The Physician Project

THE PHYSICIAN PROJECT
A Rapid Review of High Yield Facts For the Written Examination
Written by:
Robin Sia
Contributions from:
Amanda Ma, Benjamin Massouridis & Harley Owens
1 | The Physician Project

Hello!
We’re a group of physician trainees who found that the process of preparing for
the exams can be a long road and the content needed to cover is endless. It is not
possible to learn every single topic in detail but it is vital to cover the basics and
have the foundation to work out the answers. We hope this provides a guide into
what topics are essential and more detailed reading can be done around them,
but can also provide a quick reference and refresher prior to the exams.
The information has been referenced from various resources throughout

preparation (and it’s tricky to keep track of all of them, hence some have no
references) and if by chance there is a mistake or an issue, please do not hesitate
to reach out to my email below. If you think this is helpful, feel free to share
with your colleagues or juniors as we hope to help as many trainees as possible.
Good luck for the preparation, just remind yourself that you’re becoming a
better clinician and physician day by day (plus, this will help in the clinical
examination too). You’ll do great for sure!
Special thanks to Northern Health DPEs Dr Yana Sunderland, Dr Edwina

Holbeach, Dr Mueed Mian and Dr Vinita Rane for providing support and
approval for this document to be distributed.
Best wishes,
Robin Sia
BPT3 Trainee & Medical Registrar
Email: robinsiawaijen@gmail.com
© Robin Sia 2023

Disclaimer: Information in this document may change with new and rapidly advancing
research and evidence-based medicine. Hence, it is essential to stay up to date with new
articles. This document is by no means extensive and you should still do your own revision
around the topics. No material from this document can be reproduced, adapted, distributed or
stored in an electronic retrieval system or transmitted without the written consent from the
author. This document is also not for sale.

Table of Contents
Cardiology..................................................................................................................................4
Dermatology.............................................................................................................................14
Endocrinology..........................................................................................................................15
Gastroenterology......................................................................................................................21
General Medicine.....................................................................................................................29
Genetic and Metabolic Medicine.............................................................................................31
Geriatric Medicine...................................................................................................................38
Haematology............................................................................................................................40
Immunology and Allergy.........................................................................................................49
Infectious disease.....................................................................................................................50
Medical Obstetrics...................................................................................................................58
Medical Oncology....................................................................................................................62
Nephrology...............................................................................................................................71
Neurology.................................................................................................................................84
Palliative Medicine..................................................................................................................92
Pharmacology, Toxicology and Addiction Medicine..............................................................93
Respiratory and Sleep Medicine..............................................................................................97
Rheumatology........................................................................................................................104
Statistics.................................................................................................................................118

Cardiology
Heart Failure
HFrEF HFpEF
- Symptoms and signs of HF AND - Symptoms and signs of HF
LVEF<50% - LVEF>50%
- Objective evidence of heart disease
HFmrEF (Structural, diastolic dysfunction on
- EF 41-49% (treat as HFrEF although cardiac cath, ECG, echo, stress test
less evidence) or NTproBNP)

Cardiomyopathies
1. Ischaemic Cardiomyopathy
2. Non-ischaemic Cardiomyopathy (Hereditary and Acquired)
- Chemotherapy-related: Anthracycline, platinum-based agents and taxanes, 5FU,
cyclophosphomide, HER2, TKI
- Hypertrophic Cardiomyopathy (HCM)
- 50% genetics
- Variants: Asymmetrical septal, mid-ventricular, apical and concentric
- Pathophysiology: Muscle hypertrophy leading to LV outflow obstruction
causing diastolic dysfunction and arrhythmias which may lead to SCD.
Associated with myocardial bridging
- Ix: ECG, TTE, CMR, Genetic studies
- RF for SCD: Family history, recurrent syncope, NSVT, LVH>3cm, severe
obstruction, hypotension, left atrial size, specific genotypes
- Treatment: Pharmacological (Beta-blockade, Amiodarone), Device(AICD)
- Cardiac amyloid
- Pathophysiology: Beta-pleated sheets with deposits of fibrils
- Multiple types of amyloid - most common TTR amyloid
- Usually HFpEF, may be associated with hepatomegaly, periorbital purpura
- Ix: SFLC/SPEP, Congo red stain on tissue, TTE (Increased LV wall thickness,
diastolic dysfunction, dilated atria, abnormal longitudinal strain, small
pericardial eff, pulmonary HTN and speckled myocardium) , bone scan and
TTR gene sequencing
- Rx: HF - usually diuretics, ACEI and beta-blockade +/- anticoagulation
- AL Amyloid - chemotherapy ie for MM
- TTR amyloid - Tafamidis
- Restrictive Cardiomyopathy
- Predominantly Right-sided Heart failure
- Etiology can be infiltrative diseases, radiation, primary
- LV function preserved with mainly diastolic dysfunction
Functional tests for Ischaemia
Modality Sensitivity Specificity
Exercise ECG 68% 77%
Exercise Echo 86% 81%
Dobutamine Echo 85% 85%
Exercise nuclear 87% 73%
Pharmacological 89% 75%

nuclear
Cardiac CTA 95% 83%

Cardiac Physiology
JVP Waveform
Source: ESC 2015

JVP Waveforms in different pathology
Source: https://www.mdpi.com/2075-4418/12/10/2407

Source: http://www.pathophys.org/physiology-of-cardiac-conduction-and-contractility/
Duke’s Criteria for Infective Endocarditis
Major criteria Minor Criteria

1) Blood culture positive for typical 1) Predisposing heart condition
microorganism (staph aureus, 2) Intravenous drug use
enterococci, streptococcus 3) Temperature >38
viridans) 4) Immunological phenomenon (Osler’s
2) Echocardiogram showing valvular nodes, Roth Spots, Rheumatoid factor,
vegetation* Glomerulonephritis)
5) Vascular phenomenon (Janeway lesions)
6) Positive blood culture not meeting above
criteria
7) Echocardiogram finding not meeting
major criteria**
Definite IE: 2 major criteria OR 1 major + 3 minor criteria OR 5 minor
Possible IE: 1 major + 1 minor criteria OR 3 minor criteria
Rejected IE: Does not fulfil criteria above
*Vegetations, Abscess and dehiscence of valve, new valvular regurgitation
** Findings not meeting major criteria
Endocarditis prophylaxis

Endocarditis surgery indication
Source: ESC 2015

Valvular Disease Features
Aortic Stenosis Symptoms: CP, HF, Syncope

- True AS
- LFLG Signs: ESM, Slow rising pulse, aortic thrill, late peaking murmur, S4,
- Paradoxic paradoxical split S2, delayed PMI, narrow pulse pressure
al LFLG
Causes: Calcified, Bicuspid
*Refer to ESC guidelines for AS algorithm
Aortic Nocturnal chest pain

Regurgitation
Signs: Wide pulse pressure, water-hammer pulse, EDM @ Left LSE,
S3, soft S2, Austin flint murmur.
+ Multiple extracardiac manifestations ie Quinke’s, Corrigan’s
etc.
Causes; Degenerative, Endocarditis, Aortopathy (Marfan’s, EDS,

LDS), AxS, Rheumatic HD
Mitral Primary: Leaflets, MVP, RHD, CTD, Congenital, mitral annular

Regurgitation calcification
Secondary - functional from LV failure
Acute MR - infarct with flash APO (Rx: ECMO and IMPELLA)
Signs: Split S2, S3, Pansystolic murmur, pHTN
Rx: Mitraclip, MVR
Mitral Stenosis Signs: Malar flush, prominent A wave, mid-diastolic murmur, tapping
apex beat, small pulse pressure, snap close to S2, AF, pHTN
Causes: RHD, Calcific, congenital, endomyocardial fibroelastosis
Rx: Anticoagulation (risk of AF), diuresis, mitral commissuroplasty,

PBMV, MVR
Tricuspid Primary: IE, RHD, Carcinoid, Ebstein’s, Iatrogenic

Regurgitation Secondary - functional
Signs: PSM, Prominent v wave on JVP, pulsatile liver, pHTN
Pulmonary Sequelae of TOF (important for short case)

Regurgitation
Rx: Transcutaneous pulmonary valve implantation (TPVI)

Cardiac Genetics
Cardiomyopathies
1) HOCM
- Septum >15mm
- Genes: MYH7 and MYBPC3
- Rx: Medications (Amiodarone, Beta-blockade, avoid Digoxin), ablation and ICD
- HOCM Phenocopies: Noonan’s, Fabry’s, Glycogen storage disorders, Friedrich’s,
Amyloidosis, Sarcoidosis, Mitochondrial, Haemochromatosis
2) Dilated Cardiomyopathy
- 50% genetic component
- Gene: TTN, LMNA
- Associated with Alstrom syndrome, Barth syndrome, Muscular dystrophy,
Mitochondrial disorders and Metabolic disorders
3) ARVC
- Epsilon waves on ECG
- Fibrofatty infiltration
- PKP2 gene
- Associated with Naxos Disease
4) Left Ventricular Non-Compaction Cardiomyopathy (LVNC)
5) Restrictive Cardiomyopathy
Arrhythmias
1) Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT)
2) Long QT syndrome
- Risk of TdP
- Genes: KCNQ1, KCNH2, SCN5A
- Associated with Romano-Ward syndrome, Jarvell-Lienge Nilson syndrome,
Timothy Syndrome, Anderson-Tewill syndrome
3) Brugada Syndrome
- Types 1 to 3
- Ajmalin/Flecainide provocation test
- Gene: SCN5A
Aortopathies
1) Familial TAAD
- Associated with CoA, BAV, PDA, Cerebral aneurysms
- VSMC gene
2) Marfan’s
- FBN1 gene
- For more details - see Genetics section
3) Loeys-Dietz Syndrome
- TGFBR1, TGFBR2 genes
- Associated with Bifid Uvula, cleft lip and palate and aneurysms

Common Cardiology Medications
Drug Indication Side-effects Additional info
Entresto HFrEF Hyperkalemia Trial of ARB first in

(Saccubitril/Valsartan) Hypotension HFrEF and if
Angioedema (Need tolerating then
to washout with convert to Entresto.
ACEI for 36 hours)
PCSK9 inhibitor - Refractory Flu-like symptoms, Reduces total LDL

- Evolocumab hypercholesterolem rash by reducing LDL
- Alirocumab ia despite receptor
maximum statin Decreases risk of
and ezetemibe MI, stroke and
-Familial MACE
Inclisiran Familial Look at it as a “6

hypercholesterole- monthly injection of
mia PCSK9i”
P2Y12i: Second antiplatelet -Bleeding -Preferred agent over

-Clopidogrel agent in ACS, -Ticagrelor - aspirin when using
-Prasugrel Strokes. Bradycardia and with NOAC
-Ticagrelor dyspnea -Ticagrelor causes
bradycardia and
dyspnea (due to
bradykinin
accumulation)
-Prasugrel is off the
market at this
moment (similar
efficacy as
Ticagrelor but higher
bleeding risk)
SGLT2i HFrEF & HFpEF, -Euglycemic Previously used in

-Dapagliflozin T2DM, CKD, Ketoacidosis T2DM now used in
-Empagliflozin IgAN, OSA -Fournier’s gangrene CVD (DAPA-HF,
-Canagliflozin -Mycotic UTI DELIVER, EMPA-REG,
EMPEROR-HF), CKD
-Sotagliflozin -Autoamputation (DAPA-CKD), OSA
(VERTIS).
Dapagliflozin:
eGFR>25
Empagliflozin:
eGFR>30
Not to be used in
T1DM (risk of
ketoacidosis)

Ivabradine -HFrEF (EF<35% Visual changes, Inhibits lf current
and HR>77bpm) bradycardia
-Stable angina Can be used prior to
CTCA for HR target
<70bpm
Nicorandil Anti-anginal Hypotension Activates potassium

(especially when channel
combined with
nitrates)
Amiodarone -AF (Rhythm -Drug-induced liver Can be used in AF

control) injury for rhythm control in
-Monomorphic VT -T1AIT, T2AIT selected patients by
-ILD inhibiting potassium
-Photosensitivity channels.
-GIT
-CNS (Tremor, PN) Many trials now
-Corneal have supported
microdeposits rhythm over rate
-Slate-grey skin control (EAST Trial)
pigmentation
Others (extra reading):
-Tafamidis
-Patisiren
-Canakinumab
-Rilonacept
-Volanesorsen
-Vericiguat
-Omecamtiv Mecarbil
-Mavacamten
-Icosapent Ethyl
-Dobutamine
-Noradrenaline
-Levosimendan
-Anthracyclines, taxanes, platinum-based chemotherapy and HER2 antagonist on
cardiotoxicity
-CYP and P-gp interactions with common CVD drugs (important for long case)

Anticoagulant MOA PK Antidote Monitoring
Warfarin Vit-K oral Interacts with Vitamin K, INR

antagonist CYP2C9 prothrombinex
Apixaban Factor X CYP3A4 -Andexanet alfa Apixaban factor

inhibitor -Supportive Xa levels
(FFP as volume
expansion)
Rivaroxaban Factor X CYP3A4 -Andexanet alfa Rivaroxaban

inhibitor -Supportive factor Xa levels
(FFP as volume
expansion)
Dabigatran Factor II P-gp -Idarucizumab Thrombin Time

inhibitor -HDx
Vasopressors/Inotropes
Alpha-1 Beta-1 Beta-2
Adrenaline ++ +++ ++
Noradrenaline +++ +++ +
Dobutamine + +++ ++
Dopamine +++ ++ +
Isoprenaline 0 +++ +++

Dermatology
Source:https://www.grepmed.com/images/12660/diagnosis-pemphigoid-bullous-comparison-vulgaris
Skin Cancer
Basal Cell Carcinoma (BCC) Squamous Cell Carcinoma (SCC)

- Most common skin cancer - Second most common skin cancer
- Shiny pearly papule or nodule - Hyperkeratotic lesion with crusting and
- Umbilicated centre and telangiectasias ulceration
- Locally invasive and destructive - Indurated, scaling, erythematous papules
- Slow growing that occasionally ulcerate or bleed
- Bleed easily - Commonly occur on sun exposed areas but
- Located exclusively on hairy skin, also oral mucosa, oesophagus, cervix,
commonly nose vagina, lungs and anus
- More common in immunosuppressed
people
- Less than 5% metastatise to regional
nodes, generally deeply invasive and
involve subcutaneous tissue

Endocrinology
Maturity onset diabetes of the young (MODY)
Type Gene defect Frequenc Beta cell defect Features Treatment
y
1 HNF4-alpha <10% Reduced insulin Normal renal SU
secretory response to threshold for
glucose glucose
2 Glucokinase 15-31% Defective glucokinase Mild, stable, Diet
gene molecule resulting in fasting
impaired insulin hyperglycaemi
response to glucose a
3 HNF1-alpha 52-65% Abnormal insulin Low renal SU
secretion threshold for
glucose +
glycosuria
4 IPF1 Rare Reduced insulin gene Rare,
activation in response pancreatic
to hyperglycaemia agenesis
5 HNF1-beta Rare Pancreatic Insulin
atrophy, renal
dysplasia
6 NEUROD1 Rare Pancreatic Insulin
development
Bone disorder Features
Osteoporosis Low bone mass, architecture and risk of fracture - T-score <-2.5
RF: Age, menopause, concurrent illness, medications (steroids,

Tenofovir – TDF), EtOH & smoking, low BMI
Rx:
Non-pharmacological - vision, proprioception, balance, falls risk
Pharmacoligcal therapy:
- Vit D replacement
- Antiresorptives - Bisphosphonates, Denosumab, SERM,
HRT
- Anabolic agents - Romosozumab, Teriparatide
*overall important topic for long case issues list
Osteomalacia Bony pain
Causes: Vit D def, Hypophosphatemia, tumour induced, genetics

Ix:
Consider urine PO4
Low phosphate
Elevated ALP
Iron-infusion induced hypophosphatemia

- FGF23 affected - increased in Fe def and Fe infusion
prevents cleavage which causes elevated urinary PO4
excretion esp in Iron polymaltose and carboxymaltose
Paget’s disease Imbalance of osteoclast and osteoblast
Risk of osteosarcoma, HF
Rx: Bisphosphonates, calcitonin, analgesic, surgery
Hypercalcemia Causes:
- PTH dependent ( HyperPTH, FHH, autoimmune)
- PTH independent (Cancer, granulomatous disease, milk
alkali syndrome, endocrinopathy, immobilisation)
Pituitary Disorders
Work-up Panel (Determine if secretory)

ACTH (Insulin Tolerance Test)
GH (Insulin Tolerance Test, Glucagon stimulation test)
Prolactin
TSH, fT3, fT4
LH and FSH
SHBG
Symptoms:
Visual field defects
Extraocular muscle palsy
Headache
Bitemporal hemianopia
Sequelae of endocrinopathy (Amenorrhea, decreased libido,
Infertility, DI, Apoplexy)
Consider secondary causes of non-adenoma (cysts, infections,

neoplasm, vascular, inflammatory, infection, metastases,
miscellaneous)
If microadenoma - follow-up MRI 1,2,5 years

If macroadenoma - consider transsphenoidal surgery
Non-functioning Prolactin can be high due to stalk pressure

pituitary adenoma Can recur
Most common
Prolactinoma Hypogonadism
Very high prolactin
Rx: Dopamine agonist - bromocriptine, cabergoline
Acromegaly Ix: IGF-1, OGTT
Rx: Octreotide (Somatostatin analogue), Pegvisomant (GH receptor

antagonist)
Surveillance:
- Cancer surveillance - thyroid and colonoscopy
- Cardiovascular disease
Cushing’s disease Hyperpigmentation can occur due to melanocyte-stimulating

hormone, skin striae and easy bruising
Ix: 24h UFC, midnight salivary cortisol, dexamethasone

suppression test, ACTH levels, CRH stimulation, MRI, BIPSS
Rx:
- Medical - Pasireotide, Cabergoline
- Surgical - Bilateral adrenalectomy, pituitary radiotherapy
TSHoma Often T3,T4 and TSH are all high
Diabetes Insipidus Types: Central, nephrogenic

DDx: Primary polydipsia
Ix: Water deprivation test, DDAVP, Copeptin levels
Others to read Pituitary Apoplexy

about Craniopharyngioma
Lymphocytic hypophysitis
Familial (MEN1, AIP, p27 and PPKAR1A)
Thyroid disorders
Grave’s disease Autoimmune process - anti-TSHr Ab
Signs and symptoms: Thyroid acropachy, Exophthalmos (Grave’s

orbitopathy) and pretibial myxedema
Grave’s orbitopathy - increased fibroblast and worsens with

radioactive iodine or smoking, can be treated with steroids or
teprotumumab
Can occur with iodine exposure

Usually safe in pregnancy, may reactivate after

Management: Propranolol, Thionamides ie Carbimazole & PTU,
Iodine-131, Surgery
Thyroid nodule If TSH normal - FNAB
If TSH Abnormal - Uptake scan -

> not hot -> FNAB
-> hot - treat with iodine-131 (toxic adenoma)
Thyroiditis Can be caused by drugs*, post-partum, infection (De Quarvain’s)
Rx: Propranolol, pain relief
Amiodarone induced thyroiditis (AIT):

