Yr4 GenMed - Lectures Flashcards
What is Wellens Syndrome?
Wellens Syndrome is a clinical syndrome characterised by biphasic or deeply inverted T waves in V2-3, plus a history of recent chest pain now resolved. It is highly specific for critical stenosis of the left anterior descending artery (LAD).
- The pattern is usually present in the pain free state — it may be obscured during episodes of ischaemic chest pain, when there is “pseudonormalisation” of T waves in V2-3.
- Patients may be pain free by the time the ECG is taken, and have normal or minimally elevated cardiac enzymes. However, they are at extremely high risk for extensive anterior wall MI within the subsequent days to weeks
- Due to the critical LAD stenosis, these patients usually require invasive therapy, do poorly with medical management, and may suffer MI or cardiac arrest if inappropriately stress tested
What is Entresto? What is it used for?
Entresto = Sacubitril / Valsartan
Give differentials for breathlessness:
- 5 Lung diseases?
- 5 Heart diseases?
- 3 Pulmonary artery conditions?
- 5 Blood diseases?
What is Heart Failure?
- Simplest Definition?
- 4 Basic causes?
- New Universal Definition of Heart Failure?
- HFrEF? HFmrEF? HFpEF? HFimpEF?
Heart Failure
- Simplest definition: The Inability of the heart to meet the demands of the body
- Multiple causes:
1. Increased demand of the body
2. Weak pump (systolic failure)
3. Stiff pump (diastolic failure)
4. Combination
Outline a Diagnostic Algorithm for Heart Failure
- 10 possible exam findings?
- 6 initial investigations?
Outline the New York Heart Association classification of HF.
- What history would you take?
- What would you look for on examination? (6)
History of HF
- Breathlessness: How far? how much exercise? Breathless at rest; minimal exertion?
- Orthopnea, paroxysmal nocturnal dyspnea?
- Chest discomfort to suggest myocardial ischaemia
- Cough, wheeze, respiratory symptoms
- Systemic symptoms e.g. systemic diseases
- Prior history, e.g. prior diagnosis and investigations
Outline how a patient may be investigated for unexplained breathlessness in WA.
- List 5 Risk Factors and Comorbidities associated with HF?
Risk Factors and Comorbidity with HF
1. Hypertension = 53%
2. AF = 42%
3. Respiratory disease = 32%
4. Diabetes = 27%
5. Renal dysfunction = 17%
What investigations would you order for heart failure? (4)
- HF Classification by LVEF?
Investigations for Heart Failure
1. Echocardiography - Global or Regional & Valves,shunts
2. Laboratory investigations - Kidney, liver, thyroid, glucose, lipids, iron
3. Coronary imaging - Regional LV dysfunction more likely to be coronary disease
4. Assess for systemic disease - Amyloid (e.g.multiple myeloma), Toxins (e.g.alcohol), Fe and Cu studies, Hepatitis and HIV, Autoimmune screen
How does the mortality of HF compare in men vs. women?
Systolic Heart Failure and Mortality
- Men and Women are different
- More men have impaired LVEF (17.6% vs 8.3%)
- Risk in women starts at a higher LVEF (<65%) than in men (<60%)
- Heart failure is a spectrum:
1. Not all heart failure is systolic (>50% has normal LVEF)
2. Not all systolic heart failure behaves the same
3. Not everyone with systolic heart failure has the same EF
What are the severity classification of Systolic Heart Failure?
- List 8 causes of systolic HF?
Systolic Heart Failure
- Heart Failure with Reduced Ejection Fraction (HFREF)
- Ejection Fraction (EF) < 50% = Impaired EF
- …although strictly LVEF <55% abnormal
- Mild = EF 40% to 50%
- Moderate = EF 30% to 40%
- Severe = EF < 30%
- At diagnosis….Goal is to “restore normal”
What are the differences between Global LV dysfunction vs. Regional LV dysfunction? (4)
What investigation should all patients with significant LV dysfunction have and why?
Global systolic dysfunction
- All walls are affected equally and EF will decrease.
