Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Paediatrics (Y4) > 13- Paediatric surgery (2/2) > Flashcards

13- Paediatric surgery (2/2) Flashcards

1
Q

pyloric stenosis background

A
  • Progressive hypertrophy of pyloric muscle, causing gastric outlet obstruction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

pyloric stenosis pathophysiology

A

Pathophysiology
- Aetiology unknown
- The pyloric sphincter is a ring of smooth muscle the forms the canal between the stomach and the duodenum.
- Hypertrophy (thickening) and therefore narrowing of the pylorus is called pyloric stenosis.
- This prevents food traveling from the stomach to the duodenum as normal.
- After feeding, there is increasingly powerful peristalsis in the stomach as it tries to push food into the duodenum.
- Eventually it becomes so powerful that it ejects the food into the oesophagus, out of the mouth and across the room- This is called “projectile vomiting”.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

risk factors of pyloric stensosis

A

**- Male
- Family history
**

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

presentation of pyloric stenosis

A
  • Presents in first few weeks of life (4-6 weeks)
  • Failure to thrive : weightloss and dehydration
  • Non-bilious projectile vomiting after feeds
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

pyloric stenosis on examination

A

o Peristalsis can be seen by observing abdomen
o Firm, round mass -> like a large olive (hypertrophic muscles of pylorus)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

investigations for pyloric stenosis

A
  • Abdominal US -.> thickened pylorus
  • Blood gas- classic would be metabolic alkalosis (hypochloraemaic hypokalaemia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

why hypochloraemic hypoklaemia in PS

A

metabolic alkalosis as the baby is vomiting HCL from stomach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

management of pyloric stenosis

A
  • Rehydration to correct metabolic abnormalities
  • Laparoscopic pyloromyotomy (Ramstedts operation)
    o Incision is made in the smooth muscle of the pylorus to widen canal allowing food to pass from stomach to duodenum as normal
  • Excellent prognosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Oesophageal atresia (OA) and trachea-oesophageal fistula (TOF) background

A
  • Rare birth defect which occurs when the upper part of the oesophagus doesn’t connect with the lower oesophagus and stomach
  • Usually ends in a pouch
  • Means baby cant swallow safely, if at all
  • Can develop complications such as chocking and pneumonia
  • Trachea-oesophageal fistula
    Can occur alongside oesophageal atresia.
    Connects the lower part of the oesophagus with the trachea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

risk factors for oesophageal atresia (OA)

A
  • Babies who’s mother had polyhydramnios
  • More common in babies who have development problems with their kidneys, heart and spine
  • Trisomy 18 and 21
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

complications of oesophageal atresia

A
  • Air passed from the windpipe to the oesophagus and stomach -> bowel perforation due to air in the stomach and bowel
  • Stomach acid passes into the lungs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

presentation of OA

A

Presentation
- May be suspected on antenatal US
- Cannot swallow and will drool copious amounts of salvia
- Aspiration of saliva or milk
o Aspiration pneumonitis
- Can lead to acute gastric perforation
- Vomiting
- Blue tinged skin while feeding
- Rounded abdomen
- Failure to thrive – air in stomach and bowels due to trachea-oesophageal fistula

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

investigations for OA

A
  • Xray
  • Bronchoscopy
  • Oesophagoscopy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

management of OA

A
  • Will require operation in first few days of life to remove any connection between the oesophagus and trachea and have the two pouches of the oesophagus joined
  • Nutrition will be IV
  • Suction tube placed nasally to remove fluid from the pouch in oesophagus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

signs of OA on X-ray

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

types of OA and trachea-oesophageal fistula (TOF)

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

biliary atresia background

A
  • Congenital condition where section of bile duct is either narrowed or absent
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

pathophysiology of biliary atresia

A
  • Lack of bile duct causes causes cholestasis
  • Bile cannot be transported from the liver to the bowel
  • Conjugated bilirubin excreted in bile, therefore biliary atresia prevention excretion of conjugated bilirubin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

presentation of biliary atresia

A

Shortly after birth with
- Significant jaundice
- High conjugated bilirubin
- Suspect in babies with persistent jaundice >14 days in term babies and 21 days in prem babies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

investigations for BA

A

Conjugated and unconjugated bilirubin
- High proportion of conjugated suggest liver is processing bilirubin for excretion (by conjugating it), but it is not able to be excreted into the bowel

Hepatic scintigraphy radioisorope scan: Fibrosis of biliary tree

This infant with prolonged jaundice, dark urine, chalky-white stool and conjugated hyperbilirubinaemia is suspicious for an obstructive cause of jaundice. The results of the hepatic scintigraphy radioisotope scan (highlights the liver and not the bowel) is suspicious for biliary atresia. Biliary atresia is characterized by progressive fibrosis and destruction of the biliary tree

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

management of biliary atresia

A
  • Surgery: Kasai portoenterostomy
    Involved attaching a section of the small intestine to the opening of the liver, where the bile duct normally attaches
  • Definititive :full liver transplant
22
Q

Testicular torsion
Background

A
  • Occurs when the spermatic cord and its contents twists within the tunica vaginalis, compromising blood supply to the testicle
  • Surgical emergency due to infarct
  • Peak incidence 12-25 yo
23
Q

Pathophysiology of TT

A
  • Torsion occurs when a mobile testis rotates on the spermatic cord. This leads to reduced arterial blood flow, impaired venous return, venous congestion, resultant oedema and infarction to the testis if not corrected.
  • Males with a horizontal lie to their testes, often termed a ‘bell-clapper deformity’, are more prone to developing testicular torsion.
  • In this anatomical variant, the testislacks a normal attachment to the tunica vaginalis and is therefore more mobile, increasing the likelihood of it twisting on the cord structures.
24
Q

Risk factors of TT

A
  • Age
  • Previous testicular torsion
  • Family history
  • Bell clapper deformity
  • Undescended testes
25
Q

Presentation of TT

A
  • Sudden onset severe unilateral testicular pain
  • Nausea and vomiting due t pain
  • Testis have a high position
  • Lack of cremasteric reflex
  • Pain continues despite elevation of the testicle – negative Prehns sign
26
Q

Differentials of TT

A
  • Epididymo-orchitis
  • Gradual onset of pain can be associated with LUTS/ and/ or pyrexia
  • Torsion of the hydatic of Morhagni
27
Q

investigations for TT

A
  • Clinical diagnosis
  • Doppler US can be used to investigate for blood flow
  • Urine dipstick – potential infective component
28
Q

management of TT

A
  • Surgery within 4- 6 hours to salvage testis before ischaemic damage
  • Analgesia and anti-emetics, nill by mouth and maintenance fluids prescribed
  • Surgery: bilateral orchidopexy – cord and testis untwisted and both testicles fixed to the scrotum
    Complications
29
Q

complications of TT

A
  • Chronic pain
  • Infertility
  • Theoretical risk of future torsion despite fixation
30
Q

Neonatal Testicular Torsion

A

In neonates the attachment between the scrotum and tunica vaginalis is not fully formed and the entire testis and tunica vaginalis can tort; this is known as ‘extra-vaginal torsion’.
It is important to note that this can occur in-utero and new-borns must be thoroughly examined at their first check. Almost all other torsions will be ‘intra-vaginal’, with the freely moving cord and testis torting within the tunica vaginalis.

31
Q

undescended testes background

A
  • Testes which are not found in the testes
  • 5% of boys don’t have descended testes by birth
  • Can also be called cryptorchidism
  • The longer it takes for testes to descend, the less likely it is they will descend spontaneously
32
Q

pathophysiology of undescended testes

A
  • Testes develop in the abdomen and then gradually migrate down, through the inguinal canal into the scrotum.
  • Usually testes have reached the scrotum prior to birth
33
Q

risk factors of undescended testes

A
  • Family history of undescended testes
  • Low birth weight
  • Small for gestational age
  • Prematurity
  • Maternal smoking during pregnancy
34
Q

complications of undescended testes

A

Complications
- Testicular torsion
- Infertility
- Testicular cancer

35
Q

presentation of undescended testes

A
  • May be palpable in the inguinal canal (inguinal region) -> if partially descended
36
Q

management of undescended testes

A
  • Newborns: watch and weight (most will descend in first 3-6 months)
  • > 6 months: see urologist
    o Orchidopexy (surgical correction of undescended testes) – 6-12 months
37
Q

epidiymo-orchitis background

A
  • Epididymitis is inflammation of the epididymis
  • Orchitis is inflammation of the testicle
  • Usually caused by an infection in the epididymis and testicle on one side
38
Q

physiology of orchitis

A
  • At the back of each testicle is the epididymis.
  • Sperm are released from the testicle, into the head of the epididymis, connected at the top of the testicle.
  • The sperm travel through the head, then body, then tail of the epididymis.
  • Sperm mature and are stored in the epididymis.
  • The epididymis drains into the vas deferens.
39
Q

causes of orchitis

A

Causes
- Escherichia coli (E. coli)
- Chlamydia trachomatis (STI)
- Neisseria gonorrhoea (STI)
- Mumps

Need to distinguish whether likely to be an enteric organism (e.coli) or STI (chlam or gon). STI more likely if
* Age under 35
* Increased number of sexual partners in the last 12 months
* Discharge from the urethra

40
Q

presentation of orchitis

A

Presentation
Gradual onset over mins to hours.
* Testicular pain
* Dragging or heavy sensation
* Swelling of testicle and epididymis
* Tenderness on palpation, particularly over epididymis
* Urethral discharge (should make you think of chlamydia or gonorrhoea)
* Systemic symptoms such as fever and potentially sepsis

41
Q

investigations for orchitis

A
  • Urine microscopy, culture and sensitivity (MC&S)
  • Chlamydia and gonorrhoea NAAT testing on a first-pass urine
  • Charcoal swab of purulent urethral discharge for gonorrhoea culture and sensitivities
  • Saliva swap for PCR testing for mumps, if suspected
  • Serum antibodies for mumps, if suspected (IgM – acute infection, IgG – previous infection or vaccination)
  • Ultrasound may be used to assess for torsion or tumours
42
Q

Epididymo-orchitis vs testicular torsion

A

The key differential diagnosis for epididymo-orchitis is testicular torsion. Testicular torsion is a urological emergency that requires rapid treatment to avoid the testicle dying. Both present similarly, with acute onset of pain in one testicle. If there is any doubt, treat it as testicular torsion until proven otherwise.

43
Q

general management of orchitis

A
  • If patient very unwell or septic- IV antibiotics
  • Supportive measures
    o Analgesia
    o Supportive underwear
    o Reduce physical activity
    o Abstain from intercourse
44
Q

orchitis: STI likely

A

o Refer to GUM for assessment and treatment with Abx
o E.g. IM ceftriaxone
o Doxycycline
o Ofloxacin

45
Q

orchitis: E.coli more likely

A

o Ofloxacin for 14 days
 A quinolone
* Tendon damage e.g. Achilles tendon
* Lower seizure threshold
o Levofloxacin for 10 days
o Co-amoxiclav for 10 days (where quinolones are contraindicated)

46
Q

Hirschsprungs backgorund

A

Hirschsprung’s disease is a congenital condition that affects the large intestine (colon) and causes problems with passing stool. The condition is present at birth (congenital) as a result of missing nerve cells in the muscles of the baby’s colon. Without these nerve cells stimulating gut muscles to help move contents through the colon, the contents can back up and cause blockages in the bowel.

Divided into
- Short segment
- Long segment

47
Q

pathophysiology behind Hirshsprungs

A
  • Nerve cells of myenteric plexus (Auerbach’s) are absent in the distal bowel and rectum
    -> Auerbach’s forms the enteric nervous system – brain of the gut
  • Auerbach’s runs all the way along the bowel in the bowel war and is a complex network of neurones, ganglion cells, receptors, synapses and NT
    -> Causes peristalsis of the large bowel
    -> Without this stimulation -> bowel loses motility and food cannot pass food along

**- Key pathology: **absence of parasympathetic ganglion cells – responsible for peristalsis

  • Foetal development of the parasympathetic ganglion cells
    -> During fetal development these start in the upper GI tract and gradually migrate down the distal colon and rectum -> in Hirschsprung’s these cells do not travel all the way down the colon- therefore a section of the colon is left without these parasympathetic ganglion cells
    -> Aganglionic sections of the colon cannot relax-> therefore become constricted
    ->Proximal bowel will become distended and full
48
Q

risk factors for hirschsprungs

A
  • Risk factors- genetic associations
  • Family history
  • Doesn’t usually occur in isolation: Down Syndrome, neurofibromatosis, Waardenburg syndrome, MEN type II
49
Q

presentation of Hirschsprungs

A
  • Delay in passing meconium >24hrs
  • Chronic constipation since birth
  • Abdominal pain and distention
  • Vomiting
  • Poor weight gain and failure to thrive
50
Q

investigations for Hirschsprungs

A

Investigations
- Abdominal x-ray
o Intestinal obstruction
- Rectal biopsy
o Confirms diagnosis
o Bowel histology will show absence of
ganglionic cells

51
Q

management of Hirschsprungs

A

Unwell child
- Fluid resus and management of obstruction.
- Abx if Hirschsprung’s associated enterocolitis

Definitive management
- Surgical resection of a ganglionic section of bowel
- Most patients live normal life after surgery
- May be left with some degree of incontinence

Paediatrics (Y4) (42 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions