Lists Flashcards
Signs of hyperprolactinaemia may include:
Reduced libido and arousal Gynaecomastia Menstrual irregularities Amenorrhoea, and Galactorrhoea.
Capgras syndrome?
people have been replaced by exact copies of themselves.
Ganser Syndrome?
Feigns insanity by giving nonsense answers
Othello Syndrome?
Irrational belief partner is cheating
Broad features of AN?
Phobic avoidance of normal weight Relentless dieting Self-induced vomiting Laxative use Excessive exercise Amenorrhoea Lanugo hair Hypotension Denial Concealment Over-perception of body image Enmeshed families.
Features of Edwards and Patau’s (18 and 13 respectively). Which are common to both, and which are different?
Patau syndrome is associated with:
microcephaly mental retardation microphthalmia cleft lip and palate polydactyly rocker-botttom feet, and congenital heart defects.
Edwards syndrome is associated with:
mental retardation microphthalmia prominent occiput low-set ears rocker-bottom feet flexion deformities of the hands, and complex congenital heart defects.
Common to both: Mental retard Cardiac defects rocker bottom feet Microphthalmia
When are NSAID’s prefered over TXA for menorrhagia?
If there is pain.
Considerations with a woman with epilepsy and the baby?
May need to increase antiepileptic during preg as plasma levels fall.
Lamotrigine is the preferred, however we cannot say conclusively it has no side effects. However, there is probably more risk of switching during preg due to risk of seizures.
Need to supplement folate with this, and give vitamin k the month before labour.
Screening with AFP and second trimester needed. (neural tube)
Epidurals and PPH?
Nil association
Explain aspirin poisoning and it’s metabolic effects (not inc. Reye’s)
Phase 1 involves a respiratory alkalosis due to respiratory stimulation and urinary loss of sodium and potassium
Phase 2 involves acidosis due to urinary exchange of H for K (a paradoxical aciduria) despite a respiratory alkalosis
Phase 3 involves a metabolic acidosis due to accumulation of metabolic acids and dehydration.
When do most paeds cardiac defect deaths occur?
<1 year old
Which oral hypoglycaemic is continued in preg?
Diabetes in pregnancy is associated with an increased risk of fetal malformation and pregnancy-related complications. Most oral hypoglycaemic drugs should be stopped, but metformin can be continued as its benefits outweigh the risks of treatment. Treatment should be supplemented with insulin to obtain a target HbA1c <43 mmol/mol (6.1%).
Diabetes related medications which are probably safe in pregnancy include:
Metformin
Isophane (NPH) insulin
Short acting insulin analogues, such as aspart and lispro.
Many medications have insufficient safety data to be used routinely in pregnancy.
Diabetes related medications which should be avoided in pregnancy include:
All other oral hypoglycaemic drugs, such as gliclazide, pioglitazone and DPP-IV inhibitors
Long acting insulin analogues such as glargine and detemir
Injectable drugs such as exenatide or liraglutide
Statins
ACE-inhibitors.
Antiphospholipid syndrome ab’s?
Anticardiolipin
manage aspirin poisoning?
Treatment of children with salicylate poisoning includes ABC as required.
Gastric lavage is required.
Blood levels are often misleading especially if enteric coated tablets have been taken.
It is important to monitor the urine volume and pH at all times.
A forced alkaline diuresis is induced with a bicarbonate infusion.
Correction of dehydration and maintenance is calculated with haemodialysis in severe cases.
In the event of a coagulopathy vitamin K administration may be necessary.
Do twins incidence increasing with maternal age?
Dizygotes only
List some things increasing in incidence with maternal age?
Increasing maternal age sees an increase in:
Hypertension Pre-eclampsia Diabetes, and Caesarean section rates. In addition, the risk of miscarriage, ectopic pregnancy, and chromosomal abnormalities increases with maternal age.
In the confidential enquiry into maternal deaths (CEMD) between 1997-1999, maternal mortality more than doubled in women >35 years of age compared to those <30-years-old.
There is an increase in dizygotic twins with increasing maternal age.
Please discuss the mechanism of citalopram
An SSRI
Block SERT at presynaptic terminal to increase 5-HT at the synaptic cleft.
This increases post synpatic response to serotonin. However, by activating autoreceptors on the presynaptic cleft, it can lead to negative feedback, thus worsening the symptoms iniitally. However, these downregulate eventually, and the response improves.
Note this mechanism is the same for tolerance, except observed on the post synaptic membrane
What is atrophic triginitis? What othet atophic itis’ are there in this condition?
Trigone of the bladder. Also vagnitis and uretheritis
Substances causing oxidative crises in patients with G6PD
Nitrofurantoin, Fava beans, antimalarials
Symptoms of a macroadenoma?
Headache Features of raised intracranial pressure Visual disturbance Bitemporal hemianopia Suppression of other pituitary functions.
Remember it compresses the cavernous sinus i.e. nerves 3,4,6
Familial Mediterranean Fever
This boy has recurrent episodes of abdominal pain, fever and arthritis. There is hepatomegaly. All these point to familial Mediterranean fever.
If you didn’t get this, you have ligma
Antibiotics for pertussis? Why would you give these?
Consider antibiotics if:
Diagnosed in catarrhal or early paroxysmal phase (may reduce severity)
Cough for less than 14 days (may reduce spread; reduces school exclusion period)
Admitted to hospital
Complications (pneumonia, cyanosis, apnoea)
Antibiotic options:
Neonates
Azithromycin 10 mg/kg oral daily for 5 days
Children who cannot swallow tablets:
Clarithromycin liquid 7.5 mg/kg/dose (max 500mg) oral BD for 7 days
Children who can swallow tablets:
Azithromycin (for children = 6 months old): 10mg/kg (max 500 mg) oral on day 1, then 5mg/kg (max 250mg) daily for 4 days
If macrolides are contraindicated:
Trimethoprim-sulphamethoxazole (8mg-40mg per ml)
0.5ml/kg (max 20ml) BD for 7 days
Antibodies in coeliac? What other chronic diseases does it increase the risk of?
Antibodies in coeliac are anti-TTG and anti-gliadin antibodies. Also Anti-EMA but they don’t contribute to the disease process.
Chronic diseases are T cell lymphomas and small bowel cancers.
Intellectual disability has a wide differential, and causes can be divided into prenatal, perinatal and postnatal. Please list the ddx.
Over half are caused by factors prenatally, others by factors perinatally,
and some postnatally.
PRENATAL:
- Chromosomal Down’s syn, Fragile X syn, VCF syn)
- Genetic tuberous sclerosis, metabolic disorder (e.g. PKU)
- Syndromes e.g. William’s syn, Prader-Willi syn
- Infections rubella virus, CMV
- Drugs, toxins excessive alcohol
- Major structural abnormalities of the brain
PERINATAL FACTORS:
- Lack of oygen (hypoxia)
- Trauma
- Infections
- Biochemical abnormalities, e.g. hypoglycaemia
- Children with LBW are at increased risk of having these
complications after birth
POSTNATAL FACTORS:
- Head injuries MVA, near-miss drowning accidents
- Infections such as meningitis and encephalitis
- Poisons
- For mild ID the cause is often not known, although it may be
caused by any of the factors listed previously
Also, must be noted that other causes of learning difficulties include:
- hypothyroidism and diabetes
- Dyslexia, ADHD, Down’s Syndrome, Fragile X, Tuberous Sclerosis, ASD, FASD, Absence Epilepsy
Also hearing and vision difficulties can present this way. Consider causes of deafness such as neurofibromatosis
The risks of childhood obesity? Aside from sustaining obesity into adulthood and thus getting those risks.
Increasing risk of type 2 diabetes mellitus (T2DM)
Slipped femoral epiphysis
Behavioural problems (including truancy)
Depression (not schizophrenia).
Features of a congenital CMV infection pls
Microcephaly, seizures, neonatal jaundice, hepatosplenomegaly, deafness and mental retardation are some of the features that may occur.
Note the seizures are from the intracranial calcifications.
Complications of measles:
The prodromal stage fever conjunctivitis, runny nose and coughing lasts for five days. Koplik’s spots are bright red lesions with a central white dot which appear on the buccal mucosa. These are virtually diagnostic. The typical macular confluent rash appears on the face from days three to five and spreads to the rest of the body. Diagnosis is made from clinical features, viral culture from lesions and a greater than fourfold rise in antibody titres.
Otitis media, pneumonia, meningitis and very rarely several years after primary infection subacute sclerosing panencephalitis (SSPE).
Features of lead poisoning?
Anorexia Hyperirritability General apathy Vomiting Colicky abdominal pain, and Constipation.
Anaemia may be present, and there may be a history of developmental regression. The anaemia may be normocytic (due to haemolysis) or microcytic. Megaloblastic anaemia is one where there is increased numbers of lobes of granulocyte nuclei - this is specific to B12 or folate, whereas the macrocytosis caused by sideroblastic anaemia would be a macrocytosis without megaloblastosis.
Lead poisoning per se can cause a hypochromic microcytic anaemia. But lead can also cause an acquired sideroblastic anaemia, which is normo- or macro-cytic. Note that congenital sideroblastic anaemia is normo- or micro-cytic.
Neurological symptoms include behavioural problems, seizures and ataxia.
At levels greater than 100 renal tubular dysfunction can occur.
At significant exposure levels, lead can act as an enzyme inhibitor to delta amino levulinic acid dehydratase, which causes a fall in serum delta amino levulinic acid levels.
Hypertrophic scar vs keloid
Hypertrophic is a raised scar that is painles and raised, and occurs relatively soon after surg. However, it goes away.
Compartment syndrome: which occurs later: sensory or motor loss? Why do you know this?
Sensory. Cramps you get from prolonged sitting. Also motor is more heavily myelinated than spinothalamic.
When does atopic eczema usually start?
First year of life
Aside from topical steroids, what are some treatments for eczema?
Frequent bathing and hydrating of the skin avoiding strong soaps, and the liberal use of moisturisers and lubricants are first line treatments.
Clinical features of a small VSD? What about large?
Small VSDs are associated with:
Physiological splitting of S2 (S2 split during inspiration only; considered normal). Fixed splitting of S2 is associated with atrial septal defects and some larger VSDs
Harsh pansystolic murmur heard loudest at the lower left sternal edge
Normal growth and development, and
No cyanosis.
Large VSDs are associated with:
Poor neonatal weight gain
Congestive cardiac failure which can manifest initially as mild tachycardia, mild breathlessness and hepatomegaly
Palpable thrill
Harsh pansystolic murmur heard loudest at the lower left sternal edge
There may also be a mid-diastolic rumbling murmur of functional mitral stenosis when occurs when the shunt (L to R) is large. This effect is caused by the increased blood flow through the left atrium.
No cyanosis initially, although when the shunt reverses (R to L; Eisenmenger syndrome) cyanosis can occur.
Comment on the risk of infective endocarditis in VSD
Increased risk
Causes of croup pls
Causative viruses are parainfluenza (types 1,2,or 3), respiratory syncytial viruses and measles virus.
Complications of paeds iron overdoses? What is the chelator
Perf of intestines, secondary pyloric stenosis, hepatic necrosis
Note that when the iron is absorbed into liver mitochondria, they seem to improve. they will deteriorate again.
Treatment relies on the administration of desferrioxamine parenterally and supportive treatment. Gastric lavage is no longer used as iron tablets are large and sticky therefore it is unlikely to be of benefit.
Side effects of phenytoin pls. What about valproic acid?
Drug induced SLE, gingivial hyperplasia, hisutism, generalised lymphadenopathy
Haematological side effects are:
Megaloblastic anaemia Aplastic anaemia Thrombocytopenia, and Agranulocytosis. Neurological side effects include peripheral neuropathy and ataxia. In rare cases side effects may also include nystagmus and dyskinesias.
Eye involvement may occur in cases of overdosages; these include blurred vision and nystagmus.
Valproate: Alopecia, thrombocytopaenia, hepatotoxicity, pancreatitis (PATH)
https://mynotes4usmle.tumblr.com/post/76290241381/neuro-pharmacology-remember#.W-C-S_kzaHs
Foetal and Maternal complications of GDM
Foetal:
Birth trauma (obstructed vaginal delivery) increased need for c-section Macrosomia, organomegaly, polycythaemia, jaundice Hyperinsulinaemia Shoulder dystocia Neonatal hypoglycaemia Increased need for premature delivery ARDS Increased need to c-section IUFD LONG-TERM impaired glucose tolerance, T2DM, obesity
Maternal Miscarriage Preeclampsia Infection Induction of labour Trauma C-section PPH Increased risk of T2DM + HTN Increased risk of hypoglycaemia
Stridor DDX
Laryngomalacia, tracheomalacia, epiglottitis, croup, foreign body aspiration, anaphylaxis, subglottal stenosis (previous intubation), haemangioma, laryngeal web, vocal cord paraylysis, GOR, hypocalcaemia (laryngeal tetany).
