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BPT exams > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

Which gene and chromosome is associated with Wilson’s disease?

A

13q14.3 chromosome
ATP7B gene
Autosomal recessive

Carrier 1:90

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2
Q

How do Wilson’s Disease present?

A

Liver disease, coombs negative Haemolysis, tubular nephropathy, Kayser Flescher rings, Neuropsychiatric disorder

Presents typically 5 and above (need accumulation of copper for damage)

Most asymptomatic family screening

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3
Q

How do you diagnose Wilson’s disease?

A

Serum (liver) copper, Ceuroplasmin (copper carrying protein) - the lab measures the free amount of Ceuroplasm (thus, low Caeroplasmin and high copper means Wilsons), measure baseline 24 hours urinary copper excretion (and then give Pencillamine and if significant elevation -> Wilson’s disease)

ATP7 is the enzyme that attaches copper to caeroplasmin, and thus when the body isn’t able to do this , you have low levels of caeruplasmin

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4
Q

How do you treat Wilson’s disease?

A

D- Penicillamine as first line

2nd line is Trientine

(lifelong)

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5
Q

How does Bacillus Cereus infection present - in A) vomitting and B) diarrheal type?

A

Vomitting - undercoocked rice, and vomiting 1–5 hours after consumption

Diarrhea - various foods - has an 8- to 16.5-hour incubation time

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6
Q

How does Clostridium Perfrigens present?

A

Poor prepared meat and poultry - GI symptoms within 6-24 hours

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7
Q

Which Pathogen can act very quickly (within 30mins to cause GI symptoms)?

A

Staph Aureus - Foods that are frequently incriminated in staphylococcal food poisoning include meat and meat products; poultry and egg products; salads such as egg, tuna, chicken, potato, and macaroni; bakery products such as cream-filled pastries, cream pies, and chocolate eclairs; sandwich fillings; and milk and dairy products.

Heat resistant Toxin produced by Staph

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8
Q

Where is the APC gene and what role does it play?

A

It is found on chromosome 5 and mutations lead to adenomatosis polyposis coli (FAP).

It is normally a tumour suppressor gene
100% of patients will develop malignancy

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9
Q

What other malignancy is FAP associated with?

A

Hepatoblastoma

Other rare cancers; cortical dysplasia - seizure, congenital hypertrophy of retinal pigmented epithelium

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10
Q

What is Turcot syndrome?

A

Autosomal recessive + Colonic polyps + CNS tumours

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11
Q

What is Peutz Jeghers syndrome characterised by?

A

Lip freckling + gastric polyps

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12
Q

What is syndrome caused by germline mutations int he Serine Threonine Kinase tumour suppressor gene on chromosome 19p13.3?

A

Peutz Jeghers syndrome

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13
Q

How is Calprotectin produced?

A

It is present in the cytoplasm of neutrophils - it is not degraded by intestinal enzymes or bacteria

Good screening test for GI inflammation

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14
Q

What are GI complications fo CF?

A 
DIOS (15%)
Rectal prolapse (~20%)
increased risk of GI tract tumours
Fibrosing colonopathy
CF associated liver disease (spectrum of disease upto cirrhosis)
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15
Q

3 other syndromes associated with exocrine pancreatic insufficiency?

And describe their characteristics

A

Shwachman-Diamond syndrome - Triad of Pancreatic insufficiency, bone marrow dysfunction and skeletal abnormalities (OP, dysplasias)

Pearson syndrome - Pancreatic fibrosis, vacoulated erythropoetic precursors, no skeletal abnormalities

Johnson-Blizzard syndrome - EPI, hypoplasia of nasal alae

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16
Q

How do you test for Exocrine pancreatic insufficiency?

A

72 hour faceal fat or faecal elastase (false positive with diarrhea)

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17
Q

Risk factors for TPALD?

A
  • Prematurity and LBW
  • Primary GI disease
  • Lack of enteral nutrition
  • Catheter related blood stream infections
  • Small bowel bacterial overgrowth
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18
Q

Fish oil is omega- _
AND
Soy oil is omega- _

A

Fishoil - Omega 3 FA

Soy oil - omega 6 FA

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19
Q

What is the effect seen with GLP-2 analagogues (Teduglutide)?

