100% Medicine Part-1 for FMGE Aspirants by Dr. Dilip Kumar

Name: 100% Medicine Part-1 for FMGE Aspirants by Dr. Dilip Kumar
Uploaded: 2023-01-14T20:06:26.000Z
Duration: 7 h 12 min 23 s

Introduction

The speaker welcomes the audience and apologizes for a delay before starting the discussion.

Starting the Session

The speaker confirms that technical issues have been resolved and begins discussing the top 50 core topics for upcoming FMG exams.

Top 50 Core Topics

The speaker discusses how they have compiled data from previous years' FMG exams to cover all important topics.

The speaker emphasizes that they will cover almost all of the important topics required for FMG exams.

One of the first topics discussed is cardiac axis, which has been a common question in recent FMG exams.

Determination of Cardiac Axis

To determine cardiac axis, look at leads 1 and AVF.

If lead 1 is positive and lead AVF is predominantly positive, it's normal axis.

If both leads are negative, it's Northwest or extreme axis deviation.

There is no difference between FMG and NEET PG exams except for their purpose.

If lead 1 is negative and lead AVF is positive, it's right axis deviation.

To sort out confusion, look at lead 2. If it's positive, it's normal axis; if negative, left axis deviation.

Conclusion

The speaker covers an overview of important topics for upcoming FMG exams with a focus on cardiac axis determination.

Understanding Right Axis Deviation

In this section, the speaker explains how to identify right axis deviation in an ECG by looking at leads one and AVL.

Identifying Right Axis Deviation

Right axis deviation can be identified in an ECG by looking at leads one and AVL.

Acute Coronary Syndrome Management

In this section, the speaker discusses acute coronary syndrome management, including how to manage a patient with ACS and the different types of ACS.

Types of ACS

Acute coronary syndrome (ACS) is caused by plaque rupture, which leads to thrombus formation and subsequent ischemia.

There are two types of ACS: ST elevation myocardial infarction (STEMI) and non-ST segment elevation myocardial infarction (NSTEMI) or unstable angina.

Suspecting ACS

Chest pain is the most important symptom when suspecting ACS. The chest pain may be crushing or feel like someone is standing on their chest. Other symptoms include diaphoresis, pulmonary edema, hypotension, and ventricular arrhythmias.

When a patient presents with chest pain to the emergency department, an electrocardiogram (ECG) should be done within 10 minutes of admission along with cardiac markers such as troponin. Troponin is currently considered the most sensitive and specific investigation for suspected ACS or any chest pain for that matter.

Class Continuation Issue

This section addresses comments from viewers who thought that the class had ended.

Class Continuation Issue

The class has not ended; it is still ongoing.

The team confirms that the class is still continuing despite comments from viewers suggesting otherwise.

Investigations and Initial Management of Acute Coronary Syndrome

In this section, the speaker discusses how to differentiate between STEMI, NSTEMI, and unstable angina. They also explain why a normal ECG does not rule out ACS and the importance of serial troponin testing. The speaker then goes on to discuss the initial management of ACS using the mnemonic Mona BC.

Differentiating Between STEMI, NSTEMI, and Unstable Angina

STEMI patients will have ST elevation and troponin positivity.

NSTEMI patients will have elevated troponins but no ST segment elevation.

Unstable angina patients will have normal troponins and no ST segment elevation.

A normal ECG does not rule out ACS; serial ECGs and troponin testing are necessary.

Serial Troponin Testing

Serial troponin testing is necessary even if the initial troponin is normal.

Troponins take approximately 1 to 4 hours to start increasing after an event.

Troponins take approximately 5 to 14 days to come back to normal.

Initial Management of ACS Using Mona BC

The mnemonic Mona BC can be used for initial management of ACS.

M stands for morphine, which should only be used for selected patients with severe chest pain or anxiety.

O stands for oxygen, which should only be used in patients with severe shortness of breath or low saturation.

N stands for nitrates, which should be used with caution in patients who are preload sensitive.

A stands for aspirin, which should be given as soon as possible.

B stands for beta-blockers, which should be given to all patients without contraindications.

C stands for clopidogrel or ticagrelor, which should be given to all patients undergoing PCI.

Right Ventricular MI and Antiplatelet Agents

In this section, the speaker discusses how to suspect right ventricular MI and the use of antiplatelet agents.

Suspecting Right Ventricular MI

Right ventricular MI is suspected when V4R shows ST segment elevation.

If V1 shows ST elevation and V2 shows ST depression, right ventricular MI should also be suspected.

Use of Antiplatelet Agents

Aspirin is the most important antiplatelet agent. The loading dose in India is 300mg due to a lack of 81mg tablets.

Immediate release aspirin should be used instead of enteric-coated tablets.

P2Y12 inhibitors are optional for NSTE-ACS but mandatory for STEMI patients.

Clopidogrel is commonly used in India with a loading dose of 300-600mg. Prasugrel has a lower loading dose of 60mg due to its potency.

Beta Blockers

In this section, the speaker discusses beta blockers and their contraindications.

Preferred Beta Blockers

A cardioselective beta blocker is preferred, but labetalol can also be used if hypertension is present.

Contraindications for Beta Blockers

Severe COPD or bronchial asthma are contraindications for beta blockers. Recent exacerbations should also be avoided.

Patients with PR interval >0.24 seconds or second/third degree AV block should not receive beta blockers.

Bradycardia, low BP, acute heart failure signs, or hemodynamic instability are also contraindications for beta blockers.

Types of Heart Failure and Anticoagulants

In this section, the speaker discusses the different types of heart failure and anticoagulants used in acute coronary syndrome.

Types of Heart Failure

There are four classes of heart failure.

Class 1 means patients do not have any signs or symptoms of heart failure.

Class 2 means patients have signs of heart failure, such as third heart sound and jugular venous distention.

Class 3 means patients have severe heart failure with crepitations throughout the lung fields.

Class 4 means patients are in cardiogenic shock due to an MI.

Anticoagulants for Acute Coronary Syndrome

Anticoagulants used in acute coronary syndrome include infraction apparent, low molecular weight apparent, Fonda parinex, and bivalirudin.

Enoxaparin is commonly used in practice. Fonda parinex and bivalirudin are rarely used.

Bivalirudin should be given as a continuous IV infusion inside the cath lab only when other anticoagulation is contraindicated.

Management of Acute Coronary Syndrome

In this section, the speaker discusses how to manage acute coronary syndrome.

Diagnosis

Diagnosis involves ECG markers and imaging.

Types of ACS

There are two types of ACS: STEMI and NSTEMI.

Initial Management

Initial management involves MONA BC.

Reperfusion is necessary, but the technique used is not typically tested in exams.

Most exam questions focus on initial management only.

Thrombolysis and ACS

In this section, the speaker discusses the use of thrombolysis in patients with ACS.

Thrombolysis in STEMI and Stable Angina

Thrombolysis should not be used as a reperfusion strategy in patients with NSTE-ACS and stable angina.

Only primary PCI or CABG should be used.

Contradictions to Thrombolysis

The speaker does not go into detail about contraindications to thrombolysis but emphasizes that it is important for students to learn them.

Identifying STEMI on ECG

A clear-cut STEMI can be identified by convex ST segment elevation seen in leads V2-V6, lead I, and AVL.

Anterior MI indicates the culprit artery is the left anterior descending artery (LAD).