Other less common causes in older kids include bacterial tracheitis, severe tonsilitis, inhalation of hot gases in a fire, and retropharyngeal abscesses
FAp extracolonic manifestations
FAP
- Extracolonic manifestations:
o Osteoma –
o Desmoid tumours: mesenteric strangulation is an issue (in abdo wall or small bowel mesentry)
- Abdosurgery speeds up growth
o Gastroduodenal polyps – 5% develop fatal duodenal cancer
- Upper GIT scope from 20 – 5 yearly
o Retinal pigmentation (Congenital hypertrophy of the retinal pigment epithelium)
- Give total colectomy and ileorectal anastomosis à need to monitor 6 monthly rectal polyps
o Rectal cancer risk is 15% at 15 years and may develop despite surveillance, low cx rate and good bowel function
Restorative proctocolectomy and ileal pouch-anal anastomosis à eliminates risk of cancer but morbidity is worse
Surgical Complicatiosn Unique to a herniaraphy
Surgical complications
o Urinary retention
o Scrotal swelling and haematomaà oedema, swelling, bruisesà resolve
o Wound infectionà removal or mesh and Abs
o Recurrent hernia à 2%
o Nerve injury- ilioinguinal nerve (lateral cutaneous nerve to thingh in femoral)
o Persiting pain – nerve entrapment, neuroma, osteitis pubis if sutures inserted in pubic tubercle, pressure on cord
o Testicular iscahemia and atrophy- testicular artery comprimsied
o Hydrocele
- Laparoscopic technique may not be successful à open
- Damage to large blood vessels, gut or bladder
- Gas used in laproscopy can result in heart and lung complications: rare
- Testicular and scrotal swelling/bruising
- Damage to vas deferens
- Adhesions
- Recurrence of hernias or hernia formation at incision sites
- Visceral injury – viscera sliding hernia when sac is being dissected away from them
Toxic megacolon cause
- Inflammatory bowel disease (ulcerative colitis > Crohn’s disease)
- Infectious colitis
o Bacterial: C. difficile, Salmonella, Shigella, Campylobacter
o Viral: Cytomegalovirus
o Parasitic: Enterobacter histolytica - Triggers: hypokalemia, constipating agents (opioids, antidepressants, loperamide, anticholinergics), barium enema, colonoscopy
Management steps for pilonidal disease?
Conservative, I&D, and cystotomy
Types of rectal prolapse?
Type one and two. One is just the mucosa protruding past the external anal sphincter. This is more common in children. Two is complete, and involves the full thickness of the wall. and is broken up like this:
First degree: Prolapse includes the mucocutaneous junction.
2nd: Without involvement of the mucocutaneous junction
3rd: Prolapse is internal, concealed or occult. This is otherwise known as an internal intussusception.
Management of rectal prolapse?
- Type I
o Conservative: gentle manual reduction of prolapsed area, especially in children
o Mucosectomy with excision of redundant mucosa, mostly in adults - Type II
o Conservative: reduce if possible
o Surgery: Removal of segment of bowel and remaining bowel is sutured to the pelvic bone
Can be abdominal, laparoscopic, perineal (through the anus), trans sacral approaches
In general, a transabdominal repair is used for younger patients and a perineal repair for the elderly and frail patients. A full mechanical bowel preparation and parenteral antibiotic prophylaxis are essential for minimising septic complications.
Abdominal approach: rectoplexy (Ripstein operation)
• + sigmoid resection (as redundant) is the Frykman-Goldber operation
• SEPSIS RATE HIGHER BUT CONSTIPATION LOWER DUE TO NO KINKING AS IN IN RIPSTEIN
Perineal approach: perineal proctosigmoidectomy: Altemeier operation UNDER GA OR REGIONAL. In jack-knife position, circumfrential incision 1cm above dentate line. Prolapsed rectum is unfolded and redundant resected and mesorectum is ligated and divided to deliver through opening. Coloanal anastgomosis
Diff between a high and low perianal fistula and how they are managed:
A high is above the anorectal ring and usually indicates more serious pathology. A low is usually idiopathic and has a less serious aetiology.
• Low fistula
o The mainstay of treatment is to identify the internal and external openings and to ‘lay open’ the intervening track by fistulotomy. This allows the track to heal by secondary intention. Special assessment of the adequacy of the sphincter mechanism should be considered in females who have had several vaginal deliveries because occult injuries to the anal sphincters and pudendal nerve may already be present.
• High fistula: Fistulotomy is contraindicated if the internal opening is above the levator mechanism division would cause incontinence
o Caution should be exercised when more than one-third of the external anal sphincter needs to be divided
o Instead insert a seton between the two openings: silk or silastic tubing is railroaded into the track and loosely tied. The seton may act as a drain and if it is progressively tightened it may gradually divide the muscle while allowing it to heal by fibrous tissue formation. Alternatively, the seton downstages the sepsis and facilitates subsequent repair of the fistula with an advancement rectal flap. Occasionally, with more complex fistulas, a proximal stoma is constructed to divert the faecal stream, in addition to other local surgical manoeuvres.
types of perianal fistulae?
Intersphincteric
transsphinteric
suprasphincteric
Extrasphicteric
What are some risk factors for gallstones you learnt today?
Terminal ileum dmaage, weight loss (learnt why: rapid weight loss leads to excess mobilisation of cholesterol and biliary stassis), TPN (due to impaired gallbladder emptying). I would also imagine dehydration is a risk factor. Remember oestrogen slows the transit of bile in the biliary system which is the pathogenesis of cholestasis in pregnancy.
Hepatocystic triangle vs Calot’s triangle. What lies within Calot’s triangle?
Hepatocystic triangle is the one that has the free inferior border of the liver, the common hepatic duct, and the cystic duct. The Calot’s triangle replaces the cystic artery with the inferior free border of the liver. Also note that Lund’s node is contained within Calot’s triangle, and it’s commonly inflamed in cholecystitis.
What is Hartmann’s Pocuh
This is the junction of the neck of the gallbladder and the cystic duck. THis is where stones fall to be stuck.
Organisms in Cholecystitis if gets infected? Why does it get well localisedsomatic pain?
Organisms are e. coli (commonest), then klebsiella, then strep faecalis. It’s localised when it touches the peritoneum.
What is Boas’ sign?
Right subscapular pain
Two new complications of cholecystitis?
Phlegmon: when the gall bladder, bowel, and omentum adhere. Mucocoele: long term cystic duct obstruction results in a mucinous accumulation of fluid in the gallbladder.
Why would you do a hida scan?
If the USS for cholecystitis is negative. Positive result is no dye being taken up into the gallbladder.
Patient isn’t going to tolerate a general and a cholecystectomy. How can we approach this?
Percutaneous cholecystostomy is an image-guided placement of drainage catheter into gallbladder lumen. This minimally invasive procedure can aid the stabilisation of a patient to enable a more measured surgical approach with time for therapeutic planning.
The patient has a post operative fever,and pain in the RUQ after a cholecystectomy. What is the diagnosis unitl proven otherwise?
Bile duct injury
What is post cholecystectomy syndrome?
Sphincter of Oddi dysfunction. It’s a persistence or recurrence of pain after the cholecystectomy. Alternative explanations include post op adhesions.
Pre operative consideration unique to biliary tract disease?
Vitamin K supplementation or FFP if the need is urgent.
Causes of idiopathic pancreatitis?
Pancreatic divisum, microlithiasis/ sludge, stricture lesions
Role of USS and CT in pancreatitis?
Role of US is to rule out gallstones, and is commonly used in the first episode of pancreatitis. CT is to assess any complications such as a pseudocyst and to measure the extent of the necrosis. CT best done around the 72 hour mark otherwise it’s known to underestimate the extent of the disease.
Pancreatitis can be diagnosed with 2/3 of these features
Persistent epigastric pain
Elevated panc enzymes 3x normal
Radiologic findings consistent with pancreatitis. CT is better than US for this, but US will tell us the aetiology if it’s gallstones.
how do we divide the management of acute pancreatitis? Describe the steps involved?
→ Treatment with acute pancreatitis is directed four ways: general, local, complications and cause
- General
o Treat fluid loss
• If severe: careful fluid replacement with central venous pressure measurement may be necessary
• Monitor urine output: IDC
o Oxygen, Analgesia
o PPI
o AWS, thiamine
o NBM
o Nutrition- initially fast the patient, enteral nutrition has now been shown to prevent mucosal barrier breakdown and abscess formation → NG feeds if severe
- Local
o There is no specific treatment for the pancreatic inflammation
• Therefore treatment is directed at minimising the progression of the disease and preventing complications
o Antibiotics: imipenem
• Only if they have an infection, not just because they are febrile
• Prophylaxis not shown to be effective
o ERCP
• Early ERCP (<72 hours) versus conservative management extensively studies
• Benefit in cholangitis and obstructive jaundice but there has been conflicting evidence in the remainder of acute pancreatitis
o Laparoscopic cholecystectomy recommended during same admission for all groups
o Necrosectomy
• Indications
• Infected necrosis with septic complications
• Sterile necrosis with progressive deterioration
• Surgical intervention within first 2 weeks carries high mortality
- Complications
o Surgical intervention in pancreatitis is reserved for the treatment of complications and in gallstone pancreatitis for the treatment of the cause
o Severe pancreatitis with infected necrosis: Debriding necrosed tissue necessary
• As seen on a CT or the presence of organisms in tissue that as been aspirated from the pancreas following a percutaneous radiologically guided needle approach
o Pseudocysts: treated via percutaneous or endoscopic techniques or open surgery
o Abscess drainage → percutaneous or open
- Cause
o Gallstones: Cholecystectomy, ERCP
There are some procedures for the spleen: splenoraphy, arterial embolisation, a partial or total splenectomy, or even bed rest 9grade of laceration + 1 day). What are some indications for a total splenectomy?
Hereditary spherocytosis ITP (particularly if it responded to IVIG) Intractable haemorrhage Splenic vein thrombosis Hereditary spherocytosis
Blood supply of the thyroid gland
Superior thyroid artery is from the external cartoid, the inferior thyroid artery is from the subclavian artery.
What are struma ovarrii?
Literally goitre of the ovary. Cause of hyperthyroidism.
Surgical indications for Grave’s disease? Other causes of hyperthyroid?
Relapse following initial medical management
Non compliance with treatment
Ophthalmopathy
Other causes of hyperthyroid such as adenomas and TMNG are best treated with a thyroidectomy (hemi, sub total, or complete) after having their thyroid function stabilised initially.
Discuss the treatment of hyperthyroidism with PTU or carbimazole? What are the side effects, and how long do we treat for? Why is carbimazole prefered?
It’s used until we get remission. Usually about 6-18 months. Major side effects include hepatitis, agranulocytosis and fever. It can cause a rash.
Prefered Carbimazole because it’s longer duration of action, more rapid effect and lower incidence of side effects
After remission, what’s the follow up for thyroid treatment? Additionally, how do we manage opthalmopathy
Follow up after ceasing antithyroid is 1,2,3,6 months and then annualy after that.
To treat ophthalmopathy, cease smoking, prevent drying, high dose pred in severe, and consider surgical decompression.
Which cancer does TMNG increase risk of?
Follicular. This is not the most common: papillary is. It goes papillary, follicular, medullary, anaplastic. Of course, the other type is lymphoma, and this is usually if there is an underlying Hashimoto’s in the patient as well.
Commonest solitary nodule of thyroid?
TMNG
Indications for surgery of a TMNG?
- Indications for surgical treatment of a multinodular goitre include the presence of obstructive symptoms, thyrotoxicosis, suspicious or malignant changes on FNAC, a strong family history of thyroid cancer, the presence of retrosternal extension, or a past history of head and neck irradiation
- surgery is undertaken, total thyroidectomy is the preferred option, because it removes all tissue likely to cause symptoms and avoids the possibility of later recurrence, which is of the order of 30%. Lifelong thyroxine replacement is required after total thyroidectomy
Two ways to manage thyroid cancer? How does the management change when it’s medulary?
One way is to do a total thyroidectomy and follow up with a radioactive iodine ablation to remove chance of mets. The second way is to do a lobectomy, and this can only be done in young, healthy guys with a small papillary carcinoma.
That is for papillary and follicular. For the medullary, we do a total thyroidectomy and we also do a central node dissectio, lateral neck dissection, and mediastinal clearance if they have positive nodal involvement. Medullary carcinoma does not respond to the radioiodine ablation, and so we need to manage it like this.
Describe the ddx if we see a thyroid nodule?
Aside from a cancer, dominant nodule in TMNG, simple thyroid cyst, colloid cyst, adenoma, nodularity in area of thyroiditis. Only need to really operate if causing symptoms.
Secondary hyperparathyroidism is associated with hyperphosphataemia. Why? What about primary?
Hyper PTH primary increases phosphate excretion in proximal tubule for calcium reabsorption. This mechanism doesn’t work in CKD, and also we get the stimulus for high PTH due to the lack of alpha hydroxylase meaning we don’t get mature vitamin D. Thus, high phosphate and low calcium.
Signs of cancer on mammography
When do us USS when investigating lump
Spiculated lesions (radial scar)
Calcification
Mass with an irregular border
We do an USS when investigating women under 35
In Australia, how do we diagnose a syphilis infection?
We can either swab ulcers for NAAT, or we can do a blood test called EIA (enzyme immunoassay). This is specific for syphilis. After this, we do a rapid plasma reagen (RPR) and TPHA (treponema pallidum haemagglutination test) assay to look for activity.
This is from the Australian STI guidelines. The EIA is a new approach.
The old way was to do a specific first (TPPA/ TPHA) and then follow up with an RPR or a VDRL to check for disease acitivity. I will need to clarify this with Lauren.
To diagnose in babies, do an IGM.
Draw out blood supply of the brain, and discuss the strokes occurring with each artery.
If you can’t do this, you’re a howler. Go look it up.
Lithium side effects bubs?
Leukocytosis Insipidus Tremors Hypothyroidism Increased urine Mums beware (ebstein's anomaly of tricuspid)
LITHIUM
Therapeutic range of lithium
DEPENDS WHAT YOU READ
However, a safe bet is to say 0.6mmol/L - 1.0mmol/L. As long as it’s not 1.5 lol
Discuss the diabetes cycle of care. What is included in a primary care management plan for T2DM?
https://static.diabetesaustralia.com.au/s/fileassets/diabetes-australia/4732816f-9855-4c7e-bbec-ddd2f1144fea.pdf
Features of cauda equina please. What are some common mechanisms for this injury?
Cauda equina extends from L2 - S5. Tapers off from the conus medullaris.
Features depends on the severity and the level at which the deficit occurs. It includes saddle anaesthesia, weakness, anaesthesia/ sensory deficiency, pain.
Other features can include a loss of sphincter tone resulting in incontinence, sexual problems (erectile dysfunction), absent deep tendon reflexes.
Also note that the absent cremasteric reflex is L1-L2, and the absent bulbocavernosus reflex is S2-S4 (anal wink).
The number one causes of cauda equina is a disc herniation. Other causes are lumbar stenosis, trauma, cancer mets, infections or abscesses, inflammatory disease, CIDP, Paget’s, ankylosing spondylitis.
The diagnostic features of social anxiety disorder. What about specific phobias?
They have intense fear of social situations and negative evaluation and causes them to avoid it.
They always get this anixety response, and have done so for more than 6 months.
The symptoms are out of proportion, they cause impairment, and are not explained by anything else.
Specific phobias:
Intense fear of specific things that cause avoidance
Always get the anxiety response, and have done so for 6 months or more
Significant impairment, and not better explained by anything else.
GAD features in DSM?
1) Excessive worry or anixety for most days for more than 6 months which patient finds difficult to control
2) Needs three or more REMDIS features
Restlessness
Easy fatigue
Muscle tension
Difficulty concentrating/ distractibility
Irritability
Sleep disturbance
Causes significant impairment.
Not better explaned by another medical or psyche thin.
Management principles of GAD
Treatment: - Lifestyle: caffeine and alcohol avoidance, sleep hygiene - Psychological: CBT including relaxation techniques, mindfulness - Biological: o 1st line: SSRI/SNRI o 2nd line: bupropion, buspirone o 3rd: Add benzo o Beta blocker not recommended
Diagnostic elements of Anorexia Nervosa? What about bullimia?
Restriction of energy intake
Intense fear of gaining weight
Disturbance in perception of appearance
This can be the restricting or the binge eating + purging subtypes.
The specifiers are that mild is BMI > 17, mod is 16-17, severe is 15-16, and extreme is - 15
Bullimia is:
Recurrent episodes of binge eating characterised by both of the following:
eating a large amount of food in a single meal AND sense of lack of constrol over eating during this episode.
Recurrent, innappropriate compensatory behaviour in order to prevent weight gain, e.g. self induced vomiting, use of medication such as laxatives, diuretics, enemas or others, fasting or excessive exercise.
Binge eating and innappropriate behaviours both occur at least once a week for 3 months
Self-evaluation is undoubtedly influenced by body shape and weight
Disturbance does not occur during an episode of AN!
Can be in full or partial remission, and the severity is based on the number of compensatory behaviours undertaken in a single week.
Admission criteria for anorexia and bullimia?
For anorexia, it’s: Admit to medical ward if: <65% standard body weight, hypovolaemic, HR
<40, significant electrolyte abnormality
For bullimia it’s just an electrolyte abnormality.
How to manage anorexia? Bullimia?
Refer for psychotherapy, monitor weight and bloods regularly, and admit based on the criteria.
Both of them can be managed with SSRI’s, CBT, family therapy and recognition of the health risks, and regular monitoring.
Physical signs of billimia
Fatigue and muscle wasting
Tooth decay
Parotid gland swelling
Reddened knuckles/ Russell’s sign (callouses on the knuckles from the self induction of vomiting
Comment on the prognosis of Anorexia Nervosa and Bullimia?
Anorexia:
o Early intervention better
o 1 in 10 adolescents continue to have anorexia into adulthood
o 70% assume weight of at least 85% expected level, 50% resume normal
menstrual function
o Long-term mortality 10-20%
- Bulimia:
o Relapsing/remitting disease
o Good prognostic factors: onset before 15yo, achieving health weight
within 2 years of treatment
o Poor prognostic factors: later age of onset, previous hospitalisation,
individual and familial disturbance
o 60% have good treatment outcome, 30% intermediate outcome, 10%
poor outcome
Describe refeeding syndrome?
Refeeding ysndrome is when we have a low phosphate level in the body. There is a low amount intracellularly, because a lot of this is shunted to the serum to bring the levels back up. However, when we give insulin, it cannot be compensated, and all the phosphate is driven intracellularly (we get an exacerbated insulin response with long term starvation). Thus, we get hypophosphataemia. Please note that we can also get hypokalaemia with this.
Manic Diagnostic Criteria? Hypomanic?
Needs three digfast features, needs to be present for one week with a persistently elevated moood which is abnornal. Needs to cause distress or impairment and no med or substance causes.
Hypomania only has to be longer than four days and is not causing impairment.
Persistent depressive disorder is defined as a depressive disorder with less than 5 MSIGECAPS features that persists for how long?
One year in kids, two years in adults
Manic and depressive episodes need to be differentiated from what in the criterion for BPAD 1 and 2
Schizoaffective, schizophrenia and schizophreniform
Management of BPAD?
General approach:
o Psychological: long-term psychodynamic psychotherapy, CBT, IPT
o Pharmacological: lithium, anticonvulsants (valproate), antipsychotics,
Monotherapy with antidepressants should be avoided
o Other: ECT
o Social: vocational rehab, social skills training, education of family/friends
- Patient presenting with acute manic episode:
o Need to stabilise patient so admit to AMHU and give antipsychotic (1st line is
olanzapine , 2nd quetiapine) and benzodiazepine for sleep/to calm down
o Consider starting mood stabiliser with above medications if patient is in severe
manic episode, otherwise you can start these after reducing mania
o Mood stabilisers: lithium (check renal + liver + thyroid function before starting)
or anti-convulsants (eg. valproate or lamotrigine)
o ECT can be used if patient not-responding to trial of antipsychotic + benzo +
mood stabiliser
Prognosis:
- 15% suicide rate
- Relapsing and remitting: depressive symptoms seem to occur more frequently and last
longer
- 90% have recurrent manic episode within 5 years
What are the negative symptoms of schizophrenia?
Avolition, alogia, anhedonia
Mechanism of SSRI’s
4 ways it works. It inihibits pre ysnaptic uptake of serotonin. And postsynaptic. First step.
2: Increases serotonin in the synaptic cleft. More serotonin to bind to post synaptic receptors.
3: increased binding at post synapse. this is the antidepressant effect. Pre synaptic receptors get downregulated.
4: Post synaptic receptors also become downregulated which is when side effects decrease.
Theory of increased suicidality;
Two explanations. The first is that post synaptic increased serotoin activity reduces anehdonia and increases motivation - get energy to kill themselves.
2nd explanation is that presynaptic serotonin binding provides autoregulation of the neuron and reduces the serotonin response initially but over two weeks these downregulate.
Clozapine therapy is monitored how???
First, we do a baseline echo, ecg and bloods.
We do monthly FBC and clozapine levels
We do 3-6 monthly weight, waist circumference, BP, fasting blood glucose and blood lipids.
How we diagnose Cauda Equina
Spinal MRI if the patient is stable.
What is the COPDx mnemonic?
COPDX: Case finding and confirm diagnosis Optimise function Prevent deterioration Develop a plan of care Manage eXacerbations
Case finding and confirmation in COPDX includes what
Smoking is the most important risk factor.
It’s diagnosed with an FEV1/FEV of 0.7
Should be accompanied by a regular assessment of severity
If it’s reversible consider asthma. By more than 400mL.
Case finding and confirmation is followed by optimising function. What is included in this heading?
Do a proper assessment and increas the pharmacotherapy in a stepwise fashion. Adhere to the inhaler technique, and use non-pharm therapies like pulmonary rehab and exercise. Comorbid conditions are common.
Prevent deterioration
Smoking cessation is the most important intervention. Preventing exacerbations also has a role. Give them all the flu and pneumococcal vaccine. Mucolytics (such as dornase alpha) can be helpful. If the patient is having hypoxaemia, the patinet is benefitting from the oxygen therapy. REMEMBER that. It’s just if they have hypoxaemia. Prevents complications. Note that you need to have this on for 18 hours pr day. Polycythaemia, right sided heart failure, or evidence of pulmonary hypertension are also indications for this therapy.
Develop a long term care plan?
Put them on a GP management plan, with liaison with the specialists.
Manage exacerbations
Control it lol. Bronchodilators, steroids, oxygen therapy, treat with antibiotics if they have increased volume of sputum, fever, and crackles.
Failure rates of an MTOP vs STOP?
2.5% vs 0.2%.
Describe the work up for an abortion
Counselling: explore feelings and concerns, what she bases information on and get a psychologist involved to assess reasons.
Bloods: get a FBC, RH group and antibody status
USS if needed to confirm intrauterine pregnancy
Plan for contraception needs to be covered!! With any of these gynae things, make sure you cover the post op contraceptives.
Discuss the use of misoprostol and antibiotics with a surgical MTOP?
Misoprostol is used if they are being admitted overnight. That is, if they are going to be over 14 weeks. Misoprostol is given the night before or on the day, and this helps them expel any retained products of conception. Just note it can cause diarrhoea. It should also be noted that before 14/10 weeks, they are just done as day case D&C and aren’t staying overnight so no misoprostol.
Antibiotics can be used prophylactically, and used to treat anyconcommmitant STI. We do a midstream and first catch. Usually it’s doxycycline and metronidazole that’s given.
Misoprostol actions on the female reproductive system?
It cuases uterine contractions AND cervical ripening (dilation).
When do we submit the gestational sac for histology?
before 6.5 because this is when it’s easiest to miss.
Symptoms of Asherman’s?
They get subfertility, but remember they also get chronic pain usually related to the cycle.
What are some contraindications to the medical abortion?
▪ On steroids ▪ Adrenal failure ▪ Coagulopathy ▪ Hypersensitivity to prostaglandins ▪ > 9 weeks pregnant
Describe the method of a medical abortion?
Protocol/ method
1) Must have pre-work up + counselling
2) USS showing intra-uterine pregnancy
3) Mifepristone is taken
4) Sub-lingual or buccal misoprostol 36 -48 hrs. later
5) Cramps + bleeding start 1 – 2h after misoprostol
6) Abortion over in few hours
▪ must have adult carer with phone until all over
▪ Phone help-line + SMS messaging offered by MS Health
▪ must have cooperation of nearest hospital
▪ must have detailed instructions for emergencies and
follow-up
How do we follow up our medical abortion patients?
They come in 14 days later. This is when the bleeding should have stopped.
We should check to ensure there is no infection, the bleeding has diminished, and they are emotionally well.
Confirm pregnancy terminated by doing a qunatitative BHCG or USS.
Contraception has been discussed and is in place.
How to verify if there is excess bleeding?
Completely soaked pad
▪ 2 pads/hr for 2 consecutive hours
▪ Clots size of fist
▪ hypovolemia
List ALL the options for analgesia in labour?
They are divided into non pharm an pharm. Non pharm is reduction of painful stimuli, activat peripheral sensory receptors, enhance descending inhibitory pathways.
Reduce painful stimuli involves maternal movements, changing positions, counter pressure, breathing nd relaxation techniques.
Activating the peripheral sensory receptors is superficial heat, cold immersion in water, warm water shower, touch + massage, acupuncture + acupressure, aroma therapy, TENS (helpful in latent 1st stage) and intradermal sterile water injections
Enhance the descending inhibitory pathways is attention ofocusing and distraction, hypnosis, and old fashion gritting your teeth.
Pharmacological involves the inhalational analgesia, parenteral analgesia, regional anlgesia, and nerve blocks
Discuss the water immersion as a technique for labour analgesia?
It reduces the rates of spinal and epidural rates because it’s actually an effective analgesia method. People can have it if they’ve been a low risk pregnancy and labour, they have a cephalic presentation, they are post 37 weeks, they are a singleton and they are less than BMI 35.
Contraindications are narcotic analgesia in the past 4 hours, high risk pregnancy, multiple pregnancy, requirements of continuous CTG and inducted labour.
You must get consent, and confirm the labour is progressed i.e. in stage one and the cervix is more than 5cm dilated. Monitor maternal and water temp, and you must ensure you are ready to help them out of the water if they are decompensating. Be prepared for an unintended water birth.
Discuss the use of nitrous oxide:
It acts quickly, and has a really short half life. It does not affect the foetus. some side effects are nausea, vomiting, dizziness, euphoria, disorinetation, generalied tingling and sedation, and its effectiveness is very variable.
Contraindications nclude Vitamin B12 deficiency (or pernisious), if sedated and can’t hold the mask correct, history of pneuoomothorax, bowel obstruction, increased ICP or intraoccular surgery/ orbit fracutres. Must seek advice if BPAD or schizophrenia.
It must be self administed with coaching i.e. remind the patient to breath into it during a contraction, and stop when it ends. Signs of overdose are a reduced respiratory effort, so just monitor for that. Start at 50% N2O 50% O2 and can go 70% N20
Opioids in labour cpatain?
IM morphine. Provides limited pain relief, but induces a useful euphoria. it takes 30 minutes to work. Causes the usual side effects, and in the newborn, causes resp depression/ rowsiness, so will impair APGARs. Can also affect feeding. Because of this, if the birth is due within four hours or if we want a water immersion, we do not give.
Describe the types, advantages, disadvantages, contraindications, complications of an epidural
it can be caudal and lumbar. They all contain a local anaesthetic and an opioid (prevents excessive motor blockade). The reason the pain fibres are preferentially blocked is that they have less myelination than the motor fibres.
Advantages are that the woman is conscious for birth, baby has no side effects (no maternal or foetal sedaton), it controls pain very well, is most effective, allows for top up doses, allows ambulation, no increase in caesar rates, no increased back pain.
Disadvantage is that it prolongs labour (increased duration of the second stage), and it does increase the rate of instrumental vaginal delivery with either forceps or vacuum. Increased risk of post partum fever, maternal hypotension, foetal hypoxia from the maternal hypotension, foetal bradycardia, and if the epidural fails, the next logical step is to do a caesarean section.
We therefore like to do epidurals if they request it, they have multpple comribdities, they have multiple pregancy or we’re doing an assisted vaginal birth.
Contraindications are if they refuse, if there is active matenral haemorrage/ coagulopathy, if they are septic or there is a local inection at the insertion site.
Complications are divided into common, uncommon and rare.
Common;
Nausea, vomiting, headache, inadequate block, pain and bruising at the site, bloody tap, motor blockade, urinary retention, foetal brady.
uncommon is infection at the site, itching, excess bleeding, temporary nerve damage, dural puncture and subsequent post dural puncture headache.
Rare side effects include permanent nerve damage,epidural haematoma, epidural abscess, respiratory depression, and meningitis.
Epidurals will take a few hours to go away, so they must have assistance with ambulation.
We do epidurals during active stage one usually when it’s requested. it’s very uncommon to initiate after this really.
Outline the clinical approach to an epidural
If they request it around the start of the active labour stage one, here is what we do:
Informed consent + written and documented
antenatally
o Advantages + disadvantages
o Complications
o Need for IV + catheter
o Can no longer have water immersion
o Time it takes to wear off and how it feels
when it does
2) Arrange anaesthetist review
3) Inform anaesthetist when woman wants the epidural
4) Must have IV access
5) Ensure good circulatory volume
(may need IV fluids)
6) Position to avoid aorto-caval compression
7) Continuous DTG monitoring
8) Empty bladder with in-out catheter
(+ ongoing good bladder care)
9) Regular monitoring of maternal vital signs
? consider giving with subcut terbutaline or sublingual
terbutaline to ↓rates of foetal bradycardia
Remifentanil PCA is now used for ‘fall-back’ when regional
analgesia is contraindicated. The major drawback is the
danger of profound maternal respiratory depression, even
from a small overdose – this is why remifentanil was only
licensed for administration in highly monitored
environments.
What is a spinal and how is it different to an epidural?
A spinl anaesthetic is an injection of local anaesthetic into the subarachnoid space. It is just one injection, whereas epidurals are with a continuous catheter often so we can give those top up doses.
Go over those antenatal care flashcards from Dr Tucker! The one about the pre preg consult is particularly good.
yessir.
Important things to discuss on the first antenatal visit + examination
Last normal menstrual period ▪ Estimated due date (EDD) o Assists with gauging future investigation results o Naegele’s rule = 7 days + 9months after LNMP o Dating scans (accurate <12 weeks) ▪ Obstetric Hx o Any past births, issues o Abortions / misscarriages o Mode of delivery o Birth weights, gender o Complications ▪ Gynaecological Hx o Cervical procedures o Periods o Hormones ▪ PMHx + PSurgHx ▪ Family Hx o Including partner’s ▪ Medications + allergies ▪ Social o Smoking + alcohol o Finances o Social supports Initial Antenatal Examination ▪ General appearance ▪ BMI ▪ Vital Signs ▪ Neck o Goitre? o Thyroid issues? o Bruits? ▪ Chest o Lungs + heart o Breast examination ▪ Abdomen o General abdomen examination ▪ Vaginal examination o Not done routinely, only when indicated o Hx of discharge? o Bleeding? o FGM history
There are numerous investigations you order over the course of the antenatal care. Please discuss.
Booking bloods (on first visit) o FBC = ?anemia, Thalassemia, ↓plt o Group + Ab screen = for HDN o Serology ▪ Rubella ▪ Syphilis ▪ Hepatitis B + C ▪ HIV o Mid-stream urine MCS o Others ▪ Iron studies ▪ Vit D testing (<50 level) ▪ TSH ▪ Chlamydia
▪ 28 / 40 = OGTT/ FBC/ Ab
▪ 36 / 40 = FBC / Abs
▪ 18 – 22 / 40 = Morphology scan
▪ USS – 1st Trimester + 2nd Trimester
When do we do give anti-d
At 28 weeks and 34 weeks. 36 weeks is when we do ECV, and I think I often get confused between these.
What is some general advice you would give a woman at an anenatal clinic visit?
Diet o Adequate o Iodine, iron, folate o Avoid risk foods ▪ Exercise o Light to moderate exercise ▪ Smoking ▪ Alcohol ▪ Drugs = esp illicit o Placental insufficiency o Placental abruption o Early labour o Issues on the baby – e.g. opiate withdrawal ▪ Constipation o High fibre diet o Fluids o Metamusil, dietary fibre
At each antenatal checkup, what do you need to cover?
General wellbeing ▪ Symptoms o Pain o Bleeding o Fluid loss ▪ Foetal Movements o > 10 movements / day o Count movements around meals o Any changes from normal movement for you? ▪ Examination o Maternal weight – can counsel about BMI o Blood Pressure o Abdominal examination – LEOPOLD’S MANOUVRE ▪ Fundal height ▪ Fundus ▪ Back/limbs ▪ Pelvic grip – 1+2 o Comment on: ▪ Fundal Height ▪ Lie ▪ Presentation ▪ Vertex ▪ Position ▪ Engagement o Vaginal exam – NOT ROUTINE! (swabs, labour, confirm presenting part, pelvis capacity)
When is the best time to do ECV and why?
It’s around 36 weeks because before this there is a good chance it will spontaneously change it’s orientation.
What is the foetal denomentator? What is this used to describe?
The denominator is the presenting part we use to describe based on where it is related to hte maternal pelvis. For instance, if the baby is in vertex, we say it’s the occiput. If breech, it’s the sacrum, and in facial presentation it’s the mentum.
Some presentations inclue right occipitoanterior or left occipitoanterior (based on which direction the occiput is facing, right and left occipitolateral, and irght or left occipitoposterior.
What are some common complaints in pregnancy, and how do we deal with them?
Morning Sickness o Hormonal o 80% of women o Diet / anti-emetics o Assess hydration + urine ketones o Usually reduces in 2nd + 3rd trimester o Rule out other causes: multiple pregnancy, molar pregnancy, UTI ▪ Constipation o Progesterone effect o Diet / Laxitives o Most are safe in pregnancy ▪ Heart Burn o Enlarged uterus o Progesterone mediated LOS relaxation o Light meals, meals 2 – 3hrs before bed o Semi-recumbent sleep o Ant-acids ▪ Mylanta, gastrogel ▪ PPI if refractory ▪ Pelvic Pain o Physiotherapy o ? round ligament pain (in groin, lateral to uterus, ↑ on movement) o ? pubic symphisis dysfunction o MUST EXCLUDE SERIOUS CAUSES ▪ Varicose veins / haemorrhoids o Venous obstruction = ↑ venous pressure o Supportive tights, rest, elevation o Family + self-history very indicative o Usually resolve post pregnancy ▪ Carpal Tunnel Syndrome o Must exclude renal, liver, pre-eclampsia issues o May just be from fluid increase o Physiotherapy + Splints o Surgery in select cases ▪ Vaginal Discharge o ↑ vascularity of vagina / cervix = normal o Swabs for infection testing o Reassurance
What are some of the styles of antenatal care?
Search for Aus Government Department of Health Models of maternity care
Normal weight gain in pregnancy/
Make sure they know there is no normal weight. If htere is a pre normal BMI, we say 11.5-16kg total is a good amount of weight gain. Don’t just binge on unhealthy foods though because of the risk of GDM.
Please look at the normal antenatal schedule i your notes.
Thx
Assessment of a previa? They usually present with malpresentation, painless PV bleed (90%) or pain.
Do leopold’s to confirm presentation (breech is the mal), AVOID VE because this triggers bleeding, and just do a transvaginal/ transabdo USS.
How do we manage?
if diagnosed before 20 weeks, just call it a low lying placenta. It will likely move.
It it doesn’t, make the diagnosis. We need to grade it, estimate blood loss, gestational age of baby, position of baby,health of baby and health of mother need to be weighed up. We need to relive symptoms and prolong the pregnancy.
bed rest and hospitalisation can form part of the management. CTG, and high risk antenatal clinic is recommended. Blood transfusions for the mother, and avoid irritating the uterus or cervix (no sex or orgasms). Caesarean is likely the way these are delivered.
New rf’s for placental abruption?
Advanced maternal age, multiple pregnancies, Polyhydramnios, thrombophilias, amniocentesis, ECV
Can placenta previa cause conenital malformation?
yeah lol. Also IUGR, distress and iatrogenic pematurity.
Remember to admit these patients to the ward for overnight monitoring and investigation. If they are found to be okay, they can go home.
Why are multiple preganncies are risk factor for placental abruption?
Because the sudden uterine decompression from birth of first one causes a great negative pressure.
Complications of abruptio placenta inclue very shock complications. There is one more specific.
Foetomaternal haemorrhage. Do a rosette and kleihauer-betcke test to assess the amount of anti D to give in a rhesus negative woman.
The clinical presentation of an abrupted placenta?
PV bleeding Abdominal pain (or lower back pain) Labour Abdominal tenderness (woody hard) + tender uterus Foetal distress Hypovolaemia and shock Very frequent uterine contractions
Clinical diagnosis. Don’t do an USS ya berry.
Management of an abrupted placenta?
History, examination, investigations Options, resuscitation Fetal monitoring Factors to consider: o Maternal condition o Fetal condition o Gestational age o Level of neonatal care availability Difficult to diagnose in mild forms
12,15
• Consider admission for surveillance as clinically indicated
• Give Rh D immunoglobulin to all non-sensitised Rh D negative women
independent of whether routine antenatal prophylactic Rh D
immunoglobulin has been administered17 [refer to Table 9]
• Consider antenatal corticosteroids between 24 and 34 weeks + 6 days
gestation17
• Monitor for disseminated intravascular coagulopathy (DIC) and request
urgent clotting studies, platelet count as indicated44
o Do not delay treatment by waiting for coagulation results if massive
blood loss occurs44
• Significant placental abruption requires urgent delivery by CS44
o Incision – mid line preferable if other abdominal injuries suspected
o Refer to Queensland Clinical Guideline Postpartum haemorrhage for
management of PPH, blood/product replacement and MTP activation
protocols34
How do you work up a patient with a bleed in early pregnancy ya bitch?
History: LMP Pregnancy test History about bleeding/tissue passed Pregnancy symptoms History of trauma Abdominal pain Fainting / shoulder pain / dizziness Bladder and bowel symptoms Gynae history – PID/contraception Obstetric history PMHx PSHx – pelvis surgery Meds Allergies Social history Examination: General Abdominal Pelvic examination o Speculum o Bimanual Differential diagnoses: Miscarriage Ectopic pregnancy Molar pregnancy Other causes
Investigations: FBC Bhcg Blood group MSU USS
Go over the USS findings from DR Tucker’s cards and draw them out. I never remember.
Thanks
Types of miscarriage?
Complete: no medical or surgical intervention needed.
Incomplete: RPOC
Threatened: early pregnancy bleeding with other causes excluded not associated with dilation of the cervix.
Miscarriage: there is no conceptus, but there is also no bleeding.
Septic miscarriage: complicated by pelvic infection
Inevitable miscarriage is when they are in the process of happening.
Management of miscarriage can be either expectant, medical or surgical. Discuss the clinical considerations of each:
Expectant: offered if they prefer it. However, to do it, they need to have access to medical emergency care and be linked into the appropriate hospital similar to a medical abortion. Follow up is 7 days, and if there is evidence of RPOC on this follow up, we can continue current or expedite the process.
Medical management is with misoprostol. Contraindications include if it’s a suspected ectopic or gestational trophoblastic disease (the other two differentials for bleeding in early pregnancy), IUD in situ, allergy to prostaglandins, medical contraindications.
Inform them bleeding can continue for up to two weeks after (lightly).
Follow up is in 48 hours, and consider surgical management. Also on day eight, and we do FBC, BHCG, USS.
Medical review in 6 weeks.
Surgical is a D&C. If theyhave persistent bleeding, are haemodynamically unstable, or there is evidence of a suspected GTD/ RPOC or if it’s infected.
GIVE ANTI D
Go over caesareans with your dear mother.
yeah.
Efficacy of breast feeding contracpetion?
2%. This may be too high.
Which medications can effect the efficacy of the COCP
Valproate and other CP450 enzyme inducers
Antibiotics
St John’s Wort
Clomiphene citrate lol
failure rate of vasectomy and tubal ligation
Vasectomy is 1/2000, tubal ligation is 1/200. I have heard differently though in the same deck of flashcards lol
Mirena side effects
Irregular PV bleeding in the first 3-4 months, amenorrhoea in up to 30% by 1 year
Hormonal symptoms: nausea, headaches, breast tenderness, bloating
Benign and usually self-limiting ovarian cysts
Side effects of the depot provera?
Menstrual disturbance (regular, irregular or even amenorrhoea) Delayed conception (fertility may not return for 6-12 months) Weight gain (probably due to progestagen ↑ appetite) Bone loss (small risk of ↓ bone density with prolonged use)
Absolute CI’s to COCP? Relative?
< 6 weeks post partum
Smoker over age of 35
Hypertension (systolic >160mmHg or diastolic >100mg)
Current or past history of VTE
Ischaemic heart disease
History of CVA
Complicated valvular heart disease (pulmonary hypertension, atrial fibrillation, history of subacute bacterial endocarditis)
Migraine headache with focal neurological symptoms
Breast cancer (current) (pretty sure this is the progesterone component that makes this a CI i.e. in HRT if there is progesterone in it, this is what increases the risk of breast cancer)
Diabetes with retinopathy/nephropathy/neuropathy
Severe cirrhosis
Liver tumour (adenoma or hepatoma)
relative Ci’s include if they are smoker under 35, conrolled HTN, migraine >35, symptomatic gallstones, mild cirrhosis, hx of oestrogen induced cholestasis, interfering medications, and if they are less than 6 months post partum
COCP dose? Failure rate?
20-30 microg of oestorgen
50-60 microg of progesteroen
Actual failure rate is 9% and this is due to incorrect use. <1% though if it’s used correctly.
Benefits of the COCP? Risks/
Risks Benefits
Increased risk of VTE
Increased risk of cancer (cervical, breast)
Compliance issues – 9% failure rate if not
use correctly
Breast tenderness
If hypertensive – increased risk of MI +
stroke
Increased risk of hepatocellular Ca (rare)
Interactions with some other
medications
Good return to fertility
If used correctly, effective contraceptive
method
Useful in treatment of acne, menorrhagia,
dysmenorrhea, PCOS, PMS
Protective against cancer (ovarian, colon,
endometrial)
Decreased risk of benign breast disease
Important things to counsel them about before starting COCP? What about depo provera?
Counseling:
Importance of compliance – explain the packaging, how to take, when to take, discuss
active and sugar pills
OCP has no protection against STDs – use in conjunction with condoms
7d rule – when commencing, require 7 days of another contraceptive before you are
covered
Can commence on any day of the cycle
Breakthrough bleeding, even when taking active pills
Able to take active pills for up to 12m (useful in treatment of menstrual migraines)
before needling to bleed
o Recommended to use for 3m periods and then bleed
Advise women >50yo to use alternative method
No protection against STDs – use in conjunction with a condom
Importance of timed injections – needs to be given every 3 months (13 weeks)
o Two week “grace period” – patients who are =2 weeks late can just receive
the injection without the need for pregnancy testing (this is because
ovulation does not occur for at least 14/7
o If >2 weeks late for injection, recommended to do pregnancy test + back-up
contraception (e..g condom or abstinence) for 7/7
SEs: menstrual irregularities, bloating, dizziness, reduced libido
Ideal time to commence is within 7d of onset of menses of 7d before discontinuing
another method of contraception – but can be started at any time
o Always advise of need for alternative contraception in first 7d
Normal dose of paracetamol:
1g 4-6 hourly is max normal dose paracetamol for adults
Fluclox
500mg QID
Benefits of a depo provera?
Long acting (2-3m) + very effective Useful in poor compliance pts Amenorrhea Reduced pelvic pain assoc w/ periods or endometriosis Protection against endometrial and ovarian Ca, and PID Useful in pts with heavy PV bleeding, dysmenorrhea, or IDA Few drug interactions
Risks and benefits of implanon?
Risks are that you need to be a trained practioner to give it and it’s invasive, so can cause local damage. Benefits though is that it isn’t user dependent, has high continuation rates, fewer contraindications and it lasts for 3 years. The return to fertility is something like like one month.
It’s contraindicated in current breast cancer, cirrhosis, unexplained PV bleeding and in a hx of breast cancer..
Also, if hte chick palys rugby or some other highly dangerous sport, they need to be careful as this can break.
What to tell patients about emegency contraceptive?
it doesn’t protect against STi’s, it’s OTC, it loses efficacy the more you use it, and a preg test is needed in two weeks.
Absolute contraindications to the IUD?
Pregnancy, septic abortion/ postpartum sepsis, unexplained PV bleeding, gestational torphoblastic disease, endometrial cancer, distortions of the uterine cavity, and current PID
Contraindications to the mirena?
o Pts with acute liver disease or liver tumour
o Known or suspected pregnancy (if first insertion, test if pregnant)
o Current or recent PID, lower genital tract infection
o Postpartum endometriosis, cervicitis, cervical dysplasia (always do a pap smear),
uterine or cervical malignancy
o Progesterone-dependent tumours
o Undiagnosed abnormal uterine bleeding
Counselling for patients on an IUD?
No protection against STDs – use in conjunction with condoms
o Patients can check the string of their IUD to ensure in the correct place
o Keep a record of date for replacement of IUD – should not stay in any longer than
recommended time
o Return to GP if any unusual symptoms – discharge, lower abdo pain, pain during
intercourse
Remember to counsel Mum on ectopic pregnancy management.
K
Management considerations for patient with chronic diabetes mellitus pre conception?
Control it
Put them on a high risk clinic care
Take them off hypoglycaemics except for metformin and insulin
Education and refer to diaebtes educator + endocrinologist as they may need more insulin.
Fortnightly visits hehe
Maternal risks in diabetics?
Risks of caesars
Risks of increased complications, including post partum haemorrhage
Increased worsening of microvascular complications
increased risk of precclampsia and other things
Macrosomia (foetal hyperinsulinaemia, still birth)
How do you approach the risk of cardiac abnormalities in pregnant women?
Do a normal morphology scan, and then follow this up with another one at 22-24 weeks to look for cardiac defects. 50% of foetal abnormalities in pregnancy are cardiac in diabetic women. Termination of pregnancy can be offered if they are detected before 20 weeks.
Common foetal abnormalities associated with diabetes:
Macrosomia and hyperinsulinaemia Bowel Neural tube defects Cardiac Urinary tract Sacral agenesis
Perinatal diabetes care should involve?
Careful BGL control. Consult with diabetes educator and endocrinology team.
regular foetal growth scans from 24w (abnormalities and polyhydramnios),
They can have spontaneous labour up to forty weeks if they have good BGL control, normal foetal growth, and no polyhydramnios or other complications.
Also, be aware that at birth they are at risk of hypoglycaemia, ARDs, polycythaemia, neonatal jaundice, hypocalcaemia and hypomagnesaemia.
GESTATIONAL DIABETES: what is the definition in Queensland?
OGTT done at 26-28 weeks will show: fasting >5.1 mmol/L, 1hr >10mmol/L, 2 hr >8.5 mmol/L
Discuss the pathogenesis of GDM
Pregnancy is a state of insulin resistance, so there is increased insulin. This is magnified in women who are already at risk of poor glucose tolerance. Additionally, more insulin is going to the baby due to their metabolic requirements. Thus, they get more insulin and fat storage leading to macrosomia.
Please note there is also a lower renal threshold for glucose in pregnancy, so glycosuria is common.
maternal risk factors for GDM?
BMI >30
Maternal age >40yo
Previous GDM / glucose intolerance / macrosomic baby >4500g
Previous perinatal loss
PCOS
Family history diabetes (first-degree relative)
Meds – corticosteroids, antipsychotics
Multiple pregnancy
Ethnicity – South Asian, Black Carribean, Middle Eastern
What are some of the complications of GDM?
Foetal:
- Note that the structural abnormalities seen in chronic diabetes don’t apply, because GDM is theoretically occurring after the embryogenesis.
before birth: Macrosomia, IUFD,
During birth: neonatal hypoglycaemia, ARDS, prematurity iatrogenic, neonatal jaundice, shoulder dystocia, hyperinsulinaemia
After birth: impaired glucose toelrance, and increased risk of T2DM and obesity.
Maternal complications: - MIscarriage Pre ec infection Induction of labour/ trauma/ c section PPH increased irsk of T2DM + HTN Increased risk of hypoglycaemia.
Outline in detail the management of gestational diabetes mellitus?
Management:
ANTENATAL:
Multidisciplinary team approach
Targets: (to be measured QDS, and if controlled can be BD) (eTG)
o Fasting <5.3mmol/L
o 1hr post-prandial <7.8mmol/L
o 2hr post-prandial <6.7 mmol/l
Lifestyle – diet, physical activity, cease smoking + alcohol
Pharmacological
o Metformin +/- supplemental insulin PLUS lifestyle
o If high on average, or still getting 2-3 high readings each week, or if fetus is
macrosomic (>75th percentile)
Antenatal care – considered high risk, monitor regularly
Monitor growth
Monitor fetal BGL after delivery
POSTNATAL
FOLLOW-UP: OGTT @ 6 weeks post-partum to ensure normalized
Encourage breastfeeding – increased energy demands may means less insulin
required by women (insulin is safe)
Insulin requirement is ~20% less in breastfeeding women than before they were
pregnant
HAPO Study – 2008 (Hyperglycaemia and Pregnancy Outcome)
“Continuous linear relationship between maternal glucose and fetal growth and that
fetal growth can be modified by glucose-lowering therapies, with diet and lifestyle
intervention often being successful”
“ pharmacological intervention, treatment strategies starting with oral hypoglycaemic
agents (metformin or glibenclamide) but often involving progression to insulin to
ensure adequate glycaemic control are as successful but not superior to insulin alone”
“important influence of maternal glycaemia on offspring birthweight:
“Importantly, infant adiposity as estimated by sum of skin-fold thickness exhibited a
similar strong linear relationship with maternal glucose”
how diagnosis pre ec
2 measures of BP >140/90 + 1 organ system involvement. Pretty sure this has to be after 20 weeks.
reflex findings in pre ec on neuro exam?
hyperreflexia and clonus
How do we reduce the risk of pre-ecclampsia in women with risk factors?
We reduce the risk by giving them 100mg aspirin daily. We also tell them to seek helpimmediately if they feel like they have symptoms listed in pre ec.
Risk factors for pre ec
previous Older age First preg with current partner Family history pre-existing diabetes or hypertension Multiple preg Renal disease
How do we work up a pre-ecclampsia?
measure BP in clinic?
Screen for proteinuria on dipstick and quantify if positive.
FBC, LFT, LDH, urate
CTG + USS
Indications for MgSO4
Eclampsia, severe pre-ecclampsia, any signs of neuro findings. You should transfer to a high level service when giving this.
Management of HELLP
if above 34 weeks gestation, should deliver. Consider platelet transfusion.
Imminent ecclampsia is defiend as what?
Imminent eclampsia = ≥ 2 of the following symptoms: o Frontal headache o Visual disturbance o Altered LOC o Hyperreflexia o Epigastric tenderness
Management: Resus DRSABCD Goals of treatment: o Terminate the seizure o Prevent recurrence o Control HTN o Prevent maternal and fetla hypoxia MgSO4 is the anticonvulsant drug of choice Plan birth (if antepartum) ASAP!!!
Management of pre-ecclampsia after it’s been diagnosed?
multidisciplinary team approach is advocated for, and except where there is acute foetal compromise, stabilise there woman and addres the problems of pre-ecclampsia.
Timing + mode of birth:
o Recommend vaginal birth unless c-section indicated for other
obstetric indications
o Moderate HTN:
If otherwise well expectant management beyond 37w
o Preeclampsia:
Dependent of severeity and gestation
o HELLP syndrome
Plan birth ASAP!!!!
Intrapartum monitoring
o Close clinical surveillance required
o Minimum ½ hourly BP
o Continuous CTG
o IV access
o Multidisciplinary involvement
Intrapartum care:
o 2nd stage:
If BP is within target range = usual care
If BP not responsive to initial drug therapy, advise
assisted/operative birth
o 3rd stage:
Active management as increased risk of PPH
DO NOT GIVE ergometrine or syntometrine
DVT prophylaxis to you bitch.
Post partum, what do we do with our pre-ecclampsia ladies?
HTN and pre-ecclampsia may develop for the first time post partum. ask frequently about the symptoms (notably headaches and epigastric pain), and give them VTE prophylaxis.
Continue with the antihypertensives
Warn methyldopa is associated with depression (post partum depression warning)
Discharge + follow up:
o First and second line drugs are compatible for breastfeeding
o If taking ACE-I, discuss contraception
o Recommend F/U screening after 6w to ensure resolution or need for
ongoing care
o Advise to avoid smoking, maintain healthy weight and exercise,
attain healthy BMI (esp if overweight)
o Assessment for traditional CV risk markers (e.g. annula BP, serum
lipids, BGL)
o Risk reduction for future pregnancy (e.g. aspirin, change from ACE-I,
pre-conceptual advice on BP control)
types of breech? How do we manage?
Footling: one or both feet are pointing downwards and will deliver first.
Frank: foot in the face of a frank breech. Flexed hips but extended knees.
Complete: everything is flexed.
Talk me through the use of instruments when delivering. What can’t you do, what are the indictions etc.
Foreceps are used if there is failure to progress. Note: failure to progress is defined in a nulliparous woman as 0.5cm per hour (less than) and in a multip 1cm per hour. Or, if in stage 2, it’s 1 hour for a multip and 2 hours for a nulliparous woman. remember though fr second stage we allocated some leeway if they have had an epidural.
Foreceps are used if stage 2 fails to progress. Power, position, presentation need to be intact for us to use it (i.e. cannot use foreceps if less than +2 foetal descent. Syntocinin is given while we do it, and the mother MUST get an episiotomy.
Babies can get laceration and the various birth injuries which includes a fracture.
Remember the mother can have the episiotomy tears.
How do manage a breech presentation?
Often you discuss with your consultant if there is a need for a caesar.
Altenratively, to do vaginally you do:
- Hand gently supporting the emerging breech
Keep the sacrum anterior
Do the Lorsett Manoeuvere + Mariceau Smellie Veit
What is an early miscarriage? what is a late miscarriage? How many pregs have a miscarriage?
8-20%. Early is before 12 weeks and late is beyond 12.
A misscarriage is loss before 20 weeks or before 500g.
recurrent miscarriages?
3 or more consecutive
Miscarriage risk factors. Causes?
Increased age, previous, history of STI’s and PID, smoking, alcohol, BMI, fever;
chromosomal abnormality is the biggest cause, and it’s mainly aneuploidy.
Others are CONGENITAL ANOMALIES o Genetic (e.g. anencephaly) o 2* to extrinsic factors (amniotic bands) o Teratogens (mercury, ↑ BGL) ▪ CVS OR AMNIOCENTESIS ▪ ABDOMINAL TRAUMA o CVS o Amniocentesis o Fall, MVA o Domestic violence ▪ INFECTIONS o TORCH infections ▪ MATERNAL CONDITIONS o Hyperthyroidism o DM o PCOS ▪ HYPERCOAGULABLE STATE (APL – UNCLEAR…)
How does a miscarriage present?
Cramping pelvic pain, PV bleeding, PV dark discharge, amenorrhoea, loss of pregnancy symptoms, cervical shock, incidental finding
what is cervical shock?
Cervical shock is vasovagal syncope produced by stimulation of the cervical canal during dilatation. This is leading to hypotension and braydcardia. It’s usually caused when the products travel through the cervical canal.
How do we examine for and investigate a miscarriage?
Examination ▪ ABC + Vitals o IVCs +/- fluids o Analgesia for the pain ▪ Abdomino-pelvic examination o Inspect for distension o Guarding / peritonism o Tenderness o Keep open mind! Could be GIT! o Speculum o Bimanual examination ▪ Urine β-HCG Investigation ▪ FBC – assess blood loss ▪ Serum B-hcg – for confirmation ▪ Group + Hold and Rh status – for possible replacement, may need anti-D ▪ TV USS Β-HCG ▪ Serum is best doubles every 48 hours ▪ <5IU/L = normal, not pregnant ▪ 1500IU/L = should see IU pregnancy on TVUSS ▪ Need serial tests to establish viability + loss Group + Hold ▪ Determine Rhesus status ▪ May need if becomes HDS or needs surgery DR DILGIR LECTURE Ultrasound ▪ βHCG 1500 – should see an IU pregnancy (TV USS) 5000 – should see an IU pregnancy (TA USS)
how do we diagnose a miscarriage?
▪ > 25mm mean sack diameter with NO foetal
pole + yolk sac
▪ CRL >7mm with NO FHR
The management of a miscarriage can be expectant, medical, or surgical. Please discuss the intricacies of each. In addition, what are some counselling measures you would take with a woman who’s had a miscarriage
Expectant: if they are educated and aware of the consequences, can do expectant management.
Must have haemodynamic stability, be reliable, understand there will be pain and bleeding, and have access to the follow up similar to the abortion.
ALL CASES if they are beyond 12 weeks need an antiD dose.
Review in a week and do an ultrasound to see progress. 10% failure rate.
medical:
offered if it’s the preference, stable, done before 9 weeks, or as the step up if there is failure of the expectant management or there is a retained products of conception diagnosed on ultrasound follow up of the expectant management.
Need to review the medical cases in 2 weeks to ocnfirm it’s complete and no RPOC (USS).
Educate about the painfulness, and the side effects of the misoprostol (Nausea and vomiting, diarrhoea, fever).
Offer analgesia, and remember they should watch out for signs of infection.
Surgical is considerd when: - They prefer Unstable Infected Failed other options in a stepwise approach.
This is a dilatation and curetage. remember the risk of perf!
Counselling:
Educate them that they should get their period again in 4-8 weeks.
Continu folate if want to try for pregnancy again, or take contraception.
Conceive again after two normal periods.
Early USS in pregnancy in future
Social support offered
How do we defined recurrent pregnancy loss?
3 in a row if less than 35 years but 2 if older.
risk factors for recurrent pregnancy loss?
Previous pregnancy loss ▪ AMA ▪ ↑ parity ▪ Uterine factors o Congenital abnormalities o Sub-mucosal leiomyomas o Intrauterine adhesions ▪ APS – antiphospholipid syndrome (5% - 15%) ▪ Poorly controlled DM ▪ PCOS ▪ Hyperprolactinemia ▪ Genetic – Chromosomal abnormalities (e.g. balanced translocations)
How do you work up and manage?
EVALUATION ▪ Karyotype the foetus ▪ Uterine assessment (e.g. hysteroscopy, HSG) ▪ Autoimmune - ACA + LA ▪ TFT
MANAGEMENT
▪ Genetic counselling if chromosomal abnormality
▪ Surgical management of uterine anomaly
▪ Treat hyperprolactinemia
▪ APS – Aspirin + prophylactic LMWH
▪ Serial USS + support when they do fall pregnant
Types of ectopic pregnancy?
Cornual (interstitial) Tubal (isthmus) Tubal (ampullar) Infundibular ovarian Peritoneal Cervical Abdominal
Uterine activity in pregnancy is about balance between activating an inhibitory factors. List some inhibitors.
What stimulates contractions?
Progesterone, prostacyclin, relaxin, nitric oxide, PTHrP, CRH
Prostaglandins and oxytocin
Define labour?
regular uterine contraction lasting 30-60 seconds every five minutes, and progressive cervical dilaton
What are the mechanisms of labour? Discuss.
Effacement, dilatation, and the three p’s: power (uterine activity), passage (maternal pelvis + vagina), and passenger (foetal factors).
Powers:
- Normally contractions occur once every 5 minutes, and they last 30-60 seconds. They are measured using montevideo units, which is measured using a catheter. Adequate MVU is 200-250. They usually measure the sum of contractions in 10 minutes.
Interventions here include the induction of labour (prostaglandins) and augmentation using oxytocin or rupture of labour.
Passage refers to the pelvis passage and if there is cephalpelvic disproportion.
Passenger refers to the foetal head diameter (widest part), foetal attitude, foetal lie and the foetal presentation.
What are the cardinal movements of labour?
Descent (engagement), flexion, internal rotation, extension, external rotation, expulsion).
Describe the stages of labour
First stage is either latent or active. Latent phase is to 3cm, and active is beyond this to 10cm. Normal active for nulliparous is 1.2cm/ hour and for multip it is 1.5cm/hr.
The second stage is the delivery of the foetus. Remember, prolonged in a multip is going to be 1 hour and in a nullip it’s going to be 2 hours.
Third stage is placenta. mean here is 30 minutes.
The following are terms used extensively in obstetrics: failed induction, active labour, arrest of first stage. What do these mean?
Failed induction is failure to have regular contractons (every three minutes) and failure of the cervix to change after at least 24 hours of oxytocin.
Active labour is when the cervix is between 3-4cm, this is when the rate of dilation picks up greatly. However, it’s observed this can take up to 6cm or some mothers.
Arrest of first stage is when there is no change in cervixx when it’s 3-4cm dilated over 2 hours. 1st stage arrest can be diagnosed ONLY if:
⃝ Woman has reached 6 cm and the water has broken
⃝ AND there has been no cervical change for:
o 4 or more hours of adequate contractions
o OR; 6 or more hours of inadequate
contractions
If the mom is still <6 cm, then she needs additional time and
interventions before an arrest of labour can be diagnosed,
because she is still in early labour
What is the arrest in the second stage?
there are two ways we can diagnose it.
WHEN PUSHING TAKES PLACE:
▪ >3 hours in first-time moms with an epidural,
▪ >2 hours in first-time moms without an epidural,
▪ >2 hours in experienced moms with an epidural,
▪ > 1 hour in experienced moms without an epidural
NO IMPROVEMENT IN DESCENT OR ROTATION AFTER:
▪ ≥ 4 hours in first-time moms with an epidural,
▪ ≥ 3 hours in first-time moms without an epidural,
▪ ≥ 3 hours in experienced moms with an epidural,
▪ ≥ 2 hours in experienced moms without an epidural
Discuss intrapartum foetal assessment.
it can be either extenral or internal. External is either an external foetal monitor or CTG. Internal is foetal scalp electrode or intrauterien pressure catheter (to measure the montevideo units over 10 minutes and hopefully achieve 200 - 250).
What are the patterns of foetal heart rate monitoring? Discuss some trends?
Baseline is 120-160. we call that normal. higher or lower is brady or tachy.
Variability is either absent, minimal (<5bpm), moderate 5-25 or marked 25.
Periodic changes are also acceleratiosn and decelerations. We use 32 weeks to define the deceleration point, and we say that 10bpm over baselin under 32 weeks is an accel, but if over 32 it’s 15.
Decelerations are also things that we observe. These can be variable, early or late.
A variable deceleration is due to umbilical cord compression, and it’s due to either the artery or the veins compressing. If there is a vein compression, then HR goes up.If there is artery compression, heart rate drops.
An early deceleration refers to the vagal reflex during labour, and is due to the cervix compressing the head of the baby.
A late decel is when there is uteroplacental insufficiency.
umbilical vein vs arteries
2 arteries and one vein. The vein carries nutrients and oxygen TO the baby, whereas the veins carry it away.
how manage an abnormal foetal heart rate?
Hypotension o Maternal position – left lateral recumbent o IVF hydration, ephedrine 2) Maternal O2 administration 3) Cessation of contractions o Discontinue oxytocin o Uterine relaxants – terbutaline 4) Amnioinfusion 5) Expedite delivery
How can we intervene in an abnormal labour?
▪ Augmentation o Oxytocin o Achieve adequate uterine contractions o Requires reassuring foetal status ▪ AROM ▪ Therapeutic rest ▪ Operative vaginal delivery ▪ Cesarean delivery
When does obstetric cholestasis occur?
Third trimester usually when the oestrogen is at it’s highest.
How does obstetric cholestasis present? How do we diagnose?
Clinical Presentation/History:
Pruritis (onset ~28w, esp in multiple pregnancies – esp hands + soles of feet) without rash – look for excoriations
Sleep disturbance (due to pruritis)
Jaundice +/- steatorrhea (2-4w after pruritis) – rare
Dark urine + pale stools – rare
Malaise + anorexia (occasional)
Past hx gallstones +/- pruritis while on OCP
FHx obstetric cholestasis or pruritis in pregnancy and/or gallstones
Investigations:
Serum bile acids (>10mmol/L is diagnostic // >40mmol/L assoc w severe fetal risk + requires
admission)
Elevated transaminases (not diagnostic) (rules out others)
Prolonged INR/PT in severe cases
Liver + GB USS to exclude obstructive GB disease and to establish gallstones
Foetal effects of obstetric cholestasis? How do we manage?
Differential Diagnoses:
Pre-existing liver disease, alcohol or other drugs
Viral hepatitis Hep A/B/C + CMV + EBV
Autoimmune liver disease
Pre-eclampsia + acute fatty liver disease of pregnancy
Fetal effects:
Stillbirths usually after 38w with little to no warning
Severe OC (>40mmol/L serum bile acids)
o Assoc w/ increased fetal mortality + morbidity, inc;
Pre-term birth (25% vs 6.5%)
NICU admission (12% vs 5.6%)
IUFD (1.5% vs 0.5%)
Antenatal management:
Obstetrician – consider high risk care
Plan delivery (esp if dx >37w) consider delivery at 38w
Admission is severe (bile acids >40), otherwise consider outpatient Mx
Fetal surveillance:
o Report any decreased or absence of fetal mvoements
o Perform umbilical artery Doppler for changes
Pharmacological intervention:
o Ursofalk (for symptom relief, esp pruritis)
o Antihistamines (drowsy or non-drowsy)
o Recommend sorbolene, pinetarsol, aqueous craem, bicarb baths
o Vit K 10mg daily if prolonged INR/PT (if left untreated, increases the risk of PPH)
Investigations:
o Weekly serum bile acids (twice weekly in severe cases)
o Weekly LFTs (twice weekly in severe cases)
o Coags after dx of severe + before induction of labour
Counselling:
40-60% risk of recurrence in subsequent pregnancies
Reassure no long-term sequelae for mum or bub
If familial OC, at risk of chronic liver disease require long-term follow-up
Follow-up with GP review at 1/12 post-partum to check bile acids + LFTs
Physician review at 6/52 post-partum if abnormalities present
How does an ARM work? Define abortion?
Abortion: termination of pregnancy (spontaneously or intentionally) <20
weeks gestation or <500g birthweight
Artificial rupture of membrane (ARM): when membranes are ruptured
intentionally to induce labour (decreased intrauterine pressure baby’s
head moves down increased pressure on cervix PGs produced)
Which foetal lie is unstable?
Oblique
Types of cephalic presentations
Vertex, military, brow, face from order of the most flexed to the most extended.
Foetal denominators please?
Foetal occiput,
chin/mentum and sacrum are the chosen points in vertex, face and breech
presentations respectively
great grand multip?
More than 10
What is low, very low and extemely low birth weight
2500, 1500, 1000
Perinatal period?
28 days after birth
Placental attachments?
Placenta Decidua: chorionic villi attach normally to decidua
o Placenta Accreta: chorionic villi attach to myometrium
o Placenta Increta: chorionic villi invade into myometrium
o Placenta Percreta: chorionic villi invade past myometrium
Describe what is term
Pre-Term: <37 weeks gestation
o Term: 37-42 weeks gestation
o Post-Term: >42 weeks gestation
What is PPH?
Primary PPH: ≥500mL blood loss within 24 hrs of delivery
o Secondary PPH: excess blood loss from 24 hours to 6 weeks postdelivery
(no quantified volume)
What is viability in Aus?
24 weeks or 500g
List the four T’s in order of occurence.
Tone, trauma, tissue, thrombin. 70% is tone.
Causes of an atonic uterus
Large baby, polyhydramnios, multiple pregs, twins, prolonged labour, anaesthetic, mag sulf
Trauma
Laceration of cervix or vagina during a c section or instrumental delivry
Risk factors for a PPH
Over 35 Macrosomia Asian Past PPH Caesar Coag disorders Meidcation induced hypotonia like mag sulf Obeseity Prolonged labour Existing uterine abnormlaioties
Aetiology of tissue pph
Either we pull too much or there is an accreate, increta or postcreta and can’t be delivered as easily.
Signs and symptoms of PPH are as you would expect. How do we investigate?
Do HCT, weigh the kidney ishes and weigh the sheets (kidney dish is 700mL apparently), and you can also monitor vitals.
How to reduce the risk of PPH?
Use of uterotonics during the third stage of labour (active management
Early cord clamping (balance with risk of IDA) and controlled cord traction, and uterine massage after placetal birth.
To manage a PPH, you do the following standard management.
DRSABCD + get help, assess blood loss, monitor vitals, keep warm,
give O2 if necessary
o Dual IV access 14-16 gauge
o Urgent bloods: FBC, group & hold, cross match, coag profile, U&E, Ca,
lactate
o Avoid dilutional coagulopathy, 2-3L crystalloid max until RBCs ready
o Insert IDC to monitor urine output
o Identify underlying cause: 4 Ts
What is management if it’s tone?
o Fundal massage
o 5 IU IV Oxytocin over 2 minutes, repeat in 5 minutes up to total dose
10IU (DON’T DO QUICKLY, CAN CAUSE ISCHAEMIC ECG CHANGES),
plus…
o Start IV infusion of 40 IU IV Oxytocin/ 1 L of crystalloid at 125-
250ml/hr rate
o 250 microg IV Ergometrine maleate over 2 minutes
(CONTRAINDICATED eclampsia, pre-eclampsia, retained placenta
check placental borders)
o 800-1000 microg PR misoprostol
o Transfuse blood products and transfer to OT if continues
o If this doesn’t fails, transfer to OT:
Apply bimaual compression, consider intrauterine balloon
tamponade
If critical, consider B lynch suture, bilateral uterine artery
ligation or hysterectomy
Bilateral uterine artery ligation
Important management steps in a trauma, tissue or thrombin PPH?
Trauma: if stable and minor, repair as necessary. Take to OT and give blood transfusions if it’s severe.
Tissue: Give oxytocin VE and visualise placenta USS if necessary Controlled cord traction Massage fundus only after the placenta is out and whole Transfer to OT if these fail to remove.
Thrombin:
- Look for other signs of haemorrhage, as this may well be systemic
Do a coags study
Keep body temp elevaed
Give 4 units RBC 4 units ffp 10 UNITS CRYOPRECIPITATE
Clacium gluconate if low calcium
What is a secondary post partum haemorrhage. Aetiology? Management?
between 24 hrs and 6 weeks
Retained products, infection, pre-existing disease such as uterine fibroids, polyps, cervical polyps, trauma.
Manage with bed rist and IV ab’s (triples). If retained products, refer. Also use uterotonics and digital evacuation of the uterus under a GA.
Risks factors for preterm birth and PPROM?
Maternal Characteristics Medical and Pregnancy Conditions
Age <18 or >35 yo Short Cervical Length
Ethnicity: ATSI, African, Asian Previous PTB
Cigarette Smoking
Infections: bacterial vaginosis, chorioamnionitis
High or low BMI Multiple Gestation
Describe the pathogenesis of preterm labour or pprom
It’s multifactorial. Influenced by PG synthesis, oxytocin release, hormonal rations, (decreased progesterone and increased oestrogen), mechanical stretch in the uterus and changes in the uterine blood flow.
Signs and symptoms of a PPROM or preterm labour?
Signs Symptoms
SIgns include prescence of liquour on examination, cervical ripening, regular uterine activity. Symptoms include vaginal fluid loss (PPROM), pelvic pressure, lower abdo cramping and back pain.
Differential diagnoses:
- Urinary incontinence
- Physiological vaginal discharge
- Bacterial infection (eg. Bacterial vaginosis)
- Cervical mucous (sign of impending labour anyway)
How are these tihngs diagnosed?
Sterile speculum exam looking for cervical ripening and liquour or intact membranes. Assess the liquor colour and smell. If it’s mec stained it might be labour, bloody and foul smelling might be an infection.
If liquour not obvious, apply pad, encourage movement and inpspect pad later.
DO NOT DO A BIMANUAL BECAUSE THIS CAN CAUSE INFECTION.
INvestigationss needed in PPROM?
FHR and CTG monitoring for isngs of foetal distress
HIgh vaginal swab for MCS + low vaginal/ anal swab for GBS.
Midstream urine for MCS. If have these infections, you may want to keep them in because they could get a chorioamnionitis.
FBC and CRP to assess infectious signs
Foetal fibronectin: Indications: symptomatic labour between 22-36 weeks,
intact membranes, cervical dilation <3cm
Contraindications: ROM, dilation >3cm, cervical cerclage insitu
>50ng/mL = positive = increased risk of PTB
What is a cervical cerclage?
Cervical cerclage, also known as a cervical stitch, is a treatment for cervical incompetence or insufficiency, when the cervix starts to shorten and open too early during a pregnancy causing either a late miscarriage or preterm birth.
Talk about the management of PPROM?
Management:
- Admit to hospital if: fFN >50, cervical dilation present, ROM, contractions
regular and painful, foetal distress present or clinical judgment favours
- Monitor maternal and foetal obs regularly
- Antenatal corticosteroids:
o Decreased risk respiratory distress syndrome, intraventricular
haemorrhage and neonatal death
o Initial 2 doses 11.4mg IM Betamethasone 24 hours apart, if PTB
expected within 24 hours delivery doses 12 hours apart
o Repeat dose in 7 days if risk continues
- Tocolysis:
o Little evidence about use of tocolysis with PPROM before 34 weeks
associated with decreased delivery within 48 hours but increased
risk of chorioamnionitis
o Contraindications: chorioamnionitis, in-utero foetal death, preeclampsia,
placental abruption
o Nifedipine 20mg PO, repeat after 30 minutes if contractions
continue, repeat after another 30 minutes if contractions continue
o Maintenance dose 20mg PO every 6 hours for 48 hours
- Antibiotics:
o Recommended for presence of GBS, imminent PTB regardless of GBS
status and chorioamnionitis
o Ampicillin or amoxicillin 2g IV initially then 1g IV 6 hourly
(clindamycin if allergic), PLUS…
o Gentamicin 5mg/kg IV OD, PLUS…
o Metronidazole 500mg IV BD
- Magnesium sulphate:
o Neuroprotective, reduces risk of cerebral palsy
o Given if 24-30 weeks gesation
o Loading dose: 4g IV bolus over 20 minutes
o Maintenance dose: 1g/hour for 24 hours or birth
- If birth imminent, inform senior obstetric and paediatric/NICU teams
- If PTB does not occur and is not likely, discharge home with appropriate
education on signs and symptoms that warrant hospital return, eg. signs of
infection
Complications:
- Prematurity: increased risk of neonatal morbidity and mortality
- Infection: increased risk of maternal morbidity and mortality
Risk factors for shoulder dystocia? How is the diagnosis made?
Previous shoulder dystocia GDM Post-date pregnancy Macrosomia Maternal short stature High pregnancy weight gain Abnormal pelvic anatomy Prolonged 1st or 2nd stage Instrumental delivery
Diagnosis is made based on the turtle necking sign where head goes out then in, and when gentle downward traction of the foetal head fails to delivery the anterior shoulder.
Define shoulder dystocia
Usually due to anterior shoulder impacting maternal pubic symphysis AFTER BIRTH OF THE FOETAL HEAD
Management of shoulder dystocia?
HELPERR
Help
Activate instituional protocol, appropriate notification, additional staff, additional back up, neonatal resus, obs backup, anaesthesia, theatre booked.
Episiotomy
Needed to do additional manoueveres.
May not need to, do this in response to first line treatment.
Legs McRoberts Manouvere Flex maternal hips so that thighs are on abdo and knees are towards nipples - Straightens lumbosacral lordosis, increases AP diameter of pelvis, flexes foetal spine - Reduces >40% of dystocias
Pressure
Suprapubic pressure by assistant while the hips are flexed. Use a CPR style hand position for this, Attempt this for 30-60 seconds. Reduces 50% of dystocias when done with McRoberts.
Enter
Rubin II and Woodscrew.
Approach anterior foetal shoulder from
behind
- Exert pressure on scapula to adduct most
accessible shoulder and rotate to oblique positon
- Continue McRoberts
Wood Screw Manoeuvre:
- Approach posterior foetal shoulder from
front
- Gently rotate shoulder toward symphysis
Reverse Woodscrew Manoeuvre:
- Approach posterior shoulder from behind
- Rotate foetus in opposite direction from Rubin or Wood Screw manoeuvres
(apply pressure to posterior aspect of shoulder)
Remove posterior arm
Roll the woman
Roll to the McRoberts all fours position. Increases the pelvic diameter. Gravity may also contribute to dislodging. Delivery of the posterior shoulder with gentle downward traction. May attempt all enter manouveres in this position.
Last resort manourvers:
Clavicle fracture, symphysiotomy, zavanelli. (Give uterine relaxant and push baby back up
- Perform CS
- Increased risk PPH and uterine rupture)
Complications of polyhydramnios
Umbilical cord prolapse, abruption, uterine atony, malposition, PPROM,
Complications of oligohydramnios
IUGR, preterm birth, cord compression in labour, and more likely to get caesars because of worrying decompressions.
Complications of dystocia?
3rd and 4th degree tears Anal sphincter damage PPH
Uterine rupture Symphysis separation Neonatal brachial plexus
palsy (Erb’s Palsy)
Neonatal clavicular fracture Foetal acidosis
Foetal hypoxic brain injury
Classification of female sexual dysfunction
Desire disorders: Hypoactive sexual desire, sexual aversion disorder
Arousal disorders
orgasmic disorder
Dyspareunia
Causes of dyspareunia?
Superficial: vulval: infection, lichen schelrosus, atrophic vulvitis, chemical reaction, mass (bartholin’s cysts), trauma. Vaginal: vaginismus, atrophic vaginitis, trauma. Cervical: cervical mass, trauma
Deep: Cystitis, endometriosis, adenomyosis, PID, fixed retroverted uterus, pelvic mass, tumour,
IBD and IBS
Brief description of lichen sclerosus, what the signs and symptoms are, and how to diagnoses + manage?
Remember it’s a risk factor for SCC.
Signs: white, scar like lesions on the vulvar with some excoriations. Can be on perineum too.
Symptoms: dyspareunia, pruitis, pain
Investigations + diagnosis: clinical. Can do biopsy.
Manage by avoiding exacerbating factors, topical steroids, PV oestrogen and watching for changes due to SCC risk.
Atrophic Vaginitis: what are some risk factors and clinical features?
Aside from menopause and ovary failure, smoking, chemorads/ anti oest, smoking, nulliparity, decreased sexual activity.
We can get vaginal dryness, and dyspareunia with thinning of the mucosa. It’s associated with itch, bleeding, tightness, and it’s seeing increased urinary frequency and urgency due to the atrophic urethritis and trigonitis.
Diagnosis of atrophic vaginitis?
Pelvic exam, vaginal bedside pH (if alkaline it’s probs bacterial vaginosis), STI screen, PAP smear, pelvic and transvaginal USS if bleeding
Management of atorphic vaginitis:
Lubricant when having sex Topical oestrogens Reassurance Moisturisers HRT could be considered
Complications of atrophic vaginitis?
Bleeding, vaginal infections, urinary symptoms
PID has two causes. What are they, what are the clinical features and how to diagnose?
They are endometriosis and they are chronic STI. They can present with PV bleeding, deep dyspaerunia, subfertility, vaginal discharge, pelvic pain, discharge, palpable adnexal masses, cervictis etc. also fevers.
To diagnose it, I would just do an STI screen, with vaginal and urethral swabs, with midstream urine. Beta HCG, Pap smear, pelvic and transvaginal ultrasound.
Manage PID?
Temporary abstinence, may require surgical removal of the adhesions, treat partners
Complications of PID?
Chronic pain, infertility, ectopics, pelvic abscesses.
How do we diagnose endometriosis?
Definitive = on laparoscopy/ laparotomy. Presumed = dysmenorrhoea and pelvic pain even if not showing up on the exam or USS.
Most accepted theory of endometriosis pathogenesis?
Retrograde menstruation. Increased risks are menorrhagia, cervical stenosis, and outflow tract obstruction.
Commonest place for endometriosis:
In descending order, ovaries, uterosacral ligaments, ovarian fossae, then pouch of douglas.
Defintive diagnosis is on laparotomy and biopsy. What will it show?
Will show any 2 of the following 3:
- Endometrial type epithelia / glands
- Endometrial type stroma
- Evidence of cyclical activity (recent or old blood, hemosiderin laden-MACs)
Classic features of endo?
Dysmenorrhoea, dyspareunia, dyschezia
What is metorrhagia, and what is menometorrhagia?
Menometorrhagia is a combination of menorrhagia and metorrhagia, where metorrhagia is intermenstrual bleeding.
Examination findings in endometriosis?
Bluish discoloration on external genitalia ▪ Cervical motion tenderness ▪ Uterine motion tenderness ▪ Mass in / tender nodules in: o posterior vaginal fornix o adnexa o pouch of Douglas o rectovaginal ▪ Fixed or ↓ mobility of uterus ▪ Retroverted uterus
Comment on the use of laparoscopy in infertile women?
Do it. 1/2 of these will have endo, and in those who don’t, they have significant pelvic pathology anyway.
Management of endo?
Use mefanamic acid and paracetamol to control the pain.
Hormonal is also used, and we can used COCP/ progestogens, and GnRH agonists. The last line is danazol. All as effective as each other.
Use the surgical (laparoscopy) to ablate implants, excise adhesions and remove endometriomas.
Go over the stages of endometriosis?
1: scarce
3: endometriomas
4: DENSE adhesions
Things to look for in a fertility assessment?
Male factors - adequate functional and motile sperm? Ovulation diagnosis: is the woman ovulating? Tubal function tests: can the sperm and the egg meet? Uterus + cervix: can implantation persist? Ovarian reserve?
What is infertility?
1 year of unable to get preg. Primary and secondary.
What features make you think no IVF for you?
Advancing maternal age, more than 7 years of trying, and no previous female pregnancies.
History questions for infertility?
HISTORY Both ▪ Assess amount + timing of intercourse ▪ Occupational factors that may affect fertility ▪ Previous hx of STI ▪ Chronic medical conditions ▪ Drug history + prescription medications Female partner: Menstrual history ? ovulation Pelvic pain / dysmenorrhoea ? endometriosis Past abdominal surgery ? adhesions ? exposed in utero to DES ? rubella status Gyne history PCOS, fibroids, endometriosis Male partner o ? Hx of cryptorchidism o ?timing of orchiopexy o ? testicular torsion o ? inguinal hernia repair o Androgen / steroid use o STI history (+ mumps!)
Some exam findings in infertility?
EXAMINATION NOT USUALLY DONE!!! Female ▪ Obesity / ↑ BMI ▪ Thyroid dysfunction features ▪ Cushing’s features ▪ PCOS, hyperandrogenism ▪ Galactorrhoea (?↑prolactin) ▪ Abdominal surgical scars ▪ Pelvic exam o Cervical anomaly / pathology o Take STI test samples o Assess for cervical/ uterine / adnexal tenderness o Size + contour of uterus o +/- DRE is endometriosis suspected
Male ▪ Degree of 2* sexual development ▪ BMI ▪ Gynecomastia ▪ Genital exam o Size + location of urethral meatus o Structures o Evaluate testes (location + size) o Epidydimitis? o Assess for varicoceles / hydroceles ▪ DRE to assess prostate
Describe fluid make up of sperm:
70% seminal vesicle secretion, 20% prostate, 5% bulbourethral gland, 5% semen from testes. It takes less than 30 minutes for liquefaction to occur as the prostate fluids break down the coagulating factors. The longer it takes, the fewer sperm get to the ova.
Sperm concentration: what is oligozoospermia?
Less than 20 mil per mL. No sperm in the sample is azoospermia. Note that artefact is common.
Remember how in females we said we needed to assess ovulation, tubal function, uterine factors, cervical factors and ovarian reserve?
Ovulation is assessed by doing a day 21 (7 day post menses) progesterone. Basal body temperature is important, and doing it daily for three months will show a spike when we ovulate. USS follicle monitoring can be done too.
Tubal function: hysterosalpingogram. Look at the anatomy.
Uterine factors: hysteroscopy
Cervical factors: a post coitus test is done that looks at secretions.
Ovarian reserve: Can also do a day 3 FSH.
Talk to me about the De Lancey levels of support
Three levels. Level one eoncempasses sacrum, uterus and the cervix.
The levels of support here are the cardinal ligaments and the uterosacral ligaments. Things that can go wrong are dragging, fullness/ feeling a mass, bulging.
Level two encompasses the upper part of the vagina, the bladder, and the rectum (and pubis but not a part).
The methods of support here are the levator ani, pubovesicle and puborectal ligaments and the things that can go wrong are digitation (have to insert your fingers into the vagina to defaecate), urge incontinence (urge is a problem with bladder hyperactivity remember), and cystocole, UTI’s (from retention due to funny angle of the bladder).
The third level is the opening of the vagina, the genital hiatus and the anal canal.
The supports here are the perineal body (external anal sphincter, bulbospongiosus, the transverse perinealmuscles and the things that can go wrong are digitation, rectocoele, stress incontinence (hypermobility of the urethra), and a widened genital hiatus (causing flatus and reduced pleasure)
and anorectal incontinence.
All of these are having risk factors including increased intrabdominal pressure (pregnancy, obesity, NOT VAGINAL BIRTH) and weakeneded ligaments (things like Marfan’s, EHlers Danlos).
Types of incontinence. Managmeent of urge and stress?
Mixed, overflow, urge, stress, true.
Urge is through bladder training and kegel’s.
Stress is via HRT, stopping them from smoking, losing weight, or you could get them to do a suburethral tape or sling procedure.
Remember to rule out UTI’s.
