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Human Development 2 > Things to Learn > Flashcards

Things to Learn Flashcards

1
Q

what is the most common cancer in men

A

prostate

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2
Q

What do LHRH analogues do

A

LHRH analogues (also called GnRH analogues) act by desensitizing LHRH receptors in the pituitary gland, which in turn prevents the secretion of luteinizing hormone (LH), causing the body’s androgen levels to drop in the long term

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3
Q

How is prostate cancer linked to normal influences

A

Hormonal influences – prostatic adenocarcinoma is androgen sensitive because castration with surgery or LHRH analogues is associated with disease regression.
- binding of androgens induces the expression of growth factors and growth factor receptors which stimulate the progressive growth of the cancer

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4
Q

what other conditions cause a raised PSA

A

Benign prostatic hypertrophy (BPH), prostatitis, urinary tract infections (UTI), trauma etc.

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5
Q

what is the gold standard for diagnosis Prostate cancer

A

Trans Rectal Ultrasound Guided Biopsy

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6
Q

How does the Gleason score work

A

Therefore a combined Gleason Grade score is used which is the sum of:

  • The most common grade
  • The highest/dominant grade
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7
Q

what can CT be used to assess in cancer

A
  • stage of the disease and how much it has spread
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8
Q

what are the symptoms of a testicular torsion

A

Swollen, tender and erythematous testicle

Black internally

Black externally

Necrosis which also extends into the spermaticord

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9
Q

what is an orchiopexy

A

– surgical attachment of testes to scrotum to fix them into position

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10
Q

what do Sertoli cells do

A

– support cells involved in regulating spermatogenesis, spermiogenesis, blood-testes barrier, hormone production, tubular fluid secretion and phagocytosis of spermatid cytoplasm.

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11
Q

what do leydig cells do

A

– are located in the intersitium and synthesise testosterone

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12
Q

what are the risk factors for a seminoma

A

Undescended testes - poor histological development due to exposure to high temperature.

Infant hernia (indirect inguinal)

Rare genetic conditions

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13
Q

describe seminoma

A 
Macroscopic 
Hard
Well circumscribed
Pale/ White mass
Lobular
Homogenous

Microscopic

  • Nuclear pleomorphism
  • Prominent nucleoli
  • Clear cytoplasm
  • Well defined cell boundaries
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14
Q

what serum marker are used for what tumours in men

A

Seminoma – PLAP (Placental Alkaline Phosphatase)

Choriocarcinoma – hCG (human chorionic gonadotrophin)

Yolk sac tumours – AFP (alpha-fetoprotein)

Embryonal carcinoma - Oct4

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15
Q

What does cervical screening involve

A

Cervical screening involves taking a sample of epithelial cells from the transformation zone using a brush or a spatula, applying/smearing this to a slide and then staining with a Papanicolaou stain (Pap)

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16
Q

what are the types of cervical cancer

A

80% squamous cell carcinoma

15% adenocarcinoma

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17
Q

describe characteristics of kilobytes

A

Nuclear enlargement

Nuclear hyperchromasia (darker nuclei)

Peri-nuclear halo

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18
Q

what does a women above 35 breast look like

A

Older women (>35 years) – undergo changes to breast tissue as fibrous tissue in the breast gets replaced by adipose tissue which is more radiolucent (passes more X-rays) through it, hence a mammogram increases the sensitivity for the detection of a lump.

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19
Q

what two techniques are used to find an adenoma

A

ultrasound

mammogram

can also use a fine needle aspiration for cytology

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20
Q

describe a fibroadenoma

A

Commonest benign breast tumour
<30 years
Arises in the breast lobule

Firm, smooth, mobile lump - ‘breast mouse’
Painless
Benign overgrowth of collagenous tissue within the lobule
Can have multiple in one breast

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21
Q

What are the symptoms of ovarian cancer

A
  • bloating
  • feeling full quickly while eating
  • pelvic or abdominal pain
  • urinary urgency
  • abdominal vaginal bleeding or discharge
  • back pain
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22
Q

Name the three types of epithelial tumours

A

Serous

Mucinous

Endometroid

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23
Q

what are the three sex cord stomal cells

A

Granulosa cell tumour

Thecoma fibroma

Sertoli-Leydig cell tumour

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24
Q

what is the surgery of ovarian cancer

A

Total Abdominal Hysterectomy and Bilateral Salpingo-oopherectomy

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25
Q

what HPV is associated with genital warts

A

6 and 11

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26
Q

what HPV is associated with carcinoma

A

HPV 16, 18, 31, 33,

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27
Q

How does HPV cause cancer

A
  • Papillomavirus DNA is incorporated into the host genome
  • this produces the proteins E6 and E7 which form complexes with anti-oncogenes such as p53 and retinoblastoma thereby inactivating the normal cellular response to DNA damage
  • this results in accumulation of genetic abnormalities
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28
Q

when does an ovarian adenocarcinoma originate from

A

Fallopian tube

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29
Q

what are the type of cervical cancers

A

80% of being squamous cell carcinoma
15% adenocarcinoma
- the remainder are Aden-squamous and neuroendocrine carcinomas and these are caused by high oncogenic risk GPV

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30
Q

what is the transformation zone in the cervix and vaigna

A
  • changes occur with the eversion (turning inside out) of then endocervical columnar epithelium onto the ectocervix
  • the protrusion of the endocervical epithelium forms what is referred to as the endocervical columnar ectropion
  • thus at punters the original squamous-columnar junction becomes relocated outside the external os
  • in response to the acidic conditions of the vaginal vault areas of ectropion are replaced with stratified squamous epithelium by metaplasia involving stages of reverse cell hyperplasia and immature metaplastic epithelium
  • this is transformation zone
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31
Q

what type of HPV causes what type of carcinomas in the cervix

A

Squamous cell carcinomas HPV16

adenocarcinomas HPV18

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32
Q

How does HPV infect

A

HPV infect immature basal cells through epithelial breaks caused by damage
- this can directly infect metaplastic squamous epithelium but it cannot infect mature superficial squamous epithelial cells

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33
Q

what are dyskaryotic changes of the nucleus

A
  • disproportionate nuclear enlargement
  • irregularity in form and contour
  • hyperchromasia
  • irregular chromatin condensation
  • abnormalities in number, for, and size of nucleoli
  • multinucleate
  • nucleus to cytopaslm ratio increases as dyskaryosib prowesses so exfoliated cells with severe dysplasia most resemble immature basal cells
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34
Q

what two HPVs are associated with common warts

A

HPV 2 and 7

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35
Q

what are the two types of connective tissue that the breast stroma is made up of

A

1, interlobular stroma = this is comprised of a dense fibrocollagenous tissue mixed with adipose tissue
2, intra lobular stroma - this is comprised of a looser fibrocollagneous tissue contains hormonally responsive breast-specific fibroblasts important in mammary gland remodelling for example in pregnancy