- May be due to coronary disease, but more commonly caused by a cardiomyopathy (e.g. viral).
Regional LV dysfunction
- Single wall or region is abnormal
- Regional wall motion abnormality usually caused by coronary disease (impairment in coronary artery distribution).
- Occasionally regional but outside of coronary artery distribution (e.g. sarcoidosis).
- Ejection fraction may still be normal if only small region of dysfunction
Investigating LV dysfunction
- Because of the frequency of coronary artery disease, all patients with significant LV dysfunction should have coronary artery imaging
- If coronary arteries are normal, alternative causes should be sought
Diastolic Heart Failure
- What is it?
- Hallmark feature?
- 4 main causes?
- Assessment?
Diastolic Heart Failure - HFPEF
- “Failure To Relax”
- Clinical Heart Failure with Normal Ejection Fraction = HFPEF = EF>50%
- Caused by a stiff left ventricle – Like leather, will not stretch Hallmark is high filling pressure
- Abnormal myocardial relaxation occurs in many conditions, especially:
1. Myocardial ischaemia
2. Systolic dysfunction
3. Hypertrophy
4. Infiltration
4 types of Left ventricular hypertrophy?
Infiltration
- Increased LV mass may be entirely muscle, or matter deposited with muscle
- E.g. Amyloid
- Concentric hypertrophy
Outline the Mortality of Diastolic Function.
- Rule of 9s?
- 4 Markers of Diastolic dysfunction?
Diastolic Function
and Mortality - Rule of 9s
- Diastolic function is age dependent
- No significant sex-dependency
- Influenced by LVEF, valve disease, prior surgery, and AF
- Rule of 9’s, associated with higher mortality:
1. E velocity > 90cm/s
2. e’ velocity < 9cm/s
3. E:e’ ratio > 9
4. LA volume index > 34ml/m2
List 6 Complications of Heart failure.
Complications of Heart failure
1. Atrial fibrillation - Left atrial stretch produces spontaneous left atrial depolarisation and eventually atrial fibrillation. Atrial fibrillation is very common in diastolic dysfunction, so-called “substrate AF”. Stasis and risk of thrombus
2. Mitral regurgitation - secondary to a dilated left ventricle. Poor coaptation of the mitral valve leaflets due to dilatation and papillary muscle displacement / dysfunction
3. Right heart failure
4. Pulmonary hypertension - Increased pulmonary venous congestion results in pulmonary vein dilatation. Pulmonary venules and pulmonary capillaries become engorged with blood, resulting in alveolar exudates (pulmonary oedema)
5. Thrombi - Left atrial appendage in AF = A potential source of thrombus & risk of stroke
6. Renal dysfunction
Outline how heart failure can lead to pulmonary hypertension.
Pulmonary Hypertension
- ANY cause for LV diastolic dysfunction can result in heart failure:
- Hypertension or aortic stenosis
- Ischaemic or nonischaemic cardiomyopathy
- Restrictive cardiomyopathy
- Constriction
- The final common pathway of heart failure due to left heart disease is PULMONARY HYPERTENSION
- Pulmonary hypertension due to left heart disease is the commonest cause for pulmonary hypertension
- Median time from diagnosis to death is 4.1 years
Outline a simple blood test to measure heart failure.
- Role in acute breathlessness?
BNP - a simple test for heart failure
- B-type natriuretic peptide is a small hormone released by cardiac muscle (mostly LV), and causes salt and water excretion.
- BNP is released in response to wall stretch and is dependent on muscle mass: LV, then RV, with small amounts in LA and RA. Useful in both diastolic and systolic heart failure.
- High BNP levels are a strong marker of LV dysfunction, and predicts death.
Outline the Formulae for heart failure treatment (1-4).
- Outline Formula 1.
Formula 1: Reverse underlying cause
- Revascularisation in LV dysfunction
- If abnormal systolic function is caused by a coronary artery stenosis, revascularisation may restore normal systolic function
- Revascularisation may be percutaneous (angioplasty and stenting) or surgical (bypass grafting)
- Hypokinetic myocardium may return to normal
- Hibernating myocardium (akinetic) may begin to function
- LV volumes may improve, MR may decrease
Formulae for heart failure treatment
- Formula 2: 9 Lifestyle recommendations?
- Which 10 medications should be avoided in HF?
Lifestyle recommendations in HF
1. Salt intake < 3g/day
2. Fluid < 2 l/day (relax in summer and after prolonged physical activity)
3. Measure weight daily to monitor fluid status
4. Avoid illicit drugs and smoking
5. Limit alcohol to no more than 10-20g/day (2 standard drinks)
6. Abstinence from alcohol if alcohol related cardiomyopathy
7. Influenza and pneumoccal vaccinations
8. For obese patients, lose weight
9. Encourage physical activity and consider an exercise training program
Formulae for heart failure treatment
- Formula 3: Drug therapy? (8)
Drug treatment for HF
1. Breathless patients should be given loop diuretics and fluid restriction
2. ACE inhibitor at max dose, or Valsartan/Sacubitril (ARB and neprolysin inhibitor)
3. Spironolactone (as aldosterone antagonist)
4. SGLT2 inhibitors (Dapagliflozin, Empagliflozin)
5. Maximum dose β-blockers if tolerated
6. Aspirin and Statin
7. Ivabradine (If inhibitor) if sinus rhythm and resting heart rate >77bpm
8. Treat Iron Deficiency and AF if present….
Should beta blockers be given to all patients with heart failure?
What about aspirin?
Aspirin in HF
Once atherosclerosis is present, lipid lowering therapy is required to:
1. Stabilize plaque
2. Slow progression
3. Decrease risk of ACS (via plaque stabilization)
Aspirin therapy is required to: Decrease risk of ACS (via thrombus prevention)
Outline the Causes of Iron Deficiency in HF.
- Ferritin and transferrin in HF?
- Definition of iron deficiency?
- 5 effects of iron deficiency on LV function? 4 clinical effects?
Ferritin and transferrin
- Intracellular iron is stored as ferritin and haemosiderin
- Excess intracellular ferritin spills into the blood stream causing serum ferritin to rise.
- Ferritin is also an acute phase reactant - any inflammation will cause it to rise
- Transferrin transports iron.
- Transferrin saturation is the percent loaded with iron.
- Transferrin is a negative acute phase reactant - during inflammation it will fall
- During chronic illness (e.g. CHF): Ferritin rises and transferrin falls due to increased hepcidin levels and sequestration of iron
- Iron Deficiency = Ferritin <100 μg/L or Ferritin <300 μg/L if TSAT <20%
What is the role of Oral Iron in heart failure?
Use of Oral Iron in heart failure
- Heart failure alters regulation of duodenal iron transportation, decreases intestinal permeability, and decreases iron absorption.
- Oral iron (ferrous) is ineffective in restoring normal iron levels in the setting of heart failure, and further worsened with PPI use.
- Oral iron does not improve functional status, quality of life or hospital admission rate.
- IV FCM is superior to oral iron in improving iron levels.
Epilepsy
- Epidemiology?
- What is the difference between Epilepsy & Seizures?
- Incidence by age group?
Epilepsy
- a disorder of brain function
- where there is a tendency for recurrent seizures (>2 unprovoked seizures > 24hrs apart)
- Diagnosis of an “epilepsy syndrome”
- requires therapy
Seizures
- an event in which there is disruption of the normal electrochemical activity of the brain
- Sudden uncontrolled electrical discharge from neurons
- Can fire >500 times per second (>6X normal frequency) causing:
1. strange sensations
2. Emotions
3. Behaviour
4. Convulsions or abnormal movements
Classification of Seizures?
- List 10 drugs that might trigger/cause a seizure?
SOME DRUGS REPORTED TO CAUSE SEIZURES
1. Antibiotics esp PENICILLIN, Cyclosporin, Isoniazid
2. Anticholinesterases
3. Antihistamines
4. Antidepressants
5. Antipsychotics
6. Baclofen
7. Beta blockers
8. Chlorambucil
9. Cimetidine
10. General anaesthetics
11. Hypoglycaemics
12. Levodopa
13. Opioids and TRAMADOL
Classify the Epilepsy Syndromes.
DIAGNOSIS OF EPILEPSY
- Diagnostic process?
- History?
DIAGNOSIS OF EPILEPSY
Clinical diagnosis
- Relies on History
- Primarily a description of the seizures
- Ideally eye-witness account or video
- EEG is supportive (often not diagnostic – normal EEG does not exclude epilepsy)
- MRI often helpful for underlying cause but does not confirm diagnosis which remains clinical
History Taking in Seizures/Epilepsy
* Usually of an unusual event or syncopal episode that has already occurred.
* Questions directed towards:
1. Was this a seizure?
2. What type of seizure?
3. What are the patients risk factors for seizure?
4. Could it have been something else?
List 6 Differential Diagnoses of Seizures?
- How does the tempo/progression give you a clue?
- Syncope: loss of blood supply often due to drop in BP
- Epilepsy: spontaneous electrical discharge of cortical neurones
- Psychogenic/non-epileptic
- Narcolepsy/sleep attacks
- Metabolic/Endocrine – low BSL/ Low cortisol
- Migraine
Why is it so important to get the diagnosis of seizure correct? (5)
- What would you look for on examination? (5)
EXAMINATION
- Blood Pressure – lying/standing
- Pulse rate and rhythm
- Full neurological examination – any focal neurological signs
- In pregnant or post-partum patients, consider:
1. Eclampsia.
2. Structural cause e.g., meningioma (which can increase in size during pregnancy), cerebral venous thrombosis.
First Seizure
- 3 Types of Seizures?
- Definition?
- Recurrence rate?
- 10 Causes of Acute Symptomatic Seizure?
First Seizure
- Multiple events within 24 hr period are still considered “first seizure”
- Risk of Recurrent after first unprovoked seizure is approx 50%
- Risk of recurrence is highest in first 6 months after a seizure
- 30-50% of those referred have not had an epileptic seizure (most are syncope)
- Of those remaining, 30% have history suggestive of prior events (previously unrecognised) so diagnosis is epilepsy not first siezure
First Seizure
- ED investigations? (6)
- Treatment?
- Advice to patients with first seizure in the ED?
- 2 investigations for unprovoked?
- What is an EEG? Which patients is it most useful for?
- Does a normal EEG rule out epilepsy?
ED INVESTIGATIONS
1. ECG- any heart block, QT interval
2. BSL
3. Consider EUC/CMP/CK/lactate
4. CTB to rule out major structural abnormality
5. +/- others (BAL, LP)
6. If cardiogenic cause suspected – holter/loop recorder/echo
TREATMENT
- If Provoked (e.g Alcohol withdrawal, hypoglycaemia etc..) = remove provoking factors if possible
- Symptomatic (e.g encephalitis) = admit, needs further Ix
- Unprovoked (no obvious trigger) = refer to first seizure clinic/specialist for further investigations
1. EEG – most sensitive within 24 hrs of event - NOTE: Normal EEG does not rule out epilepsy
2. MRI brain – rule out structural abnormality
- What is the difference between these 2 MRIs? Whats the diagnosis?
- What is an Ictal SPECT scan?
- Left = T2 coronal MRI = CSF white (difficult to see structural pathologies)
- Right = T2 FLARE = fluid attenuated inversion recovery sequence (CSF made black so easier to see brain structure)
- Diagnosis = Medial temporal sclerosis
- Ictal SPECT = blood flow nuclear med scan
TREATMENT OF ACUTE SEIZURE?
- 4 Red flags in seizures?
TREATMENT OF ACUTE SEIZURE
- Most seizures are brief and self-limiting
- End within 1-3 mins without drug treatment
- Supportive care to all patients
- Position patient on left side
- Protect airway and maintain oxygenation
- Remove environmental hazards
- If in hospital, connect to monitoring equipment and check BSL
- Treat underlying cause - e.g ETOH withdrawal – give IV thiamine
- Anti-epileptic drugs (AED’s) may be required acutely if cause takes time to resolve
- Ongoing AED is usually NOT required or can be withdrawn
TREATMENT OF STATUS EPILEPTICUS
- When to start treatment?
- 4 Immediate goals?
- Steps 1-3?
TREATMENT OF STATUS EPILEPTICUS
- Convulsive vs Non-convulsive (less urgent)
- Start treatment after 5 mins continuous seizure activity OR Repeated seizures without recovery between
Immediate Goals
1. Resuscitate the patient
2. Stop the seizures
3. Diagnose and treat cause of seizures
4. Find and treat complications of the seizures (aspiration, trauma, rhabdomyolysis etc..)
MANAGEMENT OF EPILEPSY
- What is it influenced by? (3)
- In general which AED for focal and which for generalised?
- What is drug efficacy guided by?
- When do we do drug serum levels?
- How long can’t you drive for after ceasing an AED?
MANAGEMENT OF EPILEPSY
Influenced by:
1. Seizure Type
2. Epilepsy Syndrome
3. Patient factors (age, gender, pregnancy, cost, AE’s, drug interactions etc..)
- Aim of AED is to completely suppress seizures without adverse effects
- In general; first line therapy
- (a) Focal seizures is Carbamazepine
- (b) Generalised Seizures is Sodium Valproate (NOT in women of childbearing potential)
- No driving 6 months after cessation
2 Differentials for Seizures
- What is Syncope? Red Flags for possibiity of sinister causes of syncope?
- Non-epileptic seizures?
Causes of:
- Polyneuropathy? (11)
- Mononeuropathy? (3)
- Common drug-induced polyneuropathies? (5)
- Common Hereditary polyneuropathies? (3)
Polyneuropathy
- Summary?
- Aetiology: Hereditary, Toxins, Inflammatory, Infectious, Environmental?
Polyneuropathy is a disorder that involves damage to multiple peripheral nerve fibers. Causes include diabetes mellitus, alcohol use disorder, hereditary diseases, toxins, infection, or other inflammatory conditions. The classic presentation is a symmetrical distal burning sensation or loss of sensation. Further clinical features depend on whether an axonal or demyelinating nerve injury has occurred. Diagnosis is usually clinical, supported by laboratory studies to rule out common causes such as diabetes. Further diagnostic tests such as electrodiagnostic studies are reserved for patients with atypical clinical features, unknown etiology, and/or severe or rapidly progressive symptoms. Management involves treatment of the underlying disorder and symptomatic therapy (e.g., control of neuropathic pain).
Polyneuropathy - Clinical Features
- 6 General?
- Axonal vs. Demyelinating: Acute vs. Chronic?
General Features of Polyneuropathy
1. Symmetrical distal sensory loss (glove and stocking pattern)
2. May be accompanied by neuropathic pain, paresthesias, and motor weakness
3. Burning-foot syndrome: burning pain, tingling, pins-and-needles sensation, or formication, hyperhidrosis
4. Atrophy of muscles: e.g., stork legs in the case of Charcot-Marie-Tooth disease
5. Sensory ataxia: caused by loss of sensation, particularly proprioception, that affects the afferent limb of postural reflexes (e.g., due to vitamin B12 deficiency).
6. ↓ Deep tendon reflexes
Subtypes of Polyneuropathy
Outline the : Definition, Pathophysiology, Clinical features, & treatment for:
- Alcohol polyneuropathy?
- Refsum disease?
Hereditary motor sensory neuropathy (HMSN)
- Otherwise known as?
- Overview?
- 4 clinical features?
- HMSN type I?
-
Hereditary motor sensory neuropathy (HMSN)
- One of the most common inherited neurological diseases
- Also known as Charcot-Marie-Tooth disease
- Inheritance is usually autosomal dominant, but may be autosomal recessive or X-linked.
- Various mutations cause impaired growth or function of the axons or Schwann cells (e.g., defects in axon or myelin sheath proteins).
- Common clinical features include:
1. Distal muscle weakness and atrophy
2. Reduced or absent reflexes
3. Sensory deficits (e.g., decreased vibration, proprioception)
4. Associated with scoliosis and foot deformities (e.g., high arches, hammer toes)
Chronic inflammatory demyelinating polyneuropathy (CIDP)
- Definition?