- Type 1 - iodine related
- Type 2 - inflammation/destruction
- Can be hypothyroidism
- Rx: Stop Amiodarone, Thionamide + Steroids +/-
Cholesthyramine
- Can’t use technetium scan as amiodarone interferes with
receptors
*Drugs that may affect the thyroid- Amiodarone, Lithium,

Alemtuzumab, Immunotherapy, Tyrosine-kinase inhibitors,
IFNalpha
Subclinical Low TSH, normal T3/T4

hyperthyroidism
Can still cause osteoporosis and AF
Subclinical High TSH, normal T3/T4

hypothyroidism
Treat if TSH>10 or pregnancy, other considerations if age<65,
hyperlipidaemia, heart failure, positive antibodies
Thyroid malignancy Types:

1) Papillary - MEN1 gene, rx with BRAF/RAS inh
2) Medullary - MEN2A/2B (RET gene) - Calcitonin as marker.
Selpercatinib*
3) Follicular
4) Anaplastic - Poor prognosis
Rx: Stage the cancer, consider surgery

Radioiodine or T3 (Tertroxine) can be used for remnant cancer
Lenvatinib (Anti-VEGF TKI)
Selpercatinib (RET inh)*
Thyroglobulin is a good marker for monitoring disease progress

Investigation panels
Endocrinopathy Investigation
Hyperthyroidism 1)TFTs, fT3, fT4
2)Anti-TSHr Ab – Grave’s
3)Anti-TPO, Thyroglobulin Ab – Hashimoto’s
4)Thyroid uptake scan – Increases in Grave’s and MNG.
Reduces in thyroiditis.
Cushing’s 1) 24 hour urinary cortisol, late night salivary cortisol, low
dose dexamethasone suppression test
2) ACTH levels
3) ACTH dependent – high dose dexamethasone suppression
test, CRH stimulation test, MRI-pituitary & bilateral inferior
petrosal sinus sampling (BIPSS)
Pituitary apoplexy Pituitary screen (Prolactin, TSH, LH/FSH, ACTH) & MRI-
Pituitary
Look for Adrenal insufficiency – Early AM cortisol, Short

Synacthen test and Insulin Tolerance Test (ITT)
Osteoporosis DEXA Scan, Scout films
Marker of bone turnover: CTX, P1NP, Bone ALP

Diabetes Insipidus Urine osmolality and serum osmolality
1)Water Deprivation Test

2) DDAVP
3) Copeptin levels
Testosterone deficiency Low or normal FSH/LH, low free testosterone
(hypogonadotropic hypogonadism) – Kalman’s syndrome
High FSH/LH, low free testosterone – Klinefelter’s syndrome

Acromegaly IGF-1 gold standard
GH (fluctuates) and OGTT can be considered
MEDICATIONS
Oral Hypoglycaemic agents
Class Agents Mode of Action Side effects
Biguanides Metformin AMP Kinase activator GI symptoms, B12
deficiency, Lactic
Acidosis
Sulphonylureas Gliclazide, Katp channel Weight gain,
Glibenclamide hypoglycemia
Thiazolidinediones Glitazone PPARgamma agonist Heart failure
Bladder ca
Alpha-glucosidase Acarbose Flatulence

inhibitor
DPP-4 inhibitor Sitagliptin, Inhibitor of DPP4 Acute pancreatitis,
Linagliptin enzyme hence increasing weight neutral, no
GLP1/GIP CVD/CKD benefit.
Linagliptin can be
used in renal failure.
Saxagliptin can
cause heart failure
GLP-1 agonist Semaglutide, Promotes incretin Nausea and
Liraglutide vomiting. Benefit in
MACE.
SGLT2 inhibitor Empagliflozin, Inhibits SGLT2 at PCT UTI esp candida,
Dapagliflozin – hence promoting Fournier’s gangrene,
glycosuria and TG Euglycemic
feedback. Multiple Ketoacidosis,
mechanisms for HF and Autoamputation,
CKD. Atypical fractures
Antithyroid agents
Thionamide Propylthiouracil Additionally blocks Fulminant
(PTU) conversion from T4-> inflammatory
T3 (useful in thyroid hepatitis
storm)
Safe in pregnancy
Thionamide Carbimazole Blocks thyroid hormone Non-threatening
synthesis cholestasis,
Agranulocytosis,
MAHA, Vasculitis
Teratogenic - aplasia
cutis, omphalocoele
and other birth
defects.
Can be used in 2nd
and 3rd trimester

Gastroenterology
Inflammatory Bowel Disease
Crohn’s Disease Ulcerative Colitis
Diffuse disease Submucosal disease
Transmural disease Mainly colonic involvement, occasionally
Non-caseating granuloma backwash ileitis
Rectal involvement
Complications: Perianal fistula, strictures, Bloody diarrhea
fissures
Rx:
Rx (MORE COMPLEX): 5ASA (oral or rectal)
Early TNF inhibition preferred Steroids
No role of 5-ASA drugs Thiopurines (AZA, MMF)
MTX vs AZA can be considered for
induction
Tacrolimus (fistula)
Anti-TNFs (Infliximab, Adalimumab,
Golimumab)
Vedolizumab (MAd-CAM-1)
Ustekinumab (IL-12/23)
Tofacitinib (JAKi) Anti-TNFs (Infliximab, Adalimumab,
Golimumab)
Vedolizumab (MAd-CAM-1)
Ustekinumab (IL-12/23)
Tofacitinib (JAKi)
Others: MTX, cyclosporine (salvage therapy
vs infliximab)
3 main pathophysiology:
- Genetic predisposition
- Environmental (smoking, infection, drugs - NSAIDs, stress)
- Mucosal dysfunction
Inflammatory response
- TNF alpha, IL1, IL6, IFNgamma and IL12/23
Histopathology:
- Granuloma (non-caseating)
- Panneth cell metaplasia
- Crypt disruption
- Basal lymphoplasmacytosis

Extra-GIT involvement:
- Hepatic (choledocholithiasis, cholangitis, PSC)
- Ocular (scleritis, episcleritis, anterior uveitis)
- Pulmonary (Nodules, ILD, blebs)
- Malignancy (Lymphoma)
- SpA
- Skin (Pyoderma gangrenosum, Sweet syndrome, Psoriasis)
Consider other factors in treatment algorithm (important for long case):

- Bone health
- Vaccination
- Cancer surveillance
- Smoking cessation
- Diet (Low fat, low sugar)
- VTE prophylaxis
- Pregnancy
Cancer surveillance in IBD:

- Annual colonoscopy if PSC, FH CRC<50, Dysplastic polyp, stricture
- Every 2-3 years if inflammatory polyps, CRC>50
- Every 5 years of none of the above
Coeliac Disease
Associated with HLADQ2/DQ8
Associated with other autoimmune disease as well (Autoimmune thyroid disease, T1DM)
Other complications:
- Haematological - Fe def anaemia, pancytopenia, hyposplenism, T-cell lymphoma
- Neurological - Peripheral neuropathy, CNS dysfunction, Mood disorders
- Gastrointestinal - oral aphthous ulceration, reflux esophagitis, microscopic colitis,
pancreatic insufficiency, PSC, PBC, Metabolic-Associated Fatty Liver Disease(MAFLD)
- Bones and joints - # and osteoporosis, dental enamel defects
- Skin - Dermatitis herpetiformis
- Obstetric - miscarriage, infertility
- Others: IgAN, Down’s, Turner’s and sepsis
Ix: tTG-IgA, DGP-IgG, small bowel biopsy ( requires ongoing gluten consumption for
maximum yield - villous atrophy, intraepithelial lymphocytes, crypt hyperplasia)
DDx: Infection(Tropical sprue, H.pylori, Giardia lamblia, SIBO), CVID, Crohn’s, Cow’s
milk protein intolerance (CMPI), autoimmune enteropathy, Drugs (Olmesartan, NSAIDs,
MMF)
Subtypes: Non-responsive Coeliac Disease (NRCD), Refractory Coeliac Disease , Non-
coeliac gluten sensitivity
Rx: Gluten-free diet , complication screen and nutrition, family screening, surveillance and
vaccination

Liver Diseases Features
Hepatitis C Often becomes chronic
Target is Sustained Virilogical Response (SVR) - 12 week mark
Extrahepatic:
- Non-Hodgkin’s Lymphoma
- Cryoglobulinaemic vasculitis
- MPGN
- Sicca symptoms
- Porphyria Cutanea Tarda
- Lichen Planus
Ix:
- Screening: HepCAb = exposure, HCV RNA = current
infection
- Fibroscan/APRI
- HCC surveillance
Agents used:
- NS3A/NS4A - Glecaprevir
- NS5A – Valpatasvir
- NS5B - Sofosbuvir
-> Combinations: Sofosbuvir/Velpatasvir (Epclusa) and
Glecapravir/Pibrentasvir (Mavyret)
-> Multiple Drug-drug interaction (important for long case)
Hepatitis B Transmission based on HBe Ag
Ix:
Anti-HBs, HBs Ag, Anti-HBc
*Learn around - immunized vs prev infection vs acute and chronic
infection
Rx:
Entecavir
TDF/TAF
- TDF can cause nephropathy and osteoporosis, Fanconi
Syndrome
Autoimmune ASMA, Anti-LKM1, Anti-SLA/LP

hepatitis (Ab not specific) – gold standard is liver biopsy
Steroids + Steroid sparing immunosuppression
Careful of drugs that can mimic AIH - Minocycline, Isoniazid,

Nitrofurantoin, Methyldopa, PTU

Primary Biliary Fatigue and pruritus
Cholangitis AMA, IgM
Anti- GP210 and SP100
Associated with other autoimmune conditions
Rx: Ursodeoxycholic acid, Cholesthyramine, Rifampicin
Primary Sclerosing Associated with UC

Cholangitis Risk of cholangiocarcinoma and GB cancer
Surveillance is key
DDx: IgG4 cholangitis
Metabolic Liver Metabolic Associated Fatty Liver Disease (MAFLD) –

Disease encompasses NAFLD and Alcoholic Steatohepatitis
Histopathology: Hepatocellular ballooning
MRI can demonstrate steatosis
Fibroscan with FIB-4 score, APRI score
CVD most common cause of death
Rx (minimal evidence): Vit E, CaffeineMediterranean diet,

Pioglitazone, Obeticholic acid (FXR agonist), GLP1
Hepatocellular Surveillance is key - AFP and USS every 6 months

cancer
Quadphase CT will demonstrate arterial hyperattenuation with
venous washout
Barcelona staging and treatment strategy

https://www.journal-of-hepatology.eu/article/S0168-8278(21)02223-6/fulltext
Sorafenib and Lenvatinib

Atezolizumab + Bevacizumab
EtOH liver disease Steatosis -> Fibrosis -> Cirrhosis
Oxidative stress, acetaldehyde as main pathophysiology
Maddrey’s score (prognosis and steroid administration)
Nutrition and abstinence is key

Consider NAC and steroids
Drug-induced liver Intrahepatic:

disease (DILI) Paracetamol (CYP2E1)

- King’s college criteria for transplant
Statins (controversial)
Isoniazid
Rifampicin
Nitrofurantoin
NSAIDs
irAE hepatitis
PTU
Thiopurines
Mixed:
Mostly anti-seizure drugs
Cholestatic:
Antibiotics (Flucloxacillin)
Hormonal therapy
Chronic Liver Signs:

Disease Koilonychia
Clubbing
Palmar erythema
Dupuytren’s contracture
Spider naevi
Complications:
- Nutritional status
- Coagulopathy
- Ascites
- Renal dysfunction (Hepato-renal syndrome)
- Hepatic encephalopathy
- Pulmonary disorder (Shunt)
- Hepatic hydrothorax
- Variceal haemorrhage
- Immune dysfunction
Malnutrition - high protein low salt diet
Sarcopenia
Osteoporosis
HCC
Pregnancy related Preeclampsia

Eclampsia
HELLP
Acute fatty liver of pregnancy
Cholestasis in pregnancy
Haemochromatosis Mutated HFE gene - common mutations C282Y and H63D

Associated with Hepcidin def

Ferritin >1000 and Tsat >45%
Risk of diabetes, restrictive cardiomyopathy and infertility
Venesection is key
Commonly present with joint pain and fatigue
Aim Ferritin <100
Wilson’s Disease ATP7B gene

Movement disorders in younger age group
Ix: Keyser-Fleischer rings in eyes (Slit-lamp), Low ceruloplasmin,

high urinary copper
Complication: Associated with AIHA, Chronic Liver Disease
A1AT Deficiency SERPINA1 gene
Phenotypes: PiMM (good), PiSS (middle), PiZZ (worst)
Liver Transplant Criteria

Hepatitis serology interpretation

Malnutrition and its impact Mechanism
General infection Loss of immune function
Chest infection Loss of respiratory muscle mass, retained secretions and

reduced cough
Skin infections Skin fragility, weak barrier
Respiratory failure Loss of respiratory muscle strength, fatigue
Hypothermia Loss of subcutaneous fat insulation and impaired

thermoregulation
VTE Hypomobility and inflammatory state
Pressure ulcers Loss of skin/fat with increased pressure on bone
Wound Complications Poor skin integrity, impaired immune response
Psychological effects Central effects of undernutrition

Source: CLS 2022 - Clinical Nutrition
Antibody Disease
Anti-tTG, anti-endomysial Coeliac Disease
Ab, anti-DGP
Anti-eTG Dermatitis Herpetiformis
ASCA Crohn’s disease (pANCA for UC)
AMA Primary Biliary Cirrhosis
Anti-SMA Autoimmune Hepatitis
Anti-LKM1 Autoimmune Hepatitis (usually younger age)
Anti- SLA/LP Autoimmune Hepatitis (severe)
Anti-Actin Coeliac Disease
Faecal calprotectin IBD (UC and Crohn’s)
- Can be elevated in any active colitis
HLADQ2/DQ8 Coeliac Disease
Serum ceruloplasmin and Wilson’s disease
urinary copper levels

General Medicine
Acid base Disorders
HAGMA: GOLDMARK Metabolic Alkalosis: CLEVER PD
Glycols (ethylene glycol, propelene Contraction
glycol) Liquorice, laxatives
Oxoproline (the toxic metabolite of Endocrinopathies (Cushing’s, Conn’s)
excessive paracetamol/acetaminophen) Vomiting
L-lactate (sepsis) Excess alkali
D-lactate (gut) Renal (Barter’s, Gittelmann’s), hypokalemia
Methanol (all alcohols) Post-hypercapnia
Aspirin (Salicylates) Diuretics
Renal failure
Ketones (DKA, Alcohol, Starvation,
SGLT2i) Consider urine Cl to help with diagnosis
Steps in Interpretation:
1) Anion Gap
2) Winter’s formula = 1.5(HCO3)
+8
3) Delta-delta gap
Ref: https://www.grepmed.com/images/9343/causes-differential-
alkalosis-diagnosis-metabolic
NAGMA: HARDASS Respiratory Acidosis and Alkalosis
Hyperchloraemia
Addison’s disease/Adrenal
insufficiency
RTA
Diarrhea
Acetazolamide
Spironolactone
Saline
For CO2 prediction:= 0.7(HCO3)+20 Ref: https://litfl.com/acid-base-disorders/

Driving restrictions post cardiac/vascular event
Private Vehicle Commercial
PCI 2 days 4 weeks
AMI 2 weeks 4 weeks
Pacemaker insertion 2 weeks 4 weeks
CABG 4 weeks 3 months
Cardiac arrest/syncope 6 months 6 months
First seizure 6 months (if seizure free, 5 years (if seizure free and
with or without medications) EEG in last 6 month
demonstrate no epileptiform
activity)
Stroke 4 weeks 3 months
TIA 2 weeks 4 weeks

Genetic and Metabolic Medicine
Types of DNA changes Explanation
Deletion Vary from million base pairs to single base pairs
Frameshift mutation Affects normal triplet reading frame (deletion or insertion)
Point mutation Single base change
Silent mutation DNA sequence that does not change the amino acid sequence
Missense mutation A type of point mutation that causes single amino acid change
Nonsense mutation A type of point mutation that changes a codon to stop codon
Truncating mutation Premature stop codon and a shortened protein product
Mendelian Inheritance Conditions
Autosomal Dominant Marfan’s syndrome

NF1
VHL
Osteogenesis imperfecta
Tuberous Sclerosis Complex
Autosomal Recessive Wilson’s

Haemochromatosis
Homocystinuria
Thalassaemia
Alpha1 AT Deficiency
Friedreich's Ataxia
Phenylketonuria
Sickle Cell Disease
Gilbert’s
Cystic Fibrosis
X-Linked Recessive Bruton’s agammaglobulinaemia

Fragile X
Fabry’s Disease
Wiscott-Aldrich Disease
G6PD
Ocular albinism
Leish-Nyhan Syndrome
Duchenne MD
Haemophilia
Hurler’s

X-Linked Dominant Hypophosphatemic rickets
Incontinentia Pigmentii
*Read around non-mendelian inheritance as well as they often appear in examination ie

mitochondrial disorders, genetic imprinting, trinucleotide repeat disorders.
Neurogenetic syndromes Features

and disorders
Neurofibromatosis 1 Autosomal Dominant

(NF1) NF1 gene mutation (codes for neurofibromin)
Criteria: 2 or more of the following -

- At least 6 Cafe-au-lait patches
- At least 2 neurofibromas or 1 plexiform neurofibroma
- Axillary or inguinal freckling
- At least 2 Lisch nodules
- Osseous lesion (long bone/sphenoid wing)
- Optic glioma
- 1st degree relative
- Un-identified bright objects
- Seizures
- Learning difficulties
- CNS tumours
- Malignant Peripheral Nerve Sheath tumors
- Spinal neurofibromas
- Scoliosis
- Macrocephaly
- HTN
- Higher mortality
Can use MEK inh for Plexiform fibromas
Genetic counselling important
Neurofibromatosis 2 Autosomal dominant

(NF2)
NF2 gene (codes for Merlin)
Diagnostic criteria: One of -

- Bilateral vestibular schwannoma
- First degree relative with NF2 AND unilateral
vestibular schwannoma or any 2 of meningioma,
schwannoma, glioma, neurofibroma, posterior
subcapsular lenticular opacities
- Multiple meningiomas AND unilateral vestibular
schwannoma or any 2 of glioma, schwannoma,

neurofibroma, posterior subcapsular lenticular
opacities
- Cataracts
- Hearing loss
- Focal weakness
- Balance dysfunction
Rx: Bevacizumab (Anti-VEGF)
Tuberous Sclerosis Multiple benign hamartomas

Complex
Often Autosomal dominant (TSC1, TSC2)
Major Features:
Skin - facial angiomas, ungual fibromas, shagreen patches,
hypomelanotic macules
CNS - subependymal giant cell astrocytoma, subependymal
nodule
Others: Renal angiomyolipoma, cardiac rhabdomyoma,
retinal hamartoma, lymphangioleiomyomatosis
Minor features: Confetti skin lesions, non-renal hamartomas,

bone cysts, multiple renal cysts
Can complicate with seizures, behaviour changes
Rx: mTORi
Must always assess: Skin, MRI-B, renal USS and

ophthalmology review
Trinucleotide Repeat disorders
Fragile X Syndrome Most common inherited intellectual disability
X-linked
CGG repeats (>200)
FXTAS (Fragile X Associated Tremor and Ataxia Syndrome)

Premature ovarian failure
Features:
- Low IQ
- Behavioural problems
- Physical features - long face, large ears, testicular
enlargement
- Seizures

- Vision problems
- MVP
Friedrich’s ataxia Autosomal recessive
GAA repeats
Progressive neurological dysfunction (Cerebrellum and dorsal

root ganglia)
- Mixed UMNL and LMNL
- Posterior column dysfunction
- Cardiomyopathy and T2DM
Huntington’s Disease CAG repeats (>40 repeats)

HTT gene
Autosomal dominant
Movement disorder - Chorea
Dementia
Psychiatric conditions
Other inherited syndromes
Muscular Dystrophy X-linked

- Duchenne (DMD) Variable Penetrance and phenotype
- Becker (BMD)
DMD leads to disruption in reading frame and no functional
protein whereas BMD leads to in-frame disruption and hence
semi-functional protein
Proximal muscle weakness

Broad gait
Gower sign
Calf pseudohypertrophy
Progressive wheelchair use
Mild IQ impairment
Cardiorespiratory death
Trisomy 21 Extra chromosome 21

Others: Mosaicism, Translocation
Features:
- Dysmorphism
- Low IQ
- Hypotonia
- Hearing and vision loss
- Alzheimers dementia earlier
- Congenital Heart disease
- Hypothyroidism
- GIT (Duodenal atresia, Hirschsprung’s)
- Leukaemia (ALL and AML)

- Occipito-atlantoaxial instability
- Osteoporosis
Turner 45 XO karyotype
Features:
- Short stature
- Web neck
- Pubertal delay
- Gonadal dysgenesis
- Normal IQ
- Renal tract malformations
- Cardiac anomalies (CoA, Bicuspid aortic valve)
- Endocrinopathies
- HTN
- Congenital lymphoedema
Marfan Autosomal Dominant

FBN1 mutation
Features:
- Tall and long limbs
- Joint hypermobility
- CVS - Aortic dilation and dissection, AR/MR
- Lens dislocation
- Chest wall deformity
Rx: Prophylactic beta-blockers or RAAS blockade for aortic
root dilatation, surgical repair of aortic root/valvulopathy
Klinefelter 47 XXY
Features:
- Hypogonadotropic hypogonadism
- Eunuchoid body habitus
- Gynaecomastia
- IQ decreased
- Sexual dysfunction
- Behavioural phenotype
- Endocrinopathy
- Higher malignancy risk
Other important genetic conditions that have been asked before:

- Noonan’s syndrome
- Loeys-Dietz syndrome
- Ehlers-Danlos Syndrome
- Kallman Syndrome
- Fabry’s Disease
- Familial TAAD

Cancer syndromes Features
Knudson’s two hit hypothesis for tumour suppressor gene (Loss of Function)
Protooncogene (Gain of Function)
Usually autosomal dominant
Familial Breast and Ovarian cancer syndromes
Hereditary Breast and BRCA 1 and 2

Ovarian Cancer syndrome
(HBOC) High risk features:
Younger than 40 y/o
Triple negative
Ashkenazi/Icelandic inheritance
Male breast cancer
Risk reduction: SERM - Tamoxifen (premenopausal) or

raloxifene (post-menopausal), prophylactic surgery
Li Fraumeni syndrome Sarcoma, Breast, Adrenal gland, leukaemia
TP53 gene
Cowden Syndrome Benign cancer syndrome, follicular thyroid ca, large head
circumference, trichilemminomas, Lhermitte Duclos
PTEN gene
Rarely ovarian involvement
Familial Bowel Cancer
FAP Multiple adenomatous polyps

APC tumor suppressor gene
Congenital hypertrophy of retinal pigment epithelium

(CHRPE)
Desmoid tumors
Osteomas and cysts
Total prophylactic colectomy
MutYH Fewer polyps, phenotype similar to FAP
Lynch Syndrome (HNPCC) No increase in polyps
Extra-colonic cancer as well

MMR - MLH1, MSH2, MSH6 and PMS2
Peutz-Jeghers syndrome Hamartomatous polyposis

Lip, buccal and palm pigmentation
Intussusception in children
Increased risk of CRC and breast ca
STK11 gene
Other cancer syndromes
MEN MEN1 - Parathyroid, pituitary and pancreatic
MEN2A - Medullary thyroid ca, pheochromocytoma,

parathyroid
MEN2B - Medullary thyroid ca, pheochromocytoma
Hereditary Paraganglionoma SDHB, SDHD commonest genes

and Phaeochromocytioma Others: RET, VHL, NF1 , SDHC, SDHA
VHL CRCC
Retinal hemangioblastoma
CNS hemangioblastoma
Pheochromocytoma
Investigations in Genetics
Chromosome testing
- FISH
- MLPA
- Karyotype
- Microarray
Single gene disorders

- PCR
- Sanger sequencing
- MLPA
- Blot
Massively Parallel sequencing

- WGS
- WES
*Worthwhile going through specifics and limitations of each investigations and how it can
affect detection of large defects, or picking of VUS. Not uncommon to be tested on!

Geriatric Medicine
Dementia Features Treatment
Alzheimer’s STML Acetylcholinesterase
inhibitor – Donepezil,
Galantamine, Rivastigmine
NMDA Antagonist -
Memantine
Parkinson’s Slow progression, insidious Anti-Parkinson’s meds
onset. Established dx of PD (refer to neuro section)
Vascular Step wise decline, impaired Cholinesterase inhibitors
executive function, relative (for concomitant AD)
sparing of episodic memory
Dementia with Lewy Visual hallucinations, REM Symptomatic relief
Body(DLB) sleep behaviour disorder, (Antipsychotics mainstay)
parkinsonism (usually late
stage)
Frontotemporal Dementia Disinhibition, apathy, Nil
(bvFTD, semantic) hyperorality, compulsive
HIV Dementia Subcortical dysfunction: ART
impaired
attention/concentration/psyc
homotor speed, depressive
symptoms
Prion disease (CJD) Rapid neuropsychiatric Supportive
decline – impaired
concentration, memory,
judgement, apathy,
depression
Pathophysiology
C9ORF72 FTD-MND (Frontotemporal Dementia with Mononeuron
Disease)
Alpha Synuclein Parkinson’s, MSA, Lewy Body Dementia
Tauopathies PSP, CBD, Alzheimer’s
Neurofibrillary tangles Alzheimer’s
14-3-3 protein (CSF) Creutzfeldt-Jakob Disease
Aging physiology
Cardiovascular
- vascular sclerosis -> ↑ systolic pressure

- myocardial hypertrophy -> LV hypertrophy
- ↓ maximal HR due to ↓ catecholamine response
Respiratory

- ↑ chest wall stiffness -> chest wall compliance
- increased: A/a gradient, V/Q mismatch, functional residual capacity, residual capacity
- decreased: PaO2, FVC, FEV1
- unchanged: total lung capacity
- weakened baroreceptors/chemoreceptors
- poor response to hypoxia/hypercapnia
- weakened respiratory muscles -> ↓cough reflex
Renal
- reduced GFR and tubular excretion
Pharmacokinetic and pharmacodynamics
Prescribing in the elderly. Edwina Holbeach, Paul Yates. Australian Family Physician Vol. 39, No. 10, october 2010 p728-733.
Psychotropics on falls risk
https://www.nps.org.au/australian-prescriber/articles/combination-psychotropic-medicine-use-in-older-adults-and-risk-of-hip-fracture

Haematology
Haematological Disorder Features
Myeloproliferative disorder: Usually JAK2 V617F mutated. Others: MPL, CALR.

- Polycythaemia Rubra
Vera(PRV) Rx:
- Essential Thrombocytosis (ET) - PRV and ET involves venesection, CVD
- Primary myelofibrosis (PMF) protection and cytoreduction (Hydroxyurea,
- CML ruxolitinib).
- PMF - Ruxolitinib can be used earlier.
Allogeneic SCT.
- CML - TKIs (1st, 2nd and 3rd generation).
BCR-ABL gene on FISH.
Myelodysplastic syndrome >60 years age, bone marrow failure with peripheral
(MDS) cytopenia
May progress to AML
Subtypes: CMML, JMML
Good prognosis - Chromosome 5 abnormalities

Poor prognosis - Chromosome 7 abnormalities
Rx: Supportive (transfusion, G-CSF), Luspatercept,

Azacitidine, Lenalidomide (del 5q)
Acute Myeloid Leukaemia >20% myeloblasts on aspirate
CD13, 33
Classification:
- AML with recurrent genetic abnormalities
- AML with dysplasia-related changes
- Therapy-related myeloid neoplasms
- AML not otherwise categorised
- Myeloid neoplasm with germline
predisposition
Favourable: t(8,21), t(16,16), inv(16) mutated NPM1

without FLT3-ITD
Intermediate: Mutated NPM1 and FLT3-ITD, t(9,11)
Adverse: del5q, inversion of 5 and 7 , t(6,9), t(9,22),

Wild type NPM1 and FLT3-ITD, Mutated RUNX1,
ASXL1, TP53
Rx: 7+3 (Cytarabine and Anthracycline)

Azacitidine or Venetoclax
Midostaurin -oral TKI (FLT3 inhibitor)
Gilteritinib
APML - haematological emergency

- t(15,17), Auer Rods
- Risk of DIC
- Rx: ATRA and Arsenic - induces differentiation of
blasts into mature myeloid cells (risk of
Differentiation syndrome)
Acute Lymphoblastic >20% leucs without Auer rods in blast

Leukaemia (ALL)
Good prognosis - hyperploidy, t(12,21)
Poor prognosis - t(9,22)
Rx: TKI
Allogenic BMT
BiTE therapy (Bispecific T-cell engaging) - similar to
CAR-T cell (can cause ICANS and CRS)
Chronic Lymphocytic Good prognosis - 13q, IGHV mutant

Leukaemia (CLL) Poor prognosis - 17p, TP53 mutant
CD5, 19,23
Rx: Watch and wait usually

Commence rx when autoimmune complications,
doubling of lymphocyte in 6 months or >50% over 2
months, BM failure, disease related symptoms
Rx with Venetoclax, Ibrutinib, FCR (Fludarabine,

CYC, Ritux), Obinutuzumab
Plasma cell dyscrasias Types of paraproteinaemia:

- MGUS - MM
- Plasmacytoma - Smouldering myeloma
- POEMS syndrome - Non-secretory myeloma
- Multiple myeloma (MM) - Plasma cell leukaemia
- Plasmacytoma
- AL Amyloid

- Light/heavy chain deposition disease
- POEMS syndrome
- TEMPI syndrome
MM
- t(4,14), t(14,16)
- CD38 and 138
- BMAT - Dutcher bodies
Rx for MM
- Glucocorticoids
- IMiDs: Lenalidomide
- Proteasome inhibitors: Bortezomib
- MAb: Daratumumab
- CTx: Melphalan, CYC
- RTx
- Bisphosphonates
Aggressive B cell lymphoma Burkitt’s - t(8,14)

- DLBCL - B-cell related
- Burkitt’s - Endemic (Africa, 100% EBV) and sporadic
- ++ Tumour lysis
- Curable
DLBCL
- Rule of 1/3rds - ⅓ Adult NHL, ⅓ early stage,
⅓ extranodal, ⅓ B symptoms
- Pan-B-cell markers (CD19,20,22)
Rx: R-CHOP, ASCT, CAR-T (Kymriah, Yescarta),

Cladribine for Hairy cell
Indolent B cell lymphoma Follicular - t(14,18)

- Follicular - T-cell related
- MZL - BCL2, BCL6
- Waldenstrom
Macroglobulinemia Waldenstrom’s
- Hairy Cell Leukaemia - MyD88 gene mutation
- Can use Rituximab + Bendamustine
- Large amounts of IgM
- Be aware of hyperviscosity syndrome
- Treat with plasma exchange
Hairy-cell leukaemia
- CD25 and CD103
- BRAF V600E mutation
Rx: R-CHOP, R-CVP (cyclophosphomide, vincristine

and prednisolone), Rituximab for maintenance (or
Obinutuzumab), PLEX for Waldenstrom’s, CAR-T,

ASCT
Hodgkin Lymphoma Types:

- Nodular sclerosis
- Lymphocyte-rich
- Mixed cellularity
- Lymphocyte-depleted
Rx:ABVD, BEACOPP, Brentuximab, PD-1, ASCT
Staging for Lymphoma (both HL and NHL) - Ann-Arbor staging:

- Stage I - Single lymph node region
- Stage II - >/= 2 LNs on the same side of diaphragm
- Stage III - both side of LN
- Stage IV - Widespread disease
Tumour Lysis Syndrome

- Usually high grade lymphomas
- Hyperuricemia, hyperuricosuria, hyperkalaemia, hyperphosphatemia and
hypocalcemia
- Rx: Urate Oxidase (Rasburicase) - oxidizes uric acid to allantoin - prevents uric
acid nephropathy
Car-T cell therapy

- Axi-cel, Tisa-cel
- Side effects: Cytokine release syndrome (CRS) and Immune effector cell associated
neurotoxicity syndrome (ICANS)
- Rx for CRS - Steroids and Tocilizumab
Workup
Clinical
- detailed history and exam
- Performance status (ECOG)

- B symptoms (weight loss, fever, night sweats)
Pathology:
- Node (excisional > core biopsy), bone marrow biopsy
- Histochemistry, immunophenotyping, cytogenetics
Investigations:
- Endoscopy, MRI-B when appropriate
- CT (Chest,abdo,pelvis), FDG-PET
- LP - aggressive lymphomas/ intrathecal chemotherapy
- Pre-treatment - FBE, blood film, hepatic/cardiac/renal workup, LDH, serum-B2
microglobulin level
Etiologies: HIV, HCV and HBV testing
Pathogens involved in the development of lymphomas
Pathogens Lymphomas
HIV DLBCL
Burkitt’s lymphoma
Castleman’s disease
Hodgkin’s Lymphoma
HTLV-1 Adult T-cell leukaemia/lymphoma
EBV Burkitt’s lymphoma

T/NK-cell lymphoma
Post-transplant lymphoprofilerative disease
HHV-8 Kaposi’s Sarcoma

Castleman’s disease
Primary effusion lymphoma
HCV Splenic marginal zone lymphoma

Mixed cryoglobulinaemia
H.Pylori Gastric MALT Lymphoma
Borrelia Cutaneous MALT Lymphoma

burgdorferi
Antibodies
Anti-cardiolipin, Antiphospholipid syndrome (APLS)
lupus anticoagulant
and anti-beta2
glycoprotein
Anti-PF4 Heparin-Induced Thrombotic Thrombocytopenia (HITT), Vaccine-
induced Thrombotic Thrombocytopenia (VITT)

Transfusion-transmitted Infections
https://www.transfusion.com.au/adverse_events/risks/estimates#sthash.biFXYon0.dpuf
Multiple Myeloma
Mechanism Anticoagulant agents
Vit K Antagonist Coumadin
Direct factor Xa inhibitor Apixaban, Rivaroxaban, Edoxaban, Betrixaban
Indirect Factor Xa/IIa inhibitor LMWH, UFH, Fondaparinux, Danaparoid
Direct thrombin inhibitors Dabigatran, Argatroban, Bivalirudin

NOAC Dabigatran Rivaroxaban Apixaban
Coagulation profile TT prolonged and PT prolonged PT prolonged

APTT prolonged sometimes
Specific test Dilute thrombin Modified anti-Xa Modified anti-Xa

clotting time assay specific for assay specific for
rivaroxaban apixaban
Drug-drug interaction Potent P-gp Potent CYP3A4 Potent CYP3A4

inhibitors inhibitors and P-gp inhibitors
Half-life 9-13h 7-11h 8-15h
Time to action offset 24-96h 24-72h 24-72h
Time to peak effect 1-2h 2.5-4h 3h
Clearance/Metabolism 80% Renal 33% Renal 25% Renal
Anaemia
Microcytic (MCV<80) Normocytic (MCV 80-100) Macrocytic (MCV>100)
Iron deficiency Anaemia Reduced Production Megaloblastic

(IDA) - BM Failure - B12 deficiency
Thalassaemia - Chronic Disease - Folate Def
Haemoglobinopathy
Sideroblastic Anaemia Red cell loss Non-megaloblastic
- Haemolysis - Myelodysplasia
- Bleeding - Liver Disease
- Alcohol
- Pregnancy
- Hypothyroidism
- Drugs
Microcytic Anaemia To differentiate IDA and AoCD:

- Transferrin is high for IDA
- Tsat and ferritin low for IDA
Haemoglobinopathies:
- Quantitative - Thalassaemia
- Qualitative - HbS, HbE, HbD
Normocytic Anaemia BM Failure causes:

- Idiopathic (Aplastic)
- Medications (CTx)
- Viral
- Inherited (Diamond-Blackfan Anaemia, Fanconi)
- Haematological malignancies

- MDS
AoCD - Hepcidin related

- Renal impairment, inflammation, infection,
malignancy
Haemolysis
- Intracorpuscular - Enzyme (G6PD, PK), membrane
defect (hereditary spherocytosis), SCD, PNH, B12
deficiency, Thalassaemia
- Extracorpuscular - MAHA, Infection, Chemicals,
AIHA
-> Ix: Peripheral blood film (Reticulocytosis), LDH,
Bilirubin, Haptoglobin, urine haemoglobin/haemosiderin
(Others to consider - EMA, CD55/59, Genetic studies)
Macrocytic Anaemia B12 deficiency

- If B12 normal, can send for holotranscobalamin
levels (active B12), MMA and Homocysteine (both
high in B12 def)
Haemolytic Anaemia
G6PD Deficiency  Enzyme involved in protecting cell from oxidative

damage
 Sex-linked inheritance - most cases males
 Greece, middle east
 haemolysis triggered by
o infection
o fava beans
o oxidant drugs
 Blood film:
1. Heinz body (denatured haem)
2. Bite cells - removal of Heinz bodies by spleen
3. Hemi-ghost red cells - haem retracted to one side
4. Howell-jolly bodies - suggestive of hyposplenism
(RES overloaded)
Acquired haemolytic Warm autoimmune haemolytic anaemia

anaemia  IgG directed at RBC membranes
 RES removes IgG + pieces of cell membrane ->
spherocytes
 Ddx: hereditary haemolytic anaemia
Cold-antibody induced haemolytic anaemia
 IgM -> agglutination and complement-mediated
haemolysis
 infectious mononucleosis
 film: agglutination, spherocytes, polychromasia

Microangiopathic  Due to endothelial pathology in presence of platelets
haemolytic anaemia  keratocytes - horned cells
(MAHA) - acquired non-  schistocytes - helmet cells
immune  Types
o Valve haemolysis
o Atypical HUS (aHUS) – Rx: Eculizumab
o Typical haemolytic uraemic syndrome
(HUS)
 enterohaemorrhagic (shiga toxin
producing) e.coli – supportive care
 renal failure more predominant
feature
Thrombotic  Pathology: hyaline thrombi (platelet rich) in

thrombocytopenic purpura terminal arterioles and capillaries vs fibrin rich in
(TTP) DIC
 diagnosis
o ADAMTS-13
 low in TTP
 treatment
o steroids and rituximab if antoantibody
against ADAMTS13
o plasma exchange: MAHA +
thrombocytopenia + raised LDH
(haemolysis and cellular ischaemia)
 Symptoms - pentad
1. fever
2. microangiopathic haemolytic anaemia
3. thrombocytopenia
4. neurologic symptoms and signs
5. renal function abnormalities

Immunology and Allergy
CD4 Subsets
T-helper cells Stimulatory Cytokine Target cells Host Defence
Cytokine released
Th1 IL12, IFNgamma IFNgamma Macrophages Viruses
Th2 IL4 IL4,5,13 Eosinophils Parasites
Th17 IL6, TGF-Beta IL17,22 Neutrophils Bacteria
T Follicular IL21 Germ cell
Helper proliferation
Drug Hypersensitivity
Type A: pharmacological (80%)
Type B: hypersensitivity
- immune mediated allergic (5-10%)
- IgE mediated/mast cell activation (<1 hr): urticaria, angioedema, bronchospasm,
anaphylaxis
- T cell mediated (>1hr): maculopapular, morbilliform, SJS
- Others: immune complex, cytotoxic reaction
Hypersensitivity reactions
Type 1 IgE mediated hypersensitivity

Ag induces crosslinking of IgE bound to mast cells and basophils with release
of vasoactive mediators
Eg: systemic anaphylaxis, localised anaphylaxis (hives, hayfever, food

allergies, eczema)
Type 2 IgG-mediated cytotoxic hypersensitivity

Ab directed against cell surface Ags mediates cell destruction via complement
activation or ADCC
Eg: Blood transfusion reactions, autoimmune haemolytic anaemia
Type 3 Immune complex-mediated hypersensitivity

Ag-Ab complexes deposited in various tissues induce complement activation
and an ensuing inflammatory response mediated by massive infiltration of
neutrophils
Eg: Serum sickness, Glomerulonephritis, RA, SLE
Type 4 Cell-mediated hypersensitivity

Sensitised Th1 cells release cytokines that activate macrophages or cytotoxic
T cells which mediate direct cellular damage
Eg: Contact dermatitis, tubercular lesions, graft rejection
Conditions Features
Hereditary Rare genetic condition (SERPING1 gene): 1 in 50000

Angioedema Pathophysiology; Kallikren/Kinin System (KKS)
C1 inhibitor Deficiency
Bradykinin driven (no histamine) - hence ACEI contraindicated
Type 1: Misfolded C1 inhibitor

Type 2: Dysfunctional C1 inhibitor
Symptoms:
Asymmetrical non-pitting edema
Absence of urticaria
May manifest in any organ
Risk of laryngeal involvement
Diagnosis: C1 inhibitor assay (low), C4 (low)

Rx: C1 inhibitor, bradykinin inhibitor
Paroxysmal Acquired disease of stem cell

Nocturnal
Haemoglobinuria Pathophysiology: PIGA gene - causing Glycosyl
Phosphatidylinositol (GPI) Anchor. Loss of CD55,CD59 with absent
complement inhibitors leading to complement mediated haemolysis.
Associated with aplastic anaemia, thrombosis and smooth muscle
dystonia.

Infectious disease
Antimicrobials
Pharmacodynamics
Antifungals
Class Mechanism Examples Adverse Effects
Triozoles Inhibit ergosterol Ketoconazole, Drug-drug interactions
synthesis, Itraconazole, Fluconazole - candidaemia,
fungistatic, CYP3A4 Fluconazole, prophylaxis in SCT
inhibitors Voriconazole, Voriconazole - deranged
Posaconazole, LFTs
Isavuconazole
Polyenes Binds to ergosterol Amphotericin B Conventional: significant
nephrotoxicity
Liposomal: less
nephrotoxicity and infusion
reaction
Echinocandin Beta-D-glucan Capsofungin Drug-drug interaction
s synthetase inhibitor Covers broadly (not C.

Parapsilosis)
Culture negative Gram positive bacilli Gram positive coccus
Treponema Bacillus Catalase positive:

Rickettsia Clostridium Staph Aureus (coagulase
Mycoplasma Corynebacterium positive)
Mycobacterium Listeria Staph epidermidis
Legionella Lactobacillus (coagulase negative)
Chlamydia Staph saprophyticus
(coagulase negative)
Catalase negative:
Alpha haemolytic - Strep
pneumonia, viridans
Beta haemolytic - Strep
pyogenes, agaliactae
Gamma - enterococcus
faecalis, faecium
Gram negative coccus Gram negative bacilli Gram negative coccobacilli
Neiserria Kiebesella Haemophilus
Ecoli Bordetella
Enterobacter Brucella
Citrobacter Filaria
Serratia Pasteurella
Vibrio Legionella
Pseudomonas
Proteus
H.pylori
Campylobacter
Salmonella
Shigella
Yersinia
Cell Wall Synthesis

Class Examples Uses Do not use AE/other
Beta-lactams Penicillin: Gram positives:E faecalis E faecium –
susceptible to penicillin V/G, resistant to all
Mechanism: Penicillin V amoxycillin/ampicillin, tazocin
Target penicillin (Phenoxy)
binding proteins Some G-ves:
(transpeptidase) Penicillin G (Ben Neisseria (G-ve): susceptible to
Pen) penicillin
Flucloxacillin Pseudomonas: Tazocin

Klebsiella: Tazocin
Amoxycillin,
ampicillin Haemophilus influenzae:
amoxicillin/ampicillin

Tazocin E Coli: amoxicillin/ampicillin
Cephalosporins: G+ve G-ve with progression All enterococcus

1st: some G-ves including E (I-IV)
1st: cefazolin, Coli, Klebsiella Chlamydia
cefalexin Mycoplasma
2nd: respiratory pathogens Listeria
nd
2 : cefuroxime
(PO/IV) 3rd: G-ves (Haemophilus,
Klebsiella, Salmonella,
3rd: ceftriaxone, Shigella)
ceftazidime 4th: Pseudomonas
4th: cefepime 5th: MRSA, enterococcus
5th: ceftaroline,
ceftobiprole
Monobactams: ESCAPPM (G-ve’s, aerobes) ESBL

aztreonam Pseudomonas (CF)
Carbapenems: Note: stable against ESBL - MRSA CNS toxicity: lower

imipenem, beta lactamases (type A, C) Enterococcus seizure threshold
meropenem, Pseudomonas (not ertapenem) (mero lowest risk)
ertapenem Secondary fungal
infection
Glycopeptides Vancomycin, Gram positives only vanA Nephrotoxicity
teicoplanin enterococcus (ATN)
DRESS
Red man syndrome
*Teicoplanin can
be used in vanB
enterococcus
Fosfomycins Broad spectrum: especially
urinary pathogens
- Single dose for UTI without
bacteraemia
-Can also be used in
complicated infections
(pyelonephritis/abscess,
osteomyelitis) IV

Protein Synthesis
Subunit Class Examples Mechanism Uses Do not use AE/Other
30S Tetracyclines Tetracycline, Prevent binding Broad G+ve and Proteus Avoid with Ca/Mg/Fe
doxycycline, of tRNA prevents G-ve mirabilis: supplementation
minocycline chain elongation Intracellular incl intrinsic Hepatotoxicity,
mycoplasma resistance teratogenic, teeth, throat,
Protozoan tan
Note: resistance
common
Common
infections:
-Acne
-Cellulitis
-Bartonella
-Atypical
pneumonia
-Ticks
-STD
-Penicillin
resistant syphilis
Aminoglycosides Gentamicin, All stages of Broad spectrum Anaerobic Contraindicated M. Gravis

amikacin, protein synthesis G-ve (neuromuscular blockade)
streptomycin Synergistic effect Nephrotoxicity,
with G+ve ototoxicity,
vestibulotoxicity
Glycylcycline Tigecycline Prevent chain Resistant Increased bloodstream

elongation organisms: VRE, infections
Binds with 5x MRSA,
affinity of Acinobacter
tetracyclines
50S Macrolides Azithromycin, Prevent protein Atypicals: Clarithromycin + statin:

erythromycin, translation legionella, rhabdo risk
clarithromycin chlamydia Peristalsis, increased QT,
pneumoniae, cholestatic LFT
mycoplasma
Oxazolidinones Linezolid Proximal to the Resistant G-ves: Bone marrow suppression,

binding site of organisms: VRE, naturally serotonin syndrome,
other inhibitors MRSA, multi- resistant peripheral neuropathy
(decreased cross- drug resistant (irreversible)
resistance) strep pneumoniae
Lincosamide Clindamycin Prevent chain G+ves: including Some cross resistance

elongation community with macrolides
Also inhibits acquired MRSA High risk of C diff
toxin production Anaerobes
Invasive
GAS/toxic shock
(+ penicillin)
Streptogramins Pristinamycin Synergistic effect VRE (especially E No IV

(pristinamycin between PIA faecium), VRSA formulation
IA + (macrolide) and
streptogramin streptogramin A
A)

Membrane function
Class Examples Mechanism Uses Do not use AE/Other
Polymyxins Polymyxin Binds to LPS Colistin: multi drug G+ves: cell Caution with
B makes membrane resistant organisms wall too thick renal
Colistin more permeable to permeate impairment
osmotic lysis
Cyclic Daptomycin Binds to Ca ions Resistant organisms G-ves:
lipopeptides in cell (including linezolid, naturally
membranes rapid vancomycin) resistant
depolarisation Respiratory
inhibits DNA, illness:
RNA and protein inactivated by
synthesis surfactant
Anti-metabolites
Class Mechanism Uses Do not use AE/Other
Trimethoprim, Sequential inhibition PJP Anaerobes Rash, bone marrow
sulfamethoxazole of folate synthesis (at Parasites: With suppression, increase in
different steps) toxoplasma gondii methotrexate Cr (20%), ATN, G6PD
synergistic Nocardia
Sternotrephomonas
UTI/Cystitis
Osteomyelitis
Nucleic acid synthesis

Class Examples Mechanism Uses AE/Other
Fluoroquinolones Ciprofloxacin, Topoisomerase Ciprofloxacin: potent against Avoid in M.
norfloxacin, DNA GNB (pseudomonas, Gravis
levofloxacin, supercoiling enterobacter, haemophilus) Tendinopathy,
moxifloxacin Levofloxacin/moxifloxacin: QTc
respiratory pathogens (Strep prolongation
pneumoniae, haemophilus,
Moraxella, legionella,
chlamydia, mycoplasma)
Norfloxacin: concentrates in
urine
Ansamycins Rifampicin Prevents DNA Needs to be co-administered CYP inducer
RNA (e.g. fusidic acid): complex
staph aureus infections, TB
Single stat dose: Neisseria
meningitidis contacts
HIV Medications

Classes of ART Medications
Nucleoside RT inhibitors (NRTIs) Zidovudine

Lamivudine
Emtricitabine
Abacavir (HLAB5701 - hypersensitivity)
Tenofovir disoproxil fumarate (TDF) -
nephrotoxicity including Fanconi, Osteoporosis
Tenofovir alafenamide (TAF)
Non-nucleoside RTIs Nevirapine

Efavirenz - CNS SE
Rilpiverine
Delaverdine
Etravirine
Doravirine
Protease Inhibitors (PI) Ritonavir - helps catalyze/boost other ARTs

(CYP3A4 inh)
Lopinavir
Darunavir
Integrase inhibitor (INSTI) Raltegravir

Dolutegravir
Bictegravir
Fusion inhibitor Enfuvirtide
CCR5 antagonist Maraviroc
Tuberculosis
Epidemiology: 20% of the population has latent TB

Investigations:
1) Tuberculin Skin test/Mantoux Test
2) Interferon Gamma test
- Quantiferon Gold - Unable to differentiate activate and latent TB
- Test at least 8 weeks from last exposure
3) Sputum sample
- Ziel-Neelsen stain/Auramine stain
4) NAAT
- MTB DNA
5) Culture (Gold Standard)
6) Whole genome sequencing
Tuberculous meningitis
- All tests can be negative
- CSF features: Elevated Protein, low glucose and elevated lymphocytes
Management:
- Latent TB - 3 months Isoniazid+Rifampicin OR 4 months Rifampicin OR 9 months
Isoniazid
- Active TB - 2 months RIPE then 4 months of Isoniazid+Rifampicin
Adverse drug event:

- Isoniazid - Hepatitis, Peripheral neuropathy
- Rifampicin - Hepatitis, CYPinducer, colour change of secretions
- Pyrazinamide - Gout, Hepatitis, polyarthralgia
- Ethambutol - Optic neuropathy
MDR-TB
- Isoniazid and Rifampicin
XDR-TB
- Similar to MDR-TB + Fluoroquinolone + ⅓ Injectables
TB Complications:
- Bronchiectasis
- Pneumothorax
- Bronchopleural fistula
- Mycetomas
- Massive haemoptysis
- Cor pulmonale
- Post-obstructive pneumonia
- Lung cancer

Medical Obstetrics
Physiological change Consequence
Peripheral vasodilation Fall in SVR -> Need for increased CO
Increased CO Increased renal perfusion
Increased plasma flow Increased GFR, hyperfiltration and proteinuria
Increased blood volume Water and sodium retention and haemodilution (due to
increased RAAS activity)
Dilatation of collecting system Physiological hydronephrosis, increased frequency of

cystitis and pyelonephritis
Endocrine Increase TBG, thyroid hormone metabolism and urinary

iodine excretion
Common medical issues Examples
Hypertensive disorders in - Gestational HTN

pregnancy - Pre-eclampsia (sFLT/PIGF ratio, early aspirin)
- HELLP
Pre-eclampsia
- Methyldopa, labetalol and nifedipine
- RF: Primigravida, previous PET, CVD RF, APLS,
age>35, interpregnancy interval >10 years
- Rx: Aspirin, Calcium, management of RF
- Crisis: Eclampsia, HELLP, DIC, APO, Placenta
abruptio, PRES, ICH, Renal and hepatic failure, MAHA
CVD in pregnancy - IHD

- SCAD
- Peripartum cardiomyopathy
- Stenotic > Regurgitant lesions have issues
- Anticoagulation planning
Renal disorders in - Post-transplant management

pregnancy - CKD
CKD in pregnancy can lead to pre-eclampsia, IUGR, preterm,

perinatal mortality and polyhydramnios
-> HDx improves delivery outcomes (Improved CO, EPO and

vascular function)
Any stage of CKD affects pregnancy
Pre-eclampsia itself can cause ESKD in the future.
Statins are contraindicated in pregnancy
Optimizing CKD pre-pregnancy

- Medication planning
- Immunosuppression - ensure disease stability - use CNI
or Aza
- BP management - aim <140/90
- Proteinuria - ACEI/ARB until attempting conception
- Weight reduction
Immune system in Recommended only if disease is in remission 6-12 months.

pregnancy
SLE and MG flares, RA usually well-controlled
Anti-Ro - neonatal lupus with risk of CHB and

Cardiomyopathy (role of HCQ)
APLS in pregnancy - choice of anticoagulation and antiplatelet

- general rule of thumb is always use aspirin (antiplatelet) but
choice of anticoagulation depends on risk (therapeutic vs
prophylactic LMWH). HCQ and Pred have some role.
TNFi - no live vaccines for 6 months post-partum for baby
MS - can use Glatiramer, IFN, Natalizumab +/- Ritux
Infections in pregnancy - COVID

- Hep B (baby should get HBIg and HBV depending on
viral load)
- HCV
Liver disease in - Acute fatty liver in pregnancy

pregnancy - Cholestasis in pregnancy
- HELLP/PET
- Hyperemesis gravidarum
Consider pre-existing liver disorders ie MALD, viral hepatitis,

autoimmune
Complications: Increased risk of PET, GDM and metabolic

syndrome, increase risk of PPH, itch
Haematological disorders - Thrombocytopenia in pregnancy (PC >70 usually)

in pregnancy - TMA (TTP, HUS)
Thyroid disorders in - Hypothyroidism - need higher dose of levothyroxine

pregnancy (usually double)
- Autoimmune thyroid disease ie Grave’s TSHrAb can
cross placenta
- Postpartum thyroiditis
- Gestational Thyrotoxicosis
HCG looks like TSH

If TSH>10 (subclinical hypothyroidism) - treat
Epilepsy in pregnancy Risk of Vit K def from AED
Avoid teratogenic - safest is Levatiracetam and Lamotrigine
Folic Acid 5mg 3/12 preconception
Obesity in pregnancy High risk of adverse outcomes such as GDM, stillbirth, LGA,
NTD
Aspirin for prophylaxis for pre-eclampsia

Folate for risk of NTD
Higher risk of VTE
Risk of OSA, DM and HTN
Nausea and Vomiting in HG - 5% WL, dehydration and electrolyte imbalance

Pregnancy(NVP),
Hyperemesis Gravidarum RF: Multiple gestations, gestational trophoblastic disease
(HG)
Rx: Iodine, folate, Ginger, Vit B6, Antiemetics, PPI, Thiamine
+ Hydration + electrolyte replacement
Peripartum Pathophysiology: Cathepsin D

Cardiomyopathy
Breastfeeding may worsen
Good prognosis overall but LV function may not normalize
Systolic Dysfunction
Ix: CMR, TTE, BNP
Rx:
- Diuretics, RAAS blockade and beta-blockers
- Digoxin, MRA
- Anticoagulation where EF<35%
- ICD
- ?LVAD, ?Transplant

High risk of thrombus due to low EF
Therapeutics safe in pregnancy Agents
Hypertension Methyldopa
Labetalol
Nifedipine
Hydralazine
Thiazide diuretics (limited data)
Immunosuppression Prednisone
Azathioprine
CNI
Rituximab (limited data)
Plasmapharesis
Pre-eclampsia Prevention Low dose aspirin - 75mg

Calcium and Vit D
Nephrotic syndrome LMWH

Frusemide

Medical Oncology
Chemotherapy
Drug Target Tumour type Side effects
Alkylating agents Induces abnormal Multiple Bone marrow
-Nitrogen Mustards DNA cross-linking suppression, nausea,
(Cyclophosphamide, via alkyl groups -> alopecia, secondary
Melphalan, double strand breaks Very effective on malignancies
Ifosfamide) cancers with (cutaneous SCC,
-Nitrosoureas Act during all cell hypermethylated urothelial
(Carmustine, cycle stages MGMT (double carcinoma, AML),
Lomustine) strand break repair haemorrhagic
-Non-classical enzyme) and other cystitis + premature
(Temozolomide, homologous ovarian failure
dacarbazine, recombination (Cyclo)
procarbazine) deficiencies (i.e.
BRCA 1/2)
Platinums Permanently binds Multiple Nephrotoxicity,
(Cisplatin, DNA causing ototoxicity,
Carboplatin, abnormal DNA Very effective on neuropathy, severe
Oxaliplatin) cross-linking cancers with nausea, cold
hypermethylated dysesthesia (Oxali)
Act during all cell MGMT (double
cycle stages strand break repair
enzyme) and other
homologous
recombination
deficiencies (i.e.
BRCA 1/2)
Antimetabolites - Mimic purines, Multiple Coronary artery
purine/pyrimidine pyrimidines and spasm (5-FU, occurs
antagonists nutrients that are during or
(5-FU, capecitabine, required for DNA immediately post
gemcitabine, synthesis and cell treatment),
pemetrexed, 6-MP, division (Trojan mucositis, diarrhoea,
azathioprine, Horse approach) Hand-foot syndrome
cytarabine,
methotrexate) Act during S phase DPD deficiency
of cell cycle leads to 5-FU
overdose via limited
degradation - causes
severe
pancytopaenia,
haemorrhagic
diarrhoea
MTX-induced

hypersensitivity
pneumonitis
Antimetabolites - Inhibit DNA Multiple Pulmonary toxicity
anti-tumor synthesis (Bleo),
antibiotics cardiomyopathy
-Anthracyclines Act during S phase (Doxo)
(doxorubicin, of cell cycle
epirubicin)
-Non-anthracyclines
(bleomycin,
mitomycin,
mitoxantrone)
Anti-topoisomerase Inhibit Multiple Bone marrow
inhibitors topoisomerase suppression,
-Topoisomerase I enzyme which -tecans: diarrhoea,
inhibitors (-tecans) blocks the ligation cystitis, can
-Topoisomerase II step of the cell cycle overdose if
inhibitors in G2, generating underlying UGT1A1
(etoposide, DNA single/double deficiency (i.e.
doxorubicin) strand breaks leading Gilbert’s) due to
to apoptosis poor metabolism
Act during G2 phase

of cell cycle
Microtubule Mitotic spindle Multiple Peripheral
inhibitors poisons that bind to neuropathy,
-Stabilisers: taxanes microtubules with myelosuppression
(Docetaxel, high affinity, and cytopaenia,
Paclitaxel, enhances tubulin nausea, alopecia
Cabazitaxel) polymerization
-Destabilisers: vinca resulting in
alkaloids inhibition of mitosis
(Vinorelbine,
Vincristine, Act during M phase
Vinblastine) of cell cycle
Targeted therapy
Drug Target Tumour type Side Effects
Cetuximab, Anti-EGFR antibody CRC Acneiform rash,
panitumumab diarrhoea
Erlotinib/Gefitinib EGFR TKI - 1st Gen NSCLC Acneiform rash,
Afatinib (Erlo/Gef), 2nd Gen Can acquire diarrhoea
(Afat) resistance via T790
mutation (50-60%+
of patients)
Selpercatinib MET, RET
Crizotinib ROS1
Osimertinib EGFR TKI - 3rd NSCLC Acneiform rash,
Gen diarrhoea

Additionally targets
T790 mutation
Alectinib ALK TKI NSCLC Pneumonitis,
(Chromosome bradycardia,
fusion) hepatitis, visual
disturbance, N/V/D
Entrectinib ROS1/ALK/MET/ NSCLC
NTRK TKI
Sotorasib KRAS TKI NSCLC
Pertuzumab, Anti HER2 antibody Breast cancer Reversible
Trastuzumab (HER2 +) cardiomyopathy,
Diarrhoea
(pertuzumab)
Lapatinib Dual HER2/EGFR Breast cancer Diarrhoea,
TKI (HER2 +) mucositis, fatigue
Olaparib PARP inhibitor Breast cancer Myelosuppression,
(BRCA1/2 mutation) taste changes
Useful in
homologous
recombination
deficiency
Bevacizumab Anti-VEGF antibody Colon, Ovarian, Hypertension, bowel
Cervical, perforation,
Endometrial, proteinuria,
Glioblastoma, RCC, thrombosis, poor
NSCLC wound healing
Sorafenib, VEGF/multi TKI Renal cell ca, HCC HFS, CVD, LFT,
Lenvatinib, Hypothyroid, GI
Sunitinib, toxicity
Pazopanib, Axitinib
Alpelisib PI3K TKI Breast ca Rash,
hyperglycaemia,
N+V, diarrhoea
Dabrafenib, BRAF TKI Melanoma, CRC Dermatitis/skin
Vemurafenib, toxicity
Encorafenib
Trametinib MEK Melanoma Retinopathy
Palbociclib, CDK4/6 TKI Breast ca Neutropenia,
Ribociclib diarrhea,
transaminitis
Sonidegib, SHH gene Metastatic BCC Muscle spasm
vismodegib
Everolimus, mTOR inhibitors Clear cell RCC Proteinuria
Temsirolimus Poor wound healing
Deranged lipids
Less malignancy
risk however

Antibody-Drug Conjugates
Trastuzumab Delivers Breast ca ILD/Pneumonitis
Deruxtican (T-DXd) topoisomerase I
inhibitor via binding
to HER2
Trastuzumab Delivers DM1 HER2 met Breast ca Thrombocytopenia,
Emtansine (T-DM1) (microtubule poison) Transminitis
via binding to HER2
Sacituzumab Delivers Triple negative Neutropenia,
Govitecan topoisomerase I breast ca diarrhoea
inhibitor via binding
to TROP2
Immunotherapy
Drug Target Tumor type Side Effects
Ipilimumab CTLA4 inhibitor Melanoma, NSCLC, irAE –
MSI CRC, Bladder predominantly
ca Colitis,
hypophysitis,
dermatitis
Nivolumab, PD1 inhibitor Melanoma, NSCLC, irAE –
Pembrolizumab Prostate cancer predominantly
pneumonitis,
thyroid, pancreas
Atezolizumab, PD-L1 inhibitor NSCLC, ES SCLC As for PD1
Durvalumab
Endocrine therapy
Abiraterone Androgen synthesis Prostate ca (castrate Hypok, HTN,
in cells and adrenals resistant) peripheral edema
Enzalutamide, Androgen receptor Prostate ca (castrate Fatigue, cognitive
apalutamide, resistant) decline, seizures
darolutamide
Bicalutamide, Anti-androgen Castrate-resistant
cyproterone, Prostate Ca
flutamide,
nilutamide
Tamoxifen SERM HR+ Breast ca VTE< endometrial
ca
Letrozole, arimidex, Aromatase inh HR+ Breast ca Osteoporosis
exemestane
Post-menopausal
usually
Fulvestrant Estrogen receptor HR+ Breast ca
antagonist
Goserelin GnRH agonist Castrate-sensitive Decreased libido,

Prostate, breast ca osteoporosis, CVS
Degarelix GnRH antagonist Prostate ca Decreased libido,
osteoporosis, CVS
Chemotherapy-Induced Nausea
Severity Agents Treatment
Highly Emetogenic Cisplatin, NK-1 antagonist

Cyclophosphamide (Aprepitant) - Day 1;
5HT3 receptor antagonist
(Ondansetron, Palonosetron)
- Day 1;
Dexamethasone - Day 1-4
Moderately Emetogenic Doxorubicin, Irinotecan, 5HT3 receptor antagonist

Oxaliplatin (Ondansetron, Palonosetron)
- Day 1;
Dexamethasone - Day 1-3
Mildly Emetogenic Docetaxel, 5-FU, D2 receptor antagonist

gemcitabine (metoclopramide,
haloperidol) - Day 1;
Dexamethasone - Day 1
Common Important Features

Malignancies
Lung cancer ECOG status most important factor for prognosis
Important mutations: ALK, EGFR, ROS1, KRAS
Stage III can still consider surgery depending on ECOG
Rx:
Durvalumab (Anti-PDL1) can be used (ATLANTIC Trial)
Platinum-based chemotherapy remains basis
If stage IV
- Median survival 4-5 months with best supportive care
- Immunotherapy is still integral
- Consider targetted mutation and PDL1 status

Colon cancer FOBT>50 years old as screening
Colonoscopy every 5 years
RF:
- IBD
- Previous radiation
- Obesity
- Diabetes/insulin resistance
- Meat consumption
Mutations: RAS/RAF, KRAS/NRAS/EGFR, MSI
HNPCC - MMR
BRAF mt common in R) sided CRC, RAS/RAF wt common in

L) sided CRC
dMMR poorer prognosis
High rate of mets due to proximity of pudendal veins draining to

IVC
Surveillance:
-ctDNA
-CEA (every 3 months for 3 years)
-CT-CAP annually for 3 years
Rx:
FOLFOX/FOLFOXIRI/FOLFIRI
Bevacizumab (Anti-VEGF) - proteinuria, HTN and thrombosis
Cetuximab (Anti-EGFR) - KRAS WT - can cause acneiform
rash

Prostate cancer BRCA1, BRCA2
PARPi emerging
Rx:
Androgen deprivation therapy (ADT)
- Goserelin - CVS, Osteoporosis, low libido
Taxels for castrate-sensitive
Abiraterone/Enzalutamide for castrate-resistant
PARPi (Olaparib)
Bisphosphonates
Melanoma BRAF mutation

CNS involvement
RF:
Fair skin
UV Exposure
Dysplastic nevi
Age
Immunosuppression
Role of immunotherapy especially if BRAF negative
Renal cell carcinoma Clear cell RCC most common
VHL mutation
Rx:
1st line remains Sunitinib/Pazopanib
Can use immunotherapy, mTORi (Everolimus)
Breast cancer 50-74 yearly mammogram
BRCA1 and BRCA2

- <30 y/o metastatic
- <60 y/o triple negative
- Male
- Ashkenazi jews
- Ovarian cancer
Rx:
Early stage - premenopausal (Tamoxifen) and postmenopausal
(Aromatase inhibitor)
Surgery + Taxane/Anthracycline
Axillary clearance as well
Others: TDM-1, PI3 and CDK4/6 inh

Ovarian cancer Ix:
- Abdo/pelvic exam
- Ultrasound
- Basic bloods with Ca125*, CEA, AFP, HCG, LDH
- CXR, CT/MRI
- Biopsy
*Poor screening and can be normal >50% of stage 1 ovarian

cancer, elevated in other cancers and abnormal uterine bleeding,
liver diseases, diverticulitis
Rx:
Surgery (TAHBSO) + Carboplatin/paclitaxel
Debulking
PARPi
Endometrial cancer RF:

Nulliparity
Obesity
Early menarche
Late menopause
Tamoxifen/unopposed estrogen hormonal therapy
Genetics
Lynch syndrome
Rx:
Usually hysterectomy
Use of adjuvant RTx, of CTx (Carboplatin/Paclitaxel)
Hormonal therapy if ER/PR+
Immunotherapy for dMMR
Cervical cancer RF:

HPV 16/18
Multiparity
Increased sexual partners
Young age when first sex
Long term OCP
Smoking
HIV
Rx:
Adjuvant CTx/RTx - Cisplatin/Paclitaxel
Radical hysterectomy
Bevacizumab (Anti-VEGF)
Immunotherapy

Types of Breast Hormone- HER2-positive Triple negative
Cancer receptor positive, breast cancer
HER2- negative
Estrogen/Progesterone >1% of tumour Any <1% of tumour cells

receptor expression cells
HER2-amplification Negative Positive Negative
Proportion of new ~ 65% ~ 20% ~15%

cases
Risk of disease Good prognosis, Excellent due to Poorest prognosis,

recurrence after but late recurrences effective therapies but late recurrences
curative-intent can occur are uncommon
treatment
Effective treatments Endocrine therapy HER2-targeted Chemotherapy

+/- chemotherapy therapies
Chemotherapy +/-
endocrine therapy

Nephrology
Renovascular Disease
RVD/RAS Blood Pressure Renin Volume status
Unilateral RAS + + Normal
Bilateral RAS + Normal +
Polycystic Kidney Disease

Prevalence: 1 in 1000
10-15% have no family history
Pathophysiology:
PKD1 - Chromosome 16
PKD2 - Chromosome 4
-> Point mutations
RF for progressive Renal disease:

- Genetic Predisposition
- Male
- Early onset of symptoms
- Family history of ESKD
- Kidney size
- Proteinuria
- Hypertension
Extra-renal Manifestations:
- Aneurysms
- Cysts (Liver, Pancreas, Seminal Vesicle)
- Cardiac - MVP, AR
- Aortic dissection
- Colonic Diverticula
- Hernias
Criteria
- Positive family history AND
- 3 or more cysts total (15 to 39 y/o), 2 or more cysts in each kidney (40 to 59 y/o)
and at least 4 cysts in each kidney (60 y/o ans above)
- Negative MRI at age 18 almost always exclude PCKD
Management:
- BP and LIpid control
- Low Na and high fluid intake

- Tolvaptan
GLOMERULONEPHRITIS
Presentation Definition Examples
Nephrotic Nephrotic proteinuria with Proteinuria Minimal change

Syndrome evidence of glomerular disease <3.5g/dl +/- oedema +/ lip
3.5g/24hr + serum albumin
permeability Membranous
nephropathy
Primary FSGS
Lupus nephritis
Nephritic Mild Glomerular haematuria +/- Secondary FSGS

syndrome proteinuria +/- HTN +/- Lupus nephritis
preserved renal function Mesangioproliferativ
e GN
Severe Glomerular haematuria +/- Immune-complex

proteinuria +/- HTN +/- mediated GN
diminished renal function Infection-related GN
C3 glomerulopathy
Extreme Renal failure over days or Immune-complex

weeks + proteinura + mediated GN
glomerular haemautria Paucimmune (AAV)
Anti-GBM
Nephrotic Syndromes
Definition/Causes Characteristics
Minimal Primary/idiopathic Presentation

change - Sudden onset over days to a week of
disease Secondary the signs and symptoms of nephrotic
- Drugs: NSAIDs, Abx syndrome, often following an
(ampicillin, rifampicin, URTI/systemic infection
cephalopsorins), Lithium, - Constellation of
bisphosphonates, CPI’s proteinuria/albuminuria/weight gain
- Malignancy (particularly Bx
haematological) - Diffuse effacement of the podocyte
- Infections: syphilis, TB, foot processes on EM
HCV, Lyme disease - Normal glomeruli, no complement or
- Allergy Ig deposits on immunofluorscence
microscopy
Focal Primary Bx
segmental - Caused by a circulating - EM shows collapsed capillary loops
glomeruloscle permeability factor that is with hyaline entrapment and podoctye

rosis (FSGS) toxic to the podocyte and foot process effacement
causes generalised - More advanced form of MCD
podocyte dysfunction - suPAR (soluble plasminogen
activating receptor)
Secondary
- Maladaptive response to Rx
glomerular hypertrophy - Glucocorticoids mainstay
or hyperfiltration - Can also use CNIs
- Proteinuria often not in (tacrolimus/cyclospoin) but caution
nephrotic range with renal impairment
Membranous Autoimmune disorder Bx

nephropathy characterised by thickening of - LM shows diffuse thickening of GBM
the glomerular basement throughout all glomeruli in absence of
membrane due to subepithelial significant hypercellularity
immune complex deposition - IFM shows diffuse granular pattern of
IgG and C3 staining along the GBM
Primary - EM subepithelial electron-dense
- Autoimmune response to deposits on the outer aspect of the
PLA2R (others to be GBM
aware of
NELL1/THSD7A/SEMA PLA2R Abs classic exam Q
3B)
Secondary
- Malignancy, SLE, HBV
Amyloidosis AL amyloidosis Kidney Bx may be deferred if amyloidosis is

- Characterised by suspected in patient with a monoclonal
deposition of Ig light gammopathy - then would do an abdominal
chains fat pad aspirate to get dx of systemic AL
- Abnormal clonal amyloidosis
proliferation of plasma
cells EM shows expansions of the mesangium by
amyloid fibrils
AA amyloidosis Positive congo red staining
- Characterised by
deposition of amyloid A
- Chronic inflammatory
conditions (eg RA,
AnkSpon, IBD, FMF)

Glomerulonephritis
Definition/Causes Characteristics
IgA nephropathy Etiology largely unknown Majority present with haematuria +/- flank pain
Characterised by mesangial +/- low grade fever
deposition of IgA - Small percentage present with RPGN
- Often accompanied by HTN
Most common cause of
primary GN Bx
- IF: prominent globular deposits of IgA
Some association with CLD, in the mesangium
Coeliac, HIV, monoclonal - EM: dense deposits primarily in the
gammopathy of renal mesangium
significance
Rx
- ACEI mainstay - BP control and
reduction of proteinuria
- Commence of proteinuria
>500mg/day
- Sodium restriction, SNAP lifestyle
changes
- Use immunosuppresive agents in
patients who remain high risk for ESKD
despite maximal supportive care (eg
proteinuria >1g/day)
- Can consider SGLT2i if eGFR >30
Lupus Nephritis Most LN presents within 6-36 Class IV LN most common and most severe
months of SLE Dx form of LN
- Low C3 and high dsDNA during active
Highest risk of LN early in disease
time course - >50% glomeruli affected
- Male, <33yo at Dx,
non-white Histology features of LN
- Glomerular depositis that stain for IgG
Six histological subclasses and contain deposits of
- Class I: minimal IgA/IgM/C3/C1q
mesangial LN - Glomerulare deposits seen in
- Class II: mesangial mesangium, subendothelial and
proliferative LN subepithelial locations
- Class III: Focal LN - Extraglomerular immune deposits with
- Class IV: diffuse LN TBM, interstitium and vessels
- Class V: Membranous
LN Class V - diffuse thickening of glomerular wall
- Class VI: Advanced
sclerosing LN Rx
- MMF or cyclophosphamide initially
- Can also use MMF + CNI

Infection-related Post streptococcal GN most Presentation
GN common cause of nephritis - Gross haematuria, oedema and HTN
post infectious event
Caused by glomerular
immune complex disease Bx
induced by nephritogenic - EM: dome-shaped subepithelial deposits
strains of GAS - IF: deposition of IgG and C3 in a
diffuse granular pattern in the
Non-strep more common in mesangium and glomerular capillary
older age groups walls
Supportive Rx
Pauci-immune Granulomatosis with Can be cause of RPGN - so may see crescents

GN polyangiitis on Bx if severe enough
- ANCA associated
vasculitis (cANCA) Bx
- Crescents, segmental necrotising GN,
Microscopic polyangiits granulomas in GPA, none in MPA or
- AAV - pANCA EGPA
Rx
- Glucocorticoids + Rituximab
- If organ/life threatening disease use
GCs + Ritux +/- Cyclophosphamide
- After 3-6 months, reassess and
determine if suitable for maintenance
therapy - if yes, use either
ritux/aza/methotrexate
Anti-GBM GN Small vessel vasculitis affects Most present with RPGN, 20-60% also present
(Goodpasture’s) the capillary beds of the with alveolar haemorrhage
kidneys and lungs
Anti-GBM antibodies positive in serum or in
Directly pathogenic anti- kidney
GBM autoantibodies (non- Should also test for ANCA in all anti-GBM pos
collagenous domains of a3 patients
chain of type IV collagen)
Bx
Most often idiopathic but can - LM: Crescentic GN
follow lung or kidney injury - IF: pathognomonic linear deposition of
eg infection, inhalation of IgG along the glomerular capillaries and
hydrocarbons or other forms occasionally the distal tubules
of GN
C3 C3 Dense deposit disease C3 DDD

Glomerulopathy - Rare form of MPGN - EM characteristic sausage-shaped,
- Presence of antibodies waxy, densely osmophilic deposits
called C3 nephritic along the GBM and mesangium
factors stabilise C3
convertase C3 GN
- IF shows extensive C3 deposition along
C3 GN capillary walls with no significant Ig
- Caused by excessive deposition
activation of the
alternative Rx
complement cascade - Depends on severity of disease
due to mutations in or - Mild: supportive measures and
antibodies regulating monitoring
proteins - Mod-severe: Supportive measures + GC
- Increased activity of + MMF
C3 convertase - RPGN: supportive measures + GC +
Cyc/MMF +/- Eculizumab +/- PLEX
- Refractory disease: Eculizumab
Barter and Gittleman syndromes
Source: RACP CLS

Renal Tubular Acidosis
Type 1 Type 2 Type 4
K Low Low High
Ca High Normal Normal
Urine pH >5.5 <5.5 <5.5
Nephrolithiasis Yes No No
Location/primary Distal - defect in distal H+ Proximal - reduced Collecting duct -

defect secretion/impaired distal proximal bicarb decreased aldosterone
acidification reabsorption secretion or aldosterone
resistance
Causes Autoimminue - Sjogren’s, Monoclonal Hyporeninaemic

RA, SLE gammopathies hypoaldosteronism -
Drugs - Lithium, (myeloma), Fanconi’s Diabetic nephropathy,
Ibuprofen, Amphotericin syndrome, Amyloidosis, NSAIDs, K-sparing
Hypercalciuric conditions - PNH diuretics, ACEI/ARBs,
Hyperparathyroidism Drugs - Acetazolamide. Addisons/Primary
Topiramate, adrenal insufficiency.
oxaliplatin/cisplatin, Heparin, Severe illness,
Tenofivir acute GN
Treatment Alkali therapy with PO Much more difficult to Treat the underlying
bicarb (binds retained H+ treat, similar principles to cause if possible
ions to reduce acidosis) type 1 - Alkali therapy Fludrocortisone -
with PO bicarb caution though as can
If due to toxic agent - lead to fluid retention
may resolve on own once
culprit agent is ceased
If Fanconi - replace PO4
and VitD as well as alkali
therapy
Fanconi Syndrome
Proximal tubule physiological function:

- Reabsorption of electrolytes
- Vit D activation
- Acid/Base balance
- Recycling light chains
Feature of RTA type 2 (Proximal) - Hyperchloraemia NAGMA, hypokalemia and low HCO3
Features: glycosuria, amino aciduria, phosphaturia, uric aciduria

Causes:
- Acquired - medications (Tenofovir), Autoimmune, Myeloma, Heavy metals
- Hereditary - Wilson’s disease, Fructose intolerance

Renal Replacement Therapy (RRT)
Dialysis
- Used to support kidneys for fluid removal and waste clearance
- Doesn’t perform active transport
- Based on Diffusion (utilising a concentration gradient) and Convection (utilising
hydrostatic pressure
- Diffusion: think HD and PD - good for clearing small molecules
- Convection: think haemofiltration - good for clearing larger molecules
- Indications
- Acute: oligoanuria, fluid overload/APO, metabolic acidosis, refractory
hyperkalaemia, uraemic encephalopathy, uraemic pericarditis
- Chronic: Fatigue, difficulty concentrating, loss of appetite, metallic taste,
itch
- Long term complications
- Mineral bone disorders - more common in CKD patients on dialysis,
reiterates importance of phosphate binders if needed
- Vascular calcification
- Calciphylaxis - causes blood clots, painful skin ulcers and potential for
serious infections secondary to accumulation of calcium in small blood
vessels of the fat and skin
Haemodialysis Peritoneal dialysis
Area dialysed Blood directly though arterial Abdominal wall through a dialysing
and venous access fluid
PD solutions consist of
sodium/calcium/magnesium/chloride
Glucose is the principle osmotic agent
Access Temporary Peritoneal dialysis catheter

- Vascath, permacath Should be placed away from the
Permanent beltline, away from a skin fold, visible
- AVF (Radio-cephalic, to the patient and 2cm away from cuff
Brachio-cephalic,
Brachio-basilic), loop Continuous ambulatory PD
graft Continuous automated PD
AVF takes 6-8 weeks to mature
Frequency Few hours 3-5x/week Daily
Benefits Rapid access Lifestyle/work/travel balance

Better long term option Better for maintaining residual renal
AVF easy to cannulate function but not a lifelong option due to
likely sclerosed membrane

Complications Secondary to AVF Catheter infection
- Steal syndrome Catheter malfunction
(subclavian artery - Most common cause of failed
stenosis proximal to the PD is constipation
origin of the vertebral
artery) - results in Peritonitis
vertebrobasilar - Most common pathogens: Staph
insufficiency epi, staph aureus,
- Aneurysm enterobacteriaceae,
- Bruising/haematoma Streptococcus and enterococcus
species
Disequillibrium syndrome - IP route preferred route for Abx
- Cerebral oedema due to - Gent + cephazolin added to PD
osmotic effects of urea bag used for empiric treatment
- Common after first few - Can also use Vancomycin if
sessions of dialysis MRSA or allergy to
- Need to start dialysis cephalosporins/penicillins
slowly
Membrane sclerosis
Intradialytic hypotension Pleuroperitoneal leak
- Consider pausing or
ceasing fluid removal if
occurs
Dialysis-related amyloidosis
- Due to long term
accumulation of b2-
microglobulin
- Doesnt really happen
anymore due to newer
high-flux dialysers
Haemodialysis Prescription
- Duration
- Frequency
- Blood flow rate
- Dialyzer
- Ultrafiltration rate
- Dialysate composition
- Dialysate temperature
- Anticoagulation
- Intradialytic products - erythropoietin, iron, blood transfusion, nutrition and
antibiotics

Renal Transplant

Indications Irreversible and progressive CKD
Should be referred for transplant work up when eGFR<30
Ideally transplant should happen before dialysis is required -> improved
patient and graft survival
Options Living donor

- Blood typing and crossmatch needed, including HLA
- No CIs: age <18, uncontrolled HTN, HIV infection, T1DM, active
malignancy, high suspicion of donor coercion and others
- Need to have appropriate renal function, ideally no albuminuria or
haematuria
- Diabetes is an absolute CI to donation
Deceased
- Similar criteria
- Outcomes not as good as living donor however still improved
compared to those who remain on dialysis
- Can only use a donor kidney from a deceased person after starting
dialysis
Contraindications Absolute
- Active infection
- Active malignancy (excluding non-melanoma skin cancers)
- Active substance abuse disorder
- Reversible kidney failure
- Uncontrolled psychiatric disease
- Documented active and ongoing treatment non-adherence
Relative
- Malnutrition
- Uncontrolled ANCA vasculitis
- Severe hyperparathyroidism -> may need subtotal parathyroidectomy
prior to transplant
- Primary oxalosis
- Systemic amyloidosis -> due to high mortality
Donor age and comorbidities not necessarily CI’s but important factors to
consider when selecting donor
Immunosuppression Induction
- Rabbit Antithymocyte globulin (rATG) or Basiliximab (anti-CD25
mab)
Maintenance
- Triple immunosuppression: antimetabolite + calcineurin inhibitor +
glucocorticoids
- Eg: Azathioprine/MMF + Cyclosporine/Tacrolimus + prednisolone
Tacrolimus associated with decreased acute rejection rates and generally

better tolerated than cyclosporine

MMF preferred over azathioprine due to its superior ability to prevent acute
rejection and its better side effect profile (and do not need TPMT activity)
MMF not used in female recipients of child-bearing age unless long-acting

contraception/sterilisation/infertile
Facts about CNI (Tacrolimus and Cyclosporin)

immunosuppression - Both can cause nephrotoxicity, hypertension, hyperlipidaemia, TMA
agents - Tacrolimus more incidence of NODAT, hypomagnesemia, tremor,
neurotoxicity, hair loss compared to cyclosporin
Anti-metabolite (MMF/MPA and AZA)

- MMF/MPA higher diarrhoea and teratogenic. No issue with TPMT
deficiency compared to AZA.
mTORi (Sirolimus, Everolimus)

- Less cancer and CMV infection
- Higher wound complications, proteinuria, haematological
(cytopenia, TMA), hyperlipidaemia, mouth ulcers, oedema,
interstitial pneumonitis
Complications <1 year: IHD

>1 year: Malignancy
Infections
- Major cause of death following kidney transplant
- URTI/UTI most common
- Opportunistic infections eg CMV, BK virus, Listeria, Aspergillus,
Nocardia, PJP, HSV, EBV, TB, VZV
- Vaccinations crucial post transplant Mx -> vaccines indicated for
immunocompromised patients should be administered 3-6 months
post transplant
- Prophylaxis post transplant -> PJP
PTLD
- Secondary to outgrowth of EBV-pos B-cell proliferations in setting
of chronic T-cell immunosuppression
- Principal RF underlying development of a PTLD are the degree of
overall immunosuppression and the EBV serostatus of the patient
- Rx: if early can reduce immunosuppression, otherwise consider
Rituximab if CD20+ PTLD
Acute rejection
- Suspect when sCr rises >25% from baseline, worsening HTN,
proteinuria >1g/day, or plasma donor-derived cell-free DNA >1%
Complications T-cell mediated (TCMR)

(continued) - T cells react to donor histocompatibility antigens -> interstitial

infiltration with mononuclear cells and disruption of tubular
basement membrane
- Banff scoring system used to diagnose acute TCMR
Antibody mediated (ABMR)

- Circulating antibodies bind to donor alloantigens on graft endothelial
cells -> inflammation, cell damage, graft dysfunction
- Diagnosis requires three components
- Histological evidence of acute tissue injury
- Evidence of Ab interaction with vascular endothelium (C4d
staining in peritubular capillaries)
- Serological evidence of circulating donor-specific Abs
Malignancy
- Renal transplant recipients 3x more likely to develop cancers
- Skin cancer, PTLD, anogenital cancers, Kaposi sarcoma, RCC
BK nephropathy
- Mainstay of treatment is to reduce immunosuppression
ESKD despite transplant

- HTN and Diabetes most common cause
- Consider secondary to CNIs
Delayed graft function

- Most commonly due to ischaemic ATN
- RF for ATN - deceased donor, donor AKI, donor age, DCD and cold
ischaemia time
- Other causes: Graft thrombosis, rejection, recurred disease
New-onset diabetes after transplant (NODAT)

- Especially with Tacrolimus

Sugi, M.D. et al. (2019) ‘Imaging of renal transplant complications throughout the life of the allograft: Comprehensive multimodality review’, RadioGraphics,
39(5), pp. 1327–1355. doi:10.1148/rg.2019190096.

Neurology
UMN LMN
Tone Up Down
Power Pyramidal weakness Down

(Reduced extensors of UL
and reduced flexors of LL)
Reflexes Up Down
Plantars Up Down
Clonus Yes No
Cerebral Cortex
Frontal lobe - Primary Motor Cortex
- Personality
- Anosmia
- Optic Nerve involvement (Foster-Kennedy Syndrome)
- Gait Apraxia
- Expressive Dysphasia (Broca)
- Primitive Reflexes (palmomental, snout etc)
Parietal lobe - Primary sensory cortex
- Gerstman syndrome (Acalculia, Agraphia, L-R
disorientation, finger agnosia)
- Spatial inattention
- Construction Apraxia
- Lower quadrantanopia
Temporal lobe - Primary auditory cortex
- Receptive Dysphasia (Wernicke)
- Memory loss
- Upper quadrantanopia
Occipital lobe - Homonymous hemianopia
- Anton’s syndrome (cortical blindness and confabulation)
- Alexia without agraphia

Stroke
Management:
BP control – aim <130/90mmHg (consider permissive HTN to reduce extent of irreversible
ischaemia (Good to learn around the Lacunar syndromes as well, common among patients
with uncontrolled HTN)
Lipid control – aim LDL <1.8
Diabetes management
Antiplatelet therapy:
- DAPT 3/52 then SAPT (CHANCE and POINT trials)
- Can be started as soon as CTB excludes haemorrhage or 24/24 after tPA+CTB
Thrombolysis (tPA)
- Choice of alteplase, tenecteplase and streptokinase
- Absolute contraindications: Extensive hypoattenuation on CT, suspicion of SAH,
current or previous ICH, intracranial neoplasms, severe head trauma last 3 months,
intracranial and intraspinal surgery, PC<100, INR>1.7, APTT>40, Clexane last
24/24, suspicion of current endocarditis, active GI/internal bleeding, aortic
dissection
Recanalisation:
- ICA, MCA M1, MCA M2, Basilar
- If eligible for thrombectomy and tPA, to give tPA still
- DAWN trial – thrombectomy from 6-24 hours using perfusion imaging
- DEFUSE trial - thrombectomy 6 to 16 hours using perfusion imaging
CEA/Stenting
Hemicraniectomy – malignant MCA
Window summary:
1) tPA
- 0 – 4.5 hours – CTB -> Alteplase
- 4.5 – 9 hours – CTP/DWI-MRI to determine-> Alteplase
2) Thrombectomy (large vessel)
- 0 – 4.5 hours – tPA + thrombectomy
- 4.5 – 9 hours – if delay can tPA prior
- 9 -24 hours – CTA+CTP -> Thrombectomy
Treat etiology:
- AF
- PFO closure
- Hyperviscosity/hypercoagulable states/diseases
Other ddx: Cerebral amyloid angiopathy, cerebral venous sinus thrombosis

Movement disorders *important for short cases
Parkinson’s Disease Alpha-synucleinopathy
Pre-symptomatic stage:
- Constipation
- Anosmia
- REM SBD
- Mood changes
Symptomatic stage:
- Bradykinesia/Akinesia
- Rigidity
- Tremor (4-6 Hz)
- Supportive features: Rest tremor, L-DOPA response
and dyskinesia, olfactory loss, cardiac sympathetic
denervation on MIBG
Treatment:
- Levodopa
- Amantadine
- Dopamine agonist (pramipexole, topical rotigotine,
cabergoline, bromocriptine)
- Monoamine Oxidase Inhibitors (MAO-B)
- Symptom management (Drooling, REM SBD,
Hallucinations, Dementia, Constipation)
- Advanced – DBS, Apomorphine infusion,
Intraduodenal levodopa, sub-thalamotomy (under
USS)
Dementia with Lewy Bodies Alpha-synucleinopathy

(DLB)
Progressive cognitive decline
Visual hallucinations (Lilliputian, Pareidolias)
Less than 1 year between cognitive and movement

symptoms
Treatment: Anticholinesterases
Progressive Supranuclear Tauopathy
Palsy (PSP)
Postural instability, dementia
Vertical gaze palsy (downgaze)
Minimal tremor
Pseudobulbar palsy
MRI: Hummingbird sign

Treatment: Can try L-Dopa
Multisystem Atrophy Alpha-synucleinopathy

(MSA)
Triad of autonomic failure, parkinsonism, cerebellar signs
- Hence MSA-P, MSA-C and MSA-A subtypes
Corticobasal syndrome Tauopathy
(CBD)
Alien hand, assymetrical progressive apraxia of the hand
Epilepsy
Classification:
- Generalized
- Focal (Motor, Awareness)
Treat after second seizure
Causes:
- Genetic
- Structural
- Immune
- Metabolic
- Idiopathic
Syndromes:
- Juvenile Absence Epilepsy
- Juvenile Myoclonic Epilepsy
- Mesial temporal lobe epilepsy with hippocampal sclerosis
Medications
- Focal – Carbamazepine (Check HLAB1502 and HLA3101), Lamotrigine,
Levetiracetam, Gabapentin, Valproate, Phenytoin
- Generalized – Valproate, Levetiracetam, Lamotrigine (Child bearing age),
Ethosuximide (Absence)
- Best to combine different classes (Na channel, Ca channel etc) ie Lamotrigine and
Valproate
 Drug resistant Epilepsy – consider surgery
Complications:
- Osteoporosis, osteopenia
- SUDEP
- Psychosis
- Status Epilepticus (Convulsive and Non-convulsive, Refractory)
Obstetrics:
- Consider interaction with contraception
- Infertility risk
- Teratogenic properties of AEDs

- Best tolerated – Carbamazepine, Lamotrigine
Antibodies
Anti-GM1 Multifocal motor neuropathy with conduction block
Anti- GQ1B Miller-Fisher syndrome
Anti-AChR Ab Myasthenia Gravis
Anti-MuSK Myasthenia Gravis (more common in seronegative MG,
usually no ocular involvement)
Anti-LRP4 Myasthenia Gravis (relatively mild)
Anti-VGCC Lambert-Eaton Myasthenic Syndrome (LEMS)
Anti-Hu Limbic encephalitis (SCLC)
Anti-Yo Cerebellar degeneration (Breast ca)
Anti-Ri Opsoclonus-Myoclonus (SCLC)
Anti-Ta/Ma Rhomboencephalitis (Testicular ca)
Anti-Amphiphysin, CRMP5 Paraneoplastic myelitis
Anti-GAD Stiff-Person Syndrome
Anti-VGKC (LGI1, Autoimmune encephalitis
CASPR2)
Anti-KELCH-11 Cerebellar syndrome (Testicular seminoma)
Anti-NMDA Autoimmune encephalitis (ovarian ca)
Anti-Aquaporin 4 NMOSD
Anti-MOG NMOSD
Anti-MAG Paraproteinaemia-associated neuropathy
Neuroimmunology
MS NMOSD
Anatomy Any white-matter Optic nerves and spinal cord

Astrocytopathy
Risk factors HLADR2
Environmental: EBV, Latitude,

smoking, reduced sunlight
exposure
Attack Severity Mild Severe
Diagnosis McDonald’s Criteria - 2 lesions MRI: Longitudinally extensive

in time and space
MRI: Multiple white matter

lesions (periventricular,
infratentorial, spinal,
juxtacortical)
CSF Oligoclonal bands Pleocytosis
Permanent Late progressive phase Usually attack-related

disability
Coexisting Less common More common

autoimmunity
Serum antibodies Absent AQP4 Ab, Anti- MOG Ab
Clinical features Demyelinating attack - longer More severe than MS

than 24-48 hours with nadir of 2
weeks Optic neuritis, Acute myelitis,
Area postrema syndrome, Acute
brainstem syndrome,
symptomatic narcolepsy,
symptomatic cerebral syndrome
Treatment Injectables - Interferon beta, Aza/MMF, Rituximab,

Glatiramer Acetate Eculizumab, Inebilizumab,
Satralizumab
Orals - Fingolimod,
Teriflunomide, Cladribine,
Dimethyl Fumarate, Siponimod
MAb - Natalizumab,
Alemtuzumab, Ocrelizumab,
Rituximab
Differentials Differential diagnosis of myelitis:

Infection - HSV, VZV, HTLV1, HIV, Syphilis
Autoimmune - MS, NMO, Sarcoid, GFAP
Paraneoplastic - CRMP5, Amphiphysin
Optic Neuritis Subacute

Pain on eye movement
Decreased visual acuity, colour vision
RAPD

MG and GBS features
Myasthenia NMJ disease

Gravis Fatigable ocular, limb and bulbar weakness
Neck flexion weakness
Limb weakness - proximal and symmetric
AChR Ab, MuSK, LRP4

Thymoma
Triggers: Medications (ABx, checkpoint inh, NMJ blockers,

anaesthetics, CVD drugs), surgery, stress, infection, heat
Myasthenic crisis - Resp failure - IVIg and PLEX as Rx
Ix: Ab tests, NCS, Single-fibre EMG, Ice pack test, Edrophonium

test, CT chest
DDx: LEMS, Congenital myasthenic syndromes, Botulism, Lyme

disease, Bulbar ALS, Miller-Fisher syndrome, Pharyngeal-cervical-
brachial variant of GBS, Oculopharyngeal muscular dystrophy,
Mitochondrial disorders
Rx: Immunosuppression, Thymectomy
Guillain-Barre Inflammatory, immune mediated disease of PNS

Syndrome (GBS)
Acute onset weakness and sensory symptoms and ascending in
nature
Extraneural involvement: Dysautonomia, Respiratory involvement
Subtypes: AIDP, AMAN, AMSAN, MFS (Ataxia, Opthalmoplegia,

Areflexia), Bickerstaff encephalitis
2/3rds have antecedent respiratory or diarrheal illness
Nadir 2 weeks
>4 weeks - CIDP
DDx: Anterior horn cell disease, NMJ disorders, Myopathies,

Periodic paralysis, acute polyradiculopathies
Ix: CSF (albuminocytologic dissociation), NCS (prolonged F wave),

EMG, Antibody (GQ1B, GM1), Imaging, Sural nerve biopsy
Rx: Look for cx, IVIg, PLEX
Poor prognosis: >40 y/o, preceding diarrhea, mechanical ventilation,

high grade neurological deficits, persistentloy low CMAP amplitudes

Encephalitis
Definition:
- Major - altered mental state, personality change >24 hours with no other cause
found
- Minor (3 or more) - Fever, Seizure, Focal neurological findings, abnormal CSF,
abnormal MRI, abnormal EEG
Syndromes:
- Limbic Encephalitis - Psychiatric manifestations ie temporal lobe involvement
- Rhomboencephalitis - cranial nerve or brainstem signs
- Cerebellitis
Causes:
- Infective - Viral (HSV, VZV, Enterovirus, Flavivirus, CMV, EBV, HHV6, HIV),
Bacterial (TB, Syphilis, Listeria), Fungal (Cryptococcal)
- Autoimmune - NMDA, LGI1, CASPR2, KELCH-11, CRMP5/Ampiphysin
- Paraneoplastic - Anti-Hu, Yo, Ri,Ta/Ma

Palliative Medicine
https://www.health.wa.gov.au/~/media/Files/Corporate/general-documents/Palliative/opioid-chart.pdf

Pharmacology, Toxicology and Addiction
Medicine
Antidote Toxin
Atropine Organophosphates
Calcium CCB, Beta-blockers
Glucagon Beta-blockers
Digibind Digoxin
Flumazenil Benzodiazepines
Hydroxocobalamin Cyanide
Intralipid Local Anaesthetic Toxicity
NAC Paracetamol
Naloxone Opioids
Sodium Bicarbonate TCAs
Culprits Features
Anticholinergic Antihistamines, TCAs, first “Hot, dry, mad, blind and red”
syndrome generation antipsychotics
Cholinergic syndrome Acetylcholinesterase inhibitors Agitation, diarrhoea, urination,

(Organophosphates) or ACh bronchospasms, bronchorrhea,
agonists ie nicotinic agents, bradycardia, miosis, emesis,
mushrooms lacrimation, salivation
NMS Antipsychotic agents, CNS (confusion, delirium),

dopamine agonists autonomic dysfunction,
neuromuscular, hyporeflexia
Opioid intoxication Opioids Delirium, hypotension due to

syndrome histamine release, respiratory
depression
Serotonin syndrome SSRI, SNRI, MAOIs Similar to NMS but with

hyperreflexia
Sympathomimetics Catecholamines, Agitation, autonomic

amphetamines, cocaine dysfunction, hyperreflexia,
tremor
Clinical trial phases
Phase 1: evaluate toxicity, study drug disposition (pharmacokinetics), determine dose for
phase 2
Phase 2: estimate efficacy, further define toxicity
Phase 3: compare outcomes with usual standard of care
Phase 4: Post registration, confirm results from fast-track approval trials, additional post-
marketing safety assessment
CYP450 drugs interactions
Inhibitors - SICKFACES.COM Inducers - CRAP GPS

These drugs will increase the concentration These drugs will reduce the concentration of
of drugs metabolised by the CYP450 system drugs metabolised by CYP450 system
Sodium valproate Carbamazepine

Isoniazid Rifampicin
Cimetidine Chronic Alcohol
Ketoconazole Phenytoin
Fluconazole Griseofulvin
Acute Alcohol and grapefruit juice Phenobarbitone
Chloramphenicol Sulphonylureas
Erythromycin St Johns Wart
Sulphonamide
Ciprofloxacin
Omeprazole
Metronidazole

Pharmacology equations

Source: DeltaMed 2022

Respiratory and Sleep Medicine
Source: https://rc.rcjournal.com/content/62/11/1492
Source: Medbullets https://step1.medbullets.com/respiratory/117009/lung-volumes-and-capacities

Spirometry Interpretation
Source: https://erj.ersjournals.com/content/26/5/948.figures-only
Upper lobe fibrosis Lower lobe fibrosis
Coal worker pneumoconiosis CTD - RA, SLE

Histoplasmosis Drugs - MTX, Nitrofurantoin, Bleomycin,
Sarcoidosis Amiodarone
Aspergillosis Asbestosis
Histiocytosis X
Radiation
TB
Silicosis
Ankylosing Spondylitis
*Important for short case

Common Features
Conditions
COPD Persistent airflow obstruction (FER<0.7)

Can overlap with asthma
Non-pharmacological Rx: Smoking cessation, Pulmonary rehab

Pharmacological Rx (Minimal evidence of inhaler therapy slowing
progression):
1) LAMA monotherapy
2) LAMA/LABA combination or LABA/ICS
3) ICS/LAMA/LABA (Trelegy, Trimbow, Trilegy)
(ICS better if evidence of eosinophilia, or recurrent admissions
as it may precipitate pneumonia)
GOLD classification for severity
Asthma Variable airflow limitation
T2-high (Eosinophilic) and T2-low(Non-eosinophilic)
Associated with atopy, work-related exposures, since childhood and

bronchodilator response
Ix: RFT - FER<0.7 with bronchodilator reversibility >10% (new

guideline from 2022, previously 12%) and >200mls increase in FEV1,
Methacholine provocation test has good negative predictive value,
mannitol test has good positive predictive value, FeNO for eosinophilic
asthma
DDx: eGPA, Aspirin-related respiratory disease, ABPA, Drug-induced

(Nitrofurantoin, Ampicillin, Minocycline, Phenytoin, GM-CSF,
oxaliplatin), Chronic eosinophilic pneumonia, Acute eosinophilic
pneumonia
Classification:
- Intermittent - symptoms/SABA<2/week
- Mild persistent - symptoms/SABA>2/week
- Moderate persistent - Daily symptoms, mildly reduced FEV1
- Severe persistent - Abnormal FEV1 <60% with daily symptoms

and nocturnal features
Rx: Regular ICS or ICS/LABA PRN initially (SABA monotherapy not

recommended),
Biologics (Omalizumab, Mepolizumab, Benralizumab and Dupilumab,
Tezepelumab)
ILD Types:
- ILD of known cause - dusts (asbestosis, silicosis), CTD,
radiation-induced, drug-induced
- Granulomatous (Sarcoidosis)
- Idiopathic - IPF, COP,AIP, RB-ILD, Desquamative, NSIP
- Others - Lymphangioleiomyomatosis, Pulmonary Langerhans
cell Histiocytosis
IPF features on HRCT:

- Honeycombing
- Traction bronchiectasis
- Reticular opacities
- Subpleural and basal dominance
- No atypical features
Rx: Antifibrotics - Pirfenidone and Nintedanib
(PBS Criteria - IPF diagnosed via MDM, DLCO>30%, FVC>50%,
FER>0.7, no other causes)
*IPF can look very similar to Hypersensitivity pneumonitis and often

difficult to differentiate except with thorough history taking
NSIP features on HRCT:

- Ground glass opacity
- Reticular opacities
- Traction bronchiectasis
- Diffuse
(Now labelled as IPAF - Interstitial pneumonia with autoimmune
features)
Rx: Steroids, Thiopurines, IV Cyclophosphamide, Rituximab, Lung
transplant
Sarcoidosis
- 1:10000
- Th1 inflammation
- DDx: TB, Lymphoma, other ILD
- Generally require tissue diagnosis
- Bronch - elevated CD4:CD8 ratio, endobronchial/transbronchial
biopsy, EBUS
- Extrapulmonary involvement: Ocular, Calcium, Cardiac, CNS
- Indications for treatment - Progressive pulmonary disease,
cardiac, neurological, eye disease, symptomatic hypercalcemia

Medications in Respiratory medicine
Medications Details
CFTR Modulators Used for CF

(Ivacaftor, Tezacaftor,
Elexacaftor) Ivacaftor - Potentiator
Tezacaftor, Elexacaftor - Recruit
Omalizumab Anti-IgE
Indication: Asthma
Some role coming in chronic spontaneous urticaria, mild benefit

in eGPA
Mepolizumab, Acts on IL-5 (which mediates eosinophils)

Benralizumab
Indication: Asthma (eosinophilic asthma/Type 2 High asthma),
eGPA
Dupilumab Anti-IL-4/IL-13
Indication: Asthma
Pirfenidone Direct antifibrotic

Indication: ILD
SE: Photosensitivity
Nintedanib TKI
Indication: ILD, Scleroderma-ILD
SE: CVD, LFT derangement
Exudative Pleural Effusion Transudative Pleural Effusion
Malignant (Metastatic, mesothelioma, Heart failure

lymphoma) Hepatic hydrothorax
Infection (Bacterial, fungal, viral, Cirrhosis
parasitic, TB) Hypoalbuminaemia
CTD (SLE, RA, MCTD, FMF) Nephrotic syndrome
Drug induced (Nitrofurantoin, SVCO
amiodarone, MTX, TKIs, Clozapine) Constrictive Pericarditis
Inflammatory (Pancreatitis, PE, Renal failure
Sarcoidosis, post-cardiac surgery, ARDS) Peritoneal Dialysis
Endocrine (Myxoedema) Urinothorax
Gynae (Meigs syndrome, Ovarian Duropleural shunt

Hyperstimulation syndrome, Catamenial Ventriculopleural shunt
Hemothorax) Trapped Lung
Iatrogenic (Misplaced catheters,
sclerotherapy)
Movement of fluid (Pancreatitis,
malignant ascites)
Pleural thickening (Trapped lung,
cholesterol effusions)
Miscellaneous (BAPE, RTx)
Source: Light and Lee 2016
Sleep disorders Features
Obstructive Sleep Apnea AHI >5/hr with symptoms or >15 +/- symptoms
Daytime somnolence
Cx: MVA, Metabolic syndrome, pHTN, nocturnal

bradyarrhythmia
STOPBANG Questionaire for screening
Rx: WL, Mouth guards, CPAP, uvulopalatopharyngoplasty
Note: Read around the differences between Apnea,

Hypopnea and RERA.
Obesity Hypoventilation Triad of awake hypercapnia, BMI >30 and sleep

Syndrome disordered breathing (SDB)
Chronic hypercapnia originates from renal retention

(decreased compensatory hyperventilation)
High all cause mortality - 30% in 2 years
SDB in HF OSA vs CSA-CSR

Optimize HF therapy
Adaptive Servo Ventilation (ASV) from SERVE-HF
increases mortality for HFrEF
Narcolepsy Type 1 - at least 3 months of excessive daytime sleepiness,

cataplexy with positive MSLT and low CSF hypocretin
Type 2 - similar but no cataplexy and normal CSF
Hypocretin
Rx: Stimulant (Dexamphetamine), wake promoting agent

(Armodafinil), SSRI and SNRI can be used for cataplexy

Pulmonary Hypertension
Precapillary (1,3,4,5) - mPAP >20 mmHg, PAWP <15mmHg, PVR>3 WU

Post-capillary (2 and 5) - mPAP >20mmHg, PAWP>15mmHg, PVR< 3WU
Combined pre and post-capillary - mPAP>20mmHg, PAWP>15mmHg, PVR>3WU
Rx:
Endothelin antagonist - Bosentan
PDE5inh - Sildenafil
Prostacyclin analogue - Epoprostenol
Soluble guanylate cyclase pathway - Riociguat
Combination therapy - Ambrisentan + Tadalafil
Type 1 Idiopathic
Hereditary
Drug and toxin induced
Associated with CTD, HIV, Portal HTN, Congenital Heart
Disease, Schistosomiasis
Persistent pHTN in newborn
Responds to CCB
Associated with BMPR2 gene
Type 2 HFrEF
HFpEF
Valvular HD
Other cardiomyopathies
Type 3 Obstructive Lung disease

Restrictive Lung disease
Mixed
Pulmonary disorders
Type 4 CTEPH
Type 5 Haematological disorders

Systemic and metabolic disorders
Complex congenital heart disease

Rheumatology
Cytokine inhibition Biological agent Diseases Not effective
IL-1 Anakinra JIA, Gout RA
Canakinumab
IL-6 Tocilizumab RA, JIA, GCA
TNFalpha Infliximab RA, JIA, ANCA vasculitis
Golimumab Ankylosing
Adalimumab Spondylitis, IBD,
Etanercept Psoriasis + Psoriatic
Arhtiris, Systemic
Sarcoidosis
IL- 12/23 Ustekinumab SpA, IBD, Psoriasis
IL-17 Secukinumab SpA, Psoriasis RA and IBD
Anti-BAFF/BLYS Belimumab SLE
Anti-IFN Anifrolumab SLE
CTLA-4 Agonist Abatacept RA
JAKi Upadacitinib RA, SpA
Tofacitinib
Baricitinib
CD20i Rituximab RA, APLS, SpA,
AAV, Myositis, SLE
RANKL Denosumab Osteoporosis
Antibodies Disease
Sjogren’s,
SLE
Anti-Ro (SSA)
Congenital lupus with complete heart block
Subacute cutaneous lupus
Anti-La (SSB) Sjogren’s
Anti-HMG CoA Reductase Statin-induced necrotizing myositis
Anti-SRP Necrotizing myositis
Anti- Ro52 ILD in CTD, especially myositis
Anti-RNA polymerase III Renal crisis in systemic sclerosis
Microscopic polyangiitis (70%), Eosinophilic
pANCA
granulomatosis with polyangiitis (eGPA) (30%)
cANCA Granulomatosis with polyangiitis (GPA)
Rheumatoid arthritis (RF can be found in many others
RF, Anti-CCP
including SLE, Sjogren’s)
Anti-Histone Drug-induced Lupus

Anti-dsDNA SLE, TNFalpha inhibitor induced lupus
Anti-Sm SLE
Many autoimmune diseases particularly connective tissue
ANA diseases. Higher ANA titre the more likely it is related to
an autoimmune disease, myositis
Anti- SCL70 (Topoisomerase) Diffuse systemic sclerosis
Anti-U1 RNP, Pm-Scl, Ku Mixed Connective Tissue Disease
Anti-centromere Limited systemic sclerosis
Anti-Jo1 Anti-synthetase syndrome
Anti-synthetase syndrome (Pulmonary involvement
Anti-PL7
strongly associated)
Anti-PL12 Anti-synthetase syndrome (minimal muscle involvement)
Anti-Mi2 Dermatomyositis
Anti-TIF1gamma, Anti-NXP2 Malignancy-associated Dermatomyositis
Amyopathic Dermatomyositis (CADM) – rapidly
Anti- MDA5
progressive ILD
Anti-5NT1A Inclusion Body Myositis

Spondyloarthritis
Axial Spondyloarthritis Psoriatic Arthritis
Definition/ >3 months of back pain + age <45 yo Inflammatory articular disease:
Classification PLUS peripheral arthritis, enthesitis, axial
Criteria Sacroiliitis on imaging and >1 SpA PLUS 3 points
feature - skin psoriasis (2pt)
OR - past or FHx of psoriasis (1pt)
HLA-B27 positive and >2 SpA features - dactylitis (1pt)
 SpA features - nail changes - pitting, onycholysis
 inflammatory back pain (1pt)
 arthritis - RF negative (1pt)
 enthesitis  - juxta-articular new bone
 uveitis formation on XRAY (1pt)
 dactylitis
 psoriasis
 Crohn's/colitis
 good response to NSAIDS
 family history
 HLA-B27
 elevated CRP
Clinical Axial features: inflammatory back pain,Asymmetric
features buttock pain (alternating), restriction in
oligoarthritis/monoarthritis
spinal movement Polyarthritis -DIP, PIP
Extra-axial: peripheral arthritis Spondylo-arthritis
Extra-articular: anterior uveitis, IBD,Nail disease
psoriasis, apical fibrosis, aortic Dactylitis
regurgitation Enthesitis (particularly Achilles)
Arthritis mutilans
Investigation HLAB27: not diagnostic but 90% of AS No biomarkers or antibodies
patients will be HLAB27 positive CRP only elevated in 40%
Imaging: XRA, MRI RF and CCP negative
Imaging: bone erosion
Treatment Non-biologic NSAIDS - symptoms relief
 physiotherapy/exercise
 NSAIDS -70-80% experience csDMARDS - methotrexate,
substantial symptom management, sulfasalazine, leflunomide
no difference between diff NSAIDS
 csDMARD - only effective in Anti-TNF - adalizumab, certolizumab
peripheral arthritis pegol, etanercept, golimumab,
Biologic infliximab (all effective)
- TNF inhibitors: adalimumab,
certolizumab pegol, etanercept, Anti-IL17 - secukinumab, ixekizumab
golimumab, infliximab
 IL17A inhibitor: secukinumab Anti IL12/23 - ustekinumab
 JAK inhibitor – tofacitinib,
upadacitinib JAK inhibitor – tofacitinib,
upadacitinib

RA vs PsA
Features RA PsA
Morning stiffness >1 hour ++ +
Symmetrical arthritis ++ -
Rheumatoid nodules ++ +/-
RF ++ +/-
New bone formation - +
Dactylitis - +
DIP involved - +
Source: Dr Andrew Foote 2010
Systemic Sclerosis
Limited SSc Diffuse SSc
Skin changes Distal to elbows and knees, Proximal and distal to knees
can involve face and neck and elbows
Renal involvement Rare Uncommon (about 10%)
PAH More common - 30% Uncommon
ILD Common - 30% Common - 30%
Antibodies Anticentromere - 90% Anti-Scl-70 - 30%

Anti-Scl-70 - 10% Anticentromere - <5%
Survival Survival good, depends on Poor survival if significant

degree of PAH systemic involvement
including renal, cardiac and
lung

Imaging Features *Important for short case
Disease X-Ray features
RA Periarticular erosions
Juxta-articular osteopenia
Joint space narrowing
Sparing of DIPs
PsA DIP involvement

Pencil-in-cup deformity
Fluffy periostitis
Gout Soft tissue swelling

Sclerotic margin and overhanging edges
Rat-bitten app
Scleroderma Calcinosis
Osteolysis (destruction of bone)
No other characteristic features of other peripheral arthritis
SLE No joint changes

Jaccoud’s arthropathy (not specific for SLE) would demonstrate
subluxation of joints
OA Joint space narrowing

Periarticular sclerosis
Subchondral cyst
Osteophytes
AxS MRI more sensitive of SIJ early

Sclerosis and joint space narrowing
Squaring of vertebral bodies
Syndesmophytes
Osteopenia
Late stage - Bamboo spine

Vasculitis
Large Vessel Vasculitis
Giant cell arteritis Female to male 3:1

Only occurs >50 years old
40-50% of GCA patients will have PMR symptoms and 10-

15% of PMR will get GCA.
More common in Scandinavian and Mediterranean countries.
Pathogenesis: HLADRB1*04, Interplay between IL-6 and

IFNgamma
Features:
- Constitutional symptoms (fever, malaise, anorexia,
weight loss)
- Cranial symptoms (headache, jaw claudication, scalp
tenderness)
- Extra-cranial features (any large vessel)
Ocular complications:
- Anterior ischaemic optic neuropathy, CRAO,
Posterior circulation involvement
Ix: Thrombocytosis, high ESR (usually), Temporal artery

ultrasound, CT-angiogram, MRA, PET, Temporal Artery
Biopsy
Rx: Glucocorticoids, Tocilizumab
Takayasu’s arteritis Predominantly affects aorta and branches

<40 years old usually
F:M 9:1, Asia
Features:
Constitutional symptoms
Carotidynia
Arterial stenosis/occlusion, absent pulses
Discordant BP, bruits
Aortic dissection, aortic root dilatation, aortic valve
regurgitation
Ix: Elevated inflammatory markers, CTA/MRA

Medium Vessel Vasculitis
Polyarteritis Nodosa Main visceral arteries and branches with complications of

aneurysm
Often associated with Hep B
Features:
Constitutional symptoms
Skin involvement - purpura, panniculitis, livedo, necrotizing
vasculitis in dermis
Renal - ischemia, infarcts
Neuro - Mononeuritis multiplex, neuropathy
GI - mesenteric angina, weight loss, bowel perforation
Myopathy
Ix: ANCA negative, Aneurysms on angiography/CTA/MRA,

biopsy
Small Vessel Vasculitis
ANCA associated vasculitis (small-medium sized necrotizing vasculitis)
Common features Often can have renal involvement - Pauci-immune necrotizing

GN
Pulmonary involvement - cough, haemoptysis, alveolar
haemorrhage
Constitutional symptoms - fever, weight loss, arthralgia,
fatigue
Cutaneous - purpura
Rx:
Induction - Cyclophosphomide, Rituximab, Avacopan, ?
PLEX (If mild - MTX, MMF)
Maintenance - Rituximab, Mepolizumab (eGPA), MTX,
MMF, AZA
GPA Often ANCA positive (cANCA/PR-3 Ab)
Higher relapse and mortality rate
Features:
More common to have ENT involvement - crusting, sinusitis,
hearing loss, saddle nose
Pulmonary(15%)- Subglottic stenosis, airway stenosis
Retro-orbital pseudotumour
MPA Often ANCA positive (pANCA/MPO Ab)
Features:

Pulmonary: ILD
Peripheral nerves (70%) - mononeuritis multiplex, peripheral
neuropathy
eGPA Not uncommon to be ANCA negative

- If ANCA positive - pANCA > cANCA (MPO Ab)
- If ANCA positive tend to affect peripheral nerves,
renal involvement and purpura whereas ANCA
negative tend to have cardiomyopathy and possible
pulmonary involvement
Non-ANCA associated small vessel vasculitis
IgA Vasculitis Children and adults
Preceded by URTI
Features:
Purpura
Arthralgia/arthritis
GI (Abdo pain, nausea, GI haemorrhage)
Renal (Haematuria, proteinuria)
Ix: Skin - LCV with IgA deposition
Cryoglobulinemic May be associated with viral infections (Hepatitis B, C), CTD

vasculitis (SLE, Sjogren’s)
Triad of purpura, weakness and arthralgia

Peripheral neuropathy
Renal disease (GN)
Ix: Cryoglobulinemia, RF positive with low C4, screen for

underlying causes (HCV, HBV, HIV, ANA, ENA, dsDNA,
SPEP)
Rx: GC+ RTX, treat underlying cause

Myopathies and their Features
differentials
Dermatomyositis Heliotrope Rash

Shawl sign
V sign
Gottron sign
Gottron papules
Mechanic hands
Malignancy associated
Other system involved: Cardiac, Pulmonary, GI
Ab: Anti-Mi2, Anti-SAE, Anti-TIF1 gamma, Anti-NXP2,

Anti-MDA5
Perifascicular muscle fibre atrophy
Anti-synthetase syndrome Inflammatory myopathy

Arthritis
Fever
Raynaud’s
Mechanic Hands
ILD
Ab: Anti-Jo-1, anti-PL7, anti-PL12, Anti-Ha, Anti-Zo, Anti-

OJ, Anti-EJ, Anti-Ks
Immune-mediated Severe proximal muscle weakness

myopathies
Ab: Anti-SRP, Anti-HMG-CoA
Antibody-negative immune mediated necrotizing myopathy -
malignancy strongly associated
Myofibre necrosis
Overlap myositis Associated with other CTD - SLE, RA, SSc, Sjogren’s
Ab: Anti-Ro52, Anti-Ku, Anti-Pm-Scl, Anti-U1RNP
Polymyositis Diagnosis of exclusion
CD8 predominent
Endomysial involvement
Inclusion Body Myositis Quadriceps (Knee ext), Finger flexors and ankle dorsiflexors
(IBM) Neck, facial and bulbar involvement possible
No treatment
Ab: Anti-5NT1A (<50%)

Drug-induced Immune-checkpoint inhibitors
Anti-seizure meds (Phenytoin)
Immunosuppressants (CsA, TAC, Steroids)
CVD meds (statin, labetalol)
Anti-PD drugs (Levodopa)
CTx (Plant alkaloids, TKI)
Toxins - Cocaine, Amphetamine
Dystrophinopathies Duchenne MD and Becker MD
Progressive muscle loss

Cardiac involvement
Diaphragmatic weakness
FSHD Asymmetrical weakness of orbicularis oculi, orbicularis oris,

rhomboids, serratus anterior, biceps, triceps, paraspinalis,
rectus abdominis, tibialis anterior
Extramuscular - Retinal vasculopathy, Hearing deficit
Myotonic dystrophy Grip and percussion myotonia

Baldness
Temporalis wasting
Extramuscular: Cardiac, Cataracts, Hatchet facies, pulmonary

involvement, OSA, SIBO, hypothyroidism, DM, Malignancy
risk, GA risk
Mitochondrial disease MERRF, MELAS, CPEO, KSS
Glycogen storage Pompe disease

disorders - Autosomal Recessive
- Triggered by high protein and carbohydrate diet
- Avoid strenuous exercise
- IV alglucosidase alpha inf
- Cardiomyopathy and cardiac conduction defects
Primary Periodic Paralysis HypoK PP (CACNA1S)

HyperK PP (SCN4A)
Andersen-Tawil Syndrome (KCNJ2)

SLE
Female:Male – 9:1
10% mortality in 10 years (Sepsis, CVD, treatment complications, disease activity)
Drug induced Lupus (DIL):

Procainamide, Hydralazine, Isoniazid, Phenytoin, Penicillamine, IFN, TNFi, Minocycline,
Diltiazem, Methyldopa, Chlorpromazine
Signs and symptoms:

Mucocutaneous (acute, subacute, discoid)
Allopecia
MSK (arthralgia>arthritis – non-erosive)
CVD (Libman-Sacks, CAD, pericarditis)
Pulmonary (pHTN, vanishing lung syndrome, pneumonitis
GIT (Lupus hepatitis)
Haem (Haemolytic anaemia, pancytopenia, Evan’s syndrome)
Thrombosis (4% if combined with APLS)
Neuropsychiatric
Renal (GN)
Mx:
- Non-pharmaco – Reduce triggers (Stress, UV, sulfa), vit D, cardiovascular risk
modification, vaccination
- Pharmaco – First line therapy – HCQ
- Minor (HCQ, NSAIDs, low dose steroids, Belimumab), Major (Steroids, AZA,
MTX, LEF, CYC, CsA, Tac, MMF, Rituximab)
- Acute disease ie GN – pulse steroids + MMF/CYC. Can trial CNI/Ritux.
Associated with APLS

- If have SLE and APLS with thrombotic event, will likely require VKOA lifelong
with target INR 2.5 – 3.5
- Pregnancy counselling is key – Asymptomatic (LD Aspirin), Prior obstetrical
morbidity (LD Aspirin + LMWH) and prior thrombotic event (Therapeutic LMWH
at least 6/12 post-partum)
- Anti-Ro/La – risk of neonatal CHB – 16-26 weeks. Role of HCQ in this.
Pregnancy contraindications: Severe pHTN and restrictive lung disease, advanced CKD
and HF, previous HELLP/Pre-eclampsia despite therapy, stroke and severe disease flare in
last 6 months
Contraindication in pregnancy: LEF, MTX, NSAIDs, MMF, CYC, warfarin, ACEI/A2RB

Immunosuppressant Features
Steroids Choices of Prednisolone, Prednisone, Hydrocortisone,

Methylprednisolone, Fludrocortisone commonly
Influence gene expression
SE *Important for long case:

Cushing’s features
Weight gain
Purple striae (specific physical examination sign)
HTN
DM
Cataracts/Glaucoma
Gastritis
Pancreatitis
AVN
Osteoporosis
Immunosuppression
Myopathy
Azathioprine 6-mercaptopurine that blocks nucleotide synthesis and T

lymphocyte proliferation
Effective after 4-8 months
AE: N&V, Myelosuppression, hepatitis, pancreatitis,
infection, lymphoma
TPMT prior as deficient causes risk of myelosuppression
Careful with use of Allopurinol
Safe for pregnancy
Monitor: FBE, LFTs, regular skin check due to risk of SCC
No TPMT: Avoid Azathioprine

Increased TPMT: 6-MMP Hepatotoxicity
Decreased TPMT: 6-TGN bone marrow toxicity

MMF Inhibits monophosphate dehydrogenase
Effective after 1-2 months
AE: Abdo pain, leukopenia, anaemia
Monitor: FBC
Can use mycophenolate sodium if n&v is significant.
Leflunomide Used in RA as adjunct therapy
High risk of immunosuppression as well as teratogenicity

Other SE: Diarrhea, HTN, Peripheral neuropathy, pulmonary
and hepatotoxic
Cholestyramine washout for severe toxicity
Hydroxychloroquine Used for SLE as the basis of treatment, but adjunct for RA
Safe for pregnancy
SE: Retinal toxicity (length dependent), skin pigmentation
Sulfasalazine Used for RA as adjunct
SE: GIT sx, reversible oligospermia, careful use in G6PD

(sulfur)
Safe for pregnancy
Rituximab CD20 inhibitor
AE: Infusion reactions, Hep B reactivation, Ulcers, PML
CNI (TAC, CsA) Inhibits nuclear factor of activated T cells
SE: Nephrotoxic (esp in renal tx), metabolic syndrome,

tremor, hirsutism
Methotrexate Dihydrofolate reductase inhibitor (careful of use with other

similar agents ie TMP)
SE: Nausea, vomiting, mouth ulcers, hepatotoxic,

pneumonitis
Teratogenic
Use of folate on every other day

Folinic Acid for toxicity

Cyclophosphamide (CYC) Alkylating agent
Use in myeloma, SLE, vasculitis
SE: Bladder ca, infertility, haemorrhagic cystitis, BM

suppression, infection, malignancy, cardiac toxicity
Can use mesna with IV CYC
IV Immunoglobulin Fab and Fc
SE: Anaphylaxis, VTE, aseptic meningitis, AKI, CVD risk

Statistics
Formulas
Sensitivity (positive in disease) = Sensitivity is the ability of a test to correctly classify an
individual as ′diseased′
Sensitivity = a / a+c
= a (true positive) / a+c (true positive + false negative)
= Probability of being tested positive when disease is present.
Specificity (negative in health) = The ability of a test to correctly classify an individual as

disease- free is called the test′s specificity.
Specificity = d / b+d
= d (true negative) / b+d (true negative + false positive)
= Probability of being test negative when disease absent.
Positive Predictive Value (PPV) = It is the percentage of patients with a positive test who
actually have the disease.
PPV: = a / a+b
= a (true positive) / a+b (true positive + false positive)
= Probability (patient having disease when test is positive)
Negative Predictive Value (NPV) = It is the percentage of patients with a negative test
who do not have the disease
NPV: = d / c+d
= d (true negative) / c+d (false negative + true negative)
= Probability (patient not having disease when test is negative)
Positive likelihood ratio (LR+) = sensitivity / 1-specificity

Negative likelihood ratio (LR-) = 1-sensitivity/specificity
Pre-test odds = pre-test probability / 1- pre-test probability
Post-test odds = pre-test odds x LR+
Post-test probability = post-test odds/1+post-test odds
Absolute risk (AR) = no of events in treated or control group / number of people in that
group
Absolute risk reduction (ARR) = ARc-ARt
Relative risk (RR) = ARt/ARc = [a/(a+b)]/[c/(c+d)]
RRR = 1-RR or ARc-ARt/ARc
NNT = 1/ARR
NNH = 1/(ARt-ARc)
OR = (a/b)/(c/d)
HR = risk of outcome in exposed group / risk of outcome in non-exposed group

Study Designs
Case Control - determine if an exposure is associated with an outcome. First, identify the
cases (a group known to have the outcome) and the controls (a group known to be free of
the outcome). Then, look back in time to learn which subjects in each group had the
exposure(s), comparing the frequency of the exposure in the case group to the control
group
● calculation: case-control studies yield the odds ratio. An odds ratio is the ratio of
the odds of an exposure in the case group to the odds of an exposure in the control
group.
Randomised Control trial - is a trial in which subjects are randomly assigned to one of
two groups: one (the experimental group) receiving the intervention that is being tested,
and the other (the comparison group or control) receiving an alternative (conventional)
treatment. The two groups are then followed up to see if there are any differences between
them in outcome
Prospective Cohort Study - A research study that follows over time groups of individuals
who are alike in many ways but differ by a certain characteristic(for example, female
nurses who smoke and those who do not smoke) and compares them for a particular
outcome (such as lung cancer)
Retrospective cohort study - longitudinal study in which researchers look back to a

certain point in time to analyze a particular group of subjects who have already
experienced an outcome of interest. Data already collected

Cross Sectional study - observational study where the investigator measures the outcome
and the exposures in the study participants at the same time. Unlike in case–control studies
(participants selected based on the outcome status) or cohort studies (participants selected
based on the exposure status), the participants in a cross-sectional study are just selected
based on the inclusion and exclusion criteria set for the study. Cross-sectional designs are
used for population-based surveys and to assess the prevalence of diseases in clinic-based
samples. since this is a 1-time measurement of exposure and outcome, it is difficult to
derive causal relationships from cross-sectional analysis
Case Series - group of case reports involving patients who were given similar treatment
Meta-analysis - quantitative, formal, epidemiological study design used to systematically

assess previous research studies to derive conclusions about that body of research.
Ecological study - an observational study defined by the level at which data are analysed,
namely at the population or group level, rather than individual level. Ecological studies are
often used to measure prevalence and incidence of disease, particularly when disease is
rare.
Test Disease No disease
Positive True positive (A) false positive (B)
Negative False negative (C) true negative (D)

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THE PHYSICIAN PROJECT

A Rapid Review of High Yield Facts For the Written Examination

1 | The Physician Project

The information has been referenced from various resources throughout

Special thanks to Northern Health DPEs Dr Yana Sunderland, Dr Edwina

© Robin Sia 2023

2 | The Physician Project

3 | The Physician Project

4 | The Physician Project

Functional tests for Ischaemia

Modality Sensitivity Specificity

Exercise ECG 68% 77%

Exercise Echo 86% 81%

Dobutamine Echo 85% 85%

Exercise nuclear 87% 73%

Pharmacological 89% 75%

Cardiac CTA 95% 83%

5 | The Physician Project

Source: ESC 2015

6 | The Physician Project

Duke’s Criteria for Infective Endocarditis

Major criteria Minor Criteria

7 | The Physician Project

Source: ESC 2015

8 | The Physician Project

Aortic Stenosis Symptoms: CP, HF, Syncope

*Refer to ESC guidelines for AS algorithm

Aortic Nocturnal chest pain

Causes; Degenerative, Endocarditis, Aortopathy (Marfan’s, EDS,

Mitral Primary: Leaflets, MVP, RHD, CTD, Congenital, mitral annular

Acute MR - infarct with flash APO (Rx: ECMO and IMPELLA)

Signs: Split S2, S3, Pansystolic murmur, pHTN

Rx: Mitraclip, MVR

Causes: RHD, Calcific, congenital, endomyocardial fibroelastosis

Rx: Anticoagulation (risk of AF), diuresis, mitral commissuroplasty,

Tricuspid Primary: IE, RHD, Carcinoid, Ebstein’s, Iatrogenic

Signs: PSM, Prominent v wave on JVP, pulsatile liver, pHTN

Pulmonary Sequelae of TOF (important for short case)

9 | The Physician Project

10 | The Physician Project

Drug Indication Side-effects Additional info

Entresto HFrEF Hyperkalemia Trial of ARB first in

PCSK9 inhibitor - Refractory Flu-like symptoms, Reduces total LDL

Inclisiran Familial Look at it as a “6

P2Y12i: Second antiplatelet -Bleeding -Preferred agent over

SGLT2i HFrEF & HFpEF, -Euglycemic Previously used in

11 | The Physician Project

Nicorandil Anti-anginal Hypotension Activates potassium

Amiodarone -AF (Rhythm -Drug-induced liver Can be used in AF

Others (extra reading):

12 | The Physician Project

Warfarin Vit-K oral Interacts with Vitamin K, INR

Apixaban Factor X CYP3A4 -Andexanet alfa Apixaban factor

Rivaroxaban Factor X CYP3A4 -Andexanet alfa Rivaroxaban

Dabigatran Factor II P-gp -Idarucizumab Thrombin Time

Alpha-1 Beta-1 Beta-2

Noradrenaline +++ +++ +

Isoprenaline 0 +++ +++

13 | The Physician Project

Basal Cell Carcinoma (BCC) Squamous Cell Carcinoma (SCC)

14 | The Physician Project

Bone disorder Features

RF: Age, menopause, concurrent illness, medications (steroids,