Year 3 revision - chapter 1 Flashcards
Causes of thyrotoxicosis?
Autoimmune
- Graves
- First stage of Hashimotos thyroiditis Drugs
- Amiodarone
- Iodine in contrast
- Iodine deficiency Neoplastic
- Multinodular goitre
- Solitary thyroid adenoma Secondary hyperthyroidism
- Pituatary adenoma (high TSH)
Ix for thyrotoxicosis?
Bedside
- BGL, consider ECG Bloods and urine
- TSH
- Consider T3/T4 Thyroid antibodies
- TSH receptor auto-antibody –> Graves
- Anti-thyroglobulin –> usually Hashimotos but can be up in other thyroid dz
- Antithyroiperoxidase–> usually Hashimotos but can be up in other thyroid dz
- ESR/CRP
- Cholesterol and lipids (low chol and high FFA?)
- Coags (metabolism of clotting factors can cause high INR) Imaging
- USS Special
- Radionucleotide uptake scan
Mx of thyrotoxicosis
Basics
- Nona Place and person
- Consider endo referral Confirm dx
- Refer to Ix Definitive
- B-blocker
- carbimazole +Propylthoiouracil
- High dose iodine (paradoxical effect)
- Radioactive iodine therapy
- Thyroidectomy
Signsof thyrotoxicosis?
- Agitation/anxiety
- Acropatchy (clubbing)
- Tremor
- Sweaty/hot
- Tachycardic
- AF
- Proximal myopathy
- Hyperreflexia
- Exopthalmos/proptosis in Graves
- Lid lag
- Goitre/thyroid bruit
- Flow murmur
- Pretibial myxedema in Graves
Causes of hypothyroidism
Autoimmune (need histology to tell between these three)
- Hashimotos thyroiditis
- De Quervain thyroiditis –> painful
- Riedel’sthyroiditis
- Iodine deficiency
- Previous surgery
- Radiotherapy to the neck
- Rarely, secondary hypothyrodism, pituatary pathology, low TSH
On exam, what are the three different types of goitre?
- Diffuse
- Multinodular
- Solitary Nodule
Causes of goitre?
Graves DiseaseObstetrics: Puberty & PregnancyIdiopathic / iodine deficiencyThyroiditis (eg. Hashmoto’s, Sub-acute)Rx (drugs eg. Throxine, iodine, amioderone, lithium)Errors of thyroid hormone synthesis – Pendred’s syndrome
You find a lump in the thyroid, what are your differentials?
Benign Causes Follicular adenoma
* Slow growing, no invasion, no metastasis Thyroid cyst
* usually benign, but they occasionally contain malignant solid components
* Chronic inflammation of the thyroid (thyroiditis)
Malignant Causes Follicular Carcinoma
* Slow growing
* Metastasizes via veins to lung and bones Papillary Carcinoma
* Most common type of thyroid cancer
* Not very aggressive, but metastasizes via lymphatics to lymph nodes and lung Medullary Carcinoma
* Rare Undifferentiated/Anaplastic Carcinoma
* Rare
* Very rapidly growing and metastatses
* Wide, direct local invasion
You find a lump in the thyroid, incidentally, what tests will you do/not do
No need to perform FNA if nodule was of incidental finding and is of
What are the different types of thyroid cancer?
What is thought to be the aetiology of IBD?
It is thought that IBD develops because genetically susceptible individuals mount an abnormal inflammatory response to environmental triggers, such as intestinal bacteria. This leads to inflammation of the intestine with release of inflammatory mediators, including TNF, IL-12 and IL-23, which cause tissue damage.So not strictly autoimmune, the immune system doesn’t attack the body’s own cells, but rather ingested materials that would normally be inert.
In people who have a genetic predisposition to IBD, what factor is thought to potentially determine which type they get?
Smoker - CrohnsNon-smoker - UC
What are the pathological features of Crohns and UC?
What are the features of UC on history and exam
History
* Cardinal symptoms are rectal bleeding with passage of mucous and bloody diarrhea Pain
* can range from mild crampy pain associated with tenesmusto severe pain with either severe or complicated colitis (i.e., toxic megacolon, perforation)
Exam
* Normally - LLQ abdominal pain If severe
* anorexia, malaise, weight loss
* if the patient is toxic –> fever, tachycardia and signs of peritoneal inflammation.
Extra-intestinal signs include uveitis, ankylosing spondylitisand erythema nodosum. Clubbing can occur.
Features of Crohns on hx and exam
History
* The major symptoms are abdominal pain, diarrhoea and weight loss
* Pain is often associated with diarrhoea, which is usually watery and does not contain blood or mucus Almost all patients lose weight
* either because avoid food (since eating provokes pain), or due to malabsorbtion
Exam
* Abdo tenderness An abdominal mass may be palpable
* matted loops of thickened bowel or an intra-abdominal abscess.
* Perianal skin tags, fissures or fistulae Also
* Gallstones
* AnkSpond, anterior uveitis, erythema nodosum
Interesting note Patients tend to develop an individual phenotypic expression of the disease with one or more of the following complications as their primary problem:
* Strictures (causing bowel obstruction)
* Fistulas (often many & recurring)
* Abscesses
Investigations for IBD
Bedside
- None Bloods
- FBE –> Anemia, infection
- Iron studies –> Anemia Vit B12/Folate
- UEC/CMP –> Electrolyte disturbance
- LFTs
- CRP/ESR Imaging
- AXR - toxic megacolon, strictures
- CT Abdomen - strictures, fistula Special
- Colonoscopy/gastroscopy
Management of Crohns
Basics
* Analgesia Place and person
* If acute/severe admit to hospital
* Refer to gastro Investigations and confirm diagnosis
* See Ix page
* Repeat colonoscopy/gastroscopy and ESR/CRP to assess severity Definitive Stepwise management
* Budesonide
* Prednisolone PO
* Prednisolone IV
* Use azathioprine as a steroid sparing agent
* Vaccination and maintain general health because on long term immunosuppresion Long term follow up
* Consider changing maintenance treatment
A note on managing acute flares If patient presents with severe diarrheoa do NOT assume IBD flare and commence steroids. Perform stool culture first to rule our gastroenteritis as cause. If pt is on steroids, biologics or immunomodulators they may not be febrile or have a raised WCC. If you Rx steroids for a gastroenteritis you could cause sepsis!
Management of UC?
The key aims of medical therapy are to:
* Achieve clinical remission
* Treat acute attacks
* Prevent relapses
* Detect dysplasia and prevent carcinoma
* Select appropriate patients for surgery
Basics
* Analgesia PRN Place and person
* Refer to gastro
* Admit if septic or severe Ix
* As per investigations Management Stepwise
* Localised proctitis –> 5-ASA (mesalazine, anti-inflammatory) suppository
* More extensive disease –> Oral 5-ASA (sulfasalizine) or oral prednisolone Severe
* Admit
* Fluid rehydration
* IV prednisolone Maintenance
* MTX
* Azathioprine Intractable
* Colectomy
Extra gastrointestinal manifestations of IBD?
Musculoskeletal * Arthritis (CD > UC) * Sacroiliitis * Finger clubbing * Ankylosing spondylitis * Osteoporosis Hepatobiliary Liver * Fatty liver (steatosis) * Chronic active hepatitis * Fibrosis and cirrhosis * Abscesses Biliary tract * Primary sclerosing cholangitis * Bile duct carcinoma * Cholelithiasis Pancreatic * Crohn’s disease Amyloid * Crohn’s disease Skin lesions * Erythema nodosum * Raised reddish-blue, warm, tender nodules mostly on lower legs Pyoderm gangrenosum * UC > CD * Single or multiple deep ulcerations with a necrotic centre, with an undetermined border and violaceous skin surrounding the lesion Mucosal lesions * Aphthous ulcers -->CD Eye lesions * Uveitis * Episcleritis * Conjunctivitis Gynaecological lesions -->Crohn’s diseaseVasculitis -->Crohn’s diseaseGenitourinary * Urinary tract calculi * Ureteral obstruction * Vesicle fistulae * More common in CD Thromboembolic
What do you know about PBC and PSC?
PBC F:M 9:1 Hx
* Initial symptoms commonly FATIGUE AND PRURITIS Associated with xanthomata and xanthelasma Ix
* Small duct dz - not visible on imaging
* AMApresent in over 95% of patients. cholestatic serum biochemistry -↑ ALP ± GGT Tx
* Ursodeoxycholic acid
* treatment mainly palliates symptoms until transplant becomes necessary.
* Although 30% of patients will exhibit disease recurrence in a transplanted liver, this takes years to develop and is not a contraindication to transplant.
PSC
* Males
* Associated with UC and AnkSpond
* P-ANCA positive Continued destruction of bile ducts in PSC leads to end-stage liver disease and portal hypertension. Dx by Endoscopic retrograde cholangiopancreatography(ERCP) Wippels procedure
Tests for liver failure/disease?
Bedside
* BGL
Bloods and urine Structure
* LFTs Function
* FBE (for platelets specifically)
* Albumin Coags Autoimmune disease ASMA ANA (T1AIH) Anti-LKM1 (T2AIH) Anti-liver cytosol antibody-1 (ALC-1) (T2AIH) AMA - PBC P-ANCA - PSC Infectious
* Hep A, B and C serology Congenital
* Fe studies – Haemachromatosis Blood ceruloplasmin – Wilsons disease NASH/NAFLD FBGL Cholesterol Drugs Paracetemol level
* Blood alcohol level
Imaging
* Ultrasound
* MRCP
* ERCP
Definitive/surgical
* Biopsy –>good to determine AIH vs drugs
What are the two pathological types of liver cirrhosis and what causes each type?
Micronodular – regenerating nodules are liver involved uniformlyoften caused by ongoing alcohol damage or biliary tract diseaseMacronodular - nodules are varying sizenormal acini may be seen within the larger nodulesoften seen following chronic viral hepatitis and NASH
What are the signs of both compensated and decompensated liver disease?
Compensated Oestrogenic effects * Hair loss * Testicular atrophy * Gynaecomastia * Spider naevi * Palmar erythema * Amenorrheoa Decompensated Portal hypertension * Oesophageal varices --> malaena or haematemesis * Ascites * Caput medusa * Haemorrhoids Failure of catabolic function leading to toxic build up * Hepatic encephalopathy * Asterixis * Fetor hepaticus Failure of bilirubin metabolism * Pruritis * Jaundice Failure of anabolic function * Ascites from low albumin * Bleeding from thrombocytopenia
Investigations (and expected result) fo chronicliver disease
Explain the Child Pugh Score
What are general management strategies for patients with cirrhosis?
High protein, low salt diet
- Cirrhosis is anenormously high energy consuming state, they may not even tolerate the fast during sleep, need high protein diet
- Cirrhosis also causes extreme RAAS activation leading to massive Na retention DEXA scans and bone health monitoring
- Cirrhosis is bad for bones! Avoid
- Alcohol
- Benzodiazepines/anaesthetic agents
- Paracetemol >2g per day
Mx of cirrhosis induced ascites?
- Fluid restriction Low Na intake
- No normal saline or Hartmann’s!
- Highest tolerable dose of spironolactone
- +/- smaller doses of frusemide (
Paracentesis - For every 2L of fluid drained must give 1 unit of albumin to replace protein or else will cause hepatorenal syndrome –>death TIPS
- Completely contraindicated if the pt has ever had hepatic encephalopathy because you’re bypassing the liver’s filtration system
Transplant
Mx of hepatic encephalopathy
Treat underlying causeHepatic encephalopathy, acute and chronic, is reversible. A precipitating cause (other than worsening of hepatocellular function) can be identified in the majority of patients. Common causes = GI bleeding, increased protein intake, hypokalemic alkalosis, infection, and constipation (all of which increase arterial ammonia levels).Order blood cultures regardless of tempEnormous doses of lactuloseIf can’t swallow give via NGT with close nurse monitoringMechanism:The GIT is the primary source of ammonia, which enters the circulation via the portal vein. The intact liver clears almost all of the portal vein ammonia, converting it into glutamine and preventing entry into the systemic circulation. Reduction of the circulating ammonia level usually results in resolution of the encephalopathy.Lactulose works by lowering the pH in the bowel –>ammonia stays in NH4+ (ammonium) form and thus doesn’t get absorbed.Diarrheoa is merely a side effect!RifaximinAantibiotic to reduce bacterial burden in gut –>lowers ammonia levelsIf chronic encephalopathy limit diet to 70g protein per day
Mx of oesophageal varices?
ABC’s
- Intubation in all cases Somatostatin analogue
- MOA = splanchnic vasocontrictor Correct coagulopathy
- FFP + Vit K Do not give IV saline or Hartmann’s!!
- For every 1 litre IV saline you give you’ll create 7 litres of ascites Emergency endoscopy
- Variceal band ligation orInjection sclerotherapy If endoscopy fails
- Sengstaken-Blakemore or Minnesota Tube and retry endoscopy after ICU stabilisation
- Transjugular Intra-hepatic Portosystemic Shunt (TIPS)
- Ceftriaxone 1g per day 5 days prophylactically
- Treat underlying liver disease if feasible
What marker is used for hepatocellular carcinoma?
a-foetoproteinAlpha-Foetoprotein (AFP)200-500 ng/ml diagnostic
What is the prognosis of hepatocellular carcinoma?What complications occur?
Untreated most patients will progress within 4 months3 year survival = 12-13%Cause of death
* Progression underlying liver disease, liver failure
* Haemorrhage
* Rupture tumour
* Variceal bleed
* Metastases
What’s the epidemiology of gout?
Occurs in 1% genpop.More common in: * Caucasians * Males (M:F = 10:1) * Age 40-60 (males), 60-70 (females) * after menopause Pre-menopausal women do not get gout
Your patient has mild pain, they ask “can I take an NSAID?”What questions do you need to ask them?What side effects do you need to inform them about?
“Should I take an NSAID doc?”
* Do you have a history of stomach ulcers? Are you on warfarin/aspirin/clopidogrel?
* Do you have any kidney problems?
* Do you have heart failure?
* Do you have asthma?
1 and 2relate to bleeding risk.3 relates to the triple whammy.4 relates to NSAIDs causing salt retention5 relates to leukotriene synthesis.Side effects/ADRsRenal impairmentPeripheral oedemaGastrointestinal bleeding/PUDHypertensionN&V
If patient experiences hyperprolactinaemia on an antipsychotic which drug should you switch them to?
Aripiprazole or quetiapine
Side effects of SSRIs/SNRIs?
“DASHINS” (like dashing but dashins)DiarrhoeaAnxietySuicideHeadacheInsomniaNauseaSexual dysfunctionPlus don’t forget the serious ones ofHyponatraemiaSerotonin syndrome!Plus SNRIs can cause tachycardia, HTN
What is the most sedating 2nd gen antidepressant
Mirtazipine
Causes of sudden, painless blindness?
- Migraine
- TIA
- Giant cell arteritis
- Retinal detachment
- Central (or branch)retinalartery occlusion
- Central (or branch) retinal vein occlusion
- Vitreous hameorrhage
Can you picture what central and branch retinal vein occlusion looks like on fundoscopy?
Can you picture what a central retinal artery occlusion looks like on fundoscopy?
Buzz word is CHERRY RED SPOTSThis is basically a TIA/stroke, just in the eye!
What clinical features distinguish pre-septal from orbital cellulitis?What’s the treatment?
–Ophthalmoplegia–Pain with eye movements–ProptosisTreatment for preseptalis fluclox (just like normal cellulitis)But with orbital cellulitis you need to REFER AND ADMITThey may need surgical intervention to save their sight
Loss of vision and an ache in one eye worse on movement for the last weekWhat’s the diagnosis, treatment and management?
Diagnosis: Optic neuritisManagement: Pulsed methylprednisolonePrognosis: 30% 5 year risk of developing MS
Old patient, difficulty reading, new glasses didn’t helpWhat’s the diagnosis and management?
Diagnosis: Macular degenerationManagement:Management of dry age related macular degeneration is not particularly effective and involves modification of risk factors e.g. stop smoking, diet rich in antioxidantsIf it becomes “wet” i.e. abnormal new vessels grow which can leak and bleed then treatments are available to help regress the abnormal vessel growth–> Anti-VEGF intravitreal injectionsNB: A bleed may present as SUDDEN loss of vision
Can you visualise what macular degeneration looks like on fundoscopy?
In women at high risk or pre-eclampsia/eclampsia, what preventative measures are taken during pregnancy?
low dose aspirin 75‐150mg/dayCalcium 1g/day.
What factors place a mother at high risk of pre-eclampsia
Previous pregnancy affected by pre-eclampsiaMedical conditions including diabetes, hypertension, renal disease
Is it possible to get eclampsia without having had any signs or symptoms of pre-eclampsia?When does eclampsia occur?
Yes, it is possibleBefore, during or up to 24 hours after labour
What is the earliest gestational age that a foetal heartbeat can be detected? By what means?
6 weeks by transvaginal ultrasound
What percentage of women will have bleeding in early pregnancy
Around 20% (1 in 5)
When a woman presents with bleeding in early pregnancy, what are you thinking in terms of the probability of each of the possible outcomes?EG: How likely is ectopic, how likely is miscarriage etc?
60% will have an ongoing pregnancy30% will have pregnancy loss9.5% will have an ectopic pregnancy0.5% will have another diagnosis.
Other than ectopic pregnancy and miscarriage, what are the other causes of bleeding in early pregnancy?
Pregnancy related
- Septic miscarriage
- Throphoblastic disease
- Subchorionic haemorrhage
- Heterotropic pregnancy Non pregnancy related
- UTI
- Cervical cancer
- Vaginal trauma
What is the management/prognosis of subchrorionic haemorrhage?
Fetal outcome is dependent on size of the haematoma, maternal age, and gestational age.In most cases thehaematoma gradually decreases in size on follow-up.However, a large hematoma that has caused 30 to 40 percent of the sac surrounding the embryo to separate from the wall of the uterus may continue to get larger, causing the gestational sac to become compressed and membranes to burst, which will ultimately abort the pregnancy.
A woman presents to you with bleeding in early pregnancy, what is your history and examination?
History HOPC
* LNMP? Duration of amenorrhea? Onset of bleeding?
* Did it occur post coitus? – suggests cervical source
* Associated pain? Aggravating/alleviating?
* Products of conception passed?
* Clots? Flooding? # of pads?
* Blood loss – faint? Dizzy? Shoulder tip pain? O&G history
* Previous pregnancies and miscarriages
* How and when the pregnancy was diagnosed
* IVF or spontaneous conception
* Risk factors – PID, previous ectopic, pelvic surgery, IUD, endometriosis
* Rh status
Exam
* General inspection and vital signs to check for haemodynamic instability Abdominal exam
* Peritonitic
* Symphiofundal height Speculum PV exam Is the cervix open? Suggests miscarriage is occuring Can products of conception be visualised? Is there any obvious source of bleeding in the canal? Is there mucopurulent discharge?
Investigations to order for bleeding in early pregnancy?
Bedside
- Pregnancy test, urine dipstick Bloods
- FBE
- HCG
- Blood group and hold Imaging
- Transvaginal ultrasound Special
- none
What discrepancy is considered significant in symphysis fundal height?What are the possible causes of a discrepancy?
+/- 2 cmHowever this is really only valid between 20-34 weeksPossible causes:fetus is small/large for gestational agemultiple pregnancyinaccurate estimated due datemolar pregnanciespolyhydramnios/oligohydramniosoblique or transverse lie
What are the causes of shock in bleeding in early pregnancy?
Hypovolaemic shock – due to a ruptured ectopicNeurogenic (cervical) shock – products of conception in cervix (causes an increase parasympathetic drive and bradycardia)Septic shock – miscarriage with infection
What is a heterotopic pregnancy?
When two eggs are fertilized; one implants at an intra-uterine site, another at an extra-uterine site.Often associated with induced ovulation (IVF) (1:11,000). Otherwise rare (1:40,000)
What % of ectopic pregnancies have an identifiable risk factor?What are the risk factors?
50%Risk factors all relate to factors which would make the uterus less hospitable for implanation
- Previous ectopic
- Previous PID
- Smoking (impairs ciliary activity)
- Previous tubal surgery
- History of infertility (esp if IVF)
- Advanced maternal age
- IUDs, progesterone-only pills, tubal ligation
A pregnancy woman has a BHCG of 1200, what are the possible causes?
- a normal intrauterine pregnancy that is too early to be detected by ultrasound
- a failing intrauterine pregnancy
- an ectopic pregnancy that is resolving spontaneously
At what BHCG should a yolk sak be visible on transvaginal USS?
A B-HCG >1,500 IU/L indicates that a normal intra-uterine pregnancy should be visible on vaginal ultrasound.If uterus is empty at this reading, then the pregnancy is either ectopic or miscarried.
How common are miscarriages?
Up to 50% of biochemically diagnosed pregnanciesUp to 20% of pregnancies where the mother knows about the pregnancyBefore 5 weeks, elevated B-HCG is termed a chemical pregnancy, because it cannot yet be confirmed on U/SChemical pregnancies are often not included in studies, but have a high rate of early loss
At what gestational age to ectopic pregnancies tend to rupture?
10 weeksThe average gestational age of maternal symptoms of ectopic pregnancyis 7 weeks
How do you calculate gestational age/estimated due date?
The estimated due date (EDD)is the date that spontaneous onset of labor is expected to occur.The due date may be estimated by adding 280 days (9 months and 7 days) to the first day of the last menstrual period (LMP). This is the method used by “pregnancy wheels”.The accuracy of the EDD derived by this method depends on accurate recall by the mother, assumes regular 28 day cycles, and that conception occurs on day 14 of the cycle. This method may overestimate the duration of the pregnancy, and can be subject to an error of more than 2 weeks.In cases where the date of conception is known precisely, such as with IVF, the EDD is calculated by adding 266 days to the date of conception.Ultrasound uses the size of the fetus to determine the gestational age (the time elapsed since the the first day of the last menstrual period). The accuracy of the ultrasound estimate of the gestational age varies and is highest in the first trimester.
What is the most common cause of miscarriage ina) first trimesterb) second trimester
first trimester = foetal chromosomal abnormalitysecond trimester = ascending infection from the lower urinary tract
How would you advise an anxious expectant mother to avoid miscarriage?
In the healthy, first-time pregnant woman there is no known strategy to prevent a miscarriage.Even in women who have a significant medical or surgical disorder the concept of prevention of miscarriage is difficult to define. There is insufficient evidence on the intake of vitamins or bed rest in early pregnancy to help prevent miscarriage, stillbirth, or other maternal and infant outcomes.
Where does catamenial bleeding typically occur?
Pleura –> monthly haemoptysis +/- atelectasisBrain –> very dangerousCan be treated with OCP
How would you interpret a low beta-HCG?How would you interpret a high beta-HCG?(Remember that the normal range is enormous)
Low beta-HCG either means ectopic pregnancy or miscarriage.The level will continuously drop in miscarriage but plateu in ectopicHigh b-HCG could be trophoblastic disease
What is the treatment for trophoblastic disease?
Methotrexate
What is a blighted ovum?
Also known as an ‘anembryonic pregnancy’When a gestational sac forms but no embryo develops.The woman may experience the normal symptoms of pregnancy or some PV bleeding.Diagnosed on ultrasound.Treatment options are the same for other miscarriages.
What symptoms/features of clinical picture can miscarriage present with?
PV bleeding, clots and crampy pain in early pregnancyDisappearance of normal symptoms of pregnancy (loss of urinary frequency, nauseaHypotension, bradycardia – cervical shock due to products of conception in cervix
What are the risk factors for miscarriage?
- advanced maternal age
- Asymptomatic bacterial vaginosis
- IVF
- Alcohol intake during pregnancy
- Smoking during pregnancy
- Overweight/obese mother
Once you detect a foetal heartbeat (either because you’ve done an USS because something has caused you to worry, orjust because it’s time for the routine 12 week USS), what is the risk of miscarriage after that point?
2%That is, you start out with a risk of 50%, but once the baby has a detectable heartbeat your chance of miscarriage drops to 2%
What should you see on serial measurements of bHCG in a normal pregnancy
Doubling every 48 hoursConsidered slow if it doesnt rise by at least 50% in 48 hours
A woman has just had her third miscarriage, what are your differentials?
What conditions are associated with Group A strep infection?
URTI/strep throatImpetigo (school sorts, also caused by Staph Aureus)Scarlett feverRheumatic feverPost-strep GN
What tests can you do to screen for Group A Strep?
Anti-streptolysin O titresAnti-DNase Bis a blood test to look for antibodies to a substance produced by Group A StreptococcusASOT / Anti DNAase B
What are thediagnostic criteria for Kawasaki disease?
What are the investigations for Kawasaki disease?
Bedside testsECG – look for ischaemia / infarctionUrine dipstick – to exclude UTIBloods and urineASOT / Anti DNAase B (to exclude strep throat)FBE (often a neutrophilia, thrombocytosis, normochromic / normocytic anaemia)ESR, CRP (markedly elevated)LFT (raised ALT, hypoalbuminaemia)ImagingEchocardiographyat least twice: at initial presentation and, if negative, again at 6 - 8 weeksrecord a baseline of coronary artery dimensions at initial presentationYou’re looking for aneurysms, valvular regurgitation or hypomotilitySpecial testsNone
What is the management of Kawasaki disease?
BasicsAnalgaesia if sore hands and feetEncourage fluids if clinically dehydratedNGT if not feedingPlace and personLow threshold referral to paediatricsInvestigate and confirm diagnosisAs aboveNon-invasive managementNoneDefinitive managementIntravenous immunoglobulin (2 g/kg over 10 hours; preferably within the first 10 days of the illness.)Aspirin 3 - 5 mg/kg once a day for at least 6 to 8 weeksLong termAt least one further echocardiogram should be performed at 6-8 weeks. If this is normal, no further examinations are needed.
Old man presents with first onset stable angina, are your first thoughts in terms of management?
Stepwise management of angina?
Talk through what you would include in a peripheral vascular exam?
What medication can be used for the non-surgical management of PVD?
Pentoxifylline
Which patients should be started on CVS risk reducing pharmacotherapy?
Patients with established CVD
- Ie: Symptomatic CVA, IHD, PVD, DM with microalbuminaemia, DM if ATSI, DM if >60 years
- Patients at high absolute CVD risk
- Patients at moderate absolute CVD risk (10% to 15%) if there is a FHx of premature CVD (ie first-degree relative who developed CVD before age 60 years).
What is the eTGtarget lipid levels for patients on lipid lowering pharmacotherapy?
LDL-C and TGs should both be non-HDL-C should be Total cholesterol should be
What is the stepwise management of hyperlipidaemia?
What are the cardiovascular disease risk equivalents?
CHD “risk equivalents” - risk factors conferring an estimated 10-year risk for a cardiovascular event of more than 20%. DM
- Regardless of other Hx, confers risk equivalent to having already had an AMI Non coronary atherosclerotic disease
- PVD, CVD, AAA
- Chronic kidney disease
At what degree of occlusion of a coronary vessel does angina become symptomatic?(Roughly, obviously)
75%
Other than myocardial ischaemia, what else can cause a rise in troponin?What is the value of a CK-MB over troponin?
Surgery, sepsis, PE, pericarditis, aortic dissection or rhabdomyolysisCK-MB – the advantage of this biomarker is that it comes down after 48 hours whereas troponin stays elevated for weeks (therefore if you are worried about re-infarct CKMB might be more useful)
Name the drugs used (and when you start them)in the management of an acute coronary syndrome.
What are the different classifications of aortic dissection?
What is the aetiology/pathophys of Rheumatic Fever
Acute rheumatic fever occurs 10 days – 6 weeks after an episode of streptococcal infectionIt is caused by ‘molecular mimicary’ orantigen cross-reactionThe immune response fails to differentiate epitopes from the streptococcal pathogen from host cells, this results in a nonsuppurative inflammatory process
What are the two main strains of Group A beta haemolytic strep and who do they mainly affect?
Strep pyogenes - most commonStrep pyoderma - impoverished, high density living, associated with Rheumatic Fever
If you saw a patient with milkmaids grip, what would that look like and what condition is it associated with?
Acute Rheumatic FeverRhythmic squeezing when the patient grasps the examiner’s hands
What organisms most often cause infective endocarditis?
Streptococcus faecalis / EnterococcusStreptococcus viridansStaphylococcus aureusCandidaHACEK organisms
What are the SIGNS of infective endocarditis?
FeverClubbingSplinter haemorrhagesOsler’s NodesJaneway LesionsPetichiaeRoths spotsSigns of poor dentitionHeart murmur
What is the management of acute rheumatic fever?
Basics:Aspirin or naproxen for arthralgiaCarbemazapine or sodium valproate for choreaPlace and Person:Refer to paeds ID / cardiologyIx and Confirm Diagnosis:Definitive Management (to eradicate any existing organisms):IM benzathine penicillin G (single dose) ORPhenoxymethylpenicillin (bd for 10 days)Follow Up & Prevention:IM benzathine penicillin G (q. 3-4/52) ORPhenoxymethylpenicillin (bd)For 10 years after the most recent episode of ARF, or until 21 years of age
What are the normal ranges for the ankle-brachialpressure index?
Ratio of the (highest recorded) blood pressure in the lower legs to the blood pressure in the arms (LL BP: UL BP)Normal = 0.9 to 1.1Intermittent Claudication = 0.5 to 0.9Critical Limb Ischaemia Be careful – when using this in diabetic patients it may give a false reading as the artery cannot be compressed due to medial calcification. Or even in non-diabetic patients. A stiff/calcified/long blood vessel may have a greater than normal systolic blood pressure.https://youtu.be/KnJDrmfIXGw
What is the difference between systolic and diastolic heart failure?
Systolic =ejection fraction (Diastolic = normal ejection fraction but inadequate ventricular filling during diastole.
Describe the NYHA classification of heart failure severity
What are the top four causes of heart failure?What causes high output heart failure?
Top four causes of heart failureHypertension, ischaemic heart disease, valvular disease, cardiomyopathiesCauses of high output heart failureAnaemia, thyrotoxicosis, arteriovenous shunts
What are the top causes of acute exacerbation of heart failure?
InfectionArrythmiaAcute ischaemiaNon-compliance with fluid restriction or medication
You have a patient with heart failure and AF, what is the first line drug?
Digoxin
What is the stepwise management of heart failure?
Non-pharmacological managementFluid restriction (Salt restriction (60-100mmol/day)Weight lossReduce EtOHSmoking cessationExercise (consider cardiac rehab)VaccinationsThen:
- Biventricular pacemaker Implantable cardiac defibrillators
- Reduce risk of sudden death in chronic HF
- More effective for those with history of ventricular arrhythmia Revascularisation
- CABG or PCI Transplant
- For those with intractable HF
- Complications: rejection, infection, accelerated atherosclerosis
What is the best practice management of a patient who has ROSC after CPR but remains in a coma?
Therapeutic cooling for minimum 12-24 hours
What drugs are used in a cardiac arrest, when do you use them and at what doses?
Amiodarone - 300mg after 3rd shock, then consider another 150mg or infusion(VT or VF only)Adrenaline 1mg in 10ml after second shock then every 2 minutes in VF/VT or immediately and then every 2 mins in asystole or PEA
What is Beck’s triad and what condition does it signal?
Cardiac tamponadeIncreased JVPHypotensionDiminished heart sounds found in patients with acute onset
What are the most common causes of pericarditis?
Viruses which are most often not isolated so referred to as idiopathicNext most common is post-AMI (either 2-3 days later, or if weeks later = Dressler’s syndrome)Uraemic pericarditis is a life threatening complicant of end-stage renal failure and an urgent indication for dialysisOther rarer causes include bacterial/fungal infection, trauma and connective tissue diseases
What are the features of pain caused by pericarditis?
- Location of the pain:Central but radiating to shoulders via phrenic nerve Nature of the pain:
- Constant but pleuritic
- Sharp, Stabbing, Burning Aggravating factors:
- Side lie or supine lie
- Moving
- Breathing Swallowing
- As the oesophagus distends this may irritate the pericardium Alleviating factors:
- Sitting up or forward
What would you see on an ECG in pericarditis?
ECG changes occur in 90% of patients Widespread concave ST elevation and PR depression
- PR interval depression is a very specific indicator of acute pericarditis
- Reciprocal ST depression and PR elevation in aVR
- Sinus tachycardia
- Later there may be T-wave inversion particularly if there is a degree of myocarditis
What is the management of pericarditis?
Bacterial/purulent causeUrgent percutaneous pericardiocentesis with rinsing of the pericardial cavity and IV antibioticsNon-bacterial/non-purulent causeTreat underlying cause if possibleNSAIDs, if no response after a few weeks switch to prednisolone and cochicineNote: pericarditis is a relative contraindication to the use of anticoagulants because haemorrhagic effusion can cause cardiac tamponade. However, pericarditis tends to complicate large infarcts,in which case there is a strong indication for anticoagulation. In these cases, anticoagulation may continue with caution, with close observation and cessation if clinical signs suggest cardiac compression.
When do you hear an S3 and what does it indicate?
You heart it just have S2S3 may be normal in pregnant women, people under 40 years of age and some trained athletes but should disappear before middle age.Outside of these parameters can indicates an overly compliant/dilated left ventricle
What four aetiologies can lead to a heart murmour?
List the causes of a systolic murmur
Flow murmur (anaemia, thyrotoxicosis)Aortic or pulmonicstenosisMitral or tricuspidregurgVSDAortic outflow obstruction
List the causes of a diastolic murmur
Aortic or pulmonicregurgMitral or tricuspid stenosis
What causes a continuous murmur?
Patent ductus arteriosusOr could be a combo of both a systolic and diastolic murmur –> most commonly AS and AR
What sounds would you use the bell of the steth to hear properly?
Low pitched soundsS3 and S4Mitral stenosis (high volume, low pressure murmours are low pitched)
What are the SIGNS of severe aortic stenosis?
Narrow Pulse PressurePulsus parvus et tardus / Slow rising carotid pulseL ventricular heaveThrillEjection click no longer presentS4
What are the components of the CHADSVASC score and how do you interpret the score?
If ≥2% (≈>2 points) chance of stroke per year Rx warfarinWarfarin confers 1-2% risk of major bleed per yearReduces stroke risk by 60% per yearIf very low risk (1 point) stroke Rx aspirinReduces stroke risk by 10% per year
What is target INR for a patient on Warfarin and what do you need to tell them when they start taking it?
Target INR = 2–3 for all indications except valvular disease where the target is 2.5-3.5
- Stable dose of green leafy vegetables
- Regular blood tests, record in book, get instructions on variable dose
- Stick with the same brand (like Coumadin)
- Tell doctor/pharmacist because interacts with some antibiotics
- Tell dentist so you don’t bleed during any procedures
- Come in to ED immediately if you have any unexplained bruising, bleeding, pink, red or dark brown urine, or red or black faeces.
What are the features of LVH on ECG?
Voltage criteria =Add S segment V1 or V2 and R segment of V5 or V6. Volatage criteria if >7 large boxesInverted T waves in lateral leads (1, VL, V5 and V6)Left axis deviation
What 3 drugs can you use to revert AF?
AmiodaroneSotalolFleicanide (pro-arrythmic if there is structural heart disease like LVH)