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36
Q

What happens to the breast tissue with ageing

A
  • with ageing from approximately age 30 and through menopause the breast lobules involute and can nearly complete atrophy in the elderly
  • adipose is more prominent
  • lobules decrease in size and in number
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37
Q

describe what epithelial tumours are like and where they project

A
  • cystic with solid components
  • smooth surface or be covered in papillary projections
  • spread is often into the peritoneal cavity
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38
Q

What are the type of ovarian carcinomas

A
  • serous adenocarcinoma

- mucus adenocarcinoma

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39
Q

what plays a role in pathogenesis of prostate cancer

A
  • androgens
  • IGF-1 plays a role
  • diet as well plays a factor
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40
Q

what is the only certain risk factor for development of germ cell tumours

A

cryptorchidism

  • risk factor in germ cell tumours of the testsis mainly seminomas
  • accounts for approximately 10% of cases
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41
Q

development of the testis does not…

A

occur normally at higher temperatures

  • histological changes occur within the undescended testsis as early as 2 years of age and are evident as tubular atrophy with an arrest in germ cell development
  • in the adult, tubules are lined by a preponderance of Sertoli cells instead of having normal cellular development
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42
Q

what is a choriocarcinoma made out of

A
  • made out of giant syncytiotrophoblast cells and cytotrophoblasts
  • this is why it secretes HCG
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43
Q

what can HCG give rise to

A

gynaecomastia

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44
Q

what risk is a biopsy of a testicular neoplasm associated with

A

a risk of tumour spillage and potential spread
- therefore standard management of a solid mass in the testis is a radical orchiectomy based on the presumption of malignancy

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45
Q

What leads to hyaline membrane disease

A

 Architectural & functional immaturity of lungs ◦ preterm babies
◦ babies from diabetic mothers
◦ male gender, caesarean section
 Deficiency of pulmonary surfactant

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46
Q

what causes an increase and decrease in pulmonary surfactant

A

 glucocorticoids, thyroxine & labour increase
 insulin & Caesarean section decrease
 certain genetic polymorphisms SP-A, SP-B

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47
Q

what are the complications of hyaline membrane disease

A

◦ chronic lung disease (BPD)
◦ pneumothorax,
- pneumomediastinum,
- pneumopericardium

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48
Q

What are the causes of prematurity

A

 PROM (premature rupture of membranes) 30-40%
 Intrauterine infection 25%
 Uterine anomalies (fibroids, bicornuate)
 Cervical incompetence
 Placental problems (abruption, pl. praevia)
 Multiple gestation
 IOL for maternal or fetal disease

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49
Q

What are the major causes of death in pre-term babies(important card)

A

 Hyaline membrane disease (HMD)

 Intraventricular haemorrhage (IVH)

 Necrotizing enterocolitis (NEC)

 Neonatal sepsis
◦ early onset (up to 1 week of age)
◦ late onset (>1 week of age)

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50
Q

What factors determine survival rates in premature babies

A

 Gestational age (>35/40)

 Size
◦ BW >2500g
◦ no growth restriction

 Antenatally corticosteroids

 Exogenous surfactant at delivery

 Postnatally
◦ management
◦ treating the underlying disease

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51
Q

what happens in meningococcus septicaemia

A

◦ shock
◦ bilateral adrenal haemorrhage
◦ widespread purpura
◦ meningitis

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52
Q

what investigations do you perform to get a genetic diagnosis

A

 Antenatally
◦ chorionic villous sampling CVS
◦ amniocentesis

 Postnatally or at PM
◦ blood
◦ skin
◦ sternum

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53
Q

what does Apgar stand for

A 
o	Appearance - colour of the baby 
o	Pulse - heart rate
o	Grimace - reflex 
o	Activity (muscle tone)
o	Respiration effort
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54
Q

what happens in perinatal asphyxia

A

Tissue suffers hypoxaemia, ischaemia

- hypercarbia, metabolic acidosis

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55
Q

What are the warnings of hypoxia ischameia

A
  • Decreased fetal movement.

* Sentinel events (placenta abruption, uterine rupture, cord prolapse).

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56
Q

What does encephalopathy refer to

A

Abnormal neurologic function and consciousness level

Abnormalities of tone and reflexes

Autonomic dysfunction
Seizures

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57
Q

What are the potential targets for neuroprotection

A
  • Decrease energy depletion - increase glucose, use hypothermia and barbiturates.
  • Glutamate (inhibition of release). = via calcium channel blockers, magnesia, adenosine, hypothermia, free radical scavengers
  • Inhibition of leukocyte/microglial/cytokine effects. = hypothermia, free radical synthesis inhibitors

• Blockage of downstream cellular events.
o Free radical synthesis inhibitors
o Free radical scavengers etc…

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58
Q

what are the 5 effects that therapeutic hypothermia has

A

↓ cerebral metabolism

↓ energy use

↓ accumulation of excitotoxic amino acids

↓NO synthetase activity

↓free radical activity

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59
Q

What are the symptoms of early onset GBS

A
  • Apnea
  • Severe hypoxia
  • Cardio-respiratory failure
  • Hypotension
  • Metabolic acidosis
  • Tachycardia
  • Poor perfusion
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60
Q

How do you investigate early onset GBS

A
  • Full blood count – neutropenia
  • CRP – acute phase reactant – rise may be delayed by 12 hours
  • Blood cultures
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61
Q

What are the predisposing factors to early onset GBS

A

• 1% of babies born vaginally to mothers who carry GBS become infected
• Predisposing Factors
– Evidence of chorioamnionitis including maternal fever
– Prolonged labour
– Prolonged rupture of membranes
– Low birthweight

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62
Q

what are the organisms that cause late onset sepsis in the new-born

A
  • Coagulase-negative staphylococci
  • Staph Aureus
  • Others
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63
Q

describe the genetic and acquired reasons for a small for gestational age

A 
Genetics 
•	Normal small baby
•	Chromosomal disorders. 
o	Edwards syndrome
o	Trisomy 18. 
•	Inherited disorders.

Acquired

  • Uteroplacental insufficiency - this is the most common
  • congenital infection such as CMV
  • smoking
  • maternal chronic illness such as renal or sickle cell disease
  • multiple pregnancy
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64
Q

How does utero-placental insufficiency happen

A

o Failure of syncytiotrophoblast invasion of the high resistance spiral arteries.
o Poor placental development with raised resistance in vascular bed.

