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people have been replaced by exact copies of themselves.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.
