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)
What are the side effects of amiodarone?
Amiodarone has serious adverse effects including potential to worsen arrhythmia; these are slow to resolve after it is stopped (half-life = 1-2 months).Nausea and vomitingBlue skin discolourationPeripheral neuropathysleep disturbances (vivid dreams or nightmares)Thyroid dysfunctionhepatotoxicity (may be fatal)optic neuropathybronchospasmalveolar haemorrhage, acute respiratory distress syndromeheart failure, torsades de pointes, severe bradycardia, thrombocytopenia
What do you interpret from the “transition point” in the chest leads of an ECG?What are the possible causes of this?
The QRS complex in the chest leads shows a progession from lead V1 where it is predominantly downward, to lead V6 where it is predominantly upward. The tranisition point where the R and S waves are equal indicates the position of the interventricular septum.Chronic lung diseaseleft bundle branch blockleft anterior fascicular blockWolff-Parkinson-White syndromeright ventricular hypertrophyPneumothorax
If you saw a q wave in V1 and an R wave in V6 what would you suspect?
Left bundle branch block
What effect does LBBB have on T waves?
T wave inversion in lateral leads
What lead do you analyse to pickup a RBBB?What lead do you analyse to pickup a LBBB?
Right - V1Left - V6
Can you visualise the anatomy of the bundle of His?What do you see on ECG if you have a fasicular block?
Left anterior fasicular block = Left axis deviationRight bundle branch block = no change on cardiac axisLeft posterior fasicular block (rare) = Right axis deviationRight bundle branch block AND left anterior hemiblock = Left axis deviation
What is an accelerated idioventricular rhythm, when does it occur and what should you do about it?
Ventricular pacemaker, often associated with AMI, it is a benign rhythm and should not be treated
What would you see in an atrial escape rhythm?What would you see in a nodal/junctional escape rhythm?
Atrial - Abnormal p waveJunctional/nodal - No p wave (retrograde p wave buried in QRS)
What is the significance of ventricular extrasystoles?
They are common and usually of no clinical importance.However, when they occur early in the T wave of a preceding beat they can induce VF. This is called R on T phenomenon.
What happens to the T wave of ventricular extrasystoles?
They are inverted
What do you see on ECG in RVH?
Dominant R wave in V1Dominant S wave in V6Right axis deviationInverted T wave in V1,2,3
What sized Q wave indicate an MI?
> 1 small square wide>2mm deep
IMPORTANTWhat are the signs of a posterior MI?
In V1,2,3Horizontal ST depressionTall, broad R waves (>30ms)Upright T waves (normalyinverted in V1)
What do you know about right ventricular infarction?
- Right ventricular infarction complicates up to 40% of inferior STEMIs. Isolated RV infarction is extremely uncommon.
- Patients with RV infarction are verypreload sensitive(due to poor RV contractility) and can developsevere hypotension in response to nitratesor other preload-reducing agents. Hypotension in right ventricular infarction is treated withfluid loading, and nitrates are contraindicated.
The ECG changes of RV infarction are subtle and easily missed!The first step to spotting RV infarction is to suspect it… in all patients with inferior STEMI!ST elevation in V1– the only standard ECG lead that looks directly at the right ventricle.ST elevation in lead III > lead II– because lead III is more “rightward facing” than lead II and hence more sensitive to the injury current produced by the right ventricle.
What do you always think about in inferior STEMI?
Up to 40% of patients with an inferior STEMI will have a concomitantright ventricular infarction. These patients may develop severe hypotension in response to nitrates and generally have a worse prognosis.Up to 20% of patients with inferior STEMI will develop significant bradycardia due tosecond-orthird-degreeAV block. These patients have an increased in-hospital mortality (>20%).Inferior STEMI may also be associated withposterior infarction, which confers a worse prognosis due to increased area of myocardium at risk.
What 6 things cause T wave inversion?
- Normality
- Ischaemia
- Ventricular extrasystoles
- Bundle branch blocks
- Digoxin
What does digoxin cause on ECG?
Inverted T waveDownward sloping ST segment
What effect do calcium levels have on the ECG?
Low Ca = prolonged QTHigh Ca = short QT
What effect does high/low K/Mg have on the ECG?
Mg is same as K
What is bronchitis?
Acute bronchitis is effectively a diagnosis of exclusion, defined as a lower respiratory tract infection to distinguish this condition from common colds and other upper respiratory ailments.Bronchitis refers specifically to infections causing inflammation in the bronchial airways, whereas pneumonia denotes infection in the lung parenchyma resulting in consolidation of the affected segment or lobe.
Whilst there are no universally agreed upon diagnostic criteria, what generally are the features of bronchitis?
Acute illness Cough as predominant symptom+ at least 1 other lower respiratory tract symptomsputum productionwheezingchest painno alternative explanation for the symptoms.
What will you see on CXR of a patient with bronchitis?
Nothing
What is the management of bronchitis?
Improves spontaneously in 4-8 daysMonitor for bacterial superinfection (H. influenzae or strep pneumonia)and treat as appropriateSmoking cessationSymptom reliefParacetemol for fever/chest discomfortSABA if significant wheezingNB: Many people prescribe amoxicillin but this is not evidence based.
What is bronchiectasis?
Irreversible dilatation of the bronchi caused by destruction of the muscular and elastic tissue of the bronchial walls resulting from persistently infected mucus.Bronchiectasis usually effects medium sized airways.It is classified as an obstructive lung disease, along with emphysema, bronchitis, asthma, and cystic fibrosis.
What are the causes of bronchiectasis?
Pathophys
- A section(s) of lung supplied by a bronchus/bronchi is obstructed
- Infection occurs – stasis is the basis!
- Impaired defense mechanisms fail to clear the infection/mucus
- Prolonged and repeated bouts of inflammation –>weakening of the bronchial walls, due to proteolytic enzymes and reactive oxygen species (ROS) released from neutrophils, leading to dilatation.
What are the signs and symptoms of bronchiectasis?
Symptoms * Long term productive cough with massive sputum production * Can be haemoptysis * Dyspneoa * Fatigue * Loss of weight * Fever * Wheezing * Pleuritic chest pain Signs * Clubbing * Tachypneoa * Productive cough/massive haemoptysis * Cachexia * Febrile * Creps over the affected lobe * If severe - signs of cor pulmonale
What investigations would you order for suspected bronchiectasis?
Bedside * Peak flow, ECG to look for cor pulmonale if really sick Bloods and urine * FBE - WCC * Rh factor * Alpha 1 anti-trypsin * ELISA and Western Blot for HIV screening Imaging * CXR High rest CT chest --> diagnostic
Special
* Sweat chloride for cystic fibrosis
What is alpha-1-anti-trypsin deficiency?
Alpha 1-antitrypsin deficiency is a genetic disorder that causes defective production of alpha 1-antitrypsin (A1AT), leading to decreased A1AT activity in the blood and lungs, and deposition of excessive abnormal A1AT protein in liver cells.There are several forms and degrees of deficiency; the form and degree depend on whether the sufferer has one or two copies of the defective allele because it is a co-dominant trait.Severe A1AT deficiency causes panacinar emphysema or COPD in adult life in many people with the condition (especially if they are exposed to cigarette smoke). The disorder can lead to various liver diseases in a minority of children and adults, and occasionally more unusual problems. It is treated through avoidance of damaging inhalants and, in severe cases, by intravenous infusions of the A1AT protein or by transplantation of the liver or lungs. It usually produces some degree of disability and reduces life expectancy.
What is the management of bronchiectasis?
Basics
* O2 if required in acute exacerbation
Place and person
* Admit if acute exacerbation requiring respiratory support or IV ABx
* Respiratory physician
Definitive
* Regular vaccinations Chest physio/rehab 8-week training programme at 80% of peak heart rate
* ABx as required for infections
* SABA PRN for wheeze and dyspneoa
* Normal saline via nebuliser PRN to assist with clearing mucus
* Pulmonary resection if focal disease
Long term MDT
* Psych, GP, specialist nursing, resp physician
What rule of thumb can you use to work out what a patients PaO2 should be on an ABG?
PaO2 = 104.2–(0.27xPatient’sage)PaO2 = Roughly 100 - 1/3Ageeg: for Scott –> PaO2 = 100- 8.25PaO2 should be roughly 92
What is the diagnostic criteria on PFT for COPD
A post-bronchodilator FEV1/FVC ratio of
What 2 treatment options have a mortality benefit in COPD?
smoking cessation and oxygen supplementation
What is the management of COPD?
Basics
* O2 if acute exacerbation, be wary of suppressing respiratory drive
Place and person
* Admit if severe
* Genmed ward
Management Lifestyle
* Vaccinations to prevent infective exacerbations
* Smoking cessation
* SNAP Meds
* SABA SABA + LAMA (ipratropium bromide,Atrovent)
- SABA + LAMA + LABA SABA + LAMA + LABA/Steroid fluticasone propionate/salmeterol (Seretide) Budesonide/formoterol (Symbicort) Add theophylline (smooth muscle relaxant) Supplemental oxygen Surg Lung transplant/lung volume reduction surgery
Management of acute exacerbations O2 therapy - This improves V:Q mismatch, reducingpulmonary HT and alleviating cor pulmonale Add systemic corticosteroids
- prednisolone: 5-60 mg orally once daily
- IV hydrocortisone if oral cannot be tolerated
- Add salbutamol nebs for symptom control
- NIV when required to prevent desaturation If exacerbation is due to infection add ABx
- doxycycline or amoxicillin in community
- Ceftriaxone + azithromycin in inpatient therapy
- Pulmonary rehabilitation (chest physio)
What are the non-respiratory manifestations of cystic fibrosis?
- Sinus Disease
- Chronic rhinosinusitis due to thick secretions
GIT obstruction - Meconium ileus (pathognomonic of CF, when the meconium becomes thickened and congested in the ileum)
- In adults adultsbulky stools lead to DIOS (distal intestinal obstruction syndrome, meconium ileus equivalent) Pancreas
- loss of exocrine function leads to innsufficient secretion of digestive enzymes causingmalabsorption of fat
- steatorrhea
- Vitamin A,D,E,K (fat soluble) deficiency
- Because of potential vitamin D deficiency, BMD can be reduced.
- Can also cause protein malabsorbtion and diabetes from damage to endocrine function Liver
- Congealed bile can causefocal biliary cirrhosis (hepatomegaly,elevated ALP/GGT)
- cholelithiasis Infertility
- > 95% of males with CF are infertile due to absent vas deferens (no effect on spermatogenesis)
- 20% of females are infertile due to amenorrhea (induced primarily by malnutrition)
What tests are performed to diagnose CF?
- Newborn screening [heel prick] forImmunoreactive trypsinogen (IRT)
- The sweat chloride test = primary test for the Dx of CF
- DNA testing is used for confirmation of patients with intermediate sweat chloride results and for prognostic purposes in individuals with positive results of sweat chloride test
What are the classic symptoms of idiopathic pulmonary fibrosis?
Cough: dry and persistentBreathlessness: slowly progressive, insidious onsetDecreased exercise tolerance
What are the signs of interstitial lung disease?
Peripheries:
- Clubbing – most common in IPF but also seen in other times eg. Asbestosis Face
- Signs of central cyanosis Resp
- Fine crackles (cf coarse crackles in pneumonia, APO etc), typically bilateral and only heard at the very base of the lower lobes –>make sure to listen very low on the back or you may miss them! Cardio
- Signs of cor pulmonale in advanced disease
What investigations would you order for a patient with suspected interstitial lung disease?
Bedside
- ECG for cor pulmonale Blood and urine FBE
- Polycythemia from chronic hypoxia?
- WCC indicate infection if high or sarcoid if low
- Eosinophilia in drug reaction
- Rh factor and antibodies for connective tissue diseases Imaging CXR
- reticulonodular shadowing at peripheries HRCT Ground glass appearance + honeycombing Special
- Pulmonary function tests show a restrictive pattern
- Exercise tolerance test shows drop in sats
What is the management of interstitial pulmonary fibrosis?
To date no therapies for idiopathic pulmonary fibrosis are proven to improve survival or to modify the clinical course.Early referral to a respiratory specialist is strongly recommended.As well as instituting best supportive care, management may include drug treatment, with inclusion in a clinical trial if possible, and/or early referral for lung transplantation.Supportive CareEducationSmoking CessationOxygen TherapyPulmonary RehabilitationAcute exacerbationHigh dose corticosteroids? cytotoxic therapyConsider lung transplantation
How do you classify asthma, particular in kids?
What four main things do you assess to determine the severity of an asthma attack?
How do you assess work of breathing in kids?
What are the different types of lung cancers?
What is the staging of small cell lung cancer?
Limited stage the cancer is only in one side of the chest
* This can include one lung as well as the lymph nodes on the same side of the chest
* Can therefore be treated with a single radiation field.
* Only about 1 out of 3 people have limited stage SCC when it is first found
* These patients may benefit from combined chemotherapy and radiation therapy
Extensive stage
* cancer that is spread widely throughout the lung, to the other lung, to lymph nodes on the other side of the chest, or to distant organs (including the bone marrow)
* About 2 out of 3 people with SCC have extensive disease when their cancer is first found.
* These patients will only benefit from palliative chemotherapy, not radiation therapy. Treatment is purely palliative.
What staging system is used for non-small cell lung cancer?What are the criteria for each category of this staging system?
What paraneoplastic syndromes are associated with the different forms of lung cancer?
Small Cell Lung CancerSIADHEctopic Cushing’s SyndromeSquamous Cell CarcinomaElectrolyte imbalancesAdenocarcinomaHypertrophic osteoarthopathy
What is the definitive management of non-small cell lung cancer
Stage I & II Surgery as first line treatment for early-stage NSCLCStage IIIa Pre-operative chemotherapy or chemoradiation as first line followed by surgeryStage IIIb: Pre-operative chemotherapy + preoperative radiotherapy as first line followed by surgeryChemotherapy regime:Cisplatin + etoposideWeekly carboplatin paclitaxelTargeted drugs:Epidermal Growth Factor (EGFR) has become an important target in the management of NSCC given that 60% of NSCC are EGFR+.
Discuss the pathophysiology ofsmall and non-small cell lung cancer…
What pathogens generally cause hospital acquired pneumonia?
Most commonly aerobic gram negative-bacilli such asPseudomonas aeruginosaEscherichia coliAcinetobacterKlebsiella pneumonia
What are the most common pathogens causing atypical pneumonia?
Chlamydophila pneumoniaeMycoplasma pneumoniae - more commonLegionella pneumophiliaThese organisms are difficult to identify, they don’t grow well.
What specific/buzz word pathogens that cause pneumonia do you know?
Animal contact –>Coxiella Burnetti (Q fever)Birds –>Chlamydia PsittacosisHIV/Immunocompromise –> Pneumocystis jiroveciCystic Fibrosis –> Pseudomonas aeurginosaAlcoholism/AspirationOral flora – S. pneumoniae, S. pyogenes, mycoplasma, H. influenzaeGut flora – anaerobes
What type of pneumonia is more likely to cause pleurisy?
viralpneumonia(think: viral are smaller, get right to the edges?)
What is notable about the presentation of hospital acquired pneumonia?
The presentation of hospital-acquired pneumonia (HAP) is often unusual because it is frequently affected by advanced age, multiple chronic comorbidities and neurological disorders. Classic respiratory symptoms are often mild whereas extra-pulmonary manifestations, including mental confusion and gastrointestinal disorders, are frequent.Note that atypical pneumonias often don’t present with respiratory symptoms at all.
What tests would you order if you suspected atypical pneumonia?
- FBE: anaemia may accompany mycoplasma pneumonia
- Mycoplasma serology
- LFTs: elevated enzyme levels in mycoplasmapneumonia or Legionella pneumophila
- Urinary Legionella antigen
How do you score and interpret the CORB65?
What is the pathophysiology of acute and subacute endocarditis?
Subacute IE
* Endocardium of the valves sustain endothelial damage secondary to turbulent flow (often because they have been repaired)
* Platelets and fibrin adhere to the underlying collagen surface and create a prothrombotic milieu
* Bacteraemia –>colonisation of the thrombus –>further fibrin deposition and platelet aggregation
* This develops into a mature infected vegetation
Acute IE
* Classically caused by S. aureus
* The microorganism invades the endothelial cells, increases the expression of adhesion molecules and prothrombotic factors –>thrombus
What is the clinical picture (hx and exam) of infective endocarditis?
HistoryFevers, night sweats, rigorsMalaise/fatigue/anorexia/LOWSOB/back pain/headache/back pain/chest painIntracardiac device/prosthetic valve/IVDUExamFever (can be intermittent)ClubbingJaneway lesions/Oslo nodes/Splinter haemorrhagesRoth spotsPetechiaeMurmur
What investigations would you order for suspected infective endocarditis?
BedsideECG (1st degree heart block)Urine dipstick (blood, UTI source?)Bloods/urineFBE/UEC/LFTsCultures (x3)ESR/CRPUrinalysis (WBC/RBC casts, protein etc indicating septic emboli in kidney)ImagingCXREcho
What are the bugs and drugs for infective endocarditis?
What is the pathophysiology of HIV transmission?
After initial exposure HIV is transported by dendritic cells from mucosal surfaces to regional lymph nodes –>PERMANENT INFECTION. HIV can only infect cells bearing the CD4 receptor; these are T helper lymphocytes, monocyte-macrophages, dendritic cells and microglial cells in the central nervous system.
- HIV surface protein (gp120) recognizes the CD4+ (Th) molecule –>gp120 + CCR5 co receptors facilitate entry of the virus into the Th cell
- Viral RNA –>DNA (via host reverse transcriptase)
- Viral integrase incorporates viral DNA into host DNA
- Viral DNA transcribed to RNA via host mechanisms
- New viral RNA is used to produce viral proteins
- Assembly of the HIV virus
- Viral protease allows for the mature virus to bud off
What are the special tests on clinical exam for meningitis?
What are you looking for in the results of an LP? How would you interpret one?
What blood test can differentiate viral from bacterial meningitis?
Serum Procalcitonin –> if not raised it is NOT bacterial meningitis
What are the two types of necrotising fasciitis and who do they affect?
Type I (polymicrobial)mixture of aerobic/facultative anaerobe + anaerobic bacteriausually seen following abdominal surgery/diabeticsType 2 (monomicrobial)caused by group A streptococcusarises spontaneously in previously healthy people.
What are the criteria for Pyrexia of Unknown Origin?
- Fever of >38.3°C
- Lasting for at least three weeks.
- For which no cause can be identified after three days of investigation in hospital or after three or more outpatient visits.
What are your differentials for PUO?
What are the main forms of pneumoconiosis and what causes them?
There are fiveCoal Worker’s Pneumoconiosis – coal dust particlesSilicosis – silica particlesBerylliosis – dusts and fumes containing berylliumByssinosis - cotton or endotoxins from bacteria in raw cottonAsbestosis – asbestos dust
What is the management of pneumoconioses?
What are the different types of pneumothorax?How do the symptoms vary between types?Which groups of patients generally get each type?
You think you see a pleural effusion on CXR, what are your differentials?
What are the two types of pleural effusion?What is the pathophysiology of each?What criteria can you use to differentiate one from the other?
TransudativeEither due to pulmonary hypertension or low osmotic pressure from hypoalbuminaemiaExudativeDue to inflammed/leaky capillaries caused by infection, infarction or tumour
How big does a pleural effusion have to be to be visible on CXR?
Frontal (AP/PA) - at least 250 mlsSupine or semi-recubant - could be huge and not see it as the fluid will diffusely cover the lung fieldLateral decubitus - small effusions visible if the patient lies on their side with the affected side down
What is the management of the different types of pleural effusions?
What are the different types/categories/causes of pulmonary hypertension and their respective treatments?
Group 1: PrimaryTx - CCB, sildenafil and lung transplantGroup 2: Due to left heart failureTx of heart diseaseGroup 3: Due to lung diseasePrimary therapy consists of treatment of the underlying cause of hypoxemia and correction of the hypoxaemia with supplemental oxygen.Group 4: Due to chronic thromboembolic pulmonary hypertensionAnticoagulationGroup 5: Pulmonary hypertension with unclear multifactorial mechanismsSpecialist careGeneral treatment options for all * Diuretics * Oxygen therapy * Anticoagulation * Digoxin
What are the causes of upper and lower lobe fibrosis?
RATS SAC (upper lobe)RadiationAspergilliosisTBSarcoidosisSillicosisAnkSpondCoal miners pneumoconiosesRASCO (lower lobes)RA / radiation (depends on where you’ve radiated)AsbestosSclerodermaCryptogenic Fibrosing AlveolitisOther: drugs
Acute interstitial nephritisWhat is it?What are the most common causes?What are the features of clinical presentation?
Acute interstitial nephritis is a pattern of acute renal inflammation, usually triggered by medications, which is localised to the renal interstitium (the area between the tubules, glomeruli, and blood vessels).Caused most often by medications- B-lactam antibiotics- PPIs- NSAIDs- AntihistaminesClinical presentation:Elevated urea and creatinine but normal urine outputFever, rash, oedemaIn a patient on a medication known to cause acute interstitial nephritis
What investigations would you order for Acute Interstitial Nephritis
BedsideNABloods/urineUEC –> elevated urea and creatinineFBE –> eosinophiliaUrinalysis –> microhaematuriaImagingRenal ultrasound –> enlarged kidneysSpecialRenal biopsy
What is the management of acute interstitial nephritis?
BasicNAPlace and personProbably admit, refer to nephrologistIxFBE/UEC/Renal USS/Renal biopsyMx1) Cease causative medication2) Diuretics + Na and fluid restriction3) Oral corticosteroids4) Monitor closely, daily UECs5) Dialysis is last line therapy
What are the different stages of acute kidney injury?
At what BP does autoregulation of renal perfusion start to fail?
systolic BP
What effect does renal injury/failure have on electrolyte levels?
HyperkalaemiaHyperphosphatemiaHypocalcemiaUnable to secrete H+ –> metabolic acidosisNa is retained but because water is also retained [Na] may be normal or hyponatraemic
What symptoms are often present in acute kidney injury?
Nausea, malaise and confusionIf fluid retention –> orthopneoa
How would you differentiate pre-renal from renal acute kidney injury on urinalysis?
What can a renal USS tell you about the cause of an acute kidney injury?
What are the complications of acute kidney injury and what is the broad management of each of them?
Where does urea come from?What are the causes of a high/low urea?
NH3 (ammonia) converted to urea (blood urea nitrogen – BUN) in liverCauses of high NH3 (leading to high BUN) Increased protein load
* IV amino acids (body builder)
* Burns (catabolic state → protein breakdown)
* Corticosteroids (catabolic state → protein breakdown)
* Tetracycline Oesophageal varices
* Bleeding into GIT → digest globin in RBC → high NH3
Causes of low BUNLiver failure (can’t convert NH3 to BUN)
What are the treatment options for BPH?
Oral α-adrenoceptor blockers (tamulosin) produce rapid improvement in urinary flow in 60-70% of patients. The 5α-reductase inhibitor (finasteride) (which decreases testosterone) causes slow shrinkage of large prostate glands with improvement in symptoms. Treatment is usually required for 6-12months for symptom improvement.
What are the two different definitions of chronic kidney disease?
GFR of 3 months with or without evidence of kidney damage.ORPathological kidney damage, causing proteinuria or haematuria for >3 months
What are the most common causes of chronic kidney disease?
- DM (35%)
- GN (25%)
- Renovascular disease including HTN
- Polycystic kidney disease(10% - congenital)
- Reflux nephropathy (10% - congenital, most common cause in kids)
What is the pathophysiology of chronic kidney disease?
The pathophysiology of CKD is complex. Regardless of the method of renal injury (DM, HT, GN), once renal damage has occurred the following ensues:
* Glomerular hypertrophy
* Increase in glomerular permeability –>filtration of larger substances such as fatty acids, inflammatory markers –>mesangial matrix damage –>fibrosis and scarring
* Tubulo-interstitial damage
* Increase in angiotensin production
In summary, there is progressive renal scarring and increased angiotensin production.
What are the normal functions of the kidney and how are these effected in CKD?
Excretion of wastes and foreign substancesuraemia, reduction in clearance of drugsRegulation of fluid and electrolyte balancehypertension, oedemaMetabolic acidosisHyperphosphataemia –> hypocalcaemiaHyperkalaemiaProduction of the active form of Vitamin DRenal bone disease (NB: this is a complex disease with lots of factors)Long term regulation of BPHypertensionRegulation of production of red blood cells.Anaemia results largely from inadequate renal production of erythropoietin
Explain the pathways of PTH/Ca/Phosphate regulation
Explain the pathogenesis of renal bone disease
What is Pott’s disease?
Pott’s disease is a presentation of extrapulmonary tuberculosis whereby disease is seen in the spinal vertebrae - a kind of tuberculous arthritis of the intervertebral joints.
What is the difference between active and latent TB?What is the natural history of TB?
Latent TB has no signs or symptoms. The bacteria are not multiplying. It is diagnosed on CXR or immune tests (quantiferon or mantoux). It is not contagious. There is a 10% chance of it converting to active infection. Treat with a single drug to prevent reactivation.Active TB causes signs and symptoms from active replication of the bacteria. It is diagnosed by AFB stain and mycobacterial culture.
What are the symptoms of TB?
Prolonged cough >3/52LOW (Can be massive! Huge metabolic upregulation)Night sweatsFeversLoss of appetiteHaemoptysis
What are the top 5 causes of fever in a returned traveller
MALARIA MALARIA MALARIATyphoid feverDengue feverHepatitis AInfluenza
What is the incubation period of malaria?
10 days to 4 months
What are the history/exam findings in malaria?
HistoryFever (cyclical possibly if repeat infection)Headache/backacheNausea/vomitingDiarrheoa/Abdo painCoughExamMostly normalSplenomegaly possible if multiple exposures to malariaCheck for complications of malaria (jaundice, confusion, seizures, hypotension, respiratory distress, anuria/oliguria)
What are the four concerning complications of malaria?Which patient groups are we particularly concerned about?
Cerebal malariaDecreased consciousness is hallmark signHeadache and seizures are common features of severe malaria and do not necessarily indicate cerebral malariaARF+/- haemaglobinuria due to massive intravascular haemolysisparasite breaking out of RBC releasing hemoglobin directly into the blood vessels and into the urine, frequently leading to kidney failure= “blackwater fever”Non-cardiogenic APOHypoglycaemiaBe worried about asplenic patients, kids and pregnant women
What are the Ix for malaria?
Rapid finger prick detection testThick and thin filmAlso look for complicationsFBEUEC/LFTCoagsBGLUrinalysis – haemaglobinuria
What is the treatment for malaria?
Artemisinin derivatives: (arterunate and artemether)
- Active ingredient in absinthe!
- Rapid onset therapeutic effect
- Can use in combination with other antimalarials – chloroquine/mefloquine/doxycycline IV use for more severe infections
What are the chemoprophylactic options for travellers going to malaria endemic regions?
Wear long sleeves/pants (light colours!)Avoid outdoors at duskMosquito nets over bedNo perfume/aftershave
What is the incubation time of Dengue fever?What is the classical presentation?
Unrelenting feverRetroorbital painAbdo/Back painNausea and vomitingRarely: rash
A patient presents saying that they think they have Dengue fever after travelling to SE Asia. They had it once 10 years ago, it wasn’t as bad this time and they’re starting to feel better anyway. What do you do?
PANIC! Worry about Dengue Haemorrhagic Fever(Dengue Shock)(happens in 2nd and subsequent Dengue infections and occurs when the patient looks as thought they’re recovering)Look for:internal haemorrhage/hypotension/anaemiaFluid shifts: ascites, effusions
How do you diagnose Dengue Fever?
Dengue serology (looks for IgM)
What do you know about Typhoid?
Typhoid infection is a faecal-oral transmissible disease caused by the bacterium Salmonella entericaSx = fever, headache, abdo pain + diarrhoea or constipation, relative bradycardiaIx = Culture blood, stool, urineTx = Ceftriaxone or azithromycin + supportive care
What tests would you order in a febrile returned traveller?
BedsideBGL (malaria can cause hypoglycaemia)Bloods and urineFBEUECLFTsBlood culturesHep A and B serologyDengue serologyThick and thin filmsFaecal MCSCXRInfluenza
What are the most common pathogens of food poisoning and what are their associated features?
Preformed toxin –>Staphylococcus aureus or Bacillus cereusStaph is usually from sliced meat, pastries and sandwichesB cereus is almost always from poorly reheated rice8 to 16 hoursClostridium perfringensFrom beef and poultry> 16 hoursViral or bacterial infection (enterotoxigenic or enterohemorrhagic E. coli)Salmonella/Shigella/Campylobacter (all can be bloody)
What are the Ix for suspected C. difficile infection?
Review previous medications (causative ABx could have been taken months ago!)FBEFOBT (+ve)Stool immunoassay for toxins A and B (specificity 95-100%)Stool PCRAbdo xray or CT (if severe)
What is the Mx of c. diff infection?
Stop causative ABxMild-moderateMetronidazole 400mg orally or via NGT, 8-hourly for 10 daysCan be given IVSevereVancomycin 125mg orally or via NGT, 6-hourly for 10 daysCannot be given IVIf complicated by shock, ileus or toxic megacolon à ADD metronidazole 500mg IV, 8-hourly for 10 days
What is the defining feature of cholera diarrheoa and what is the treatment?
‘rice water’ diarrhea with mucusRehydration and Doxycycline
How does bladder cancer normally present?
Bladder cancer most commonly presents with GROSS or MICROSCOPIC haematuria.Gross haematuria is characteristically intermittent, which may lead to the incorrect conclusion that an intervention such as antibiotic administration has been effective.Signs and symptoms apart from haematuria:
* urinary urgency
* dysuria
* back or abdominal pain
* loss of appetite and weight
KEY – Any haematuria – INVESTIGATE BLADDER CANCER
What are the main treatment options for bladder cancer?
instillation of BCG vaccine
- mechanism is unclear but can induce a local immune reaction against bladder tumour cells.
- Radical cystectomy
- Treated with chemotherapy and radiation
What type of cancers are bladder cancers normally?
UROTHELIAL CARCINOMA (a.k.a transitional cell carcinoma).
What is the most common form of kidney cancer?How is it normally diagnosed?
Clear cell carcinomas (80%)50% of renal cell carcinomasare diagnosed incidentally, and renal masses are usually only symptomatic late in the disease.Often no symptoms until metastatic spread or paraneoplastic symptoms prompt investigation
What is the management of chronic kidney disease (according to stage)?
Stage 1-2:Manage CVS risk factorsACEi/ARBStatins – regardless of lipid levels, statins show cardioprotective effects e.g. simvastatin, 5-40mg/day orallyIf target BP is not achieved with ACEi addb-blockers/centrally acting CCB (e.g. diltiazem, verapamil)Stage 3-4:Same as above, however there may be additional complications:Anaemia – EPOMetabolic acidosis – oral bicarbonate to correct acidosisSecondary hyperparathyroidism – hypocalcaemia results in secondary hyperparathyroidism; treat with phosphate-binding drugs, ergocalciferol, calcitriolStage 5, or if patient is uraemic/symptoamticDialysisKidney transplant
What is the most common cause of nephrotic syndrome in adults?
DM
Does DM cause typically cause a nephritic or nephrotic picture?
nephrotic
What one main test would you order to monitor the kidneys of an otherwise healthy person with T1DM?
Early morning urinary albumin to creatine ratio (ACR)
What are the core features of nephrotic syndrome?
Proteinuria (>3.5 g/day)Hypoalbuminaemia (Generalised oedemaHyperlipidaemia/Lipiduria (caused by increased hepatic production)
What complications of nephrotic syndrome do you worry about?
Intravascular volume collapse / shockMonitor BP/HRImmunocompromise/sepsisLosing proteinous IgG in urineThromboembolism (especially cerebral vein thrombosis)you also loose intrinsic anticoagulants such as protein C, protein S AND the liver is upregulating synthetic functions so increased production of clotting factors
What are the core features of nephritic syndrome?
Acute renal failureHypertensionHaematuriaSub-nephrotic proteinuria(These patients can also get odematous)There is active sediment with casts
What is active sediment?
What degree of proteinuria is diagnostic of a nephrotic syndrome?
> 3.5 g/24 hours (24 hour urine collection)orProtein:Creatinine ration (PCR) >300 mg/micromol
What are the causes of nephrotic syndrome?
Minimal change nephropathyFocal segmental glomerulosclerosisMembranous nephropathyDiabetic nephropathyAmyloidosisCould cause nephrotic or nephritic:Mesangiocapillary GN, SLE
What is the management of minimal change disease?
BasicsNonePlace and personAdmit, contact paeds nephrologyIxUrinalysisFBE/UEC/LFTs/AlbuminANA if considering SLEMxSteroids, 6 month course tapering downAspirin for thrombotic riskBenPen for sepsis riskIV albumin if hypotensiveSteroids - tapered o
What are the diagnostic criteria of SLE?
A RASH POINts anMDHaving 4 out of the 11 features has an 85% sensitivity and 95% specificity for the diagnosis
What are the small vessel vasculitides?What is the triad associated with each of them?
What are all of the causes of renal failure? (think of the tree diagram)
https://drive.google.com/file/d/0B1rcMgBpTQG7bkJoM3ZvQ1d3S0E/view?usp=sharing
What are the causes of nephritic syndrome?
Primary GNIgA NephropathyMesangiocapillary GNSecondary GNPost-streptococcal GNVasculitisLupus nephritisGoodpasture’s
What are the key components of management of diabetic nephropathy?
Glycaemic control to maintain HbA1c ACE inhibitors or ARBsNutritionDietary protein restriction of 0.8g/kg of ideal body weight per day is suggestedSmoking cessationStatins
What are the key management points in nephrotic syndrome?
Low salt and low protein dietACEi or ARBFrusemide +/- hydrocholorothiazideStatinCorticosteroid + cytotoxic or immunosuppressive therapyAspirinAntibiotics
What zones of the prostate does BPH occur in?What zones of the prostate does prostate Ca occur in?
Benign prostatic hypertrophy: occurs within the transitional zoneProstate cancer: occurs in the peripheral zone – this makes it less symptomatic but easier to feel on DRE
Where does prostate cancer metastasise to?
Metastases of prostate cancer tend to be in:bone (90%)lung (46%)liver (25%)pleura (21%)adrenals (13%)
Who shouldbe offered PSA testing?
there is a reduced risk of prostate cancer death with PSA testing and treatment in those patients in the 55-69 year age group, who also have a greater than 7 year life expectancy
What causes membranous GN?
85% idiopathicCan be infection, autoimmune or drug related
What is the prognosis of membranous GN?
20 years after diagnosis, 1/3 of patients will be in complete remission, and 1/3 will have progressed to end-stage renal disease and need dialysis. Another 1/3 will be somewhere in the middle.
DoesMembranoproliferative glomerulonephritis cause nephrotic or nephritic syndrome?
Nephritic
What are the buzz words for membranoproliferative GN?
“tram tracking”Hep C
What are the small vessel vasculidites?
Wegener’s granulomatosis (granulomatosis with polyangiitis)Microscopic polyangiitisChurg-Strauss Syndrome/ Allergic GranulomatosisHenoch-Scholein Purpura
What is the clinical picture of granulomatosis with polyarngiitis? (Wegners)
Rhinitis/epistaxis/saddle nose deformityTracheal collapse/stenosisPulmonary haemorrhage/haemoptysisRapidly progressive GN
What is the clinical picture of microscopicpolyangiitis?
No nasopharyngeal involvement / no granulomas (distinct from granulomatosis with polyangiitis)TheFIVEmost common clinical manifestations of MPA are:Rapidly progessive GN (~ 80% of patients).Weight lossSkin lesionsNerve damageFevers
What antibody is positive in granulomatosis with polyangiitis?What antibody is positive in microscopic polyangiitis?
Granulomatosis w polyangiitis –> c-ANCAMicroscopic polyangiitis –> p-ANCA
What is Goodpasture syndrome?
arareautoimmune diseasein which antibodies attack thebasement membranein lungs and kidneys, leading to rapidly progressive GN and haemoptysis
What is achalasia?Who does it normally affect?
Achalasia is an oesophageal motor disorder which is characterized by:
* oesophageal aperistalsis (absence of peristalsis)
* insufficient lower oesophageal sphincter (LOS) relaxation in response to swallowing
This is the result of the loss of inhibitory nitrinergic neurons in the oesophageal myenteric plexus (Auerbach’s plexus) –>loss of oesophageal relaxation.Normally affects people > 60-70 years of age
What is angiodysplasia? Where in the gut does it normally occur?What causes it?
Angiodysplasia is a degenerative vascular malformation of the GIT characterized by fragile and leaky blood vessels –>GI bleeding /anaemia. Can be anywhere from small occult bleed to acute haemorrhage.Lesions are located most commonly in the Caecum and Ascending colon.Cause is unknown, but happens to older people –> ?part of aging?
What are the classic signs of appendicitis?
Central abdominal pain migrating to RLQNauseaAnorexiaConstipationLow grade feverUrinary symptoms
What signs would you look for if you suspected appendicitis?
- Localised tendernesss to one finger palpation +/- slight guarding
- Rebound tenderness @ McBurney’s point
- Percussion tenderness (= peritonism)
Obturator sign - Pain in the RLQ by internal rotation of the flexed right thigh Rosvings sign / cross tenderness
- LLQ pressure elicits RLQ pain from gas backflow irritating the appendix Psoas sign
- Extending the right thigh in left lateral position elicits pain in the RL
- Absent bowel sounds due to the bowel becoming shocked
What is Barret’s oesophagus?Why do we care about it?
Barrett’s Oesophagus is a change (metaplasia) in the epithelium of the oesophagus to a cell type that is usually found in the lower GIT.Stratified squamous epithelium –>Simple columnar epithelium with goblet cellsBarretts oesophagus has a strong association with oesophageal adenocarcinoma. The five year survival rate of oesophageal adenocarcinoma is 8%, this is largely due to commonly late diagnosis.
What two segments of gut are most susceptible to ischaemia?
Splenic flexure and rectosigmoid junction
What are the progressive phases (in terms of clinical picture) of transmural ischaemic colitis?
- A hyper active stage occurs first, in which the primary symptoms are severe abdominal pain and the passage of bloody stools.
- A paralytic phase can follow if ischemia continues; in this phase, the abdominal pain becomes more widespread, the belly becomes more tender to the touch, and bowel motility decreases, resulting in abdominal bloating, no further bloody stools, and absent bowel sounds on exam.
- Finally, a shock phase can develop as fluids start to leak through the damaged colon lining. This can result in shock and metabolic acidosis with dehydration, low blood pressure, rapid heart rate, and confusion. Patients who progress to this phase are often critically ill and require intensive care.
What are the most common causes of large and small bowel obstructions in adults and paeds?
What is the clinical picture of:- high small bowel obstruction- low small bowel obstruction- colonic bowel obstruction?
AllEither failure to pass faeces/flatus (complete obstruction: obstipation) or successful passing of some flatus or faeces (partial obstruction) +High small bowel
* Acute onset
* frequent, profuse vomiting
* central crampy abdo pain
* minimal distension
* High pitched tinkling bowel sounds (early)
* Absent bowel sounds (late)
* Diarrhoea (early due to hyperperistalsis) or constipation (late)
* Rebound, guarding, localized tenderness -> peritonitis -> surgical emergency
Lower small bowel
* Acute onset
* colic pain
* moderate vomiting (may be faeculent)
* Faeculent breath odor
* moderate distension
* High pitched tinkling bowel sounds (early)
* Absent bowel sounds (late)
* Diarrhoea (early due to hyperperistalsis) or constipation (late)
* Rebound, guarding, localized tenderness -> peritonitis -> surgical emergency
Large bowel
* Gradual onset
* Less common than SBO
* abdominal distension
* lower abdo pain (may be minimal)
* minimal vomiting
* Normal or absent bowel sounds
* Empty rectum on PR exam Screen for malignancy Sx
* Recent LOW
* Change bowel habit
* PR bleeding
* FHX colon Ca
What are the investigations for bowel obstruction?
BedsideUrine MCSBloodsFBE, UEC, LFTLactateGroup and hold if severeImagingSupine and erect AXR/CXR (screen for pneumoperitoneum)Consider CT/MRI/endoscopy/barium swallow
How could you tell from an AXR if the bowel is dilated?
3:6:9 ruleIf small bowel is greater then 3cm, large bowel is greater then 6cm and caecum is greater then 9cm it is dilated and there is likely to be some obstruction
How do you assess air fluid levels on AXR?
More than 5 fluid levels, greater than 2.5 cm in length is abnormal and associated with obstruction, ileus, ischaemia and gastroenteritis.
The radiologist phones and says the AXR has a coffee bean sign, what is the likely diagnosis?
Sigmoid volvulus - ‘coffee bean’ signThe sigmoid colon is very dilated because it is twisted at the root of its mesentery in the left iliac fossa (LIF). The proximal large bowel is also dilated (asterisks).The twisted loop of sigmoid colon is said to resemble a coffee bean. As in this case the loop of dilated sigmoid colon - or ‘coffee bean’ - usually points upwards towards the diaphragm.This patient is at high risk of perforation and/or bowel ischaemia.
What pathogens are typically responsible for cholecystitis?
Asually aerobic gram negative bowel flora (e.g. E. coli, Klebsiella species)Less commonly, Enterococcus faecalis.Anaerobes are found infrequently, unless biliary obstruction is present.
What is the clinical picture of biliary colic/acute cholecystitis?
Biliary colic
* Term used for pain associated with the temporary obstruction of the cystic or common bile duct by a stone, usually migrating from the gall bladder
* Severe and constant (NOT COLICKY)
* Worse post prandially, especially with high fat content food
* Usually occurs at night
* Initially epigastric, may have right upper quadrant component, may be poorly localized
* Radiation may occur over the right shoulder and subscapular region
* +/- Nausea and vomiting
* Cessation spontaneous or after opiate analgesia administration
If associated with obstruction, may also have:
* Jaundice
* Pruritis
* Nausea
* Pale stools
* Dark urine
Acute cholecystitis
* More protracted pain +/- fevers and rigors –>cholecystitis
* Parietal peritoneal involvement in inflammatory process/ empyema/ gangrenous cholecystitis
* Progression with localized right upper quadrant pain.
What are the investigations for suspected cholecystitis?
Bedside * Preg test * Urine dipstick Bloods * FBE (leukocytosis) * UEC * LFTs (obstructive pattern) * ESR/CRP * Amylase/lipase (check for pancreatitis) * Lipids (risk factor) Imaging Abdominal USS * Must be after fasting, as otherwise the gallbladder will be contracted and you won’t see much * Sonographic Murphy’s sign is a very reliable finding of acute cholecystitis, with a specificity >90%. Look for pericholecystic fluid, distended gallbladder, thickened gallbladder wall, dilated bile ducts HIDA scan * CT cholangiogram * uses contrast called Biliscopinwhichis removed by the liver into the bile. Allows visualisation of the gall bladder. * MRCP
What is the mx of cholecystitis?
BasicsDiclofenac or opiodsAntiemesisNBMIV rehydrationPlace and personAdmit, refer to gastroIx and confirm DxBloods, abdo USS, CT cholangiogram or MRCPDefinitiveLaporascopic cholecystectomyThe pathophysiology of acute cholecystitis is cystic duct obstruction, which causes an acute sterile inflammation. Antibiotics are required if infection is suspected on the basis of laboratory and clinical findings.
How can you differentiate cholecystitis from choledocolithiasis clinically?
If choledocolithiasis will have:Scleral icterusJaundicePruritisClay coloured stoolDark urine
What is the management of choledocolithiasis?
Basics * Diclofenac or opiods * Antiemesis * NBM * IV rehydration Place and personAdmit, refer to gastroIx and confirm DxFBEUECLFTsLipase/AmylaseDefinitiveERCP + sphincterotomy
What complication do you worry about in choledocolithiasis?How does it present and what would you do about it?
PancreatitisAscending cholangitisFever, jaundice, and RUQ pain (Charcot’s triad)Cholangitis can quickly become an acute, septic, life-threatening infection that requires rapid evaluation and treatment.Antibiotics alone do not provide sufficient treatment in the majority of patients. Drainage of the biliary tree is the most critical step in management.If untreated, sepsis with shock, vascular collapse, multi-organ failure, and potentially death can occur.
What are the complications of cirrhosis? What frequency do they occur at?
What foodstuffs contain gluten?
Gluten is found in wheat, rye, barley, oats and related grains (Mnemonic = BROW).
What are the risk factors for coeliac dz?
FemaleInfancy or 40s/50sFHx of coeliac diseaseIgA deficiencyType 1 diabetesAutoimmune thyroid diseaseInflammatory bowel diseaseSjogrens syndromeDowns syndrome
What do you know about the aetiology of coeliac dz?
Almost all people with coeliac disease have ONE of TWO MHC-II molecules (HLA-[DQ2 or DQ8]).These MHC-II molecules are required to present gluten peptides to activate an antigen-specific T cell response.Other factors thought to play a role include: the timing of initial gluten exposure, GI infection leading to gluten antigen mimicry, or direct damage to the intestinal epithelial barrier à abnormal exposure of the mucosa to gluten peptides.
What part of the bowel does coeliac usually affect?
Coeliac disease generally affects the proximal small bowel.
What is the pathology of coeliac dz?
Immune activation in the small intestine –>villous atrophy, hypertrophy of intestinal crypts, numbers of lymphocytes in the epithelium + lamina propria.
What is the clinical presentation of coeliac dz?What conditions are associated with coeliac?
gastrointestinal symptoms e.g. diarrhoea, constipation, nausea, vomiting, flatulence, cramping, bloating, abdominal pain, steatorrhea fatigue, weakness and lethargy iron deficiency anaemia and/or other vitamin and mineral deficiencies failure to thrive or delayed puberty in children weight loss (although some people may gain weight) bone and joint pains recurrent mouth ulcers and/or swelling of mouth or tongue altered mental alertness and irritability skin rashes such as dermatitis herpetiformis easy bruising of the skin
The long term consequences of untreated coeliac disease are related to chronic systemic inflammation, poor nutrition and malabsorption of nutrients.Fortunately, timely diagnosis of coeliac disease and treatment with a gluten free diet can prevent or reverse many of the associated health conditions.
What are the tests for coeliac dz?
Before testing – ensure the patient is ingesting gluten!all tests will normalize on a gluten-free dietSerology Immunoglobulin A - tissue transglutaminase (IgA-tTG) titre should be evaluated
* Very sensitive (85-95%) –>a normal IgA-TTG is adequate to exclude a diagnosis in patients with a low clinical index of suspicion
* Must measure IgA levels concurrently as IgA deficient patients will have false negative
* Cannot be used in kids under 2, use anti-gliaden instead
Duodenal biopsyPatients with IgA-tTG should be advised to remain on a gluten-containing diet and referred for duodenal biopsy. Duodenal biopsy is the gold standard for diagnosis. The presence of typical coeliac changes in duodenal histology + clinical improvement on a gluten free diet = COELIAC DISEASEOther tests HLA testing
* may be used to rule out coeliac disease in patients already on a gluten free diet – not helpful for diagnosis FBE
* May show microcytic or macrocytic anaemia from iron or folate deficiency U&E
* mayreveal reduced concentrations of calcium, magnesium, total protein, albumin or vitamin D
How do you stage colorectal cancer?
T = TumourTX = primary tumour can’t be assessedTis = tumour is in situ, only involves the mucosaT1 = tumour extends into the submucosaT2 = tumour extends into the muscularisT3 = tumour extends into the serosa, but not through itT4a = tumour has extended through the serosaT4b = tumour has extended through the serosa and is attached to or has invaded nearby tissuesN = NodesNX score = lymph nodes can’t be assessedN0 = no cancer in the lymph nodesN1 = Cancer cells found in 1-3 nearby lymph nodesN2 = Cancer cells found in 4 or more nearby lymph nodesM = metastasesM0 = no metastasisM1 = is metastasis
What are the risk factors for colorectal ca?
Increasing age
- is the greatest risk factor for sporadic colorectal adenocarcinoma with 99% of cancers occurring in people aged 40 years or over. FHx of colorectal Ca
- The majority of colorectal cancers are sporadic rather than familial, but next to age, FHx is the most common risk factor. Obesity
- confers a 1.5-fold increased risk
- Inflammatory Bowel Disease (sp. UC) Diet
- High in red meats (like beef, pork or lamb) and processed meats (like hot dogs, bacon or cold cuts)
- High in fruit and vegetables lowers risk
What are the investigations for suspected colorectal cancer?
What are the causes/differentials for constipation?
Primary constipation
* disordered regulation of colonic and anorectal neuromuscular functions as well as brain –GIT neuroenteric function dyssynergistic defacation
Secondary constipation Metabolic disturbances (hypercalcaemia, hypothyroidism) Medicines
* opiates/Ca channel blockers/ anti-psychotics Neurological disorders
* Diabetes, spinal cord lesions, parkinsonism Primary disease of the colon
* Stricture, cancer, anal fissure Infectious
* Typhoid and others GIT
* Irritable bowel syndrome
What history questions would you ask for a patient with constipation?
description of the patients bowel habits
- frequency
- consistency (Bristol stool chart)
- stool size
- urge to defecate
- degree of straining
- sensation of incomplete evacuation
- duration
- severity of symptoms
- any history of precipitating events, including medication history
Describe the treatment algorithm (etG flowchart) for constipation?
If alarm features –> investigateIf no alarm features consider and investigate for dysynergistic defacation syndrome or IBSPossible testsFBE/UEC/LFTs/CMPTFTsBGL (DM?)ConoloscopyBarium enema
What general advice/management strategies could you offer to a pt with constipation?
- Patient education
- Advice to eat a high fibre diet
- Advice to drink lots of fluids
- Advice to regularly exercise
- Bulk laxatives
If unresponsive to dietary and lifestyle modificationsLAXATIVESBulk Laxatives/ stool softeners (1st line)Prunes are a natural alternative to laxativesIf >6 weeks of therapy:osmotic laxatives such as lactulose, polyethylene glycol (macrogol) or magnesium containing laxatives can be used.
What are the different types of laxatives and when would you use them?
1st line - bulk laxatives2nd line - stool softeners3rd line - osmotic laxative4th line - prokineticBulk laxatives = insoluble fibre and equivalent = metamucilStool softener = like detergent = docusate sodium (Coloxyl)Osmotic laxative= draw water into the gut =magnesium or lactuloseProkinetic = increase enteric secretion and peristalsis = not often used?
What are the different causes of chronic diarrheoa?
DOMESDeranged motilityHyperthyroidDiabetesIBSOsmoticFructose/Lactose intoleranceLaxative abuseMalabsorbtionPancreatisis/pancreatic insufficiencyCoeliacExudative/InflammatoryIBD (UC/Crohns)DiverticulitisCancerSecretoryInfectiousZollinger-Ellison syndrome
What is the management of coeliac disease?
Exclusion of gluten (Barley, rye, wheat, and oats)Dietary fortification – iron, folate, calcium and vitamin D
