Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Gastro > intestinal > Flashcards

intestinal Flashcards

(63 cards)

Start Studying
1
Q

two features of ileum histology not seen in duodenum/jejunum

A

1) peyer’s patches - lymphoid tissue in lamina propria
2) lacteals - white core of villi that house lymphatic system

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

four hormones found in duodenum in intestinal phase of digestion, and their jobs

A

1) Secretin: inc NaHCO3 from pancreas + bile from liver
2) CCK: inc pancreas enzymes + bile from GB, slows gastric emptying
3) GIP: main role to inc insulin
4) motilin: moves things along

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

what are tinea coli and haustra?

A

a. Tinea coli – muscularis externa concentrated in three thickened strips
b. Tinea coli contract to form haustra (non-permanent infoldings of mucosa and submucosa)

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

examples of: mono, di and polysaccharides

A

1) mono: fructose, galactose, glucose
2) di:
- Sucrose = glucose + fructose
- Lactose = glucose + galactose
- Maltose = glucose + glucose
3) poly: glycogen

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

breakdown of carbohydrates: explain process

A

1) mouth: salivary amylase
2) CCK -> pancreatic alpha amylase
- amylases can only break from poly to di (1,4 links only)
3) intestinal brush border:
a - Glucoamylase + dextrinase = maltose
b - Sucrase-isomaltase
i) Sucrose  glucose + fructose
ii) Maltose  glucose + glucose
c- Lactase

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

when does lactase action drop usually?

A

5-7yo

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

how are monosaccharides absorbed in the SI?

A
  • Glucose + galactose – Na+ dependent glucose transporter (SGLT1) [basis of ORS]
  • Fructose – facilitated diffusion via GLUT5
  • All monosaccharides are transported across basal border by GLUT 2 transport
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

breakdown of protein in digestion: explain the process

A

1) chief cells > pepsinogen > (gastric acid)//pepsin
2) AA in duo/jej > CCK > panc zymogens
3) enterokinase in epithelium activates trypsinogen -> trypsin, which autocatalyses and actives other zymogens
4) panc peptidases at brush border: oligopeptides into tri, di and single AAs

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

types of pancreatic peptidases

A
  1. Endopeptidases = trypsin, chymotrypsin, elastase
    a. Act at interior peptide bonds
  2. Exopeptidases = pancreatic carboxypeptidases
    a. Act on terminal amino acids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

how efficient is fat absorption, and how much exocrine function do we need for normal fat absorption?

A
  • Fat absorption >95% efficient (85% in infants)
  • 2-3% exocrine function allows normal fat absorption
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

breakdown of fats: explain the process

A

1) lingual lipase + gastric lipase&raquo_space; (TG)&raquo_space; glycerol+FA
3) CCK > panc enzymes (panc lipase, chol ester hydrolase + phospholipase A2) + bile salts
4) colipase binds to panc lipase to prevent bile salts from acting
left with: glycerol, FA, monoglycerides, cholesterol
5) micelle formation by bile acids

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

absoprtion of fats: explain the process

A

1) micelle transports lipids to apical membrane
2) then can dissolve, and TG+MGs enter
3) then:
SCFA (FA <12 C) direct to portal system (ie. MCT)
FA >12 C re-esterified to TG > chylomicrons > lacteals > lymphatic system

i.e. no active transport required

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

stool fat globules vs crystals - what does it mean?

A

Fat globules = maldigestion eg. pancreatic insufficiency, cholestatic liver disease
Fat crystals = malabsorption

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

length of bowel at birth vs adult

A

At birth length of the bowel = 200-250cm
Adulthood = 300-800cm

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

bowel resection in infant: how little does one need to be able to survive and wean off TPN?

A

15cm with IC valve, or 20cm without

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

in short gut - what is the worst part of the SI to lose? What happens when you lose that bit?

A

Ileum - jej can’t compensate for it:
- no distal ileum = no bile salts / b12
- net Na+H2O absorption ++ in ileum -> malabsorption

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

prox jej is responsbile for what absorption

A

first 100-200cm responsible for CHO, protein, iron and water soluble absorption

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

5 causes of short gut - most to least common

A
  1. NEC
  2. mec ileus
  3. abdo wall defect e.g. gastroschisis
  4. intestinal atresia
  5. volvulus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

pattern of age distribution of IBD

A

bimodal - 10-20yo (20% all cases for both UC and CD <18yo), then 50-80yo

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

paeds: which more common - UC vs CD

A

CD higher incidence

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

4 factors involved in IBD pathogenesis

A

i. Genetic susceptibility
ii. Environmental triggers
iii. Changes in gut microbiota and dysbiosis (defining event); shift from symbiote microbes (friendly) to pathobiome microbes (harmful)
iv. Immune response

