Gastroenterology Flashcards

1
Q

What are the sites of absorption in the intestine for iron,

A

IRON = proximal duodenum
-> needs acidic environment

FOLIC acid = first 1/3 small intestine (duodenum/jejunum)

VITAMIN B12 = ileum
-> needs intrinsic factor

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2
Q

Which part of the small intestine has maximal absorption of zinc?

A

Proximal jejunum

All three segments (duodenum, jejunum and ileum) have the ability to absorb zinc

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3
Q

What is the MoA of cholera in producing diarrhoea?

A

(1) Cholera enterotoxin -> activation of ADENYLATE CYCLASE -> increase cAMP in intestinal epithelial cells
(2) cAMP on intestinal epithelial transport -> stimulation of active Cl secretion (crypts) and inhibition of Na-Cl absorption (villi)

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4
Q

Why is ORS important in treating cholera?

A

Cholera enterotoxin (cAMP) does NOT inhibit glucose-stimulated Na (and thus fluid) absorption

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5
Q

What is the MoA of ORS?

A

Glucose to stimulate Na and fluid absorption in the small intestine via cyclic AMP-independent process

Glucose absorption requires luminal Na -> absorption markedly enhanced by the presence of luminal glucose

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6
Q

Which part of the small intestine (microscopic) does electrolyte absorption vs secretion take place?

A

Electrolyte ABSORPTION = villi (peaks)

SECRETION = crypts

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7
Q

What is the major site of the intestine for absorption?

A

Jejunum

Majority of nutrient absorption takes place in jejunum, EXCEPT:

Iron = duodenum 
Folate = duodenum and jejunum 
Calcium = duodenum and upper jejunum (transcellular active transport process); throughout length of intestine (paracellular, passive process) 
Vitamin B12 = terminal ileum 
Bile salts = terminal ileum
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8
Q

Name the disaccharides and their components (monosaccharides)

A

Maltose = glucose + glucose

Lactose = glucose + galactose

Sucrose = glucose + fructose

*Remember, glucose in all; two of the three monosaccharides start with ‘G’

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9
Q

What syndromes are associated with Hirschsprung disease?

A
Mowat Wilson syndrome
Down syndrome (T21) 
Bardet-Biedl syndrome 
Smith-Lemli-Opitz syndrome 
Waardenburg syndrome
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10
Q

What are the symptoms caused by deficiency in the fat-soluble vitamins?

A

A = night blindness (late), scaly skin, infection susceptibility of epithelia (lung, GI, GU)
-> vitamin A involved in maintenance of epithelial functions

D = rickets, craniotabes (softening skull), rachitic rosary, growth plate widening

E = haemolysis (usually 2nd month life), neurologic manifestations (cerebellar disease, posterior column dysfunction, retinal disease)
-> vitamin E functions as in antioxidant

K = bleeding (GI, mucosal, cutaneous)
-> required for clotting factors

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11
Q

What is the initial finding (usually) in vitamin E deficiency?

A

Loss of deep tendon reflexes

-> limb ataxia, truncal ataxia, dysarthria, opthalmoplegia (limited UPward gaze), decreased proprioception

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12
Q

What is an example of diarrhoea getting worse with ORS instead of IVT?

A

Glucose-galactose malabsorption

Autosomal RECESSIVE disorder = inheritance of two defective copies of the SGLT1 gene (chromosome 22)

MoA = lack of transportation (the protein product of SGLT1) of the broken down lactose (into glucose and galactose by lactase) from the lumen into intestinal cells -> osmotic diarrhoea

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13
Q

What syndromes is coeliac disease associated with?

A

Down (T21)
Turner
William

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14
Q

What are the types of autoantibodies seen in autoimmune hepatitis type 1 vs. 2?

A

Type I

  1. Antinuclear (ANA) antibodies
  2. Anti-smooth muscle (anti-SMA) antibodies

Type II

  1. Antiliver-kidney microsomal-1 antibodies (anti-LKM-1)
  2. Antiliver cytosol-1 antibodies (anti-LC-1)

Both typically have hyPERGAMMAglobulinaemia (IgG levels >16g/L)

Type II > I in severity 
Type II (almost exclusively) female
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15
Q

What are the 3 Rome criteria functional disorders for abdominal pain?

A
FUNCTIONAL ABDOMINAL PAIN 
(school age) 
1. Periumbilical pain 
2. Normal growth 
3. Appetite not usually affected 
4. Symptoms better on weekend/vacation
5. Social stressors exacerbate
FUNCTIONAL DYSPEPSIA 
(school age/adolescent) 
1. Midepigastric 
2. Correlation to meals 
3. Normal growth 

IRRITABLE BOWEL

(adolescent)
1. Lower abdomen
2. Female
3. Pain improves with defacation
4. Frequent changes in stool caliber/frequency
5. Normal growth and appetite

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16
Q

What disease is abdominal pain that wakes from sleep typically seen in?

A

H. pylori infection

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17
Q

What are the major differences between omphalocele vs. gastroschisis?

A

OMPHALOCELE

  1. Central defect (umbilical ring)
  2. Covering membrane (peritoneal membrane internal, amniotic membrane external)
  3. Congenital anomalies (thoracoabdominal syndorme, BWS, lower midline syndrome, trisomies)
  4. Staged surgery
  5. +/- midgut volvulus
  6. Lower survival rate (affected by congenital)

GASTROSCHISIS

  1. Lateral (right) - accident involving right umbilical vein or omphalomesenteric artery
  2. No membrane
  3. Midgut volvulus
  4. Immediate surgery
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18
Q

Where are the two vomiting centers of the brain located?

A

Vomiting center (neural) = in the nucleus solitarius in MEDULLA

Chemoreceptor trigger zone (chemical) = floor of 4th ventricle

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19
Q

What is the best test for chronic vomiting?

A

Endoscopy

Main causes = oesophagitis, gastritis
Less common = duodenitis, giardiasis

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20
Q

What other disease is cyclic vomiting associated with?

A

Migraines

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21
Q

What is the treatment for cyclic vomiting?

A

Cyproheptadine (1st choice < 5 years)
Propanolol
Amitriptyline

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22
Q

Which grains contain gluten?

A

BRWS

B - barley
R - rye
W - wheat
S - spelt (a species of wheat)

Oats previously thought to be harmful - but appears to be from contamination with wheat flour
-> still included in gluten-free diet

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23
Q

Which patients are at high-risk for coeliacs?

A
  1. First and second-degree relatives with coeliacs
  2. Down syndrome (T21)
  3. T1DM
  4. Selective IgA deficiency
  5. Autoimmune thyroiditis
  6. Turner syndrome
  7. William syndrome
  8. Juvenile chronic arthritis
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24
Q

What is the best serologic test for diagnosis of coeliac disease?

A

IgA antibodies against tissue transglutaminase (tTG-IgA)

= highly specific, sensitive and cost-effective

OTHER
= IgA antibodies to endomysium (EMA)
-> as accurate as tTG-IgA, but more expensive and operator interpretation-dependent

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25
Q

What does gluten react with in coeliac disease?

A

Intestinal damage due to immunological cross-reaction

= reaction to human transglutaminase (hence serology test)

26
Q

What lesion is pathognomonic for coeliac disease?

A

Dermatitis herpetiformis

= itchy, vesicular rash
-> erupts symmetrically on extensor surface of arms, legs and buttocks

27
Q

What are the 2 mandatory requirements for diagnosis of coeliac disease?

A
  1. Characteristic histology on small-intestine biopsy
    a) increased epithelial lymphocytes
    b) crypt hyperplasia
    c) villous atrophy
  2. Complete clinical remission with a gluten-free diet
28
Q

What is the enzyme that conjugated bilirubin in the liver (from unconjugated to conjugated)?

A

Glucuronyltransferase

29
Q

Does Dubin-Johnson syndrome cause conjugated or unconjugated bilirubinaemia?

A

Conjugated

= ABCC2 gene affected
-> provides instructions for making a protein that transports bilirubin out of hepatocytes into bile -> accumulation in body

30
Q

What is the most common genetic cause of liver disease in children?

A

Alpha1-antitrypsin deficiency

31
Q

What is giant cell hepatitis seen in?

A

Alpha1-antitrypsin deficiency

32
Q

What is periodic acid-Schiff positive staining of the liver seen in?

A

Alpha-1 antitrypsin deficiency

33
Q

Are ceruloplasmin levels low or high in Wilson disease?

A

Low

Failure of copper to be incorporated into ceruloplasmin leads to a plasma protein with shorter half life, and therefore reduced steady-state concentration of ceruloplasmin in the circulation

Wilson = absence/malfunction of ATP7B -> decreased biliary copper excretion -> accumulation of copper in cytosol of hepatocytes

34
Q

What is the difference between progressive familial intrahepatic cholestasis (PFIC) 1 and 2 vs. 3?

A

PFIC3 has elevated GGT, 1 and 2 do not

PFIC = inherited disorders where bile is not properly formed

35
Q

What is used for hepatitis A prophylaxis?

A

Hepatitis A vaccine OR immunoglobulin

Given within 2 weeks of exposure

HepA vaccine = preferred >/= 12 months

IG = preferred < 12 months

HepA vaccine given universally at 1 year of age -> protection for 20 years

36
Q

Which hepatitis virus is DNA?

A

Hepatitis B

37
Q

How do you interpret hepatitis B serology?

A

HepB SURFACE antigen
= either carrier or early hepatitis B
-> IgG antibodies to surface antigen means (1) past exposure; (2) immunity

HepB CORE antigen
= free core antigen does not circulate in serum
-> antibodies (first IgM, then IgG) appears early in disease; persist for life
= most reliable marker for previous exposure

HepB e antigen
= marker of actively replicating virus -> infectivity/inflammation
-> found in serum

38
Q

What is the first hepatitis B marker detectable in serum when infected?

A

HepB surface antigen

  1. HBsAg
    (WINDOW PERIOD)
  2. HBcAb

Best test during window period = anti-HBc IgM

39
Q

What autoimmune disease in hepatitis B associated with?

A

Polyarteritis nodosa

40
Q

Which of the 2 hepatitis viruses cause chronic infection that potentially leads to cirrhosis and carcinoma?

A

Hepatitis B and C

41
Q

What hepatitis virus requires a concomitant or previously existing HBV infection to become pathogenic?

A

Hepatitis D

42
Q

What are the tests for each of the hepatitis viruses in an ACUTE infection?

A

Hepatitis A = IgM HAV

Hepatitis B = HBsAg & IgM HBc (window period)

Hepatitis C = anti-HCV antibody

43
Q

What are the two types of exocrine secretory cells in the stomach?

A

PARIETAL
= secrete HCl and intrinsic factor

CHIEF
= secrete pepsinogen and chymosin

44
Q

Is celiac disease B cell or T cell mediated?

A

T-cell mediated chronic inflammatory disorder

45
Q

What skin manifestation is pathognomonic for coeliac disease?

A

Dermatitis herpetiformis

46
Q

What is the most common extraintestinal manifestation of coeliac disease?

A

Iron deficiency anaemia

47
Q

What are examples of extraintestinal manifestations of coeliac disease?

A
THIAMINE/B12 DEFICIENCY 
Peripheral neuropathy 
Epilepsy 
Cerebral calcifications 
Cerebellar ataxia 

AUTOIMMUNITY
Dermatitis herpetiformis
Alopecia
Erythema nodosum (rare)

CALCIUM/VIT D MALABSORPTION
Short stature
Secondary hyperparathyroidism

OTHER
Arthritis/arthralgia
Cardiomegaly
Aphthous stomatitis

48
Q

What is the main cause of death in coeliac disease patients?

A

Non-Hodgkin lymphoma

49
Q

What histologic changes are seen on biopsy of intestine in coeliac disease?

A

Small bowel mucosal inflammation = short, often flattened, villi + crypt hyperplasia

50
Q

What are the radiological findings of intussusception?

A

USS
1. ‘Target’ sign

XR

  1. Crescent sign = soft tissue density projecting into gas of large bowel
  2. Obscured liver margin
  3. Meniscus-shaped mass outlined by air in the colon
51
Q

What anatomic structure marks the formal division between the first and second parts of the small intestine (i.e. duodenum and jejunum)?

A

Ligament of Trietz
= normally to LEFT of spine (at level of gastric antrum)

a.k.a. suspensory muscle of duodenum

***In malrotation, ligament is on right of spine + inferior to duodenal bulb -> thus contrast fills the jejunal loops on RIGHT side of abdomen

52
Q

What is the ‘rule of 2’s’ for Meckel diverticulum?

A

Present in 2% of population

Located within 2 feet of ileocoecal valve

Measures 2 inches in length

Measures 2 cm in diameter

2:1 = M:F

Usually symptomatic before 2 years of age

53
Q

What is the main symptom of Meckel divertucula?

A

PAINLESS GI bleeding (bright red or maroon)

= from ectopic gastric mucosa

+/- colicky abdominal pain

54
Q

How do you diagnose a Meckel diverticula?

A

Technetium-99m pertechnetate scan (a.k.a. Meckel scan)

= technetium-99m pertechnetate concentrates in parietal cells of gastric mucosa and bladder

-> +ve if uptake outside stomach and bladder

55
Q

Is a Meckel diverticulum associated with other congenital abnormalities?

A

Yes

Oesophageal atresia (6x) 
Imperforate anus (5x) 
Neurologic anomalies (3x) 
Cardiovascular anomalies (2x)
56
Q

Which of the following is associated with congenital anomalies - duodenal or jejunal atresia?

A

Duodenal

(D)uodenum -> (D)own syndrome

Also: cardiac, GU, anorectal, oesophageal

57
Q

What disease has periodic acid -Schiff positive granules in the lamina propria (of intestine)?

A

Whipple disease = Tropheryma whipplei

58
Q

Where is lactase found in the intestine?

A

On the brush border near the tips of the intestinal villa

59
Q

What is the most common reliable diagnostic test for lactase deficiency?

A

Breath hydrogen test

When carbs malabsorbed, bacteria in colon produce hydrogen gas -> absorbed across colon into blood and expired in lungs

Abx give false -ve

Too early rise in H+ = bacterial gut overgrowth

60
Q

What are the different types of jejunoileal atresia?

A

4 types. Not associated with T21

Type 1 = mycosal obstruction cased by intraluminal membrane

Type 2 (35%) = a solid, fibrous cord connects blind ends of the proximal and distal bowel

Type 3 = blind ends of distal and proximal bowel separated by small (type IIIa) and extensive (type IIIb) mesenteric defects

Type 4 = multiple segments of bowel atresia