Finals Medicine Surgery Flashcards
Managing hyper kalmia
10ml 10% calcium chloride/gluconate over 5-10 min Insulin/glucose infusion Salbutamol Calcium resinous Identify and manage underlying cause
Hyperkalemia on ECG
4 features
Tall tented T wave
QRS a complex broaden
PR prolonged
P wave flattened
Wolf Parkinson white syndrome
Delta wave (characteristic slurred up slope)
(Pre-excited AF sometimes)
PR short
(Accessory pathway: bundle of Kent)
ECG changes of ACS (chronological)
Normal Peaked T wave ST segment elevation Q wave formation and loss of R wave (anterior chest leads) T wave inversion
4 criteria for STEMI/Emergency re perfusion
2 mm ST elevation in 2 or more contiguous chest leads
1 mm ST elevation in 2 or more limb leads of same territory
New LBBB or LBBB in clinical MI
True posterior MI
RV hypertrophy on ECG
R axis deviation
Dominant R wave in lead V1
Inverted T waves spreading from right side of the heart
Axis deviation
Look at I and avF
If away from each other then L axis deviation
If towards each other then R axis deviation if both positive then normal
IE bacteria
Strep
Staph
HACEK
The HACEK organisms are a group of fastidious Gram-negative bacteria that are an unusual cause infective endocarditis (IE), which is an inflammation of the heart due to bacterial infection.[1] HACEK is an abbreviation of the initials of the genera of this group of bacteria: Haemophilus, Aggregatibacter (previously Actinobacillus), Cardiobacterium, Eikenella corrodens, Kingella.[1] The HACEK organisms are a normal part of the human flora, living in the oral-pharyngeal region.[2]
Causes of dominant R wave in V1/V2
Posterior MI
PE
RBBB
RVH
DUchenne muscular dystrophy
Dectrocardia
WPW
Why is it important to diagnose posterior MI?
Posterior MI can cause back pressure and raise JVP.
Usually when we see JVP elevation, we tend to give diuretics because we think it’s R heart failure. However diuretics can be fatal for posterior MI as we’re decreasing the preload, ie stretching… (Sterling law)
Mesenteric ischemia (classic triad)
GI emptying
Abdo pain
Underlying cardiac disease
JVP waves
http://youtu.be/cLETr8qmXPQ
How to differentiate a jugular venous pulse from the carotid pulse
JVP: Not palpable. Obliterated by pressure. Characterised by a double waveform. Variable with respiration - it decreases with inspiration. Enhanced by the hepatojugular reflux
Waveforms of JVP
Waves[2][3][4]
a - presystolic; produced by right atrial contraction.
c - bulging of the tricuspid valve into the right atrium during ventricular systole (isovolumic phase).
v - occurs in late systole; increased blood in the right atrium from venous return.
Descents
x - a combination of atrial relaxation, downward movement of the tricuspid valve and ventricular systole.
y - the tricuspid valve opens and blood flows into the right ventricle.
The a and v waves can be identified by timing the double waveform with the opposite carotid pulse. The a wave will occur just before the pulse and the v wave occurs towards the end of the pulse. Distinguishing the c wave, x and y descents is an almost impossible task.
Causes of raised jugular venous pressure
Heart failure.
Constrictive pericarditis (JVP increases on inspiration - called Kussmaul’s sign).
Cardiac tamponade.
Fluid overload, eg renal disease.
Superior vena cava obstruction (no pulsation).
Abnormalities of jugular venous pressure
Abnormalities of the a wave: disappears in atrial fibrillation.
Large a waves occur in any cause of right ventricular hypertrophy (pulmonary hypertension and pulmonary stenosis) and tricuspid stenosis.
Extra large a waves (called cannon waves) in complete heart block and ventricular tachycardia.
Prominent v waves
Tricuspid regurgitation - called cv or v waves and occurring at the same time as systole (a combination of v wave and loss of x descent); there may be earlobe movement.
Slow y descent
Tricuspid stenosis.
Right atrial myxoma.
Steep y descent Right ventricular failure. Constrictive pericarditis. Tricuspid regurgitation. (The last two conditions have a rapid rise and fall of the JVP - called Friedreich's sign.)
Austin-flint murmur
soft mid-diastolic rumble heard at the apical area. It appears when regurgitant jet from the severe aortic insufficiency renders partial closure of the anterior mitral leaflet.(in similar way to MS)
AR signs
large-volume, ‘collapsing’ pulse also known as: Watson’s water hammer pulse
Corrigan’s pulse (rapid upstroke and collapse of the carotid artery pulse)
low diastolic and increased pulse pressure
de Musset’s sign (head nodding in time with the heart beat)
Quincke’s sign (pulsation of the capillary bed in the nail; named for Heinrich Quincke)
Traube’s sign (a ‘pistol shot’ systolic sound heard over the femoral artery; named for Ludwig Traube)
Duroziez’s sign (systolic and diastolic murmurs heard over the femoral artery when it is gradually compressed with the stethoscope)
Drugs not to be used in severe AS
Nitrates (risk of syncope)
TAVI
Transcatheter aortic valve implantation
AF definition
Uncoordinated and disordered contraction of atria at fast rate which leads to initiation of ventricular contraction through the AV node at varying intervals… Thus leading to an irregularly irregular pulse
NY Heart Association classification of HF
I Cardiac disease, but no symptoms and no limitation in ordinary physical activity, e.g. shortness of breath when walking, climbing stairs etc.
