Quiz
GI - Pancreas
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Perguntas do quiz (26)
1Describe the functional anatomy of the exocrine pancreas
Groups of [blank_start]acini[blank_end] ([blank_start]sac-like cavity[blank_end] in a gland, surrounded by [blank_start]secretory cells[blank_end])
[blank_start]Simple cuboidal epithelium[blank_end] surrounding an [blank_start]excretory duct[blank_end]
Several excretory ducts [blank_start]combine with increasing dimension[blank_end] to terminate as [blank_start]pancreatic duct[blank_end] / [blank_start]accessory pancreatic duct[blank_end]- Aacini
- Bsac-like cavity
- Csecretory cells
- DSimple cuboidal epithelium
- Eexcretory duct
- Fcombine with increasing dimension
- Gpancreatic duct
- Haccessory pancreatic duct
2What does the microscopic structure of endocrine pancreas consist of
lots of isolated clumps of [blank_start]cells surrounding a capillary[blank_end] (islets of Langerhans)
2 Major functions
• [blank_start]Digestion[blank_end] ([blank_start]exocrine pancreas[blank_end])
• Regulation of [blank_start]metabolism[blank_end] ([blank_start]endocrine pancreas[blank_end])- Acells surrounding a capillary
- Bendocrine pancreas
- CDigestion
- Dexocrine pancreas
- Emetabolism
3Explain the regulation of the exocrine pancreas and its role in digestion
[blank_start]Pancreatic juice[blank_end] - 2 major components
[blank_start]HCO3-[blank_end] to [blank_start]neutralise stomach acid[blank_end] thereby protecting small intestinal mucosa
Also provide the [blank_start]correct pH[blank_end] for digestive enzymes to function
Enzymes to [blank_start]digest food material[blank_end] for [blank_start]absorption in the small intestine[blank_end]
Involved in [blank_start]carbohydrate / protein / fat[blank_end] digestion- APancreatic juice
- BHCO3-
- Cneutralise stomach acid
- Dcorrect pH
- Edigest food material
- Fabsorption in the small intestine
- Gcarbohydrate / protein / fat
4What is the relevance of pancreatic juice in the horse/pig
substantial amounts of pancreatic juice produced – create large [blank_start]intestinal environment[blank_end] suitable for [blank_start]fermentation[blank_end].
- equivalent to [blank_start]saliva[blank_end] production in ruminants- Aintestinal environment
- Bfermentation
- Csaliva
5What is the Ionic composition of Pancreatic juice
Similar to [blank_start]blood[blank_end]
• [blank_start]HCO3-[blank_end] actively transported into duct lumen in exchange for [blank_start]Cl-[blank_end]
• Water follows by [blank_start]osmosis[blank_end]
• [blank_start]H+[blank_end] correspondingly transported into [blank_start]blood stream[blank_end]
• Negates the [blank_start]alkaline tide[blank_end]
• At normal flow rates [blank_start]HCO3-[blank_end] reabsorbed into [blank_start]acinar cells[blank_end]
• At [blank_start]high flow rates[blank_end] (eg during digestion) not enough time for [blank_start]HCO3-[blank_end] reabsorption so [blank_start]pancreatic juice[blank_end] remains highly [blank_start]alkaline[blank_end]
• [blank_start]Na+ / K+[blank_end] composition constant whatever the flow rate- Ablood
- BHCO3-
- CCl-
- Dosmosis
- EH+
- Fblood stream
- Galkaline tide
- Hacinar cells
- IHCO3-
- Jhigh flow rates
- KHCO3-
- Lpancreatic juice
- Malkaline
- NNa+ / K+
6What is the Enzymatic composition of pancreatic juice
• Secretion of [blank_start]digestive enzymes[blank_end] for c[blank_start]arbohydrate / fat / protein[blank_end] breakdown
• Proteases secreted in [blank_start]inactive[blank_end] form to prevent auto-digestion (as in stomach)
• Amylase breaks down [blank_start]starch[blank_end] (continues where salivary amylase left off!) to [blank_start]maltose[blank_end]
• Lipases / phospholipases break down fat to [blank_start]glycerol / fatty acids[blank_end]- Adigestive enzymes
- Barbohydrate / fat / protein
- Cinactive
- Dstarch
- Emaltose
- Fglycerol / fatty acids
7What happens to trypsinogen
• Duodenal epithelial surface contains [blank_start]enteropeptidase[blank_end]
Trypsinogen ⇒ [blank_start]Trypsin[blank_end]
• [blank_start]Trypsin[blank_end] auto-catalyses itself as well as [blank_start]activating other proteases[blank_end]- Aenteropeptidase
- BTrypsin
- CTrypsin
- Dactivating other proteases
8What do pancreatic cells produce
“[blank_start]trypsin inhibito[blank_end]r” to prevent [blank_start]auto-digestion[blank_end]- Atrypsin inhibito
- Bauto-digestion
9What are the 3 stages of digestion
• [blank_start]Cephalic[blank_end] phase
• [blank_start]Gastric[blank_end] phase
• [blank_start]Intestinal[blank_end] phase- ACephalic
- BGastric
- CIntestinal
10How is cephalic /gastric phase mediated
mediated by [blank_start]vagus / gastrin[blank_end]
• [blank_start]Carnivores[blank_end] - only enzymatic component
• [blank_start]Horse / Pig[blank_end] - ionic component as well (for large intestinal fermentation)- Avagus / gastrin
- BCarnivores
- CHorse / Pig
11What is theIntestinal phase mediated by
[blank_start]secretin / CCK[blank_end]
• Causes largest [blank_start]increase[blank_end] in secretion- Asecretin / CCK
- Bincrease
12What does vasco active inhibitory peptide (VIP) inhibit
effect of [blank_start]secretin[blank_end]- Asecretin
13What is the effect of secretin
Released from [blank_start]duodenum[blank_end] in response to [blank_start]H+[blank_end]
Increases [blank_start]HCO3-[blank_end] secretion
[blank_start]Negative feedback[blank_end] mechanism
As acid chyme gradually [blank_start]neutralised[blank_end] stimulus for secretin [blank_start]release[blank_end] diminishes- Aduodenum
- BH+
- CHCO3-
- DNegative feedback
- Eneutralised
- Frelease
14What is the effect of CCK
• Released from [blank_start]duodenum[blank_end] in response to [blank_start]fat / protein metabolites[blank_end] (fatty acids / monoglycerides / peptides / amino acids)
• Increases [blank_start]enzyme[blank_end] secretion
• Also causes [blank_start]gall bladder[blank_end] to contract (see Liver lecture)
• [blank_start]Positive feedback[blank_end] mechanism
• Increased enzyme secretion produce more [blank_start]metabolites[blank_end] which in turn stimulate further [blank_start]CCK[blank_end] release- Aduodenum
- Bfat / protein metabolites
- Cenzyme
- Dgall bladder
- EPositive feedback
- Fmetabolites
- GCCK
15What is the fucntion of insulin
• [blank_start]Peptide[blank_end] hormone released in response to [blank_start]increased plasma levels[blank_end] of [blank_start]glucose & amino acids[blank_end]
• Overall [blank_start]ANABOLIC[blank_end] effect
• Produced in [blank_start]pancreatic β-cells[blank_end]
• Synthesised as [blank_start]pre-pro-hormone[blank_end]
• Converted to [blank_start]pro-insulin[blank_end]
• Inactive due to [blank_start]c-peptide[blank_end] (blue)
• Secreted as [blank_start]active insulin[blank_end] by [blank_start]cleavage[blank_end] of the C-peptide
• Plasma half life of [blank_start]5-8 mins[blank_end]
• Deactivated in [blank_start]liver[blank_end] by cleavage of [blank_start]di-sulphide bonds[blank_end]- APeptide
- Bincreased plasma levels
- Cglucose & amino acids
- DANABOLIC
- Epancreatic β-cells
- Fpre-pro-hormone
- Gpro-insulin
- Hc-peptide
- Iactive insulin
- Jcleavage
- K5-8 mins
- Ldi-sulphide bonds
- Mliver
16Regulation of insulin
• Stimulated by increase in [blank_start]plasma glucos[blank_end]e and increase in [blank_start]plasma amino acids[blank_end]
• [blank_start]Direct feedback[blank_end] mechanism independent of other factors
• [blank_start]Bi-phasic[blank_end] secretion
• Initial immediate secretion of [blank_start]stored insulin[blank_end] lasting [blank_start]5-15 mins[blank_end]
