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Gastro Flashcards

1
Q

type of CMPA

A
  1. IgE mediated - type 1 hypersensitivvity reaction, atopy related
  2. non IgE mediated - activates T cells (osmotic diarrhoea due to damage to absorptive area)
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2
Q

presentation of CMPA

A

GI symptoms within 2 hours of cows milk in first 4 weeks of life
wheeze/ rhinitis
atopic eczema/ rash
crying, irritable, milk refusal
failure to thrive
blood in stool - non IgE mediated

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3
Q

presentation of GORD

A

excessive regurg or vomiting
irritability e.g. back archin
faltering growth
excessive hiccups
apnoeas/ breath holding/ cyanotic episodes

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4
Q

what is sandifers syndrome

A

abnormal posturing + deviation of head and neck + discomfort with feeds

needs upper GI endoscopy

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5
Q

GORD diagnosed

A

clinical diagnosis but can do ph study or barium swallow
ph < 4 for 15 secs

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6
Q

management of GORD

A
  1. lifestyle - feed upright, reduce feed volume
  2. add feed thickener for 1-2 weeks e.g. carobel, gaviscon
  3. add PPI for 4 week trial if flatering growth
  4. add domperidone
  5. fundoplication
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7
Q

type of bacteria h.pylori

A

gram negative flagellated bacteria
(lipopolysaccharide layer, O antigen and lipid A)
releases urease to neutralise stomach acid and releases toxins to mucosal damage

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8
Q

presentation of h.pylori

A

dysspepsia
epigastric pain and tenderness
nausea
intolerance of fatty food

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9
Q

diagnosis of h.pylori

A
  1. urea breath test *- detects CO2 (h.pylori produces urease to convert urea to ammonia + CO2)
  2. stool antigen test
  3. endoscopy - affects lesser curvature of stoamch
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10
Q

management of h.pylori

A

omeprazole + amoxicillin + metro/ clarithromycin for 1-2 weeks (4 weeks if haematemesis)

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11
Q

what is zollinger ellison syndrome

A

ectopic gastrin secrteion from a gastrinoma
multiple peptic ulcers >2cm diameter

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12
Q

lining og stomach

A

columnar epithelium

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13
Q

function of parietal cells

A

produce HCl + intrinsic factor

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14
Q

function of G cells

A

produce gastrin

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15
Q

function of enterochromaffin like cells

A

produce histamine (binds to parietal cells to activate)

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16
Q

function of D cells

A

produce somatostatin which inhibits gastrin secretion

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17
Q

function of mucus neck cells

A

produce bicarbonate and mucus

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18
Q

function of chief cells

A

produce pepsinogens

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19
Q

epidemiology of coeliac

A

1% population

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20
Q

risk factors for coeliac

A
  • HLA-DQ2 or DQ8
  • 1st degree family
  • autoimmune disease e.g. vitiligo (lack of melanocytes in epidermis)
    -Ig A deficiency
  • Downs syndrome
  • Turner syndrome
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21
Q

presentation of coeliac

A

GASTRO - abdo pain and distension, diarrhoea, vomiting, buttock wasting, constipation, faltering growth
SKIN - dermatitis herpetiformis, aphthous stomatitis, vitiligo
OTHER - vit b12 deficiency, dental enamel defects, iron deficiency, dilated cardiomyopathy

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22
Q

diagnosis coeliac disease

A

IgA tissue transglutaminase positive*** +/- anti endomysial antibodies

if IgA deficiency -> test IgG ttG
if <10 x maximum, upper Gi endoscopy and duodenal biopsy

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23
Q

findings on duodenal biopsy of coeliac disease

A

intra epithelial lymphocytosis ***
subtotal villous atrophy
crypt hypertrophy
lamina propria cell infiltrate
enteropathy

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24
Q

complications of coeliac

A

amenorrhoea
delayed puberty
osteopenia and osteoporosis
hyposplenism
T cell lymphoma

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25
Q

risk factors of pyloric stenosis

A

male ** -first born
first degree relative (female pass on higher risk)
prematurity
maternal smoking
IUGR
macrolide abx use

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26
Q

presentation of pyloric stenosis

A

present 4-6 weeks of life with…
projectile vomiting
hungry baby
weight loss
dehydration
palpable olive shaped mass in RUQ