Reperfusion Strategy for STEMI

Ideally, within two hours of diagnosis, a patient with STEMI should undergo some form of reperfusion therapy.

Primary PCI is preferred over thrombolysis but if primary PCI will be delayed, then thrombolysis can be done instead.

Window Period for Thrombolysis and Bradycardia Management

In this section, the speaker discusses the window period for thrombolysis and management of bradycardia.

Window Period for Thrombolysis

The window period for thrombolysis is 12 hours but there are other guidelines involved as well. It's unlikely that exam questions will focus on when to do thrombolysis or PCI.

Management of Bradycardia

A gap between two QRS complexes greater than five large boxes indicates bradycardia.

The patient in the ECG has two conducted P waves, indicating some form of heart block.

In exams, questions may focus on the management of bradycardia rather than diagnosis.

Understanding Mobitz Type 2 Block and Brady Management

In this section, the speaker discusses how to diagnose Mobitz Type 2 block and why it is more dangerous than Mobitz Type 1. They also explain the diagnosis of a patient with both Mobitz Type 2 block and ST elevation myocardial infarction (STEMI), as well as the acute management of bradycardia.

Diagnosing Mobitz Type 2 Block

Look at the PR interval to determine if it is constant or varying.

If the PR interval is constant, it is likely Mobitz Type 2 block.

Patients with Mobitz Type 2 block are more likely to be hemodynamically unstable and may convert to complete heart block.

Diagnosis of Patient with STEMI and Mobitz Type 2 Block

The patient has ST elevation myocardial infarction (STEMI) causing right bundle branch block and Mobitz Type 2 block.

This combination of diagnoses requires immediate attention.

Acute Management of Bradycardia

Observe stable patients with acute bradycardia.

If unstable, administer atropine immediately (0.5mg/dose up to a maximum total dose of approximately 3mg).

If atropine does not work, try transcutaneous pacing before converting to transvenous pacing once an expert is available.

Management of Bradycardia and Tachycardia

In this section, the speaker discusses the management of bradycardia and tachycardia. They explain how to determine if a patient is stable or unstable and what medications can be used to manage these conditions.

Management of Bradycardia

If the patient is stable, observe them. If they are not stable, give a drop in. If that doesn't work, go for a pacemaker.

Stability means looking at the systolic blood pressure. If it's less than 90, then the patient is unstable.

The most commonly tested area in exams is systolic BP of less than 90 which indicates instability in the setting of any bradism or even attack element.

Adenosine is not an ordinary drug because it's not very good at increasing heart rate.

Diagnosis of Tachycardia

Atrial fibrillation is a very common rhythm in exams.

To diagnose tachycardia, look for less than three large boxes between two QRS complexes which means it's a tachycardia.

A regular narrow complex tachycardia without p waves before QRS may be AV nodal re-enter and tachycardia.

Ventricular tachycardia can be identified by its wide complex beating at almost 300 beats per minute.

Management of Tachycardia

Atrial fibrillation is the most common tachyarrhythmia.

AV nodal re-enter and tachycardia can be diagnosed by seeing the P wave that is buried within the QRS.

Treatment for AV nodal re-enter and tachycardia may include vagal maneuvers, adenosine, or calcium channel blockers.

Polymorphic Ventricular Tachycardia and Long QT Syndrome

In this section, the speaker discusses polymorphic ventricular tachycardia and long QT syndrome. They explain how to diagnose these conditions and what causes them.

Polymorphic Ventricular Tachycardia

Polymorphic ventricular tachycardia is a type of ventricular attack where the QRS complexes are different from each other.

If a patient has polymorphic ventricular tachycardia along with long QT syndrome, it is called Torsades de Pointes (TdP).

Long QT Syndrome

To diagnose long QT syndrome, calculate the QT interval by measuring from the beginning of the QRS complex to the end of the T wave on an ECG strip.

Corrected QT (QTc) should be calculated using Bazett's formula. A normal QTC value is less than 0.44 seconds in males and less than 0.46 seconds in females.

The most common cause of Long QT Syndrome is drugs, followed by electrolyte imbalances.

Drugs that Cause Long QT Syndrome

Many drugs can cause Long QT Syndrome, including anti-psychotics, antihistamines, antibiotics like macrolides and quinolones, antitubercular drug bedaquiline, and antifungal drug fluconazole.

Class I and class III antiarrhythmic drugs can also cause Long QT Syndrome.

Hypokalemia, Hypocalcemia, and Hypomagnesemia

In this section, the speaker discusses how high pose can cause longevity and mentions the importance of hypocalcemia in exams. The speaker also talks about metabolic problems that can cause longevity such as hypokalemia, hypocalcemia, hypomagnesemia, and hypothermia.

Metabolic Problems That Can Cause Longevity

High pose can cause longevity.

Hypokalemia, hypocalcemia, hypomagnesemia, and hypothermia are metabolic problems that can cause longevity.

Hypercalcemia produces longitude not shot QT.

Management of Tachyarrhythmias

In this section, the speaker discusses the management of tachyarrhythmias using the ACLS protocol. The speaker explains how to determine if a patient is stable or unstable and what steps to take based on their condition. They also discuss different types of tachycardia and which drugs to use for each type.

Determining Patient Stability

Rule out sinus tachycardia before starting treatment because it is often caused by an underlying issue.

Determine if the patient is stable or unstable. If they are unstable (e.g., systolic BP less than 90), proceed with synchronized DC cardioversion. If they are stable, try drugs or vehicle maneuvers depending on QRS width.

Narrow Complex Tachycardia

If the QRS width is less than 0.12 seconds, it is narrow complex tachycardia.

Try vehicle maneuvers like valsalva or carotid sinus massage. If those fail, try adenosine.

AV nodal blockers, beta blockers, and non-dihydropodin calcium channel blockers can also be used.

Wide Complex Tachycardia

If the QRS width is more than 0.12 seconds, it is wide complex tachycardia.

Use antiarrhythmic drug infusions such as amiodarone, procainamide, or sotalol.

Special ECGs

In this section, the speaker discusses special ECGs and their importance in diagnosing certain conditions.

No bullet points provided for this section.

Diagnosing Bundle Branch Block Patterns and Morphology

In this section, the speaker explains how to diagnose left bundle branch block pattern and morphology as well as right bundle branch block pattern and morphology.

Left Bundle Branch Block Pattern and Morphology

QRS and V1 with a predominantly negative complex with white QRS is indicative of LBB morphology or LBB pattern.

T wave inversions in anterior leads like V1-V4 can also be evidence of LBB dysfunction.

Right Bundle Branch Block Pattern and Morphology

A predominantly positive complex in V1 or a typical M pattern or rsr pattern that is equivalent to RBB morphology or RBB pattern.

T wave inversions beyond V3 or V4 are indicative of RV dysfunction which can be diagnosed as RVC unless proven otherwise.

ECGs That Can Cause Sudden Death

In this section, the speaker discusses two important ECG patterns that can cause sudden death in young individuals: arithmogenic right ventricular cardiomyopathy (ARVC) and Brugada syndrome.

Arithmogenic Right Ventricular Cardiomyopathy (ARVC)

ARVC is characterized by epsilon waves, which are small wavelet-like appearances at the J point in V1.

Evidence of RV dysfunction includes T wave inversions in anterior leads like V1-V4.

The investigation of choice for ARVC is cardiac MRI, while the treatment of choice is an implantable cardioverter-defibrillator (ICD).

Brugada Syndrome

Brugada syndrome is characterized by a pseudo right bundle branch block pattern with ST segment elevation and coving with T wave inversion in V1-V2.

Brugada syndrome is most commonly due to SCN5A gene mutations, has autosomal dominant inheritance, and typically affects males.

Glucose Syndrome and Sudden Death

In this section, the speaker discusses glucose syndrome and its potential to cause sudden death at rest or during sleep. The treatment of choice for glucose syndrome is an ICD implantable cardiometric defibrillator.

Causes of Sudden Death

Hypertrophic cardiomyopathy, arithmogenic right ventricular cardiomyopathy (ARVC), long QT syndrome, Brugada syndrome, and catecholaminergic polymorphic ventricular tachycardia (CPVT) are important causes of sudden death.

HCM, ARVC, and ERVC are structural problems in the heart. Long QT syndrome is a channelopathy. CPVT is also a channelopathy due to calcium or sodium channel mutations.

Most of these problems have a strong genetic basis.

Genetic Basis

Mutations in certain sarcomeric genes contribute to 70%+ cases of HCM. Beta myosin heavy chain and cardiac myosin binding protein C are two important sarcomeric gene mutations that occur in HCM.

ARVC is due to desmosomal mutations which are cell-to-cell adhesion molecule addition things.

Long QT syndrome is caused by sodium, potassium or calcium channel mutation but most commonly potassium Channel mutation. CPVT occurs due to calcium channel mutations.

Gene Mutations Associated with Syndromes

This section covers gene mutations associated with different syndromes such as Long QT Syndrome, Brugada Syndrome, and CPVT.

Gene Mutations

Long QT syndrome is caused by sodium, potassium or calcium channel mutation but most commonly potassium Channel mutation.

Brugada syndrome is autosomal dominant and Long QT syndrome also predominantly autosomal dominant. Some syndromes are there which are autosomal recessive like your general Lange Nielsen syndrome but the majority of the longitude syndromes will be autosomal dominant.

In HCM, you will see left ventricular hypertrophy and septal hypertrophy in ECG. In ARVC, you will see epsilon waves and T wave inversion.

ECG and Imaging Findings in Cardiac Disorders

In this section, the speaker discusses the ECG and imaging findings in various cardiac disorders.

Echocardiogram Findings in HCM

LVH and septal hypertrophy are common findings.

The most important finding is systolic anterior motion of anterior mitral leaflet (SAM) of AML.

Imaging Findings in ARVC

Right ventricular dysfunction is a common finding.

Channelopathies vs. Structural Problems

LQTS, Brugada syndrome, and CPVT are channelopathies while HCM and ARVC are structural problems.

Imaging will be normal for channelopathies as they do not involve structural heart disease.

Diagnosis of CPVT

If a young patient dies due to exertion with normal baseline ECG and echo, the diagnosis is likely to be CPVT.

It is important not to misdiagnose it as HCM.

Causes of Death in Cardiac Disorders

HCM and ARVC cause death during exertion.

CPVT causes death during exertion or at rest/sleep.

LQTS type 1 causes death during swimming/diving.

LQTS type 2 causes death when the patient hears a loud noise.

LQTS type 3 and Brugada syndrome can cause death at rest/sleep.

Treatment for Sudden Death Prevention

Most of these disorders will be treated with an implantable cardioverter-defibrillator (ICD).

Pointers for HCM Diagnosis in Exams

Pulses bispherians is a common finding in HCM.

Dynamic changes and dynamic obstruction are also important findings.

The speaker mentions a South Indian movie called Vikram to explain LQTS type 2. This is not relevant to the summary and has been omitted.

Conditions that Affect Preload and Afterload

In this section, the speaker discusses conditions that can reduce or increase preload and afterload.

Preload

Valve cell wall Salva is a maneuver that can reduce preload.

Squatting and leg raising maneuvers can increase preload.

Squatting pushes blood back into central circulation, increasing preload.

Afterload

Amyl nitrate inhalation or any vasodilator can reduce afterload.

Isometric hand grip increases afterload.

Exercise increases contractility, which in turn increases obstruction.

Tamponade and Pulsus Paradoxus

In this section, the speaker discusses tamponade and pulsus paradoxus.

Tamponade

Tamponade occurs when fluid around the heart compresses it.

Clinical features of tamponade include Big Strad (jugular venous distention, hypotension, muffled/distant heart sounds).

Patients with tamponade may also experience severe tachycardia, dyspnea, hypotension/shock.

Pulsus Paradoxus

Pulsus paradoxus refers to an inspiratory fall in blood pressure by more than 10 mmHg.

Temporary is the most important cause of pulsus paradoxus in exams.

Understanding Pulse Paradoxes and Tamponade

In this section, the speaker discusses pulse paradoxes and tamponade. They explain what pulse paradoxes are, how to diagnose tamponade, and the treatment options available.

Pulse Paradoxes

Pulse paradoxes occur when there is a fall in SVP by more than 10mmHg during inspiration.

This is a typical sign of tamponade.

Other conditions that can cause pulse paradoxes include severe respiratory problems like acute exacerbation of bronchial asthma and acute exacerbation of COPD.

Treatment for pulse paradoxes caused by tamponade is pericardiocentesis.

Diagnosing Tamponade

The clinical diagnosis of tamponade can be made at the bedside if there is a compatible clinical presentation.

The investigation of choice for diagnosing tamponade is a simple 2D echocardiogram called trans-thoracic echocardiogram.

If the patient is stable, there's no need to perform pericardial synthesis. However, if they have signs of hemodynamic instability or jugular organ distension, pericardiocentesis may be necessary.

JVP Findings in Tamponade

A deep X descent with blunted Y descent is characteristic of tamponade.

Electrical alternates are seen on ECG in patients with tamponade.

Differentiating Constriction from Tamponade

Deep white descent with constriction produces Friedrich sign.

Deep X descent plus deep Y descent differentiates constriction from tamponade.

Understanding JVP Findings

In this section, the speaker explains JVP findings and their causes.

JVP Wave Pattern

A wave: due to atrial contraction

C wave: due to isovolumetric ventricular contraction

X descent: due to rapid ejection of the ventricles along with atrial relaxation

V wave: due to venous filling of the right atrium

Y descent: due to rapid passive filling of the right ventricle

JVP Findings in Tamponade

A deep X descent with blunted Y descent is characteristic of tamponade.

Electrical alternates are seen on ECG in patients with tamponade.

English JVP Findings

In this section, the speaker discusses the important findings related to Jugular Venous Pulse (JVP).

A Waves

Absent in atrial fibrillation

Large areas seen in right ventricular inflow tract obstruction or outflow obstruction

Very large areas seen in AV dissociation and AVNRT

Complete heart block is a cause of AV dissociation

Ventricular Brady with AV decision complete unblock tacky with every decision

Irregular cannon waves seen in AV dissociation, regular cannon waves seen in AB and RB

C Waves

Smooth CV wave seen in severe tricuspid regurgitation

X descent lost and large V wave present in severe tricuspid regurgitation

X Descent

Prominent X descent seen in constrictive pericarditis and tamponade

Attenuated X descent seen in tricuspid regurgitation and right heart failure

V Wave

Large V wave commonly caused by tricuspid regurgitation

Venous filling of the right atrium causes V wave

Prominent Y wave seen in constrictive pericarditis and TR, blunted Y descent is most important finding for tamponade

The speaker emphasizes that these are common exam findings related to JVP.

Understanding Pulse Alternation

In this section, the speaker explains the different types of pulse alternation and how to differentiate between them.

Types of Pulse Alternation

Electrical alternates: Only the QRS amplitude changes, not the pulse amplitude.

Pulses by Gemini: A ventricular examination equivalent that produces a powerful sinus beat and a small volume premature ventricular contraction beat.

Pulses alternates: Regularly alternating large and small volume pulses.

Differentiating Between Pulse Alternations

Pulses alternates are regular, while pulses by Gemini are irregular.

Irregularly irregular pulse is one of the classic examples of pulses by Gemini.

Acute Aortic Dissection

In this section, the speaker discusses acute aortic dissection, its symptoms, and diagnostic clues.

Symptoms of Acute Aortic Dissection

Chest pain that radiates to the back in between the shoulder blades (interscapular region).

Quality of chest pain can be piercing or tearing.

Diagnostic Clues for Acute Aortic Dissection

Unequal pulse and blood pressure between arms and legs.

Chest x-ray may show mediastinal widening due to dissection aneurysm formation.

Diagnostic Tests for Acute Aortic Dissection

Three diagnostic tests include:

CT angiogram or CCT of the chest

MR angiogram of the chest

Transesophageal Echo

Iot Dissection

This section covers the diagnosis and treatment of iot dissection.

Diagnosis

Unstable patients require a transesophageal echo.

Stable patients can undergo a CT angiogram, which is comparable to an MR angiogram.

False lumen will have lesser contrast compared to the true lumen.

Treatment

Primary treatment for both Standford A and B is reducing blood pressure and heart rate.

Target systolic blood pressure should be less than 120 mmHg, and target heart rate should be less than 60 bpm.

IV beta blockers are used to achieve these targets. Labetalol is commonly used in India.

Surgery is required for Standford A, but only in special situations for Standford B.

Venous Thromboembolism

This section covers the diagnosis of venous thromboembolism.

Diagnosis

The Wells probability score determines whether a definitive investigation or D-dimer test is needed.

Definitive investigations include compression ultrasound or lower limb venous Doppler for DVT, while pulmonary embolism requires computed tomography pulmonary angiography (CTPA).

Venous Thromboembolism

This section covers the signs and symptoms of deep vein thrombosis (DVT) and pulmonary embolism (PE), as well as important investigatory findings. It also discusses the treatment options for venous thromboembolism.

Signs and Symptoms of DVT and PE

The most important sign of DVT is asymmetric calf swelling, which may be accompanied by calf tenderness.

The most important sign of PE is unexplained shortness of breath, which may be accompanied by positive clinical signs such as breathlessness.

Other signs of PE include sinus tachycardia, right ventricular hypertrophy, tall P waves indicating right atrial enlargement, RV strain pattern with T wave inversions in multiple leads, and S1 Q3 T3 pattern.

Investigatory Findings

CT pulmonary angiogram is the investigation of choice for diagnosing PE.

Inappropriate situations can lead to a diagnosis of right ventricular hypertrophy based on a large R wave in V1 without a wide QRS complex.

A saddle embolus can be seen occluding the pulmonary arteries on CT imaging.

Treatment Options

Anticoagulation is the treatment of choice for any venous thromboembolism.

IVC filters are used only if anticoagulation is contraindicated or ineffective.

Thrombolysis can be considered if a patient has PE with systolic blood pressure less than 90.

Diagnosing and Treating ARDS

In this section, the speaker discusses how to diagnose and treat Acute Respiratory Distress Syndrome (ARDS).

Diagnosing ARDS

ARDS is diagnosed using the New Berlin criteria.

The criteria include acute onset of illness within seven days, non-cardiogenic pulmonary edema, bilateral infiltrates in chest x-ray, and severe hypoxemia with a PF ratio less than 300.

PF ratio should be calculated based on PEEP. PEEP should be at least five centimeters of water.

Causes of ARDS

The most common cause of ARDS is sepsis, especially gram-negative sepsis causing endotoxic shock.

The second most common cause is direct lung injury due to pneumonia.

Treating ARDS

Low tidal volume ventilation is important for treating ARDS. Tidal volume must be 4 to 6 ml per kilogram.

PEEP should be titrated based on Arts net protocol according to the needs of the patient.

Conservative fluid management has been proven to be efficacious even though survival impact is not that great.

Early use of paralytic agents has been shown to have some effect in patients who are having ventilator patient dysentery.

Prone positioning for at least more than 16 hours a day can also help treat ARDS.

Corticosteroids have no effect in treating ARDS. Morphine should not be used either.

Understanding Lung Disease

In this section, the speaker explains the differences between obstructive and restrictive lung diseases. They also discuss how to identify large airway obstruction using flow volume loops.

Obstructive vs Restrictive Lung Disease

Obstructive lung disease refers to small airway obstruction, which produces a curving appearance on flow volume loops.

Restrictive lung disease has a relatively normal curve shape but appears smaller due to reduced FVC and FEV1.

The speaker emphasizes that small airway obstruction is different from large airway obstruction.

Identifying Large Airway Obstruction

Flow volume loops can be used to identify large airway obstruction.

If the inspiratory limb is flattened, it suggests variable extra-thoracic obstruction.

If the expiratory limb is flattened, it suggests variable intra-thoracic large airway obstruction.

If both limbs are flattened, it indicates fixed obstruction.

Oxygen Delivery Devices

This section covers different oxygen delivery devices and their recommended flow rates.

Simple Nasal Cannula

Recommended flow rate: 1-6 L/min

Can deliver an FiO2 of 24%-44%.

Simple Face Mask (Hudson Mask)

Minimum oxygen flow rate: 5 L/min

Patient must breathe through both nose and mouth; minimum recommendation is to start at 5 L/min.

Non-Rebreather Mask (NRBM)

Recommended flow rate: 10-15 L/min

Can theoretically deliver an FiO2 of 70%-100%, depending on the number of walls.

Practically speaking, it delivers 62.85% FiO2.

Oxygen Delivery Devices

In this section, the speaker discusses different oxygen delivery devices and their advantages.

Venturi Mask

A fixed performance device that delivers a fixed FIO2.

Color-coded for easy identification.

Delivers 24 to 40% oxygen.

Self-Inflation Bag (SIB)

Also known as Ambu, but Ambu is a company name.

Used in OT rooms by anesthetists.

Can be used by anyone, but requires expertise.

Called flow inflation bags because the bag can only be expanded with adequate oxygen flows.

High Flow Nasal Oxygen (HFNO)

Provides humidified oxygen easily.

Delivers FIO2 from 21 to 100% as a fixed performance device.

Used as an alternative to CPAP or BPAP in certain patients.

Acute Exacerbation of COPD

In this section, the speaker discusses how to manage acute exacerbation of COPD.

Causes of Acute Exacerbation

Most common cause is infection, with H. influenzae and Streptococcus pneumoniae being the most common pathogens.

Treatment of Acute Exacerbation

Bronchodilators

Short acting muscarinic antagonists are more effective than beta agonists in COPD.

SABA can also be used.

Systemic Corticosteroids

Oral prednisolone or IV methylprednisolone can be used depending on whether treating as OPD or IP basis respectively.

Antibiotic Treatment and NIV

In this section, the speaker discusses when to consider starting antibiotics for a patient with fever or increased WBC count. They also explain what non-invasive ventilation (NIV) is and when it should be used.

Antibiotic Treatment

Empirically, antibiotics should be considered if the patient has a fever, increased total leukocyte count, high CRP, new infiltrates in chest x-ray imaging, or is clinically sick.

Macrolides can be started initially but antibiotic choice should depend on local microbiological expertise.

Antibiotic choice should depend on local culture patterns.

Non-Invasive Ventilation (NIV)

NIV is very effective in patients with acute COPD exacerbation.

Indications for NIV include pH less than 7.35 and PaCO2 over 45 mmHg.

If pH is less than 7.25, it's better to avoid NIV due to high rates of failure.

A typical NIV device includes a mask that needs to be sealed tightly by closing the patient's nose as well as mouth.

Interstitial Lung Disease Classification

In this section, the speaker explains how interstitial lung disease (ILD) can be classified based on known causes.

ILD Due to Known Causes

Occupational ILDs are important and can be caused by hypersensitivity pneumonitis or pneumoconiosis due to organic or inorganic dust exposure.

Certain drugs like bleomycin, anti-cancer drugs, and methotrexate can cause ILD.

Connective tissue disorders like rheumatoid arthritis and scleroderma can also cause ILD.

ALDS Treatment

In this section, the speaker discusses the five-step treatment for patients with acute respiratory failure due to interstitial lung disease.

Five-Step Treatment

The five-step treatment for patients with acute respiratory failure due to interstitial lung disease includes bronchodilation, systemic corticosteroids, antibiotics, NIV, and endotracheal intubation.

Endotracheal intubation is only used in cases of severe respiratory failure.

Pulmonary Langerhans Cell Histiocytosis and Sarcoidosis

In this section, the speaker discusses two types of interstitial lung diseases (ILDs): pulmonary Langerhans cell histiocytosis (PLCH) and ILDs due to unknown causes, specifically sarcoidosis.

PLCH

PLCH is a cystic disease that typically involves upper lobes.

Biopsy is necessary for diagnosis, which will show malignant Langerhans cells.

Electron microscopy will show characteristic Birbeck granules. CD207 (Langerin) will also be positive.

Smoking cessation is the treatment of choice. Corticosteroids may be used short-term.

Sarcoidosis

Sarcoidosis is an ILD due to unknown causes that produces non-caseating granulomas. It can affect multiple organs in the body.

There are two syndromes associated with sarcoidosis:

Lofgren syndrome, which has bilateral hilar lymphadenopathy and arthritis and has an excellent prognosis.

Heerfordt-Waldenstrom syndrome, which presents with fever, uveitis, parotid gland enlargement, and seventh nerve palsy.

Uveitis will be granulomatous.

Lupus pernio skin lesions can occur but are not part of the classic triad.

Both syndromes are acute forms of sarcoidosis.

Sarcoidosis can produce Central diabetes insipidus if it affects the pituitary gland and can produce both Central as well as nephrogenic diabetes insipidus.

Investigation of choice is biopsy, which will show non-caseating granulomas. Serum calcium may be elevated due to hyper vitaminosis D from granulomas containing 1-alpha hydroxylase activity. High serum Angiotensin converting enzyme may also be present but is not sensitive or specific.

Sarcoidosis and Idiopathic Interstitial Pneumonias

In this section, the speaker discusses sarcoidosis and idiopathic interstitial pneumonias (IIPs), including their diagnosis and treatment.

Sarcoidosis

CD4/C8 ratio more than 2.5 is diagnostic of sarcoidosis.

Prednisolone is the first-line therapy for sarcoidosis.

Idiopathic Interstitial Pneumonias (IIPs)

IIPs are unknown causes, similar to sarcoidosis.

Examples of IIPs include idiopathic pulmonary fibrosis (IPF), non-specific interstitial pneumonia (NSIP), cryptogenic organizing pneumonia (COP), and acute interstitial pneumonia (AIP).

Anti-fibrotic therapy is the treatment of choice for IPF, with TGF beta inhibitor periphenidone and tyrosine kinase inhibitor nintedanib being two options.

Corticosteroids are not effective in the setting of IPF.

Diagnosis of IPF requires ruling out secondary causes like connective tissue disorders.

Biopsy may be required to see a usual interstitial pneumonia pattern.

Diagnosis and Treatment

HRCT is the radiological investigation of choice for any IILDS.

Investigation of choice for any ILD is going to be HRCT.

CT scan will show subpleural basal fibrosis with honeycombing appearance and traction bronchiectasis.

Fibrosis itself will dilate the bronchus and it will look like as if its bronchiectasis but it is not.

Panchos Tumor and Lung Cancer

In this section, the speaker discusses Panchos tumor, a type of squamous cell cancer that occurs in the apex of the lung. The speaker also talks about different types of lung cancer and their characteristics.

Panchos Tumor

Panchos tumor is a type of squamous cell cancer that occurs in the apex of the lung.

It can cause wasting of small muscles of the hand, pain in the neck and arm, and rib destruction due to brachial plexus involvement.

It can also cause Horner syndrome and hardness syndrome.

This is a classic feature of Honda Centro because of sympathetic plexus involvement in the brachial plexus.

Lung Cancer Types

There are two main types: non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC).

NSCLC includes squamous cell carcinoma and adenocarcinoma. SCLC is less common than NSCLC but tends to produce more paraneoplastic syndromes.

Squamous cell carcinoma and SCLC occur exclusively in smokers while adenocarcinoma can occur in both smokers and non-smokers.

Adenocarcinoma is most common among non-smokers while squamous cell carcinoma is typically central tumors near hilar region.

Paraneoplastic Syndromes

Paraneoplastic syndromes are more important than types when discussing lung cancer.

They can produce endocrine problems, skeletal problems, or neurological problems such as Lambert-Eaton myasthenic syndrome (LEMS).

Small cell lung cancer tends to produce more paraneoplastic syndromes than NSCLC.

Perineoplastic Syndromes and Emergency Medicine

In this section, the speaker discusses perineoplastic syndromes associated with lung cancer, including hypercalcemia and skeletal manifestations. They also cover neurological manifestations and hematological complications. Finally, they discuss emergency medicine protocols for cardiac arrest.

Perineoplastic Syndromes

Hypercalcemia is a common perineoplastic syndrome associated with squamous cell cancer, not small cell lung cancer. It is caused by PTH-related peptide.

Skeletal manifestations can include clubbing or hypertrophic osteoarthropathy in any non-small cell lung cancer. Hypertrophic pulmonary osteoarthropathy is specific to adenocarcinoma.

Neurological manifestations are typically only seen in small cell lung cancer and can include Lambert-Eaton myasthenic syndrome (LEMS), peripheral neuropathy, and cerebellar degeneration.

Antibodies that produce cerebellar degeneration include anti-Yo, anti-Hu, anti-Ma1/Ma2, anti-CRMP5, anti-Tr, and anti-GAD65.

Hematological complications such as hypercoagulability and DIC are more common in adenocarcinoma than other types of lung cancer.

Emergency Medicine Protocols for Cardiac Arrest

The AC less protocol involves placing paddles on the right side in the anterior direction and on the left side in the lateral position. Other paddle positions include right anterior/left posterior.

Hot embedded external defibrillators may be used to assess patients with cardiac arrest.

Scene Safety and Basic Checklist

In this section, the speaker emphasizes the importance of scene safety and provides a basic checklist to follow in case of an emergency.

