medicine

approach to managing a COPD exacerabation resulting in resp failure

1. correct resp failure ( oxygenation/ventilation)

- oxygen, NIV

2. identify and treat underlying triggers

- antibiotics, allergies, PE, inhaled CSt

3. optimise recovery and prevent further exacerbations

- smoking cessation/nicotine replacement

- bronchodilators

- pulm rehab, Asthma/COPD aciton plan

- vaccine

mechanisms of hypoxia

- reduced Fio2 - high altitude

- obstruction / ventilation failure

- perfusion/ diffusion failure

- V/Q mismatch - causing shunting

- right to left heart shunt

approach to spirometry

check FEV1/FVC - target is 0.7

- below is obstructive

- above is normal or restrictive

check FEV1 against predicted ( severity of obstruction)

- post broncodilator improvement of 12% and 200ml = asthma

- non improvement = incomplete reversible obstruction = COPD

what to ask when px presents with dyspnea and wheeze

Dyspnea:

orthopnea,

exertional vs dysnpnea at rest,

paroxysmal noctural dyspnea

additional symptoms

wheeze ( small airways disease)

- inspiratory or expiratory

diagnosis of osteoperosis vs osteopenia

osteoperosis : DEXA scan , T score : ≤ -2.5

osteopenia : T score : -1 to -2.5

osteoclast activity > osteoblast activity

common osteoperotic fractures and complications

• Vertebral compression fractures (most common, often asymptomatic)

- Hip fractures

- Distal radius fractures

• Proximal humerus fractures

Clinical Consequences

• Morbidity: chronic pain, deformity (kyphosis), reduced mobility

• Mortality: hip fracture 1-year mortality ≈ 20- 30%

• Psychosocial: loss of independence, nursing home placement

prevention and management of osteoperotic fractures

Primary prevention

- Diet |exercise | falls prevention

Secondary prevention

- Calcium & Vitamin D

- Bisphosphonates ( bind to hydroxyappetite reducing OCs),

Denosumab (inhibits RANK ligand) ,

Teriparatide (severe - Parathyroid hormone)

• Orthopaedic input

hip fracture classification

intracapsular:

head

neck ( subcaptial, midcervical, basic cervical)

*worse outcomes

extracapsular:

intertrochanteric

subtrochanteric

garden classification and treatment of intracapsular vs extracapsular fractures

Femoral neck fractures Intracapsular

Garden 1-2 ( undisplaced, stable)

- internal fixation ( dynamic hip screw/pin & plate)

Garden 3-4 ( displaced , unstable)

- internal fixation ( young), hemi arthoplasty or THR ( elderly)

extracapsular

- intertrochanteric (DHS or IM nail)

- subtrochanteric IM nail

system to desribe wrist fracture

Patient → Bone/location → Side → Pattern → Displacement/Angulation → Intra-articular? → Open/Closed → Named fracture → Associated injuries.

23 female - fracture of distal radial - right side - volar displacement with radial shortening ( distance compared to ulna) - closed fracture - consistent with smiths fracture- bruising on right elbow.

fracture healing

factors influencing?

direct vs indirect healing?

phases of healing

factors influencing:

Patient :

• age, smoking, nutrition,

Fracture:

• Adequate stability • Allow some motion, biomechanically stable

direct: anatomic fixation with compression - bone heals directly

indirect: callous formation

phases: haematoma, callous ( soft), bone remodelling

principles of paediatric fractures

aim

periosteum

types

classification

principles of paediatric fractures

aim : avoid growth disturbance

periosteum : thicker - rapid healing

types: torus, buckle

classification: salter harris

Definition of cirrhosis and 4 aetiologies

Cirrhosis

- final stage CLD characterised by regenerative nodules and fibrous septal in liver parenchyma due to chronic hepatic injury

Aetiology

- ethol abuse

- NAFLD

- autoimmune hepatitis

- Hep c

- Primary biliary cirrhosis

Rarer causes

_hameachromatosis

- Alpha -1 antitrysin deficiency

- Wilson disease

cirrhosis

Name 4 symptoms and complications

Symptoms

- ascites

- Hepatosplenomegaly

- Jaundice

- Spider nevi

- Palmar erythema

- Gynacomastia , hypogonadism ?? - increase in estrogen

- Pruritis

- Dupentren contracture

-

Complications

- hepatic ensephalopathy

- Hepatorenal syndrome - acute or non acute kidney injury ( need liver transplant)