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27
Q

investigations pyloric stenosis

A
  1. gas - metabolic alkalosis - hypokalaemia, hypochloraemia
  2. USS abdomen - wall thickness 4mm, length 17mm, diameter 15mm
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28
Q

management of pyloric stenosis

A
  1. rehydration with IVF prior to surgery
  2. surgical correction with Ramstedt pylomyotomy
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29
Q

viral causes of gastroenteritis

A
  1. rotavirus - childcare settings, cause dehydration, doubel stranded rNA virus
  2. noravirus - healthcare
  3. adenovrirus
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30
Q

bacterial causes of gastroenteritis

A
  1. salmonella - poulty (typhi - travel abroad + salmon pink rash)
  2. campylobacter *
  3. e.coli - undercooked meat
  4. shigella
  5. staph aureus -ingestion of inadequately reheated food
  6. cholera - vibrio cholerae, large volume, rice water stools
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31
Q

risk of e.coli enterotoxi 0157

A

haemolytic uraemic syndrome - reduced renal function + pale + anaemia + bloody stool

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32
Q

type of diarrhoea

A
  1. osmotic diarrhoea = damage to intestinal microvilli causing malabsorption, if stop eating, diarrhoea stops
  2. secretory = enterocyte binding toxin causing release of Cl into intestinal lumen, even if continue eating, diarrhoea continues
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33
Q

type of fluid loss

A
  1. hypotonic - highly concentrated urine, high sodium, causes water depletion
  2. isotonic - water and Na loss causing increased haematocrit
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34
Q

most common sites of crohns

A

proximal colon and terminal ileum

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35
Q

presentation of crohns

A
  1. GI - diarrhoea, abdo pain, weight loss , growth failure, mouth ulcers
  2. skin - erythema nodosum, pyoderma gangrenosum , psoriasis
  3. blood - iron deficiency
  4. eye - episcleritis
  5. bone - ank spondylitis, sacroilitis, osteoporosis
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36
Q

diagnosis of crohns

A

upper and lowe endoscopy + biopsy *

non caseating granulomas, multiple lymphoid aggregates, transmural inflammation with skip lesions, fissures, strictures, aphous / linear ulcers

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37
Q

inducing remission in crohns disease

A
  1. 1st presentation = glucocorticoids e.g. prednisolone , methylpred, IV if severe
  2. 6 week enteral nutrition (protein based formula,polymeric 1st line)
  3. 5-ASA
  4. azathioprine
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38
Q

maintenance therapy in crohns

A

1st line = AZATHIORPINE

side effects:
myelosuppression
pancreatitis
hepatitis

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39
Q

indications for surgery in crohns

A
  • ileocaecal disease
  • strictures
  • fissures
  • failure of medical treatment
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40
Q

pathophysiology of UC

A

diffuse continuous inflammation of intestinal mucosa (usually rectal and colon) and exaggerayed T cell response

associated with HLA-DRB in extensive disease
90% pancolitis !!!!

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41
Q

presentation of UC

A
  • bloody diarrhoea
  • night stools
  • abdo pain
  • weight loss
  • erythema nodoum
  • iritis, uveitis
    -sclerosing cholangitis
  • autoimmune hepatitis
  • arthritis
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42
Q

diagnosis of UC

A

endoscopy and biospy (sigmoid colon **)

friable mucosa, submucosal and mucosal inflammation, crypts abscesses, goblet cell depletion, ulceration

affects the mucosa layer

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43
Q

complications of UC

A

toxic megacolon - fever, tachycardia, dilated transverse colon
colon cancer
oxalate renal stones
osteoporosis

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44
Q

management of UC

A

induction: mesalazine (5-ASA)

maintenance: mesalazine or sulfasazlaline

15% require surgery 5 years from diagnosis

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45
Q

pathophysiology of duodenal atresia

A

abnormal developement of intestine - failure of canalization of duodenum at 7 weeks gestation

usually occurs at ampulla of vater

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46
Q

associations with duodenal atresia

A

trisomy 21
prader willi
congenital heart disease
CF
diaphragmatic hernia

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47
Q

presentation of duodenal atresia

A

present in 1st few days of life with bilious vomiting (non bilious in 20% if above ampulla of vater)
abdo distension

