Year 3 revision - chapter 1 Flashcards

Question

Explain the Child Pugh Score

Answer 1

High protein, low salt diet * Cirrhosis is an enormously 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

Answer 2

* 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

Answer 3

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

Answer 4

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 or Injection 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

Answer 5

a-foetoproteinAlpha-Foetoprotein (AFP)200-500 ng/ml diagnostic

Answer 6

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

Answer 7

``` 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 ```

Answer 8

“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 2 relate to bleeding risk.3 relates to the triple whammy.4 relates to NSAIDs causing salt retention5 relates to leukotriene synthesis.Side effects/ADRsRenal impairmentPeripheral oedema Gastrointestinal bleeding/PUDHypertensionN&V

Answer 9

Aripiprazole or quetiapine

Answer 10

"DASHINS" (like dashing but dashins)DiarrhoeaAnxietySuicideHeadacheInsomniaNauseaSexual dysfunctionPlus don't forget the serious ones ofHyponatraemiaSerotonin syndrome!Plus SNRIs can cause tachycardia, HTN

Answer 11

Mirtazipine

Answer 12

* Migraine * TIA * Giant cell arteritis * Retinal detachment * Central (or branch) retinal artery occlusion * Central (or branch) retinal vein occlusion * Vitreous hameorrhage

Answer 13

Buzz word is CHERRY RED SPOTSThis is basically a TIA/stroke, just in the eye!

Answer 14

–Ophthalmoplegia–Pain with eye movements–Proptosis Treatment for preseptal is fluclox (just like normal cellulitis)But with orbital cellulitis you need to REFER AND ADMITThey may need surgical intervention to save their sight

Answer 15

Diagnosis: Optic neuritisManagement: Pulsed methylprednisolonePrognosis: 30% 5 year risk of developing MS

Answer 16

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

Answer 17

low dose aspirin 75‐150mg/dayCalcium 1g/day.

Answer 18

Previous pregnancy affected by pre-eclampsiaMedical conditions including diabetes, hypertension, renal disease

Answer 19

Yes, it is possible Before, during or up to 24 hours after labour

Answer 20

6 weeks by transvaginal ultrasound

Answer 21

Around 20% (1 in 5)

Answer 22

60% will have an ongoing pregnancy30% will have pregnancy loss9.5% will have an ectopic pregnancy0.5% will have another diagnosis.

Answer 23

Pregnancy related * Septic miscarriage * Throphoblastic disease * Subchorionic haemorrhage * Heterotropic pregnancy Non pregnancy related * UTI * Cervical cancer * Vaginal trauma

Answer 24

Fetal outcome is dependent on size of the haematoma, maternal age, and gestational age. In most cases the haematoma 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.

Answer 25

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?

Answer 26

Bedside * Pregnancy test, urine dipstick Bloods * FBE * HCG * Blood group and hold Imaging * Transvaginal ultrasound Special * none

Answer 27

+/- 2 cm However this is really only valid between 20-34 weeks Possible causes: fetus is small/large for gestational agemultiple pregnancyinaccurate estimated due datemolar pregnanciespolyhydramnios/oligohydramniosoblique or transverse lie

Answer 28

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

Answer 29

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)

Answer 30

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

Answer 31

* a normal intrauterine pregnancy that is too early to be detected by ultrasound * a failing intrauterine pregnancy * an ectopic pregnancy that is resolving spontaneously

Answer 32

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.

Answer 33

Up to 50% of biochemically diagnosed pregnancies Up 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

Answer 34

10 weeks The average gestational age of maternal symptoms of ectopic pregnancy is 7 weeks

Answer 35

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.

Answer 36

first trimester = foetal chromosomal abnormalitysecond trimester = ascending infection from the lower urinary tract

Answer 37

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.

Answer 38

Pleura --> monthly haemoptysis +/- atelectasisBrain --> very dangerous Can be treated with OCP

Answer 39

Low beta-HCG either means ectopic pregnancy or miscarriage.The level will continuously drop in miscarriage but plateu in ectopic High b-HCG could be trophoblastic disease

Answer 40

Methotrexate

Answer 41

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.

Answer 42

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

Answer 43

* advanced maternal age * Asymptomatic bacterial vaginosis * IVF * Alcohol intake during pregnancy * Smoking during pregnancy * Overweight/obese mother

Answer 44

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%

Answer 45

Doubling every 48 hours Considered slow if it doesnt rise by at least 50% in 48 hours

Answer 46

URTI/strep throatImpetigo (school sorts, also caused by Staph Aureus)Scarlett feverRheumatic feverPost-strep GN

Answer 47

Anti-streptolysin O titresAnti-DNase B is a blood test to look for antibodies to a substance produced by Group A Streptococcus ASOT / Anti DNAase B

Answer 48

Bedside testsECG – look for ischaemia / infarctionUrine dipstick – to exclude UTI Bloods 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 hypomotility Special testsNone

Answer 49

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.

Answer 50

Pentoxifylline

Answer 51

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).

Answer 52

LDL-C and TGs should both be non-HDL-C should be Total cholesterol should be

Answer 53

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

Answer 54

Surgery, sepsis, PE, pericarditis, aortic dissection or rhabdomyolysis CK-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)

Answer 55

Acute rheumatic fever occurs 10 days – 6 weeks after an episode of streptococcal infectionIt is caused by ‘molecular mimicary’ or antigen cross-reactionThe immune response fails to differentiate epitopes from the streptococcal pathogen from host cells, this results in a nonsuppurative inflammatory process

Answer 56

Strep pyogenes - most commonStrep pyoderma - impoverished, high density living, associated with Rheumatic Fever

Answer 57

Acute Rheumatic Fever Rhythmic squeezing when the patient grasps the examiner’s hands

Answer 58

Streptococcus faecalis / EnterococcusStreptococcus viridansStaphylococcus aureusCandidaHACEK organisms

Answer 59

FeverClubbingSplinter haemorrhagesOsler’s NodesJaneway LesionsPetichiaeRoths spotsSigns of poor dentitionHeart murmur

Answer 60

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

Answer 61

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

Answer 62

Systolic = ejection fraction (Diastolic = normal ejection fraction but inadequate ventricular filling during diastole.

Answer 63

Top four causes of heart failureHypertension, ischaemic heart disease, valvular disease, cardiomyopathiesCauses of high output heart failureAnaemia, thyrotoxicosis, arteriovenous shunts

Answer 64

InfectionArrythmiaAcute ischaemiaNon-compliance with fluid restriction or medication

Answer 65

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

Answer 66

Therapeutic cooling for minimum 12-24 hours

Answer 67

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

Answer 68

Cardiac tamponadeIncreased JVPHypotension Diminished heart sounds found in patients with acute onset

Answer 69

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

Answer 70

* 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

Answer 71

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

Answer 72

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.

Answer 73

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

Answer 74

Flow murmur (anaemia, thyrotoxicosis)Aortic or pulmonic stenosisMitral or tricuspid regurgVSDAortic outflow obstruction

Answer 75

Aortic or pulmonic regurgMitral or tricuspid stenosis

Answer 76

Patent ductus arteriosus Or could be a combo of both a systolic and diastolic murmur --> most commonly AS and AR

Answer 77

Low pitched soundsS3 and S4Mitral stenosis (high volume, low pressure murmours are low pitched)

Answer 78

Narrow Pulse PressurePulsus parvus et tardus / Slow rising carotid pulseL ventricular heaveThrillEjection click no longer presentS4

Answer 79

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

Answer 80

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.

Answer 81

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

Answer 82

AmiodaroneSotalolFleicanide (pro-arrythmic if there is structural heart disease like LVH)

Answer 83

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

Answer 84

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 disease left bundle branch blockleft anterior fascicular blockWolff-Parkinson-White syndromeright ventricular hypertrophyPneumothorax

Answer 85

Left bundle branch block

Answer 86

T wave inversion in lateral leads

Answer 87

Right - V1Left - V6

Answer 88

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

Answer 89

Ventricular pacemaker, often associated with AMI, it is a benign rhythm and should not be treated

Answer 90

Atrial - Abnormal p waveJunctional/nodal - No p wave (retrograde p wave buried in QRS)

Answer 91

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.

Answer 92

They are inverted

Answer 93

Dominant R wave in V1Dominant S wave in V6Right axis deviationInverted T wave in V1,2,3

Answer 94

>1 small square wide>2mm deep

Answer 95

In V1,2,3Horizontal ST depressionTall, broad R waves (>30ms)Upright T waves (normaly inverted in V1)

Answer 96

* Right ventricular infarction complicates up to 40% of inferior STEMIs. Isolated RV infarction is extremely uncommon. * Patients with RV infarction are very preload sensitive (due to poor RV contractility) and can develop severe hypotension in response to nitrates or other preload-reducing agents. Hypotension in right ventricular infarction is treated with fluid 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.

Answer 97

Up to 40% of patients with an inferior STEMI will have a concomitant right 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 to second- or third-degree AV block. These patients have an increased in-hospital mortality (>20%). Inferior STEMI may also be associated with posterior infarction, which confers a worse prognosis due to increased area of myocardium at risk.

Answer 98

* Normality * Ischaemia * Ventricular extrasystoles * Bundle branch blocks * Digoxin

Answer 99

Inverted T waveDownward sloping ST segment

Answer 100

Low Ca = prolonged QTHigh Ca = short QT

Answer 101

Mg is same as K

Answer 102

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.

Answer 103

Acute illness Cough as predominant symptom+ at least 1 other lower respiratory tract symptomsputum productionwheezingchest painno alternative explanation for the symptoms.

Answer 104

Improves spontaneously in 4-8 days Monitor for bacterial superinfection (H. influenzae or strep pneumonia) and treat as appropriateSmoking cessationSymptom reliefParacetemol for fever/chest discomfortSABA if significant wheezing NB: Many people prescribe amoxicillin but this is not evidence based.

Answer 105

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.

Answer 106

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.

Answer 107

``` 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 ```

Answer 108

``` 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

Answer 109

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.

Answer 110

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

Answer 111

PaO2 = 104.2–(0.27xPatient’sage)PaO2 = Roughly 100 - 1/3Age eg: for Scott --> PaO2 = 100- 8.25PaO2 should be roughly 92

Answer 112

A post-bronchodilator FEV1/FVC ratio of

Answer 113

smoking cessation and oxygen supplementation

Answer 114

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, reducing pulmonary 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)

Answer 115

* 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 adults bulky stools lead to DIOS (distal intestinal obstruction syndrome, meconium ileus equivalent) Pancreas * loss of exocrine function leads to innsufficient secretion of digestive enzymes causing malabsorption 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 cause focal 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)

Answer 116

* Newborn screening [heel prick] for Immunoreactive 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

Answer 117

Cough: dry and persistentBreathlessness: slowly progressive, insidious onsetDecreased exercise tolerance

Answer 118

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

Answer 119

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

Answer 120

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

Answer 121

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.

Answer 122

Small Cell Lung CancerSIADHEctopic Cushing’s SyndromeSquamous Cell CarcinomaElectrolyte imbalancesAdenocarcinomaHypertrophic osteoarthopathy

Answer 123

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 surgery Chemotherapy regime:Cisplatin + etoposideWeekly carboplatin paclitaxel Targeted drugs:Epidermal Growth Factor (EGFR) has become an important target in the management of NSCC given that 60% of NSCC are EGFR+.

Answer 124

Most commonly aerobic gram negative-bacilli such asPseudomonas aeruginosaEscherichia coliAcinetobacterKlebsiella pneumonia

Answer 125

Chlamydophila pneumoniaeMycoplasma pneumoniae - more commonLegionella pneumophiliaThese organisms are difficult to identify, they don’t grow well.

Answer 126

Animal contact --> Coxiella Burnetti (Q fever)Birds --> Chlamydia PsittacosisHIV/Immunocompromise --> Pneumocystis jiroveciCystic Fibrosis --> Pseudomonas aeurginosa Alcoholism/AspirationOral flora – S. pneumoniae, S. pyogenes, mycoplasma, H. influenzaeGut flora – anaerobes

Answer 127

viral pneumonia(think: viral are smaller, get right to the edges?)

Answer 128

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.

Answer 129

* FBE: anaemia may accompany mycoplasma pneumonia * Mycoplasma serology * LFTs: elevated enzyme levels in mycoplasma pneumonia or Legionella pneumophila * Urinary Legionella antigen

Answer 130

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

Answer 131

HistoryFevers, night sweats, rigorsMalaise/fatigue/anorexia/LOWSOB/back pain/headache/back pain/chest painIntracardiac device/prosthetic valve/IVDU ExamFever (can be intermittent)ClubbingJaneway lesions/Oslo nodes/Splinter haemorrhagesRoth spotsPetechiaeMurmur

Answer 132

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

Answer 133

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

Answer 134

Serum Procalcitonin --> if not raised it is NOT bacterial meningitis

Answer 135

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.

Answer 136

* 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.

Answer 137

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

Answer 138

TransudativeEither due to pulmonary hypertension or low osmotic pressure from hypoalbuminaemiaExudativeDue to inflammed/leaky capillaries caused by infection, infarction or tumour

Answer 139

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

Answer 140

``` 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 care General treatment options for all * Diuretics * Oxygen therapy * Anticoagulation * Digoxin ```

Answer 141

RATS SAC (upper lobe)RadiationAspergilliosisTBSarcoidosisSillicosisAnkSpondCoal miners pneumoconioses RASCO (lower lobes)RA / radiation (depends on where you’ve radiated)AsbestosSclerodermaCryptogenic Fibrosing AlveolitisOther: drugs

Answer 142

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

Answer 143

BedsideNABloods/urineUEC --> elevated urea and creatinineFBE --> eosinophiliaUrinalysis --> microhaematuriaImagingRenal ultrasound --> enlarged kidneysSpecialRenal biopsy

Answer 144

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

Answer 145

systolic BP

Answer 146

HyperkalaemiaHyperphosphatemiaHypocalcemiaUnable to secrete H+ --> metabolic acidosisNa is retained but because water is also retained [Na] may be normal or hyponatraemic

Answer 147

Nausea, malaise and confusionIf fluid retention --> orthopneoa

Answer 148

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)

Answer 149

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.

Answer 150

GFR of 3 months with or without evidence of kidney damage.ORPathological kidney damage, causing proteinuria or haematuria for >3 months

Answer 151

* DM (35%) * GN (25%) * Renovascular disease including HTN * Polycystic kidney disease (10% - congenital) * Reflux nephropathy (10% - congenital, most common cause in kids)

Answer 152

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.

Answer 153

Excretion of wastes and foreign substances uraemia, 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

Answer 154

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.

Answer 155

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.

Answer 156

Prolonged cough >3/52LOW (Can be massive! Huge metabolic upregulation)Night sweatsFeversLoss of appetiteHaemoptysis

Answer 157

MALARIA MALARIA MALARIATyphoid feverDengue feverHepatitis AInfluenza

Answer 158

10 days to 4 months

Answer 159

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)

Answer 160

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 APOHypoglycaemia Be worried about asplenic patients, kids and pregnant women

Answer 161

Rapid finger prick detection testThick and thin filmAlso look for complicationsFBEUEC/LFTCoagsBGLUrinalysis -- haemaglobinuria

Answer 162

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

Answer 163

Wear long sleeves/pants (light colours!)Avoid outdoors at duskMosquito nets over bedNo perfume/aftershave

Answer 164

Unrelenting feverRetroorbital painAbdo/Back painNausea and vomitingRarely: rash

Answer 165

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

Answer 166

Dengue serology (looks for IgM)

Answer 167

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

Answer 168

BedsideBGL (malaria can cause hypoglycaemia)Bloods and urineFBEUECLFTsBlood culturesHep A and B serologyDengue serologyThick and thin filmsFaecal MCSCXRInfluenza

Answer 169

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 hours Viral or bacterial infection (enterotoxigenic or enterohemorrhagic E. coli) Salmonella/Shigella/Campylobacter (all can be bloody)

Answer 170

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)

Answer 171

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

Answer 172

‘rice water’ diarrhea with mucus Rehydration and Doxycycline

Answer 173

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

Answer 174

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

Answer 175

UROTHELIAL CARCINOMA (a.k.a transitional cell carcinoma).

Answer 176

Clear cell carcinomas (80%) 50% of renal cell carcinomas are diagnosed incidentally, and renal masses are usually only symptomatic late in the disease. Often no symptoms until metastatic spread or paraneoplastic symptoms prompt investigation

Answer 177

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 add b-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

Answer 178

Early morning urinary albumin to creatine ratio (ACR)

Answer 179

Proteinuria (>3.5 g/day)Hypoalbuminaemia (Generalised oedemaHyperlipidaemia/Lipiduria (caused by increased hepatic production)

Answer 180

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

Answer 181

Acute renal failureHypertensionHaematuriaSub-nephrotic proteinuria (These patients can also get odematous)There is active sediment with casts

Answer 182

>3.5 g/24 hours (24 hour urine collection)orProtein:Creatinine ration (PCR) >300 mg/micromol

Answer 183

Minimal change nephropathyFocal segmental glomerulosclerosisMembranous nephropathyDiabetic nephropathyAmyloidosisCould cause nephrotic or nephritic: Mesangiocapillary GN, SLE

Answer 184

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

Answer 185

A RASH POINts an MDHaving 4 out of the 11 features has an 85% sensitivity and 95% specificity for the diagnosis

Answer 186

https://drive.google.com/file/d/0B1rcMgBpTQG7bkJoM3ZvQ1d3S0E/view?usp=sharing

Answer 187

Primary GNIgA NephropathyMesangiocapillary GNSecondary GNPost-streptococcal GNVasculitisLupus nephritisGoodpasture’s

Answer 188

Glycaemic control to maintain HbA1c ACE inhibitors or ARBsNutritionDietary protein restriction of 0.8g/kg of ideal body weight per day is suggestedSmoking cessationStatins

Answer 189

Low salt and low protein dietACEi or ARBFrusemide +/- hydrocholorothiazideStatinCorticosteroid + cytotoxic or immunosuppressive therapyAspirinAntibiotics

Answer 190

Benign prostatic hypertrophy: occurs within the transitional zone Prostate cancer: occurs in the peripheral zone – this makes it less symptomatic but easier to feel on DRE

Answer 191

Metastases of prostate cancer tend to be in:bone (90%)lung (46%)liver (25%)pleura (21%)adrenals (13%)

Answer 192

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

Answer 193

85% idiopathicCan be infection, autoimmune or drug related

Answer 194

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.

Answer 195

"tram tracking"Hep C

Answer 196

Wegener’s granulomatosis (granulomatosis with polyangiitis)Microscopic polyangiitisChurg-Strauss Syndrome / Allergic GranulomatosisHenoch-Scholein Purpura

Answer 197

Rhinitis/epistaxis/saddle nose deformityTracheal collapse/stenosisPulmonary haemorrhage/haemoptysisRapidly progressive GN

Answer 198

No nasopharyngeal involvement / no granulomas (distinct from granulomatosis with polyangiitis)The FIVE most common clinical manifestations of MPA are:Rapidly progessive GN (~ 80% of patients).Weight lossSkin lesionsNerve damageFevers

Answer 199

Granulomatosis w polyangiitis --> c-ANCAMicroscopic polyangiitis --> p-ANCA

Answer 200

a rare autoimmune disease in which antibodies attack the basement membrane in lungs and kidneys, leading to rapidly progressive GN and haemoptysis

Answer 201

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

Answer 202

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?

Answer 203

Central abdominal pain migrating to RLQNauseaAnorexiaConstipationLow grade feverUrinary symptoms

Answer 204

* 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

Answer 205

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 cells Barretts 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.

Answer 206

Splenic flexure and rectosigmoid junction

Answer 207

* 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.

Answer 208

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

Answer 209

BedsideUrine MCSBloodsFBE, UEC, LFTLactateGroup and hold if severeImagingSupine and erect AXR/CXR (screen for pneumoperitoneum)Consider CT/MRI/endoscopy/barium swallow

Answer 210

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

Answer 211

More than 5 fluid levels, greater than 2.5 cm in length is abnormal and associated with obstruction, ileus, ischaemia and gastroenteritis.

Answer 212

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.

Answer 213

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.

Answer 214

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.

Answer 215

``` 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 Biliscopin which is removed by the liver into the bile. Allows visualisation of the gall bladder. * MRCP ```

Answer 216

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.

Answer 217

If choledocolithiasis will have:Scleral icterusJaundicePruritisClay coloured stoolDark urine

Answer 218

``` Basics * Diclofenac or opiods * Antiemesis * NBM * IV rehydration Place and personAdmit, refer to gastroIx and confirm DxFBEUECLFTsLipase/AmylaseDefinitiveERCP + sphincterotomy ```

Answer 219

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.

Answer 220

Gluten is found in wheat, rye, barley, oats and related grains (Mnemonic = BROW).

Answer 221

FemaleInfancy or 40s/50sFHx of coeliac diseaseIgA deficiencyType 1 diabetesAutoimmune thyroid diseaseInflammatory bowel diseaseSjogrens syndromeDowns syndrome

Answer 222

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.

Answer 223

Coeliac disease generally affects the proximal small bowel.

Answer 224

Immune activation in the small intestine --> villous atrophy, hypertrophy of intestinal crypts, numbers of lymphocytes in the epithelium + lamina propria.

Answer 225

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.

Answer 226

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 * may reveal reduced concentrations of calcium, magnesium, total protein, albumin or vitamin D

Answer 227

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

Answer 228

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

Answer 229

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

Answer 230

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

Answer 231

If alarm features --> investigateIf no alarm features consider and investigate for dysynergistic defacation syndrome or IBS Possible testsFBE/UEC/LFTs/CMPTFTsBGL (DM?)ConoloscopyBarium enema

Answer 232

* 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 laxatives If >6 weeks of therapy:osmotic laxatives such as lactulose, polyethylene glycol (macrogol) or magnesium containing laxatives can be used.

Answer 233

1st line - bulk laxatives2nd line - stool softeners3rd line - osmotic laxative4th line - prokinetic Bulk 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?

Answer 234

DOMESDeranged motilityHyperthyroidDiabetesIBSOsmoticFructose/Lactose intoleranceLaxative abuseMalabsorbtionPancreatisis/pancreatic insufficiencyCoeliacExudative/InflammatoryIBD (UC/Crohns)DiverticulitisCancerSecretoryInfectiousZollinger-Ellison syndrome

Answer 235

Exclusion of gluten (Barley, rye, wheat, and oats)Dietary fortification – iron, folate, calcium and vitamin D