): CN VII - facial nerve
b) general sensory (pressure etc): CN V - trigeminal nerve (V3, mandibular nerve)
c) motor sensory: hypoglossal nerve - CN XII
for posterior 1/3 tongue:
nerve supplies the
a) special sensory (taste): glossopharnyngeal nerve (CN IX)
b) general sensory (pressure etc): glossopharnyngeal nerve (CN IX)
c) motor sensory: hypoglossal nerve - CN XII