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48
Q

antenatal signs of duodenal atresia

A

polyhydramnios
double bubble sign of USS

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49
Q

management of duodenal atresia

A
  1. NG tube - decompress stomach, NBM
  2. duodenoduodenostomy by open laparotomy
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50
Q

pathophysiology of necrotising enterocolitis

A

acute inflammatory injury of small intestine and invasion of enteric organisms and causing ischaemic necrosis of intestinal mucosa

commonly affects terminal ileium, caecum and sigmoid colon

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51
Q

factors contributing to necrotising enterocolitis

A
  1. premature gut motility
  2. reduced igA and reduced barrier function -> initiate mucosal injury _> invasion of gas producing bacteria
  3. gut hypoxia
  4. metabolic substarte in gut lumen
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52
Q

risk factors for necrotising enterocolitis

A
  1. prematurity (<32 weeks)
  2. low birth weight , iUGR
  3. hypothermia
  4. PROM
  5. artificial feeds or rapid increase in enteral feeds
  6. placenta insufficicency, abruption
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53
Q

presentation of necrotising enterocolitis

A

feed intolerance with gastric residuals
bilious vomiting, diarrhoea
rectal bleeding
abdo distension, abdo tenderness
leading to perforation and shock, mortality 10%

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54
Q

investigations for necrotising enterocolitis

A
  1. abdo x ray - pneumoperitoneum, portal venous gas, bowel wall oedema, intramural gas of nitrogen and hydrogen (= pneumatosis intestinalis)
  2. blood cultures
  3. gas - metabolic acidosis, high lactate
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55
Q

management of necrotising enterocolitis

A
  1. NBM
  2. NG suctioning
  3. parental nutrition and IVF
  4. IV antibiotics 14 days
  5. +/- surgery if perforation or failure of medical treatment
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56
Q

what is hirschsprungs disease

A

absence of ganglion cells in the distal part of colon and rectum due to failure of neural crest cells (derived from neuroectoderm) to migrate and populate distal colon

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57
Q

associations with hirschsprungs disease

A
  • downs syndrome
  • waardenburg syndrome
  • bardet biedl
  • males
  • mutations in RET and EDNRB
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58
Q

pathophysiology of hirschsprungs disease

A

lack of ganglion cells in submucosa and myenteric plexus (auerbach ) muscular layer causes….
1. functional obstruction as no contraction of muscles
2. enterocolitis - stool accumulates and causes extension of proximal bowel and bacetria

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59
Q

presentation of hirschsprungs disease

A

failure to pass meconium in 1st 48 hours of life
abdo distension
poor feeding
enterocolitis - fever, explosive diarrhoea

60
Q

investigations for hirschsprungs disease

A

rectal suction biopsy * - lack of ganglion cells
AXR with contrast enema - reveals transition zone

61
Q

management of hirschsprungs disease

A
  1. antibiotics for enterocolitis
  2. surgical rectal washout and resection of anganglionic segment
62
Q

pathophysiology of malrotation

A

intestine in abnormal position in peritoneal cavity - intestine completed by 8-11 weeks and rotates around superior mesenteric artery.

63
Q

presentation of malrotation

A

VOLVULUS !! - bilious vomiting, abdo distension, peritonitis, fresh blood in rectum

30% present by 1 month age, 58% present by 1st year of life

64
Q

investigation of malrotation

A

AXR - proximal intestine obstruction

upper gI contrast study ** - corkscrew sign, dilated proximal duodenum with failure to pass contrast into 2nd part

65
Q

management of malrotation

A
  1. NG tube on free drainage
  2. NBM
  3. iVF
  4. surgery - laparotoy, resect necrotic bowel +/- stoma
66
Q

what is exomphalos

A

herniation of abdominal contents (stomach, intestine, liver or spleen) through umbilical defect and contained in membranous sac from amniotic membrane.

67
Q

exomphalos associations

A

trisomy 21, 13, 18
cardiac abnormalities
beckwith wiedeman syndrome

68
Q

what is gastroschisis

A

defect in rectus muscle leading to herniation of intestine to right of abdomen

69
Q

risk factors for gastoschisis

A

low maternal age
maternal drugs and smoking
low socio-economic class

70
Q

management of anorectal malformation

A
  1. defunctioning colostomy
  2. MCUG
  3. staged prolonged surgery 3-6 months old
71
Q

Tracheo-oesophageal atresia associations

A
  1. VACTERL syndrome
  2. duodenal atresia
  3. CHARGE syndrome
  4. trisomy 13,18,21
  5. diaphragmatic hernia
  6. cardiac abnormalities
72
Q

types of oesophageal atresia

A

type a - oesophageal atresia
B - proximal fistula and distal atresia
C - proximal oesophageal atresia with distal oesophageal fistula *****
D - atresia with fistula between trachea
E - isolated fistula

73
Q

oesophageal atresia presentation

A

in 1st few hours of life:
resp distress
excessive salivation + lots of secretions + frothing at mouth
abdo distension
choking on feeds
inability to pass NG

74
Q

presentation of oesophageal atresia antenatally

A

polydydramnios
absence of fetal bubble

75
Q

management of oesophageal atresia

A

x ray - nG coiled up in proximal oesophagus
echo prior to surgery
replogle tube - suction and aspirate
surgery

76
Q

causes of pancreatitis

A
  1. Idiopathic **
  2. trauma
  3. gallstones - cholesterol (obesity), calcium bilirubin
  4. viral infections - mumps,, enterovirus
  5. metabolic - hypercalcaemia
    6.medications - valproate, steroids, azathioprine
77
Q

pathophysiology of pancreatitis

A

inflammation of pancrease due to injury from overactivation of trypsinogen and pancreatic enzymes
Amylase made in acinar cells

causes release of histamine, braydkinin and trypsin

causing vasodilation and fluid loss

78
Q

presentation of pancreatitis

A

epigastric abdominal pain
vomiting
jaundice
shock
hypovolaemia
fever

79
Q

diagnosis of pancreatitis

A
  1. raised amylase ( 3 x normal, take 48 hours to reach peak)
  2. USS - identify gallstones
  3. CT abodmen - oedema, retroperitoneal fat stranding
  4. MRI and ERCP
80
Q

management of pancreatitis

A
  1. IV fluids
  2. analgesia
  3. bowel rest and TPN
  4. surgery if complications
81
Q

cause of wilsons disease

A

autosomal recessive - mutation in ATB7B on chromosome 13

copper not able to transferred intracellularly so copper accumulates and deposits leading to liver damage

82
Q

presentation of wilsons disease

A
  1. liver disease, cirrhosis, chronic hepatitis
  2. kayser fleischer rings
  3. asymmetrical tremor (early sign), ataxida, clumsy
  4. mood disorder and personality change (1st presentation)
83
Q

diagnosis of wilsons disease

A

liver biopsy *** - copper deposits
low caeruloplasmin
basal 24 hr urinary excretion of copper elevated

84
Q

management of wilsons disease

A
  1. penicillamine
  2. reduced copper containing food - liver, chocolate, nuts, mushrooms
  3. liver transplant
85
Q

presentation of biliary atresia

A

cholestatic jaundice ** - most common causes in first 3 months life
clay coloured stools
dark urine
hepatomegaly

86
Q

investigations biliary atresia

A
  1. high conjugated bilirubin
  2. HIDA - no excretion of bile ***
  3. USS - absent gallbladder/ irregular outline
  4. high GGT and high ALP
87
Q

management of biliary atresia

A
  1. ursodeoxycholic acid (promotes flow of bile)
  2. fat soluble vitamins
  3. nutrition
  4. kasai surgical procedure *** - performed 60 days post birth
88
Q

what is intussusception

A

proximal bowel telescopes into distal bowel = most commonly ileocaecal junction
present 4 month - 1 y/o, usually boys

89
Q

presentation of intussusception

A

abdominal pain - drawing knees up
red currant jelly stool
palpable abdo pain
vomiting

90
Q

diagnosis of intussusception

A

USS abdomen ** - target lesion

91
Q

management of intussusception

A
  1. NG tube on free drainage
  2. NBM
  3. IVF
  4. triple antibiotics
  5. surgery = rectal air enema **
    complication = perfroation and pneumoperitoneum -> immediate needle compression
92
Q

presentation of appendicitis

A

abdo pain : peri umbilical _. RIF
rosvings sign : pain in RIF on palpation of LLQ
psoas sign : pain on extension of right hip whilst laid on left
fever
vomiting
anorexia

93
Q

causes of constipation

A

poor fluid intake
low fibre diet
child behaviour
ADHD
medications
medical conditions e.g. coeliac, hypothyroidm, CMPA, spina bifida