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

does UC or CD have more genetic infuence

A
  • CD more genetic influence
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

first IBD gene identified

A

NOD2 (CARD15); but up to 70% CD don’t have it

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

inheritance of IBD:
- risk if both parents affected
- risk with affected sibling

A
  • both parents: >35%
  • single sibling: CD 30%, UC 10%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
genetic disorders associated with IBD (3)
turners GSD Immunodeficiency
26
what must we always think about that can mimic ileitis
abdominal TB - esp Asian/African origin
27
ASCA vs pANCA association in IBD
ASCA - CD pANCA - UC
28
most common EIM of IBD? most common skin EIM?
- most common: arthritis (30%) - skin: erythema nodosum
29
EIM of IBD: mnemonic
A PIE SAC: Arthritis, Ankylosing spondylitis, anaemia Pyoderma gangrenosum/vegetans ,Perianal skin tags, Psoriasis, Pleuritis, Pericarditis, Pancreatitis I for eye signs: Iritis, uveitis, episcleritis, conjunctivitis Erythema nodosum Sclerosing cholangitis, Sacroilitis Aphthous ulcers Clubbing of fingers, Cholelithiasis, renal Calculi
30
EIM that correlate with disease activity, and those that don't
Correlate with disease activity: - peripheral arthritis - erythema nodosum - anaemia Don't correlate: - PSC - pyoderma gangrenosum - hepatitis - ank spond
31
more common EIM with CD vs UC
CD: aphthous ulcers, fevers, erythema nodosum, gall/renal stones, OROFACIAL CD, peripheral arthritis UC (4): pyoderma gang, sclerosing cholangitis, ank spond, hepatitis
32
compare UC vs CD features
UC: • rectum always, limited to colon. continuous • No granulomas, skip lesions • Mucosal inflammation • Cx: TMG (abscess/structure rare) • no recurrence post-colectomy CD: • Any part of GIT, Discontinuous • Non-caseating granulomas, skip lesions, cobblestoning • Transmural inflammation • Cx: strictures, fistulae, perf, abscess • Perianal disease more common • cramping, watery diarrhoea / steatorrhoea • can recur post-colectomy
33
pathogenesis of growth failure in IBD (esp CD)
1. malabsorption 2. inc losses 3. steroids 4. inflammation
34
what increases risk of malignancy in IBD
time of disease length of colon presence of sclerosing cholangitis FHx of CRC
35
what is stool calprotectin?
leukocyte derived protein
36
calpro: - sensitivity and specificity - when not to use it
- sensitivity = 96% - specificity = 87% - don't use: <4yo, likely infection, nsaids/ppi
37
classic presentation diarrhoea / abdo pain / wt loss - more common UC or CD?
UC. only 20% present with this in UC
38
most common part of GIT for CD involvement
ileocolonic 50%
39
most common presenting complaint of CD
growth failure - can precede other symptoms by 1-2 years, and much more common in CD
40
conditions a/w coeliac
• first-degree relatives with CD • autoimmune conditions: T1DM, thyroid disease, liver disease • Down syndrome • Turner syndrome • Williams-Beuren syndrome • IgA deficiency
41
Rx for crohn's disease
Induction 1st line - complete EEN 2nd line - steroids Maintenance - mild: 5-aminosalicylates (mesalazine) - mod/severe: Immunomodulators 1) thiopurines (aza / 6-MP) - effect 3-4 months 2) MTX (+folic acid) - effect 6-8 weeks Biologics: - infliximab / adalimumab - vedo / usteikinumab
42
describe role of allopurinol in thiopurines
- AZA -> 6MP 1) ---(TMPT)-> 6MMP - hepatotoxic 2) --- (hPMT) -> TGN 3) ---(xanthine oxidase) -> byproduct -ppl with higher TMPT activity make lots of 6-MMP - so allopurinol will shunt active 6-MP towards making more TGN
43
side effects of thiopurines
dose dependent - bone marrow suppression - hepatotoxicity dose independent - nausea - pancreatitis - infection: HSV, HPV - malignancy: HSTCL, lymphoma, melanoma, EBV associated lymphoma
44
risks of biologics
1. HSTCL (esp with AZA) 2. TB - screen with CXR + QFN 3. cytopaenia 4. lupus
45
when is screening indicated for CRC in Crohn's / UC?
Crohn's: after 10 years of colonic disease, needing regularly colonoscopies UC: after 8-10yrs of disease duration
46
xray findings of UC
may show loss of haustral markings in an air filled colon or marked dilatation in toxic megacolon (in an adult diameter > 6cm)
47
Rx for UC
