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3ayeeeee > Paeds Gastro > Flashcards

Paeds Gastro Flashcards

1
Q

What is the cause of jaundice in the first 24 hours ?

A
  • Pathological
  • Rhesus haemolytic disease
  • ABO haemolytic disease
  • Hereditary spherocytosis
  • Glucose-6-phosphodehydrogenase
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2
Q

What is the cause of jaundice 2-14 days post birth ?

A
  • Very common (40%) of baby and usually due to a combination of factors including more red blood cells, more fragile red blood cells and less developed liver function
  • More commonly seen in breastfed babies
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3
Q

When does prolonged jaundice occur ?

A
  • After 14 days
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4
Q

What are the causes of prolonged jaundice ?

A
  • Biliary atresia
  • Hypothyroidism
  • Galactosaemia
  • UTI
  • Breast milk jaundice
  • Prematurity – due to immature liver function
  • Congenital infections e.g. CMV
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5
Q

What is the risk with jaundice and prematurity ?

A
  • Kernicterus
  • Brain damage occurring as a result toxic levels of unconjugated bilirubin
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6
Q

How is pathological jaundice managed ?

A
  • Phototherapy
  • Exchange transfusion
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7
Q

What is necrotising enterocolitis ?

A
  • A life threatening emergency caused by death of the bowel tissue
  • Surgical emergency which could lead to peroration, peritonitis and shock
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8
Q

RFs for necrotising enterocolitis ?

A
  • Very low birth weight or premature
  • Formula feeds
  • Respiratory distress and assisted ventilation
  • Sepsis
  • PDA or other congenital heart defects
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9
Q

Presentation of necrotising enterocolitis

A
  • Feeding intolerance
  • Abdominal distension
  • Bloody stools
  • Quickly progresses to abdominal discolouration, perforation and peritonitis
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10
Q

X-ray signs of necrotising enterocolitis

A
  • Dilated bowel loops
  • Bowel wall oedema
  • Pneumatosis intestinalis
  • Portal venous gas
  • Air both inside and outside the bowel (Rigler sign)
  • Air outlining the falciform ligament (football sign)
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11
Q

Investigations for necrotising enterocolitis

A
  • FBC – thrombocytopenia and neutropenia
  • CRP – inflammation
  • Capillary BG – metabolic acidosis
  • Blood cultures – for sepsis
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12
Q

Management for necrotising enterocolitis

A
  • If suspected then nil by mouth, IV fluids and total parenteral nutrition and ABs to stabilize
  • NG tube can drain fluid from stomach and intestines
  • Surgical emergency
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13
Q

Complications of necrotising enterocolitis

A
  • Sepsis
  • Death
  • Perforation and peritonitis
  • Abscess formation
  • Recurrence
  • Long term stoma
  • Short bowel syndrome
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14
Q

Why are babies more susceptible to GORD ?

A
  • Immaturity of the lower oesophageal sphincter, allowing stomach contents to more easily reflux
  • Reflux in babies is normal provided there is normal development
  • Usually improves as babies grow and 90% of infants will stop after 1 year
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15
Q

GORD presentation in babies ?

A
  • Chronic cough
  • Hoarse cry
  • Distress, crying or unsettled after feeding
  • Reluctance to feed
  • Pneumonia
  • Poor weight gain
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16
Q

GORD presentation in infants over 1 year

A
  • Similar to adults
  • Heartburn
  • Acid regurgitation
  • Retrosternal or epigastric pain
  • Bloating and nocturnal cough
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17
Q

DDs of vomiting in infants

A
  • Overfeeding
  • GORD
  • Pyloric stenosis
  • Gastritis or gastroenteritis
  • Appendicitis
  • Infections such as UTI, tonsilitis or meningitis
  • Intestinal obstruction
  • Bulimia
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18
Q

Vomiting red flags

A
  • Not keeping down any feed
  • Projectile vomiting or forceful vomiting
  • Bile stained
  • Haematemesis or melaena
  • Abdominal distention
  • Reduced consciousness, bulging fontanelle or neurological signs
  • Respiratory symptoms
  • Blood in stools
  • Signs of infection
  • Rash, angioedema or other signs of allergy
  • Apnoeas – serious cardiac pathology
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19
Q

GORD management

A
  • Simple = explanation, reassurance and practical advice – small frequent meals, burping, not-over-feeding, keep the baby upright after feeding
  • More problematic = Gaviscon mixed with feeds, thickened milk or formula, PPIs
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20
Q

What is Sandifer’s syndrome ?

