Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Physiology for Anaesthetists > GIT - digestion and absorption > Flashcards

GIT - digestion and absorption Flashcards

1
Q

What is the length of the GIT

A

9m

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Where are most nutrients absorbed

A

Jejunum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Where is B12 absorbed

A

Terminal Ileum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

where is iron absorbed

A

duodenum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Where is dietary fat and water absorbed

A

Throughout

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe the layers of the small intestine

A 
ADVENTITIA
MUSCULARIS EXTERNA (Peristalsis)
- Outer longitudinal smooth muscle
- Myenteric plexus
- Inner Circular smooth muscle
SUBMUCOSA
- Meissner's plexus (secondary enteric nervous system plexus) blood vessels, lymphatics, elastic connective tissue
MUCOSA
- Muscularis mucosae 
- Lamina propria
- Epithelium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the difference between muscularis externa and muscularis mucosa

A

Muscularis externa

  • longitundinal muscles
  • myenteric plexus
  • circular muscles

–> responsible for peristalsis

Muscularis Mucosa

  • Within the submucosa
  • innervated by Meissner’s plexus
  • Agitate mucosa increasing contact with luminal content and preventing their adherence
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Where are Peyer’s patches and what do these do

A

Lymphoid nodules within the lamina propria of the mucosa of the terminal ileum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Where is Meissner’s plexus. What else is contained in this layer of the intestine

A

Within the submucosa

also
Blood vessels
Lymphatic vessels
Elastic connective tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the length and surface areaof the small intestine. How is this achieved

A

Length - 7m

SA: 250 m^2

  1. Valvulae conniventes - mucosal folds that project into the lumen of the SI
  2. Villi - Tiny finger-like projections of the intestinal wall
  3. Microvilli - microscopic projections on top of villi (brush border)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What structures lie between the villi in the small intestine and what is the function of these structures

A

Goblet cells –> secrete mucus

Intestinal crypts –> secrete brush border enzymes and contain stem cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe blood and lymphatic supply to each villi

A

A single arteriole –> capillaries –> single venule

Lacteal = a single lymphatic capillary which transports absorbed fats as chylomicrons to the thoracic duct.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Where does digestion of CHO begin and how

A

Mouth

Salivary amylase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

After the mouth when does CHO digestion recommence and how

A

Duodenum

Pancreatic amylase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Subsequent to salivary amylase and pancreatic amylase, how does CHO digestion proceed?

A

Brush border enzymes

  • Sucrase
  • Maltase
  • Lactase

–> Disaccharides to monosaccharides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe the sucrose, maltose and lactose monomers

A

Sucrose –> glucose + fructose
maltose –> glucose + glucose
Lactose –> glucose + galactose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What causes lactose intolerase

A

Brush border enzyme lactase deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Which CHO passes through the GIT undigested and why

A

Cellulose –> no brush border enzymes present for hydrolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How are glucose and galactose absorbed

A

Enterocyte

SGLT - 1
Sodium Glucose Linked Transporter- 1

This is secondary active transport subsequent to basolateral Na/K+ ATPase activity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How is fructose absorbed

A

facilitated diffusion (not by Na+ transport)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How are pentose sugars (like ribose and deoxyribose) absorbed

A

Simple diffusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Once secondary active transport via the SLGT-1 has transported the glucose and galactose into the enterocyte, how does absoprtion continue

A

Down concentration gradient. Pass through the basolateral membrane via the GLUT-2 glucose transporter (facilitated diffusion) Into the capillary network within the villi –> venule –> portal vein –> Liver

monosaccharides are osmotically active so co-absorption of water occurs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Where does protein digestion begin. Name the cells enzyme and cofactors involved

A

Stomach - Pepsin

Chief cells —> pepsinogen + low pH (HCl) –> pepsin

Parietal cells –> HCl

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How is protein digstion continued in the duodenum

A

Pancreatic trypsin and chymotrypsin cleave polypeptides –> dipeptides and tripeptides

25
Q

How is protein metabolism continued at the brush border?