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65
Q

Name some problems that neonates have if they are small for gestational age

A
  • temperature control
  • polycythemia
  • poor nutritional status
  • hypoglycaemia
  • increased risk of necrotising enterocolitis
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66
Q

why do spontaneous preterm births happen

A
  • Infection or ruptured membranes
  • Cervical incompetence
  • Polyhydramnios
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67
Q

what are the 3 main respiratory problems

A

structurally immature

  • primaritve alveolar development
  • susceptibility to oxygen toxicity

functionally immature

  • surfactant deficient
  • lack of respiratory drive - intercostal and diaphragm are weak

susceptibility to infection
 Immature immune system.
 Instrumentation of airway. - e.g. mechanical ventilation used can provide an easy way for pathogens to enter

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68
Q

what are the symptoms of respiratory distress syndrome

A

tachypnoea
expiratory grunting
recession

  • happens within 4 hours of birth
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69
Q

How do you prevent respiratory distress syndrome

A
  • Ante-natal steroids
  • Avoidance of intrauterine hypoxia
  • Prophylactic surfactant treatment
  • Keep warm, avoid acidosis – acidosis can denatures surfactant
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70
Q

What happens in chronic lung disease of the infancy

A

 Oxygen dependency in a preterm baby at 36weeks post menstrual age
 Lung injury in the preterm infant
 Inflammation, fibrosis, emphysema

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71
Q

what are the signs and symptoms for necrotising enterocolitis

A
  • abdominal distension, tenderness, discolouration
  • blood in stools
  • generalised collapse
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72
Q

What are the risk factors for necrotising enterocolitis

A
  • prematurity, hypoxia, infection, enteral feeding
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73
Q

what is the preterm central nervous system at risk of

A

Periventricular Haemorrhage (PVH)

Periventricular leucomalacia (PVL)

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74
Q

what are the risk factors for a periventricular haemorrhage

A
  • Prematurity (very rare after 34 weeks)
  • RDS
  • Pneumothorax
  • Hypercapnia
  • Acidosis
  • Hypotension
  • Instability and handling
  • Severe bruising at birth
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75
Q

overall what are the 4 main causes of death for children under 5 years

A
  1. Preterm birth complications
  2. Pneumonia.
  3. Intrapartum related events.
  4. Diarrhea.
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76
Q

How do you reduce chance of pneumonia

A
  • Breastfeeding promotion

* Hemophilus influenzae type b and pneumococcal vaccines

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77
Q

What does polymorphism mean

A

• they are polymorphic when the frequency of the minor allele in the population is >1%.

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78
Q

name the three ways how you can identify disease genes

A

positional candidates
• Identified through genome wide genetic linkage analysis.

functional candidates
- Identified by a functional association with previously identified disease genes

exome/genome sequencing

  • Identified as having rare variants in multiple unrelated affected individuals – an allelic series
  • for example you remove all the common variants and this leaves the candidates genes
  • you then get multiple people with the same condition and compare the cases to see which genes are shared between the individuals
  • eventually you end up with on candidate gene that causes the condition
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79
Q

What does diphtheria act on

A

Acts on:
o Heart: myocarditis and heart block.
o Nerves further difficulty swallowing, paralysis, diplopia.

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80
Q

what does the endotoxin do

A

 Released during lysis of the organisms.

 Leads to macrophage activation

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81
Q

describe the pathogenesis of meningococcal disease

A
  • Activation of inflammatory cascade via LPS
  • Causes release of pro-inflammatory cytokines such as. IL-6 and TNF- alpha
  • This causes myocardial depression
  • Endothelial dysfunction which causes capillary leakage and shock
  • Causes a coagulopathy – takes a long time for the blood to clot as the whole coagulation cascade is abnormal

= therefore this inflammatory reaction to LPS causes most the symptoms of septic shock

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82
Q

Name some slow bacterial infection

A 
–	Tonsillitis 
–	Otitis media
–	Urinary tract infection
–	Gastroenteritis
–	Impetigo
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83
Q

What the three common causing meningitis and septicaemia

A
  • streptococcus pneumonia
  • neisseria meningitides
  • haemophilus influenza B
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84
Q

What are the clinical symptoms of septicaemia

A
  • Tachycardia.
  • Tachypnoea.
  • Prolonged capillary refill- blood being sent to organs
  • Low BP (late sign) - common to drop blood pressure due to shock whereas in children this is a pericardia a rest and late sign that they are going to decompensate
  • Rash - doesn’t disappear usually, but you can have septicaemia without any rash
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85
Q

What are the clinical symptoms of meningitis

A
  • High temperature
  • Headaches
  • Vomiting
  • Not able to tolerate bright lights = photophobia
  • Drowsiness
  • Stiff Neck.
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86
Q

What are the symptoms of meningitis in infants

A
  • Tense or bulging soft
  • High temperature
  • Breathing fast and difficulty breathing
  • Extreme shivering
  • Cold hands and feet
  • Vomiting and refusing to feed
  • Blotchy skin getting paler or turning blue
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87
Q

what vaccinations take place at

  • 8 weeks old
  • 12 weeks old
  • 16 weeks old
  • one year
A

8 weeks old

  • Diphtheria, tetanus, peruses, polio, Hib, HepB,
  • pneumoccoal (13 serotypes)
  • Meningococcal group B
  • rotavirus, gastroenteritis

12 weeks old

  • Diphtheria, tetanus, peruses, polio, Hib, HepB,
  • rotavirus

16 weeks old

  • Diphtheria, tetanus, peruses, polio, Hib, HepB,
  • pneumoccoal (13 serotypes)
  • Meningococcal group B

one year

  • Men B
  • Hib and MenC
  • pneumococcal
  • MMR
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88
Q

What are the top 3 organisms that can cause problems in young infants before vaccination

A
  • Group B streptococcus
  • E.coli
  • Listeria
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89
Q

what are the vulnerable groups of people that are predisposes to developing pneumococcal infection

A

• Absent / non-functional spleen
– Congenital asplenia – born without a spleen
– Traumatic removal
– Hyposplenism (eg sickle cell) – spleen gets ruined as well

  • Hypogammaglobulinaemia
  • HIV infection
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90
Q

what bacteria does not having a spleen leave you vulnerable to and how do you treat it

A 
•	Vulnerable to encapsulated bacteria
–	Pneumococcus
–	HiB
–	Meningococcus
•	Vaccination
•	Lifelong penicillin daily
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91
Q

what are the invasive and non invasive features of pneumoccoal

A 
Non invasive 
•	Acute otitis media 
•	Sinusitis
•	Conjunctivitis
•	Pneumonia
Invasive 
•	Septicaemia
•	Meningitis
•	Peritonitis
•	Arthritis
•	Osteomyelitis
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92
Q

What are the symptoms of neonatal tetanus

A
  • Weak
  • Lethargic
  • Poor suck
  • Spams
  • Fits
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93
Q

what are the two types of fungi and give examples

A

Yeasts
- such as candida

Moulds
- such as aspergillum

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94
Q

what are common suerpiical mycosis

A 
•	Common
o	Candidiasis: nappy rash.
o	Tinea Corporis: ring worm.
	Treat both with topical antifungal (nystatin). 
•	Occurs in Normal Hosts
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95
Q

what are invasive mycosis

A

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.

