MET EOYS1 Flashcards by patrick ellis

Name the cells bordering the lumen [1]

paneth cell

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what region of the GI tract is this? [1]
how can you tell? [1]

duodenum [1]
brunners glands [1]

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label A-E

A = **enterocyte brush border**
B = **lacteal**
C = **goblet cell**
D = **immune cells (lymphocytes)**
E = **lamina propria**

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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.

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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

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what is the name for what dietary lipid is transported in? [1]
which system are dietary lipids transported in? [1]

chylomicrons [1]
lymphatic system [1]

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B12 can be only observed where? & what must it first be complexed with?

what is B12 aka?

describe the absorptive pathway of B12 :)

B12: absorbed only in terminal ileum, after being complexed with stomach-derived intrinsic factor
B12: aka cobalamin

absorptive pathway:

bound to dietary protein
first dissociated by HCl and pepsin, in stomach
reattaches itself via haptocorrin (from saliva thats now in stomach)
dissociated from haptocorrin and binds with stomach-derived intrinsic factor
absorbed only in terminal ileum in enterocytes (although 60-80% still goes into faeces)
reassociates with transcobalamin and then goes to portal circulation

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which 3 antibodies do you get high levels of in CD patients? [3]

antigliadin, tissue transgluataminase, anti endomysial

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how do commensal bacteria regulate digestion?

what happens if we have bacterial overgrowth?

dynamic equilibrium between diet-gut microbiome-bile acid pool size:

normally - we have conjugated bile acids, created by liver. Conjugated bile acids (primary bile acids): more efficient in emulsifying fats because at intestinal pH they become more ionized than the unconjugated bile acids.

Commensal bacteria: participate in the synthesis of bile acids. Microbial enzymes de-conjugate bile acids & make them less effecient: (secondary bile acids).

so we have a pool of primary and secondary bile acids: if have bacterial overgrowth in gut: form too much secondary bile acids = struggle to digest fats

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what do mutations in:

LCT gene
SLC5A1 gene

cause?

which phase of digestion they effect?

mutation in gene LCT - affects mucosal phase of dissachardide absorption. lactose intolerance

gene SLC5A1 - encodes for Sodium dependent GLucose tranpsorter one: SGLT1. so mutation causes glucose-galactose malabsorption. again: mucosal phase

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why does muscle not have a role in raising blood glucose levels? [2]

free glucose cannot be produced / released from skeletal muscle bc **it doesnt have glucose-6-phosphatase (to convert G6P -> glucose) [1]
muscle doesnt have glucagon receptors [1]**

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where is glucagon made?

it is produced by the alpha cells, found in the islets of Langerhans, in the pancreas

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what is glycogen breakdown aka?
explain how this occurs (4)

glycogenolysis:

debranching enzyme: breaks down the a-1,6 glycosidic bonds (the branches of glucose)
glycogen phosphorylase: breaks down a-1,4 glycosidic bonds: free G1Ps
phosphoglucomutase: converts G1P to G6P
in the liver: glucose-6-phosphatase removes the P group = free glucose
(but step 4 does not occur in the muscle - instead, it is immediately used in glycolysis)

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what do two starting materials do you need before glycogen synthesis?

*glycogen synthesis needs:**
a primer (protein that glucose will attach to): glycogenin.
*- glucose-6-phosphate (G6P)**

BUT: NEED TO CONVERT G6P -> UDP-glucose before can be added to glycogen:

*a) G6P –> G1P
b) G1P –> UDP-glucose**

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what do two starting materials do you need before glycogen synthesis?