- Varices, caput medusa, haemorroids

- HCC

What labs would you order and what would expect to see in cirrhosis

LFTs

- raised enzymes

- hyperbilirubineamia

INR

- prolonged PT time

Ultrasound

- atrophic heterogenous liver with nodular surface

- CT abdo if ultrasound inconclusive

CBC

- thrombocytopenia, leukopenia

CMP

- low albumin, hyponatremia

* liver chemistries may be normal in early cirrhosis

Prognosis and management of cirrhosis

MELD and Child - Pugh scores ( used to prioritise patients for liver transplant - determine 3 month mortality rate)

Score 6-40

Child's ABCDEs:

Albumin, bilirubin, coagulopathy (INR), distended abdomen ( ascites), encephalopathy

Management:

- treat underlying disease - avoid toxins, antivirals

- reconcile medications list - avoid NSAIDs , opioids, benzos

- immunise

- treat complications - oesophageal varices ( non selective beta blockers - reduce CO & vasoconstriction - propranolol)

- parecentesis

- liver transplant

contraindications of NIV

reduced consciousness

Recent facial trauma

Signifcant hypotension

Pneumothorax

clinical features of pneumonia

- dyspnea

- chest pain

- cough

- radiographic evidence of consolidation

antibiotics for CApneumonia

mild - monotherapy doxycycline

moderate ( in ED) - dual therapy - benzopenicillin and doxycycline

severe- ceftriaxone ( broader coverage including gram neg)

- cefalexin doesnt penetrate lungs

common. organisms in CAP

HAP

px with high dose prednisone/immunosuppressed

cap - strep pneumoniae, myocoplasma,

HAP - staph aureus

immunosuppressed/prednisone - pneumocystitis jerovicis

describe curb 65

tool used for pneumonia management

causes of hypercalcemia

1. primary hyperparathyroidism

2. maliganacy

3. prolonged bed rest ( reduced osteoblast activity from mechanical loading, osteoclasts unopposed)

4. medications

- thiazide diuretics ( reduce Ca2 excreation

- lithium ( shift PTH set point up)

- vit a toxicity ( increases OC act)

5. VIT D toxicity ( increases Ca uptake)

What are the key presentations of ischaemic stroke and haemorrhagic stroke (ICH + SAH)?

A:

Ischaemic:

-sudden focal deficit

- negative symptoms - loss of function

(hemiparesis, facial droop, aphasia, Visual loss - amorsis fugax, ataxia)

ICH:

- sudden onset of neurosymptoms

-vomiting, ↓ consciousness, severe hypertension.

- hyperdensity within brain parenchyma

SAH: thunderclap headache, neck stiffness, photophobia, collapse.

- circle of willis shadowing

* Epidural - lucid period

subdural - gradual decline

Q: What are major risk factors for ischaemic stroke and haemorrhagic stroke?

A:

Ischaemic: hypertension (strongest), AF, diabetes, hyperlipidaemia, smoking, age, prior TIA/stroke, carotid stenosis.

Haemorrhagic: hypertension, amyloid angiopathy, anticoagulation, berry aneurysms - SAH, AVMs, heavy alcohol use.

Q: What common conditions mimic stroke and how do they present?

A:

Seizure (Todd's paresis): transient unilateral weakness post-ictal usually resolving in 24 hours ( brain exhaustion)

Migraine aura: gradual spread of positive symptoms (visual zig-zags, tingling).

Hypoglycaemia: altered consciousness ± focal deficits.

Functional neurological disorder.

Q: What are the indications and limitations of CT, CTA, and CT perfusion?

A:

CT (non-contrast): first-line to rule out haemorrhage; limited sensitivity early in ischaemia.

CTA: identifies large vessel occlusion (ICA/M1) for EVT.

CTP: defines infarct core vs salvagable penumbra ( scans blood flow); extends reperfusion window to 24h.

Q: When is MRI (especially DWI) used in acute stroke and what are its limitations?

A:Use: highest sensitivity for acute ischaemia, posterior circulation events, uncertain diagnosis.

Limitations: slower, less available, contraindications (implants), not ideal for unstable patients.

What is the FAST stroke protocol?

1. FAST-positive = Code Stroke activation

Triggers:

- Immediate triage to resus bay

- Urgent neuro exam

- Non-contrast CT within 20 minutes ( rule out bleed)

- CT angiography if stroke suspected ( not sensitive for acute ischemic stroke)

- Notification of stroke team

2. determine eligbility for reperfusion

- assess for IV thrombylysis ( up to 4.5 hours)

- assess for endovascular thrombectomy ( up to 24 hrs with favourable imagine - CTP)

* better in large vessel occlusion

In FAST protocol , how do you assess a patient?