• Also stimulated by [blank_start]GI[blank_end] hormones (e.g. [blank_start]gastric inhibitory peptide[blank_end]) released when food enters duodenum
• Thus insulin secreted in [blank_start]anticipation[blank_end] of increased absorption of [blank_start]glucose / amino acids[blank_end]
• Insulin secretion greater when [blank_start]glucose[blank_end] administered [blank_start]orally or intra-venously[blank_end]- Aplasma glucos
- Bplasma amino acids
- CDirect feedback
- DBi-phasic
- Estored insulin
- F5-15 mins
- GGI
- Hgastric inhibitory peptide
- Ianticipation
- Jglucose / amino acids
- Kglucose
- Lorally or intra-venously
17Descibe ANS regulation
• [blank_start]Parasympathetic[blank_end] activity (via [blank_start]vagus)[blank_end] increases [blank_start]insulin[blank_end] secretion
• Part of [blank_start]long-reflex arc[blank_end]
• Amplifies hormonally-regulated secretion
• [blank_start]Sympathetic[blank_end] activity & [blank_start]adrenaline[blank_end] release [blank_start]decreases[blank_end] insulin secretion- AParasympathetic
- Bvagus)
- Cinsulin
- Dlong-reflex arc
- ESympathetic
- Fadrenaline
- Gdecreases
18Actions of insulin
• Binds to receptors on [blank_start]target cells[blank_end]
• Receptor functions as [blank_start]tyrosine kinase[blank_end] upon activation
• [blank_start]Phosphorylation[blank_end] of intra-cellular proteins mediates different actions of insulin
• Stimulates cell uptake of nutrients during [blank_start]absorptive[blank_end] phase
• Most important [blank_start]anabolic[blank_end] mediator
• Glucose uptake enhanced by mobilisation of [blank_start]glucose transporter[blank_end] ([blank_start]GLUT4[blank_end]) to cell membranes
• Nearly all tissues (especially [blank_start]skeletal muscle / adipose tissue[blank_end])
• [blank_start]Brain[blank_end], [blank_start]liver[blank_end], [blank_start]intestines[blank_end], [blank_start]kidney[blank_end] & [blank_start]mammary tissue[blank_end] insulin-independent
• Glucose uptake mediated by different GLUT transporters
• [blank_start]anabolic[blank_end] effect
• Increases concentration / activity of intra-cellular enzymes involved in [blank_start]metabolism[blank_end] of glucose / amino acids / lipids
• Increases [blank_start]glycogenesis[blank_end] in liver / skeletal muscle
• Increases formation of [blank_start]glycerol[blank_end] / [blank_start]FFA[blank_end] for tri-glyceride synthesis
• Inhibits enzymes that breakdown [blank_start]tri-glycerides[blank_end] (e.g. hormone sensitive lipase)- Atarget cells
- Btyrosine kinase
- CPhosphorylation
- Dabsorptive
- Eanabolic
- Fglucose transporter
- GGLUT4
- Hskeletal muscle / adipose tissue
- IBrain
- Jliver
- Kintestines
- Lkidney
- Mmammary tissue
- Nanabolic
- Ometabolism
- Pglycogenesis
- Qglycerol
- RFFA
- Stri-glycerides
19What is Diabetes mellitus
• Plasma [blank_start]glucose[blank_end] elevated ([blank_start]hyperglycaemia[blank_end]) due to [blank_start]decreased[blank_end] uptake by cells
• Capacity for [blank_start]kidneys[blank_end] to re-absorb glucose [blank_start]exceeded[blank_end] ([blank_start]glucosuria[blank_end])
• Fairly rare but occurs most often in [blank_start]carnivores / omnivores[blank_end]- Aglucose
- Bhyperglycaemia
- Cdecreased
- Dkidneys
- Eexceeded
- Fglucosuria
- Gcarnivores / omnivores
20What are the 2 types of DM
• Type I - [blank_start]Insulin-dependent (IDDM)[blank_end]
Insulin production [blank_start]impaired[blank_end]
Treated by [blank_start]insulin injections[blank_end] (not orally)
• Type II - [blank_start]Non-insulin-dependent (NIDDM)[blank_end]
Insulin production [blank_start]normal[blank_end] but cells [blank_start]resistant[blank_end] to its effects- AInsulin-dependent (IDDM)
- BNon-insulin-dependent (NIDDM)
- Cimpaired
- Dinsulin injections
- Enormal
- Fresistant
21What type is most common
[blank_start]IDDM[blank_end] most common
What is it caused by
• Caused by [blank_start]pancreatic[blank_end] inflammation, [blank_start]hyper-secretion[blank_end] of hormones [blank_start]antagonistic[blank_end] to insulin (e.g. [blank_start]cortisol / growth hormone[blank_end]) & [blank_start]obesity[blank_end]- AIDDM
- Bpancreatic
- Chyper-secretion
- Dantagonistic
- Ecortisol / growth hormone
- Fobesity
22What is Hyperglycaemia
• Results in [blank_start]polyuria / polydypsia[blank_end]
• Would expect urine specific gravity to be [blank_start]low[blank_end] but artificially [blank_start]normal / high[blank_end] due to [blank_start]glucosuria[blank_end]- Apolyuria / polydypsia
- Blow
- Cglucosuria
- Dnormal / high
23In hyperglycemia, what does increase of degradation of lipids lead to
• Incomplete metabolism of [blank_start]FFAs[blank_end] results in production of [blank_start]ketone bodies[blank_end] (normally [blank_start]ketone bodies[blank_end] oxidised to [blank_start]CO2 / H2O[blank_end])
• Some [blank_start]ketones[blank_end] are acidic resulting in [blank_start]metabolic acidosis[blank_end]
• Impaired brain function can lead to [blank_start]diabetic coma / death[blank_end]- AFFAs
- Bketone bodies
- Cketone bodies
- DCO2 / H2O
- Emetabolic acidosis
- Fketones
- Gdiabetic coma / death
24What is Hypoglycaemia
• Plasma [blank_start]glucose[blank_end] below [blank_start]normal physiological range[blank_end] ([blank_start]5mM[blank_end])
• Most often caused by insulin [blank_start]overdose[blank_end]
• Also insulinoma ([blank_start]tumour of pancreatic β-cells[blank_end])
• Treated by [blank_start]oral / intravenous[blank_end] glucose
• [blank_start]Ruminants[blank_end] less sensitive to hypoglycaemia- Aglucose
- Bnormal physiological range
- C5mM
- Doverdose
- Etumour of pancreatic β-cells
- Foral / intravenous
- GRuminants
25What is the function of Glucagon
• Peptide hormone released in response to [blank_start]decreased[blank_end] levels of [blank_start]glucose & amino acids[blank_end]
• Overall [blank_start]CATABOLIC[blank_end] effect
• Produced in [blank_start]pancreatic α-cells[blank_end]
• Synthesised as [blank_start]pre-pro-hormone[blank_end]
• Converted to [blank_start]pro-glucagon[blank_end]
• Secreted as [blank_start]active glucagon[blank_end]
• Plasma half-life of [blank_start]5-6 mins[blank_end]
• Deactivated by metabolism in [blank_start]liver / kidneys[blank_end]- Adecreased
- Bglucose & amino acids
- CCATABOLIC
- Dpancreatic α-cells
- Epre-pro-hormone
- Fpro-glucagon
- Gactive glucagon
- H5-6 mins
- Iliver / kidneys
26What ar the regulation/actions of glucagon
• Stimulated by [blank_start]decrease[blank_end] in plasma glucose
• Also stimulated by [blank_start]increase[blank_end] in plasma amino acids & [blank_start]increased[blank_end] sympathetic activity
• Binds to receptors on [blank_start]target cells[blank_end]
• Activates [blank_start]adenyl cyclase[blank_end]
• Actions of glucagon are [blank_start]reverse[blank_end] of insulin
• Net effect on metabolism depends on ratio of [blank_start]insulin : glucagon[blank_end]
• Increases plasma glucose by stimulating liver [blank_start]glycogenolysis[blank_end] and [blank_start]gluconeogenesis[blank_end]
• Little effect on any tissues other than the [blank_start]liver[blank_end]- Adecrease
- Bincrease
- Cincreased
- Dtarget cells
- Eadenyl cyclase
- Freverse
- Ginsulin : glucagon
- Hglycogenolysis
- Igluconeogenesis
- Jliver
Informações
- Descrição
- GI (GI) Quiz sobre GI - Pancreas , criado por hanna sayedi em 29-01-2019.
- Autor
- hanna sayedi
- Idioma
- English
- Visualizações
- 3
- Etiquetas
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