Scene Safety

Scene safety is crucial when responding to an emergency.

Call for help immediately by contacting local emergency medical services.

Check for responsiveness. If the patient is responsive, no CPR is needed. Wait for the Emergency crew to arrive.

If the patient is not responsive, check for pulse and breathing together.

Basic Checklist

Verify scene safety

Check for responsiveness

If patient is responsive, wait for Emergency crew

If patient is not responsive, check pulse and breathing together

CPR Steps

This section covers what to do if a patient does not have a pulse or is not breathing normally.

No Pulse or Not Breathing Normally

If there's no pulse, start CPR immediately.

If there's a pulse but the patient isn't breathing normally (primary respiratory arrest), give rescue breaths only.

Continue CPR until the Emergency crew arrives.

Adult CPR Guidelines

This section outlines guidelines for performing adult CPR.

Adult CPR Ratio

The ratio for adult CPR is 30 chest compressions to 2 breathes.

Chest Compression Rate and Depth

The chest compression rate should be between 100 to 120 per minute.

The depth of compression should be five to six centimeters or two to two and a half inches.

Advanced Airway

If the patient has an advanced airway, the breath rate can be around 10 per minute.

AED and Shockable Rhythms

This section covers what to do when an Automatic External Defibrillator (AED) arrives at the scene and how to identify shockable rhythms.

AED Arrival

Once the AED arrives, follow instructions and identify what rhythm is going on.

Shockable Rhythms

Shockable rhythms include pulseless ventricular tachycardia, ventricular fibrillation, and pulseless ventricular tachycardia with no pulse.

Non-Shockable Rhythms

Non-shockable rhythms include pulseless electrical activity and asystole.

CPR After Shocking

This section covers what to do after shocking a patient's heart.

After Shocking

After shocking, don't look at the monitor. Instead, perform CPR for two minutes before checking the rhythm again.

If there's no change in rhythm (asystole), continue performing CPR.

Depending on whether it's a shockable or non-shockable rhythm, continue with the same cycle of CPR.

Drugs Used in CPA

This section covers the drugs used in Cardiopulmonary Arrest (CPA).

Drugs Used

The most important drug used in CPA is epinephrine.

Cardiac Arrest Protocol and Acid-Base Analysis

In this section, the speaker discusses the Cardiac Arrest protocol and Acid-Base Analysis.

Cardiac Arrest Protocol

Chest compressions are the most important priority in Cardiac Arrest.

Intubation can be done later on after initial CPR is done.

Adrenaline dose is 1mg given intravenously and can be repeated every 3 to 5 minutes.

Amiodarone dose is 300mg for the first dose and 150mg for the second dose. It should be given IV as a bolus form.

Lignocaine should only be given in shockable rhythms.

Acid-Base Analysis

The pH level determines if it's acidosis or alkalosis.

If pH <7.4, it's acidosis; if pH >7.4, it's alkalosis.

Bicarbonate levels determine metabolic status:

Low bicarbonate = metabolic acidosis

High bicarbonate = metabolic alkalosis

Pco2 levels determine respiratory status:

High Pco2 = respiratory acidosis

Low Pco2 = respiratory alkalosis

This concludes the summary of the transcript on Cardiac Arrest Protocol and Acid Base Analysis.

Understanding Acid-Base Disorders

In this section, the speaker explains how to diagnose respiratory acidosis and alkalosis, and when compensation formulas are required.

Diagnosing Respiratory Acidosis and Alkalosis

Respiratory alkalosis occurs when the pH is more than 7.45.

A bicarbonate level of 31 indicates chronic respiratory acidosis, while a bicarbonate level of less than 24 indicates acute respiratory alkalosis.

Compensation formulas are not required for NEET PG/FMG levels. It is important to know how to identify the problem and whether it is acute or chronic respiratory acidosis.

Mixed Disorders

When arrows move in opposite directions (one component increasing while the other decreases), it's a mixed disorder.

Anion Gap Metabolic Acidosis

Anion gap is important for metabolic acidosis patients.

The mnemonic "RAD" stands for renal tubular acidosis, Addison disease, diarrhea, and other gastrointestinal causes that can cause normal anion gap metabolic acidosis.

The mnemonic "GOLDMARK" stands for glycols (ethylene glycol/propylene glycol), oxoproline metabolite (acetaminophen poisoning), lactic acidosis (lactate), D-lactic acidosis (D-lactate), methanol poisoning, aspirin/salicylate poisoning, renal failure, ketoacidosis.

Differentiating Pre-Renal AKA from Acute Tubular Necrosis

No bullet points provided.

English Tubular Functions in AK and Vitamin Deficiencies

In this section, the speaker discusses tubular functions in pre-renal AK and acute tubular necrosis. They also discuss fat-soluble vitamin deficiencies.

Tubular Functions in Pre-Renal AK and Acute Tubular Necrosis

In pre-renal AK, the urinary concentration increases, resulting in a specific gravity of more than 1.020 and Uranus multi of usually more than 350 to 500.

In acute tubular necrosis, the tubular function is lost, resulting in a specific gravity of less than 1.010 and Uranus multi of less than 350.

The fractional excretion of sodium will be less than one percentage in pre-renal AK because they can reabsorb solutes better due to intact tubular function.

The fractional excretion of sodium will be more than two percentages in acute tubular necrosis because they cannot absorb solutes well due to lost tubular function.

Fat-Soluble Vitamin Deficiencies

Vitamin A Deficiency

Vitamin A deficiency produces night blindness, xerophthalmia, and keratomalacia.

Vitamin D Deficiency

Vitamin D deficiency produces rickets and osteomalacia. Elevated alkaline phosphates are an early sign of complicated vitamin deficiency like rickets or osteomalacia.

Tocopherol (Vitamin E) Deficiency

Tocopherol deficiency can produce hemolytic anemia.

Thiamine and Other Vitamin Deficiencies

In this section, the speaker discusses different types of vitamin deficiencies and their symptoms.

Types of Beriberi

Dry beriberi produces peripheral neuropathy.

Wet beriberi typically produces high output cardiac failure.

Causes of Thiamine Deficiency

Alcoholics are prone to thiamine deficiency.

Pregnant women with hyperemesis gravidarum may develop thiamine deficiency.

Patients with malignancy or long-standing cancer pain may also develop thiamine deficiency.

Symptoms of Wernicke Encephalopathy

Confusion and altered mental status

Ophthalmoplegia

Ataxia

Treatment for Thiamine Deficiency

Ophthalmoplegia is the first symptom to resolve after giving thiamine.

Confusion resolves next, followed by ataxia.

Other Vitamin Deficiencies

Riboflavin Deficiency (Riboflavinosis)

Can produce local symptoms like mouth sores and small skin changes.

Niacin Deficiency (Pellagra)

Also called four D's: diarrhea, dermatitis, dementia, death.

Pantothenic Acid Deficiency

Produces paresthesia only.

Pyridoxine (B6) Deficiency

Can produce anemia (specifically sideroblastic anemia) and peripheral neuropathy.

Suspect in alcoholics and patients taking INH treatment for tuberculosis.

Biotin Deficiency

Produces dermatitis only.

Folic Acid and Folate Acid Deficiency

Produces neural tube defects in newborns.

Anemia will be megaloblastic type not cytoplastic type globlastic anemia.

Cyanocobalamin (B12) Deficiency

Produces megaloblastic anemia and neurological complications like dementia and peripheral neuropathy.

Ascorbic Acid (Vitamin C) Deficiency

Produces scurvy, which causes growth problems in children and skin changes causing petechiae.

Vitamin Deficiency and Heat-Related Illnesses

In this section, the speaker discusses vitamin deficiencies and heat-related illnesses.

Subacute Combined Degeneration of the Cord

Subacute combined degeneration of the cord is a neurological complication of vitamin B12 deficiency.

Key Environmental Issues

There are three key environmental issues to discuss: heat-related illness, alternated illness, and cold-related illness.

Heat-related illness can present as either heat exhaustion or heat stroke.

Differences Between Heat Exhaustion and Heat Stroke

The main difference between heat exhaustion and heat stroke is that in heat exhaustion, the core body temperature will be less than 40.5 degrees Celsius, while in heat stroke it will exceed 40.5 degrees Celsius.

Patients with heat exhaustion may have tachycardia and tachypnea but their vital signs will be stable, while patients with heat stroke may be hypotensive and have altered mental status.

Patients with classic heat stroke tend to be elderly and it occurs during times of epidemics such as during a heat wave. Rapid cooling is the treatment of choice for patients with classic heat stroke.

Treatment for Heat Exhaustion and Heat Stroke

Treatment for heat exhaustion involves hydration, shifting the patient to a cooler environment, and giving fluids.

Rapid cooling is necessary for treating patients with classic heat stroke using active or passive cooling methods such as injecting cold saline or normal saline into iced water at 0 to 4 degrees Celsius respectively.

Active cooling should be stopped when the patient starts shivering or when the temperature reaches around 102 degrees Fahrenheit.

English High Altitude and Cold-Related Problems

In this video, the speaker discusses high altitude and cold-related problems. The key features of high altitude pulmonary edema are crepitations in the lungs and low spo2. Patients with high altitude cerebellar edema will have a headache and altered mental status. The core body temperature can be measured by putting a probe in the pulmonary artery or lower part of the esophagus, but rectal temperature is commonly used in field settings.

High Altitude Pulmonary Edema

Key features: crepitations in lungs, low spo2

Treatment:

Oxygen is important

Temporary hyperbaric chambers can be used to pressurize the bag so that it mimics as if the patient is at a lower altitude.

Dexamethasone can be given to most patients.

Non-invasive ventilation (NIV) like CPAP or BPAP can also be tried.

Nifedipine can be tried.

Acetazolamide cannot be used as prophylaxis or treatment for high-altitude pulmonary edema.

High Altitude Cerebral Edema

Key features: headache, altered mental status, seizures

Acetazolamide cannot be used as prophylaxis or treatment for high-altitude cerebral edema.

Cold-related Problems

Frostbite

Symptoms: numbness, wooden block feeling in hands/feet

Treatment: re-warming with a solution at 37 to 40 degrees Celsius is excruciatingly painful but the number one treatment of choice.

Hypothermia

Symptoms: shivering, confusion, loss of coordination

Treatment: remove wet clothing and warm the person with blankets or a sleeping bag.

Diabetic Emergencies and Environmental Problems

In this section, the speaker discusses diabetic emergencies and environmental problems that may be asked in FMG exams.

Diabetic Emergencies

There are two important diabetic emergencies: Diabetic Ketoacidosis (DK) and Hyperosmolar Hyperglycemic Syndrome (HHS).

DK is common in type 1 diabetes compared to type 2 diabetes. The hallmark of DK is ketosis and acidosis.

Plasma ketones should be measured to diagnose DK. Beta-hydroxybutyrate is the best ketone to measure.

HHS is usually a complication of type 2 diabetes. Patients with HHS will not have ketosis.

Environmental Problems

Local areas of occlusion can be treated with IV thrombolysis or IV DPA within 24 hours. After 24 hours, bone scans or FDJ PET can be used to look for areas of devitalization. Amputation may also need to be considered.

One question on environmental problems will likely appear on FMG exams.

Hyperglycemic Emergencies

In this section, the speaker discusses the differences between diabetic ketoacidosis (DK) and hyperosmolar hyperglycemic state (HHS), their symptoms, and how to treat them.

Symptoms of DK and HHS

Abdominal pain, nausea, vomiting are common in DK but not in HHS.

Breath that smells like fruit is characteristic of DK.

High serum osmolality causing intracellular brain dehydration is what brings patients with HHS to the hospital.

CBG levels are usually higher in HHS than in DK.

Mortality Rates

HHS has a higher mortality rate than DK due to late presentation and severe dehydration.

Mortality rates for HHS can be more than 15%, while for DK it's less than 3-4%.

Treatment for Hyperglycemic Emergencies

FLIP Therapy

Fluids, insulin, and potassium (FLIP) therapy is used to treat hyperglycemic emergencies.

Fluid Treatment

Normal saline or half-normal saline can be used depending on capillary blood glucose levels.

In HHS, fluids are the most important treatment due to severe dehydration.

Insulin Treatment

Regular insulin is used to treat both DK and HHS.

Insulin is the most important treatment for correcting ketosis doses in DK.

Potassium Treatment

Potassium is given to almost all patients, and the amount depends on their potassium levels.

Treatment of Hyperglycemic Emergency

In this section, the speaker discusses the treatment of hyperglycemic emergency and explains the importance of flip therapy.

Flip Therapy for Hyperglycemic Emergency

KCl should be given first in hyperglycemic emergency.

Careful monitoring of potassium is required before adding insulin.

Once potassium levels become more than 3.5, insulin can be added.

For potassium levels between 3.5 to 5, insulin and KCl can be given together.

For potassium levels above 5, insulin motor protection can be added later on.

If potassium levels are less than 3.5, KCl should be given first.

Adrenal Insufficiency

In this section, the speaker talks about adrenal insufficiency and explains how to differentiate between primary and secondary adrenal insufficiency.

Primary vs Secondary Adrenal Insufficiency

Key feature of primary adrenal insufficiency is hyperpigmentation.

In primary adrenal insufficiency, cortisol levels are low which increases ACTH levels as a reflex.

In secondary adrenal insufficiency, ACTH levels are low which causes low cortisol levels.

Aldosterone levels will also be low in primary adrenal insufficiency leading to salt wasting states with hypovolemic hyponatremia and hyperkalemia.

Patients with secondary adrenal insufficiency will have normal aldosterone levels leading to no salt wasting or electrolyte changes.

Diagnosis and Treatment

The investigation of choice for diagnosing any type of adrenal insufficiency is an ACTH stimulation test.

Hydrocortisone replacement therapy is used for primary adrenal insufficiency.

In secondary adrenal insufficiency, only hydrocortisone is enough as aldosterone levels are normal.

Adrenal Insufficiency and Crisis

This section covers the management of adrenal insufficiency and crisis.

Management of Adrenal Crisis

Patients with adrenal crisis present with shock that is out of proportion to the severity of their acute illness.

The first treatment for adrenal crisis is always IV fluids, followed by corticosteroids. Hydrocortisone is used if the patient is a known case of adrenal insufficiency, while dexamethasone is used if the patient is not a known case.

If the patient is not a known case, an ACTH stimulation test should be performed to diagnose whether they have adrenal insufficiency or not.

Diagnosis of Adrenal Insufficiency

An ACTH stimulation test involves injecting ACTH and checking serum cortisol after one hour. Hydrocortisone can interfere with cortisol measurements, so dexamethasone should be used instead if performing an ACTH stimulation test.