- Epidemiology?
- Aetiology?
- 4 Predisposing factors?
- Pathophysiology?
- Clinical features?
- Diagnostics?
- Treatment?
CIDP
* Cause identified in <30%
* Onset is less well defined than GBS
* Involves motor system with proximal and distal muscles involved simultaneously and with graded sensory involvement at onset (more vibration and position sense)
* Less significant airway involvement
* Tends to be slowly progressive after 8 weeks
* More common in older males, but all ages and sexes
* Treatment: IVIG or plasma exchange
Investigation of a patient with Polyneuropathy
- Lab studies?
- Electrodiagnostic studies?
- 4 Additional tests?
- Identify the cause
- All patients warrant an EMG/NCS
- CSF examination if disease process involves the nerve roots (GBS, CIPD, for diagnosis)
- Nerve biopsy: vasculitis, amyloid, sarcoidosis, leprosy
- Skin biopsy: if distal small fibre sensory neuropathy
- MRI: nerve roots
- Full diagnostic evaluation if: asymmetric, rapidly progressive, motor predominance, acute onset, no obvious cause, prominent autonomic involvement, non-length dependence
Additional testing
1. Sural nerve biopsy: performed in diagnostic uncertainty or prior to starting aggressive treatments
2. Skin biopsy: may be performed in patients with a burning sensation or painful neuropathy
3. Genetic testing: for suspected hereditary disorders
4. Cerebrospinal fluid analysis: for suspected infections or CIDP
Management of Polyneuropathy
- Nonpharmacological methods?
- Pharmacological therapy?
Management of polyneuropathy
- Treat the cause!
- Demyelinating inflammatory polyneuropathies: IVIG or plasma exchange
- Treat symptoms: gabapentin, tricyclics, duloxetine, pregabalin, carbamazepine
- Avoid falls
- Walking aids
- Protection of feet (podiatrist)
- Preserve respiration
Whats important in
Haematological Malignancy? (7 points)
- What is the ECOG Score?
Whats important in Haematological Malignancy
1. Cure or Palliation? “remission”
2. Biological age - ECOG score (describes a patient’s level of functioning in terms of their ability to care for themself, daily activity, and physical ability (walking, working, etc.).
3. Prognostic factors and staging including clinical, blood, cytogenetics and gene/ microRNA expression profiling
4. Survival and statistics
5. Quality of life
6. Risk of treatment –side effects
7. Expense of new therapies
List 6 treatment options for haematological malignancies?
- Outline the Normal Haemopioetic Cell Differentiation and where each of the haem malignancies fall in this?
- Chemotherapy
- Targeted therapy bcr-abl gene “Glivec”
- Biological therapy (CD20) – “Mabthera”
- Stem cell rescue
- Allogeneic transplantation
- Radiotherapy
Outline the Clinical Assessment of a patient with suspected haematological malignancy?
- What are you looking for on examination? (6)
- Which staging investigations will you consider? (7)
Clinical Assessment
- Bone marrow failure (Hb, WCC, platelet)
- Systemic process weight loss, night sweats
- Excess proliferation leading to organ enlargement/involvement, vessel occlusion
- Examination
- Review Histology
- Staging and prognosis
Acute Leukaemia
- Morphological classification?
- Clinical features?
- 3 Prognostic factors?
Acute Leukaemia
1. FBC changes
2. Bone marrow failure
3. Coagulopathy
4. CNS involvement
5. Oportunistic infection
Prognostic factors:
1. Age
2. WCC (higher = worse)
3. Type/ Cytogenetic abnormality/ Mutational analysis
Treatment of Acute Leukaemia
- Acute Lymphoblastic Leukemia? (5)
- Myeloid?
Treatment of Acute Lymphoblastic Leukaemia
1. Intensive chemotherapy for 6-8 months
2. CNS prophylaxis
3. CR 80-90% long term 40-50%
4. Stem cell uncertain role
5. Allogeneic transplantation if high risk
If a patient presents with lymphadenopathy, what do you need to describe?
- 3 differentials?
Lymphadopathy
1. Location
2. Age
3. Consistency
4. Associated features
DDx
1. Lymphoma
2. Chronic lymphocytic leakaemia (FBC)
3. Others (connective tissue, infective)
Lymphoproliferative disorders
- List 4?
- What investigation should you order?
- Which disease are they associated with?
- Outline the Rai and Binet staging of CLL?
Lymphoproliferative disorders
1. Chronic lymphocytic leukaemia
2. Prolymphocytic leukaemia
3. Hairy cell leukaemia
4. Circulating lymphoma
- Blood film and flow cytoemtry for T and B cell antigens important
- Associated with autoimmune disease (Haemolytic anaemia)
Chronic Lymphocytic Leukemia
- Treatment?
- Evolution of CLL treatment — from chemoimmunotherapy to targeted
and individualized therapy?
Treatment of CLL
- Treat symptoms - no impact on survival
- Monoclonal antibody CD20
- Mabthera plus cyclophoshamide and fludarabine
- Targeted therapy Ibrutinib, venetoclax
- Immunosuppression
Staging of Lymphoma/Hodgkins Disease?
Lymphoma
- Histology important (T and B cell)
- Non Hodgkins and Hodgkins Lymphoma
- Stage important
- Bulky, B symptoms, abnormal blood count, high LDH
- Treatment radiotherapy, chemotherapy, biological therapy
Non-Hodgkin’s Lymphoma
- 3 types/grades?
- Compare follicular vs. large cell (8)?
Hodgkins Lymphoma
- Which cell type?
- Epidemiology?
- What determines treatment intesity?
- Treatment options?
- What should you try to minimise?
Hodgkins Lymphoma
- Reed Sternberg Cell (malignant B cell)
- Bimodal peak age
- Histology important
- Stage determines intensity of treatment
- Curable with chemotherapy >80% depending on stage, B symptoms, LDH, cell counts, albumin
- Radiotherapy used in bulky disease/ early stage
- Minimising long term side effects fertility, second cancer, heart disease
Multiple Myeloma
- What is it?
- Clinical features?
- Treatment targets?
Multiple Myeloma
- Plasma cell tumour
- Paraprotein plasma/urine
- Lytic lesions, hypercalcaemia
- Renal involvement, bone marrow failure
- Stage B2 microglobulin, albumin
- Treatment chemotherapy, thalidamide/ lenolidamde, bortezomib /anti CD38/other
- Biphosphonates
- Improved outlook
- MGUS versus smouldering myeloma
- CRAB = Calcium, Renal, Anaemia, Bone
Myeloproliferative disorders
- List 5?
- Clinical features?
- Treatment?
- WHO classification?
Myeloproliferative Disorders
Myeloproliferative neoplasms (MPN) are a group of hematological malignancies characterized by clonal proliferation of bone marrow stem cells and are classified into subgroups, including polycythemia vera, essential thrombocythemia (ET), primary myelofibrosis, chronic myeloid leukemia, and MPN unclassifiable. While the risk of developing acute myeloid leukemia is well known in patients with MPN, over the past 10 years, various studies have also reported on the increased risk of other cancers.
- Abnormal FBC
- JAK 2/Calreticulin/mpl mutation
- Splenomegaly
- Thrombosis and bleeding
- Treatment: hydroxyurea, jak2
inhibitors venesection, anticoagulants, anti-platelet
Myelodysplastic disorders
- Clinical features?
- What is MDS?
- MDS Scoring and Treatment?
Myelodysplastic disorders
- Common in elderly age
- Present with anaemia, infection, bleeding or organomegaly
- Half asymtomatic
- Can be secondary to chemotherapy
Myelodysplastic syndrome (MDS) is a heterogeneous group of hematologic neoplasms classically described as a clonal disorder of hematopoietic stem cells leading to dysplasia and ineffective hematopoiesis in the bone marrow. Some patients with MDS may have a transformation into acute myeloid leukemia (AML).