Induction: 1. 5-aminosalicylates (mesalazine / sulfasalazine) 2. steroids Maintenance: mild - 5-aminosalicylates (oral, rectal combo better than just oral) mod - thiopurines, biologics Salvage: biologics, cyclosporin, tacro *probiotics - adjuvant to 5-asa *curcumin!
48
long term prognosis for UC better if ...
... if achieve clinical remission (PUCAI <10) within first 3 months
49
what concommitant condition with IBD increases risk of CRCdramatically?
PSC: so annual or bi-annual surveillance colonoscopy should be initiated from the time of PSC diagnosis
50
what cancer does PSC inc risk of?
cholangiocarcinoma - Serial CA19.9 and liver ultrasound/MRCP testing may thus be considered every 1 to 2 years
51
what is pyoderma gangrenosum?
neutrophilic dermatosis - not infectious/gangrenous!
52
diagnostic criteria of TMC
1) radiological evidence of colonic distension - right colon > 6cm, absence of haustral markings 2) + at least 3 of: fever, HR >120, neutrophilic leukocytosis, anaemia 3) + at least one of: dehydration, altered GCS, electrolyte disturbances, hypotension
53
tpmt genotypes
90% homozygous for wild type TPMT = rapid metabolism of thiopurines, higher doses for clinical effect 10% heterozygous for wild type TMPT = metabolise slowly and respond to much lower doses 0.3% can't metabolise
54
compare osmotic vs secretory diarrhoea: - pathogenesis - response to fasting - volume - Na - osmotic gap - reducing substances - pH
osmotic: - non-absorbed nutrients pulling water out - Response to fasting (as no more sugar) - <200 ml/ay - Na <70 meq/L - High >100; > (Na + K) x 2 - reducing substances present and pH <5 secretory: - secreted ions pulling water out - no response to fasting - >200 ml/day - Na >70 meq/L - Low <50 osmotic gap; = (Na + K) x 2 - Absent reducing substances, pH >6
55
causes of osmotic vs secretory diarrhoea
Osmotic: - laxatives - mucosal injury - infective (eg. post-rotavirus), inflammation (IBD), immune mediated (celiac), vascular - sugar transport defects Secretory: - congenital ion transport defects e.g. chloridorrhoea - secretagogues - bile acid malabsorption - turn on cAMP - tumours e.g. producing VIP - fast transit
56
describe how intestinal secretion of Na and water is mediated by chloride
- Cl enters crypt cell with Na/K/Cl transporter - Cl >>> activation of cAMP - cAMP activates CFTR > Cl secreted into lumen - Cl accumulates in lumen > negative electric potential > Na pulled into lumen>water
57
how does vibrio cholerae cause diarrhoea
- have flagella, swim to attach to enterocyte, produce cholera toxins - toxin B unit binds > enter the cell via endocytosis - toxin A unit activates G protein > activates AC > inc cAMP - high cAMP > CFTR > Cl secretion
58
how does ORS work?
Has salts, glucose and starch Na/glucose co-transporter remains even in terrible infections -> brings water in more effectively Starch that fermentable is added -> SCFA -> Na+fluid absorption
59
how quick should Na fall during hyperNa corrections
no quicker than 0.5mmol/hr
60
EIM of enteric infections, and which bugs cause them
1) Focal infections from systemic spread (all) 2) Reactive arthritis - Salmonella, Shigella, Yersinia, Campylobacter, Cryptosporidium, C difficile - 1-3 weeks after infection 3) Guillain-Barre - campylobacter; few weeks after 4) Glomerulonephritis - Shigella, Campylobacter, Yersinia 5) IgA nephropathy - campylobacter 6) Erythema nodosum - Yersinia, Campylobacter, Salmonella 7) HUS - Shigella dysenteriae 1,EHEC O157:h7 8) Haemolytic anaemia -camp,yersinia
61
DDx infant/toddler PRbleeding
Anal fissure Food protein induced colitis Intussusception Meckel’s diverticulum Lymph nodular hyperplasia GI duplication cyst Infantile and VEO IBD
62
DDx older children PR bleeding
Infectious colitis HUS IgA vasculitis (HSP) Juvenile polyps Anal fissure Infectious colitis /IBD Meckel's Diverticulum
63
DDx PR bleeding by aetiology
Vascular - AVM, HSP, HUS, coagulopathy Inflam/infectious - infection, allergic colitis, IBD, NEC Neoplastic - rare D - not really Iatrogenic - c.diff Congenital - hirschprung, Anatomic - meckel's, fissures, malrotation, intuss,haemorrhoids,polyps, duplication cyst Trauma Endocrine - not really

Gastro (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions