Collapse radiological signs

Direct signs

1.Displacement of interlobar fissures

2.Crowding of vessels and bronchi

Indirect signs

1.local increase in opacity

2.elevation of hemidiaphragm

3.displacement of the mediastinum

4.compensatory over inflation

4 Approximation of the ribs

5.Absence of  an air bronchogram(resorption atelectasis only)

6.Absence of visibility of interlobar artery(in lower lobe atelectasis only)

Reference -Fraser volume 1 page 529

Physiology of evening rise of temperature

 Physiology of the Evening Temperature Rise

​Circadian Rhythm Control: The 24-hour body clock, regulated by the suprachiasmatic nucleus (SCN) in the hypothalamus, naturally shifts the body's thermal set-point throughout the day. It is not fixed at a single temperature.

​Diurnal Variation: Temperature follows a predictable daily wave. It reaches its lowest point (nadir) between 4:00 AM and 6:00 AM during deep sleep, and steadily climbs to its highest point (peak) between 4:00 PM and 8:00 PM.

​Cumulative Metabolic Activity: Throughout the waking hours, ongoing cellular metabolism, physical movement, and muscle contractions continuously generate heat. This thermal energy accumulates in the body over the course of the day.

​Diet-Induced Thermogenesis: Eating meals (specifically lunch and afternoon snacks) triggers metabolic breakdown and digestion, a process that inherently releases heat as a byproduct.

​Delayed Heat Dissipation: During the day, the body prioritizes keeping the core warm. It is only after the evening peak that the hypothalamus signals the blood vessels in the hands and feet to dilate (widen) so the body can shed core heat and cool down for sleep.

​Amplification During Illness: When a person has a fever, immune chemicals (pyrogens) instruct the hypothalamus to raise the baseline temperature. The natural evening circadian peak stacks on top of this elevated baseline, which is why fevers frequently spike and feel much worse at night.

The evening rise of temperature in Tuberculosis (TB) is a classic clinical feature. It occurs because the immune response to the Mycobacterium tuberculosis bacteria essentially hijacks and amplifies the body’s natural 24-hour circadian rhythm.

Here is the physiology behind why this happens:

The Release of Pyrogens: When you have TB, your immune cells (specifically macrophages and T-lymphocytes) are constantly fighting the bacteria inside the lungs or other tissues. As they fight, these immune cells release signaling proteins called pyrogens (such as Interleukin-1, Interleukin-6, and Tumor Necrosis Factor-alpha).

Resetting the Hypothalamus: These pyrogens travel through the bloodstream to the brain, where they stimulate the production of Prostaglandin E2 (PGE_2) in the hypothalamus. PGE_2 acts directly on the body's thermostat, tricking it into setting a higher target temperature (a fever).

Synergy with the Circadian Rhythm: Under normal conditions, everyone's body temperature naturally peaks in the late afternoon and evening (between 4:00 PM and 8:00 PM) due to the brain's internal clock. In a TB patient, the immune system's pyrogen production is not constant; it fluctuates in tandem with this daily biological clock, causing a massive release of inflammatory cytokines that perfectly coincides with the natural evening temperature surge.

Why it Causes "Night Sweats": The dramatic drop in temperature after this evening spike explains another classic TB symptom. A few hours after the evening peak (usually past midnight), the hypothalamus resets back toward a normal level. Because the body is suddenly much hotter than its new set-point, it desperately tries to dump heat. It does this by widening blood vessels and triggering profuse sweating, leading to the characteristic drenching night sweats.

Bronchial breath sounds

When the lung tissue between the central airways and the chest wall is airless as a result of consolidation, atelectasis or fibrosis the breath sounds are transmitted to the stethoscope with relatively little loss by attenuation or filtration. They resemble the sounds heard over the trachea in that they are loud, with the higher frequencies preserved and are audible throughout expiration as well as inspiration. In all these respects bronchial breathing differs from the normally transmitted breath sounds, which are faint, low pitched and inaudible during the latter half of expiration. Bronchial breathing is often heard over an airless upper lobe, whether the lobar bronchus is patent or obstructed, because the mediastinal surface of the upper lobes is in contact with the trachea and the sound is directly transmitted to solid lung. There is no direct path of transmission to the lower lobes so that the tracheal sounds do not reach them unless the intervening bronchi are patent. Bronchial breathing is usually absent, therefore, when the lower lobe is consolidated or atelectatic as a result of bronchial obstruction.

Reference- Paul forgax

Lady Windermere Syndrome

Middle lobe syndrome

Right middle lobe syndrome is a pulmonary condition characterized by the chronic or recurrent collapse (atelectasis) and inflammation of the right middle lobe of the lung, often accompanied by bronchiectasis. It occurs due to anatomical vulnerabilities and can be caused by obstructive or non-obstructive factors. 

* Anatomy: The right middle lobe bronchus is relatively long, narrow, and surrounded by a ring of lymph nodes, making it highly susceptible to blockage or poor collateral ventilation. [

* Causes:

* Obstructive: External compression from enlarged lymph nodes (due to infections like tuberculosis or histoplasmosis), tumors, or internal blockages like foreign bodies and mucus plugs.

   * Non-obstructive: Persistent inflammation, chronic bronchitis, or atypical bacterial infections (such as Mycobacterium avium complex).

* Symptoms: Patients may experience a chronic "wet" cough, recurrent pneumonia, hemoptysis (coughing up blood), chest pain, and shortness of breath. 

* Diagnosis: Diagnosed using chest X-rays (revealing a classic triangular, wedge-shaped opacity) and high-resolution CT scans. Bronchoscopy is often performed to rule out tumors or obstructions. 

* Treatment: Management generally involves airway clearance techniques, antibiotics for infection, and bronchodilators. In severe, recurrent, or obstructive cases, surgical removal of the lobe (lobectomy) may be required.

Pesticides and insecticides

 Pesticides vs Insecticides

Pesticides

Pesticides are substances used to prevent, destroy, repel, or control pests.

The term "pest" includes:

Insects

Weeds

Fungi

Rodents

Mites

Nematodes

Other harmful organisms

Thus, pesticide is a broad umbrella term.

Insecticides

Insecticides are pesticides specifically designed to kill or control insects.

Therefore:

All insecticides are pesticides

Not all pesticides are insecticides

Classification of Pesticides

1. Insecticides

Used against insects.

Examples:

Malathion

Parathion

Chlorpyrifos

Permethrin

Cypermethrin

DDT

2. Herbicides

Used against weeds and unwanted plants.

Examples:

Glyphosate

Paraquat

Atrazine

2,4-D

3. Fungicides

Used against fungi.

Examples:

Mancozeb

Copper sulfate

Carbendazim

Fluconazole (agricultural use is uncommon)

4. Rodenticides

Used against rats and mice.

Examples:

Zinc phosphide

Warfarin

Brodifacoum

5. Acaricides

Used against mites and ticks.

Examples:

Amitraz

Dicofol

6. Nematicides

Used against nematodes.

Examples:

Aldicarb

Carbofuran

7. Molluscicides

Used against snails and slugs.

Examples:

Metaldehyde

Niclosamide

Classification of Insecticides

A. Based on Chemical Class

1. Organophosphates

Mechanism:

Inhibit acetylcholinesterase

Examples:

Malathion

Parathion

Chlorpyrifos

Diazinon

Clinical features:

Cholinergic crisis

SLUDGE syndrome

Miosis

Bronchorrhea

2. Carbamates

Mechanism:

Reversible acetylcholinesterase inhibition

Examples:

Carbaryl

Propoxur

Aldicarb

3. Pyrethroids

Mechanism:

Prolong sodium channel opening

Examples:

Permethrin

Cypermethrin

Deltamethrin

Features:

Relatively safer in humans

Paresthesias common

4. Organochlorines

Mechanism:

Alter sodium channel function

Examples:

DDT

Lindane

Endosulfan

Features:

Neurotoxicity

Environmental persistence

5. Neonicotinoids

Mechanism:

Nicotinic acetylcholine receptor agonists

Examples:

Imidacloprid

Thiamethoxam

P pulmonale and mitrale

P pulmonale 

Ecg - Tall, peaked, and sharp P waves.

Criteria: Amplitude >2.5mm in inferior leads(Lead 2, 3 aVF), >1.5mm in leads V1 and V2.

P Mitrale

ECG-Broad, notched, or "bifid" (camel-hump-like) P waves

Criteria -P wave duration > 110 ms with a distinct notch in Lead II, and a wide, deep terminal negative component in lead V1

Cough Reflex and Neural Control

Cough Reflex and Neural Control

- Rapidly Adapting Receptors: Located in the epithelial and submucosal layers of the larger airways, these receptors produce cough and laryngeal narrowing in response to stimuli like dust, ammonia, histamine, and increases in inspiratory airflow.

Bronchial C Receptors: Located in the airway wall, these receptors project centrally through unmyelinated fibers and produce a cough when activated by capsaicin or bradykinin.

 Upper Airway Receptors: Receptors located in the pharynx initiate the cough reflex when stimulated by cold air.

 Afferent Pathway: Afferent signals originating from lung mechanoreceptors travel via the vagus nerve.

Cough Centre (Central Processing):

 *While a singular "cough centre" is not explicitly named, afferent signals from the peripheral receptors enter the pontomedullary network of the brain stem.

 * Sensory signals specifically terminate in the nucleus of the solitary tract (nTS), which is situated within the dorsal respiratory group (DRG).

 * This sensory input is processed by the respiratory central pattern generator (rCPG), a neuronal network in the central nervous system responsible for generating and modulating respiratory motor acts.

Efferents (Motor Output):

 * Neural output from the rCPG central controller drives the activity of specific motor neuron pools to execute the physical cough.

 * Efferent signals travel to brain stem motor neurons that innervate and control upper airway muscles.

 * Efferent signals also project to spinal motor neurons (phrenic, intercostal, and lumbar) to drive the respiratory pump muscles necessary for expulsion.

Cardiac asthma, renal asthma and uremic lung

 Cardiac asthma

Cardiac asthma is wheezing, cough, and breathlessness caused by left heart failure, especially acute LV failure, rather than primary bronchial asthma.

Mechanism

Left ventricular dysfunction → ↑ left atrial pressure → pulmonary venous congestion → interstitial edema around bronchioles → airway narrowing and reflex bronchoconstriction.

Clinical features

Paroxysmal nocturnal dyspnea

Orthopnea

Wheeze (“cardiac wheeze”)

Basal crackles

Pink frothy sputum in severe pulmonary edema

Often elderly with hypertension/CAD/valvular disease

Renal asthma

Renal asthma is an older clinical term describing paroxysmal dyspnea/wheezing due to pulmonary congestion from renal failure, usually because of:

Fluid overload

Severe hypertension

Heart failure secondary to kidney disease

Essentially, it is a form of cardiogenic pulmonary edema precipitated by renal dysfunction.

Pathophysiology

Renal failure → sodium and water retention → volume overload → pulmonary venous hypertension → pulmonary edema → wheeze and dyspnea.

Typical setting

Advanced CKD

Acute kidney injury with fluid overload

Missed dialysis

Important point

“Renal asthma” is not true asthma; it is pulmonary edema from renal disease.

Uremic lung

Uremic lung refers to pulmonary edema occurring in severe uremia/advanced renal failure, classically before dialysis era.

Pathogenesis

Combination of:

Fluid overload

Increased pulmonary capillary permeability due to uremic toxins

LV dysfunction/hypertension

Reduced oncotic pressure (sometimes)

Pathology

Interstitial and alveolar edema

Fibrinous alveolar exudates may occur

Clinical features

Severe dyspnea

Tachypnea

Hypoxemia

Crackles

Sometimes wheeze

Imaging

Classic chest X-ray:

Bilateral perihilar fluffy opacities

“Bat-wing” or “butterfly” pattern

May resemble cardiogenic pulmonary edema.

Management

Urgent dialysis

Oxygen/NIV if needed

Fluid removal

Treat hypertension and heart failure

Relationship between the three

Cardiac asthma → pulmonary edema from heart failure causing wheeze.

Renal asthma → pulmonary edema from renal disease/volume overload causing wheeze.

Uremic lung → pulmonary edema and lung injury specifically associated with severe uremia.

So, renal asthma and uremic lung overlap substantially, while cardiac asthma emphasizes the wheezing phenotype from heart failure.

dyspnea aggregating factors

Common aggravating factors:

Physical exertion, like walking or climbing stairs.

Supine position, especially if orthopnea is present

Environmental triggers, such as smoke, dust, pollution, cold air, or allergens.

Respiratory infections or worsening bronchospasm.

Anxiety or panic, which can intensify the sensation of breathlessness.

Anemia

obesity, and poor fitness, which can reduce exercise tolerance and worsen symptoms 

CNS - Cardinal symptoms

Cardinal symptoms of CNS

1. Syncope

2.Dizziness

3.vertigo

4.Fatigue

5.Muscke weakness and paralysis

6.numbness

7.Tingling sensation 

8.sensory loss

9.Gait disorder 

10.Imbalance and fall

11.confusion

12.delirium

13.coma

14.dementia

15.aphasia, dysarthria

16.memory loss

17.headache

18.sleep disorders.