94
Q

management of constipation

A
  1. conservative - increase fluid intake, reward system, increase fibre
  2. if impacted stool (faecal mass/ overflow) -> movicol disimpaction regime
  3. can add stimulatnt e.g. senna, bisacodyl. picosulfate
  4. surgical - appendicostomy for anterior continence enemas
95
Q

transmission of hepatitis

A

hep A - faecal oral route
hep B - vertical or blood
hep c - blood and bodily fluids

96
Q

presentation of hepatitis

A

hep A - self resolve, dont progress to chronic disease
Hep B - most self resolve, jaundice, abdo pain, N&v
Hep c - 80% progress to chronic infection and 50% develop chronic liver disease

97
Q

vaccination of heb B serology

A

hep B surface antibodies +ve

98
Q

acute infection Heb B serology

A

core antibody IgM +ve
surface antigen +ve
high ALT in immune clearance phase

Hep B e antigen = high level of virus

99
Q

chronic infection Heb B serology

A

core antibody IgG +ve
surface antigen +ve

100
Q

inheritance of gilbert syndrome

A

autosomal recessive
mutation in UGT1A1 gene on chromosome 2q27 which is responsible for conjugation of bilirubin

101
Q

gilbert syndrome presentation

A

incidental finding on LFT
mild jaundice at time of stress/ cold/ illness/ alcohol/ dehydration

102
Q

investigations gilbert syndrome

A

bilirubin (80-90
FBC normal

103
Q

causes of jaundice <24 hours old

A
  1. sepsis **
  2. ABO incompatability *
  3. rhesus haemolytic disorders
  4. G6PD deficiency, spherocytosis
  5. congenital infections - conjugated
104
Q

causes of jaundice 2 days - 2 weeks of age

A
  1. infection - sepsis, toxoplasmosis, UTI
  2. breast milk jaundice ***
  3. physiological - low glucoronyl transferance levels, low UDPT, low ligandin
  4. dehydration
  5. crigler najjar syndrome - absence of glucornyl transferase
105
Q

causes of prolonged jaundice (> 2 weeks)

A

UNCONJUGATED **
1. haemolytic anaemia e.g. sickle cell, thalasaaemia
2. hypothyroid
3. infection
4. CF
5. breast milk

CONJUAGTED
1. viral hepatitis
2. biliary atresia
3. neonatal hepatitis
4. alagille syndrome - bile duct malformation, dysmorphic, pulomonary stenosis, butterfly vertebra
5. alpha 1 anti trypsin deficiency

106
Q

presentation of kernicterus

A

build up of unconjugated bilirubin can cross blood brain barrier

athetoid cerebral palsya
hearing loss
paralysis
upward gaze
dental dysplasia
learning disability

107
Q

signs of conjugated jaundice

A

pale stools (lack of stercobilin)
dark urine

108
Q

tests for jaundice

A
  1. split bilirubin levels
  2. FBC
  3. urine MC&s
  4. TFTs
  5. viral screen
  6. blood group and DCT
109
Q

side effects with exchange transfusion

A

hyperkalaemia
catheter related complications - emboli, acidosis, hypocalcaemia
hypo/ hyper glucose
haemodynamic instabolity

110
Q

short gut syndrome complications

A
  1. osmotic or secretory diarrhoea
  2. abdo distesnion
  3. foul smelling stool
  4. flatulences
  5. fat soluble vitamin and vit B12 deficiency
111
Q

ileum function

A
  1. majority of water absorbed here
  2. bile acids absorbed - help fat absorotion inc fat soluble vitamins
  3. B12 absorption (terminal ileum)
112
Q

vit A deficiency signs

A

night blindness
dry eyes, corneal ulceration
hyperkeratosis
immune dysfunction
growth failure

113
Q

vit D deficiency signs

A

ricket - muscle weakness, growth retardation, skeletal deformities (genu varum)

114
Q

vit E deficiency signs

A

neuroaxonal degeneration -> ataxia
progressive neuropathy
retinopathy

115
Q

vit K deficiency

A

deranged coagulation - Fcator VII, IX,X), bleeding

116
Q

laxative abuse finding on colonoscopy

A

dark brown pigmentation of colonic mucosa = melanosis coli and pigment laden macrophages

117
Q

breakdown of haemoglobin produces..