Facial droop

- ask patient to smile

Arms weakness or drift

- pronator drift test, ask patient to hold out arms

Assess speech coherence/slurring

what is the role of magnesium

50% in bone , 20% in muscle

antagonises calcium influx - cell metabolism

inhibits glutamate from binding to NMDA recepetors - reduced excitablity ( neuroprotective)

e.g status epilepticus - give mag sulphate Iv

hypomagnesium = <0.75 - give oral or iv mag

mechanism of calcium and symptoms of hyper /hypo calcemia

what is an ecg sign for severe hypocalcemia

stabilises sodium channels

needed for osteoblast activity

symptoms

hypercalcemia ( >2.6), severe > 3.5

stones(renal), bones(pain), groans/thrones(pancreatitis, consipation, psychiatric undertones (anxiety/altered

conciousness)

hypocalcemia

- reduced sodium channel stability - lowered threshold - muscle twitching, contraction - tetany

* tausaddes du point - prolonged QTC

most common esophageal cancer?

clinical symptoms/signs

adenocarcinoma- GORD

- PROGRESSIVE DYSPHAGIA ' i was fine drinking coffee 2 weeks ago but now i can't swallow food properly'... cancer invaded muscles causing dysmotility

haematological emergencies:

febrile neutropenia vs leukostasis

definition and action

febrile neutropenia

<0.5 neutrophils and fever may be the only sign of sepsis

action : cultures, antibiotics within 1 hour

leukostasis

blast count >100 WCC

( sludging in brain and lung capillaries)

- hypoxia, headache, confusion

action: emergent cytoreduction ( leukapheresis)

definition, signs of tumour lysis syndrome and treatment

definition:

rapid cell death releasing toxic contents

labs : high potassium, phosphate, uric acid, low calcium

management

aggressive hydration, allopurinol, raburicase

signs pointing to Acute Promyelocytic Leukemia ( APML) - medical emergency

blasts > 20% abnormal and presence of abnormal coagulopathy - DIC

treat immediately with ATRA ( all-trans retinoic acid)

- forces cell to mature and stop releasing granules - 95% cure rate

diagnostic genetic confirmation:

t(15:17)

investigations and diagnostics for leukemia:

FBC & smear

coag profile ( DIC)

metabolic panel ( tumour lysis syndrome)

viral serologies ( pre chemo screening)

bone marrow biopsy

MPO stain + = AML

MPO stain - = ALL

flow cytometry/ immunophenotyping

cytogenetics -classifcation to determine if favourable or adverse prognosis

>20% blasts and presence of auer rods, gum hypertrophy is indicative of ?

AML

* median diagnostic age 67 years old

clinical presentation of leukemia

- anemia ( pale, fatige , SOB)

-thrombocytopenia

( bruising, petechia, gum bleeding)

- neutropenia ( fever, recurrent infections)

why do you need a lumbar puncture in AML

what makes is a confirmatory LP test for AML

treatment?

to see if leukemia has crossed the BBB and affected CNS

- CSF > 5 WCs with blasts confirmatory

manage with prophylactic intrathecal chemotherapy

( treatment is 2-3 years )

immediate vs delayed compensatory mechanisms of the heart

immediate - within mins

- TPR & CO

- Arteriole & venous constriction

- HR & contractility - PSNS - inhibitory centre + SNS accelatory centre via baroreceptors cartoid & aortic arch

delayed ( hours to days

RAAS, ADH release, Thirst stimulation

4 classifications of shock

Oxygen Delivery Can't Happen

Obstructive - pipes are blocked

Distributive ( septic, anaphylactic, neurogenic) * warm shock

Cardiogenic - pump no good

Hypovolemic - tank is empty

*cytotoxic shock- poison related, oxygen delivered but can't be utilised

aetiology of hypovolemic shock and explain the lethal diamond of severe blood loss

inadequate intake

haemorrage

fluid loss - burns

lethal diamond

hypothermia- impaired clotting and platelets

coaguloapathy - impaired oxygen tissue delivery

acidosis - further degrades clotting

hypocalcemia - acidodic intracellular shift

management and resus for haemorrage

1. ABCDE

2. 2x large bore IV access

3. FBC, G+H

4. monitering ecg + art line , TTE

5. MAP target 50-60mmHG ( unless TBI >80)

6. Early source control ( direct pressure, torniquet, code crimson)

7. correct coagoloapthy

8. temp control (WARMED FLUIDS)

9. damage control resus ( 1:1:1, minimal crystalloid , prioritise blood, TXA 1g, MTP activation, permissive hypotension)

targets for MTP

temp

fibrinogen

iCal

pH

lactate

Plt

PT/APTT

INR

temp >35

fibrinogen >2

iCal >1

pH > 7.2

lactate ><4

Plt >50

PT/APTT <1.5 normal

INR <1.5

symptoms and investigations for

- malaria

-dengue

- typhoid

- measels

malaria

-microscopy thick and thin films (gold standard)

rapid test for plasmodium falciparum

- variety of symptoms , splenomegaly

dengue - serology IGM , NS1 antigen test

- break bone fever ( arthralgia), biphasic rash ( handprint stays)

- typhoid - blood cultures

- fever , rose spots , salmon rash, constipation

* food contamination

Measles

Pcr , IGM ( + indicates recent infection/vaccination)

high fever , coryzal symptoms, rash

at rsk groups for syphilis

MSM

indigenous or those living in such communities

women of child bearing age

IV drug users

* notifiable disease, contact tracing

routes of transmission of syphilis( treponema palladium)

- contact with infected lesion

e.g condomless sex

- verticle transmission ( crosses placenta) - screen every trimester , can occurr as early as 8 weeks gestation. 90-100% transmission if untreated

- contact with infected blood

symptoms and complications of syphilis( treponema palladium)

chancre sores ( anything that looks like an ucler/sore - TEST)

- truncal red rash, patchy hairloss ( scalp eyebrows)

pathophys: widespread inflam/immune response

complications:

neurosyphilis - hearing, vision loss, menigitis, cog impaired

cardiovascular issues - aneurysm, valve damage

skin problems, infertility

staging, diagnostics and treatment of syphilis

staging

-early latent - <2 years since first transmission

-late latent - >2 years "

-tertiary syphilis - symptoms develop 7-30 years after transmission

DIAGNOSTICS

-PCR dry swab on lesion

-serology - TPPA antibodies

* can take 2-4 weeks to be detected in blood, swab first!

99% specificity

TREATMENT

penicillin

* monitor for JH jarisch-Herxheimer reaction ( transient fever, headache malaise, worsening rash)

transmission routes of HIV

unprotected vaginal or anal sex

* anal mucosa highest risk area

Percutanous contact

- needle sharing, transfusions

Mother to child

- intrauterine, perpartum, breastfeeding

*not by hugging kissing, urine, saliva

what cell does HIV target

screening test?

diagnostic ?

CD4

screening : Enzyme Immunoassay EIA

- test by 6 and 12 weeks since last high risk exposure

confirmatory: western blot

What regimine is given before and after HIV exposure

before - PREP ( 2 pil regimine daily or 1 injection every 2months)

after - PEP (within 72 hours of exposure) post exposure prophylaxis

signs of raised ICP

what is cushings triad?

.deteriorating level of consciousness

abnormal posturing ( decoricate or decerebrate)

abnormal pupillary response, uni/bilateral dilatation

abnormal breathing patterns

cushings triad - LATE SIGN

hypertension

bradycardia

irregular breathing

extradural hematoma

epidemiology?

bleeding from where?

epidural haemorrage

younger population - dura becomes more fused to skull as you get older

can be a torn venous sinus but mostly from middle meningeal artery

* bleeding cant cross a suture line

definition of cholecystitis vs choliangitis

investigations

cholecystitis: inflammation of the gall bladder

choliangitis: infection of the common bile duct

- jaundice must be present

investigations

US

CRP, WCC, LFTs, amylase, lipase ( >3x normal suggests pancreatitis)

pathophys of gallstones

cholstrol stones

- supersaturation ( high fat diet, pregnancy)

- biliary stasis ( high fat diet, rapid weight loss)

pigmented stones

- haemolysis

- cirrhosis

cholecystitis clinical presentation vs choliangitis ( name charcots + raynauds)

gall stones

RUQ, fever, nausea, vomiting, pain self limits <4 hours, biliary colic, murphys sign, bloating ,dyspepsia ( indigestion)

choliangitis

charcots triad

- Fever

-RUQ pain

- JAUNDICE

raynauds - late sign emergency

- charcots

- hypotension

- confusion

diagnosis on ultrasound of cholecystitis

presence of gall stones

thickened wall

pericholecystic fluid

management of cholecystitis

( which antibiotics)

Inital and definitive

initial:

- admit

- nil by mouth

- IV fluids

- pain releif

- IV antibiotics ( ceftriaxone and metronidazole)

definitve

cholecystectomy

management of choleangitis

initial:

- admit

- nil by mouth

- IV fluids

- pain releif

- IV antibiotics ( ceftriaxone and metronidazole)

Decompress/removal of obstruction

- ERCP or percutaneous drainage ( if not fit for surgery)

definitve

cholecystectomy

oncology referral if inidicated

pathophys of pancreatitis

signs of mild , moderate ,severe

obstruction of pancreatic duct causing congestion and ductal hypertension resulting in autodigestion and necrosis

mild - minimal symptoms

moderate - raised WBC and amylase

severe - shock, organ failure, raised CRP & lactate

treatment for pancreatitis

supportive care

- IV fluids

- pain control

- nil by mouth

enteral feeding

Address cause

- ERCP for stones

- stop alcohol

classifcation for HF

HFrEF - <40%

HFpEF >50%

NYHA

symptoms & signs of HF

symptoms

fatigue

exertional dyspnea/ reduced exercise tolerance

orthopnea

parosymal noctural dyspnea

ankle swelling

signs

elevated JVP, HJ reflux

displaced apex beat

fine bibasal crackles

3rd heart sound

heart murmur

pitting oedema ( ankle, sacrum)

investigations for HF

bedside

bloods : FBC, EUC, CMP, Pro BNP

ecg

imaging

CXR

Transthoracic Echo

management for HFrEf and HFpEf

- treat underlying cause

HFrEF

mortality reducing agents - 4 pillars

- ace/arni - Entresto

- beta blocker - Carvedilol

- Mineralcorticoid receptor antagonist MRA - finerenone, spironlactone

- SGLT2 inhibitors - empagliflozin

symptom reducing - loop diuretic

HFpef

- SGLT2 inhibitors - empagliflozin

- symptom relief - diuretics

Front: Addison’s disease – pathophysiology & signs/symptoms

Pathophysiology: Primary adrenal insufficiency → ↓ cortisol + ↓ aldosterone + ↑ ACTH (usually autoimmune destruction)

Mechanisms: ↓ aldosterone → ↓ Na⁺, ↑ K⁺ → hypotension ↑ ACTH → ↑ MSH → hyperpigmentation

Signs/Symptoms: Fatigue, weakness, weight loss Nausea, vomiting, abdominal pain Hyperpigmentation Hypotension, salt craving Hyponatraemia, hyperkalaemia, ± hypoglycaemia

Addison's disease - investigations & management

Investigations: ↓ morning cortisol Short Synacthen test → no rise in cortisol (confirms) ↑ ACTH (primary) Electrolytes: ↓ Na⁺, ↑ K⁺

Management:

Chronic: Hydrocortisone (glucocorticoid) Fludrocortisone (mineralocorticoid) Sick day rules + medical alert

Addisonian crisis: IV hydrocortisone + IV normal saline ± treat trigger ( surgery,infection, illness, non adherence meds)

infective endocarditis

signs/symp, investigations, RFs, complications

diagnosing criteria, management

Front: How does radiotherapy kill cancer cells & what is the oxygen effect?

Ionising radiation → free radicals → DNA double-strand breaks

Oxygen fixes DNA damage → prevents repair

Hypoxic tumours = radioresistant

Why is radiotherapy given in fractions & what are the 4 Rs?

Fractionation allows normal tissue recovery while damaging tumour

4 Rs:

Repair (normal cells recover)

Reoxygenation (tumour becomes more sensitive)

Redistribution (cell cycle)

Repopulation

What are key side effects and oncologic emergencies of radiotherapy?

Acute: skin erythema, mucositis, fatigue

Late: fibrosis, infertility, secondary malignancy (irreversible)

Emergencies:

Spinal cord compression → steroids + urgent RT

SVC obstruction → RT ± chemo

Front: What are the major Duke criteria for diagnosing infective endocarditis?

Positive blood cultures with typical organisms

(e.g. Staph aureus, viridans strep, enterococcus, HACEK)

Evidence of endocardial involvement:

- Vegetation/abscess on echo (TOE > TTE)

- New valvular regurgitation

📌 Memory: “Blood + Echo”

Front: What are the major & minor Duke criteria and how is infective endocarditis diagnosed?

major:

postive blood cultures + changes on echo

Minor criteria:

- Predisposition

(IVDU, valve disease)

- Fever ≥38°C

- Vascular phenomena (emboli, Janeway lesions)

- Immunological phenomena (Osler nodes, Roth spots, GN)

Diagnosis:

Definite:

- 2 major

- OR 1 major + 3 minor

- OR 5 minor

Possible:

1 major + 1 minor

OR 3 minor

What is the initial and medical management of infective endocarditis?

empirical therapy for native and prosthetic valve

if suspected MRSA ( iv drug user), what change in antibiotic?

Back:

Take ≥3 blood cultures before antibiotics

-Start empiric IV antibiotics (then tailor to cultures)

Prolonged therapy: 4–6 weeks IV

TG empiric cover:

Native valve:

Benzylpenicillin 1.8g 4hrly + flucoxacillin 2g 4hrly + gentamycin

prosthetic valve

flucoxacillin 2g 4 hrly + vancomycin + gentamycin

MRSA: replace benzyl with vancomycin

Monitor:

Blood cultures (clearance)

Renal function (drug toxicity)

📌 Key principle: “Culture first, then treat long and IV”

antibiotic therapy for MSSA in IE

- include standard, non severe + severe reaction

standard = flucox 2 g 4 hrly

non severe = cefazolin 2g 8hourly

severe = vanc -

triad of cardiac tamponade

common blood pressure sign?

Beck's triad

hypotension, raised JVP, muffled heart sounds

- widened pulse pressure

pericarditis features associated with poor prognosis

- high fever >38 degrees

-subacute course—symptoms developing over several days

-without a clear acute onset

-large pericardial effusion

-cardiac tamponade

-failure to respond within 7 days to drug therapy.

What are the epidemiology, risk factors, and key investigations/diagnostic features of acute pericarditis?

📊 Epidemiology

Most common cause of acute pericarditis: viral

⚠️ Risk factors / causes

-Viral infections (Coxsackie most common)

- non infectious - autoimmune, malignancy ,metabolic, traumatic, iatrogenic ( covid vaccine)

🔬 Investigations

ECG: diffuse ST elevation + PR depression

Troponin: may be mildly elevated (myopericarditis)

CRP/ESR: elevated inflammatory markers

TTE: assess effusion/tamponade

CXR: may show enlarged cardiac silhouette if effusion

🧠 Diagnosis (clinical)

need 2 of following:

- Pleuritic Chest pain -pericardial rub

-ECG changes

- effusion

What is the management and complications of acute pericarditis?

💊 Management

First-line:

Colchicine (reduces recurrence)

NSAIDs (ibuprofen high dose)

If severe/refractory:

Corticosteroids (careful: ↑ recurrence risk)

Treat underlying cause (e.g. TB, uraemia)

Restrict strenuous exercise until resolution

🚨 Complications

Pericardial effusion

Cardiac tamponade (emergency)

Recurrent pericarditis

Constrictive pericarditis (chronic fibrosis)

risk factors and complciations of IE

RFs:

prosthetic valves

congenital heart defects, intravenous drug use,

iatrogenic

poor dental hygiene

immunosuppressed

complications

heart failure

stroke

septic emboli- kidney, spleen limb

immune mediated GN

Haematuria

Front: Causes and key features of haematuria?

Glomerular:

Glomerulonephritis

Dysmorphic RBCs, RBC casts

Non-glomerular:

Stones

Infection

Malignancy

📌 Exam clues:

Painful → stones/infection

Painless → malignancy until proven otherwise

Reduced GFR

: Causes and consequences of reduced GFR?

Causes:

AKI (pre/intra/post renal)

CKD

Hypoperfusion

Consequences:

Uraemia

Hyperkalaemia

Fluid overload

Metabolic acidosis

Flashcard 7: Dialysis Indications (in renal replacement therapy)

Front: What are the indications for dialysis?

AEIOU:

Acidosis (refractory)

Electrolytes (↑K⁺, Ca2) refractory

Intoxication of poisons ( lithium)

Overload (fluid) refractory to medical management

Uraemia (encephalopathy, pericarditis)

haemodyalysis, peritoneal, kidney transplant

Complications of CKD

Front: What are the major complications of chronic kidney disease (CKD)?

