Brainscape's Knowledge GenomeTM

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


See full index

Semester 3 > GI Session 8 > Flashcards

GI Session 8 Flashcards

1
Q

How is the large SA needed for absorption in the intestines achieved?

A

Mucosa permanent folded in pliae circulares

Enterocytes have microvilli –> brush border

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

Say does the intestinal epithelia consist of?

A

Enterocytes
Goblet cells
Intestinal glands/crypts between villi

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

What cells are present in the intestinal crypts?

A 
Intestinal stem cells
Paneth cells
Transit amplifying cells
Goblet cells
Enteroendocrine cells
Enterocytes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the function of Paneth cells?

A

Part of innate immune system which possess antivirals and antimicrobials in eosinophilic granules

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

What happens to cells in the intestinal crypts?

A

Start from bottom of crypt and migrate and matured urging transit becoming more differentiated as they reach the surface

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

What happens to cells when they reach the top of the intestinal crypts?

A

Undergo anoikis - programmed cell death due to loss of contact with cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Why does the intestinal mucosa have a high turnover of cells?

A

Sloughed off into faeces and replaced every 3-6 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the function of cells on the villi in the intestines?

A

V. actively secrete enzymes into the brush border to break down carbohydrates and proteins in order to complete digestion

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

Describe the stages of carbohydrate digestion.

A

Starch broken down by alpha-amylase (saliva) and amylase (pancreas) –> glucose, maltose and alpha dextrins –> brush border enzymes –> monosaccharides–> enterocyte absorption

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

What form do carbohydrates have to be in to be absorbed by the gut?

A

Monosaccharides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Why is alpha-amylase short acting?

A

Due to stomach acid

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

What binds do amylase act in in carbohydrate digestion?

A

Alpha 1-4

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

Why does amylase action on amylopectin result in?

A

Alpha dextrins

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

What brush border enzymes are found in the intestines?

A 
Isomaltase: alpha 1-6
Maltase
Alpha dextrinase
Sucrase: sucrose--> glucose and fructose
Lactase: lactose--> glucose and galactose
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the role of the intestines?

A

Absorb nutrient, water and electrolytes from conditioned chyme
Barrier to pathogen entry for innate immune defence

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

How are monosaccharides absorbed?

A

Na+/K+-ATPase on basolateral membrane maintains low intracellular sodium –> SGLT1 binds sodium which allows glucose binding and both move into cell –> GLUT-2 transports glucose down gradient into capillary –> GLUT-5 allows facilitated diffusion of fructose

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

Why does a mixture of glucose and salt stimulate maximum water uptake?

A

Monosaccharide absorption involves sodium uptake so water will follow

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

What form must proteins be in to be absorbed?

A

A.a.
Dipeptide
Tripeptide

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

How is protein digestion carried out by the stomach?

A

Chief cell releases pepsinogen –> HCl converts it to pepsin –> pepsin on proteins –> dipeptides and a.a. absorbed by small intestine

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

How does the pancreas function in protein digestion?

A

Trypsinogen converted by enteropeptidase –> trypsin –> activates other proteases from zymogens –> chymotrypisn and elastase hydrolyse interior peptide bonds, exopeptidases caboxypeptidase A+B hydrolyse from C terminal end

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

What breaks down oligopeptides further so they can be absorbed?

A

Brush border enzymes

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

How are a.a. transported into cells during absorption?

A

Via neutral/acidic/basic/imino Na+-acid cotransporters using active and passive mechanisms

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

How are dipeptides and tripeptides absorbed?

A

Moved into cells by H+ cotransporter and converted by cytolsolic peptidases –> a.a.

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

What happens in the process of isosmotic fluid uptake in the intestines?

A

Sodium AT out across basolateral membrane –> sodium diffuses into epithelial cells and paracellular electrolyte movement–> osmotic gradient due to all absorption –> water move in

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How do the sodium transporters found in the small and large intestine differ?

A

Small: Na+ cotransporters on apical membrane which absorbed more sodium
Large: sodium channels induced by aldosterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How is calcium absorbed by active transcellular mechanisms in the gut?

A

Ca2+ATPase removes calcium across BLM –> gradient allows facilitated diffusion of calcium by binding to calbindin

27
Q

What is needed for calbindin to function?

A

Vitamin D

28
Q

In which parts of the gut do active transcellular and passive paracellular absorption of calcium occur?

A

Active in proximal

Passive in distal

29
Q

How is iron mainly absorbed in the GI tract?

A

In haem/Fe2+ absorbed across apical membrane –> binds to apoferritin –> across BLM –> binds to transferrin in circulation

30
Q

What determines levels of iron absorption from the GI tract?

A

Levels of transferrin in blood

31
Q

How are vitamins absorbed in the GI tract?

A

Water soluble by sodium cotransport e.g. Vit C and B

B12 in terminal ileum bound to intrinsic factor

32
Q

What are the three mechanisms of small intestine motility?

A

Intestinal gradient
Segmentation
Peristalsis

33
Q

What is intestinal gradient in small intestine motility?

A

Between meals intestinal pacemakers have a higher frequency proximally which drives slow caudal progression of contents

34
Q

What is segmentation in small intestine motility?

