Haematology
What is the staging criteria utilised for a SOLID ORGAN tumour? Describe the staging criteria with relevant numerics.
TNM Classification:
T: Tumour (T1 - T4) Describes the size of the primary tumour and how far it has invaded into the organ or surrounding tissues.
N: Node (NX - N2b) Indicates whether the cancer has spread to regional lymph nodes.
M: Metastasis (M0 - M1c) Denotes whether the cancer has metastasized to distant organs or tissues
What is the mechanism behind Bilateral Eyelid Oedema in Primary Hypothyroidism?
Mechanism
What is an Aschoff Body?
- Cluster of T-Lymphocytes, Occ. Plasma Cells, & Activated Macrophages (Anitschkow Cells).
- Pathognomonic for Rheumatic Heart Disease.
What is the purpose behind the Abdominojugular Reflux Test? What is a positive AJRT?
A sustained rise in JVP of ≥3 cm throughout abdominal compression (typically maintained for at least 10 seconds).
Why are Ca2+ Channel Blockers contraindicated in Pre-excited Atrial Fibrillation (e.g., Wolff–Parkinson–White syndrome)?
Calcium channel blockers (particularly verapamil and diltiazem) are contraindicated because they slow conduction through the AV node but do not slow conduction through the accessory pathway. This can force more atrial impulses down the accessory pathway, resulting in extremely rapid ventricular rates, degeneration into ventricular fibrillation, and sudden cardiac death.
An accessory pathway (the bundle of Kent) provides an alternative electrical connection between the atria and ventricles.
Unlike the AV node, this pathway:
As a result, impulses can bypass the AV node and directly activate the ventricles.
Q: I stand at the gateway, first in the line, Uniting two partners by metabolic design. When iron-rich treasure and haem abound, My work slows down and I'm scarcely found. Yet when red pigment is needed anew, The pathway looks first and foremost to who?
What am I?
ALA Synthase
The pituitary calls, but I answer with little. TSH climbs high while my hormones dwindle. Weight may increase, reflexes slow their race, And cold becomes an unwelcome embrace. What am I?
Hypothyroidism
Otitis media is most common in which patient age demographic?
1. Children (<2 Years of Age (Peak Incidence: 6 - 18 Months Old)
2. Common in First Nations Children
What are the 4 locations you will check for bony tenderness in a haematological checklist?
Clavicles and sternum, shoulder girdles, spine, and pelvis
A patient has Severe Malaria despite taking chemoprophylaxis. Provide five varying explanations.
1. Poor adherence to chemoprophylaxis (most common)
Chemoprophylaxis is only effective if taken correctly.
Examples include:
Mechanism: Drug concentrations fall below therapeutic levels, allowing blood-stage parasites to multiply.
2. Drug-resistant parasites
The infecting parasite may have reduced susceptibility to the prophylactic drug.
Examples:
Mechanism: The parasite survives despite adequate drug levels and continues its lifecycle.
3. Inadequate drug absorption or reduced bioavailability
Even if the patient is adherent, sufficient blood concentrations may not be achieved.
Causes include:
Mechanism: Subtherapeutic plasma concentrations fail to suppress parasite replication.
4. Incorrect prophylactic regimen for the destination
The chosen prophylaxis may not have been appropriate for local malaria epidemiology.
Examples:
Mechanism: The prophylactic agent is ineffective against the local parasite population.
5. No chemoprophylactic drug is 100% protective
Current prophylactic agents primarily suppress the blood stage of malaria and reduce, but do not eliminate, the risk of infection.
Factors increasing the chance of breakthrough infection include:
Mechanism: Despite adequate prophylaxis, some parasites successfully establish blood-stage infection and proliferate.
Name ONE Anthracycline & outline their MOA.
1. Doxorubucin, Epirubicin (derv. Streptomyces spp.)
2. Cell Cycle Non-Specific Cytotoxic (Intf. w/ DNA Metabolism)
- Inhibit Topoisomerase II Enzyme (Allows for DNA Repair)
- Prevents relaxation of Supercoiled DNA, Blocking Transcription/Replication
What is the additional effect of propylthiouracil (PTU) compared to carbimazole?
It has an additional effect of preventing the conversion of T4->T3 in the peripheral tissues.
Infective Endocarditis is most commonly caused by which three microorganisms? Bonus points for their origin.
1. Streptococcus viridans (Oral Cavity Flora)
2. Staphylococcus aureus (Skin Commensal)
3. Enterococci (GIT Flora)
4. HACEK Group (Oropharyngeal Flora)
Describe the sounds of auscultations associated with Mitral Regurgitation.
Mitral regurgitation produces a high-pitched, pansystolic (holosystolic) murmur that begins with S1 and extends to S2 without changing intensity. It is best heard at the cardiac apex using the diaphragm of the stethoscope and typically radiates toward the left axilla.
What are the features of Papillary Carcinoma?
1. Psammoma Body
2. Enlarged Overlapping Nuclei with Pale/Empty Appearing Chromatin ("Orphan Annie Eye" Nuclei")
3. Associated w/ Prior Ionising Radiation Exposure
Incidence: 25 - 50 Years of Age, Asymptomatic Thyroid Nodule w/ Enlarged Cervical LN.
I am a neoplasm, chronic and slow, Making haematocrit and haemoglobin grow. Erythropoietin falls, but production won't cease, For mutated kinase signalling grants no relief. Splenomegaly may join me, and clotting may ensue What myeloproliferative disorder am I to you?
Polycythemia vera
What are the names of the proteins that T3 and T4 bind to in the bloodstream?
Albumin, thyroxine binding globulin, and transthyretin
What is the standard treatment given to someone who presents with chest pain and whose ECG is normal?
300mg aspirin orally, GTN, IV morphine for pain
Name all the required symptoms you need to ask for in the Haematological Checklist
Fatigue, Light-headedness/dizziness, Dyspnoea, Bruising, Exanthem, Pruritus, Bleeding, Lymphadenopathy, Bone Pain, Recurrent Infection, B-Symptoms
A 56-year-old man is diagnosed with Chronic Myeloid Leukemia and is found to have the BCR-ABL fusion gene resulting from the Philadelphia chromosome [t(9;22)]. Following treatment with a tyrosine kinase inhibitor, he achieves complete clinical remission.
Five years later, highly sensitive PCR testing still detects the BCR-ABL fusion gene in a small population of bone marrow cells.
Explain why the continued presence of the BCR-ABL fusion gene does not necessarily indicate active leukaemia.
The presence of the BCR-ABL fusion gene indicates that the genetic mutation is still present, but the presence of a gene does not necessarily mean it is actively expressed. Disease depends on gene expression, not simply the DNA sequence.
For BCR-ABL to drive leukaemia, the fusion gene must first be transcribed into mRNA and then translated into the constitutively active BCR-ABL tyrosine kinase protein. If transcription is reduced or absent, little or no oncogenic protein is produced, limiting its biological effect.
Gene expression depends on several regulatory mechanisms. An accessible promoter is required for RNA polymerase II and general transcription factors to assemble and initiate transcription. Enhancers and activator transcription factors further increase transcription, whereas repressors reduce it.
Epigenetic modifications can also silence gene expression without altering the DNA sequence. For example, DNA methylation of promoter CpG islands recruits methyl-CpG-binding proteins and histone deacetylases (HDACs), producing condensed chromatin that is inaccessible to the transcriptional machinery. Conversely, histone acetylation relaxes chromatin and promotes transcription.
In this patient, residual cells containing the BCR-ABL fusion gene may remain transcriptionally inactive, produce minimal oncogenic protein, or exist as dormant leukaemic stem cells that are not actively proliferating. In addition, the tyrosine kinase inhibitor prevents the BCR-ABL protein from signalling even if small amounts are produced, suppressing uncontrolled cell division.
Therefore, gene sequence alone does not determine phenotype. The development of disease depends on whether the gene is expressed, how it is regulated, and whether the resulting protein is functionally active. This illustrates the distinction between genetics (DNA sequence) and gene regulation/epigenetics (control of gene expression)
I masquerade as iron deficiency, yet iron is not my plight. My MCV is low, but ferritin may be just right. One globin chain is lacking, while its partner accumulates, Causing ineffective erythropoiesis and destruction at the gates. What haemoglobin disorder am I?
Thalassemia
What are the names of the 8 branches that arise from the external carotid artery?
Superior thyroid, ascending pharyngeal, lingual, facial, occipital, posterior auricular, maxillary and superficial temporal
Name one difference and one commonality between Amiodarone & Sotalol?
1. Commonality: Both Amiodarone and Sotalol are Class III Antiarrhythmic drugs that prolong cardiac repolarisation by blocking potassium (K⁺) channels, increasing the action potential duration and effective refractory period. Both are used to treat atrial and ventricular arrhythmias and can prolong the QT interval, increasing the risk of Torsades de Pointes.
2. Difference: Sotalol also has Non-Selective β-Blocking (Class II) Activity, whereas Amiodarone has actions from all four Vaughan Williams classes (I, II, III, and IV).
Name ALL additional testing required following a Cardiovascular PES Examination.
1. Height, Weight, BMI
2. Urinalysis, Fundoscopy
3. ECG
4. Fluid Balance Chart
5. Test for Postural Hypotension
5. Blood Glucose Level
Tay–Sachs Disease has a carrier frequency of approximately 1 in 30 in the Ashkenazi Jewish population. Using principles of Population Genetics, explain why the carrier frequency of Tay-Sachs Disease has remained relatively high in this population despite the disease being fatal in early childhood.
A small ancestral population carried the pathogenic HEXA variant at a relatively high frequency (Founder Effect). Over generations, Genetic Drift allowed the allele frequency to remain elevated, while limited gene flow due to endogamy reduced the introduction of alternative alleles.
Although affected individuals (aa) have reduced reproductive fitness, heterozygous carriers (Aa) are asymptomatic and reproduce normally. As a result, natural selection removes affected individuals but has little effect on the mutant allele when it is carried in heterozygotes.
Together, these population genetics mechanisms explain why the Tay-Sachs allele has persisted at a relatively high frequency despite the disease's severe phenotype