IV fluids are important in treating adrenal crisis because ABCs (airway, breathing, circulation) are crucial.

Hyperthyroidism and Hypothyroidism

This section covers hyperthyroidism and hypothyroidism, focusing on Graves disease.

Graves Disease

Patients with Graves disease will present with hyperthyroidism and extra-thyroidal manifestations such as Graves ophthalmopathy (orbitopathy), pretibial myxedema, thyroid acropachy (clubbing and bone changes).

Orbital MRI is the investigation of choice for diagnosing Graves ophthalmopathy.

Corticosteroids (dexamethasone) are the treatment of choice for moderate to severe cases of Graves ophthalmopathy.

Treatment of Graves' Disease

In this section, the speaker discusses the different treatment options for Graves' disease and their contraindications.

Anti-Thyroid Drugs

Propyl thyrosine, carbimazole, and methimazole are anti-thyroid drugs used to treat Graves' disease.

Methimazole is the first-line drug except in the first trimester of pregnancy where propyl thyrosine is used instead.

Radioactive Iodine Ablation (RAIA)

RAIA is a second-line treatment option for Graves' disease.

Contraindications for RAIA include pregnancy, lactation, suspected cancer, and moderate to severe ophthalmopathy.

Surgery

Surgery is rarely performed nowadays for Graves' disease.

Investigations

TFT will show hyperthyroidism with low TSH.

Radioactive iodine uptake will be increased diffusely and homogeneously.

Ultrasound will show increased vascularity.

The most specific investigation is thyroid receptor antibodies (TRAb).

De Quervain's Thyroiditis

In this section, the speaker discusses De Quervain's thyroiditis or subacute granulomatous thyroiditis.

De Quervain's thyroiditis presents with painful gland and pyrotoxic picture.

TFT shows a hyperthyroid feature with high T4 and low TSH.

Radioactive iodine uptake will be low only.

Biopsy showing granuloma mass that is decreased confirms diagnosis.

Conservative management with NSAIDs and dexamethasone for pain relief is the treatment of choice.

Approach to a Patient with Primary Immunology

In this section, the speaker discusses how to approach a patient with primary immunology who has not experienced menses.

Steps for Evaluation

The first step is to evaluate secondary sexual characteristics.

The second step is to examine breast development using the Tanner staging system.

If the patient has secondary sexual characteristics and good breast development, the next step is an ultrasound to look for Mullerian structures, specifically the uterus.

If Mullerian structures are absent in ultrasound, karyotyping should be done. An XXY karyotype indicates complete androgen insensitivity syndrome while an XX karyotype indicates Mullerian agenesis or MRKH syndrome.

Differentiating Between MRKH Syndrome and Androgen Insensitivity Syndrome

This section discusses how to differentiate between MRKH syndrome and complete androgen insensitivity syndrome.

Key Points

MRKH syndrome refers to utero vaginal agenesis while complete androgen insensitivity syndrome results from defective androgen receptors.

Patients with MRKH will have normal axillary and pubic hair while patients with complete AIS will have absent axillary and pubic hair.

Evaluating Short Stature in Patients without Secondary Sexual Characteristics

This section discusses how to evaluate short stature in patients without secondary sexual characteristics.

Key Points

The first step is to evaluate height on a growth chart.

If FSH levels are low, it indicates a central cause like pituitary or hypothalamic issues.

If FSH levels are increased, Turner syndrome should be considered.

Endocrine Issues

In this section, the speaker discusses various endocrine issues and syndromes that are commonly asked in exams.

Turner Syndrome

The classic triad of Turner syndrome is short stature, streak ovaries, and cardiovascular problems.

Patients with Turner syndrome will be on average 20 centimeters shorter than their peers after completing puberty.

If a patient's height is normal, FSH levels should be checked to determine if there are any central causes of gonadotropin deficiency.

If FSH levels are high, it indicates gonadal dysgenesis.

Klinefelter Syndrome

Klinefelter syndrome is 47 XXY and affects males.

The most common cause of Klinefelter syndrome is meiotic non-disjunction.

Patients with Klinefelter syndrome will actually be tall and won't have breast development due to fried gonads during embryonic development.

Other Syndromes

Four syndromes that should be remembered for exams are: Turner syndrome, Klinefelter syndrome, Marfan syndrome, and Liddle's syndrome.

Features of Klinefelter syndrome include testicular failure due to extra X effect.

Clinical Pearls

Remembering these syndromes can be helpful in exams.

Characteristics and Risks of Klinefelter Syndrome

In this section, the speaker discusses the characteristic features of Klinefelter syndrome, including gynecomastia, tall stature, and lack of male pattern baldness. The speaker also mentions the increased risk of cardiovascular problems, autoimmune disorders, and male breast cancer associated with Klinefelter syndrome.

Key Features of Klinefelter Syndrome

Patients with Klinefelter syndrome often have gynecomastia and are generally tall.

Lack of testosterone at puberty can cause delayed fusion of epiphysis leading to tall stature.

Testosterone deficiency in patients with Klinefelter syndrome leads to a lack of male pattern baldness and reduced facial hair growth.

Patients with Klinefelter syndrome are at an increased risk for cardiovascular problems such as mitral valve prolapse and autoimmune disorders like thyroiditis. They also have a 50 times higher risk for male breast cancer.

Reproductive Endocrine Issues in Klinefelter Syndrome

In this section, the speaker discusses reproductive endocrine issues associated with Klinefelter syndrome. The speaker explains that testosterone replacement therapy is used to treat these issues.

Reproductive Endocrine Issues in Klinefelter Syndrome

Male breast cancer is a significant risk factor for patients with Klinefelter syndrome.

Treatment for reproductive endocrine issues in patients with Klinefelter syndrome involves testosterone replacement therapy.

Management of Rheumatoid Arthritis

In this section, the speaker discusses the management of rheumatoid arthritis. The speaker explains that corticosteroids are used to treat acute flares, while methotrexate and leflunomide are used for long-term maintenance therapy.

Management of Rheumatoid Arthritis

Ulnar deviation of fingers is the most common deformity in a rheumatoid hand.

The DIP joint and thoracolumbar spine are not involved in patients with rheumatoid arthritis.

Acute flares of rheumatoid arthritis are treated with corticosteroids like prednisolone or methylprednisolone.

Long-term maintenance therapy for rheumatoid arthritis involves methotrexate and leflunomide.

Treatment of Rheumatoid Arthritis

In this section, the speaker discusses the treatment options for rheumatoid arthritis.

Triple Therapy

Triple therapy is a combination of methotrexate, hydroxychloroquine, and sulfasalazine.

If the patient does not respond to triple therapy, biological drugs can be used.

Biological Drugs

Biological drugs are approved for monotherapy or in combination with methotrexate.

There are five anti-tumor necrosis factor alpha drugs available. Infliximab is commonly used in India.

IL-6 receptor inhibitors tocilizumab and sarilumab are also available in India.

Anti-cd20 therapies such as rituximab can also be used.

Novel Therapies

JAK inhibitors such as tofacitinib and baricitinib are oral drugs that block the JAK receptor pathway.

CTLA4 fusion antibodies such as abatacept and belatacept are a new class of drugs that can be used for transplant patients.

Conclusion

The speaker concludes by thanking the audience and wishing them success on their exams.