A
  • Rare condition causing brief episodes of abnormal movements associated with gastro-oesophageal reflux in infants
  • The infants are usually neurologically normal
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21
Q

What are key features of Sandifer’s syndrome ?

A
  • Torticollis – forceful contractions of the neck muscles causing twisting of the neck
  • Dystonia – abnormal muscle contractions causing twisting movements, arching of the back or unusual posture
  • Tends to resolve as reflux is treated or improves
  • Generally the outcome is good
  • DD is infantile spasms and seizures so it is worth referring for specialist assessment
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22
Q

What is pyloric stenosis ?

A
  • Hypertrophy (thickening) and therefore narrowing of the pylorus a ring of smooth muscle that forms the canal between the stomach and the duodenum
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23
Q

Epidemiology of PS ?

A
  • 4 per 1000
  • 4x more common in males
  • 10-15% of infants have a positive family history
  • 1st borns more commonly affected
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24
Q

Features of Pyloric Stenosis ?

A
  • Projectile vomiting typically 30 minutes after a feed
  • Constipation and dehydration may also be present
  • A palpable olive sized mass may be present in the upper abdomen
  • Hyperchloremic hypokalemic acidosis due to persistent vomiting
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25
Q

How is PS diagnosed and managed ?

A
  • US
  • Ramstedt pyloromyotomy
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26
Q

What is Gastroenteritis ?

A
  • Gastroenteritis = inflammation all the way from the stomach to the intestines and presents with nausea, vomiting and diarrhoea
  • Very common in children MCC is viral
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27
Q

DDs of gastroenteritis

A
  • Infection
  • IBD
  • Lactose intolerance
  • Coeliac disease
  • CF
  • Toddler’s diarrhoea
  • IBS
  • Medications e.g. antibiotics
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28
Q

MCC of gastroenteritis

A
  • Rotavirus
  • Norovirus
  • (E.coli less common associated with bloody diarrhoea)
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29
Q

Principles of gastroenteritis management

A
  • Patient isolation, barrier nursing and infection control
  • Stay off school 48 hours or until symptoms have completely resolved
  • Stool microscopy, culture and sensitivities
  • Maintain hydration and attempt fluid challenge
  • If can handle PO fluids then send home otherwise IV hydration
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30
Q

DDs for constipation in infant

A
  • Idiopathic or functional
  • Hirschsprung’s
  • CF
  • Hypothyroidism
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31
Q

Constipation presentation

A
  • Less than 3 stools a week
  • Hard stools that are difficult to pass
  • Rabbit dropping stools
  • Straining and painful passages of stools
  • Abdominal pain
  • Holding an abnormal posture, referred to as retentive posturing
  • Rectal bleeding associated with hard stools
  • Faecal impaction causing overflow soiling, with incontinence of particularly loose smelly stools
  • Hard stools may be palpable in abdomen
  • Loss of the sensation of the need to open the bowels
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32
Q

What is encopresis ?

A
  • A term for faecal incontinence
  • Not considered pathological until 4 years of age
  • Usually a sign of chronic constipation where the rectum becomes stretched and looses sensation
  • Large hard stools remain in the rectum and only loose stools are able to bypass the blockage and leak out causing soiling
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33
Q

Conditions that can present with encopresis ?

A
  • Spina bifida
  • Hirschsprung’s disease
  • Cerebral palsy
  • Learning disability
  • Stress and abuse
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34
Q

Lifestyle factors that can contribute to constipation

A
  • Habitually not opening the bowels
  • Low fibre diet
  • Poor fluid intake and dehydration
  • Sedentary lifestyle
  • Psychosocial problems such as a difficult home or school environment (always keep safeguarding in mind)
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35
Q

Constipation red flags

A
  • Not passing meconium within 48 hours of birth (cystic fibrosis or Hirschsprung’s disease)
  • Neurological signs or symptoms, particularly in the lower limbs (cerebral palsy or spinal cord lesion)
  • Vomiting (intestinal obstruction or Hirschsprung’s disease)
  • Ribbon stool (anal stenosis)
  • Abnormal anus (anal stenosis, inflammatory bowel disease or sexual abuse)
  • Abnormal lower back or buttocks (spina bifida, spinal cord lesion or sacral agenesis)
  • Failure to thrive (coeliac disease, hypothyroidism or safeguarding)
  • Acute severe abdominal pain and bloating (obstruction or intussusception)
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36
Q

Complications of constipation

A
  • Pain
  • Reduced sensation
  • Anal fissures
  • Hemorrhoids
  • Overflow and soiling
  • Psychosocial morbidity
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37
Q

Management of constipation

A
  • Correct any reversible contributing factors, recommend a high fibre diet and good hydration
  • Start laxatives (movicol is first line)
  • Faecal impaction may require a dis-impaction regimen with high doses of laxatives at first
  • Encourage and praise visiting the toilet. This could involve scheduling visits, a bowel diary and star charts.
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38
Q

When is peak incidence for appendicitis ?

A
  • 10-20 years
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39
Q

How does appendicitis classically present ?

A
  • Abdominal pain that starts centrally and then moves down to the right iliac fossa over time
  • On palpation the abdomen is tender in McBurney’s point (one third the distance from the anterior superior iliac spine (ASIS) to the umbilicus
  • Rovsing’s sign (palpation of the left iliac fossa causes pain in the RIF)
  • Rebound tenderness is increased pain when quickly releasing pressure on the right iliac fossa
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40
Q

How is diagnosis of appendicitis made ?

A
  • Based on the clinical presentation and raised inflammatory markers
  • Performing a CT scan be useful in confirming the diagnosis, particularly where another diagnosis is more likely
  • US scan is often used in female patients to exclude ovarian or gynecological pathology
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41
Q

Key DDs for appendicitis

A
  • Ectopic pregnancy
  • Ovarian cysts
  • Meckle’s Diverticulum
  • Mesenteric Adenitis
  • Appendix mass
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42
Q

Management of appendicitis

A
  • Urgent admission to hospital under the surgical team
  • Removal of the inflamed appendix (appendicectomy) is the definitive management for acute appendicitis.
  • Laparoscopic surgery is associated with fewer risks and faster recovery compared to open surgery (laparotomy).
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43
Q

Complications of appendicectomy

A
  • Bleeding, infection, pain and scars
  • Damage to bowel, bladder or other organs
  • Removal of a normal appendix
  • Anesthetic risks
  • VTE
44
Q

Which 2 conditions are included in IBD

A
  • Ulcerative colitis
  • Crohn’s disease
45
Q

Pneumonic for Crohn’s disease ?

A
  • N = no blood or mucus
  • E = entire GI tract
  • S = skip lesions on endoscopy
  • T = Terminal ileum most affected and Transmural (full thickness) inflammation
  • S = Smoking is a RF (don’t set the nest on fire)
46
Q

Pneumonic for ulcerative colitis ?

A
  • C = continuous inflammation
  • L = limited to the colon and rectum
  • O = only the superficial mucosa
  • S = smoking is protective
  • E = excrete blood and mucus
  • U = use aminosalicylates
  • P = primary sclerosing cholangitis
47
Q

How would children with IBD present ?

A
  • Children and teenagers present with perfuse diarrhoea, abdominal pain, bleeding, weight loss or anaemia
  • They may be systemically unwell during flares with fevers and dehydration
48
Q

How would extra-intestinal manifestations of IBD present in children ?

A
  • Finger clubbing
  • Erythema nodosum
  • Pyoderma gangrenosum
  • Episcleritis and iritis
  • Inflammatory arthritis
  • Primary sclerosing cholangitis (ulcerative colitis)
49
Q

How would a child be investigated for IBD

A
  • FBC, infection screening, TFT, LFT, KFT
  • Faecal calprotectin = 90% sensitive
  • Endoscopy = gold standard
  • Imaging with US, CT or MRI can look for complications such as fistulas, abscesses and strictures
50
Q

General management for a child with IBD ?

A
  • MDT – pediatricians, specialist nurses, pharmacists, dieticians and surgeons
  • Essential to monitor growth and pubertal development especially when they have exacerbations or are being treated with steroids – this is where input from dietician can help
  • Management involves combination of inducing remission during flares and maintaining remission when well
51
Q

Management of Crohn’s

A
  • Remission – oral prednisolone or IV hydrocortisone 1st line
  • Maintain remission – Azathioprine or mercaptopurine
52
Q

Management of UC – Mild-moderate

A
  • First line: aminosalicylate (e.g. mesalazine oral or rectal)
  • Second line: corticosteroids (e.g. prednisolone)
53
Q

Management of UC – Severe disease

A
  • First line: IV corticosteroids (e.g. hydrocortisone)
  • Second line: IV ciclosporin
54
Q

Maintaining Remission UC

A
  • Aminosalicylate (e.g. mesalazine oral or rectal)
  • Azathioprine
  • Mercaptopurine
55
Q

What is failure to thrive

A
  • Poor physical growth and development in a child
56
Q

What is faltering growth

A
  • A fall in wight across:
  • One or more centile spaces if their birthweight was below the 9th centile
  • Two or more centile spaces if their birthweight was between the 9th and 91st centile
  • Three or more centile spaces if their birthweight was above the 91st centile
57
Q

Causes of failure to thrive

A
  • Inadequate nutritional intake
  • Difficulty feeding
  • Malabsorption
  • Increased energy requirements
  • Inability to process nutrition
58
Q

Causes of inadequate nutritional intake (failure to thrive)

A
  • Maternal malabsorption if breastfeeding
  • Iron deficiency anemia
  • Family or parental problems
  • Neglect
  • Availability of food
59
Q

Causes of Difficulty Feeding (failure to thrive)

A
  • Poor suck, e.g. cerebral palsy
  • Cleft life or palate
  • Genetic conditions with an abnormal facial structure
  • Pyloric stenosis
60
Q

Causes of malabsorption (failure to thrive)

A
  • Cystic fibrosis
  • Coeliac disease
  • Cows milk intolerance
  • Chronic diarrhoea
  • Inflammatory bowel disease
61
Q

Causes of increased energy requirement (failure to thrive)

A
  • Hyperthyroidism
  • Chronic disease e.g. congenital heart defect or cystic fibrosis
  • Malignancy
  • Chronic infections for example HIV or immunodeficiency
62
Q

Causes of inability to process nutrition

A
  • Inborn errors of metabolism
  • T1DM
  • Glucose-6-phosphate dehydrogenase
63
Q

Hx/assessment of a patient with a failure to thrive

A
  • Pregnancy, birth, developmental and social history
  • Feeding or eating history
  • Observe feeding
  • Mums physical and mental health
  • Parent-child interactions
  • Height, weight and BMI (if older than 2 years) and plotting these on a growth chart
  • Calculate the mid-parental height centile
64
Q

What should be included in a feeding history

A
  • Breast or bottle feeding, feeding times, volume and frequency and any difficulties with feeding. An eating history involves asking about food choices, food aversion, meal time routines and appetite in children. Asking the parent to keep a food diary can be helpful.
65
Q

Investigations for failure to thrive

A
  • Urine dipstick, for urinary tract infection
  • Coeliac screen (anti-TTG or anti-EMA antibodies)
  • TFTs
  • DM
  • FBC
66
Q

Management for inadequate nutrition

A
  • Encouraging regular structured mealtimes and snacks
  • Reduce milk consumption to improve appetite for other foods
  • Review by a dietician
  • Additional energy dense foods to boost calories
  • Nutritional supplements drinks
67
Q

What is Coeliac disease ?

A
  • A condition where exposure to gluten causes an immune reaction that creates inflammation in the small intestine
  • It usually develops early in childhood but can start at any age
68
Q

2 key ABs associated with Coeliac disease ?

A
  • Anti-TTG
  • Anti-EMA
69
Q

Pathophysiology with Coeliac disease ?

A
  • In coeliac disease autoantibodies are created in response to exposure to gluten
  • These autoantibodies target the epithelial cells of the intestine and lead to inflammation
  • It causes atrophy of the intestinal villi. particularly the jejunum.
  • Damage to the villi causes malabsorption of nutrients and disease related symptoms
70
Q

Symptoms that could suggest coeliac

A
  • Failure to thrive in young children
  • Diarrhoea
  • Fatigue
  • Weight loss
  • Mouth ulcers
  • Anaemia secondary to iron, B12 or folate deficiency
  • Dermatitis herpetiformis is an itchy blistering skin rash that typically appears on the abdomen
  • Neurological (Rare) Peripheral neuropathy, Cerebellar ataxia, Epilepsy
71
Q

What other condition are all new T1DM patients tested for ?

A
  • Coeliac disease
72
Q

Investigations to confirm coeliac disease ?

A
  • Must be carried out on a patient whist they remain a diet containing gluten
  • Check total immunoglobulin A levels to exclude IgA deficiency
  • Raised anti-TTG (1st line)
  • Raised anti-EMA
73
Q

Endoscopy and intestinal biopsy findings for coeliac disease

A
  • “Crypt hypertrophy”
  • “Villous atrophy”
74
Q

Other conditions associated with coeliac ?

A
  • Type 1 diabetes
  • Thyroid disease
  • Autoimmune hepatitis
  • Primary biliary cirrhosis
  • Primary sclerosing cholangitis
  • Down’s syndrome
75
Q

Complications of Coeliac disease

A
  • Vitamin deficiency
  • Anaemia
  • Osteoporosis
  • Ulcerative jejunitis
  • Enteropathy-associated T-cell lymphoma (EATL) of the intestine
  • Non-Hodgkin lymphoma (NHL)
  • Small bowel adenocarcinoma (rare)
76
Q

What is Hirschsprung’s ?

A
  • A congenital condition where the parasympathetic ganglion nerve cells of the myenteric plexus are absent in the distal bowel and rectum
  • The myenteric plexus is responsible for stimulating peristalsis of the large bowel and without the stimulation the bowel looses mortality and stops being able to pass food along its length leading to functional obstruction
77
Q

What conditions is Hirschsprung’s associated with ?

A
  • Down’s syndrome
  • Neurofibromatosis
  • 3 times more common in males
78
Q

How can Hirschsprung’s present ?

A
  • Delay in passing meconium (more than 24 hours)
  • Chronic constipation since birth
  • Abdominal pain and distention
  • Vomiting
  • Poor weight gain and failure to thrive
79
Q

What is Hirschsprung’s associated enterocolitis ?

A
  • Inflammation and obstruction of the intestine occurring in around 20% of neonates with Hirschsprung’s disease
  • 2-4 weeks (old) with fever, abdominal distention, diarrhoea (bloody) and sepsis
  • Life threatening and can lead to toxic megacolon and perforation of the bowel
  • Treat with ABs, fluid resuscitation and decompression of the obstructed bowel
80
Q

How is Hirschsprung’s investigated and managed ?

A
  • Rectal biopsy is gold standard
  • Histology will show an absence of ganglionic cells
  • Abdominal X-ray can show the initial obstruction
  • Definitive management if surgical removal of the aganglionic sections of the bowel
81
Q

What is Intussusception ?

A
  • The invagination of one portion of the bowel into the lumen of the adjacent bowel
  • Most commonly around the ielo-caecal region
82
Q

How is most likely to present with intussusception

A
  • Typically affects between 6-18 months old
  • Boys 2x more likely to be affected
83
Q

How does intussusception present ?

A
  • Intermittent, severe, crampy, progressive abdominal pain
  • Inconsolable crying
  • During paroxysm the infant will characteristically draw their knees up and turn pale
  • Vomiting
  • Bloodstained stool – red currant jelly – is a late sign
  • Sausage-shaped mass in the right upper quadrant
84
Q
  1. What conditions is Intussusception associated with ?
A
  • Concurrent viral illness
  • Henoch-Schonlein purpura
  • CF
  • Intestinal polyps
  • Mechel Diverticulum
85
Q

How in intussusception investigated and what would be seen ?

A
  • US
  • Will show target shaped mass
86
Q

How is Intussusception managed ?

A
  • Reduction by air insufflation under radiological control
  • Surgery is 2nd line
87
Q

What are potential complications of Intussusception ?

A
  • Obstruction
  • Gangrenous bowel
  • Perforation
  • Death
88
Q

What is Meckels Diverticulum ?

A
  • A congenital diverticulum of the small intestine
  • The remnant of the omphalomesenteric duct and contains ectopic ileal, gastric and pancreatic mucosa
89
Q

What is the rule of 2s for Meckels Diverticulum ?

A
  • Occurs in 2% of the population
  • Is 2 feet form the ileocecal valve
  • Is 2 inches long
90
Q

How does Meckels Diverticulum present ?

A
  • Abdominal pain mimicking appendicitis
  • Rectal bleeding – MCC cause of painless massive GI bleeding requiring a transfusion in children between the ages 1 and 2 years
  • Intestinal obstruction
91
Q

How is Meckels Diverticulum investigated ?

A
  • If the child is hemodynamically stable with less severe or intermittent bleeding then a Meckel’s scan should be considered
  • Uses 99, technetium pertechnetate which has an affinity for gastric mucosa
92
Q

How is Meckels Diverticulum managed ?

A
  • Removal if narrow neck or symptomatic
  • Options are between wedge excision or formal small bowel resection and anastomosis
93
Q

What are red flags for colic ?

A
  • Persistent or bilious vomiting
  • Severe chronic diarrhoea
  • Fever
  • Rectal bleeding
  • Weight loss or flatering growth
  • Dysphagia
  • Nighttime pain
  • Abdominal tenderness
94
Q

How would you investigate colic ?

A
  • Anaemia – can indicate IBD or coeliac disease
  • Raised ESR or CRP – IBD
  • Raised anti-TTG or anti-EMA – coeliac disease
  • Raised faecal calprotectin – IBD
  • Positive urine dipstick – UTI
95
Q

What is an abdominal migraine ?

A
  • Occurs in children before they develop traditional migraines as they get older
  • Abdominal migraine present with episodes of central abdominal pain lasting more than 1 hour
  • This may be associated with Nausea and vomiting, Anorexia, Pallor, Headache, Photophobia and Aura
96
Q

How is an abdominal migraine treated ?

A
  • Low stimulus environment (quiet, dark room)
  • Paracetamol
  • Ibuprofen
  • Sumatriptan
97
Q

How is an abdominal migraine prevented ?

A
  • Pizotifen, a serotonin agonist
  • Propranolol, a non-selective beta blocker
  • Cyproheptadine, an antihistamine
  • Flunarazine, a calcium channel blocker
98
Q

When does a cow’s milk protein allergy typically present ?

A
  • Occurs in 3-6% of all children
  • Typically presents in the first 3 months of life in formula-fed infants, although rarely it is seen in exclusively breastfed infants
99
Q

What are the features of cow’s milk protein allergy ?

A
  • Regurgitation and vomiting
  • Diarrhoea
  • Urticaria, atopic eczema
  • ‘Colic’ symptoms: irritability, crying
  • Wheeze. Chronic ough
  • Rarely angioedema and anaphylaxis may occur
100
Q

How is diagnosis of cow’s milk protein allergy made ?

A
  • Often clinical e.g. improvement with cow’s milk protein elimination
  • Investigations include
  • Skin prick/patch testing
  • Total IgE and specific IgE (RAST) for Cow’s milk protein
101
Q
  1. How is cow’s milk protein allergy made ?
A
  • If breastfed then eliminate cow’s milk protein from maternal diet, use eHF when breastfeeding stops until 12 months of age
  • If formula-fed – extensively hydrolyzed formula is 1st line
  • Amino-acid-based formula is 2nd line
102
Q
  1. What is the prognosis with cow’s milk protein allergy ?
A
  • CMPI usually resolves in most children
  • If IgE mediated intolerance around 55% will be milk tolerant by the age of 5 years
  • In children with non-IgE mediate intolerance most children will be milk tolerant by the age of 3 years
103
Q

What is biliary atresia ?

A
  • Congenital condition where a section of the bile duct is ether narrowed or absent
  • This results in cholestasis where the bile cannot be transported from the liver tot the bowel
  • Conjugated bilirubin is excreted in the bile, therefore biliary atresia prevents the excretion of conjugated bilirubin
104
Q
  1. How does biliary atresia present ?
A
  • Shortly after birth with significant jaundice due to high conjugated bilirubin levels
  • Suspect biliary atresia in babies with persistent jaundice lasting more than 14 days in term babies and 21 days in premature babies
105
Q
  1. How is biliary atresia investigated ?
A
  • Conjugated and unconjugated bilirubin
  • A high proportion of conjugated bilirubin suggests the liver is processing bilirubin but cannot get rid of it due to bile duct blockage
106
Q
  1. How is biliary atresia managed ?
A
  • Kasai Portoenterostomy – involves attaching a small section of the small intestine to the opening of the liver, where the bile duct normally attaches
  • This is somewhat successful and can clear jaundice and prolong survival
  • Often patients require a full liver transplant to resolve the condition

3ayeeeee (12 decks)

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