A

haem + globin

haem broken down to carbon monoxide and bilverdin which turned into bilirubin

118
Q

treatment for giardia infection

A

metronidazole

steattorhoea, watery diarrhoea, nutrient deficiency

119
Q

tests for lactose intolerance

A

hydrogen detected in breath
stool sample within 1-2 hours of ingestion

120
Q

diagnosis of CMPA IGE mediated

A

skin prick
blood specific IgE testing

121
Q

management of CMPA

A
  1. if breast feeding, strict maternal cows milk free diet
  2. exclusively hydrolysed formula 2-6 weeks
  3. amino acid based formula
122
Q

marker to measure protein losing enteropathy

A

ALPHA 1 ANTI TRYPSIN
resistant to degradation of proteases
measurement indicates leakage of plasma proteins in the gut

123
Q

presentation of autoimmune hepatitis

A

7-10 y/o
acute hepatitis - jaundice, abdo pain, easy bruising
arthritis
skin rash
presence of auto antibdodies

124
Q

presentation of lymphageictasia

A

= protein losing enteropathy
oedema + diarrhoea

125
Q

bloods of refeeding syndrome

A

hypokalaemia
hypophosphateaemia
hypomagnesium
normal Na and Ca

126
Q

Mechanism of action fo PPI

A

inhibit gastric acid secretion by inhibiting H+/K+ ATP pump in gastric parietal cell

127
Q

mechanism of phototherapy in eczema

A

targets inflammatory cells, alters cytokine production and antimicrobial

127
Q

calories in breast milk

A

70 Kcl/100 mls
high in vit A

128
Q

BMI diagnosis of obesity

A

BMI >98TH CENTILE = OBESE
BMI >91ST CENTILE = OVERWEIGHT

129
Q

Management of umbilical hernia

A

usually resolves by 1 y/o
surgery at 3-4 y/o

130
Q

role of GGT

A

enzyme involved in glutathione metabolsim and acts as transporter molecule and assists in lievr metabolism

131
Q

role of prebiotics

A

non digestable food products that stimulate growth + activity of bacteria in digestive system

132
Q

signs of vitamin C deficiency

A

curly hair
petechiae and bruising
lethargy
gingivitis
impaired wound healing

133
Q

signs of zinc deficiency

A

poor wound healing
eczmea, nappy rashes, dry scaling skin
increased risk of infections
oral ulcers and stomatitis
tremor, nystagmus
delayed puberty
chronic diarrhoea

134
Q

where is zinc found

A

red meat, oysters, poultry, beans and nuts
stored in skeletal muscle and bone

135
Q

causes of B12 deficiency

A
  1. vegan diet (found in meat, fish, eggs)
  2. intrinsic factor deficiency (absorbed in distal ileum) - pernicious anaemia (autoimmune)
  3. toddlers diarrhoea
  4. malabsorption e.g. coeliac, IBD
136
Q

signs of B12 deficiency

A

failure to thrive, lethargy
peripheral neuropathy
developmental d=regression
glossitis (beefy red tongue)
depression
subacute combined degeneration of the cord

137
Q

where is iron absorbed

A

jejunum
- give with vit C to help absorption
- excessive zinc can reduce absorption

138
Q

signs of B1 deficiency (thiamine)

A

peripheral neuritis
reduced tendon reflexes
loss of vibration sense
muscular cramps
restless
soundless cry

139
Q

what should be monitored when starting tPN

A
  1. glucose in first 1- 2 hours of starting TPN
  2. potassium, chloride, ph and calcium measured daily when starting TPN
  3. LFT weekly
140
Q

presentation of kwashiokor

A

protein energy malnutrition (calorie intake adequate)

oedematous
muscular atrophy
hepatomegaly

141
Q

hormone changes in anorexia

A
  • elevated circulating cortsiol
  • reduced T3, NORMAL TSH
  • reduced FSH/LH
  • increased resting GH
  • reduced GnRH
  • reduced oestrogen
142
Q

histology of cows milk enteropathy

A

patchy enteropathy with mild disturnace of crypt villous architecture, mucosal lymphocytes and increased eosinophils

143
Q

histology of lymphangiectasia

A

dilated ectatic villous lacteals with distortion of villi (normal length) and no inflammatory markers

144
Q

histiological findings of biliary atresia

A

bile duct proliferation
fibrosis
portal duct oedema
fibrosis
inflammation
bile duct bile plugs

FOP/TAS (12 decks)

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