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Gastro > intestinal > Flashcards

intestinal Flashcards

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

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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

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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)

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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

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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

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6
Q

when does lactase action drop usually?

A

5-7yo

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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
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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

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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
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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
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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

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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

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13
Q

stool fat globules vs crystals - what does it mean?

A

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

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14
Q

length of bowel at birth vs adult

A

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

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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

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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

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17
Q

prox jej is responsbile for what absorption

A

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

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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
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19
Q

pattern of age distribution of IBD

A

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

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20
Q

paeds: which more common - UC vs CD

A

CD higher incidence

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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

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22
Q

does UC or CD have more genetic infuence

A
  • CD more genetic influence
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23
Q

first IBD gene identified

A

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

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24
Q

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

A
  • both parents: >35%
  • single sibling: CD 30%, UC 10%
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25
Q

genetic disorders associated with IBD (3)

A

turners
GSD
Immunodeficiency

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26
Q

what must we always think about that can mimic ileitis

A

abdominal TB - esp Asian/African origin

27
Q

ASCA vs pANCA association in IBD

A

ASCA - CD
pANCA - UC

28
Q

most common EIM of IBD? most common skin EIM?

A
  • most common: arthritis (30%)
  • skin: erythema nodosum
29
Q

EIM of IBD: mnemonic

A

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
Q

EIM that correlate with disease activity, and those that don’t

A

Correlate with disease activity:
- peripheral arthritis
- erythema nodosum
- anaemia

Don’t correlate:
- PSC
- pyoderma gangrenosum
- hepatitis
- ank spond

31
Q

more common EIM with CD vs UC

A

CD: aphthous ulcers, fevers, erythema nodosum, gall/renal stones, OROFACIAL CD, peripheral arthritis
UC (4): pyoderma gang, sclerosing cholangitis, ank spond, hepatitis

32
Q

compare UC vs CD features

A

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
Q

pathogenesis of growth failure in IBD (esp CD)

A
  1. malabsorption
  2. inc losses
  3. steroids
  4. inflammation
34
Q

what increases risk of malignancy in IBD

A

time of disease
length of colon
presence of sclerosing cholangitis
FHx of CRC

35
Q

what is stool calprotectin?

A

leukocyte derived protein

36
Q

calpro:
- sensitivity and specificity
- when not to use it

A
  • sensitivity = 96%
  • specificity = 87%
  • don’t use: <4yo, likely infection, nsaids/ppi
37
Q

classic presentation diarrhoea / abdo pain / wt loss - more common UC or CD?

A

UC. only 20% present with this in UC

38
Q

most common part of GIT for CD involvement

A

ileocolonic 50%

39
Q

most common presenting complaint of CD

A

growth failure - can precede other symptoms by 1-2 years, and much more common in CD

40
Q

conditions a/w coeliac

A

• first-degree relatives with CD
• autoimmune conditions: T1DM, thyroid disease, liver disease
• Down syndrome
• Turner syndrome
• Williams-Beuren syndrome
• IgA deficiency

41
Q

Rx for crohn’s disease

A

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
Q

describe role of allopurinol in thiopurines

A
  • 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
Q

side effects of thiopurines

A

dose dependent
- bone marrow suppression
- hepatotoxicity

dose independent
- nausea
- pancreatitis
- infection: HSV, HPV
- malignancy: HSTCL, lymphoma, melanoma, EBV associated lymphoma

44
Q

risks of biologics

A
  1. HSTCL (esp with AZA)
  2. TB - screen with CXR + QFN
  3. cytopaenia
  4. lupus
45
Q

when is screening indicated for CRC in Crohn’s / UC?

A

Crohn’s: after 10 years of colonic disease, needing regularly colonoscopies

UC: after 8-10yrs of disease duration

46
Q

xray findings of UC

A

may show loss of haustral markings in an air filled colon or marked dilatation in toxic megacolon (in an adult diameter > 6cm)

47
Q

Rx for UC

A

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
Q

long term prognosis for UC better if …

A

… if achieve clinical remission (PUCAI <10) within first 3 months

49
Q

what concommitant condition with IBD increases risk of CRCdramatically?

A

PSC: so annual or bi-annual surveillance colonoscopy should be initiated from the time of PSC diagnosis

50
Q

what cancer does PSC inc risk of?

A

cholangiocarcinoma - Serial CA19.9 and liver ultrasound/MRCP testing may thus be considered every 1 to 2 years

51
Q

what is pyoderma gangrenosum?

A

neutrophilic dermatosis - not infectious/gangrenous!

52
Q

diagnostic criteria of TMC

A

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
Q

tpmt genotypes

A

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
Q

compare osmotic vs secretory diarrhoea:
- pathogenesis
- response to fasting
- volume
- Na
- osmotic gap
- reducing substances
- pH

A

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
Q

causes of osmotic vs secretory diarrhoea

A

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
Q

describe how intestinal secretion of Na and water is mediated by chloride

A
  • Cl enters crypt cell with Na/K/Cl transporter
  • Cl&raquo_space;> activation of cAMP
  • cAMP activates CFTR > Cl secreted into lumen
  • Cl accumulates in lumen > negative electric potential > Na pulled into lumen>water
57
Q

how does vibrio cholerae cause diarrhoea

A
  • 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
Q

how does ORS work?

A

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
Q

how quick should Na fall during hyperNa corrections

A

no quicker than 0.5mmol/hr

60
Q

EIM of enteric infections, and which bugs cause them

A

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
Q

DDx infant/toddler PRbleeding

A

Anal fissure
Food protein induced colitis
Intussusception
Meckel’s diverticulum
Lymph nodular hyperplasia
GI duplication cyst
Infantile and VEO IBD

62
Q

DDx older children PR bleeding

A

Infectious colitis
HUS
IgA vasculitis (HSP)
Juvenile polyps
Anal fissure
Infectious colitis /IBD
Meckel’s Diverticulum

63
Q

DDx PR bleeding by aetiology

A

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)

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