A

Brush border integral membrane proteins attached to villi called peptidases cleave dipeptides and tripeptides into single amin oacids

26
Q

How are amino acids absorbed into the enterocyte

A

Similar to glucose:

Secondary active transport (driven by basolateral Na/K ATPase)

Sodium lined co-transport.
There are different co-transporters for neutra, acidic and basic amino acids

Short peptides ( 2 or 3 linked aa’s) are also absorbed by an H linked transport system

27
Q

What happens to the short peptides once absorbed into the enterocyte

A

Broken down into single amino acids inside the enterocyte

28
Q

How are amino acids transported into portal circulation

A

facilitated diffusion through the basolateral membrane

Water absorbed as amino acids are osmotically active

29
Q

What is a triglyceride

A

Glycerol backbone with three fatty acid residues attached

30
Q

What other forms of dietary lipid are there

A

Triglycerides
Cholesterol
Fat-soluble vitamins
Phospholipid

31
Q

What is emulsification. Where does it occur, How does it occur, why does it occur

A

Lipids are insoluble in water.
Form large droplets in the aqueous environment of the GIT.
Bile acids (secreted by the liver, stored and then released from the gall bladder) coat lipid droplets dividing them into multiple smaller droplets so increasing the surface area for digestive enzymes to work.

32
Q

What is the name of the enzyme breaks down triglycerides. Describe this process

A

Pancreatic lipase covers the outer surface of the smaller lipid droplets and acts on TG molecules resulting in the formation of two free fatty acids and a 2 - monoglyceride.

33
Q

What is a Micelle

A

Micelle formation

The ffa’s and 2-monglycerides released from TG combine with BILE SALTS forming micelles containing small balls of mixed lipids and bile salts

34
Q

What happens when a micelle makes contact with an enterocyte

A

The lipid contained within is absorbed by simple diffusion.

the bile salts remain in the gut lumen until the terminal ileum when they are reabsorbed and returned to the liver - recycled.

35
Q

What is a chylomicron

A

Monoglycerides and fatty acids travel to the smooth endoplasmic reticulum in the cytoplasm of enterocytes where they are recombined to form a TG. The TG is packaged with CHOL and phospholipid and a cellular label called APOLIPOPROTEIN to form lipid balls called chylomicrons.

36
Q

What happens to chylomicrons once formed in the enterocytes

A

Released from enterocytes into lacteals (the lymphatic capillaries that service each villus).

Chylomicrons then flow through the lymphatic system until they are released into systemic circulation at the thoracic duct.

37
Q

What is Orlistat

A

Orlistat is a pancreatic lipase inhibitor. Prevents breakdown of TGs and hence prevents TG absorption. TG remains undigested and unabsorbed in the GIT resulting in Steatorrhoea

Pancreatic insufficiency also presents with steatorrhoea

38
Q

Describe the cells, and % cell mass, of the endocrine pancreas

A

The cells with endocrine function are call the ISLETS OF LANGERHANS
- Make up 1 - 2 % of pancreatic cell mass

alpha cells - glucagon
beta cells - Insulin
delta cells - somatostatin
PP cells - pancreatic polypeptide

39
Q

What volume of pancreatic juice produced per day

A

1.5 L which drains into the duodenum via the pancreatic duct

40
Q

Describe the main cell types of the exocrine pancreas

A

Acinar cells = produce digestive enzymes

Ductal cells = secrete HCO3- and water

41
Q

What is the difference between exocrine and endocrine

A

Exocrine - secretes substances via a ductal system to an epithelial surface

Endocrine - secretes substances directly into the blood stream

42
Q

What proenzymes and enzymes do acinar cells produce

A
  1. Protein: Trypsinogen and chymotrypsinogen
  2. CHO: Pancreatic amylase
  3. Fat: Pancreatic lipase
43
Q

How are trypsinogen and chymotrypsinogen activated

A

After secretion into the duodenal lumen, enterokinase (mucosa of small intestine) cleaves trypsinogen into trypsin, a powerful peptidase.

Trypsin then cleaves both trypsinogen and chymotrypsinogen, resulting in chymotrypsin and more trypsin

Trypsin –> more trypsin = autocatalysis

44
Q

What is autocatalysis

A

The process where by trypsin results in further formation of trypsin by catalysis of trypsinogen.

45
Q

What is the role of trypsin in acute pancreatitis

A

In acute pancreatitis there is inappropriate activation of proenzymes within the pancreas.

Trypsin activates more trypsin (autocatalysis)

Trypsin also activates:
1. Phospholipase A2 –> breaks down pancreatic cell membrane phospholipids –> necrosis

  1. Elastase –> digests blood vessel walls –> haemorrhage

Massive release of inflammatory mediators TNF alpha and IL -1 into systemic circulation –> SIRS.

  1. Pancreatic lipase is releasedinto the interstitium where it digests retroperitoneal fat –> retroperitoneal haemorrhagic necrosis –> Grey-Turner’s sign (discoloration flanks) and Cullen’s sign (Periumbilical discoloration
46
Q

What is Grey-Turner sign

What is Cullen’s sign

A

Indicate severe pancreatitis
Result from release of pancreatic lipase into instersitium –> haemorrhagic necrosis of fat

Grey-Turner’s sign: discolouration of flanks
Cullen’s sign: Periumbilical discolouration

47
Q

What do the ductal cells of the pancreas secrete and why

A

HCO3- and water

HCO3- is to neutralize the acidic pH from the stomach which would denature the pancreatic enzymes rendering them unable to digest their respective food groups.

48
Q

Describe the process of HCO3- formation and secretion in the pancreatic ductal cells

A
  1. CO2 diffuses in
  2. CO2 + H2O –> H2CO3 –> H+ + HCO3- (Carbonic anhydrase)
  3. H+ exchanged for Na+ (H+/Na+ exchanger - basolateral). Gradient for Na+ provided by Na+/K+ ATPase
  4. HCO3- into pancreatic duct lumen in exchange for Cl-. Cl- then returns to pancreatic duct lumen via CFTR

CFTR = Cystic Fibrosis Transmembrane conductance Regulator

This is defective in cystic fibrosis

HCO3- is osmotically active so water moves with HCO3-

49
Q

How is pancreatic secretion controlled

A

Neural and Humoral

Neural
1. VAGUS
Meal anticipation –> Vagus –>increase acinar cell activity

Humoral
1. GASTRIN
Gastric distension –> Gastrin (G cells) –> stimulates pancreatic acinar cells to secrete digestive enzymes (feed-forward control system)

  1. CHOLECYSTOKININ (CCK)
    Chyme in duodenum –> CCK secretion (Mucosa)
    a) Increase bile production in liver
    b) stimulate contraction gall bladder
    c) Slow gastric emptying
    d) Stimulate pancreatic acinar cells to secrete digestive enzymes
  2. SECRETIN
    Chyme in duodenum –> secretin secretion (Mucosa)
    a) Slow gastric emptying
    b) Stimulate ductal cells of pancreas to secrete HCO3- + Water
50
Q

What are the functions of Cholecystokinin

A

a) Increase bile production in liver
b) stimulate contraction gall bladder
c) Slow gastric emptying
d) Stimulate pancreatic acinar cells to secrete digestive enzymes

51
Q

What are the functions of secretin

A

a) Slow gastric emptying

b) Stimulate ductal cells of pancreas to secrete HCO3- + Water

52
Q

How does intestinal motility differ between the fed and the fasted states

A

Fed
1. Segmental contractions x 2 compartmentalises followed by continuous longitudinal contraction-relaxation for mixing/contact

  1. Propulsive contractions: Co-ordinated circular then longitudinal contraction-relaxation

Fasted

  1. Infrequent, regular contractions of the small intestine
    - Every 90 minutes there is a period of intense co-ordinated intestinal contraction spreading from the duodenum to the ileocaecal valve = Migrating Motor Complex
53
Q

What is the Migrating Motor Complex

A

Infrequent, regular contractions of the small intestine in the fasted state.
- Every 90 minutes there is a period of intense co-ordinated intestinal contraction spreading from the duodenum to the ileocaecal valve = Migrating Motor Complex

54
Q

What is the resting membrane potential of smooth muscle cells of the small intestine and when does contraction of smooth muscle occur

A

-40 to -70 mV

When membrane potential exceeds threshold potential –> opening of voltage gated sodium and calcium channels –> sudden influx Na and Ca –> depolarizes cell membrane and causes contraction

55
Q

What are slow waves and describe the process of depolarization in the smooth muscle of the small intestine

A

This is a pattern of fluctuation of the membrane potential of the smooth muscle membrane of the small intestine.

The fluctuations are not enough to exceed threshold –> Instead they help to CO-ORDINATE depolarizations and contractions of the small intestine

Food bolus –> release of ntmtrs –> small depolarization + at the time of next ‘slow wave’ –> threshold will be exceeded –>spike potential –>smooth muscle contraction

56
Q

Describe the neural control of intestinal motility

A

NEURAL
Enteric nervous system - extensive network of afferent and efferent neurons converging on two types of ganglion:
- Myenteric (Auerbach’s) plexus
- Submucosal (Meissner’s) plexus

Semi-autonomous with input from ANS

  • SNS: Reduced GIT motility / secretions /blood flow
  • PSNS (Vagus): Increase motility / secretion / blood flow
57
Q

Describe the humoral control of intestinal motility

A

CCK + Secretin –> slow gastric emptying

Motilin - released from duodenal mucosa every 90 minutes –> Migrating Motor Complex.

Vasoactive intestinal peptide (VIP) - Increase GIT secretion of water an electrolytes

58
Q

Which drug is a motilin agonist

A

Erythromycin

Physiology for Anaesthetists (61 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions