HD Flashcards

1
Q

Anterior and posterior divisions of the Internal iliac

A

Anterior division.
- Obturator artery.
- Uterine Artery:
• Goes into a circuit with the ovarian artery (comes directly from the abdominal aorta).
• Gives off the vaginal branch (1/3 of vagina and cervix) and ascending branch (supplies uterus).
- Vaginal Artery (supplies lower 2/3 of vagina).
• Can also be branch of the uterine a.

Posterior Division

  • Superior Gluteal
  • Inferior Pudendal
  • Inferior Gluteal
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2
Q

Lumbar Plexis important branches

A

Femoral: anterior compartment of thigh (L2, 3, 4)

Obturator: medial compartment of thigh (L2, 3, 4)

Genitofemoral: skin of scrotum/cremaster muscle/labium majorum (L1, 2)

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3
Q

Lumbosacral Trunk

A

fibres from L4 and L5 join = lumbosacral trunk, which emerges medial to the psoas, runs inferiorly over the pelvic brim and joins the sacral plexus

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4
Q

Pudendal Nerve to pelvic floor

A

(S2, 3, 4): leaves the pelvis through the greater sciatic foramen and then enters the perineum through the lesser sciatic foramen (goes around the sacrospinous ligament)

Travels through the pudendal canal - also, contains the pudendal artery/vein (IIA).

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5
Q

Pelvic parasympathetic to pelvic floor

A

(S2, S3, S4) to pelvic viscera.

Micturition, defecation, genital erection (point and shoot).

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6
Q

Sympathetic supply to pelvic floor

A

Allows filling of bladder and contraction of internal urethral sphincter (hypogastric), simulates contraction of the seminal vesicles and vas deferens.

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7
Q

Obstetric Anaesthetic Options

A

Spinal Aesthesia: subarachnoid space (L4-L5) - Complete anaesthesia below waist monitoring of uterine contractions

Pudendal Nerve Block:
Peripheral nerve block S2-S4: perineum and lower ¼ vagina - Mother can feel/assist contractions.

Caudal Epidural Block:
Administered to catheter in sacral canal (S1-S5) - Limbs unaffected.

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8
Q

Penis and Ovarian/testes Lymphatic drainage

A

Penis = drained by deeper Inguinal lymph nodes

Ovarian/testes = drained by Preaortic lymph nodes.

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9
Q

Infertility Definition

A

The failure to achieve a clinical pregnancy within 12 months of unprotected sex.

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10
Q

Primary infertility

A

Unable to ever bear a child

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11
Q

Secondary infertility

A

Unable to bear/ability to carry a child following a previous pregnancy

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12
Q

Spermatic Cord contents

A

Contains the vas deferens, testicular artery, genital branch (of the genitofemoral nerve), Pampiniform plexus, lymphatic vessels, tunica vaginalis.

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13
Q

Testes Blood supply and drainage

A

Supply:
Abdominal artery branches to form the gonadal testicular artery

Venous Drainage:
Right testicle = drained by to the inferior vena cava (also lies on the right side)
Left testicle = drained to the left renal vein (a lot longer).

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14
Q

Ovarian Cycle

A

Follicular phase: days 1 to 10
• 5-12 primordial follicles stimulated each month: one grows and matures.
• GnRH secreted from hypothalamus: stimulates anterior pituitary to secrete LH and FSH.
o These stimulates follicle to grow.
• Mature follicle secretes oestrogen.
o Inhibits further LH and FSH secretion by anterior pituitary (negative feedback).
o Stimulates growth of endometrium.

Ovulatory phase: days 11 to 14
• Negative feedback is temporary: oestrogen stimulates HPA resulting in burst of LH and FSH.
o Completion of meiosis I, onset of meiosis II in the oocyte.

Luteal phase: days 15 to 18
• Granulosa cells of mature follicle divide and form the corpus luteum
• Secretes progesterone and oestrogen. Prepares uterine endometrium for implantation

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15
Q

Menstrual Cycle

A
Menstrual phase (day 1-5): 
•	Due to withdrawal of steroid support (oestrogen/progesterone) the endometrium collapses. 
•	Endometrium is shed with blood from ruptured arteries (blood loss: 50-150ml). 
Proliferative phase (day 6-14): 
•	Oestrogen from mature follicle stimulates thickening of the endometrium. 
•	Glands/spinal arteries form. 
•	Oestrogen also causes the growth of progesterone receptors on endometrial cells. 
Secretory phase (day 15-28):
•	Progesterone from corpus luteum: acts on endometrium. Enlargement of glands --> secret mucus and glycogen in preparation for implantation of fertilised oocyte. 
•	No fertilisation = corpus luteum degenerates --> corpus albicans. Progesterone levels fall.
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16
Q

Conception Advice

A

Intercourse throughout the cycle (not just at certain parts)
No smoking, alcohol.
Reduce weight, stress, drugs.
Take folic acid (400mg).

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17
Q

Causes of Infertility

A

Ovulatory Causes (25%)

Tubal and Uterine Causes of Infertility (30%)

Unexplained Fertility

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18
Q

Ovulatory Causes of Infertility

A

Type 1: Hypopituitary failure (anorexia).
Management:
- Increase weight, decrease exercise.
- Consider pulsatile GnRH

Type 2: Hypopituitary dysfunction (e.g. PCOS, hyperprolactinaemia)
Management for HP: bromocriptine

Type 3: Ovarian Failure (premature ovarian failure if under 40 years).
- Involves persistent FSH raised.
Management: donor eggs, alternative parenting.

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19
Q

Polycystic Ovarian Syndrome

A

Diagnostic Criteria:
Clinical hyperandrogenaemia (excessive testosterone)
Oligomenorrhoea (infrequent periods)
Polycystic ovaries on ultrasound.
Menstrual disturbance, acne.
Raised LH with normal FSH, raised testosterone

Management:
First line: Clomiphene or metformin

Second line: combined clomiphene and metformin, laparoscopic ovarian drilling and Gn theraphy.

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20
Q

Tubal and Uterine Causes of Infertility

A

Pelvic Inflammatory Disease:

  • Symptoms (NOTE: may be asymptomatic):
    o Pelvic pain
    o dyspareunia (painful sexual intercourse)
    o fever.
    (Investigate with full blood count and raised ESR).

Caused bacteria and STIs (chlamydia and gonorrhoea).
- Management: antibiotics, rest and abstinence.

Endometriosis
Symptoms:
o Pain
o Dysmenorrhoea (painful menstruation).
o Menorrhagia (abnormally heavy bleeding)
o Dyspareunia (difficult/painful sexual intercourse).

Management
• NSAIDs, COCP, GnRH agonists, surgery

Fibroids
• Benign tumours of smooth muscle of the myometrium (uterine leiomyoma).
o Complain of heavy, regular periods.
• Treated with (COCP), LARCs, surgical.

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21
Q

Male Factors of Infertility

A
  • Testicular (infection, cancer, surgical, congenital and trauma)
  • Azoospermia (absence of motile sperm).
  • Reversal of vasectomy.
  • Ejaculatory problems (retrograde and premature).
  • Hypogonadism.
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22
Q

Assisted Conception

A
Intrauterine Insemination (IUI):
Sperm is separated in lab, removal of slower speed sperm before partner is inseminated - tried 12 cycles before IVF
In-Vitro Fertilisation (IVF):
o	Women under 40 who have not conceived after 2 years of unprotected intercourse
o	Women 40-42 offered one cycle if:
	Never had IVF. 
	6 or more UII cycles.  
	No evidence of low ovarian reserve.

Intracytoplasmic Sperm Injection (ICSI):
• Single sperm injected directly into egg.
• Is offered to:
o Severe deficits in semen quality
o Obstructive and non-obstructive azoospermia.
o Failure of IVF treatment.

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23
Q

Function of the Prostate

A

Makes about 30% of alkaline seminal fluid that contains an anticoagulant (PSA) to that sperm can swim and survive in the female vaginas acidic environment.

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24
Q

Regions of the Prostate

A
Peripheral Zone (PROSTATE CANCER)
Central Zone
Transition Zone (BENIGN PROSTATE ENLARGEMENT)
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25
Q

Testosterone Proliferation and Apoptosis in Benign Prostatic Hyperplasia

A

Stromal cells: converted to estradiol
• Causes stromal cell proliferation (binds to ER alpha).

Epithelial cells: converted to DHT and prevents apoptosis.

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26
Q

Signs and Symptoms of Benign Prostatic Hyperplasia

A
•	Weak/interrupted flow of urine.
•	Frequent urination (nocturia).
•	Trouble urinating.
•	Pain/burning during urination. 
   o	Blood in urine/semen
SHITE = slow stream, hesitancy, intermittent flow, terminal dribbling, emptying incomplete. 
FUN = frequency, urgency, nocturia.
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27
Q

Diagnosis of Benign Prostatic Hyperplasia

A

Diagnosis:
• History
• Digital Rectal Exam (DRE)
• Ultrasound (biopsy) = allows an estimate of the width/height/length of prostate.
• Blood test = PSA (gamma-seminoprotein or kalikrein-3)

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28
Q

Treatment of Benign Prostatic Hyperplasia

A

Pharmacotherapy.
o Alpha-1 adrenergic blockers - Relaxes smooth muscle in bladder and prostate (Tamulosin).
o 5-Alpha-reductase inhibitors - Tries to block conversion of testosterone to its active form (dihydrotestosterone). DHT normally binds to androgen receptor causing cell proliferation.
Two types: dutasteride and finasteride

Surgery
o Transurethral resection of the prostate - Cuts out transitional zone but leaves PZ
Done when:
• Urinary tract infection.
• Recurrent gross haematuria.
• Failed voiding trials.
• Renal insufficiency secondary to obstruction

Open Prostatectomy
o For very large prostates (>75g)

Laser Ablation/Transurethral Microwave/High Energy US Therapy
• Going through urethra with laser (will cook TZ cells and kill them so you can increase size).

Urolift: opening of urethra

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29
Q

Prostate Cancer

A

Symptoms of BHP may be like prostate cancer - PSA tends to be much higher than in BPH

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30
Q

Mechanism of Smooth Muscle Relaxation in Erection

A
  1. Non-adrenergic non-cholinergic parasympathetic neuron releases nitric oxide.
    a. Diffuses across to smooth muscle
  2. NO binds to soluble guanylyl cyclase and produces cGMP
  3. This causes smooth muscle relaxation (decreases calcium inflow).
    a. Signals from the sympathetic neuron does the opposite.
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31
Q

Treatment of Erectile Dysfunction

A
Can target cGMP and stop its breakdown to cause relaxation. E.g.
•	Phosphodiesterase type 5 inhibitor:
o	Sildenafil (Viagra) 
o	Vardenafil (Levitra)
o	Taladafil (Cialis)
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32
Q

Peyronie’s Disease (Bent Penis)

A

Scar tissue forms on shaft of penis

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33
Q

Where do varioceles in the testes usually develop

A

ALWAYS in the left testis.

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34
Q

Types of Miscarriage

A

Threatened: light/painless bleeding from vagina (PV)
• Fetus is alive - cervical os is closed

Inevitable: bleeding heavier vs threatened.
• Fetus may be alive at this point - cervical os is open.
o Miscarriage about to occur.

Incomplete: only some of the fetal parts have passed.
• Cervical os is open.
• PV bleeding continues.

Complete: All fetal tissues have been passed.
• Bleeding has diminished stopped.
• Uterus no longer enlarged - cervical os is closed

Septic: contents of uterus infected = endometritis.
• Tender uterus, fever may be absent.
• May progress to pelvic infection.

Missed
• Fetus has not developed and died in utero.
o Cervical os is closed

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35
Q

Causes of Recurrent Miscarriage

A
Causes:
•	Autoimmune disease (e.g. anti-phospholipid syndrome): 25%. 
•	Chromosomal defects (4%). 
•	Hormonal factors
•	Anatomic factors. 
•	Infection.
•	Others
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36
Q

Presentation of Ectopic Pregnancy

A

Clinical Presentation
• Women of reproductive age with PV bleeding.
• Lower abdominal pain.
• Collapse (shoulder tip pain).
• Amenorrhoea for 4-10 weeks (absence of menstruation)

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37
Q

Molar Pregnancy/Gestational Trophoblastic Disease

A

When trophoblastic tissue that forms part of blastocyst proliferates more aggressively than normal

Hydatidiform mole: no fetus, only the placenta forms
Partial Hydatiform: some evidence of embryonic development can be found

Examination
• Large uterus
• Early pre-eclampsia and hyperthyroidism may occur.

Investigations
• Ultrasound: snowstorm appearance.

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38
Q

Infections in Pregnancy

A

TORCH

Toxoplasmosis
Other (influenza, parvovirus B19) 
Rubella
Cytomegalovirus (CMV)
Herpes Simplex Virus, HIV, Hepatitis.
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39
Q

Congenital Cytomegalovirus Symptoms

A

Wide Range Symptoms
• Severe: intra uterine growth retardation (IUGR) –> very non-specific.
o Hepatosplenomegaly, microcephaly.
o Sensorineural deafness (commonest congenital cause)

Treatment:
•	IV Ganciclovir OR
•	Valganiclovir (pro-drug of Ganciclovir)
   o	   Inhibits DNA synthesis. 
   o	   Oral medication.
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40
Q

Congenital Varicella Syndrome Symptoms

A

Symptoms:
• Skin lesions (73%): limb hypoplasia
• CNS (62%): microcephaly, hydrocephaly, neurodevelopmental delay.
• Cataracts/other eye problems.
• GI, Genitourinary and cardiac abnormalities

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41
Q

Neonatal HSV Infection treatment

A

Acquire infection while passing through birth canal (and kissing the child)

Management
• Mortality (untreated) 65% reduced to 25% with aciclovir treatment

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42
Q

Congenital Rubella

A
The risk is greater the earlier there is contraction. 
Risks involve:
o	Microcephaly
o	Heart disease
o	Petechiae and purpura.
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43
Q

Congenital Toxoplasmosis

A

Mother infection due to parasite toxoplasma gondii ( Natural host is cat)

Clinical Features: IUGR (intrauterine growth restriction), hydrocephalus, cerebral calcification, microcephaly, hepatosplenomegaly.

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44
Q

Syphilis

A

Sexually transmitted infection due to spirochete Treponema pallidum.

Treatment: penicillin

Congenital Syphilis:
Early 0 to 2 years
•	Rash
•	Rhinorrhoea (thin clear nasal discharge)
•	Osteochondritis
•	Perioral fissures
•	Lymphadenopathy 
Late i.e. >2 years
•	Hutchinson’s teeth
•	Clutton’s joints
•	High arched palate
•	Deafness
•	Saddle nose deformity
•	Frontal bossing
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45
Q

Stages of Labour

A
1st Stage of Labour
Latent Phase: 0-3cm cervical dilatation.
Active Phase: 3-10cm cervical dilatation. 
•	Primigravida: 1-3cm/hr.
•	Multigravida: 3-6cm/hr. 

2nd Stage of Labour
Primigravida: 40 minutes
Multigravida: 20 minutes.
• Propulsive phase: from full dilation to present part reaching pelvic floor.
• Expulsive Phase: from reaching the pelvic floor to delivery of the baby

3rd Stage of Labour
• From delivery of the baby to expulsion of the placenta (30 mins)

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46
Q

Macrosomia causes

A
  • Maternal diabetes (common).
  • Maternal Obesity
  • Previous large babies
  • Prolonged pregnancy
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47
Q

Management of Failure to Progress in pregnancy

A

Powers: Uterine Inertia (absence of effective contractions).
o Give syntocinon (oxytocin)

Passenger: Malpresentation or malposition.
o Consider ECG/rotation forceps/C-section

Passages: contracted pelvis/rigid cervix.
o C-section.

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48
Q

Signs of Foetal Distress in Labour:

A

• Meconium (faeces in abdomen due to distress)

• Fetal heart rate abnormalities
o Bradycardia <110/mt, tachycardia >160/mt

• Decelerations.

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49
Q

Closure of Foetal circulatory vessels

A

Closure of ductus arteriosus (increased oxygen levels).
o In utero ductus is kept open under influence of PG E1

• Closure of foramen ovale.
o Due to drop in pressure in pulmonary circulation/right side of heart.
 Shunting is reversed and valve closes

• Closure of ductus venosus.
o Due to decrease in blood flow in inferior vena cava.

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50
Q

What causes the blue look in cyanosis

A

Amounts of deoxygenated Hb

Deoxygenated Hb >50g/l in capillaries OR >34/l in arterial blood

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51
Q

Eisenmenger shunt

A

Pulmonary oedema impairs gas exchange (increased PAP from left –> right shunts)

Pulmonary hypertension causes right to left shunting as there is higher pressure on right side

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52
Q

Neural Tube Defects

A

Spina Bifida Occulta = failure of one or more vertebrae in spine to form properly
o Myelomengocoele is the most serious form (neural tissue exposed on babies back)

Meningocoele = meninges protruding from spinal column.

Encephalocoele = protrusion of neural tissue (brain) from head.

Anencephaly = absence of major portion of brain, skull, and scalp.

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53
Q

Treatment and consequences of Myelomeningocele

A

Closure reduces risk of infection but does not restore normal neural function.
Also: closure may lead to hydrocephalus (build-up of CSF).
o Treated with a plastic catheter that is put through the valve and runs under the skin into the peritoneal cavity to be rapidly absorbed into the circulation

Consequences:
Mixed sensory, motor and autonomic problems.
o Dependent on level of lesions and degree of neural disruption.
Loss of bladder control, faecal incontinence and loss of sensation in legs.

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54
Q

Abdominal Wall Defects

A

Gastroschisis (abdominal cavity open)

Exomphalos (Herniation through umbilical cord)

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55
Q

Causes of Primary Post-Partum Haemorrhage (PPH)

A

Are traditionally the 4Ts:
T: Tone = uterus not contracting (70%)

T: Tissue = placenta/membranes left behind (20%)

T: Trauma = episiotomy/tear which keeps bleeding (9%)

T: Thrombin = clotting disorders that need to be corrected (1%).

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56
Q

Management of Primary PPH

A
Uterotonics
•	Syntometrine (oxytocin and Ergemetrine). 
o	Syntocinon (synthetic oxytocin). 
o	Ergemetrine (vasoconstriction). 
•	Misoprostol (prostaglandin E1)
•	Carboprost (prostaglandin F2alpha). 

Surgery
• Bakri Balloon: device used for the temporary control and reduction of PHH (inflates: keeps uterus contracted and stops bleeding).
• B-Lynch: mechanical compression of atonic uterus using sutures.

Uterine Artery Embolization (catheter to deliver small particles that block the blood supply to uterine body).
(!) Resort to hysterectomy (removal of uterus) sooner rather than later
• Especially in cases of placenta accreta (vessels grow too deeply into uterine wall)/uterine rupture.

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57
Q

Causes of Secondary PPH

A

Infection: endometritis (Commonest cause of postnatal morbidity)

Tissue: Retained products of conception (RPOC).

58
Q

Psychiatric Disorders in pregnancy

A

Postpartum Blues

Postpartum/Perinatal depression

Postpartum/Puerperal psychosis

59
Q

Pregnancy-Induced Hypertension (PIH)

A

Gestational hypertension: late onset hypertension, without proteinuria.

Pre-eclampsia: hypertension with proteinuria and after 20 weeks of pregnancy.

Eclampsia: pre-eclampsia and convulsions (one or more).

60
Q

Control of Fits treatment in eclampsia

A

Loading Dose: MgSO4 (8mls + 12mls saline) over 20 minutes

Maintenance Dose: 1-2g MgSO4/hr (20 + 30)
o Maintain for 24 hours post-delivery

Therapeutic Levels: 2-4mmol/litre.

61
Q

Apgars Scoring

A
o	Appearance
o	Pulse
o	Grimace
o	Activity
o	Respiration 
o	Skin Colour
62
Q

Perinatal Asphyxia/Hypoxic-Ischaemic Encephalopathy

A

Medical condition result from deprivation of O2 to a newborn infant (usually harm to brain)

Clinical Presentation:
•Infant needs resuscitation at birth. Presents with
o Absent heart rate, infant not breathing
o May require airway, respiratory and haemodynamic support
o Infant subsequently encephalopathic.
 Abnormal neurological function.
 Abnormalities of tone and reflexes
 Autonomic dysfunction
 Seizures.

63
Q

Prevention of Secondary Energy Failure after Perinatal Asphyxia

A
Decrease energy depletion.
Glutamate (inhibition of release). 
Inhibition of leukocyte/microglial/cytokine effects.
Blockage of downstream cellular events. 
o	Free radical synthesis inhibitors
o	Free radical scavengers etc…
64
Q

Infection of the Newborn

A

Major cause of mortality and morbidity

GBS (group B streptococcus) and E. Coli.

Early-Onset GBS:
•	Apnea (stop breathing in sleep)
•	Severe hypoxia
•	Cardio-respiratory failure
•	Hypotension
•	Metabolic Acidosis
•	Tachycardia
•	Poor perfusion 

Treatment
• Amikacin and gentamicin.

65
Q

Low birthweight classes

A

Low Birthweight (LBW) = <2500g

Very Low Birthweight (VLBW) = <1500g

Extremely Low Birthweight (ELBW) = <1000g.

66
Q

Edwards syndrome affects which chromosome

A

Trisomy 18

Presents with:
Decreased muscle tone, low set ears, overlapping fingers or clubfeet

67
Q

Neonatal Problems with SGA Baby

A

Temperature control:
Increase SA to volume ratio
Reduced adipose tissue insulation
Reduced capacity for thermogenesis.

Polycythaemia (increased RBCs) - Due to being hypoxic in utero –> thickened blood

Poor nutritional status = URGENT: treated with:

  • Feeds
  • Bolus of dextrose + IV infusion.
68
Q

Respiratory distress syndrome (RDS)

A

Surfactant deficiency

Signs of respiratory distress: tachypnoea, expiratory grunting, recession.
- Within 4 hours of birth.

Presentation
o X-Ray = ground glass appearance
 Air bronchogram (air in villus not in lung).
Acute Complications of HMD
o Air leaks to increased pressure to inflate lungs.
o Pneumothorax if air leaks through pleura.
o Pulmonary intestinal emphysema.
 Air in interstitium (increased respiratory distress).

Prevention:
Ante-natal steroids.
Avoidance of intrauterine hypoxia.
Prophylactic surfactant treatment.
Keep warm, avoid acidosis. 

Treatment:
Surfactant and respiratory support.

69
Q

Cardiovascular problems with premature

A

PPHN (Persistent Pulmonary Hypertension of the Newborn) - Lung vessels do not relax and are constricted: blood flow is suboptimal

Failure to maintain blood pressure

Patent Ductus Arteriosus - Connects the pulmonary artery and the aorta.
• Can cause excessive pulmonary blood.

70
Q

What can excess feeding in the premature cause

A

may precipitate necrotising enterocolitis (NEC)

71
Q

Necrotising Enterocolitis

A

Acute bacterial invasion/ inflammation/necrosis of bowel gas formation in bowel wall (pneumotosis)

Clinical Presentation
o Abdominal distension, tenderness, discolouration.
o Blood in stools.
o Generalised collapse

72
Q

Hospital Acquired Infections in premature

A

Coagulase negative staphylococci.

Gram negative organisms (colonise the intestine).

73
Q

Neurological problems in the premature

A

Susceptibility to periventricular haemorrhage (PVH)
• Poor control of brain perfusion.
• If sudden increase (release of pneumothorax) increased flow.
o On the walls of the third ventricle: germinal matrix.
 Lots of neurons that migrate to the cortex.
 Susceptibility to bleeding (no scaffolding).

Risk of Periventricular Leucomalacia (PVL).
• Ischaemia of periventricular white matter.
o Area where ACA and MCA meet: very susceptible.

IVH Classification
Stage I: haemorrhage in the matrix.
Stage II: IVH without ventricular dilatation.
Stage III: IVH with enlarged ventricles.
Stage IV: IVH with parenchymal haemorrhage.

74
Q

Fanconi anaemia

A

failure of DNA to repair itself properly.
o Genetic cause; FANC as well as FANCA.
 Work together to ubiquitinate two proteins.

75
Q

Aetiology of Gestational Diabetes

A

Pregnancy, intrinsically, is a state of insulin resistance and glucose intolerance.
o Due to placental secretion of anti-insulin hormones (HPL, cortisol and glucagon)

Gestational diabetes: exaggeration of this.
o Often due to increased genetic and environmental risk.

76
Q

When to screen for Gestational Diabetes

A

26-28 weeks - Don’t screen earlier: physiological drivers that are diabetogenic not yet present.

77
Q

Gestational Diabetes effect on the baby

A

Mother has higher blood sugar levels

Glucose is small –> crosses placenta into fetus

Macrosomic Baby: fetus will get fat as it stores glucose.
o Also, large for gestational age

Polyhydramnios: because baby is bigger it will urinate more

(Unexplained Stillbirth): because baby is too big it will not have enough nutrients.

78
Q

Gestational Diabetes Fetal Complications

A
  1. Macrosomia (birth asphyxia and traumatic birth injury).
  2. Respiratory Distress Syndrome (low surfactant)
  3. Hypoglycaemia (baby loses flood of glucose supply).
  4. Hyperbilirubinemia (jaundice).
79
Q

Drug used for Gestational Diabetes treatment

A

Metformin (only one not teratogenetic)

80
Q

Urinary Tract Infections in pregnancy

A

More common in pregnancy (pressure of fetus on tubes (ureter and urethra) and bladder causes stasis)

Treatment matters (even if asymptomatic) because of risk of complications:
o	Maternal: pyelonephritis (infection of one or both kidneys)
o	Fetal: growth restriction, preterm labour. 

Treatment:
• Penicillin’s
• Cephalosporins
• Nitrofurantoin.

81
Q

Listeriosis

A

Rare but can be fatal.

Often asymptomatic or just “virus” symptoms.

82
Q

Criteria for Further Assessment for Growth in the child

A

Weight/height or BMI is below the or 0.4th centile.
 Unless already investigated

Height centile is more than 3 centile spaces below mid-parental centile

Drop in Height Centile Position of more than 2 centile spaces.

83
Q

Phase of Growth and driving factors

A

Infancy: rapid growth (nutritionally determined, up to two years)

Childhood: relatively steady (primarily regulated by GH and T4)

Puberty: acceleration and then cessation (GH, sex steroids, T4).

84
Q

Turner’s Syndrome

A

Missing whole/part of X syndrome.
Benefit from growth hormone (early diagnosis is key).
o Therefore, all short stature girls need karyotype analysis

Short stature
Webbed neck
Widely-spaced shield nipples
Cubitus valgus (angulation of forearm)
Lymphedema of hands
Knock knees
Shortening of 4th/5th metcarpal
85
Q

Management of Idiopathic Short Stature in Children

A

Administration of GH
Oxandrolone
o Very little change in most cases.

Do not recommend growth hormone therapy unless immense psychological effects.

86
Q

Tests for Systemic Disorders in Children

A

Complete blood count, Na/K+/Cl/Bicarbonate.

Kidney function tests (blood urea nitrogen)

Insulin-like growth factor -1

Immunoglobulin A (IgA), tissue transglutaminase (CD).

87
Q

Action of Somatostatin on Growth Hormone

A

Inhibitory –> determines peak pulses of GH (every 3-4 hrs)

88
Q

Most Common cancer in:
0-14 Year Olds
15-19 Year Olds

A

0-14:
• Leukaemia (31.1%),
• CNS (25.4%),
• Lymphomas (10%).

15-19:
•	Lymphomas (20.7%), 
•	Carcinomas and Melanoma (19.6%)
•	CNS (18.7%)
•	Leukaemia (13.8%).
89
Q

Oncogenes activation

A
DOMININANT (One allele activation)
A gain of function. Activated by:
o	Mutation
o	Chromosome Translocation
o	Gene Amplification
o	Retroviral Insertion.
90
Q

Tumour Suppressor Inactivation

A
RECESSIVE (both allele dysfunction - no functional gene)
Inactivated by
o	Mutations
o	Deletions
o	DNA Methylation (epigenetic)
91
Q

Wilms Tumour

A

Aggressive tumour of the kidney (known as Nephroblastoma) consisting of pluripotent embryonic renal precursors (Blasterma, Epithelia, Stroma)

Asymptomatic abdominal mass without metastasis.
o Spreads by growth or via lymphatics/blood stream

Somatic genetic alterations:
• Inactivated WT1, WTX, TP53 genes.
• Activated CTNNB1 (beta catenin) gene (oncogene).
• Epigenetic alterations at IGF2/H19 locus.

(!) WT1 has a key role in ureteric branching.
• WT1/WNT (activated by beta catenin): key roles in epithelial induction of metanephric mesenchyme.

92
Q

Retinoblastoma

A

Tumour of the retina (Loss of RB1)

Symptoms: leukocoria (white pupil when light shone into it), eye pain or redness, vision problems.

Cancer Cells without RB1: if you don’t have RB1: E2F is free to induce G1-S transition.

Activation of MYCN: proliferation.

93
Q

Neuroblastoma

A

Tumour of the SymNS in adrenal gland/sympathetic ganglia

Derived from sympatho-adrenal linage of the neural crest during development.
o Originates from incompletely committed precursor cell.

Key genes: MYCN, ALK.

Treatment:
Surgery, chemotherapy, radiation theraphy.

Targeted Theraphy
• Crizotinib against ALK mutations

Immunotherapy

94
Q

Acute Lymphoblastic Leukaemia

A

MOST COMMON MALIGNANCY in children

Symptoms
• Bruising/bleeding.
• Pallor or fatigue due to anaemia.
• Infection due to neutropenia (few white blood cells)

Pro-B: CD19+ on the cell surface.
Pre-B: CD19+ and CD10+.

These have very specific genetic changes that cause different types of leukaemia’s.
• ALL: MLL translocation (19) (most common)
• TEL-AML1 translocation (19 and 10)

Standard Treatment Phases
•	Induction 
•	Consolidation
•	Maintenance 
•	Bone marrow transplantation.
95
Q

Chlamydia Trachomatis

A

Serovars D-K
• Males: urethritis, epididymitis, prostatitis
• Females: cervicitis, PID (pelvic inflammatory disease), Fitz-Hugh Curtis (inflammation of stomach and liver lining)
• Neonate: conjunctivitis (pink eye) and pneumonia.

Serovars L1-3
• Lymphogranuloma Venereum (chronic infection of the lymphatic system) (LGV).
o Buboes = swollen inflamed lymph node
o Proctitis = inflammation of the rectum/anus

Complications
• Reactive arthritis
• Infertility

Treatment
• Azithromycin
• Doxycycline

96
Q

Genital Warts

A

Human Papilloma Virus (DNA)
Some are associated with carcinoma (16, 18, 31, 33)

Management.
o Topical Podophyllotoxin
o Imiquimod
o Cryotherapy

97
Q

Neisseria Gonorrhoea

A

Symptoms:
• Males: urethritis, prostatitis, sore throat, epididymitis, prostatitis
• Females: cervicitis, PID, peri-hepatitis, septic abortion (infected while pregnant)
• Neonates: conjunctivitis

Complications: septic arthritis (bacteria spreads through the joints), blindness, infertility, septicaemia (blood poisoning by bacteria) –> meningitis, endocarditis.

Management:
Ceftriaxone: antibiotic.

98
Q

Herpes Simplex Virus 1 and 2

A
HSV-1 = Oral
HSV-2 = Genital. 

Blisters that scab over

Two main presentations: 
Disseminated HSV
•	Sepsis-like syndrome
•	Hepatitis, coagulopathy
•	High mortality
•	IV aciclovir

HSV Encephalitis
• Fever, seizures
• Haemorrhagic infarction of white matter/cortex
o Particularly in temporal lobes.

Management (Not curable)
• Aciclovir
• Famciclovir
• Valaciclovir.

99
Q

Treponema Pallidum (Syphilis)

A

Primary:
Chancre (genital ulcer disease - painless so unnoticed)
o Highly infectious ++

Secondary:
Condyloma Lata (wart-like lesions on genitals)
o Highly infectious ++

Latent, Tertiary, Congenital.
o Often asymptomatic in early stages.

Diagnosis depends on serology.

Treatment (Curable)
• Penicillin.
• Doxycycline.

100
Q

HIV

A
HIV infects CD4+ T cells (T-helper cells), macrophages and dendritic cells. 
o	Acute (primary) HIV infection leads to massive loss of CD4+ cells. 
o	Chronic HIV infection leads to on-going loss of CD4+ cells, decline in immune function and progressive immunosuppression

HIV-associated disease incorporates:
o Direct effect of HIV: wasting, diarrhoea, neurological problems
o Opportunistic Infections: viral, fungal, bacterial, mycobacterial and parasitic infections
o Malignancies: lymphoma, cervix carcinoma.

Retroviral Theraphy
• HAART: highly active antiretroviral theraphy.
o 6 classes of antiretroviral drugs.
 Nucleoside Reverse Transcriptase Inhibitors (NRTIs)
 NNRTIs (Non-NRTIs)
 PIs (Protease Inhibitors).
 Fusion Inhibitors.
 Integrase Inhibitors.
 Co-receptor antagonists.
o Always combine at least 3 from 2 classes.
• Act during viral replication cycle.

101
Q

Problems with HAART therapy (against HIV)

A

Side Effects
Short-Term:
• Nausea/vomiting/headache.
• Sleep disturbance.

Long-Term 
•	Lipodystrophy (lose fat in some parts and gain in others)
•	Renal dysfunction.
•	Peripheral neuropathy.
•	Lactic acidosis.
102
Q

Wheezing in intra and extra-thoracic airways

A

Anything related to obstruction of intrathoracic airways = wheeze of expiration
Wheezing is fluttering between slight and greater narrowing:
• Can be caused by airway swelling

Anything related to obstruction of extrathoracic airways = wheeze of inspiration
• Often related to croup. – upper airway infection, characteristic barking cough

103
Q

Preschool Wheeze

A

Episodes of wheeze usually triggered by cold

Treatment:

1) Short-acting beat 2 agonist
2) Inhaled steroid or Leukotriene receptor agonist (LTRA)
3) Inhaled steroid and LTRA
4) Paediatrician

104
Q

Asthmatic cellular effects

A
  • Goblet cell hyperplasia.
  • Thick subbasement membrane.
  • Cellular infiltrate.
105
Q

Bacteria with exotoxins

A

o Exotoxins: bacterial toxins secreted by the host.

Cholera: opening of CL- channels that lead to water into gut.

Diphtheria: sore throat with pseudo membrane
• Diphtheria Toxin A inhibits protein synthesis. Acts on:
o Heart: myocarditis and heart block.
o Nerves further difficulty swallowing, paralysis, diplopia (d. vision)

106
Q

Septicaemia and Meningitis in children causes and symptoms

A

Steptococcus pneumoniae
Neisseria meningitides
Haemophilus influenza B (HiB)

Clinical Symptoms of Septicaemia
•	Tachycardia.
•	Tachypnoea.
•	Prolonged capillary refill.
•	Low BP (late sign)
•	Rash. 
Clinical Symptoms of Meningitis
•	High temperature
•	Headaches
•	Vomiting
•	Not able to tolerate bright lights. 
•	Drowsiness
•	Stiff Neck. 

Meningitis official diagnosed through lumbar puncture (>3 months)

107
Q

Tetanus causes

A

Gram-positive bacillus

Spores found in soil.

108
Q

Organisms in Young Infants

A
  • Group B streptococcus.
  • E. coli.
  • Listeria

Young infants = combination of Cefotaxime/Ceftriaxone AND Amoxicillin (needed for listeria cover).
• Older children just need Ceftriaxone.

109
Q

Immune Defects Predisposing to Pneumococcal Infection in childhood

A

Absent/non-functional spleen.
o Vulnerable to encapsulated bacteria (pneumococcus, HiB, meningococcus).
 Congenital asplenia
 Traumatic removal
 Hyposplenism
o Need vaccination and lifelong penicillin.

Hypogammaglobulinaemia. (low immunoglobulins)

HIV Infection.

110
Q

Invasive and non-invasive streptococcal diseases in childhood

A

Non-invase: acute otitis media, sinusitis, conjunctivitis, pneumonia.

Otitis Media: normally pneumococcus sit in the nasopharynx.
o Children tube: more straight.

Invasive: pneumonia, septicaemia, meningitis, peritonitis, arthritis.

Pneumococcal Pneumonia: lobar and empyema.
o Empyema: chest drain and Urokinase.
 Also, managed by VATS.

111
Q

Vaccination for streptococcal diseases

A

Pneumococcal Polysaccharide Vaccine (PPV)

Pneumococcal Conjugate Vaccine (PCV)

112
Q

Fungal Infections

A
Superficial Mycosis (Common):
o	Candidiasis: nappy rash.
o	Tinea Corporis: ring worm.
	Treat both with topical antifungal (nystatin). 
•	Occurs in Normal Hosts 

Invasive Mycosis (Rare):
o Candidaemia: extremely preterm infant, effects kidneys and brain.
o Pulmonary Aspergillosis: child with chronic granulomatous disease.
 Impaired neutrophil function

• Opportunistic infections in immunocompromised hosts.

113
Q

Protozoa Infections in childhood

A

Malaria
Four main species of Plasmodium species:
- falciparum, viva, ovale and malariae

Toxoplasma gondii (toxoplasmosis)

Cryptosporidium (diarrhoea).

114
Q

What can be used in rapid diagnosis of trisomy 21

A

fluorescence in situ hybridization (FSH

115
Q

Down Syndrome important considerations

A
Cardiac Assessment (echocardiogram): between 40-60% = congenital heart defect. 
o	30-40% are complete atrioventricular septal defects
  • Hearing Tests: sensorineural hearing loss
  • Ophthalmology: tenfold increase in congenital cataract/infantile glaucoma
  • GI Check: 7% have GI problems

Assessed again at three months.

116
Q

A1555G Mutation

A

Penetrance of hearing loss following aminoglycoside (antibacterial) exposure

Leads to:
• Communication difficulties
• Academic difficulties
• Social functioning difficulties.

117
Q

Types of Sudden Unexplained Death in childhood

A
Baby is found dead in the cot:
o	SIDs. 
o	Congenital heart disease.
     	   Acute myocarditis. 
     	   Fibromuscular dysplasia of CAs. 
o	Respiratory infections. 
o	CNS infections
o	Septicaemia 
o	Unsuspected liver tumour

Baby dies in parents/carers arms (instantaneous death):
o Cause of death is obvious
o Cause of death is not apparent

Rapid death due to a recognised illness:
o	Respiratory infections
     	   Severe bronchopneumonia
o	CNS infections
     	   Meningitis (see micro). 
•	Waterhouse-Friderichsen (group of symptoms due to adrenal dysfunction)
•	DIC: disseminated intravascular coagulation 
o	Gastroenteritis. 
o	CNS Haemorrhage.
118
Q

How does Petechiae in the thymus look

A

Starry sky pattern.

 White: macrophages eating up lymphocytes (dark).

119
Q

Sudden infant death syndrome (SIDS) triple risk hypothesis

A

Critical Developmental Period
• Developmental immaturity.
• Rapid changes between 2 and 4 months.

Vulnerable Infant
•	Males 60%. 
•	Abnormality of serotonergic network.
•	Slower responses to changes. 
o	Increases in heart rate/breathing. 
•	Alterations in heart ions channels. 
External Stressor
•	Minor URTI (upper respiratory tract infection)
•	Prone position
•	Bed-sharing
•	Overheating
•	Hyperthermia.
120
Q

Enveloped and non-enveloped viruses

A
Enveloped
Herpes virus:
•	Herpes simplex virus
•	Cytomegalovirus
•	Varicella Zoster 
•	CMV
•	Epstein-Barr
•	HHV 6/7/8. 
Hepatitis B
Poxviruses. 
Non-enveloped
PAP:
•	Papillomavirus
•	Adenovirus
•	Parvovirus.
121
Q

Epstein-Barr Virus

A

Usually asymptomatic in early life.
o The older you are the more infectious it tends to be

Spread by saliva

Infectious mononucleosis (glandular fever)

Sub-Saharan Africa: Burkitt’s Lymphoma

122
Q

HHV-6 and 7: Roseola Infantum

A
Also, known as exanthema subitum.
Common between 6 months and 2 years of age. 
o	Sudden onset of high fever. 
o	Lasts few days then suddenly stops.
o	Followed by rash appearing.
123
Q

Consequences of Chronic Hep B Infection

A

Cirrhosis.

Hepatocellular carcinoma.

124
Q

Papillomavirus serotypes

A

Cause of cervical cancer.
Serotypes 16 and 18 = carcinogenic
Serotypes 6 and 11 = genital warts.

Cervarix vaccine
Gardasil quadrivalent vaccine
o For 6, 11, 16 and 18.

125
Q

Adenovirus symptoms

A

URTI/pneumonia.
Conjunctivitis.
Diarrhoea

126
Q

Parvovirus (Slapped Cheek)

A

Single-stranded DNA

P Antigen
• Attaches to P antigen.
o If lacking individual not susceptible.
• If P antigen: replicates in rapidly dividing cells (red cell precursors).
o Leads to aplastic crisis in people with haematological problems.

Newborns/Children
• Asymptomatic
• “Slapped cheek”

Adults
• Arthroplasty (adults)
• Fetal loss.

127
Q

Important RNA Enveloped and Non-enveloped Viruses

A
Enveloped:
MMR
RSV, Influenza, Parainfluenza
Hepatitis C
HIV 

Non-enveloped:
Rotavirus
Enteroviruses (polio)
Hepatitis A.

128
Q

Measles Symptoms

A

1) Conjunctivitis
2) Couple of days: Koplik spots (inside the buccal mucosa).
3) 2 Days later: Rash (always starts behind the ears.

• Rare complication: Subacute Scleorising Pan-Encephalitis (SSPE)
o Present years later with neurodegenerative disease.

129
Q

Rubella Symptoms

A

Fever, occipital lymphadenopathy

Mild rash.

Congenital Rubella - Triad of symptoms (EEH)
o Eyes: cataracts, micro-opthalmia, glaucoma
o Ears: sensineural deafness
o Heart: pulmonary artery stenosis, VSD

• Can also be more non-specific
o Low birth weight, rash, microcephaly.

130
Q

Bronchiolitis

A

• Viral infection of infants (70% RSV, can also be Influenza, Parainfluenza).
• Inflammation of bronchioles.
• Cough, respiratory distress, wheeze.
• Can be severe in preterm
o Congenital heart disease.
o Try to prevent it with Palivizumab (monoclonal Ab) for prevention of RSV.

131
Q

Rotavirus

A

Fever, vomiting, watery diarrhea.

Vaccines:
RotaTeq
RotaRix

132
Q
Causes of Common Paediatric GI Symptoms:
Abdominal Pain
Chronic Vomiting/Haemetemesis:
Chronic Diarrhoea:
Failure to Thrive/Weight Loss
Rectal Bleeding/Blood Stools
A
Abdominal Pain:
•	Constipation
•	Functional/RAP (recurrent abdominal pain)/IBS
•	Duodenal ulcers/Helicobacter Pylori
•	Inflammatory Bowel Disease

Chronic Vomiting/Haemetemesis:
• Gastro-oesophageal Reflux
• Intestinal Obstruction (if bile) intermittent.
• DU (rare).

Chronic Diarrhoea:
•	IBD
   o	   Weight loss
   o	   Abdominal pains
   o	   Tiredness
   o	   Rectal bleeding

Failure to Thrive/Weight Loss
• Coeliac
• Cystic Fibrosis

Rectal Bleeding/Blood Stools
•	IBD 
•	Chron’s/UC
•	Fissures/haemorrhoids
•	Polyps/polyposis syndromes
•	Infection (bacterial).
133
Q

Constipation Definition

A

Passing less than 3 stools per week OR painful bowel movements due to hard/large stools and stool retention in spite of passing >3 times per week

134
Q

Organic disease causes of Constipation

A
  • Hirschsprungs.
  • Hypothyroidism.
  • Neurologic.
  • Anal stenosis.
135
Q

Gastro-oesophageal Reflux treatment in infants

A
•	Positioning
•	Thickening of feeds
•	Reduce acid
   o	   H2 antagonists
   o	   Proton pump inhibitors
   o	   Promotility agents (e.g. domperidone)
136
Q

Eosinophillic Oesophagitis

A

Treatment resistant symptoms of GORD

Treatment
•	Dietary
   o	   Food exclusions
   o	   Pragmatic trials. 
•	Oral budesonide
•	Monteleukast
137
Q

Gastritis

A

Inflammation of the gastric mucosa
Due to infection with Helicobacter pylori.

Presentation 
•	Vomiting
•	Abdominal pain
•	Haemetemesis
•	Anaemia. 

Treatment:
Non-steroidal anti-inflammatories (NSAIDS)

138
Q

C13 Breath Test

A

Used to detect H. pylori

If H. pylori is present, urea is metabolized to ammonia and C-labeled CO2

139
Q

Treatment of H. pylori

A

2 weeks: amoxicillin, clarithromycin

+ 6/52 H2 antagonists OR PPIs

Repeat breath test/stool.

140
Q

Chron’s Disease (IBD)

A
  • Mouth to anus, patchy disease “skip lesions”
  • Transmural inflammation
  • Granulomas
Presentation 
•	Abdominal pain
•	Weight loss
•	Diarrhoea 
•	Insidious onset
•	Growth failure
•	Raised ESR/CRP/low albumin/Hb. 
•	Fever/clubbing/PR bleeding/oral ulcers/abdominal mass, other upper GI symptoms. 
    o	   Pyoderma gangrenosum - painful ulcers
141
Q

Ulcerative Colitis (IBD)

A

Only rectum/colon
Continuous disease
Mucosal inflammation.

Presentation
•	Chronic bloody diarrhoea 
•	Abdominal pain. 
•	Weight loss. 
•	Sclerosing Cholangitis
•	Arthropathy
142
Q

Medical Treatment of Inflammatory Bowel Disease

A
Induce Remission
•	Exclusive enteral nutrition (Chron’s)
o	Reduce inflammation
o	Correct undernutrition
o	6/52 of milk based formula 
•	Steroids
•	5-ASA
•	Biologicals (e.g. anti-TNF infliximab). 

Maintain Remission
• 5-ASA (UC)
• Immunosuppressants
• Biologicals