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96
Q

what are the symptoms of malaria

A

• Can be non-specific
– Fever, lethargy, vomiting, diarrhoea

•	Severe disease
–	Anaemia
–	Respiratory distress
–	Cerebral malaria (coma, seizures)
–	Hypoglycaemia
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97
Q

What is the presentation of toxoplasmosis in the neonate

A
  • Hepatosplenomaegaly
  • Funducosopy – nasty retinitis
  • Ultrasound scan of the brain – ventricular dilation that can cause hydrocephalus
98
Q

what does the frequency of a wheeze depend on

A
  • degree of narrowing
  • elasticity of airway wall
  • local airflow
99
Q

describe congenital lobar emphysema

A
  • Over distension of lobe

* Partial bronchial obstruction

100
Q

describe what bronchogenic Cyst present

A

o Early with respiratory distress.

o Later with infection.

101
Q

What problems can cancers affect later on

A 
Growth and development 
Psychosical 
Organ function 
Cacner 
Fertility and reproduction
102
Q

what is the most common cancers in 0-14 year olds

A
  • Leukaemia (31.1%),
  • CNS (25.4%),
  • Lymphomas (10%).
103
Q

what is the most common cancer in 15-19 year olds

A
  • Lymphomas (20.7%),
  • Carcinomas and Melanoma (19.6%)
  • CNS (18.7%)
  • Leukaemia (13.8%).
104
Q

if you have wilms tumour what syndromes are you predisposed to

A

WAGR

  • Wilms tumour
  • Aniridia
  • Genito-urinary abnormalities
  • Mental retardation

Can also have
- Beckwith-wiederman syndrome (BWS)

105
Q

why is the WT1 gene linked to kidney tumours (wilms tumour)

A
  • WT1 plays a crucial role in ureteric branching
  • WT1 and the WNT pathway (activated by beta catenin) have key roles in epithelial induction of the metanephric mesenchyme
106
Q

what are the symptoms to retinoblastoma

A
  • Leukocoria – white pupil when light is shone onto it
  • Eye pain
  • Redness
  • Vision problems
107
Q

what are chemotherapy related complications

A

hearing loss, infertility, cardiac toxicity and second malignancies

108
Q

How does the patient present with acute lymphoblastic leukaemia and where does it metastasis to

A
  • Bruising/bleeding.
  • Pallor or fatigue due to anaemia.
  • Infection due to neutropenia.
  • liver, spleen, lymph nodes and mediastinum
109
Q

what are the causes of abdominal pain

A
  • Constipation
  • Functional/RAP (recurrent abdominal pain)/IBS
  • Duodenal ulcers/Helicobacter Pylori
  • Inflammatory Bowel Disease
110
Q

what are the causes of chronic vomiting/haemetemesis

A
  • GOR.
  • Intestinal Obstruction (if bile) intermittent.
  • DU (rare)
111
Q

what are the causes of rectal bleeding/blood stools

A
  • IBD
  • Chron’s/UC
  • Fissures/haemorrhoids
  • Polyps/polyposis syndromes
  • Infection (bacterial).
112
Q

what are the symptoms of IBD

A

o Weight loss
o Abdominal pains
o Tiredness
o Rectal bleeding

113
Q

what are organic causes of constipation and how would you investigate them

A
  • Hirschsprungs - rectal biopsy
  • hypothyroidism - growth failure so check TSH
  • neurologic - examines the spine and lower limbs
  • anal stenosis - examination
114
Q

what does reflex present like with children who are greater than three years old

A
  • heart burn
  • brash
  • vomiting
  • oesophagi’s
  • usually have history of reflux as an infant
115
Q

what are the RED flags and pink flags for GORS

A 
Red Flags
o	Haemetemesis
o	Failure to thrive
o	Sandifers syndrome (back arching in infants) 
o	Aspiration pneumonia.

Pink Flags
o Daily symptoms for longer than 12 months
o Failed empiric theraphy

116
Q

name 3 ways in which you can assess GORD

A
  • pH study/impedence
  • barium swallow
  • upper GI endoscopy
117
Q

how do you use a clinical score to mark GORD

A
  • the I-GERQ-R is used
  • this is a list of 12 questions that can be filled out by carers
  • measures how significant refluxes are at home over the last week
118
Q

what is the treatment of eosinophilic oesophagitis

A

• Dietary
o Food exclusions
o Pragmatic trials.

  • Oral budesonide
  • Monteleukast.
119
Q

what is the symptoms of gastritis

A
  • Vomiting
  • Abdominal pain
  • Haemetemesis
  • Anaemia.
120
Q

How do you diagnose gastritis

A
  • Endoscopy
  • Stool antigen
  • C13 breath test
121
Q

what is the presentation of crohns disease

A 
•	Abdominal pain
•	Weight loss
•	Diarrhoea 
•	Insidious onset
•	Growth failure
•	Raised ESR/CRP/low albumin/Hb. 
- raised calprotectin greater than 20
122
Q

what is the presentation of ulcitis colitis

A
  • Chronic bloody diarrhoea
  • Abdo pain
  • Weight Loss
  • Usually diagnosed within 2 months
123
Q

when should you use surgical treatment for iBD

A

– Medical treatment not working
– Obstruction or other surgical emergency
– Poor growth and localised disease in Crohn’s

124
Q

who are the two groups of children that are most likely to die at the hands of their carers

A
  • vulnerable children and children in need
125
Q

what is vulnerable children

A

A vulnerable child is defined as being under the age of 18 years and currently at high risk of lacking adequate care and protection.

126
Q

what are the risk factors for physical abuse

A

Unrelated adult male in the house

Single, young, unsupported parents

Mental health problems

Domestic violence

Drug and or alcohol Abuse

Previous parental police records

Disabled child

127
Q

what can neglect include

A

Failure to provide adequate food, shelter and clothing

Failing to protect a child from physical harm or danger

Failure to provide adequate supervision

Failure to ensure access to appropriate medical assessment and treatment

Unresponsive to a child’s basic emotional needs

128
Q

what can emotional abuse involve

A

It may involve conveying to children that they are worthless or unloved, inadequate, or valued only insofar as they meet the needs of another person.

It may feature age or developmentally inappropriate expectations being imposed on children.

It may involve seeing or hearing the ill-treatment of another.