II Mild symptoms (mild shortness of breath and/or angina) and slight limitation during ordinary activity.
III Marked limitation in activity due to symptoms, even during less-than-ordinary activity, e.g. walking short distances (20–100 m).
Comfortable only at rest.
IV Severe limitations. Experiences symptoms even while at rest. Mostly bedbound patients.
What sign is pathognomic of HF?
3rd heart sound
Most common causes of HF in UK
CAD
HTN
Alcohol
Valvular disease
Lifestyle modifications in HF?
Smoking
Alcohol
Salt intake
Limit fluid intake (<2L)
TTT of HF
ACEI/ARB
Betablockers
Spironolactone/eplerenone
Diuretics for fluid overload but don’t impact prognosis
Other ttt for HF
Revascularisation if CAD
Bi ventricular pacemaker /defibrillator if dysynchrony
Transplantation
LVAD
Symptoms of IE
Lethargy
Fever
Night sweats
Less common:
New heart failure
Embolic phenomena (stroke)
IE on examination
New murmur
Splenomegaly
Embolic phenomena (splinter hges, osler’s nodes, janeway lesions, petechiae
Evidence of aetiology: IVDA, infected cannula, recent surgery
Ix in IE
3 blood cultures (different sites / different times) Echo (find vegetation) Baseline blood test (CRP) ECG Urine (hematuria)
Transoesophageal Echo (TOE) vs TTE in IE
TTE (60% sensitive) vs TOE (90% sensitive)
Dx of IE
Modified Duke criteria
2 major
1 major + 3 minor
5 minor
Major criteria:
1) evidence of endocardial involvement with either vegetarians/abscess on echo or new murmur
2) typical microorganism from 2 separate blood cultures
Minor criteria
1) predisposition (cardiac lesion/IVDU/line)
2) fever (>38)
3) vascular phenomena (arterial emboli)
4) immunological phenomena (glomerulonephritis)
5) echo abnormalities but no vegetation/abscess
Surgical replacement of infected valve in IE: when?
Evidence of HF (caused by infected valve, abscess or collection)
Heart block (caused by infection with virulent organisms unlikely to be cleared with antibiotics)
Large vegetation at risk of embolisation
Prosthetic valve endocarditis (always almost requires surgical Mx)
Prognosis of IE
Mortality 20%
Worse prognosis:
prosthetic valve
Embolic phenomena
Staph aureus
Causes of MR
Acute MR:
from papillary muscule rupture or dysfct following MIA, perforation or valve leaflet during IE
Chronic MR:
Causes: Rh fever, mitral heart disease prolapse. Functional MR in HF
Examination findings of MR
Pansystolic murmur
?third heart sound
Apex beat displaced
Basal creps + peripheral edema (HF)
MS finding on ECG
Bifid P wave = P mitrale
Due to LA enlargement
Surgical Mx of MS
PBMV: percutaneous balloon mitral valvotomy
Mitral valve repair
Mitral valve replacement
Causes of TR
Rh heart disease
Endocarditis (mainly IVDA)
Carcinoid heart disease
Most common: Dilation of RV (usually due to L heart failure, PHTN or RV infarct)
Carcinoid heart disease
Carcinoid heart disease is common in patients with carcinoid syndrome, and occurs in up to 50% of these patients.iiiIt is characterised by right sided cardiac involvement, caused by plaque-like deposits of fibrous tissue which are thought to be caused by serotonin, via action on the 5HT2b receptoriv.These deposits are most commonly seen on valve cusps and leaflets, but can be anywhere in the cardiac chambers, and even in the pulmonary arteries or aorta. The left side of the heart is relatively protected, with the pulmonary circulation filtering out the majority of the serotonin produced by the tumour. Overt left sided disease has been described in patients with a patent foramen ovale, bronchial carcinoid and patients with very high levels of serotonin
Signs in TR
Pansystolic murmur at L sternal edge
Prominent systolic wave in JVP
Pulsatile hepatomegaly (pathognomic)
Carcinoid syndrome
Carcinoid tumour in GI tract or bronchi that secrete 5-HT.
5-HT leads to flushing wheezing and diarrhea
Cardiac causes of syncope
HAPE HOCM AS PE Atrial Myxoma
AF
Heart block
Patients who don’t get classical chest pain
Elderly
DM
Atypical presentation of MI (in DM and elderly)
SOB
Syncope
Sweating
N&V
Complications of MI
FAM
Failure
Arrhythmias (commonest VT/VF… DC cardioversion)
Murmur (MR or VSD)
Approach to systolic murmurs
Chest pain…?
Chest pain + palpitations…?
Dizziness + chest pain…?
Chest pain…? AS
Chest pain + palpitations…? Mitral
Dizziness + chest pain…? AS
Symptoms of AS
Syncope
Angina
Dyspnea
Stenosis vs Sclerosis
Sclerosis:
No radiation
Normal pulse
Normal in elderly
Causes of malar flush
MS Pregnancy SLE Parvovirus Any hyperdynamic state (thyrotoxicosis)
Graham steel murmur
Leakage of pulmonary valve… Pulmonary regurgitation… Early diastolic murmur
Increased JVP a
R sided heart failure TR/TS SVC obstruction Heart block CCF
When JVP elevated, how to differentiate between TR/TS and SVC obstruction
SVC obstruction is non pulsatile while TR/TS is
VSD murmur
Usually asymptomatic in finals
Very loud pansystolic murmur throughout precordium + thrill
Murmur louder at sternal edge compared to apex
Machinery like murmur
Signs of previous CABG in exams
Midline sternotomy scar
LIMA
Legs (saphenous)
Arms (radial artery)
Prosthetic valve signs
Median sternotomy scar (no leg scar)
Bruised skin (on warfarin)
Audible clicks from end of bed
Prosthetic first heart sound
Complications of prosthetic valve
Failure (valve dehiscence) Infection Bleeding Anaemia (from anticoagulant, hemolytic anemia, secondary to IE) Theomboembolic
CHA2DS2VASC
C Congestive heart failure (or Left ventricular systolic dysfunction) 1
H Hypertension: blood pressure consistently above 140/90 mmHg (or treated hypertension on medication) 1
A2 Age ≥75 years 2
D Diabetes Mellitus 1
S2 Prior Stroke or TIA or thromboembolism 2
V Vascular disease (e.g. peripheral artery disease, myocardial infarction, aortic plaque) 1
A Age 65–74 years 1
Sc Sex category (i.e. female sex) 1
Electrolytes disturbance causingbTdP
Hypokalemia
Hypomagnesemia
Bifascicular block
RBBB + LAD
Trifascicular block
RBBB + LAD + 1st degree heat block
WPW
AVRT (1% mortality vs 0% mortality in AVNRT)
Definition of MI
Detection of rise or fall of cardiac biomarker (trop) + at least 1 of the following:
- symptoms of ischemia
- ST changes or new LBBB
- pathological q waves
- imaging evidence of new loss of viable myocardium or new regional wall motion abnormality
Cardiac sounding chest pain
- constricting discomfort in front of chest, neck shoulders jaw or arms
- precipitated by physical exertion
- relieved by rest or GTN within about 5 min
DD of chest pain
MS chest pain Pneumonic/pleuritic chest pain Pericarditic chest pain GORD/Gastric/Upper abdo Aortic dissection/AAA
STEMI Definition & Management
Def:
- ST elevation > 2 mm in anterior leads in 2 consecutive leads
- or ST elevation 1 mm in 2 consecutive limb leads,
- or new onset of LBBB
Mx:
- PAMI and CP<12h or pt still complaining of CP
- far from PAMI then thrombolysis (streptokinase, alteplase, tinctplase)
Post-reperfusion:
- beta blockers
- DAPT (dual antiplatelet therapy) 12 months
- Statin high intensity
- ACEI/ARB
Mx of NSTEMI
MONAC (initially) Assess risk (GRACE score for risk of death/MIA) Start beta blockers, anti-coagulation, high intensity statin, ACEI/ARB
Definition of HF
Abnormality of cardiac structure and or function leading to failure of the heart to deliver xylem at a rate equivalent to the requirement of the metabolising tissues.
Clinically, typical symptoms are (SOB, swelling and oedema, fatigue) and signs (raised JVP, pulmonary crackles) resulting from abnormality of cardiac structure / fct
HF types
- HFREF vs HFPEF (reduced vs preserved ejection fraction)
- Acute vs chronic
- left vs right
- severity (NYHA grade I to IV)
Causes of HF
- Myocardial disease: CAD, cardiomyopathy
- Valvular heart disease
- Pericardial disease
- Endocardial disease
- Arrhythmia
- conduction disorder
- high output status / volume overload / congenital HD
Pathophysiology of HF
Pathological re-modelling of the ventricle with dilation and impaired contractility
Signs of HF
SOB exertion Raised JVP Pulse abnormalities (irregular/ tachycardia) Murmur S3 gallop Displaced apex Pulmonary creps Hepatomegaly Oedema Ascites
Digoxin ttt effects on ECG
Reduced wave amplitude
ST segment depression
Increased u wave amplitude
Shortened QT interval
Pleural tap Ix
Protein
Glucose
LDH
Cell count, culture and microscopy cytology
AAFB and culture if suspecting TB
Ligth’s criteria
Used when protein 25-35g/l or patients with abnormal serum protein
Transudate < 30g/L
Exudate > 30 g/L
Simultaneous measurement of pleural fluid and serum
- pleural fluid protein/serum protein > 0.5
- pleural fluid LDH/serum LDH>0.6
- pleural fluid LDH>2/3 upper limit of normal
Any criteria met… Effusion=exudate
Causes of transudates
CCF Cirrhosis Hypoalbuminemia Nephrotic syndrome Hypothyroidism
Causes of exudate
Infection (pneumonia) Empyema (pleural pH of <7.2 is highly suspicious) TB Neoplastic RA Trauma Sarcoidosis Pancreatitis Esophageal rupture
CAP: typical and atypical bacteria
Typical: Strep pneumoniae H influenzae S aureus G- organisms
Atypical: Mycoplasma pneumoniae Legionella Pneumophilia Chlamydia pneumoniae/psittaci
CURB 65
Confusion +1
Blood Urea Nitrogen (BUN) > 19 mg/dL (> 7 mmol/L) +1
Respiratory Rate ≥ 30 +1
Systolic BP < 90 mmHg or Diastolic BP ≤ 60 mmHg +1
Age ≥ 65 +1
0-1: Treat as an outpatient
2-3: Consider a short stay in hospital or watch very closely as an outpatient
4-5: Requires hospitalization with consideration as to whether they need to be in the intensive care unit
HAP causative organisms
G- Enterobacteria
S Aureus
Klebsiella
Risk factors for aspiration pneumonia
Reduced GCS
Neurological conditions: stroke , bulbar palsies, MG, drug alcohol misuse
Signs of CF
Underweight Cyanotic Finger clubbing Coarse crackles throughout both lung fields Wheeze
Mx of CF
MDT approach Dietitian (malnutrition) Physio (postural drainage) Pancreatic enzymes supplements IV/nebulised antibiotics Bronchodilators Inhaled recombinant DNAase (improve FEV1) Lung transplant
Causes of bronchioecstasis
Genetic (CF, Karatgener’s, primary ciliary dyskinesia)
Post-infective (pneumonia, TB)
Post childhood infection (measles, pertussis)
Bronchial obstruction (foreign body, tumour)
Hypogammaglobulinemia
Allergic bronchopulmonary aspergillosis
AI disorders (RA)
Risk factors for PE
Recent surgery (hip/knee, pelvic/abdo) Recent lower limb fracture Malignancy Recent hospitalisation Previous Hx of VTE Pregnancy Prolonged immobility Long-haul travel OCP
Signs of PE
Breathlessness Pleuritic chest pain Cough Haemoptysis Clinical evidence of DVT Tachypnea Tachycardia Raised JVP Hypotension Raised JVP Pleural rub on auscultation
ECG pattern in PE
Tachycardia
Right heart strain/RBBB
S1Q3T3 (large S wave in lead I, a large Q wave in lead III, and an inverted T wave in lead III)
Definition of sarcoidosis
Multi-system disorder characterised by non-caseating granulomas. Aetiology unknown
Sarcoidosis: Respiratory signs and symptoms
Breathlessness Chest pain Malaise / reduced exercise tolerance Cough - usually dry Low grade Pyrexia Bilateral hilar lymphadenopathy on CXR Lung fibrosis
Sarcoidosis: non pulmonary manifestation
Erythema nodosum Lymphadenopathy Hypercalcemia Hepatosplenomegaly Lupus pernio Posterior or anterior uveitis Keratoconjunctivitis sicca Enlargement of parotid glands Neurosarcoidosis Cardiomyopathy/Arrhythmia Arthralgia
Causes of interstitial lung disease
Idiopathic pulmonary fibrosis Hypersensitivity pneumonitis Sarcoidosis Pulmonary eosinophilia Coal workers pneumoconiosis Malignancy Previous infection Cryptogenic organising pneumonia Langerhans cell histiocytosis Drugs (amiodarone, cyclophosphamide, bleomycin)
Treatment of Idiopathic pulmonary fibrosis
Triple therapy: steroids + azathioprine + n-acetylcysteine
Lung transplant
Hypersensitivity pneumonitis
= extrinsic allergic alveolitis
Farmer’s lung most common
Horner’s syndrome
Ptosis
Miosis
Anhydrosis
Caused by Pancoast tumour
SVC obstruction s&s
Facial suffusion
Upper limb swelling
Distended jugular veins
Para neoplasticism drone
PTH-RP: hypercalcemia (SCC)
SiADH: hyponatremia
Eaton-Lambert syndrome (Lambert-Eaton myasthenic syndrome (LEMS) is a disorder of neuromuscular transmission caused by impaired presynaptic release of acetylcholine).
Ectopic ACTH production - Cushing (SCLC)
TB extrapulmonary manifestations
CNS: meningeal TB Genitourinary TB Bone TB (Potts disease) Skin TB (lupus vulgaris) Peritoneal TB Pericarditis (active or constrictive) GI TB
TB Ix
Sputum samples (AAFB smear and culture) Early morning krone for AAFB if renal disease suspected CXR Mantoux Bronchial washing or biopsy
TB Drug side effects
Rifampicin: liver function, urine orange
Isoniazid: peripheral neuropathy (give pyridoxine)
Ethambutol: retrobullar neuritis
Pyrazinamide: abnormal liver enzymes
Wegener granulomatosis TTT
Steroids
Cyclophosphamide
Infliximab
Aspergillosis six
Serum precipitins
Acute exacerbation of asthma: Mx
Oxygen Nebs Salbutamol 5 mg Nebs Ipratropium 0.5 mg IV hydrocortisone 200 mg Back to back Nebs Theophylline (check they're not already on it) Magnesium (1.2-2g IV)
If treating a patient that looks like acute exacerbation of asthma… And after giving all treatment no improvements, what can it be?
Pneumothorax (do Xray): asthmatic at higher risk of developing pneumothorax
Super added Infection
S&s in PE not usually asked
Syncope
PE
Coma due to resp failure
Cardiac arrest
Na and K daily requirements:
Na 100mmol/24h (1.5-2 mmol /kg/24h)
K 60 mmol/24h (1 mmol/kg/24h)
Fever and fluid requirement
Give 1 extra litre of fluid saline per degree rise every 24h
Adequate urine output
0.5 ml/kg/h
Wells score for PE diagnosis
clinically suspected DVT — 3.0 points
alternative diagnosis is less likely than PE — 3.0 points
tachycardia (heart rate > 100) — 1.5 points
immobilization (≥ 3d)/surgery in previous four weeks — 1.5 points
history of DVT or PE — 1.5 points
hemoptysis — 1.0 points
malignancy (with treatment within 6 months) or palliative — 1.0 points
Traditional interpretation[9][10][15]
Score >6.0 — High (probability 59% based on pooled data[16])
Score 2.0 to 6.0 — Moderate (probability 29% based on pooled data[16])
Score 4 — PE likely. Consider diagnostic imaging.
Score 4 or less — PE unlikely. Consider D-dimer to rule out PE.
BTS pre-test probability score for PE
Pt has clinical features compatible with PE: raised RR, hemoptysis, pleuritic chest pain
Plus 2 other factors:
1- absence of another reasonable clinical explanation
2- presence of a major risk factor
If 1 and 2 high probability
If 1 or 2: intermediate probability
If none: low probability
In what circumstances do u use thrombolysis in PE?
In Massive PE with cardiac instability
Signs of PE
Tachycardia Tachypnea RV strain / pulmonary hypertension - high JVP - RV heave - loud P2 - TR Systemic hypotension (SBP<100) Cyanosis
On ECG: - Sinus tachy (commonest) - R sided strain - AF/atrial flutter/atrial tachycardia - RAD - partial or complete RBBB - TWI anteriorly +- laterally +- inferiority - S1Q3T3 - ST depression - P pulomonale - ST elevation (V1-V3) 1 reported case ECG can be completely normal
JVP anatomical position
The Jugular Venous Pressure (JVP) is found between the sternal and clavicular heads of the Sternoclavicular Muscle (SCM); usually just above the clavicle.
Coronary arteries and MI
RCA infarct:
- inferior MI (leads II, III and aVF)
- posterior MI (prominent R wave in V1/V2)
LAD infarct:
- anteroseptal (V1/V2)
- anterior (V3/V4)
- anterolateral (I, aVL, V3-6)
- excessive anterior (I, aVL, V1-6)
Circumflex infarct:
- lateral (I, aVL, V5-6)
- isolated posterior (prominent R wave in V1-2)
ST elevation in aVR?
Left stem occlusion (very dangerous)… ST elevation probably in All leads then
How is a fluid challenge done?
250 ml bolus of colloid administered as quickly as possible. Response in CVP or urine output should be seen within min. (Importance of size and duration of CVP response rather than the actual values recorded)
Shock: definition and types
Abnormality of the circulatory system that results in inadequate organ perfusion and tissue oxygenation (ie cardiac output is unable to meet the tissues metabolic requirements)
Hypovolemic (most common: hemorrhagic shock after injury)
Septic
Cardiogenic (from blunt injury, tamponade, air embolus, infarct).
Anaphylactic
Neurogenic (spinal injury causes shock because of loss of sympathetic tone (presenting as hypotension and bradycardia) which may compound and present hypovolemia)
Addisonian (withdrawal from steroids)
Quantifying Hypovolemic Shock
Class I: 0-15% blood loss (750ml)
Class II: 15-30% blood loss (750-1500ml)
Class III: 30-40% blood loss (1.5-2l)
Class IVA: >40% >2l
BP starts falling at >30%
Hypernatremia and urine osmolality
If urine osmolality is high: hyponatremia due to dehydration
If urine osmolality is low: diabetes insipidus
Causes of cardiogenic pulmonary oedema
Remember acronym HAVM
1- hypertension
2- arrhythmia
3- valve disease (aortic/mitral)
4- MI/IHD
5- failure of prosthetic heart valve 6- cardiomyopathy 7- VSD 8- negatively inotropic drugs 9- pericardial disease
T wave morphology
Normal
Inverted (new old MI)
Biphasic (ischemia)
Tented peak (in hyperkalemia, hyperacute in ischemia)
VT vs SVT (with aberrancy)
More likely VT if Concordance Very wide qrs > 150 msec Captured beats Fusion beats
LVH on ECG
S1R6 > 35 mm
RVH on ECG
Prominent R V1 > 10 mm
Shock definition
Inadequate tissue perfusion and oxygenation
Definition/Dx of cardiac arrest
2 things
- unresponsive
- no major pulse
Diagnosis of tamponade clinically
Beck’s triad: low arterial blood pressure, distended neck veins, and distant, muffled heart sounds
Causes of PEA (pulseless electrical activity)
These possible causes are remembered as the 6 Hs and the 6 Ts
Hypovolemia Hypoxia Hydrogen ions (Acidosis) Hyperkalemia or Hypokalemia Hypoglycemia Hypothermia Tablets or Toxins (Drug overdose) Cardiac Tamponade Tension pneumothorax Thrombosis (Myocardial infarction)(Pulmonary embolism) Tachycardia Trauma (Hypovolemia from blood loss)
Signs of cerebellar disease
DANISH T
- Dysdiadochokinesis - impairement of rapid alternating movements
- Ataxia-broad based gait, falling to side of lesion
- Nystagmus - horizontal nystagmus with fast beat towards side of lesion
- Intention tremor (finger to nose and heel to shin testing)
- Stoccato speech-usually with bilateral lesions (cerebellar dysarthria)
- hypotonia
- titubation (rhythmic tremor of head)
Causes of cerebellar disease
Demyelination (MS)
Space-occupying lesion in posterior fossa
Brainstem vascular disease
Infection - HIV abscesses
Toxicity (alcohol, anticonvulants, CO, lead)
Inherited (friedrich’s ataxia, sca (spinocerebellar ataxias)
Degenerative
Charcot-Marie tooth disease (peroneal muscular dystrophy)
Distal limb weakness : pes cavus Wasting of small muscles (hands, arms...) Hyporeflexia Absent ankle jerks High stepping gait
Azathioprine: what test before starting?
Test TPMT
Thiopurine methyltransferase (TPMT) is the main enzyme responsible for inactivating toxic products of azathioprine …
Adrenaline dose for cardiac arrest
1 mg IV
1/10000 concentration
Speed of anaphylactic reactions
Food reaction=Resp arrest in 30-35 min
Insect stings: shock 15 min
IV meds: within 5 min
Anaphylaxis : adrenaline dose?
0.5 mg IM
1/1000
Mix of UMN and LMN degeneration symptoms and no sensory abnormalities…?
Think Motor neurone disease
Heart failure – Chest X ray signs
ABCDE
Heart failure – Chest X ray signs
ABCDE
Alveolar oedema (bat’s wings) kerley B lines (interstitial oedema) Cardiomegaly Dilated prominent upper lobe vessels Effusion (pleural)
Causes of blackout
CRASH
Cardiac (stokes Adams)
Reflexes (vagal overactivity, postural hypotension)
Arterial (migraine, Tia, shock…)
Systemic (glucose drop, resp(hypoxia), blood (anemia)
Head (epilepsy…)
Chorea (definition and causes)
Non rhythmic purposeless jerky flitting movements Causes Huntington Sydenhan Wilson L-dopa
Sparing of forehead wrinkling and blink
Frontales and orbicularis muscle have bilateral UMN representation
(LMN lesion: the final common pathway is destroyed)
Drug induced SLE
CHIMP Carabamazepube Hydralazine Isoniazidr Minocycline Procaibamide, pyrazinamide
Causes of fractured neck of femur
Osteoporosis
Trauma
Combination
What to know in Hx of fractured neck of femur
Age
Comorbidity
Preinjury mobility
Social hx
Describing a fracture radiograph
Location: (which bone and part) Pieces: simple/multifragmentory Pattern: transverse/oblique/spiral Displaced/undisplaced Transverse/angulated
Red flag for bone pain
Malignancy
Infection
severity pain
Hx to ask about in OA
Pain (exertional, rest, night)
Disability (walking distance /stairs…)
Deformity
Previous history (trauma and infection)
Treatment given (physio injection operation)
Other joints affected
Problem as a child (development dysplasia of the hip)
OA management
Conservative : analgesics, physio, walking aids, avoidance of exacerbating activity, injections (steroid, viscosupplementation)
Operative : 1- replace (knee/hip) 2- realign (knee/big toe) 3- excise (toe) 4- fuse (big toe) 5- synovectomy (rheumatoid) 6- denervate (wrist)
Most common causes of large bowel obstruction
Cancer
Diverticular disease
Volvulus
Bird’s beak sign on barium swallow
Achalasia
Fourth heart sound
Long standing aortic stenosis or hypertension
Third heart sound
Heart failure: rapid ventricular filing
Signs of chronic liver disease
- General: cachexia, icterus, excoriation, bruising
- Hands: leuconychia, clubbing, dupuytren, Palmar erythema
- Face: xanthelasma, parotid swelling, fetor hepaticus
- Chest and abdomen: spider naevi, caput medusa, reduced body hair, gynecomastia, testicular atrophy
Signs of hepatomegaly
palpation and percussion:
- mass in r upper quadrant, moves with respiration, not able to get above, dull to percussion
- estimate size: finger breaths below diaphragm
- Smooth our craggy/nodular (malignancy cirrhosis)
- Pulsatile (TR in CCF)
Auscultation
- Bruit over liver (hepatocellular carcinoma)
Evidence of an underlying cause of hepatomegaly
Tattoos and needle marks Pigmentation Cachexia Midline sternotomy scar Infectious hepatitis / alcohol Haemochromatosis Malignancy CCF
Evidence of DECOMPENSATED chronic liver disease
AAA
Ascites (shifting dullness)
Asterixis (liver flap)
Altered consciousness (encephalopathy)
Causes of hepatomegaly
- Big 3
Cirrhosis (alcoholic)
Carcinoma (secondaries)
CCF - Other
Infectious (hep b c)
Immune (pbc, psc, autoimmune hepatitis)
Infiltrative (amyloid and myeloproliferative disorders)
What do patients with portal hypertension die of
Variceal bleeding which would be a medical emergency
What it’s major hemorrhage protocol
Hh
Urobilinogen in obstruction
Is negative (we all have a tiny amount)
What happen to bile salts in obstruction
They leak into bloodstream
What are true liver enzymes
Albumin
Bilirubin
Alkaline phosphatase
ALT (alanine amino transferase)
In addition need to measure AST and GGT
What does polio do
Old polio which damages the nucleus of the lower motor neuron
Mixed upper and lower motor neurone disease
ALS
Child pugh score
Classification score for cirrhosis
Based on
Bilirubin Albumin INR Ascites Encephalopathy
Felty’s syndrome
is characterized by the combination of rheumatoid arthritis, splenomegaly and neutropenia.
Causes of unilateral kidney engagement
Polycystic kidney disease
Renal Cell carcinoma
Simple cysts
Hydronephrosis (due to ureteric obstruction)
Causes of bilateral kidney enlargement
Polycystic kidney disease Bilateral renal Cell carcinoma Bilateral Hydronephrosis Tuberous sclerosis Amyloidosis
Evidence of immunosuppressive
Ciclosporin: gum hypertrophy and hypertension
Steroids: cushingoid appearance, thin skin ecchymoses…
Top 3 causes for renal transplantation
Glomerulonephritis
Diabetic nephropathy
Polycystic Kidney disease
Top 3 causes for liver transplantation
Cirrhosis
Acute hepatic failure (hepatitis a b, paracetamol overdose)
Hepatic malignancy
Causes of gum hypertrophy
Drugs: ciclosporin, phenytoin, nifedipine Scurvy Aml Pregnancy Familial
Dorsal columns
Vibration
Proprioception
Spinothalamic tract
Pain
Temperature
Tabes dorsalis
Tabes dorsalis, also known as syphilitic myelopathy, is a slow degeneration (specifically, demyelination) of the nerves primarily in the dorsal columns (posterior columns) of the spinal cord (the portion closest to the back of the body). They help maintain a person’s sense of position (proprioception), vibration, and discriminative touch.
Horner’s syndrome causes
Causes of Horner syndrome may also be classified as involving first-order, second-order, or third-order neuron lesions.
First-order neuron lesions that may give rise to the syndrome include the following:
Arnold-Chiari malformation
Basal meningitis (eg, syphilis)
Basal skull tumors
Cerebral vascular accident (CVA)/Wallenberg syndrome (lateral medullary syndrome)
Demyelinating disease (eg, multiple sclerosis)
Lesions in the hypothalamus or medulla
Intrapontine hemorrhage
Neck trauma (eg, traumatic dislocation of cervical vertebrae or traumatic dissection of the vertebral artery) - Horner syndrome occurring in association with spinal cord trauma suggests a high cervical cord lesion because it does not occur with lesions below T2 or T3
Pituitary tumor
Syringomyelia
Second-order neuron lesions that may give rise to Horner syndrome include the following:
Pancoast tumor (tumor in the apex of the lung, most commonly squamous cell carcinoma)
Birth trauma with injury to lower brachial plexus[6]
Cervical rib
Aneurysm or dissection of the aorta
Lesions of the subclavian or common carotid artery
Central venous catheterization
Trauma or surgical injury (eg, from radical neck dissection, thyroidectomy, carotid angiography, or coronary artery bypass grafting)[7]
Chest tubes
Lymphadenopathy (eg, Hodgkin disease, leukemia, tuberculosis, or mediastinal tumors)
Mandibular tooth abscess
Lesions of the middle ear (eg, acute otitis media)
Neuroblastoma[8]
Austin flint murmur
In cardiology, an Austin Flint murmur is a low-pitched rumbling heart murmur which is best heard at the cardiac apex.[1] It can be a mid-diastolic[2] or presystolic murmur[3] It is associated with severe aortic regurgitation, although the role of this sign in clinical practice has been questioned.[4]
Pericardiris on ECG
St elevation (,notchz,) Pr deression
Meeran eye slide
Micro aneurysm
Hard exudate
Blot hemorrhages
Background diabetic nephropathy
Patient needs good diabetic control: diet exercise maybe metformin (add gliclazide if needed)
Pros and cons ctpa vs vq scan
Ctpa: More radiation (not pregnant,) More available in hospitals Vq scan can be done only if xrays normal Ctpa can give more info (pleural effusion...) If pe wrong diagnosis
Commonest bacteria in teeth that might cause problems
Strep viridans
Pleurisy in paces
Pleural rub heard… Crunch… Walking on snow
Usually from: Primary infarction, or following pneumonia or following pulmonary embolus.
Horner syndrome
Horner syndrome is due to a deficiency of sympathetic activity. The site of lesion to the sympathetic outflow is on the ipsilateral side of the symptoms. The following are examples of conditions that cause the clinical appearance of Horner’s syndrome:
First-order neuron disorder: Central lesions that involve the hypothalamospinal tract (e.g. transection of the cervical spinal cord).
Second-order neuron disorder: Preganglionic lesions (e.g. compression of the sympathetic chain by a lung tumor).
Third-order neuron disorder: Postganglionic lesions at the level of the internal carotid artery (e.g. a tumor in the cavernous sinus or a carotid artery dissection).
Partial Horner’s syndrome In case of a third-neuron disorder, anhidrosis is limited to the middle part of the forehead or can be absent, resulting in a partial Horner’s syndrome.[3]
Eye out and down
Third nerve palsy
Surgical or medical
Look at pupil size
Surgery: posterior aneurysm…
In a squint
The outside image is from the weak eye
By doing cover test
Probably 6th nerve palsy or 3rd or complex ophtalmoplegia
Cause of complex opthalmoplegia
Graves disease (commonest)
MG
Retro-orbital tumour
Miller-Fisher syndrome (orbital guillain Barre syndrome) (one patient is usually in exams)
Eye slide Number 2
NOrmal fundus
What to see in background retinopathy
Hard exudates,(cholesterol)
Micraneyrysms,z(dots
Blot hemorrhages
Third slide eye Meeran
Cotton wool spots (used to be called soft exudates)
What are cotton wool spots
Retinal ischemia
Slide 4 Meeran eye
New vessels
Silver wiring
Diabetes
They present wiyh hyperosmolar… Weren’t diagnosed before
Slide 5 eye Meeran
Hdhdhd
Management of diabetic retinopathy
Background
Pre-proliferative: cotton wool spots. Suggests General ischemia. If left alone New vessels will grow. Needs Pan retinal phosphorylation
Proliferative: visible New vessels (this is an emergency weight be seen in exam)
Needs Pan retinal photocoagulation
Eye slide 6
See laser spots
Can ask if they have diabetes but might be shouted at
Pan retinal photocoagulation…
Older laser black burns
Newer lasers are paler
Pan retinal photocoagulation
Carefully avoid burning the macula
So we are sacrificing some peripheral vision tip maintain central vision
Eye slide 7
Retinitis pigmentosa
Retinitis pigmentosa
Retinitis pigmentosa (RP) is an inherited, degenerative eye disease that causes severe vision impairment and often blindness.[1] The progress of RP is not consistent. Some people will exhibit symptoms from infancy, others may not notice symptoms until later in life.[2] Generally, the later the onset, the more rapid is the deterioration in sight.[citation needed] Those who do not have RP have 90 degree peripheral vision, while some people who have RP have less than 90 degrees.
Retinitis pigmentosa with photonic acid
Chelsea and westminster site
Heritable
Many genetic syndromes example usher syndrome
(Deafness)
Refsum’s disease (failure to metabolize phytanic acid)
Can lead to blindness and would like to take Family history
Causes for hirner syndrome
Damage to sympathetic chain
Trauma to carotid sheeth (central line)
Apical lung tumour
Stages of hypertensive retinopathy
1- Silver wiring
2- av nipping
3- cotton wool and flame shaped hemorrhages
4- Papilloedema
