CR PBLs Flashcards
Types of CoA
Pre-ductal
Juxtaductal
Post-ductal
Which type of CoA is most common?
Juxtaductal
Defects associated with CoA
Left sided obstructive defects
VSD
Bicuspid aortic valve
Aortic arch hyperplasia
Surgical treatments for CoA
Resection and end-end anastomosis
Patch aortoplasty
Left subclavian flap angioplasty
Bypass graft repair
Symptoms of second degree heart block
Lightheadedness, dizziness, syncope
Chest pain
Irregular heart beat
Bradycardia
Causes of heart block
Electrolyte imbalances MI Coronary artery disease Myocarditis or cardiomyopathy Heart enlargement from heart failure
Indications for pacemaker in heart block
Persistant bradycarida
Asystole for >3 seconds
Heart failure
Associated with neuromuscular disease
When is CRP commonly raised?
Late pregnancy
Mild inflammation
Bacterial and viral infection
Burns
Reversible risk factors or angina
Smoking Hypertension Hyperlipidameia Obesity Physical inactivity
Irreversible risk factors for angina
Family history
Older age
Male sex
Diabetes mellitus
Signs of angina on ECG stress test
ST depression
T wave inversion
Short and spikey T waves
Drugs used in angina treatment
Aspirin CCBs BBs Statins Nitrates Beta blockers ACEIs ARBs
Characteristics of unstable angina
Pain comes on suddenly
Not triggered by exertion
Does not go away with rest
Gets worse over a short period of time
ST elevation
= ongoing active damage
>2mm in chest leads
>1mm in limb leads
Must be present in 2 or more contiguous leads
Pathological Q waves
= irreversible damage >0.04s >2 small squares in depth >25% of the depth of the QRS complex Present in V1-3
Troponin subtypes
T and I
When is troponin released and when do levels return to normal?
First released 4-6 hours after attack
May remain elevated for 2 weeks
Myocardial creatine kinase
= CK-MB
When is CK released and when do levels return to normal?
3-12 hours after infarct
Return to normal after 48-72 hours
When is AST released and when do levels return to normal?
Peaks around 48 hours
Returns to normal after 5 days
When is LDH released and when do levels return to normal?
Peaks around 72 hours
Returns to normal after 6 days
When is myoglobin released?
As early as 2 hours after infarct
Pain felt in AMI
Intense and consistent for 30-60 minutes Retrosternal Radiates --> neck, jaw, back, arm May be felt as indigestion Felt as a weight on the chest as squeezing pain
AMI immediate treatment
Aspirin
Pain relief and sedation
Thrombolysis or PCI
Beta blockers
Secondary prevention
Aspirin
Beta blocker
Statin
ACEI
Short term complications of AMI
Arrhythmia
Heart failure
Rupture
Mural thrombosis
Long term complications of AMI
Aneurysm
Heart failure
Pericarditis
Adverse prognostic features of AMI
Advanced age Anterior AMI Larger AMI Heart failure Systolic hypotension Complex ventricular arrhythmias >24h after infarct History of previous infarct(s)
Causes of heart failure
Coronary artery disease Valve disease Cardiomyopathy Congenital defects Toxins (alcohol, cocaine) Drugs (BBs, CCBs) Anaemia Pregnancy Hyperthyroidism
Major criteria for heart failure
PND Weight loss with treatment Neck vein distention Hepatojugular reflux Rales S3 gallop Cardiomegaly
Minor criteria for heart failure
Nocturnal cough Dyspnoea on normal exertion Decrease in VC by 1/3 Pleural effusion Tachycardia Bilateral ankle oedema
Why do you get PND?
Return of peripheral oedema fluid to circulation due to gravity
Reduced respiratory drive during sleep
Reduced sympathetic bronchodilation during sleep
ECG features of heart failure
LVH (high R waves in V4-6)
ST depression showing ischaemia
LBBB
CXR findings
Cardiomegaly Bat wing sign Kerley B lines Pleural effusions Upper lobe diversion
Echo findings
Reduced eject fraction Dilated ventricles Valve dysfunction Pulmonary artery pressure raised Reduced/increased wall thickness
Drugs for heart failure
Diuretics ACEIs Beta blockers ARB Aldosterone blocker Digoxin
Heart failure prognosis
50% die within 5 years
Asthma characteristics
Airflow limitation
Airway hyper responsiveness
Inflammation on bronchi
Raised cells in asthma
Eosinophils
Mast cells
T cells
Signs of severe asthma
SaO2 <92% PEFR <33% predicted Tachycardia PaO2 <8kPa PaCO2 normal or raised Silent chest Cyanosis Inability to complete sentences in one breath Feeble respiratory effort
Treatment ladder of asthma
Salbutamol Inhaled steroid LABA Leukotriene antagonist Antimuscarinic Theophylline Oral steroid
Risk factors for DVT
Previous DVT Hospitalisation Surgery Active cancer Lower limb trauma Increasing age Pregnancy COCP/HRT Obesity Thrombophilia Long haul travel Family history
Signs and symptoms of DVT
Limb pain Tenderness Swelling Pitting oedema Distention of superficial veins Increased temperature Erythema Cord like palpable vein
What is D dimer?
Breakdown product of cross-liked fibrin produced by plasmin
DVT treatment
LMWH then warfarin
Complications of DVT
PE
Active bleeding from treatment
Post-thrombotic syndrome
Heparin induced thrombocytopaenia
Forms of embolus
DVT Fat Air Amniotic fluid Tumour
Symptoms of PE
Dyspnoea
Pleuritic chest pain
Haemoptysis
Atypical symptoms of PE
Syncope Seizures Abdominal pain Fever Confusion Delirium
Signs of PE
Tachycardia Tachypnea Hypoxia Pyrexia Raised JVP Pleural rub Accentuated second heart sound Hypotension and shock
Differential diagnosis of PE
Pneumonia Acute coronary syndrome Aortic dissection Cardiac tamponade Pneumothorax
ECG signs of PE
Tachycardia RBBB RV strain RAD Large P waves S1Q3T3 pattern Atrial arrhythmia
CXR signs of PE
Dark lung fields Focal oligaemia Prominent central artery Basal wedge shaped opacities Pleural effusion
Type of respiratory failure in PE
1
Treatment of PE
Heparin or fondaparinux
Then warfarin
Thrombolysis in massive PE
Can thrombolysis be used in pregnancy?
YES
Sites of RBC production
Yolk sac
Liver and spleen
Bone marrow
Forms of haemoglobin
Hb Gower 1 = zeta 2 epsilon 2
HbF = alpha 2 gamma 2
HbA = alpha 2 beta 2
HbA2 = alpha 2 delta 2
Genetics of alpha thalassaemia
Gene deletions on chromosome 16
Usually 4 genes present
Consequences of alpha thalassaemia
1-2 deletions = no symptoms
3 deletions = HbH disease –> severe microcytic anaemia
4 deletions = hydrops foetalis –> death
Hb levels in beta thalassaemia major
Low HbA
High HbF
Normal or slightly high HbA2
Sites of extra medullary haematopoiesis
Spleen
Liver
Consequences of haemolysis
Jaundice
Reticulocytosis
Hepatosplenomegaly
Treatment of beta thalassaemia major
Regular blood transfusions
Iron chelation therapy
Bone marrow transplant
Splenectomy
Iron chelating agents
Desferrioxamine (SQ)
Deferiprone (oral)