*glycogen synthesis needs:**
a primer (protein that glucose will attach to): glycogenin.
*- glucose-6-phosphate (G6P)**

BUT: NEED TO CONVERT G6P -> UDP-glucose before can be added to glycogen:

*a) G6P –> G1P
b) G1P –> UDP-glucose**

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glycogen production and breakdown is carried out by which hormone signalling molecules (4) and which do they act on - liver or muscle?

insulin: muscle and liver - builds glycogen stores
glucagon: only liver - breaks down glyocgen stores to release glucose
adrenaline: muscles via a & b adrergic receptors - release glucose

4 calcium: muscles via a & b adrergic receptors - release glucose

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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**

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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)

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what are the two pathways that insulin causes glycogen synthase to be activated and cause glucose -> glycogen?

insulin:

activates phosphodiesterase
activates protein phosphastase

which are two different pathways that both end up in the glucose –> glycogen

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Mc Ardle’s disease:

what type of disease (autosomal dom etc?)
caused by?

what does this mean with regards to exercise ? second wind can occur from?

Herrs Disease

same>?

Mc Ardle’s disease:

autosomal recessive disease

caused by: deficiency in glycogen phosophorylase gene: PYGM. cant breakdown glycogen in the muscle = muscle weakness

when exercise: can only exercise in short bursts, otherwise muscles will cramp, lock and they will fall over in intense pain. This is due to their muscles running out of energy.

second wind: muscles use alternative fuel to glucose

Her’s disease:

caused by: deficiency in glycogen phosphorylase in liver = severe problems maintaining their blood glucose

Treatment: regular, often feeding. This is because they cannot maintain their blood glucose like we can

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what is von Gierkes disease? [1]

deficiency in glucose-6-phosphastase: means liver cant produce glucose via glycogen breakdown.

feed patients with carbs day and night

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*gastrooesphageal reflux disease (GERD):**
caused by?
associated with? (3)
what can chronic condition lead to? (3)
treatments?

Study These Flashcards

gastrooesphageal reflux disease (GERD):

- caused by:

a) movement of stomach contents from fundus -> distal oesophagus after lower oesophagus sphincter is relaxed
b) then get increased frequency of transient relaxations of lower oesph. sphincter

- associated with:

**weight gain
gastroparesis
stress**

- chronic condtion leads to:

*a) ulcer formation
b) inflammation**
treatment: antacids and alginates - like gaviscon

gastroparesis:

caused by?
symptoms?
which disease is it associated with?
what can it lead to?

Study These Flashcards

- caused by: delayed gastric emptying

- inability to remove stomach content causes: nausea, vomiting, feeling of fullness, pain and bloating

- associated with diabetes: diabetic gastroparesis

- subsquently can lead to malnutrition (bc people dont eat) and changes in blood sugar

gastroparesis:

caused by?
symptoms?
which disease is it associated with?
what can it lead to?

Study These Flashcards

- caused by: delayed gastric emptying

- inability to remove stomach content causes: nausea, vomiting, feeling of fullness, pain and bloating

- associated with diabetes: diabetic gastroparesis

- subsquently can lead to malnutrition (bc people dont eat) and changes in blood sugar

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 are the two pathways that insulin causes glycogen synthase to be activated and cause glucose -\> glycogen? [2]

insulin: * *- activates phosphodiesterase - activates protein phosphastase** which are two different pathways that both end up in the glucose --\> glycogen

which cells in stomach secrete: - pepsinogen? - HCl? where in the stomach do u find them? how do u differientate? (2)

- **pepsinogen**: chief cells - **HCl**: parietal cells * *- chief cells:** deep in fundic glands * *- parietal cells:** neck of fundic segment - **chief cells**: smaller, paler * *- parietal cells**: bigger, darker

how do u tell the difference between paneth cells and endocrine?

**Paneth granules** are **above nucleus** (supranuclear) & **appear pink** **endocrine granules** are **beneath** the **nucleus** (subnuclear)

how do u tell the difference between paneth cells and endocrine?

**Paneth granules** are **above nucleus** (supranuclear) & **appear pink** **endocrine granules** are **beneath** the **nucleus** (subnuclear)

name the 5 different types of celsl find in the body / fundic mucosa?