A

It is a trophic hormone normally secreted by enteroendocrine cells -

It is shown to increase villous height in SBS patients and increase serum citrulline levels

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20
Q

SPINK 1 associated with ________

A

Familial pancreatitis

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21
Q

NOTCH 2 and JAG1 associated with _______

A

Allagile syndrome

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22
Q

SERPINA 1 associated with ________

A

A1AT deficiency

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23
Q

STK11 associated with _________

A

Peutz Jeghers

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24
Q

UGTP81 associated with ___________

A

Gilberts

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25
Q

SBDS associated with ______

A

Schwaman Diamond Syndrome

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26
Q

What is the rule of 4-4-9?

A 
Carbohydrates = 4kcal/gram
Protein = 4kcal/gram
Fat = 9kcal/gram
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27
Q

Lactose = ______ + _______ (broken down by _______)

A

Glucose + Galactose (by lactase)

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28
Q

Breath test for carbohydrate malabsorption peaks at ______ hours. An earlier peak at 1 hour may suggests…

A

Breath test for carbohydrate malabsorption peaks at 2-4 hours. An earlier peak at 1 hour may suggest bacterial overgrowth or intestinal pathology

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29
Q

Glucose and galactose are transported by which transporter?

A

SGLT1 which requires Na and ATP

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30
Q

Fructose is transported by _______ and ________ across the basolateral membrane

A

Fructose is transported by GLUT2 (also transports glucose) and GLUT5

Transported via passive diffusion across the apical membrane

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31
Q

How does Mycophenolate mofetil work?

A

Prevents guanosine nucleotide synthesis preventing proliferation of T and B cells

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32
Q

Massive hepatic haemangiomas are associated with _________.

This is in relation to tumour expressing __________ which acts to _______

A

Associated with hypothyroidism.

The tumour expresses type 3 iodothyronine deiodinase which results in an increased rate of inactivation of thyroid hormone

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33
Q

The _ _ variant of A1AT overwhelmingly associated with liver disease

A

The ZZ variant

MM normal

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34
Q

Crigler-Najjar Syndrome 1 is due to ________

A

Absent enzyme that conjugates bilirubin - also UGTA1A gene

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35
Q

In Crigler-Najjar Syndrome 2 - the bilirubin levels are responsive to treatment with ______

A

Phenobarbitol because it increases the activity of the enzyme

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36
Q

IL-__ deficiency in VEO-IBD seen with significant perianal disease

A

IL-10

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37
Q

Which extra-manifestinal are more common in Crohns Disease than ulcerative colitis?

A

Erythema nodosum

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38
Q

Which bacteria can mimic RIF pain/appendicitis?

A

Yersinia enterocolitca

Also presents with erythema nodosum

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39
Q

Which is the investigation of choice when looking for fructose intolerance?

A

Serum Aldolase B enzyme measurement

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40
Q

What are the two chelating agents used for copper?

A

Pencillamine and Trientine

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41
Q

How do you treat hyperammonia?

A

Sodium Benzoate

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42
Q

Goat’s milk is deficient in _______

A

Folate

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43
Q

______ mutation increases the likelihood of developing Crohn’s disease

A

NOD2

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44
Q

Most common food associated with EI?

A

Cow’s milk

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45
Q

What is the recommended treatment for EI?

A

PPI, Elimination diet, swallowed corticosteroids

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46
Q

Difference between Type I and Type II and Type III Progressive familial intrahepatic cholestasis

A

Type I and II - normal GGT

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47
Q

What does bowel histopathology with Rotavirus show?

A

Histopathology of rotavirus-induced gastroenteritis show that the jejunal and duodenal mucosa appear to have patchy irregularities, which consists of shortening and blunting of the villi, and increased infiltration of the lamina propria with mononuclear cells.

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48
Q

In faecal screen:

Fat globules = ___________________

Fatty acid crystals = ________________

A

Fat globules = intraluminal problem e.g. failure of enzyme process or bile to suspend fats = maldigestion

Fatty acid crystals = mucosal/brush border problem (fatty acid not absorbed) = malabsorption

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49
Q

___________ is a form of idiopathic familial intrahepatic cholestasis associated with lymphedema of the lower extremities

A

Aagenaes syndrome

Affected patients usually present with episodic cholestasis with elevation of serum aminotransferase, alkaline phosphatase, and bile acid levels. Between episodes, the patients are usually asymptomatic and biochemical indices improve.

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50
Q

Generalized hypotonia with psychomotor retardation. Abnormal head shape and unusual facies, hepatomegaly, renal cortical cysts, stippled calcifications of the patellas and greater trochanter, and ocular abnormalities. Hepatic cells on ultrastructural examination show an absence of peroxisomes.

Which syndrome?

A

Zellweger (cerebrohepatorenal) syndrome

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51
Q

What is the pathophysiology behind neonatal haemachromatosis?

A

This is an alloimmune disorder with maternal antibodies directed against the fetal liver. Liver injury results in decreased hepatic hepcidin expression and thus dysregulation of placental iron flux

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52
Q

Affected patients present with steatorrhea, pruritus, vitamin D-deficient rickets, gradually developing cirrhosis, and low γ-glutamyl transpeptidase (GGT) levels

A

PFIC 1

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53
Q

The mutation for PFIC 1 occurs on chromosome __ and the pattern of inheritance is _______. This has an impact on _________

A

Chromosome 18q21 and inheritance is autosomal recessive. This affects protein FIC1 which is responsible for ATP dependent aminophospholipid flippase

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54
Q

What are some differences in presentation fo PFIC 1 and PFIC 2?

A

PFIC 2 presents with rapidly progressive cholestatic giant cell hepatitis, growth failure, pruritus.

Key differences are that PFIC 2 is rapidly progressive and PFIC 1 has impact on colon and thus you have more diarrhea

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55
Q

In contrast to PFIC I and PFIC 2, patients with PFIC type 3 (MDR3 disease) have _________

A

High levels of GGT

It is more often later-onset cholestasis, portal hypertension, minimal pruritus, intraductal and gallbladder lithiasis

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56
Q

How does benign recurrent intrahepatic cholestasis (BRIC) type I present?

A

Recurrent bouts of cholestasis, jaundice, and severe pruritus. Same mutation that involves PFIC1 but has

non-sense, frame shift, and deletional mutations cause PFIC type I; missense and split-type mutations result in BRIC type I

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57
Q

___________ is characterized by an elevated serum bile acid concentration, pruritus, failure to thrive, and coagulopathy

A

Familial hypercholanemia is characterized by an elevated serum bile acid concentration, pruritus, failure to thrive, and coagulopathy

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58
Q

___________ is characterized by an elevated serum bile acid concentration, pruritus, failure to thrive, and coagulopathy

A

Familial hypercholanemia is characterized by an elevated serum bile acid concentration, pruritus, failure to thrive, and coagulopathy

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59
Q

SGLT1 helps absorb ______________

A

glucose and galactpse

60
Q

How does congenital sucrase-isomaltase deficiency present?

A

Infant begins to have diarrhea after starting fruits and juices

61
Q

What is the genetic manifestation of glucose/galactose malabsorption?

A

Autosomal recessive disorder with SGLT1 gene anomaly (found on chromosome 22)

62
Q

Hereditary fructose intolerance is caused by deficiency in which enzyme and what is the genetic basis?

A

It is caused by deficiency of Aldolase B which is important in conversion of fructose 1-P into glyceraldehyde (issue inside the hepatocytes)

Autosomal recessive condition

63
Q

How is the digestion of MCT different to LCT?

A

You don’t need emulsification process and also MCT’s goes straight into the blood stream.

LCT’s get absorbed as chylomicrons through the lymphatics

64
Q

Low albumin, low lymphocyte count and low IgG? + diarrhea/oedema

A

Primary intestinal lymphangiectasia

65
Q

Which stool test helps look for protein losing enteropathy?

A

Alpha-1 antitrypsin

66
Q

How do you treat protein losing enteropathy?

A

Treat underlying condition
Alter diet to MCT rich diet to put less pressure on lymphatic pressures
Can also use Octreotide to reduce pressures

67
Q

What are non-GI manifestations of Coeliac disease?

A 
Dermatitis Herpetiformis
Dental enamel hypoplasia
Delayed puberty
Osteopenia/Osteoporosis
Fe Deficiency
Epilepsy with occipital calcifications
68
Q

What are some associated conditions with Coeliac deficiency?

A 
Down syndrome
Turner syndrome
Williams Syndrome
T1DM
Thyroiditis
69
Q

Most sensitive serology test for coeliac?

Most specific serology test for coeliac?

A

Sensitive - tTG IgA

Specific - EMA IgA, DGP IgA and then tTG IgA

70
Q

DQ _ found in 95% of coeliac patients and DQ _ in remaining

A

DQ 2 found in 95% of coeliac patients and DQ 8 i n remaining

Present in 30-40% of general population - used to rule out but not rule in

71
Q

___% of people can be serology negative and still have Coeliac disease

A

5%

72
Q

How does Schwannman diamond syndrome cause pancreatic insufficiency?

A

Acinar cell failure -parenchymal fatty infiltration of the pancreas

73
Q

__________ is caused by a gene mutation in UBR1 gene and is associated with pancreatic failure; other clinical signs associated with this are imperforate anus, hypoplastic alae nasi, hypothyroidism, ectodermal scalp defect, deafness

A

Johanson Blizzard syndrome

No haematological or skeletal anomalies

74
Q

_______ is associated with defects in acinar and duct cell function leading to pancreatic insufficiency. Other clinical signs can be refractory sideroblastic anaemia.

This is a mitochondrial disease

A

Pearson marrow pancreas syndrome

75
Q

Most common cause of recurrent pancreatitis is genetic - what is the causative gene?

A

PRSS1 (autosomal dom) - 80%

SPINK1 is the autosomal recessive - less common

76
Q

Why does coeliac disease reduce pH?

A

Lactose fermentation (secondary lactose intolerance) thus stool pH is low

That’s why carbohydrate malabsorption reduce stool pH

77
Q

Estimated caloric requirements;

Neonate - XX kcal/kg/day,
6yo - XX kcal/kg/day,
12yo - XX kcal/kg/day.

Carbs = Xcal/g
Protein = Xcal/g
Fat = Xcal/g
A

Neonate - 100kcal/kg/day,
6yo - 75kcal/kg/day,
12yo - 50kcal/kg/day.

Carbs = 4 cal/g
Protein = 4 cal/g
Fat = 9cal/g
78
Q

What is Sandifer syndrome?

A

Sandifer syndrome is a condition that involves spasmodic torsional dystonia with arching of the back and rigid opisthotonic posturing, associated with symptomatic gastroesophageal reflux, esophagitis, or hiatal hernia

79
Q

How does PPI work?

A

Irreversibly bind to and inhibit the parietal cell enzyme hydrogen potassium stimulated ATPase “gastric proton pump”

80
Q

How does erythromycin work to help with gastric motility?

A

Antidopaminergic effects and motilin agonist

81
Q

How does Baclofen work for dysmotility?

A

Cholinergic agent - GABA receptor agonist

82
Q

What is achalasia?

A

Reduction in inhibitory ganglion cells in the myenteric cells - reduced NO (increased collagen and lymphocytes)

83
Q

Which syndrome?

Achalasia + ACTH insensitivity + Alacrima = ______

A

Allgrove syndrome

84
Q

Hypophosphatemic rickets + deafness + vitiligo + achalasia = ______ which syndrome?

A

Rozychi

85
Q

Which infective disease can cause achalasia?

A

Chagas disease

86
Q

What are pathognemonic findings for EO?

A
  • rings “trachialisation” of the oesophagus
  • Furrows
  • There may be white exudate
  • Crepe paper like mucosa
  • Or normal in 1/3 of the cases
87
Q

When eliminating food in EO; which food do you eleminate first?

A

First eliminate Dairy and Gluten - 43% efficacy

Then you eliminate legumes and egg as well - 64% efficacy in children

88
Q

First line treatment for H Pylori treatment?

A

Amoxi- Clarithro - PPI

Use metro instead of Clarithromycin if there is resistance

Confirmation of clearance with hydrogen breath test

89
Q

What is the most common type of oesophageal fistula?

A

Type C - Oesophagus dead end; distal oesophagus connected to trachea (84%)

Second most common - Type A - both dead end

90
Q

Vascular malformation occur in ___% of ToF

A

18%

91
Q

Which genetic condition does Hirschsprung disease commonly occur in?

A

including trisomy 21, Joubert syndrome, Goldberg-Shprintzen syndrome, Smith-Lemli-Opitz syndrome, Shah-Waardenburg syndrome, cartilage-hair hypoplasia, multiple endocrine neoplasm 2 syndrome, neurofibromatosis, neuroblastoma, congenital hypoventilation (Ondine’s curse)

+ increased familial incidence

92
Q

What is the histopathological findings in Hirschprung disease?

A

Observed histologically is an absence of Meissner’s and Auerbach’s plexuses and hypertrophied nerve bundles with high concentrations of acetylcholinesterase between the muscular layers and in the submucosa

93
Q

What is the Curriano triad?

A

Currarino triad must be considered, which includes anorectal malformations (ectopic anus, anal stenosis, imperforate anus), sacral bone anomalies (hypoplasia, poor segmentation), and presacral anomaly (anterior meningoceles, teratoma, cyst).

  • Often detected when investigating for Hirschprung disease in older children
94
Q

What is the diagnosis?

Normal ganglion on the rectal suction biopsy, normal ACTHe activity, but absence of recto-sphinteric reflex on anal manometry

A

Internal anal sphincter achalasia

95
Q

Which variants of Protease inhibitor phenotype gives you liver disease?

A

PiZZ and PiSZ

96
Q

How does alpha 1 antitrypsin deficiency present?

A

11% have neonatal cholestasis +/- acholic stools
25% develop early liver failure and cirrhosis

Assoc with biliary atresia

Increased risk of HCC

97
Q

What do you see in histopath for A1 antitrypsin def?

A

Period acid Schiff +ve diastase resistance globules in ER of hepatocytes

98
Q

Low elastase in stool means?

A

Pancreatic insufficiency

99
Q

What is the specific gene involved in Lynch syndrome?

A

MLH1 or MSH2 gene

Autosome dominant

100
Q

What is the specific gene in Peutz Jeghers?

A

STK11

101
Q

What is the second most common cancer in Lynch syndrome after cololncancer?

A

Endometrial cancer

102
Q

If a button battery is in the _______ the it needs to be taken out ASAP

A

Oesophagus!

if in stomach we normally repeat XRAY in 24 hours, to check it is moving out of the stomach. If it isn’t -> endoscopy

103
Q

Most common side effects with Sulfalazine?

A

Rash

104
Q

Most common side effect of Mesalazine?

A

Elevated creatine, renal function issues, LFT rise and pancreatitis

105
Q

Gold standard diagnosis of CMV colitis is________

A

colonic biopsies - you see Apoptosis

106
Q

Primary sclerosing cholangitis is more in ______

A

More common in males, ulcerative colitis

107
Q

Uveitis, arthritis and erythema nodosum is more common in ______

A

Crohn’s disease!

108
Q

Anti-LMK 1 and Anti-LMK 3 and Anti-LC 1 are associated with _______

A

Type 2 Autoimmune hepatitis

109
Q

What antibodies are associated with Type 1 autoimmune hepatitis?

A

ANA, Anti-SM, Antiactin antibody

110
Q

Which form of autoimmune hepatitis is more severe?

A

Type 2

111
Q

Several human leukocyte antigen class II molecules―particularly DR_, DR_, and DR_ isoforms―confer susceptibility to autoimmune hepatitis

A

DR 3, DR 4, DR 7

112
Q

What are some extrahepatic manifestations of Autoimmune hepatitis?

A

Extrahepatic manifestations can include arthritis, vasculitis, nephritis, thyroiditis, Coombs-positive anemia, and rash

113
Q

AMA +ve might also be seen in

A

Primary biliary cholangitis

114
Q

What are the most common drugs that can induce pancreatitis?

A

Valproic acid
6MP
Azathioprine
Aspiriginase

115
Q

What are the symptoms of Thiamin (B1 deficiency)?

A

o May have ptosis and atrophy of optic nerve
o Hoarseness secondary paralysis of laryngeal nerve characteristic
o Later: Raised ICP, meningismus, coma
o Severe deficiency -> beriberi disease

  • Wet beriberi= undernourished, pale, edematous child with dyspnoea, vomiting and tachycardia, urine has albumin and casts
  • Dry beriberi= plump, pale flabby, listless with dyspnoea, tachycardia and hepatomegaly
116
Q

Low RBC transkelotase activity is best indicator of body tissue ___________

A

Thiamine deficiency

117
Q

Which vitamin deficiency is associated with cheilosis and glossitis

A

Riboflavin (B2)

118
Q

Which vitamin B deficiency?

classic triad of dermatitis, diarrhoea and dementia

A

Niacin - B3

119
Q

Normal milk/formula/ breast milk has how many calories?

A

20kcal/30mL or 67kcal/100mL

120
Q

The ____ acts as the major haematopoeitic organ until week 6, after which the bone marrow takes over

A

The liver

121
Q

The pancreases starts excreting insulin from week __

A

Week 10

122
Q

Gut rotation normally begins around week __ and ends week ___.

Normally the caudal portion (forms the cecum) of the midgut rotates ___degrees _____.

The most common type of malrotation involves failure of the cecum to move into the _________

A

Week 5 - Week 12

The Caecum rotates 270 degrees counterclockwise

Failure of caecum to move to RLQ

123
Q

ATP7 A =

ATP7 B =

A

ATP7 A = Menke’s

ATP7 B = Wilson’s

124
Q

As per guidelines, first line treatment for Wilson’s in an asymptomatic person?

A

ZInc salts

125
Q

Coca Cola breaks down….

A

Fruit and vegetable bezoars

126
Q

What drugs in Crohn’s disease cause mucosal healing?

A

EEN
Prednisolone
Infliximab

All of the above used for induction

127
Q

Ways to differentiate osmotic vs secretory diarrhea?

A

Osmotic = loosing water alongside electrolytes

Secretory = “loosing serum”. Affected by feeds

Stool osmolal gap=
Stool Osm - (2x (Na+K))
If >100 = osmotic (losing electrolytes)
<100 = secretory

Simple way:

  • 2 x (serum sodium + potassium)
  • If >250 = secretory
  • If <200 = osmotic
128
Q

Most infectious agents cause secretory diarrhea, but in what instance can it cause osmotic diarrhea?

A

In salmonella and malabsorption disorders = you get osmotic diarrhea because losing nutrients and water

129
Q

Which hormone is inappropriately high in PWS?

A

Grehlin

130
Q

What is the role of gastrin?

A

Gastrin is a peptide hormone that stimulates secretion of gastric acid (HCl) by the parietal cells of the stomach and aids in gastric motility

131
Q

Which cells release acid?

A

Parietal cells

132
Q

What is the role of secretin and CCK?

A

Secretin stimulates the flow of bile from the liver to the gallbladder. CCK stimulates the gallbladder to contract, causing bile to be secreted into the duodenum, as shown below.

In the pancreas, secretin stimulates the secretion of bicarbonate (HCO3), while CCK stimulates the secretion of digestive enzymes

Released by duodenum in response to chyme

133
Q

What is the step up with medications UC and CD?

A

UC: Mesalazine -> azathioprine (steroid sparing)-> Infliximab (reserved for steroid requiring disease)

CD: Azathioprine -> Methotrexate (steroid sparing) -> Infliximab (reserved for steroid requiring disease)

134
Q

EPCAM gene occurs in ….

A

Lynch syndrome

135
Q

MYO5B is associated with…

A

PFIC, microvillous inclusion disease

136
Q

What is the mechanism of action of cholestyramine?

A

Increased excretion of bile salts through he gut. Binds to the bile salts and prevent them from being absorbed in the ileum.

137
Q

90% of bile salts are reabsorbed through the ____ as urobilogen

A

Ileum

138
Q

Name the important channels:

Channels on the apical enterocyte absorption:

  • _____ - sodium cotransporter - absorbs glucose and galactose
  • ______ - absorbs fructose

Channels on the basolateral enterocyte membrane:

  • ________ - glucose, galactose, fructose
  • ________ - fructose
A

Channels on the apical enterocyte absorption:

  • SGLT2 - sodium cotransporter - absorbs glucose and galactose
  • GLUT 5 - absorbs fructose

Channels on the basolateral enterocyte membrane:

  • GLUT 2 - glucose, galactose, fructose
  • GLUT 5 - fructose
139
Q

Liver histology =

Periductal fibrosis of liver = _______

Proliferation of bile ducts = _________

Paucity of bile ducts = __________

Periportal fibrosis = ___________

PAS negative staining = ________

A

Periductal fibrosis of liver = Primary sclerosing cholangitis

Proliferation of bile ducts = Biliary atresia

Paucity of bile ducts = Alagilles syndrome

Periportal fibrosis = NAFD

PAS negative staining = A1AT

140
Q

ABCB4 gene is associated with ______

A

PFIC type 3

141
Q

What do pareital cells secrete?

A

Intrinsic factor and hydrochloric acid

142
Q

What do chief cells secrete?

A

Pepsinogen

143
Q

What do G cells secrete?

A

G-cells are enteroendocrine cells which produce gastrin.

Gastrin causes stimulation of acid secretion from gastric parietal cells and stimulation of mucosal growth in the acid-secreting part of the stomach

144
Q

Is Sucrose a reducing sugar or not a reducing sugar?

A

Sucrose is not

Most of the others are

145
Q

Crypt lesions are seen in _______

A

Ulcerative colitis

146
Q

Granulomas on bowel biopsy are seen in _______

A

Crohn’s disease

BPT exams (24 decks)

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