❤️ Cardiovascular (most common cause of death)

Hypertension

Accelerated atherosclerosis

Heart failure

🩸 Haematological

Anaemia → ↓ erythropoietin ( give EPO stim + iron)

⚡ Electrolyte / metabolic

Hyperkalaemia

Metabolic acidosis

Fluid overload

🦴 Bone & mineral (CKD-MBD)

↓ vitamin D activation

↑ phosphate → ↑ PTH (secondary hyperparathyroidism)

Renal osteodystrophy, fractures

🧠 Uraemia

Encephalopathy

Pericarditis

📌 Memory: “Blood, Bones, Electrolytes, Heart, Uraemia”

risk factors, signs ( nemonic) and mangement of serotonin syndrome

risk factors:

- use of serotonergic drugs or combo use of cyp450 inhibitors e.g MAOs, SSRIs, ondanz, MDMA, tramadol, merepiridine

signs

SHIVERS

shivering

hyperreflexia + myoclonus

increased temp < 41

vitals unstable ( ↑HR, ↑ RR, labile BP)

Encephalopathy - altered/LOC

Restless

Sweating

management

cease causative drugs

supportive care e.g oxygen , IV fluids, agitation ( benzos), active cooling ( fan + mist, ice bath, ice packs, cold IV fluids)

What are the 4 H’s in cardiac arrest and how are they managed?

🟠 Hypoxia

Oxygen, airway support, ventilation/intubation

🟡 Hypovolaemia

IV fluids ± blood products

Control bleeding

🔵 Hypo-/Hyperkalaemia (± metabolic)

Hyperkalaemia: IV calcium, insulin + glucose, dialysis( refractory)

Hypokalaemia: IV potassium

Acidosis: treat cause ± sodium bicarbonate

🟣 Hypothermia

Active rewarming

Warm IV fluids

📌 Key idea: Fix oxygen, volume, electrolytes, temperature

What are the 4 T’s in cardiac arrest and how are they managed?

⚡ Tension pneumothorax

Immediate needle decompression → chest drain

❤️ Cardiac tamponade

Urgent pericardiocentesis

🫁 Thrombosis

Pulmonary embolism → thrombolysis

Coronary (MI) → PCI/thrombolysis

☠️ Toxins

Antidotes (e.g. naloxone, sodium bicarbonate(TCAs))

Supportive care

📌 Key idea: Relieve pressure, remove fluid, treat clots, reverse toxins

Discontinuation Syndrome

Front: What is discontinuation syndrome and how is it recognised and managed?

🧠 Definition

Symptoms after abrupt cessation or rapid dose reduction of antidepressants

Common with short half-life drugs (e.g. paroxetine, venlafaxine)

⚡ Symptoms (FINISH)

Flu-like symptoms

Insomnia

Nausea

Imbalance (dizziness)

Sensory disturbances (“brain zaps”)

Hyperarousal (anxiety, irritability)

⏱️ Timing

Onset: 1–3 days after stopping

Duration: ~1–2 weeks

💊 Management

Prevention: gradual taper

If occurs:

Restart drug → taper slowly

Consider switching to fluoxetine ( long acting SSRI)

Discontinuation Syndrome vs Relapse

Front: How do you differentiate discontinuation syndrome from depression relapse after stopping antidepressants?

⏱️ Timing

Discontinuation: rapid onset (1–3 days)

Relapse: gradual (weeks)

⚡ Symptoms

Discontinuation: physical + neurological

Dizziness, nausea, “brain zaps”, flu-like

Relapse: psychological

Low mood, anhedonia, hopelessness

💊 Response to restarting meds

Discontinuation: improves quickly (days)

Relapse: improves slowly (weeks)

Fast + physical = discontinuation

Slow + psychological = relapse

Pathophys + Symptoms and ecg changes for angina/ CAD

CAD Pathophysiology

Endothelial injury → LDL oxidation → foam cells → plaque

Plaque → stenosis → ↓ coronary flow

Demand > supply → ischaemia → angina

Plaque rupture → thrombosis → MI

Angina Features

Central, crushing pain

Radiates to arm/jaw

Exertional ( can measure metres they can walk until)

Relieved by rest/GTN

Ischaemia ECG

ST depression, T inversion ( v2-25)

MI ECG

ST elevation, Q waves

DDx + Ix + Management of angina

DDX

Life-threatening chest pain

ACS, PE, aortic dissection, tamponade, pneumothorax

Mimics

GORD, oesophageal spasm, costochondritis, anxiety

Key Investigations

ECG (first)

Troponin (serial)

CXR ± CTangio/aorta ( rule out PE)

Stable Angina Management

Lifestyle changes- SNAP

GTN (symptom relief)

Beta blockers (↓ demand)

Aspirin + statin

PCI/CABG if severe

ecg signs for pericarditis?

criteria for STEMI

Diffuse ST elevation + PR depression.