**body / fundic mucosa:** mucous neck cells: secrete mucous - chief cells: deep at bottom of fundic glands. secrete pesinogen ! - parietal cells: neck of fundic segment: secrete HCl and intrinsic factor ! - stem cells - endocrine cells

what are the small intestine cells? (5)? roles

- **enterocytes**: secretory and absorb functions - **goblet** **cells**: secrete mucous - **paneth** **cells**: secrete antimicrobe substances; H&E= pink **-** **enteroendocrine** **cells**: release horomones - **m** **cells**: modified enterocytes that cover lymphoid nodules

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: a**trophy of villi (1), hyperplasia of intestinal crypts, more lymphocytes

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)

what happens to C&L muscle in anal sphincter?

circ muscle: **becomes internal anal sphincter** long muscle**: extends over sphincter & attaches to CT**

what are the three zones of the anal canal? what are the cells like there?

_colorectal zone:_ simple columnar epi _anal transitional zone_: transition betwen simple columnar and and stratified squamous epi _squamous zone:_ stratified squamous

which two things signify hunger in ur body? [2]

- release of hormone **ghrelin** - **phase three of migrating motor complex**

which cells cause depolarisation to initiate stomach muscle contraction? [1]

**interstitial cells of cajal**

functions of the proximal stomach: - what happens when bolus enters stomach? (2 steps) - what is each step innervated by? - what method can u do to relieve pressure of stomach? - how does this occur? functions of the distal stomach? (3)

**functions of the proximal stomach:** - **receptive relaxation**: makes proximal stomach **stretch** so not immediatly full _(vagal-vagal relflex, causes release of CCK)_ - a**daptive relaxation**: **ENS** releases **NO** to allow relaxation - can relieve pressure by **burping** (lets gas out of stomach) via **relaxation** of **LOS** * *functions of the distal stomach:** - propulsion, retropulsion and further grinding and mixing (propels food agaisnt closed pylorus) - gastric acid digestion - only particles of 1-2 mm empty into duodenum

## Footnote what anatomical features of the colon ensure that peristalsis is modified? (2)

- get bulges of outer circular muscle (**haustra**), which are held together by three bands of circular muscle: **taenia** ## Footnote **- taenia can contract in either direction**

## Footnote what anatomical features of the colon ensure that peristalsis is modified? (2)

- get bulges of outer circular muscle (**haustra**), which are held together by three bands of circular muscle: **taenia** ## Footnote **- taenia can contract in either direction**

explain what the duodenal and jejunal breaks are

**dudenal and jejunal brakes:** 1. food goes into the duodenum, might be too big - like long chain fatty acids / amino acids. causes the release of CCK **2. release of CCK activates vagal efferents** * *3. as a result of vagal efferents:** - reduces opening of pyloric sphincte - reductions contractions in corpus - enhances relaxation of fundus

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

IgA anti-gliadin, anti-tTG and anti-endomysial\* (EMAs) are produced by which immune cell? [1]

B cells

\* What is the rate controlling step of glycolysis? What factors regulate it’s function. [3] \*

**Fructose-6-phosphate** to **Fructose-1,6-bisphosphate** via the enzyme **Phosphofructokinase-1**. Is regulated by: 1.**ATP:AMP ratio** 2.**Citrate** (decreases activity) 3**.Fructose-2,6-bisphosphate** (increased activity)

where does bile enter the dudeonum? which part of the duodenum?

**at the Ampulla of Vater: 2nd part of duodenum**

what are th 5 pancreatic enyzmes made?

- Procarboxypeptidase - Trypsinogen - Chymotripsinogen - Amylase - Lipase

which cells release pepisogen? how is it activated?

**Chief cells** (1) release **pepsinogen** --\> activated to **pepsin** using **hydrochloric acid** released from **parietal cells!!**

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**

**pink = parietal !!**

Vitamin B12 - absorbed where? which population needs supplementts/

* Complexed with intrinsic factor in stomach * Absorbed in **_terminal ileum!!_** * Vegans need to be supplemented with vitamin B12

which cells transport gut antigens from lumen across epithelium?

**M cells** (microfold cells) transport gut antigens from the lumen across epithelium into the tissue.

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.**

MET EOYS1 Flashcards

(54 cards)