A

Following a meal contraction proximally then distally move contents back and forth so contents is mixed and absorption time is increased

35
Q

What is segmentation in large intestine motility?

A

In proximal colon contraction of haustra causes agitation and mixing of contents so most of the remaining water can be removed from faeces

36
Q

What is mass movement?

A

Coordinated contraction 1-3x daily which moves contents rapidly from transverse colon to rectum, often triggered by eating

37
Q

What is the gastro-colic reflex?

A

Trigger of mass movement caused by eating

38
Q

What happens in the process of defecation?

A

Rectum normally empty –> fills to 25% –> urge to defecate –> PNS relaxes internal sphincter, somatic NS relaxes external sphincter, intra-abdominal pressure increases –> expulsion of faeces

39
Q

What is IBD?

A

Group of conditions characterised by idiopathic inflammation of the GI tract

40
Q

What diseases are included in the term IBD?

A 
Crohn's
Ulcerative colitis
Diversion colitis
Pouchitis
Microscopic colitis
41
Q

What is microscopic colitis?

A

No visible disease process but inflammatory cells are present in the mucosa

42
Q

What extra-bowel symptoms are commonly experienced in IBD?

A

Arthropathy
Erythema nodosum/pyoderma gangrenosum/psoriasis
Primary sclerosing cholangitis
Scleritis or episcleritis

43
Q

What extra-bowel symptom is commonly linked with ulcerative colitis?

A

Primary sclerosing cholangitis due to fibrosis of bile duct

44
Q

What can trigger IBD?

A

Abx
Infections
Smoking
Diet

45
Q

How do the impacts of smoking differ in Crohn’s and UC?

A

Increases risk of Crohn’s

Impromptus UC symptoms

46
Q

What is the gross pathology of Crohn’s disease?

A 
Hyperaemia --> erythema
Mucosal oedema
Discrete superficial ulcers
Deeper ulcers
Transmural inflammation --> thickening of bowel wall
Cobblestone mucosa
Fistulas
47
Q

What is the gross pathology of UC?

A 
Chronic inflammatory infiltrate of LP
Crypt abscesses due to inflammatory cells in crypt and surrounding oedema
Decreased goblet cells
Pseudopolyps
Loss of haustra
48
Q

What are pseudopolyps?

A

Oedematous healthy mucosa

49
Q

What causes cobblestone mucosa in Crohn’s disease?

A

Ulcers/oedematous tissue pushing through

50
Q

What is the microscopic pathology of Crohn’s?

A

Epithelioid granulomas are pathognomonic but not present in all cases

51
Q

What is seen on investigation of Crohn’s?

A

Bloods: macrocytic anaemia due to B12 deficiency
CT/MRI: bowel wall thickening, obstruction, extramural problems
Barium enema: strictures, fistulae, string sign
Colonoscopy: cobblestone mucosa, ulcer formation

52
Q

What is the limit of colonoscopy?

A

Terminal ileum

53
Q

What is seen on investigation of UC?

A

Bloods: iron deficiency aneamia, ANCA
Stool cultures: no infection
AXR/CT/MRI: not useful as only mucosal involvement
Colonoscopy: ulceration connected between patches

54
Q

What does detection of ANCA in UC suggest?

A

Autoimmune disease

55
Q

What is indeterminate colitis?

A

IBD pts with features of Crohn’s and UC but no defining features on investigation

56
Q

What are the distinguishing characteristics of Crohn’s disease?

A 
No rectal involvement but anywhere in GI tract
Gross bleeding in 25%
Perianal disease in 75%
Fistulae
Malnutrition
Transmural inflammation
Granulomas >75%
Fibrosis common but crypt abscesses rare
Skip lesions
Aphthous and linear ulcers
Contact bleeding rare
Cobblestone appearance
57
Q

What are the distinguishing characteristics of UC?

A 
Rectum almost always involved +/- colon
Gross bleeding common
Perianal disease rare
No fistula or malnutrition
Transmural inflammation rare
No granulomas or fibrosis but crypt abscesses seen
Continuous mucosal involvement
Linear and apthous ulcers rare
Friable mucosa
No cobblestone appearance
58
Q

What are the main classes of Tx option for IBD?

A

Lifestyle changes
Medical Tx
Surgical Tx

59
Q

What medical Tx can be used in IBD?

A
  1. Aminosalicylates for flares and remission
  2. Corticosteroids for flares only due to steroid S/E
  3. Immunomodulators for active disease or remissive pts who don’t tolerate aminosalicylates
60
Q

Why are Abx with anti-inflammatory effects not used to Tx IBD?

A

Lack of infective cause

61
Q

When is surgery used in Crohn’s?

A

Repair of strictures of fistulae

Remove small section of bowel in v. active disease

62
Q

Why is surgery avoided in Crohn’s?

A

Reduce risk of short bowel disorder

Reduce risk of painful adhesions for repeated surgery

63
Q

When is surgery used in UC?

A

Curative via colectomy for unsettling inflammation, precancerous change and toxic megacolon

64
Q

What is toxic megacolon?

A

Acute and rapid distension to point of perforation, a systemic condition

Semester 3 (50 decks)

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