ST elevation in ≥2 continguous leads

sawtooth pattern on ecg is suggestive of which cardiac condition?

management?

atrial flutter

* often misdiagnosed as SVT

ventricular rate ≥150 bpm + narrow QRS

management

unstable = cardiovert

stable - same as AF, rate vs rhythm control

QRS width = differentials for narrow vs wide

management of SVT

Narrow (<120 ms)

Supraventricular

AF (irregularly irregular)

Flutter (sawtooth)

SVT (regular, fast)

Wide (>120 ms)

Ventricular tachycardia (assume first)

- monomophic VT , polymorphic tausades

SVT with aberrancy/ BBB ( narrow but appears wide)

WPW - delta wave

SVT managemment

- vagal maneurvers ( carotid sinus massage, valsalva)

- adenosine 6mg IV bolus followed by saline flush, give 12mg if ineffective after 2 mins ( continue titration)

ecg recognition of types of blcok Heart block

QUICK ECG RECOGNITION

Long PR only → 1st degree

PR progressivly longer then drop → Mobitz I - atropine if symptomatic

Sudden drop, PR constant → Mobitz II 🚨pacemaker

P & QRS unrelated → Complete heart block 🚨- urgent pacing , syncope

PATHOPHYS + DDx of restrictive lung disease

aetiologies of interstitial lung disease

how does spironmetry look in restrictive disease

Restrictive lung disease

↓ compliance → ↓ lung volumes → dyspnoea

Intra-thoracic

ILD, fibrosis, sarcoidosis

Crackles present

↓ DLCO ( diffusion of gas across membrane)

Extra-thoracic

Obesity, neuromuscular MG/MND, chest wall, kyphoscoliosis

- Normal DLCO

aetiologies

idiopathic

environmental - asbestos, silica, smoking

autoimmune - RA, scleroderma

drugs - methotrexate, amioderone ( pulm toxic)

spirometry

volumes reduced but normal ratios

management of interstitial lung disease vs restrictive

Goals:

Slow fibrosis

Reduce inflammation

Improve oxygenation

General

Smoking cessation

vaccinations

Pulmonary rehab - physio

Oxygen

Drugs

Anti-fibrotic (pirfenidone, nintedanib) → IdiopathicPF

Steroids/immunosuppressants → inflammatory ILD

Advanced

Lung transplant

restrictive

- improve mechanics

obesity - weight loss, CPAP

neuromuscular - treat underylying cause (immunosuppress in MG), BiPAP

scoliosis- physiotherapy

Causes of AKI and general management

Causes

60% Pre-renal → ↓ perfusion

- hypovolemia ( haemorrage, dehydration)

- hypotension ( shock, sepsis)

- decreased circulating volume ( heart,liver failure, nephrotic syndrome(>3.5g protein/day)

- renal artery stenosis

- drugs ( Ace, Arbs, NSAIDs)

35% Intrinsic → internal damage

ATN (85% cause of intrinsic AKI) - muddy casts

- ischemia ( prolonged hypotension

- nephrotoxic drugs (contrast, amingoglycosides, methotrexate)

- endogenous toxins ( myoglobin- rhabdo, haemoglobin in haemolysis, bence jones proteins - multiple myeloma)

AIN

- medication( antibiotics, PPIs, Phenytoin, interferon)

- infection

- infiltrative disease ( amyloid/sarcoidosis)

Vascular disease ( scleroderma, hypertensive emergency)

GN - RBC casts

5% Post-renal → obstruction

acquired- stones, BPH, clots, tumor, iatrogenic

neurogenic - MS, spinal cord lesion, peripheral neuropathy

congenital malformation ( posterior urethral valves )

Management

Treat cause

Stop nephrotoxic drugs (NSAIDs, ACEi)

Fluid balance

Monitor electrolytes

investigations you would order in AKI?

urinalysis in AKI

what would you see in pre renal, ATB, GN & interstitial nephritis

bloods :

-FBC, UEC, albumin:creatinine ratio (ACR), egfr

-ultrasound to rule out post renal

-biopsy in suspected GN, nephrotic syndrome(>3.5g protein/day), unexplained AKI

🚽 Urinalysis

Bland urine

No cells/casts

ATN

Muddy brown casts

GN

RBC casts + haematuria

Interstitial nephritis

WBCs ± eosinophils