It may involve serious bullying (including cyber-bullying), causing children frequently to feel frightened or in danger

129
Q

what is the role of a doctor in child protection

A

Complete a child protection report

Opinion-­‐ Accidental/Non-­‐accidental injury Maintain a holistic approach

Assess for other medical problems

Assess growth and development

Ensure siblings are assessed

Attend Strategy meeting

Contribute to Child Protection Conference

130
Q

what is an impairment

A

any loss or abnormality of psychological, physiological or anatomical structure or function. ( e.g. paralysis of the legs)

131
Q

what is a disability

A

any restriction or lack (resulting from impairment) of ability to perform an activity in the manner or within the range considered normal for a human being. (e.g. Inability to walk)

132
Q

what is a handicap

A

the impact of the impairment or disability on the person’s pursuit or achievement of the goals which are desired by him/her or expected of him/her by society. (e.g. unable to work in a job that requires mobility)

133
Q

iN the international classification of functioning disability and health (ICF) what are the three levels of it

A
  • Impairment in body function/structure.
  • A limitation in activity. - such as the inability to read or move around
  • A restriction in participation such as exclusion from school
134
Q

describe the 4 development screening/assessment questionnaires

A

ASQ ages and stages questionnaire – at 9 months and 2 years, parents complete, paper based, and health visitor/community nurse

SGS – schedule of growing skills - simple toys, crayons etc up to 5 years, screening tool relay

Griffiths.- formal assessment up to 6 years – takes 1 hour

Baylye – up to 2 years often used for ex premature

135
Q

what does fetal alcohol spectrum disorder look like

A
  • small head
  • flat face
  • small eye opening
  • short nose
  • low nasal bridge
  • underdeveloped jaw
  • thin upper lip
  • smooth philtrum
136
Q

what is executive function

A

An ability to organize and plan

An ability to focus and maintain attention

An ability to store and retrieve memories

An ability to inhibit inappropriate actions

An ability to prevent emotions from getting out of control

An ability to understand social situations and social behaviour

137
Q

How does fetal alcohol spectrum disorder present

A
  • Sleep disturbances, poor wake/sleep cycle
  • Poor sucking responses/feeding problems
  • Failure to thrive
  • Hyper/hypo sensitivity to light cold pain
  • Delays in walking and talking
  • Delayed toilet training
  • Difficulty in following directions
  • Temper tantrums and disobedience
  • Distractibility
138
Q

what is a conduct disorder

A

Disorder of behaviour characterised by repetitive and persistent pattern of dissocial, aggressive or defiant conduct

139
Q

who’does conduct disorder affect usually

A

Boys&raquo_space; girls

Inner cities > rural areas

Socio-economic disadvantage

Family conflict and poor communication in the family

Increased incidence in looked after children

“Difficult” temperament

Specific reading disability

140
Q

what are the three symptoms of attention deficit hyperactive disorder (ADHD)

A
  • Hyperactivity
  • inattention
  • impulsivity

Hyperactivity

  • Restless and fidgety
  • Unable to wait

Impulsivity

  • Acts without thinking
  • Answers before questions finished

Inattention

  • Jumps from task to task
  • Makes carless mistakes
  • Doesn’t listen properly
141
Q

what are the risk factors of ADHD

A
  • Boys > girls (4:1)
  • Genetic factors
  • Neuro-developmental abnormalities
  • Maternal depression
  • Smoking during pregnancy
142
Q

How do you monitor ADHD

A

Height and weight - drugs can cause growth restriction

CVS – HR and BP

Sleep - drugs can cause sleep disturbance

Tics - can develop tics with the medication so you change which medication you are giving

143
Q

describe the 4 aspects that you use to evaluate short stature

A
  1. Height centile vs weight centile.
    • Failure to thrive vs failure to grow.
2.	When started.
•	In utero
•	In infancy
•	In childhood
•	In puberty
  1. Body proportions.
    • Primary or secondary growth disorder
  2. Presenting signs.
    • Idiopathic
144
Q

What an cause disproportionate growth

A

Skeletal dysplasia

  • achondroplasia - FGFR3 mutation - due to inhibition of ossification at the growth plates resulting in the long bones not elongating
  • hydrochondroplasia FGFR3 mutation - due to structural and function receptor affected - milder and noticed later
  • leri-welli dyschonrosteosis - reduced subischial length and madelung deformitiy, due to modparts of the limb shortening

rickets - caused by Vitamin D deficiency

145
Q

describe madelung deformity and what its consists of

A
  • Bowing of the radius
  • Dorsal dislocation of the ulna
  • Premature epiphyseal fusion
146
Q

what can cause propionate growth failure

A
  • psychosocial assessment = psychical growth retardation
  • Syndrome features karyotypes = such as turners syndrome, Noonan, Williams
  • tests for systemic disorders = such as chronic renal insufficiency, gastrointestinal disease, nutritional deficiency

test for endocrine disorder s= hypothyroidism and hypercortisolism

147
Q

what are the phenotypes of turner syndrome

A
  • short stature due to SHOX haplo-insufficiency
  • webbed neck
  • shield chest, widely spaced nipples
  • cubitus valgus
  • lymphedema of the hands
  • shortening of 4th/5th metacarpal
  • knocked knees
  • gonadal dysgensis
148
Q

What are the key features of Larons syndrome

A 
Normal size at birth
Severe growth 
restriction in infancy
Distinctive facial features
Blue sclerae 
Hypoglycaemia (Insulin sensitivity
149
Q

How do you manage idiopathic short stature

A

• Administration of GH

• Oxandrolone - anabolic steroid used for a long time and extradites growth but doesn’t increase adult height
o Very little change in most cases.

150
Q

what are the symptoms of Kawasaki disease

A

Medium vessel vasculitis of childhood in those aged less than 5 years old

  • fever for at least 5 days with 4 or the following
  1. bilateral conjunctival injection, non-exudative
    - cervical lymphadenopathy
    - polymorphous rash (not petechial bulls or vesicular)
    - oral inflammation and irritation (not discrete lesions or exuate)
    - ertherma and oedema of extermetieis progression to desquamination int he second week

If not treated you end up with a giant coronary artery aneurysm

151
Q

What are the triple risk for SIDS

A
  • vulnerable infant (male, prematurity, low birth weight)
  • cortical developmental period
  • external stressor (prone position, bed sharing, minor illnesses e.g. URTI, overheating, parental smoking)
152
Q

what are mimics of abuse that you have have which are not abuse

A

Fractures

  • Sometimes seen in vaginal delivery
  • Osteopenia of prematurity
  • Vitamin D deficiency especially in breast fed babies
  • Osteogenesis imperfecta
  • Resuscitation

Shaken baby syndrome

    • Triad of encephalopathy, subdural haemorrhage (SDH), retinal haemorrhages
  • SDH - 25-46% of asymptomatic newborn babies;
  • retinal haemorrhages 34% of newborn babies (clear up to 2 months?)
153
Q

what are the risks of STIs

A

Age - depends on age, anyone can get one but shift towards younger ages

Sexual partner - male will depend on whether they have exclusively male or female parterres, sex between men has a higher risk of STIs

Sexual practice - type of sex that you have, certain sort of sex have a higher risk - anal and vaginal sex has a higher transmission than oral sex

Condom usage - present STIs

Ethnicity

Area of residence

154
Q

What are the types of chlamydia trachomatis -

A

serovars D-K

serovars L1-3 cause

155
Q

what symptoms can serovars D-K

A

Males - Urethritis - clear watery discharge, epipdidymitis, prostatitis

Females - Cervicitis(increase in vaginal discharge, spotting after sexual intercourse), Pelvic Inflammatory Disease, Fitz-Hugh Curtis - intra-abdominal syndrome

Neonate - conjunctivitis and pneumonia

156
Q

what symptoms can serovars L1-3 cause

A 
Lymphogranuloma venereum (lymphatic issues)
-   Buboes, proctitis
  • usually rectally acquired, can cause abdominal pain and change in bowel habits
157
Q

What are the symptoms of Neisseria gonorrhoea

  • males
  • females
  • neonates
A

Males – Urethritis, proctitis (rectally acquired), sore throat, epididymitis, prostatitis

Females – Cervicitis, PID, Peri-hepatitis, septic abortion

Neonates – Conjunctivitis

158
Q

How do you treat neisseria gonorrhoea

A

– Ceftriaxone

Drug resistance increasing

159
Q

How do you manage genital warts

A

Vaccination

Management

  • Topical podophyllotoxon, imiquimod
  • Cryotherapy - freeze them of
160
Q

What is the treatment of HSV

A

Aciclovir
Famciclovir - prodrugs
Valaciclovir - prodrugs

161
Q

what is another word for syphilis

A

Treponema pallidum

162
Q

Describe primary syphilis

A

Chancre usually single, painless

Dark ground positive - see organisms under the microscope

Lymphadenopathy

Serology may be negative

Infectious++

163
Q

Describe secondary syphilis

A

Rash, fever, lymphadenopathy

Condyloma lata

Serology positive

Infectious++

  • effects soles of hand and feet can cause redness
164
Q

name some DNA enveloped viruses

A

Herpes viruses

  • Herpes simplex
  • Varicella zoster
  • CMV
  • Epstein-Barr
  • HHV 6/7/8

Hepatitis B

Poxviruses

165
Q

name some non-enveloped DNA viruses

A

Papillomavirus

Adenovirus

Parvovirus (ssDNA)

  • spell out PAP, cervical smar for papillomarvirus
166
Q

how does Herpes simplex virus present in neonates

A

Disseminated HSV

  • Sepsis-like syndrome
  • Hepatitis, coagulopathy

HSV encephalitis

  • Fever, seizures
  • Haemorrhagic infarction of white matter and cortex
167
Q

How do you treat disseminated HSV

A
  • IV Aciclovir
168
Q

what are the problems with the treatment of CMV

A
  • Neutropenia,
  • thrombocytopenia
  • IV access
  • Long term fertility/malignancy risk
169
Q

what are the symptoms of CMV

A
  • sensioruneal deafness
  • calcification in the brain
  • hydrocephalus
  • extra medullary haemopoitesis
  • hepatosplenomeagly
170
Q

what are the symptoms of varicella zoster virus

A
  • rash - lasts 4-5 days

- once the lesions have crusted over they are no longer transmittable

171
Q

what are the symptoms of EBV in early life versus older children

A 
Usually asymptomatic in early life
Infectious mononucleosis (glandular fever), typically 15-25 yrs old
172
Q

What cancer can EBV cause

A

Burkitts lymphoma

173
Q

what are the symptoms of Roseola infantum

A
  • caused by HHV 6 and 7

- sudden onset of high fever which lasts a few days then suddenly stops and the rash disappears

174
Q

what are the consequences of chronic Hep B infection

A

Cirrhosis

Hepatocellular carcinoma

175
Q

How do you reduce the risk hipB of transmission at birth

A
  • give Hep B virus vaccine at birth and then at 1 month of age
  • and HBIG as well (hepatitis B immunoglobulin)
176
Q

what does poxvirus cause

A

smallpox

molluscum contagiosum - found in groin and axilla areas, spread by direct contact

177
Q

what can adenovirus cause

A

URTI / pneumonia

Conjunctivitis

Diarrhoea

Disseminated disease in immunocompromised hosts

178
Q

What are the symptoms of parovirus B19

A

Asymptomatic

‘Slapped cheek’ syndrome

Arthropathy (adults) - present with disabling arthritis

Aplastic crisis

Fetal loss in pregnant women

179
Q

What are important RNA enveloped virus

A

Measles, mumps, rubella

RSV, influenza, parainfluenza

Hepatitis C

HIV

  • MMR, RSV, influenza, parainfluenza - respiratory in presentation
  • Hepatisis C, HIV - blood infections
180
Q

What are non enveloped RNA viruses

A

Rotavirus

Enteroviruses (includes polio)

Hepatitis A

  • broadly cause enteric infections and gut infections
181
Q

what are the original symptoms of measles

and then what happens after 2 days and then 2 days after

A

Fever
Cough
Conjunctivitis
Miserable

then after 2 days get kopek spots
then after another 2 days a rash develops - usually starts behind the ear and spread downwards

182
Q

what are the symptoms of rubella

A
  • Fever
  • occipital lymphadenopathy
  • Mild rash
183
Q

what are the symptoms of congenital rubella

A

EYES: cataracts, micro-ophthalmia, glaucoma

EARS: sensorineural deafness

HEART: pulm artery stenosis, VSD

  • Low birth weight, rash, microcephaly
184
Q

How does bronchiolitis present

A
  • cough
  • respiratory distress
  • wheeze
185
Q

how do you measure the perinatal mortality rate

A

number of stillbirths and early neonatal deaths per 1000 total births

186
Q

describe how prematurity can lead to neonatal death and perinatal mortality

A
  • Surfactant deficiency
  • Periventricular haemorrhage
  • Infection
  • Necrotising enterocolitis
187
Q

What is meckel-gruber syndrome

A

Meckel-Gruber syndrome is a rare and lethal autosomal recessive disorder characterized by occipital encephalocele, postaxial polydactyly and bilateral dysplastic cystic kidneys

188
Q

List the maternal causes of still birth

A
  • diabetes
  • hypertensive disorder
  • lupus
  • APS
  • cholestasis
  • drug misuse
189
Q

what are external finings of SIDS

A
  • Body well developed and nourished
  • Frothy fluid around nose
  • Cyanosis of lipids and nail beds
190
Q

what ligament is important in preventing uterine prolapse

A
  • utter-sacral ligament
191
Q

where does a lumbar block happen

A

L4/L5

192
Q

what is the Rotterdam criteria for PCOS

A

 i)Clinical hyperandrogenaemia
 ii) oligomenorrhoea (less than 6-9 menses per year)
 Iii) 12 or more polycystic ovaries on ultrasound. Or ovaries greater than 10ml

193
Q

describe PID symptoms

A
  • Asymptomatic
  • pelvic pain
  • deep dyspareunia
  • malaise
  • fever
  • purulent vaginal discharge
194
Q

what are the symptoms of endometriosis

A

 Pain, dysmenorrhoea, menorrhagia, dyspareunia

 Ex: pelvic tenderness or mass, fixed uterus

195
Q

what are the NICE guidelines for referring someone with subfertility

A

“Offer an earlier referral for specialist consultation to discuss options for attempting conception, further assessment and appropriate treatment if:

  1. The woman in aged 36 years or over, and
  2. There is a known clinical cause of infertility or a history of predisposing factors for infertility
196
Q 
how do you assess 
- ovarian function 
- tubal function 
- uterine function 
in secondary care
A

 To assess ovulatory function:
• Bloods not done in primary care;
• Ovarian reserve testing-how female would respond to Gonadotrophin stimulation in IVF;

 To assess tubal function: Hysterosalpingogram – this is when dye is injected in the room to look at the patency of the fallopian tubes – this can be painful

 To assess uterine function: laparoscopy – for endometrioses to understand how significant things are

197
Q

what are the NICE guides for unexplained infertility

A

Do not offer clomiphene-no increased chance of pregnancy or live birth (NOTE INTERNET PURCHASES - watch out that they don’t do these).

To continue having regular unprotected intercourse for 2 years (investigations after 1 year).
Offer IVF after 2 years.

198
Q

who should you offer IVF to

A
  • Offer 3 cycles to Women under 40 who have not conceived after 2 years of unprotected intercourse or 12 cycles of artificial insemination (6 IUI).
  • Offer one cycle to 40-42 year old women if 2 years unprotected intercourse,12 cycles AI (6 or more IUI), never previously had IVF & no evidence of low ovarian reserve.
199
Q

what are the symptoms of ovarian hyper stimulation syndrome

A

 Mild: Lower abdo discomfort/distention, with or without nausea.
 Severe: Abdo pain/distention, ascites, pleural effusion, venous thrombosis

200
Q

when do you offer intracytoplasmic sperm injection (ICSI)

A
  • Severe deficits in semen quality
  • Obstructive azoospermia
  • Non-obstructive azoospermia
  • Couple in whom previous IVF treatment cycle has resulted in failed or very poor fertilisation
  • Appropriate investigations (eg semen analysis) for dx.
  • Consider genetic issues (karyotype for Kallman’s) and microdeletions on Y-chromosome.
201
Q

Who do you offer intrauterine insemination IUI to

A
  • People who are unable to have vaginal intercourse (disability).
  • Requiring specific consideration (eg sperm wash in HIV pos men)
  • Same-sex relationships
202
Q

what is the difference between a primary post part haemorrhage and a secondary post part haemorrhage

A

Primary
>500ml blood loss from the genital tract within 24 hours of delivery
- commoner

secondary
abnormal bleeding from the genital tract, from 24 hours after delivery - 6 weeks

203
Q

what are the 4 causes of primary PPH

A

 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%).

204
Q

What are the predisposing factors to a primary PPH

A

Antepartum haemorrhage in this pregnancy

Placenta praevia (15x risk)

Multiple pregnancy (5x risk)

Pre-eclampsia (4x risk)

Nulliparity (3x risk)

Previous PPH (3x risk)

Maternal obesity (2x risk)

Maternal age (increases with age)

Multiparity (parity > 4)

205
Q

what are the intrapartum risk factors for a PPH

A

Emergency Caesarean section (9x risk)

Elective CS (4x risk)

Retained placenta (5x risk)

Episiotomy (5x risk)

Operative vaginal delivery (2x risk)

Labour >12 hours (2x risk)
>4kg baby (2x risk)

Maternal pyrexia in labour (2x risk)

206
Q

What are pre-exisitng and pregnancy risk factors for thromboembolic disease

A 
1, Previous VTE
2, Thrombophilia Congenital /Acquired
3, Age over 35 years
4, Obesity (BMI >30)
5, Parity >4
6, Gross varicose veins
7, Paraplegia
8, Sickle cell disease
9, Inflammatory disorders
Pregnancy related complications 
1, Surgical procedure eg LSCS, MROP
2, Dehydration
3, Sepsis e.g. pyelonephritis
4, Pre-eclampsia
5, Excessive blood loss
6, Prolonged labour
7, Immobility after delivery
207
Q

when does post partum psychosis happen

A

o Usually first 10 days following childbirth.

208
Q

Explain the mechanism of action behind proliferation versus apoptosis of the cells in the prostate gland

A
  • in the stomal cell testosterone is converted to estradiol via aromatase this causes cell proliferation when estradiol binds to ER alpha
  • some of the oestradiol leaks across into the basal and luminal epithelium through the basement membrane and this causes apoptosis when the estradiol binds to ERbeta
  • But Testosterone is converted to DHT via 5 alpha reductase in the basal epithelium, then testosterone can either bind directly to AR or bind to AR by DHT
  • the binding to AR prevents epithelial cell apoptosis
  • but in old age too much DHT and testosterone is produced therefore there is too much proliferation and not enough oestraiol causing apoptosis
209
Q

What is the three finger test for hernias

A

index finger on DIR, middle finger on SIR and ring finger on saphenous opening. Ask cough:
 Indirect: deep inguinal ring
 Direct: superficial inguinal ring.
 Femoral: at the saphenous.

210
Q

describe the mechanism fo action of the smooth muscle relaxation during an erection

A
  • Parasympathetic neurone which is non adrenergic and non cholinergic allows calcium to enter the synapse and causes the release of nitric oxide
  • the nitric oxide then diffuses across the smooth muscle
  • NO binds to soluble gauntly cylases and produces cGMP this causes the smooth muscle to relax and decreases calcium inflow
  • then signals from the sympathetic neurone does the opposite
211
Q

what are the effects of congenital varicella syndrome

A 
Skin lesions (73%)
•	leading to limb hypoplasia

CNS (62%)
• microcephaly, hydrocephaly, neurodevelopmental delay

• cataracts/other eye problems

  • also GI, genitourinary & cardiac abnormalities
  • miscarriage
212
Q

what does toxoplasmosis cause

A

• IUGR

  • hydrocephalus,
  • cerebral calcification
  • microcephaly
  • hepatosplenomegaly
213
Q

What are the symptoms of congenial syphilis

A
  • Early i.e. 0 to 2 years
  • rash
  • rhinorrhoea
  • osteochondritis
  • perioral fissures
  • lymphadenopathy
  • GN
  • Late i.e. > 2 years
  • Hutchinson’s teeth
  • Clutton’s joints
  • high arched palate
  • deafness
  • saddle nose deformity
  • frontal bossing
214
Q

What are the risk factors of gestational diabetes

A

 Previous GDM
 FH of Diabetes
 Previous macrosomic baby - babies are larger as they receive more glucose for growth, baby can produce a large amount of amniotic fluid
 Previous unexplained stillbirth
 Obesity
 Glycosuria
 Polyhydramnios - larger baby can produce more urine and therefore cause polyhydraminos
 Large for Gestational Age (LGA) in the current pregnancy

215
Q

what are the maternal complications of gestational diabetes and type two diabetes (more likely complications if you have gestational diabetes)

A

1) Hyperglycaemia/hypoglycaemia
2) Pre-eclampsia
3) Infection
4) Thromboembolic disease

216
Q

What are the foetal complications of gestational diabetes and type 2 diabetes

A

1) Macrosomia (birth asphyxia and traumatic birth injury)
2) Respiratory Distress Syndrome
3) Hypoglycaemia - used to an rich sugary environment and then when there born they are not exposed to as much sugar
4) Hyperbilirubinaemia (Jaundice)

Congenital abnormalities ( this is to do with poor glucose control (due to pre-exisiting diabetes) in the first 12 weeks of the pregnancy)

217
Q

Group B streptococous effects on the neonate

A
  • Pneumonia
  • Meningitis
  • Non-focal sepsis
  • death
218
Q

what makes up the risk pro-life for group B streptococcus

A
  • Preterm ruptured membranes
  • Prolonged ruptured membranes
  • Previous GBS neonatal infection
  • Intrapartum fever
  • GBS bacteruiria in pregnancy
219
Q

what can cause macrosomia

A
  • macrosomia is when the baby is larger than the 95% percentile

causes
Maternal diabetes – espically if not diagnosed or controlled

Maternal obesity

Previous large babies

Prolonged pregnancy

220
Q

what are the problems with passage

A

Contracted pelvis – malnourished or have babies younger when the pelvis haven’t formed yet

Placenta praevia – haemorrhage

Soft tissue tumours = fibroids blocking the way or a big fibroid in the lower part of the uterus

Pendulous abdomen- those that have lots of babies before have lost the muscle tone in the tummy it is not as easy for the baby to come out

221
Q

what are the different problems you can have with the power of contraction

A

Uterine inertia

Inco-ordinate contractions

Hypertonic contractions

Uterine Rupture

222
Q

what are the signs of a poor fit when giving brith

A

Failure of progressive cervical dilatation

Failure of descent of the presenting part

Moulding

Caput

223
Q

what are the two signs of fatal distress in labour

A
  • Meconium-stained liquor - made out of bowel contents and disquemnetated cells
  • fetal heart rate abnormalities
224
Q

what are the problems with the 3rd stage of labour

A

Retained placenta – placenta should be out before an hour and normally within 30 minutes if not out in this time then manaual removal of the placneta

Uterine atony – cytosnoe?, emptying the bladder

Soft tissue lacerations

Uterine inversion

225
Q

what are the 6 types of miscarriage

A

Threatened

  • cervical os is closed
  • bleeding light

Inevitable

  • cervical OS open
  • bleeding heavier than threatened

Incomplete

  • cervical os is open
  • some fetal tissue has passed

Complete

  • cervical os shut and uterus is no longer open
  • not fetal tissue remaining
  • no longer bleeding

Septic

  • tender uterus, fever may be absent
  • contents of the uterus is infected

Missed

  • cervical OS closed
  • fetus has not developed and died in utero
226
Q

what are the symptoms of a septic miscarriage

A
  • Contents of uterus infected causing endometritis
  • Vaginal loss offensive
  • Tender uterus
  • May be present with sings of pelvic infection
227
Q

what are the investigations that you do in a miscarriage

A

Ultrasound scan
- Detects the location and viability – may show retained tissue, if any doubt repeat scan after 1 week (NICE)

Serum B HCG
- Increases in greater than 66% in 48 jrs in viable pregnancy

Other bloods

  • FBC
  • G+ S
  • Rhesus status - give Anti D to rhesus negative women
228
Q

How do you manage a miscarriage

A

Expectant
 Wait for spontaneous resolution
o Resuscitation if blood loss is substantial

Medical Management
 Removal of fetal tissue (using prostaglandins such as misoprostol).

Surgical Management
 Curettage (scraping instrument)/surgical aspiration.= this can cause scarring of the womb which will cause fertility problems
= done under ultrasound guidance

229
Q

What are the causes of a recurrent miscarriage

A
  • problems in the uterine cavity e.g. large fibroids
     Autoimmune disease (e.g. anti-phospholipid syndrome): 25%.
     Chromosomal defects (4%).
     Hormonal factors
     Infection.
     Others (obesity, smoking, maternal age, drug abuse
230
Q

What are the risk factors for an ectopic pregnancy

A
  • Smoking
  • Scarring in womb and previous structures
  • Previous ectopic – 10-15% chance that you will have another
  • STIs
  • Emergency contraction
  • IVF
  • Pelvic surgery
  • IUCD in situ
231
Q

How do women present with ectopic pregnancies

A

Women of reproductive age

  • Positive pregnancy test/ Amenorrhoea 4-10 weeks
  • PV bleeding
  • Low abdo pain
  • Collapse +/- shoulder tip pain

find
 Tachycardia, abdominal tenderness.
 Uterus is smaller than expected gestation
 Cervical os is closed.

232
Q

what do you manage the complete molar pregnancy

A
  • surgery to remove the molar tissue
  • 15% of molar tissue remains in the deeper tissue of the body and this can result in a gestational tumour
  • need to have chemotherapy to get rid of it
233
Q

How do you manage a partial molar pregnancy

A
  • surgery to remove the molar tissue
  • only 1% will have abnormal cells remaining in the deep tissue and have a persistent gestational tumour - this will need to have chemotherapy to get rid of it
234
Q

What are the clinical features of a molar pregnancy

A

 PV Bleeding
 HG (excess HCG production)
o HCG secreted by syncytiotrophoblast.
 Passage of vesicles per vaginum.

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

235
Q

what are the causes of an antepartum haemorrhage

A 
Placenta abruption
Placental praevia
Incidental genital tract pathology
Uterine rupture
Vasa praevia
236
Q

what are the risk factors for placenta abruption

A
  • Prev abruption,
  • ↑ BP, Trauma
  • Smoking
  • idiopathic
  • Multiparity
  • ECV
  • Polyhydramnios
237
Q

Why are the clinical features of placental abruption

A
  • Intense constant abdo pain
  • +/- PV bleeding
  • Shock, Oliguria, DIC
  • Tense ‘woody’ uterus
  • Fetal heart rate weak or absent
238
Q

what are the risk factors of a placenta praevai

A

Prior praevia

Multiparity

Multiple pregnancy

Advanced maternal age

Prev LSCS

Smoking

239
Q

what are the clinical signs of a placenta praevia

A
  • Painless vaginal bleeding: usually between 32-37 weeks
  • Uterus soft and non tender
  • Malpresentation is common
  • Requires c section delivery
  • May result in pre-term delivery
240
Q

What are the risk factors for pre-eclampsia

A
  • age
  • previous
  • diabetes
  • obesity
  • hypertension
  • autoimmune diseases
  • sickle cell disease
  • high age gap between pregnancies e.g. not having a pregnancy for 10 years

placental abnormalities

  • hypoxia
  • ischemia repercussion injury
  • damage to the placental vili
241
Q

what are the signs and symptoms of pre eclampsia

A
  • Headaches
  • Seeing spots
  • Stomach pain
  • Feeling nausea and throwing up

Human Development 2 (34 decks)

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