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Phase 3a topics > Bits and bobs > Flashcards

Bits and bobs Flashcards

1
Q

gene and chromosome cystic fibrosis

A

CFTR - codes a cAMP-regulated chloride channel

F508 on the long arm of chromosome 7

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2
Q

Organisms which may colonise CF patients?

A

Staphylococcus aureus
Pseudomonas aeruginosa
Burkholderia cepacia
Aspergillus

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3
Q

Diagnostic test cystic fibrosis

A

sweat test - high sweat chloride
normal value < 40 mEq/l,
CF indicated by > 60 mEq/l

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4
Q

Cystic fibrosis drug

A

Lumacaftor/Ivacaftor (Orkambi)

Fluclox to prevent s.aureus

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5
Q

Investigation bronchiolitis

A

immunoflurescence of nasal secretions may show RSV

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6
Q

Investigation - pyloric stenosis

A

Ultrasound to visualise thickened pylorus

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7
Q

Blood gas pyloric stenosis

A

Hypochloric, hypokalaemic metabolic alkalosis

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8
Q

Management pyloric stenosis

A

laparoscopic pyloromyotomy

known as Ramstedt’s pyloromyotomy

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9
Q

management of transposition of the great arteries

A
  1. prostaglandin infusion
  2. Balloon septostomy
  3. Open heart surgery
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10
Q

Fever pain score?

A

A score of 2 – 3 gives a 34 – 40% probability (consider abx) and 4 – 5 gives a 62 – 65% probability of bacterial tonsillitis (give abx)

Fever during previous 24 hours
P – Purulence (pus on tonsils)
A – Attended within 3 days of the onset of symptoms
I – Inflamed tonsils (severely inflamed)
N – No cough or coryza

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11
Q

recurrent tonsilitis tonsilectomy criteria

A

> 3 episodes per year for 3 years
5 episodes per year for two years
7 episodes in a single year

  • refer to ENT
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12
Q

what lobe?
seizure

Hallucinations (auditory/gustatory/olfactory), Epigastric rising/Emotional, Automatisms (lip smacking/grabbing/plucking), Deja vu/Dysphasia post-ictal)

A

Temporal lobe (HEAD)

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13
Q

What lobe seizure?

Head/leg movements, posturing, post-ictal weakness, Jacksonian march

A

Frontal lobe (motor)

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14
Q

what lobe seizure?

paraesthesia

A

Parietal lobe (sensory)

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15
Q

what lobe seizure?

floaters/flashes

A

Occipital lobe (visual)

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16
Q

What contraceptives are unaffected by enzyme inducing anti-epleptic drugs?

A

Copper intrauterine device
Progesterone injection (Depo-provera)
Mirena intrauterine system

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17
Q

criteria for diagnosis of rheumatic fever

A

A diagnosis of rheumatic fever can be made when there is evidence of recent streptococcal infection, plus:

Two major criteria OR
One major criteria plus two minor criteria

The mnemonic for the Jones criteria is JONES – FEAR.

Major Criteria:
J – Joint arthritis
O – Organ inflammation, such as carditis
N – Nodules
E – Erythema marginatum rash
S – Sydenham chorea

Minor Criteria:
Fever
ECG Changes (prolonged PR interval) without carditis
Arthralgia without arthritis
Raised inflammatory markers (CRP and ESR)

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18
Q

investigations rheumatic fever

A

Throat swab for bacterial culture
ASO antibody titres
Echocardiogram, ECG and chest xray can assess the heart involvement

A diagnosis of rheumatic fever is made using the Jones criteria

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19
Q

Brain scan where does encephalitis classically affect

A

temporal lobe

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20
Q

inheritance percentages children carrier and affected - autosomal recessive

A

autosomal recessive condition there is a 50% chance that their next child will be a carrier

25% chance that the child will actually have the disease (be homozygous).

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21
Q

pathophysiology ITP

A

Antibodies are directed against the glycoprotein IIb/IIIa or Ib-V-IX complex. It is an example of a type II hypersensitivity reaction.

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22
Q

when is management indicated for ITP? what are options?

A

If the platelet count is very low (e.g. < 10 * 109/L) or there is significant bleeding.

  • oral/IV corticosteroid eg prednisolone
  • IV immunoglobulins
  • platelet transfusions can be used in an emergency (e.g. active bleeding) but are only a temporary measure as they are soon destroyed by the circulating antibodies
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23
Q

when can children with scarlet fever return to school?

A

24 hours after commencing abx

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24
Q

Hypsarrhythmia on EEG

A

Infantile spasms (west’s syndrome)

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25
Q

What birth defects are sodium valproate associated with

A

neural tube defects

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26
Q

epilepsy management pregnancy

A

aim for mono therapy

lamotrigine is often best choice

5mg folic acid prior to getting pregnant if possible

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27
Q

Sections of APGAR score?

A

Appearance, Pulse, Grimace, Activity, and Respiration
each either 2/1/0

Appearance/Colour: pink, peripheral blue, all blue

Pulse: >100, <100, absent

Reflex irritability: cries on stimulation/sneeze/cough, grimace, nil

Muscle tone:active movement, limb flexion, flaccid

Respiratory effort:Strong crying, weak irregular, nil

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28
Q

Osteogenesis imperfecta on xray

A

Radiology may show translucent bones, multiple fractures, particularly of the long bones, wormian bones (irregular patches of ossification) and a trefoil pelvis.

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29
Q

Normal lumbar puncture result

A

clear appearance

glucose 70% of plasma

protein 0.3 g/l

WCC 2 per mm^3 (neuts)

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30
Q

Bacterial meningitis LP result

A

Cloudy

Glucose low (< 1/2 plasma) bacteria using up the glucose

Protein high (> 1 g/l) bacteria releasing proteins

WCC 10 - 5,000 polymorphs/mm³ the immune system releases neutrophils in response to bacteria

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31
Q

Viral meningitis LP result

A

Clear/cloudy

Glucose 60-80% of plasma glucose* viruses don’t really use glucose

Protein normal/raised viruses may release a small amount of protein

WCC 15 - 1,000 lymphocytes/mm³ the immune system releases lymphocytes in response to viruses

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32
Q

Tuberculous LP result

A

Slight cloudy, fibrin web

glucose Low (< 1/2 plasma)

Protein high >1g/l

WCC 30-300 lymphocytes/mm3

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33
Q

Management of brain abscess?

A

surgery - craniotomy

IV antibiotics: IV 3rd-generation cephalosporin + metronidazole

intracranial pressure management: e.g. dexamethasone

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34
Q

Pathophysiology Duchenne’s muscular dystrophy and beckers?

A

It is caused by a defective gene for dystrophin on the X-chromosome. Dystrophin is a protein that helps hold muscles together at the cellular level.

Becker’s muscular dystrophy is very similar to Duchennes, however the dystrophin gene is less severely affected and maintains some of its function.

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35
Q

Inheritance Duchenne’s and beckers?

A

X-linked recessive

If a mother is a carrier and she has a child, that child will have a 50% chance of being a carrier if they are female and 50% chance of having the condition if they are male

Given that boys have a single X-chromosome and girls have two, girls have a spare copy of the dystrophin gene. Female carriers of the condition do not usually notice any symptoms. This makes Duchenne’s muscular dystrophy an X-linked recessive condition.

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36
Q

when does a limp warrant urgent same day assessment?

A

if child is <3 years old

if child is febrile

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37
Q

triad of the shaken baby syndrome

A

Retinal haemorrhages
Subdural haematoma
Encephalopathy

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38
Q

EEG : 3Hz generalized, symmetrical

A

absence seizures

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39
Q

EEG centro-temporal spikes

A

Benign rolandic epilepsy

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40
Q

GI conditions associated with down’s?

A

duodenal atresia
hirschsprung’s disease

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41
Q

Cardiac complications in down’s

A

multiple cardiac problems may be present
endocardial cushion defect (most common, 40%, also known as atrioventricular septal canal defects)
ventricular septal defect (c. 30%)
secundum atrial septal defect (c. 10%)
tetralogy of Fallot (c. 5%)
isolated patent ductus arteriosus (c. 5%)

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42
Q

Monitoring in down’s

A

Regular thyroid checks (2 yearly) - at risk of hypothyroidism

Echocardiogram - cardiac defects

Audiometry regular - hearing impairment - recurrent otitis media and glue ear etc.

Regular eye checks - myopia, strabismus, cataracts

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43
Q

What type of jaundice causes dark urine and pale stools

A

In obstructive jaundice (both intrahepatic cholestasis and extrahepatic obstruction) the serum bilirubin is principally conjugated. Conjugated bilirubin is water soluble and is excreted in the urine, giving it a dark colour (bilirubinuria).

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44
Q

Defintion nephrotic syndrome

A

the presence of proteinuria (>3.5 g/24 hours)

hypoalbuminaemia (<30 g/L)

peripheral oedema.

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45
Q

Philadelphia chromosome t(9;22)

A

chronic myeloid leukemia

65+

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46
Q

Most common leukemia in children? triad?

A

Acute lymphoblastic leukemia

anaemia, thrombocytopenia, neutropenia

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47
Q

Genetics and inheritance sickle cell

A

autosomal recessive

abnormal variant called haemoglobin S (HbS)

abnormal gene for beta-globin on chromosome 11

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48
Q

Definitive diagnosis sickle cell disease

A

haemoglobin electrophoresis

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49
Q

Management sickle cell

A

General:
- avoid dehydration and triggers
- vaccines inc pneumococcal polysaccharide vaccine every 5 years
- abx prophylaxis eg penicillin V
- hydroxycarbamide (stimulate fetal HbF)
- blood transfusion
- bone marrow transplant can be curative

vaso-occlusive pripism:
- aspiration of blood

splenic sequestration:
- blood transfusion and fluid resus

aplastic:
- blood transfusion

acute chest:
- abx and antivirals
- blood trans
- ventilation

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50
Q

reticulocyte count sickle cell anaemia?

A

high (needing to constantly make new rbc)

may be low in aplastic crisis

normal is 0.45–1.8 percent

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51
Q

cause of aplastic crisis sickle cell

A

parovirus B19

reticulocytes may be low

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52
Q

gold standard investigations sickle cell

A

Haemaglobin electrophoresis

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53
Q

blood film sickle cell

A

A blood film shows target cells and Howell-Jolly bodies.

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54
Q

ehlers danlos syndrome

inheritance
pathophysiology
cardiac
hypermobile scoring

A

hypermobile, stretchy skin

autosomal dominant

type 3 collagen

aortic regurg,dissection, mitral prolapse

beighton score

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55
Q

Rotterdam critera

A

The Rotterdam criteria are used for making a diagnosis of polycystic ovarian syndrome. A diagnosis requires at least two of the three key features:

Oligoovulation or anovulation, presenting with irregular or absent menstrual periods (generally defined as fewer than six to nine menstrual cycles per year)

Hyperandrogenism, characterised by hirsutism and acne

Polycystic ovaries on ultrasound (or ovarian volume of more than 10cm3)

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56
Q

Invetsigations PCOS

A

pelvic ultrasound: transvaginal

FSH, LH, prolactin, TSH, and testosterone are useful investigations

(raised LH:FSH ratio is a ‘classical’ feature but is no longer thought to be useful in diagnosis. Prolactin may be normal or mildly elevated. Testosterone may be normal or mildly elevated - however, if markedly raised consider other causes)

2-hour 75g oral glucose tolerance test (OGTT)

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57
Q

General management PCOS

A

weight loss, orlistat if bmi>30

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58
Q

Investigations to establish diagnosis of ALL/leukemias

A

Full blood count, which can show anaemia, leukopenia, thrombocytopenia and high numbers of the abnormal WBCs
Blood film, which can show blast cells
Bone marrow biopsy
Lymph node biopsy

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59
Q

murmur turners

A

ejection systolic murmur due to bicuspid aortic valve

A bicuspid aortic valve is an aortic valve that has two flaps (cusps) instead of three. It may cause a narrowed or obstructed aortic valve opening (aortic valve stenosis),

or systolic subclavicular from coarctation

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60
Q

rotavirus vaccine information

A

it is an oral, live attenuated vaccine

2 doses are required, the first at 2 months, the second at 3 months

the first dose should not be given after 14 weeks + 6 days and the second dose cannot be given after 23 weeks + 6 days due to a theoretical risk of intussusception

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61
Q

Contraindications to lumbar puncture

A

focal neurological signs
papilloedema
significant bulging of the fontanelle
disseminated intravascular coagulation
signs of cerebral herniation

For patients with meningococcal septicaemia a lumbar puncture is contraindicated - blood cultures and PCR for meningococcus should be obtained.

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62
Q

Degenerative cervical myelopathy

A

Presentation: myelopathy: pain (affecting the neck, upper or lower limbs) loss of fine motor function (dexterity, clumsy) loss of sensory function causing numbness, loss of autonomic function, hoffmans

Causes: Cervical spondylosis (osteophyte), disc herniation

Investigation: MRI

Management: decompressive surgery

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63
Q

Neoplastic spinal cord compression

A

Presentation: cancer patient, back pain, bilateral weakness, UMN signs. First symptom: back pain

Investigation: MRI of whole spine

Management: high dose dexamethasone and oncology assessment

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64
Q

Brown-sequard syndrome

A
  • ipsilateral dorsal column signs
  • ipsilateral corticospinal tract signs
  • contralateral spinothalamic tract signs
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65
Q

Subacute combined degeneration of spinal cord

A

Presentation: bilateral dorsal column signs, may have bilateral corticospinal tract signs (affects posterior cord)

Cause: B12 deficiency

Prevention: Always replace vitamin B12 before folate - giving folate to a patient deficient in B12 can precipitate subacute combined degeneration of the cord

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66
Q

Friedrich’s ataxia

A

Presentation: teenage corticospinal, spinocerebellar, dorsal column and peripheral nerves

Information: autosomal recessive trinucleotide repeat disorder resulting in reduced level or function of the frataxin protein.

Investigation: genetic analysis

Management: supportive

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67
Q

Syringomyelia

A

Pathophysiology: development of a fluid-filled cyst (a syrinx) around the spinal canal.

Causes: Chiari malformation, tumour, trauma

Presentation: ‘central cord syndrome’ bilateral spinothalamic and/or bilateral corticospinal tract symptoms. The upper limbs are affected first whilst the lower limbs are spared until much later. As the fibres of the spinothalamic tract enter the spinal cord and immediately decussate, they pass close to the spinal canal, meaning they are often the first of these white matter fibres to be compressed and damaged. As the cervical cord is the most likely location of the lesion, there is classically said to be a “cape-like” loss of pain and temperature sensation.

Investigation: full spine MRI with contrast and brain MRI

Management: treat cause. If persistent : shunt

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68
Q

Lumbar spinal stenosis

A

Presentation: back pain, bilateral leg weakness or unilateral, positional element: better on walking up hill and sitting forward. Ddx claudication

Investigation: MRI

Management: Laminectomy

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69
Q

Ankylosing spondylitis

A

Presentation: young man, lower back pain and stiffness, worse in morning
Investigation: plain x ray of sacroiliac joints
Management: encourage regular exercise such as swimming, NSAIDs are the first-line treatment, physiotherapy

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70
Q

Myelopathy vs radiculopathy

A

Myelopathy: bilateral as spinal cord and bladder/bowel, not always painful “clumsiness” “loss of manual dexterity”

Radiculopathy: radiating limb pain, often in the pattern of the dermatome, sharp/shooting in character, with only a small proportion (about 5%) having associated neurologic symptoms such as dermatomal sensory loss, and even less commonly myotomal muscle weakness.

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71
Q

Myotomes upper limb

A

C5 – Elbow flexion (and shoulder abduction)
C6 – Wrist extension (and shoulder adduction) (and elbow flexion)
C7 – Elbow extension (and wrist flexion)
C8 – Finger flexion and thumb extension
T1 – Finger abduction

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72
Q

Myotomes lower limb

A

L2 – Hip flexion
L3 – Knee extension
L4 – Ankle dorsiflexion
L5 – Great toe extension
S1 – Ankle plantarflexion

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73
Q

Dermatome Thumb + index finger

A

C6

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74
Q

Dermatome middle finger + palm of hand

A

C7

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75
Q

Dermatome ring + little finger

A

C8

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76
Q

Dermatome nipples

A

T4

T4 at the Teat Pore

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77
Q

Dermatome xyphoid process

A

T6

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78
Q

Dermatome umbillicus

A

T10

BellybuT-TEN

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79
Q

Dermatome inguinal ligament

A

L1

L for ligament, 1 for 1nguinal

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80
Q

Dermatome knee caps

A

L4

Down on aLL fours - L4

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81
Q

Dermatome big toe, dorsum of foot (except lateral aspect)

A

L5

Largest of the 5 toes

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82
Q

Dermatome Lateral foot, small toe

A

S1

the smallest 1

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83
Q

Dermatome genetalia

A

S2, S3

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84
Q

Cauda equina most common cause

A

central disc prolapse at L4/5 or L5/S1

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85
Q

newborn resus steps

A
  1. Dry baby and maintain temperature
  2. Assess tone, respiratory rate, heart rate
  3. If gasping or not breathing give 5 inflation breaths*
  4. Reassess (chest movements)
  5. If the heart rate is not improving and <60bpm start compressions and ventilation breaths at a rate of 3:1
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86
Q

child resuscitation

A
  1. Safety
  2. Stimulate - put hand on head, shake a limb, flick fingers and toes
  3. Shout - 2222
  4. Open airway - head tilt-chin lift, jaw thrust if ?spinal injury
  5. Look, listen, feel
  6. 5 rescue breaths (pinch nose and breathe into their nose)
    CPR 15 chest compressions, 2 ventilations (1 hand or 2 hands) ⅓ to ½ of chest 100-120 per minute, allow for recoil, lower sternum (for one minute, if no help yet go get help yourself)
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87
Q

Parkinsons disease tremor

A

Unilateral resting tremor (improves with voluntary movement)

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88
Q

Causes of drug-induced parkinsonism

A

Antipsychotics or antiemetic metoclopramide can cause EPSE.

In patients with parksinons, prescribe antiemetic domperidone as it doesn’t cross BBB therefore doesn’t cause EPSE

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89
Q

Invetsigation lewy-body

A

SPECT/DaTSCAN

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90
Q

When is expectant management of ectopic pregnancy indicated?

A

size < 35
no pain
unruptured
no heart beat
hCG <1,000IU/L
another intrauterine pregnancy

Expectant management involves closely monitoring the patient over 48 hours and if B-hCG levels rise again or symptoms manifest intervention is performed.

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91
Q

When is methotrexate management of ectopic pregnancy indicated?

A

size < 35
minimal pain
unruptured
no heart beat
hCG <1,500IU/L
must be willing to attend follow up

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92
Q

When is surgical management of ectopic pregnancy indicated? options?

A

size > 35
pain
unruptured or ruptured
fetal heart beat
hCG >5,000IU/L

Salpingectomy is first-line for women with no other risk factors for infertility

Salpingotomy should be considered for women with risk factors for infertility such as contralateral tube damage

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93
Q

Risk factors for ectopic pregnancy

A

damage to tubes (pelvic inflammatory disease, surgery)
previous ectopic
endometriosis
IUCD
progesterone only pill
IVF (3% of pregnancies are ectopic)

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94
Q

Most common site of ectopic pregnancy

A

ampulla of fallopian tube

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95
Q

The investigation of choice for ectopic pregnancy

A

transvaginal USS

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96
Q

Management of miscarriage <6 weeks gestation?

A

expectant then pregnancy test in 7-10 days to confirm

refer if any pain etc (ectopic?)

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97
Q

Management of miscarriage >6 weeks gestation?

A

refer to early pregnancy assessment service
transvaginal USS

Expectant : if no infection risk/bleeding risk. pregnancy test in 3 weeks

Medical : misoprolol (prostaglandin analogue –> stimulate contractions)

Surgical : Manual vacuum aspiration under local anaesthetic as an outpatient or electric vacuum aspiration under general anaesthetic

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98
Q

Management of incomplete miscarriage

A

Medical : misoprolol
Surgical: Evacuation of retained products of conception (ERPC)

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99
Q

Management intestinal malrotation with volvulus

A

Ladd’s procedure

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100
Q

causes pulmonary hypoplasia

A

oligohydramnios
congenital diaphragmatic hernia

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101
Q

what is enuresis

A

‘involuntary discharge of urine by day or night or both, in a child aged 5 years or older, in the absence of congenital or acquired defects of the nervous system or urinary tract’

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102
Q

ToF features

A

ventricular septal defect (VSD)
right ventricular hypertrophy
right ventricular outflow tract obstruction, pulmonary stenosis
overriding aorta

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103
Q

When do pregnant women need prophylaxis for VTE? what prophylaxis is given?

A

Low molecular weight heparin eg dalteparin, enoxaparin, and tinzaparin

If previous DVT

Or x number of risk factors:
Age > 35
Body mass index > 30
Parity > 3
Smoker
Gross varicose veins
Current pre-eclampsia
Immobility
Family history of unprovoked VTE
Low risk thrombophilia
Multiple pregnancy
IVF pregnancy

4 or more risk factors warrants immediate treatment with low molecular weight heparin continued until six weeks postnatal. I

3 risk factors low molecular weight heparin should be initiated from 28 weeks and continued until six weeks postnatal.

If diagnosis of DVT is made shortly before delivery, continue anticoagulation treatment for at least 3 month, as in other patients with provoked DVTs.

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104
Q

An abortion can be performed before 24 weeks if ?

A

continuing the pregnancy involves greater risk to the physical or mental health of:

The woman

Existing children of the family

The threshold for when the risk of continuing the pregnancy outweighs the risk of terminating the pregnancy is a matter of clinical judgement and opinion of the medical practitioners.

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105
Q

An abortion can be performed at any time during the pregnancy if?

A

Continuing the pregnancy is likely to risk the life of the woman

Terminating the pregnancy will prevent “grave permanent injury” to the physical or mental health of the woman

There is “substantial risk” that the child would suffer physical or mental abnormalities making it seriously handicapped

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106
Q

trimesters of pregnancy

A

First Trimester (0 to 13 Weeks)
Second Trimester (14 to 26 Weeks)
Third Trimester (27 to 40 Weeks)

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107
Q

criteria hyperemesis gravidarum

A

More than 5 % weight loss compared with before pregnancy

Dehydration

Electrolyte imbalance

assess severity with Pregnancy-Unique Quantification of Emesis (PUQE) score. This gives a score out of 15:
< 7: Mild
7 – 12: Moderate
> 12: Severe

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108
Q

when to admit someone with hyperemesis gravidarum

A

admission should be considered in cases of ketonuria and/or weight loss despite use of oral anitemetics

Unable to tolerate oral antiemetics or keep down any fluids

More than 5 % weight loss compared with pre-pregnancy

Ketones are present in the urine on a urine dipstick (2 + ketones on the urine dipstick is significant)

Other medical conditions need treating that required admission

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109
Q

associations with hyperemesis gravidarum?

A

multiple pregnancies
trophoblastic disease
hyperthyroidism
nulliparity
obesity

Smoking is associated with a decreased incidence of hyperemesis.

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110
Q

Types of molar pregnancy

A

complete - 2 sperm, no genetic material in ovum

partial - 2 sperm, genetic material in ovum

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111
Q

Presentation, invetsigation and management of molar pregnancy?

A

More severe morning sickness
Vaginal bleeding
Increased enlargement of the uterus
Abnormally high hCG
Thyrotoxicosis (hCG can mimic TSH and stimulate the thyroid to produce excess T3 and T4)

Ultrasound of the pelvis shows a characteristic “snowstorm appearance”. histology of material after for diagnostic.

  1. referred to the gestational trophoblastic disease centre
  2. evacuation of uterus
  3. effective contraception is recommended to avoid pregnancy in the next 12 months
  4. monitor hCG until normal
  5. check for choriocarcinoma
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112
Q

Glasgow coma scale components and scoring

A

Glasgow coma scale (GCS) out of 15

Motor response
6. Obeys commands
5. Localises to pain
4. Withdraws from pain
3. Abnormal flexion to pain (decorticate posture)
2. Extending to pain
1. None

Verbal response
5. Orientated
4. Confused
3. Words
2. Sounds
1. None

Eye opening
4. Spontaneous
3. To speech
2. To pain
1. None

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113
Q

MRC power grades

A

Grade 0
No muscle movement

Grade 1
Trace of contraction

Grade 2
Movement at the joint with gravity eliminated

Grade 3
Movement against gravity, but not against added resistance

Grade 4
Movement against an external resistance with reduced strength

Grade 5
Normal strength

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114
Q

Reflex nerve roots

A

Ankle = S1
Miss out 2
Knee = L3,4
Brachioradialis = C5,6
Biceps = C5,6
Triceps = C7

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115
Q

Causes and ddx features cranial third nerve palsy

A

Surgical third nerve palsy : painful, dilated pupil

Diabetes : not painful, reactive pupil

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116
Q

Bell’s palsy

presentation and management

A

lower motor neuron facial nerve palsy - forehead affected

oral prednisolone within 72 hours

if the paralysis shows no sign of improvement after 3 weeks, refer urgently to ENT

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117
Q

Triple assessment breast

A

Clinical assessment (history and examination)

Imaging (ultrasound or mammography)

Histology (fine needle aspiration or core biopsy)

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118
Q

When should IV thrombolysis with mechanical thrombectomy be offered for ischaemic stroke?

A

Thrombectomy within 6 hours of onset
Thrombolysis within 4.5 hours onset

Both if occlusion if proximal anterior circulation on CTA or MRA

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119
Q

Wernikes aphasia

Presentation
Location

A

Receptive aphasia

Fluent speech, doesn’t make any sense, comprehension impaired

Lesion in superior temporal gurus

Supplied by inferior division of left MCA

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120
Q

Brocas aphasia

Presentation
Location
Blood supply

A

Non-fluent laboured and halting speech. Repetition impaired (expressive)

Inferior frontal gyrus
Superior division of left MCA

Spoken word is heard at the ear. This passes to Wernicke’s area in the temporal lobe (near the ear) to comprehend what was said. Once understood, the signal passes along the arcuate fasciculus, before reaching Broca’s area. The Broca’s area in the frontal lobe (near the mouth) then generates a signal to coordinate the mouth to speak what is thought (fluent speech).

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121
Q

Conduction aphasia

Presentation
Location

A

Speech fluent but repetition is poor
Aware of errors

Arcuate fasiculus (connection between brocas and wernikes)

Spoken word is heard at the ear. This passes to Wernicke’s area in the temporal lobe (near the ear) to comprehend what was said. Once understood, the signal passes along the arcuate fasciculus, before reaching Broca’s area. The Broca’s area in the frontal lobe (near the mouth) then generates a signal to coordinate the mouth to speak what is thought (fluent speech).

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122
Q

UMN signs

A

Minimal muscle atrophy

Weakness ‘Pyramidal’ pattern i.e. weakness of upper limb extensors, lower limb flexors So upper limb is flexed and lower limb extended (think hemiplegic gait)

Slightly reduced power

Hyperreflexia of deep tendon reflexes- as no UMN regulating that reflex

Absent superficial reflex - babinski positive

Hypertonia + or - clonus (Spasticity occurs in pyramidal tract lesions) such as clonus and clasp-knife rigidity

Pronator drift

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123
Q

management of extradural hematoma

A

stabilising the patient followed by surgical intervention with a burr hole or craniotomy to evacuate the haematoma.

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124
Q

blood vessel implicated by extradural hematoma

A

middle meningeal artery

eminem getting hit by a lemon

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125
Q

ct scan subdural hematoma

A

concave crescent-shaped

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126
Q

blood vessel implicated in subdural hematoma

A

bridging veins

old man drinking alcohol in a cave with a bridge outside and a crescent moon in the sky

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127
Q

management subdural hematoma

A

Small or incidental acute subdurals can be observed conservatively.

If big or signs then surgical options include monitoring of intracranial pressure and decompressive craniectomy.

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128
Q

Causes SAH

A

Ruptured cerebral aneurysm or trauma

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129
Q

conditions associated with berry aneurysms

A

adult polycystic kidney disease

Ehlers-Danlos syndrome

Coarctation of the aorta

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130
Q

ct scan for SAH

A

Acute blood (hyperdense/bright on CT) is typically distributed in the basal cisterns, sulci and in severe cases the ventricular system.

may be normal - do LP

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131
Q

lumbar puncture for SAH

A

LP is performed at least 12 hours following the onset of symptoms to allow the development of xanthochromia (the result of red blood cell breakdown).

Xanthochromia helps to distinguish true SAH from a ‘traumatic tap’ (blood introduced by the LP procedure).

As well as xanthochromia, CSF findings consistent with subarachnoid haemorrhage include a normal or raised opening pressure

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132
Q

invetsigation after spontaneous SAH confirmed?

A

CT intracranial angiogram

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133
Q

Management SAH

A
  1. referral to neurosurgery after confirmation
  2. coil by interventional radiologists
  3. or craniotomy
  4. 21-day course of nimodipine (a calcium channel inhibitor targeting the brain vasculature)
  5. Hydrocephalus is temporarily treated with an external ventricular drain
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134
Q

treatment of radiculopathy

A

Similar to that of other musculoskeletal lower back pain: analgesia, physiotherapy, exercises

If symptoms persist after 4-6 weeks then referral for consideration of MRI is appropriate

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135
Q

narcolepsy associations

A

associated with HLA-DR2

it is associated with low levels of orexin (hypocretin), a protein which is responsible for controlling appetite and sleep patterns

early onset of REM sleep

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136
Q

features narcolepsy

A

typical onset in teenage years
hypersomnolence
cataplexy (sudden loss of muscle tone often triggered by emotion)
sleep paralysis
vivid hallucinations on going to sleep or waking up

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137
Q

investiagtions narcolepsy

A

multiple sleep latency EEG

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138
Q

management narcolepsy

A

daytime stimulants (e.g. modafinil) and nighttime sodium oxybate

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139
Q

Managing Hirsutism PCOS

A

weight loss
Co-cyprindiol (Dianette) for 3 months*
Topical eflornithine

Specialist:
Electrolysis
Laser hair removal
Spironolactone (mineralocorticoid antagonist with anti-androgen effects)
Finasteride (5α-reductase inhibitor that decreases testosterone production)
Flutamide (non-steroidal anti-androgen)
Cyproterone acetate (anti-androgen and progestin)

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140
Q

Management acne PCOS

A

Co-cyprindiol (Dianette) for 3 months*

Topical adapalene (a retinoid)
Topical antibiotics (e.g. clindamycin 1% with benzoyl peroxide 5%)
Topical azelaic acid 20%
Oral tetracycline antibiotics (e.g. lymecycline)

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141
Q

Managing infertility PCOS

A

weight loss

Clomifene (causes ovulation, selective estrogen receptor modulator (SERM).)

Laparoscopic ovarian drilling

In vitro fertilisation (IVF)

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142
Q

reducing risk of endometrial cancer pcos

A

Mirena coil for continuous endometrial protection

Inducing a withdrawal bleed at least every 3 – 4 months with either:
Cyclical progestogens (e.g. medroxyprogesterone acetate 10mg once a day for 14 days)
Combined oral contraceptive pill

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143
Q

PCOS blood results

A

high LH
high LH:FSH ratio

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144
Q

turners blood results

A

high LH and FSH

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145
Q

management turner syndrome

A

Growth hormone therapy can be used to prevent short stature

Oestrogen and progesterone replacement can help establish female secondary sex characteristics, regulate the menstrual cycle and prevent osteoporosis
Fertility treatment can increase the chances of becoming pregnant

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146
Q

inheritance androgen insensitivity syndrome?

A

x linked

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147
Q

blood results androgen insensitivity syndrome

A

High LH, High/normal testosterone

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148
Q

diagnostic invetsigation androgen insensitivity

A

buccal smear or chromosomal analysis to reveal 46XY genotype

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149
Q

Presentation of CAH neonate? why?

A

Hyponautramia, shocked, hyperkalaemia
Poor feeding
Vomiting
Dehydration
Arrhythmias

as aldosterone is low so not adequate resorption of sodium and water/excretion of potassium

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150
Q

most common cause CAH?

others?

A

21-hydroxylase deficiency

11-beta hydroxylase deficiency (5%)
17-hydroxylase deficiency (very rare)

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151
Q

inheritance CAH

A

autosomal recessive

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152
Q

Management CAH

A

Hydrocortisone- Cortisol replacement

Fludrocortisone - Aldosterone replacement

Female patients with “virilised” genitals may require corrective surgery

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153
Q

Pathophysiology CAH

A

21-hydroxylase deficiency (90%) (responsible for biosynthesis of aldosterone + cortisol)

21-hydroxylase is the enzyme responsible for converting progesterone into aldosterone and cortisol. Progesterone is also used to create testosterone, but this conversion does not rely on the 21-hydroxylase enzyme. In CAH, there is a defect in the 21-hydroxylase enzyme. Therefore, because there is extra progesterone floating about that cannot be converted to aldosterone or cortisol, it gets converted to testosterone instead. The result is a patient with low aldosterone, low cortisol and abnormally high testosterone.

High progesterone also seems to inhibit menstruation and so leads to primary or secondary amenorrhoea.

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154
Q

Most common cause of secondary amenorrhoea

A

pregnancy

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155
Q

what is hypothalamic amenorrhoea

A

The hypothalamus reduces the production of GnRH in response to significant physiological or psychological stress. This leads to hypogonadotropic hypogonadism and amenorrhoea. The hypothalamus responds this way to prevent pregnancy in situations where the body may not be fit for it, for example:

Excessive exercise (e.g. athletes)
Low body weight and eating disorders
Chronic disease
Psychological stress

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156
Q

what type of amenorrhoea would prolactin secreting pituitary tumour cause

A

High prolactin levels act on the hypothalamus to prevent the release of GnRH. Without GnRH, there is no release of LH and FSH. This causes hypogonadotropic hypogonadism.

eg pituitary adenoma

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157
Q

what is sheehans syndrome

A

Sheehan’s syndrome (SS) is postpartum hypopituitarism caused by necrosis of the pituitary gland. It is usually the result of severe hypotension or shock caused by massive hemorrhage during or after delivery. Patients with SS have varying degrees of anterior pituitary hormone deficiency.

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158
Q

definition secondary amenorrhoea

A

Cessation of menstruation for 3-6 months in women with previously normal and regular menses, or 6-12 months in women with previous oligomenorrhea

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159
Q

define premature ovarian insufficiency

A

menopause before the age of 40 years

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160
Q

blood results premature ovarian insufficiency

A

Raised LH and FSH levels (gonadotropins)
Low oestradiol levels

hypergonadotrophic hypogonadism

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161
Q

diagnosis of premature ovarian insufficiency

A

FSH level persistently raised (more than 25 IU/l) on two consecutive samples separated by more than four weeks to make a diagnosis.

menopause symptoms

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162
Q

Management of premature ovarian insufficiency

A

Traditional hormone replacement therapy
Combined oral contraceptive pill
Adequate vitamin D and calcium intake

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163
Q

Diagnosing menopause

A

A diagnosis of perimenopause and menopause can be made in women over 45 years with typical symptoms, without performing any investigations.

NICE guidelines (2015) recommend considering an FSH blood test to help with the diagnosis in:
Women under 40 years with suspected premature menopause
Women aged 40 – 45 years with menopausal symptoms or a change in the menstrual cycle

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164
Q

Ashermans presentation

A

presents following recent dilatation and curettage, uterine surgery or endometritis with:
Secondary amenorrhoea (absent periods)
Significantly lighter periods
Dysmenorrhoea (painful periods)

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165
Q

Ashermans diagnosis and management

A

Hysteroscopy is the gold standard investigation, and can involve dissection and treatment of the adhesions

reoccurence is common

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166
Q

treatment vasomotor symptoms menopause

A

fluoxetine, citalopram or venlafaxine

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167
Q

hCG

interuterine pregnancy
ectopic
miscarriage

A

The developing syncytiotrophoblast of the pregnancy produces hCG. In an intrauterine pregnancy, the hCG will roughly double every 48 hours. This will not be the case in a miscarriage or ectopic pregnancy.

A rise of more than 63% after 48 hours is likely to indicate an intrauterine pregnancy. A repeat ultrasound scan is required after 1 – 2 weeks to confirm an intrauterine pregnancy. A pregnancy should be visible on an ultrasound scan once the hCG level is above 1500 IU / l.

A rise of less than 63% after 48 hours may indicate an ectopic pregnancy. When this happens the patient needs close monitoring and review.

A fall of more than 50% is likely to indicate a miscarriage. A urine pregnancy test should be performed after 2 weeks to confirm the miscarriage is complete.

168
Q

Blood results rickets?

vit D
calcium
phosphate
ALP
parathyroid hormone

A

Serum 25-hydroxyvitamin D - less than 25 nmol/L is deficient

Serum calcium may be low
Serum phosphate may be low
Serum alkaline phosphatase may be high
Parathyroid hormone may be high

169
Q

management rickets

A

Vitamin D (ergocalciferol).

children between 6 months and 12 years is 6,000 IU per day for 8 – 12 weeks.

170
Q

diagnosis rickets

A

need xray

171
Q

most common cause of disproportionate short stature

A

achondroplasia

172
Q

maintenance fluids neonates

A

10% dextrose
Day 1 – 60 mls/kg/day
Day 2 – 90 mls/kg/day
Day 3 – 120 mls/kg/day
Day 4 – 150 mls/kg/day

From day 2
Na 3 mmol/kg/day
K 2 mmol/kg/day
Ca 1 mmol/kg/day (rarely)

173
Q

estimating weight ?

A

(Age + 4) x2 = weight in kg

174
Q

maintenance fluids children

A

0.9% sodium chloride + 5% glucose (+/- KCl)
Weight Daily (ml/24h)

First 10 kg 100 ml/kg
Next 10 kg 50 ml/kg
Every other kg 20 ml/kg

Rate (ml/h): Total (ml) / 24

175
Q

signs of shock

% defecit?

A

Reduced consciousness
Cold, mottled peripheries
Low blood pressure
Prolonged capillary refill time
Weak peripheral pulses
Anuria

10%

176
Q

signs of dehydration

%defecit?

A

Thirst
Dry lips
Restlessness, irritability
Sunken eyes
Reduced skin turgor
Decreased urine output
Altered responsiveness
Normal blood pressure
Normal CRT
Skin colour normal

5%

177
Q

calculating fluids to correct deficit

A

Deficit(%) x 10 x Wt(kg)

+ maintenance

178
Q

hydration if can tolerate oral

A

give 50 ml/kg low osmolarity oral rehydration solution (ORS) solution over 4 hours, plus ORS solution for maintenance, often and in small amounts

continue breastfeeding

consider supplementing with usual fluids (including milk feeds or water, but not fruit juices or carbonated drinks)

179
Q

what bolus would you give in shock

A

20 mls/kg of 0.9% sodium chloride bolus

(note: no glucose)

10ml/kg more appropriate on some occasions eg cardiac, kidneys, DKA
Seek expert advice (for example, from the paediatric intensive care team) if 40–60 ml/kg of IV fluid or more is needed as part of the initial fluid resuscitation.

180
Q

signs of hypernautraemic dehydration?

A

jittery movements
increased muscle tone
hyperreflexia
convulsions
drowsiness or coma

181
Q

What is PPH

A

bleeding after delivery of the baby and placenta

500ml after a vaginal delivery
1000ml after a Caesarean section

182
Q

Severity of PPH blood loss

A

Minor <1000
Moderate 1000-2000
Major >2000

183
Q

Primary vs secondary PPH

A

Primary - within 24 hours of birth
Secondary > 24 hours after birth

184
Q

Causes of PPH

A

T – Tone (uterine atony – the most common cause)
T – Trauma (e.g. perineal tear)
T – Tissue (retained placenta)
T – Thrombin (bleeding disorder

185
Q

Risk factors PPH

A

Previous PPH
Multiple pregnancy
Obesity
Large baby
Failure to progress in the second stage of labour
Prolonged third stage
Pre-eclampsia
Placenta accreta
Retained placenta
Instrumental delivery
General anaesthesia
Episiotomy or perineal tear

186
Q

Preventing PPH

A

Treating anaemia during the antenatal period

Giving birth with an empty bladder (a full bladder reduces uterine contraction)

Active management of the third stage (with intramuscular oxytocin in the third stage)

Intravenous tranexamic acid can be used during caesarean section (in the third stage) in higher-risk patients

187
Q

Management PPH

A

Resuscitation with an ABCDE approach
Lie the woman flat, keep her warm and communicate with her and the partner
Insert two large-bore cannulas
Bloods for FBC, U&E and clotting screen
Group and cross match 4 units
Warmed IV fluid and blood resuscitation as required
Oxygen (regardless of saturations)
Fresh frozen plasma is used where there are clotting abnormalities or after 4 units of blood transfusion

188
Q

Mechanical treatments to stop bleeding in PPH

A
  • rubbing uterus/fundus
  • catheter
189
Q

Medical treatments to stop bleeding in PPH

A

Oxytocin (slow injection followed by continuous infusion) 40 units in 500ml

Ergometrine (intravenous or intramuscular) stimulates smooth muscle contraction (contraindicated in hypertension)

Carboprost (intramuscular) is a prostaglandin analogue and stimulates uterine contraction (caution in asthma)

Misoprostol (sublingual) is also a prostaglandin analogue and stimulates uterine contraction

Tranexamic acid (intravenous) is an antifibrinolytic that reduces bleeding

190
Q

Surgical management to stop bleeding PPH

A

Intrauterine balloon tamponade – inserting an inflatable balloon into the uterus to press against the bleeding

B-Lynch suture – putting a suture around the uterus to compress it

Uterine artery ligation – ligation of one or more of the arteries supplying the uterus to reduce the blood flow

Hysterectomy is the “last resort” but will stop the bleeding and may save the woman’s life

191
Q

Causes of secondary PPH

A
  • retained products of conception
  • infection (endometritis)
192
Q

Investigations for secondary PPH

A
  • USS for RPOC
  • high vaginal swab for infection
193
Q

Abdo USS whirlpool pattern

A

Ovarian torsion

194
Q

When do you give anti-D to non-sensitised Rh -ve mother’s?

A

28 and 34 weeks

195
Q

In what situations should an anti-D be given within 72 hours

A

delivery of a Rh +ve infant, whether live or stillborn

any termination of pregnancy

miscarriage if gestation is > 12 weeks
ectopic pregnancy (if managed surgically, if managed medically with methotrexate anti-D is not required)

external cephalic version

antepartum haemorrhage

amniocentesis, chorionic villus sampling, fetal blood sampling

abdominal trauma

196
Q

Tests for rehusus sensitisation ?

A

all babies born to Rh -ve mother should have cord blood taken at delivery for FBC, blood group & direct Coombs test

Coombs test: direct antiglobulin, will demonstrate antibodies on RBCs of baby

Kleihauer test: add acid to maternal blood, fetal cells are resistant (do after a sensitisation event to see if further foses of anti-d are required)

197
Q

How will an affected fetus present - rhesus sensitisation

A

oedematous (hydrops fetalis, as liver devoted to RBC production albumin falls)
jaundice, anaemia, hepatosplenomegaly
heart failure
kernicterus
treatment: transfusions, UV phototherapy

198
Q

Mittelschmerz?

A

Ovulation pain

199
Q

Missed miscarriage

A

the fetus is no longer alive, but no symptoms have occurred

200
Q

Threatened miscarriage

A

vaginal bleeding with a closed cervix and a fetus that is alive

201
Q

Inevitable miscarriage

A

vaginal bleeding with an open cervix

202
Q

Incomplete miscarriage

A

retained products of conception remain in the uterus after the miscarriage

203
Q

Complete miscarriage

A

a full miscarriage has occurred, and there are no products of conception left in the uterus

204
Q

Anembryonic pregnancy

A

a gestational sac is present but contains no embryo

205
Q

Diagnosing miscarriage

A

transvaginal ultrasound

206
Q

Gravida (G)

A

is the total number of pregnancies a woman has had

207
Q

Primigravida

A

refers to a patient that is pregnant for the first time

208
Q

Multigravida

A

refers to a patient that is pregnant for at least the second time

209
Q

Para (P)

A

refers to the number of times the woman has given birth after 24 weeks

210
Q

Nulliparous (“nullip”)

A

refers to a patient that has never given birth after 24 weeks gestation

211
Q

Primiparous

A

technically refers to a patient that has given birth after 24 weeks gestation once before (see below)

The term primiparous, or “primip” is a bit confusing. Technically, it refers to a woman that has given birth once before. However, it is often used on the labour ward to refer to a woman that is due to give birth for the first time (and has never given birth before). You may hear patients referred to on the labour ward as a “primip” when they have never given birth before.

212
Q

when do fetal movements start?

A

20 weeks

If fetal movements have not yet been felt by 24 weeks, referral should be made to a maternal fetal medicine unit

213
Q

vaccines in pregnancy?

A

Whooping cough (pertussis) from 16 weeks gestation

Influenza (flu) when available in autumn or winter

Live vaccines, such as the MMR vaccine, are avoided in pregnancy.

214
Q

what is part of ‘booking bloods’ antenatal?

A

A set of booking bloods are taken for:

Blood group, antibodies and rhesus D status
Full blood count for anaemia
Screening for thalassaemia (all women) and sickle cell disease (women at higher risk)

Patients are also offered screening for infectious diseases, by testing antibodies for:

HIV
Hepatitis B
Syphilis

Screening for Down’s syndrome may be initiated depending on the gestational age. Bloods required for the combined test are taken from 11 weeks onwards.

215
Q

What congenital abnormality is lithium associated with, especially in first trimester?

A

ebsteins anomaly

216
Q

features of congenital rubella

A

Congenital deafness
Congenital cataracts
Congenital heart disease (PDA and pulmonary stenosis)
Learning disability

217
Q

chickenpox in pregnancy complications

A

More severe cases in the mother, such as varicella pneumonitis, hepatitis or encephalitis

Fetal varicella syndrome

Severe neonatal varicella infection (if infected around delivery)

218
Q

exposure to chicken pox during pregnancy? Investigation and management

A

When they are not sure about their immunity, test the VZV IgG levels. If positive, they are safe.

When they are not immune, they can be treated with IV varicella immunoglobulins as prophylaxis against developing chickenpox. This should be given within ten days of exposure.

219
Q

chickenpox rash in pregnancy and > 20 weeks gestastion

A

oral aciclovir

220
Q

congenital varicella syndrome

A

Fetal growth restriction
Microcephaly, hydrocephalus and learning disability
Scars and significant skin changes located in specific dermatomes
Limb hypoplasia (underdeveloped limbs)
Cataracts and inflammation in the eye (chorioretinitis)

221
Q

why should pregnanct women avoid foods such as blue cheese, unpasteurised foods, processed meats

A

Listeriosis in pregnant women has a high rate of miscarriage or fetal death. It can also cause severe neonatal infection.

222
Q

parovirus b19 in pregnancy?

A

Miscarriage or fetal death
Severe fetal anaemia
Hydrops fetalis (fetal heart failure)
Maternal pre-eclampsia-like syndrome

223
Q

Category 1 caesarean sections should occur within how long of decision?

A

30 minutes

224
Q

pathophysiology parovirus b19 and fetal anaemia

A

Fetal anaemia is caused by parvovirus infection of the erythroid progenitor cells in the fetal bone marrow and liver.

These cells produce red blood cells, and the infection causes them to produce faulty red blood cells that have a shorter life span.

Less red blood cells results in anaemia. This anaemia leads to heart failure, referred to as hydrops feta

225
Q

what babies are at risk of respiratory distress syndrome

A

below 32 weeks gestation

Other risk factors for SDLD include
male sex
diabetic mothers
Caesarean section
second born of premature twins

226
Q

cxr respiratory distress syndrome

A

ground glass appearance

227
Q

prevention/management respiratory distress syndrome

A

dexamethasone to mum before delivery

endotracheal surfactant
CPAP
O2 to maintain sats between 91-95

228
Q

defintion bronchopulmonary dysplasia/CLDP

A

Infants who still have an oxygen requirement at a post-menstrual age of 36 weeks are described as having bronchopulmonary dysplasia (BPD) or chronic lung disease.

229
Q

investigation bronchopulmonary dysplasia

A

cxr widespread opacification, hyperinflation and atelectasis, may have cystic changes

A formal sleep study to assess their oxygen saturations during sleep supports the diagnosis and guides management. Babies may be discharged from the neonatal unit on a low dose of oxygen to continue at home, for example 0.01 litres per minute via nasal cannula. They are followed up to wean the oxygen level over the first year of life.

230
Q

Pneumatosis intestinalis

A

gas in bowel wall - sign of NEC

231
Q

investigation for NEC

A

abdo xray
dilated loops of bowel

232
Q

diagnostic test g6pd deficiency

A

G6PD enzyme assay around 3 months after an acute episode of hemolysis

RBCs with the most severely reduced G6PD activity will have hemolysed → reduced G6PD activity → not be measured in the assay → false negative results

233
Q

things that can ppt a crisis in g6pd

A

anti-malarials: primaquine
ciprofloxacin
sulph- group drugs: sulphonamides, sulphasalazine, sulfonylureas

infections
broad (fava) beans

234
Q

diagnosis of spherocytosis

A

family history + blood results :MCHC high, high reticulocytes, spherocytes

if ambiguous: EMA binding test and the cryohaemolysis test
for atypical presentations : electrophoresis analysis of erythrocyte membranes is the method of choice

235
Q

congenital defect in the anterior abdominal wall just lateral to the umbilical cord

A

Gastroschisis

vaginal delivery may be attempted
newborns should go to theatre as soon as possible after delivery, e.g. within 4 hours

236
Q

the abdominal contents protrude through the anterior abdominal wall but are covered in an amniotic sac formed by amniotic membrane and peritoneum.

A

Exomphalos (omphalocoele)

caesarean section is indicated to reduce the risk of sac rupture
a staged repair may be undertaken as primary closure may be difficult due to lack of space/high intra-abdominal pressure

Associations
Beckwith-Wiedemann syndrome
Down’s syndrome
cardiac and kidney malformations

237
Q

triad of features toxoplasmosis

A

Intracranial calcification
Hydrocephalus
Chorioretinitis

238
Q

defintion neonatal hypoglycaemia

management

A

glucose < 2.6 mmol/L

asymptomatic
encourage normal feeding (breast or bottle)
monitor blood glucose

symptomatic or very low blood glucose
admit to the neonatal unit
intravenous infusion of 10% dextrose

239
Q

causes cleft lip/palate

A

polygenic inheritance
maternal antiepileptic use increases risk

240
Q

definiton recurrent miscarriage

A

three or more consecutive miscarriages.

241
Q

main causes of recurrent miscarriage

A

Idiopathic (particularly in older women)
Antiphospholipid syndrome
Hereditary thrombophilias eg factor V leidin
Uterine abnormalities

242
Q

Chronic Histiocytic Intervillositis

A

Chronic histiocytic intervillositis is a rare cause of recurrent miscarriage, particularly in the second trimester. It can also lead to intrauterine growth restriction (IUGR) and intrauterine death.

The condition is poorly understood. Histiocytes and macrophages build up in the placenta, causing inflammation and adverse outcomes. It is diagnosed by placental histology showing infiltrates of mononuclear cells in the intervillous spaces.

243
Q

Small for gestational age vs intrauterine growth restriction

A

Small for gestational age is defined as a fetus that measures below the 10th centile for their gestational age (doesn’t state if pathoplogical or not)

intrauterine growth restriction (IUGR), is when there is a small fetus (or a fetus that is not growing as expected) due to a pathology

244
Q

causes of placenta mediated growth restriction

A

Idiopathic
Pre-eclampsia
Maternal smoking
Maternal alcohol
Anaemia
Malnutrition
Infection
Maternal health conditions

245
Q

causes of non-placenta mediated growth restriction

A

Genetic abnormalities
Structural abnormalities
Fetal infection
Errors of metabolism

246
Q

complications of fetal growth restriction

A

Short term complications of fetal growth restriction include:
Fetal death or stillbirth
Birth asphyxia
Neonatal hypothermia
Neonatal hypoglycaemia

Growth restricted babies have a long term increased risk of:
Cardiovascular disease, particularly hypertension
Type 2 diabetes
Obesity
Mood and behavioural problems

247
Q

How is growth of fetus measured

A

symphysis fundal height (SFH) from 24 weeks

serial growth scans with umbilical artery doppler if need closer invetsigation due to:
- SFH being < 10th centile at 24 weeks
- Three or more minor risk factors
- One or more major risk factors
- Issues with measuring the symphysis fundal height (e.g. large fibroids or BMI > 35)

248
Q

when is early delivery considered for small for gestational age?

A

when growth is static

249
Q

defintion of low birth weight

A

less than 2500g

250
Q

main risk for large for gestational age

A

shoulder dystocia

251
Q

Investigations for a large for gestational age baby ?

A

Ultrasound to exclude polyhydramnios and estimate the fetal weight
Oral glucose tolerance test for gestational diabetes

252
Q

causes macrosmia

A

Constitutional
Maternal diabetes
Previous macrosomia
Maternal obesity or rapid weight gain
Overdue
Male baby

253
Q

defintion large for gestational age

A

large for gestational age (also known as macrosomia) when the weight of the newborn is more than 4.5kg at birth.

An estimated fetal weight above the 90th centile is considered large for gestational age.

254
Q

what type of twin pregnancy has best outcomes?

A

diamniotic, dichorionic twin pregnancies

255
Q

lambda sign or twin peak sign pregnancy

A

diamniotic, dichorionic

256
Q

T sign pregnancy

A

Monochorionic diamniotic

257
Q

no membrane separating twins pregnancy

A

monochorionic, monoamniotic

258
Q

when are monoamniotic twins delivered, how?

A

elective caesarean section at between 32 and 33 + 6 weeks.

259
Q

when are diamniotic twins delivered?

A

36 and 36 + 6 weeks for uncomplicated monochorionic diamniotic twins

37 and 37 + 6 weeks for uncomplicated dichorionic diamniotic twins

Vaginal delivery is possible when the first baby has a cephalic presentation (head first)
Caesarean section may be required for the second baby after successful birth of the first baby
Elective caesarean is advised when the presenting twin is not cephalic presentation

260
Q

what do UTIs in pregnancy increase the risk of?

A

pre-term birth

261
Q

testing for UTIs in pregancy

A

MSU for sensitivities and cultures routinely (at booking and at appointments) - treat asymptomatic bacteraemia during pregnancy

MSU and dip when symptomatic

262
Q

folic acid dosage pregnancy

A

400mcg per day from prior to getting pregnant

Women with folate deficiency/epileptic drugs/pre-existing diabetes/BMI>30 are started on folic acid 5mg daily.

263
Q

when are pregnant women screened for anaemia

A

Booking clinic
28 weeks gestation

264
Q

cut offs for treating anaemia in women? in pregnancy and post partum

A

Hb
<115 non-pregnant
<110 first trimester (booking appt)
<105 2nd/3rd trimester
<100 post partum

265
Q

anaemia treatment pregnancy

A

ferrous sulphate 200mg three times daily

266
Q

what should people with B12 deficiency be tested for?

A

pernicious anaemia (checking for intrinsic factor antibodies).

267
Q

investigation of choice DVT?

A

Doppler ultrasound

The Wells score is not validated for use in pregnant women. D-dimers are not helpful in pregnant patients, as pregnancy is a cause of a raised D-dimer.

268
Q

investigations for pulmonary embolism : initial and definitive

A

Chest xray
ECG

There are two main options for establishing a definitive diagnosis: CT pulmonary angiogram (CTPA) or ventilation-perfusion (VQ) scan.

CTPA is the test for patients with an abnormal chest xray
CTPA carries a higher risk of breast cancer for the mother (minimal absolute risk)
VQ scan carriers a higher risk of childhood cancer for the fetus (minimal absolute risk)

Patients with a suspected deep vein thrombosis and pulmonary embolism should have a Doppler ultrasound initially, and if a DVT is present, they do not require a VQ scan or CTPA to confirm a PE. The treatment for DVT and PE are the same.

The Wells score is not validated for use in pregnant women. D-dimers are not helpful in pregnant patients, as pregnancy is a cause of a raised D-dimer.

269
Q

Management of venous thromboembolism in pregnancy

A

low molecular weight heparin (LMWH). Examples of LMWH are enoxaparin, dalteparin and tinzaparin. The dose is based on the woman’s weight at the booking clinic, or from early pregnancy.

LMWH should be started immediately, before confirming the diagnosis in patients where DVT or PE is suspected and there is a delay in getting the scan. Treatment can be stopped when the investigations exclude the diagnosis.

When the diagnosis is confirmed, LMWH is continued for the remained of pregnancy, plus six weeks postnatally, or three months in total (whichever is longer). There is an option to switch to oral anticoagulation (e.g. warfarin or a DOAC) after delivery. An individual risk assessment is performed before stopping anticoagulation, with advice from a haematologist if necessary.

270
Q

Management pregnant women with PE and haemodynamic compromise

A

Unfractionated heparin
Thrombolysis
Surgical embolectomy

271
Q

pathophysiology pre-eclampsia

A

Pre-eclampsia is caused by high vascular resistance in the spiral arteries and poor perfusion of the placenta. This causes oxidative stress in the placenta, and the release of inflammatory chemicals into the systemic circulation, leading to systemic inflammation and impaired endothelial function in the blood vessels.

272
Q

pre-eclampsia definition

A

NICE guidelines for diagnosis:
Systolic blood pressure above 140 mmHg
Diastolic blood pressure above 90 mmHg

PLUS any of:
Proteinuria (1+ or more on urine dipstick)

Organ dysfunction (e.g. raised creatinine, elevated liver enzymes, seizures, thrombocytopenia or haemolytic anaemia)

Placental dysfunction (e.g. fetal growth restriction or abnormal Doppler studies

Triad : hypertension after 20 weeks, proteinuria, oedema

273
Q

what is eclampsia

A

seizures due to pre-eclampsia

274
Q

which factors mean women will be offered aspirin for pre-eclampsia prophylaxis? how long given for?

A

From 12 weeks until birth

One high-risk factors:
Pre-existing hypertension
Previous hypertension in pregnancy
Existing autoimmune conditions (e.g. systemic lupus erythematosus)
Diabetes
Chronic kidney disease

2 or more moderate risk factors:
Older than 40
BMI > 35
More than 10 years since previous pregnancy
Multiple pregnancy
First pregnancy
Family history of pre-eclampsia

275
Q

proteinuria in pregnancy values

A

Urine protein:creatinine ratio (above 30mg/mmol is significant)

Urine albumin:creatinine ratio (above 8mg/mmol is significant)

276
Q

test to rule out pre-eclampsia

A

The NICE guidelines (2019) recommend the use of placental growth factor (PlGF) testing on one occasion during pregnancy in women suspected of having pre-eclampsia.

Placental growth factor is a protein released by the placenta that functions to stimulate the development of new blood vessels. In pre-eclampsia, the levels of PlGF are low.

NICE recommends using PlGF between 20 and 35 weeks gestation to rule-out pre-eclampsia.

277
Q

management of pre-existing diabetes in pregnancy

A

folic acid 5mg
stick to metformin and insulin
aim for same levels as in gestational diabetes
retinopathy screening after booking and at 28 weeks
planned delivery between 37 and 38 + 6 weeks

278
Q

complications of gestational diabetes

A

hypoglycaemia of newborn
macrosmia

279
Q

gram positive colour

A

purple

stays purple, stay positive

280
Q

what does blood spot heel prick test for?

A

9 things

CF
congenital hypothyroidism
sickle cell
metabolic diseases: maple syrup, PKU etc

281
Q

posterior triangle of neck swelling

anterior triangle of neck swelling

A

cystic hydroma

branchial cyst

282
Q

test for thrush

A

Often treatment for candidiasis is started empirically, based on the presentation.

Testing the vaginal pH using a swab and pH paper can be helpful in differentiating between bacterial vaginosis and trichomonas (pH > 4.5) and candidiasis (pH < 4.5).

A high vaginal charcoal swab with microscopy can confirm the diagnosis.

283
Q

gold standard investigation osteomyelitis

A

MRI

284
Q

management thrush

A
  1. oral fluconazole 150 mg as a single dose first-line

clotrimazole 500 mg intravaginal pessary as a single dose if oral therapy is contraindicated

If there are vulval symptoms, consider adding a topical imidazole in addition to an oral or intravaginal antifungal

  1. if pregnant then only local treatments (e.g. cream or pessaries) may be used - oral treatments are contraindicated
285
Q

diagnosis gonnorrhoea

A

NAAT

A standard charcoal endocervical swab should be taken for microscopy, culture and antibiotic sensitivities before initiating antibiotics. This is particularly important given the high rates of antibiotic resistance.

286
Q

Management gonorrhoea

A

A single dose of intramuscular ceftriaxone 1g if the sensitivities are NOT known

A single dose of oral ciprofloxacin 500mg if the sensitivities ARE known

287
Q

test of cure gonorrhoea

A

This is with NAAT testing if they are asymptomatic, or cultures where they are symptomatic. BASHH recommend a test of cure at least:

72 hours after treatment for culture
7 days after treatment for RNA NATT
14 days after treatment for DNA NATT

288
Q

Disseminated Gonococcal Infection

A

Various non-specific skin lesions
Polyarthralgia (joint aches and pains)
Migratory polyarthritis (arthritis that moves between joints)
Tenosynovitis
Systemic symptoms such as fever and fatigue

289
Q

test for chlamydia

A

NAAT

290
Q

management of chlamydia

A

First-line for uncomplicated chlamydia infection is doxycycline 100mg twice a day for 7 days.

The guidelines previously recommended a single dose of azithromycin 1g orally as an alternative.

291
Q

management of chlamydia in pregnancy and breast feeding

A

Azithromycin 1g stat then 500mg once a day for 2 days

292
Q

Lymphogranuloma Venereum

A

Lymphogranuloma venereum (LGV) is a condition affecting the lymphoid tissue around the site of infection with chlamydia. It most commonly occurs in men who have sex with men (MSM). LGV occurs in three stages:

The primary stage involves a painless ulcer (primary lesion). This typically occurs on the penis in men, vaginal wall in women or rectum after anal sex.

The secondary stage involves lymphadenitis. This is swelling, inflammation and pain in the lymph nodes infected with the bacteria. The inguinal or femoral lymph nodes may be affected.

The tertiary stage involves inflammation of the rectum (proctitis) and anus. Proctocolitis leads to anal pain, change in bowel habit, tenesmus and discharge. Tenesmus is a feeling of needing to empty the bowels, even after completing a bowel motion.

Doxycycline 100mg twice daily for 21 days is the first-line treatment for LGV recommended by BASHH

293
Q

unilateral conjunctivitis

A

Chlamydial conjunctivitis

294
Q

what is trichomonas

A

Trichomonas vaginalis is a type of parasite spread through sexual intercourse. Trichomonas is classed as a protozoan, and is a single-celled organism with flagella.

295
Q

complications of chlamydia?

A

Pelvic inflammatory disease
Chronic pelvic pain
Infertility
Ectopic pregnancy
Epididymo-orchitis
Conjunctivitis
Lymphogranuloma venereum
Reactive arthritis

296
Q

trichomonas complications

A

Contracting HIV by damaging the vaginal mucosa
Bacterial vaginosis
Cervical cancer
Pelvic inflammatory disease
Pregnancy-related complications such as preterm delivery.

297
Q

pregnancy complications chlamydia

A

Preterm delivery
Premature rupture of membranes
Low birth weight
Postpartum endometritis
Neonatal infection (conjunctivitis and pneumonia)

298
Q

investigation trichomonas

A

high vaginal charcoal swab with microscopy

299
Q

management trichomonas

A

metronidazole

300
Q

raised vaginal pH - value? indicate?

A

> 4.5

  • BV
  • trichomonas
301
Q

investigation genital herpes

A

clinical but can do:

Viral PCR swab from a lesion can confirm the diagnosis and causative organism.

302
Q

management genital herpes

A

Aciclovir

303
Q

genital herpes and pregnancy

A

Primary HSV-2 <28 weeks gestation
- aciclovir during the initial infection
- regular prophylactic aciclovir starting from 36 weeks gestation
- if asymptomatic at delivery can have a vaginal delivery (provided it is more than six weeks after the initial infection)

Primary HSV-2 >28 weeks gestation
- aciclovir during the initial infection followed immediately by regular prophylactic aciclovir.
- Caesarean section

Recurrent HSV-2
carries a low risk of neonatal infection (0-3%), even if the lesions are present during delivery. Regular prophylactic aciclovir is considered from 36 weeks gestation to reduce the risk of symptoms at the time of delivery.

304
Q

tests for syphillis

A

Antibody testing for antibodies to the T. pallidum bacteria can be used as a screening test for syphilis.

Patients with suspected syphilis or positive antibodies should be referred to a specialist GUM centre for further testing.

Samples from sites of infection can be tested to confirm the presence of T. pallidum with:
Dark field microscopy
Polymerase chain reaction (PCR)

The rapid plasma reagin (RPR) and venereal disease research laboratory (VDRL) tests (assessing for active infection) 2481632 thing

305
Q

treatment syphillis

A

deep intramuscular dose of benzathine benzylpenicillin (penicillin)

306
Q

Mycoplasma genitalium (MG)

A

bacteria that causes non-gonococcal urethritis

307
Q

investigation mycoplasma genitalium

A

Nucleic acid amplification tests (NAAT)

308
Q

management mycoplasma genitalium

A

Course of doxycycline followed by azithromycin for uncomplicated genital infections:

Doxycycline 100mg twice daily for 7 days then;
Azithromycin 1g stat then 500mg once a day for 2 days (unless it is known to be resistant to macrolides)

Moxifloxacin is used as an alternative or in complicated infections. Azithromycin alone is used in pregnancy and breastfeeding (remember doxycycline is contraindicated).

309
Q

testing for HIV

A

Antibody testing for screening (blood test) - needs 3 months to show up

Testing for the p24 antigen. This can give a positive result earlier in the infection compared with the antibody test.

PCR testing for the HIV RNA levels tests directly for the number of viral copies in the blood, giving a viral load.

310
Q

CD4 count

A

500-1200 cells/mm3 is the normal range

Under 200 cells/mm3 is considered end-stage HIV (AIDS) and puts the patient at high risk of opportunistic infections

311
Q

Viral load HIV - undetectable level?

A

Viral load is the number of copies of HIV RNA per ml of blood.

“Undetectable” refers to a viral load below the lab’s recordable range (usually 50 – 100 copies/ml).

The viral load can be in the hundreds of thousands in untreated HIV.

312
Q

management of HIV

A

Two NRTIs (e.g. tenofovir and emtricitabine) plus a third agent.

313
Q

management if CD4 is less than 200

A

Prophylactic co-trimoxazole (Septrin) to protect against pneumocystis jirovecii pneumonia (PCP)

314
Q

cervical smears women with HIV

A

Yearly cervical smears

315
Q

how to prevent transmission of HIV during birth

A

Normal vaginal delivery is recommended for women with a viral load < 50 copies / ml

Caesarean section is considered in patients with > 50 copies copies / ml and in all women with > 400 copies / ml

IV zidovudine should be given during the caesarean if the viral load is unknown or there are > 10000 copies / ml

316
Q

can you breastfeed with HIV

A

not recommended

317
Q

what is PEP

A

PEP involves a combination of ART therapy. The current regime is Truvada (emtricitabine and tenofovir) and raltegravir for 28 days.

PEP is not 100% effective and must be commenced within a short window of opportunity (less than 72 hours)

HIV tests are done immediately and also a minimum of three months after exposure to confirm a negative status. Individuals should abstain from unprotected sexual activity for a minimum of three months until confirmed as negative.

318
Q

Pathophysiology BV

A

Lactobacilli are the main component of the healthy vaginal bacterial flora. These bacteria produce lactic acid that keeps the vaginal pH low (under 4.5). The acidic environment prevents other bacteria from overgrowing. When there are reduced numbers of lactobacilli in the vagina, the pH rises. This more alkaline environment enables anaerobic bacteria to multiply.

319
Q

Risk factors BV

A

Multiple sexual partners (although it is not sexually transmitted)
Excessive vaginal cleaning (douching, use of cleaning products and vaginal washes)
Recent antibiotics
Smoking
Copper coil
Bacterial vaginosis occurs less frequently in women taking the combined pill or using condoms effectively.

320
Q

Investigations BV

A

Vaginal pH can be tested using a swab and pH paper. The normal vaginal pH is 3.5 – 4.5. BV occurs with a pH above 4.5.

321
Q

Management BV

A

Metronidazole is the antibiotic of choice for treating bacterial vaginosis

This is given orally, or by vaginal gel. Clindamycin is an alternative but less optimal antibiotic choice.

322
Q

What do you need to remember to say when prescribing metronidazole

A

Whenever prescribing metronidazole advise patients to avoid alcohol for the duration of treatment. This is a crucial association you should remember, and something examiners will look out for when you are explaining the treatment to a patient. Alcohol and metronidazole can cause a “disulfiram-like reaction”, with nausea and vomiting, flushing and sometimes severe symptoms of shock and angioedema.

323
Q

What is pelvic inflammatory disease

A

inflammation and infection of the organs of the pelvis, caused by infection spreading up through the cervix

Most common causes:
Neisseria gonorrhoeae tends to produce more severe PID
Chlamydia trachomatis
Mycoplasma genitalium

324
Q

Invetsigation markers pelvic inflammatory disease

A

Pus cells on microscopy. The absence of pus cells is useful for excluding PID.

Raised CRP/ESR

325
Q

Management PID

A

refer to GUM

A single dose of intramuscular ceftriaxone 1g (to cover gonorrhoea)
Doxycycline 100mg twice daily for 14 days (to cover chlamydia and Mycoplasma genitalium)
Metronidazole 400mg twice daily for 14 days (to cover anaerobes such as Gardnerella vaginalis)

326
Q

management genital warts

A

topical podophyllum or cryotherapy are commonly used as first-line treatments depending on the location and type of lesion

multiple, non-keratinised warts are generally best treated with topical agents

solitary, keratinised warts respond better to cryotherapy

327
Q

pathogen genital warts

A

HPV 6 and 11

328
Q

whats a double/triple swab

A

Double swabs: a NAAT swab (endocervical or vulvovaginal) and a high vaginal charcoal media swab.

Triple swabs: a NAAT swab (endocervical or vulvovaginal), a high-vaginal charcoal media swab and an endocervical charcoal media swab.

329
Q

What CF colonising bacteria is bad

A

Pseudomonas aerginosa

330
Q

Haemolysis
Elevated Liver enzymes
Low Platelets

A

HELLP SYNDROME - COMPLICATION OF PRE-ECLAMPSIA

331
Q

management of gestational diabestes

A

Four weekly ultrasound scans to monitor the fetal growth and amniotic fluid volume from 28 to 36 weeks gestation.

The initial management:

Fasting glucose less than 7 mmol/l: trial of diet and exercise for 1-2 weeks, followed by metformin, then insulin

Fasting glucose above 7 mmol/l: start insulin ± metformin

Fasting glucose above 6 mmol/l plus macrosomia (or other complications): start insulin ± metformin

332
Q

What can obstetric cholestasis cause?

A

still birth

333
Q

Shoulder dystocia management

A

Immediately after shoulder dystocia is recognised, additional help should be called.
Fundal pressure should not be used.
An episiotomy is not always necessary.
Induction of labour at term can actually reduce the incidence of shoulder dystocia in women with gestational diabetes.
McRoberts manoeuvre is the first line intervention as it is known to be simple, rapid and effective in most cases

334
Q

Category 2 caesarean section occur within?

A

75 minutes

335
Q

diagnosis gestational diabetes

A

Gestational diabetes can be diagnosed by either a:

fasting glucose is >= 5.6 mmol/L, or
2-hour glucose level of >= 7.8 mmol/L
‘5678’

336
Q

cholestatic picture of liver tests

A

High ALP and GGT, with a lesser rise in ALT.

337
Q

what screening tool is used for postnatal depression

A

Edinburgh scale

338
Q

when would you test for gesttaional diabetes

A

OGTT 24-28 weeks

339
Q

Histology cervical cancer

A

squamous cell cancer (80%)
adenocarcinoma (20%)

340
Q

Biggest risk factor in developing cervical cancer?

A

HPV 16,18 & 33

341
Q

What virsuses cause genital warts

A

HPV 6 & 11

342
Q

How does HPV cause cervical cancer?

A

HPV 16 & 18 produces the oncogenes E6 and E7 genes respectively
E6 inhibits the p53 tumour suppressor gene
E7 inhibits RB suppressor gene

343
Q

screening pathway for cervical cancer

A
  1. Test for high-risk human papillomavirus strains (hrHPV)
    If negative return to normal recall
  2. If positive → cytology
    If cytology negative, retest hrHPV in 12 months
    If hrHPV is then negative return to recall, if hrHPV positive repeat again in 12 months
    If hrHPV is positive at 24 months, cytology is normal refer to colposcopy anway
  3. If cytology positive → colposcopy
344
Q

If sample is inadequate HPV cervical screening, what do you do?

A

Retest in 3 months
If inadequate again –> colposcopy

345
Q

Normal recall for cervical screening

A

Age 25 years: first invitation.
Age 25-49 years: screening every 3 years.
Age 50-64 years: screening every 5 years.
Women 65 years of age or older if they have not had a cervical screening test since 50 years of age or a recent cervical cytology sample is abnormal.

346
Q

cervical screening and pregnancy

A

cervical screening in pregnancy is usually delayed until 3 months postpartum unless missed screening or previous abnormal smears.

347
Q

women with HIV and cervical screening

A

Cervical cytology at diagnosis.

Cervical cytology should then be offered annually for screening.

348
Q

What is the test of cure pathway for cerviclal cancer?

A

Individuals who have been treated for CIN1, CIN2, or CIN3 should be invited 6 months after treatment for a test of cure repeat cervical sample in the community

349
Q

Management of cervical intraepitlealial neoplasia

A

Large loop excision of the transformation zone (LLETZ)

350
Q

Cervical cancer stage 1A

A

Confined to cervix, only visible by microscopy and less than 7 mm wide:
A1 = < 3 mm deep
A2 = 3-5 mm deep

Gold standard of treatment is hysterectomy +/- lymph node clearance
Nodal clearance for A2 tumours

For patients wanting to maintain fertility, a cone biopsy with negative margins can be performed

Radical trachelectomy is also an option for A2

351
Q

Cervical cancer stage 1B

A

Confined to cervix, clinically visible or larger than 7 mm wide:
B1 = < 4 cm diameter
B2 = > 4 cm diameter

Radiotherapy with concurrent chemotherapy is advised
Radiotherapy may either be bachytherapy or external beam radiotherapy
Cisplatin is the commonly used chemotherapeutic agent

For B2 tumours: radical hysterectomy with pelvic lymph node dissection

352
Q

Stage II and III cervical cancer

A

Stage 2: Extension of tumour beyond cervix but not to the pelvic wall
A = upper two thirds of vagina
B = parametrial involvement

Stage 3: Extension of tumour beyond the cervix and to the pelvic wall
A = lower third of vagina
B = pelvic side wall

NB: Any tumour causing hydronephrosis or a non-functioning kidney is considered stage III

Radiation with concurrent chemotherapy
Radiotherapy may either be bachytherapy or external beam radiotherapy
Cisplatin is the commonly used chemotherapeutic agent

If hydronephrosis, nephrostomy should be considered

353
Q

Stage IV cervical cancer

A

Extension of tumour beyond the pelvis or involvement of bladder or rectum
A = involvement of bladder or rectum
B = involvement of distant sites outside the pelvis

Radiation and/or chemotherapy is the treatment of choice
Palliative chemotherapy may be best option for stage IVB

354
Q

What complications is there with LLETZ and cone biopsy

A

pre term labour in future pregnancies

355
Q

What does FSH do?

A

development of follicle beyond secondary
stimulates granulosa cells to multiply and produce oestrogen
Induces LH receptors on granulosa cells of the dominant follicle

356
Q

What does oestrogen do?

A

stimulates proliferation of granulosa cells
exerts negative feedback on the secretion of gonadotrophins
works with progesterone to maintain lining in luteal phase

357
Q

What does LH do?

A

stimulates theca cells to synthesise androgens
the mid-cycle surge in LH causes ovulation

358
Q

What does progesterone do?

A

Helps to build and maintain endometrial lining
progesterone is produced in large amounts by the corpus luteum to maintain the lining

the drop in progesterone due to degeneration of corpus luteum (due to no hCG) causes endmetrial shedding

359
Q

what are the 4 key follicular stages

A

Primordial follicles
Primary follicles
Secondary follicles
Antral follicles (also known as Graafian follicles)

360
Q

Histology of most endometrail cancers

A

adenocarcinoma

361
Q

risk factors for endometrial cancer

A

obesity
Nulliparity (Nulliparity is a risk factor for endometrial cancer. This is because during pregnancy, the balance of hormones shifts towards progesterone, which is a protective factor.)
early menarche
late menopause
unopposed oestrogen. The addition of a progestogen to oestrogen reduces this risk (e.g. In HRT). The BNF states that the additional risk is eliminated if a progestogen is given continuously
diabetes mellitus
tamoxifen
polycystic ovarian syndrome
hereditary non-polyposis colorectal carcinoma

362
Q

2 week wait criteria for ?endometrial cancer

A

Age over 55 with post menopausal bleeding (must be >12 months since last period)

Consider if over 55 and:
Unexplained vaginal discharge
Visible haematuria plus raised platelets, anaemia or elevated glucose levels

363
Q

Investigations for endometrial cancer?

A

Transvaginal ultrasound for endometrial thickness (normal is less than 4mm post-menopause)

Hysteroscopy with endometrial biopsy

Pipelle biopsy, which is highly sensitive for endometrial cancer making it useful for excluding cancer

364
Q

Stages of endometrial cancer?

A

Stage 1: Confined to the uterus
Stage 2: Invades the cervix
Stage 3: Invades the ovaries, fallopian tubes, vagina or lymph nodes
Stage 4: Invades bladder, rectum or beyond the pelvis

365
Q

Managemnet of endometrial cancer

A

total abdominal hysterectomy with bilateral salpingo-oophorectomy, also known as a TAH and BSO (removal of uterus, cervix and adnexa).

progestogen therapy is sometimes used in frail elderly women not consider suitable for surgery

366
Q

how may endometrial hyperplasia present?

A

intermenstrual bleeding

367
Q

What is endometrial hyperplasia ?

types?

A

abnormal proliferation of the endometrium in excess of the normal proliferation that occurs during the menstrual cycle. A minority of patients with endometrial hyperplasia may develop endometrial cancer

types:
hyperprolifertaion without atypia
atypical hyperplasia

368
Q

Management of endometrial hyperplasia?

A

Intrauterine system (e.g. Mirena coil)
Continuous oral progestogens (e.g. medroxyprogesterone or levonorgestrel) and retest in 3 months

If atypia : hysterectomy advised

369
Q

Invetsigations for ovarian cancer?

A

CA-125

If CA-125 is over 35 the do abdo USS

Diagnosis is difficult and usually involves CT for staginh and diagnostic laparotomy

370
Q

risk factors for ovarian cancer

A

Family history: mutations of the BRCA1 or the BRCA2 gene

many ovulations*: early menarche, late menopause, nulliparity

371
Q

Most common ovarian cancer histlogy

A

epithelial cell tumour - serous tumour

372
Q

What are teratomas?

A

germ cell tumours

373
Q

Particular complication with teratomas?

A

ovarian torison

374
Q

Blood tests in teratomas

A

raised alpha-fetoprotein (α-FP)
raised human chorionic gonadotrophin (hCG)

375
Q

Risk factors for ovarian cancer

A

Age (peaks age 60)
BRCA1 and BRCA2 genes (consider the family history)
Increased number of ovulations
Obesity
Smoking
Recurrent use of clomifene

Factors that increase the number of ovulations, increase the risk of ovarian cancer. These include:
Early-onset of periods
Late menopause
No pregnancies

376
Q

2 week wait criteria for ovarian cancer

A

Ascites
Pelvic mass (unless clearly due to fibroids)
Abdominal mass

377
Q

What investigation should women under 40 years with a complex ovarian mass have

A

?teratoma

Alpha-fetoprotein (α-FP)
Human chorionic gonadotropin (HCG)

378
Q

What can raise CA-125?

A

Endometriosis
Fibroids
Adenomyosis
Pelvic infection
Liver disease
Pregnancy

379
Q

Management ovarian cancer

A

Ovarian cancer will be managed by a specialist gynaecology oncology MDT. It usually involves a combination of surgery and chemotherapy.

380
Q

Management ovarian cancer

A

Ovarian cancer will be managed by a specialist gynaecology oncology MDT. It usually involves a combination of surgery and chemotherapy.

381
Q

Stages of ovarian cancer

A

Stage 1: Confined to the ovary
Stage 2: Spread past the ovary but inside the pelvis
Stage 3: Spread past the pelvis but inside the abdomen
Stage 4: Spread outside the abdomen (distant metastasis)

382
Q

Most common histology vulval cancer

A

squamous cell carcinomas

383
Q

Invetsigations for vulval cancer

A

Biopsy of the lesion
Sentinel node biopsy to demonstrate lymph node spread
Further imaging for staging (e.g. CT abdomen and pelvis)

384
Q

management of lichen sclerosus

A

topical steroids and emollients

385
Q

Presentation of vaginal cancer?

A

abnormal discharge

386
Q

management vulval cancer?

A

Wide local excision to remove the cancer
Groin lymph node dissection
Chemotherapy
Radiotherapy

387
Q

IUD vs IUS?

A

IUD - copper coil
IUS - things like mirena coil

388
Q

Risk factors for placental abruption?

A

A for Abruption previously;
B for Blood pressure (i.e. hypertension or pre-eclampsia);
R for Ruptured membranes, either premature or prolonged;
U for Uterine injury (i.e. trauma to the abdomen);
P for Polyhydramnios;
T for Twins or multiple gestation;
I for Infection in the uterus, especially chorioamnionitis;
O for Older age (i.e. aged over 35 years old);
N for Narcotic use (i.e. cocaine and amphetamines, as well as smoking)

389
Q

“chocolate cysts”

A

A lump of endometrial tissue outside the uterus is described as an endometrioma. Endometriomas in the ovaries are often called “chocolate cysts”.

390
Q

Blood reuslts rickets

A

Low calcium, low phosphate, high ALP and high PTH

391
Q

Inheritance of thalassemia?

A

autosomal recessive

392
Q

What does FBC show thalassemia?

A

microcytic anaemia

393
Q

Investigations thalassmeia

A

Full blood count shows a microcytic anaemia.
Haemoglobin electrophoresis is used to diagnose globin abnormalities.
DNA testing can be used to look for the genetic abnormality

Pregnant women in the UK are offered a screening test for thalassemia at booking.

394
Q

On what chromosome is defect that causes alpha thalassemia?

A

chromosome 16

395
Q

On what chromosome is defect that causes beta thalassemia?

A

chromosome 11

396
Q

Thalassemia minor pathophysiology, presentaiton and management

A

Patients with beta thalassaemia minor are carriers of an abnormally functioning beta globin gene. They have one abnormal and one normal gene.

Thalassaemia minor causes a mild microcytic anaemia and usually patients only require monitoring and no active treatment.

397
Q

Thalasssemia intermedia - pathophysiology, presentation, management

A

Patients with beta thalassaemia intermedia have two abnormal copies of the beta-globin gene. This can be either two defective genes or one defective gene and one deletion gene.

Thalassaemia intermedica causes a more significant microcytic anaemia and patients require monitoring and occasional blood transfusions. If they need more transfusions they may require iron chelation to prevent iron overload.

398
Q

Thalassemia major - pathophysiology, presentation, manageement

A

Patients with beta thalassaemia major are homozygous for the deletion genes. They have no functioning beta-globin genes at all. This is the most severe form and usually presents with severe anaemia and failure to thrive in early childhood.

Thalassaemia major causes:
Severe microcytic anaemia
Splenomegaly
Bone deformities

Management involves regular transfusions, iron chelation and splenectomy. Bone marrow transplant can potentially be curative.

399
Q

What is haemophilia A caused by

A

deficiency in factor VIII

400
Q

What is haemophilia B caused by

A

Deficiency in factor IX

401
Q

Diagnosis of haemophilia

A

bleeding scores
coagulation factor assays
genetic testing.

402
Q

Management of haemophilia

A

Infusions of the affected factor (VIII or IX) - either prophylacticly or in response to bleeding

Desmopressin to stimulate the release of von Willebrand Factor

Antifibrinolytics such as tranexamic acid

403
Q

Requirements for instrumental delivery

A

FORCEPS acronym

Fully dilated cervix generally the second stage of labour must have been reached

OA position preferably OP delivery is possible with Keillands forceps and ventouse. The position of the head must be known as incorrect placement of forceps or ventouse could lead to maternal or fetal trauma and failure

Ruptured Membranes

Cephalic presentation

Engaged presenting part i.e. head at or below ischial spines the head must not be palpable abdominally

Pain relief

Sphincter (bladder) empty this will usually require catheterization

404
Q

contributing factors anaemia of prematurity

A

Less time in utero receiving iron from the mother
Red blood cell creation cannot keep up with the rapid growth in the first few weeks
Reduced erythropoietin levels
Blood tests remove a significant portion of their circulating volume

405
Q

Most common causes of anaemia in older children?

A

Iron deficiency anaemia secondary to dietary insufficiency. This is the most common cause overall.
Blood loss, most frequently from menstruation in older girls

406
Q

Worldwide, a common cause of blood loss causing chronic anaemia and iron deficiency is?

management?

A

helminth infection, with roundworms, hookworms or whipworms.

This can be very common in developing countries and those living in poverty. It is more unusual in the UK.

Treatment is with a single dose of albendazole or mebendazole.

407
Q

what is fanconi anaemia?

A

autosomal recessive aplastic anaemia (pancytopaenia)

408
Q

what does high total iron binding capacity indicate?

A

iron deficicency

A total iron-binding capacity (TIBC) test measures the blood’s ability to attach itself to iron and transport it around the body. A transferrin test is similar. If you have iron deficiency anaemia (a lack of iron in your blood), your iron level will be low but your TIBC will be high.

409
Q

relationship between iron and stomach acid

A

Iron is mainly absorbed in the duodenum and jejunum. It requires the acid from the stomach to keep the iron in the soluble ferrous (Fe2+) form. When there is less acid in the stomach, it changes to the insoluble ferric (Fe3+) form. Therefore, medications that reduce the stomach acid, such as proton pump inhibitors (lansoprazole and omeprazole) can interfere with iron absorption.

410
Q

Myasthenia gravis associations

A

thymomas 15%

autoimmune conditions

411
Q

Diagnostic investigation myasthenia gravis

A

Specific antibodies against the acetylcholine receptors AChR antibodies

If negative test anti-muscle-specific tyrosine kinase antibodies
single fibre electromyography: high sensitivity (92-100%)
CT thorax to exclude thymoma
CK normal

412
Q

Mnagement myasthenia gravis

A

long-acting acetylcholinesterase inhibitors:
pyridostigmine is first-line

immunosuppression is usually not started at diagnosis, but the majority of patients eventually require it:
prednisolone initially
azathioprine, cyclosporine, mycophenolate mofetil may also be used
thymectomy

413
Q

Management of a myasthenic crisis

A

plasmapheresis
intravenous immunoglobulins

​​Plasmapheresis removes circulating antibodies, including the autoimmune antibodies responsible for the disease. Immunotherapy with intravenous gammaglobulin appears to diminish the activity of the disease.

414
Q

MG implications for anaesthesia?

A

Suxamethonium is a depolarising NMBD - it acts by binding to and activating the receptor, at first causing muscle contraction, then paralysis. Due to a decreased number of available receptors, MG patients are typically resistant to depolarising NMBDs and may require significantly higher doses.

415
Q

What drugs should be avoided in MG?

A

beta blockers
lithium
phenytoin
antibiotics: gentamicin, macrolides, quinolones, tetracyclines

416
Q

most common fractures associated with NAI

A
  • Radial
  • Humeral
  • Femoral

Phase 3a topics (39 decks)

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