Hantavirus pulmonary syndrome

Hantavirus Pulmonary Syndrome (HPS) is an acute febrile illness (i.e., temperature greater than 101.0 F [greater than 38.3 C]) with a prodrome consisting of fever, chills, myalgia, headache, and gastrointestinal symptoms,and one or more of the following clinical features: Bilateral diffuse interstitial edema, or

- Clinical diagnosis of acute respiratory distress syndrome (ARDS), or

- Radiographic evidence of noncardiogenic pulmonary edema, or

- An unexplained respiratory illness resulting in death, and includes an autopsy examination demonstrating noncardiogenic pulmonary edema without an identifiable cause, or

- Healthcare record with a diagnosis of hantavirus pulmonary syndrome, or

- Death certificate lists hantavirus pulmonary syndrome as a cause of death or a significant condition contributing to death

Laboratory Criteria For Diagnosis

- Detection of hantavirus-specific immunoglobulin M or rising titers of hantavirus-specific immunoglobulin G, or

- Detection of hantavirus-specific ribonucleic acid in clinical specimens, or

- Detection of hantavirus antigen by immunohistochemistry in lung biopsy or autopsy tissues

Pleuritic chest pain - features

 Pleuritic Chest Pain — Classical Features

Pleuritic chest pain is pain arising from irritation/inflammation of the parietal pleura. It has a characteristic clinical profile:

Key Features

Sharp, stabbing pain

Often described as “knife-like” or “catching”

Worsens with respiration

Increased by:

Deep inspiration

Coughing

Sneezing

Yawning

Laughing

Localized pain

Patient can often point with one finger to the painful area

Sudden onset is common

Especially in conditions like pneumothorax or pulmonary embolism

Reduced by shallow breathing / splinting

Patients avoid deep breaths because of pain

May radiate

To shoulder or neck if diaphragmatic pleura involved (via phrenic nerve)

Associated pleural rub

A scratching/grating sound on auscultation in pleuritis

Subpulmonic effusion -Radiological sign

Radiological Signs (Erect Chest X-ray):

1.Pseudodiaphragm Appearance: The dome of the diaphragm appears elevated, often creating a smooth, "flatter" contour.

2.Lateral Diaphragmatic Peak: The peak of the diaphragm is displaced laterally rather than being in the middle, creating a "hump".

3.Increased Left Lung-Gastric Bubble Distance: On the left side, the distance between the lung base and the stomach bubble (air-fluid interface) is increased, usually > 2cm

SURFACE ANATOMY

Apex: lung apex and pleural cupola extend about 2–3 cm above the medial third of the clavicle into the root of the neck. 

Anterior margin (right): follows the right side of the sternum from about the 2nd to the 4th costal cartilages then slopes laterally to reach the 6th right costal cartilage. 

Anterior margin (left): similar but deviates laterally to form the cardiac notch and reaches approximately 3 cm lateral to the left sternal edge at the upper margin of the 6th costal cartilage (the cardiac notch produces the lingula). 

Inferior margins (costal landmark lines)

Mid-clavicular line: inferior border of lung at 6th rib (pleural reflection ~2 ribs lower). 

Mid-axillary line: inferior border of lung at 8th rib. 

Posteriorly (paravertebral): inferior border reaches roughly the 10th rib/vertebral level. 

Note: the parietal pleura extends ~2 ribs lower than the lung at these points, creating the costodiaphragmatic recess. 

miliary tb ct finding

Nodule size and number: Numerous micronodules usually 1–3 mm (sometimes up to ~4–5 mm) and often too many to count. 

Distribution: Random (hematogenous) distribution with no centrilobular clustering or polygonal secondary-lobule pattern; nodules are bilateral and diffuse across all lung zones (may show mild basilar predominance acutely and mild upper-zone predominance chronically). 

Margins and background: Nodules often sharply marginated but can be ill-defined; ground-glass attenuation or interlobular septal thickening/reticular change may be present superimposed on the nodules. 

Pulsus paradoxus

Paradoxical pulse refers to an inspiratory decline in systolic pressure greater than 10 mmHg. In normal circumstances, inspiration results in an increase in venous return as blood is ‘sucked into’ the thorax by the decline in intrathoracic pressure. This increases right ventricular stroke volume, but left ventricular stroke volume falls slightly (ventricular interdependence). When the heart is constrained in a ‘fixed box’ by a pericardial effusion (cardiac tamponade) or by thickened pericardium (pericardial constriction), the increased inspiratory right ventricular blood volume reduces left ventricular compliance, resulting in a more pronounced reduction in left ventricular filling stroke volume and systolic blood pressure during inspiration. ‘Pulsus paradoxus’ therefore represents an exaggeration of the normal inspiratory decline in systolic pressure and is not truly paradoxical. Pulsus paradoxus in acute severe asthma is thought to be due to negative pleural pressure increasing afterload and thereby impedance to left ventricular emptying. It is measured by inflating a blood pressure cuff until no sounds are heard. The pressure is then slowly decreased until systolic sounds are first heard during expiration but not during inspiration – note this reading. The pressure is slowly decreased further until sounds are heard throughout the respiratory cycle (inspiration and expiration) – note this second reading. If the pressure difference between the two readings is >10 mmHg, it can be classified as pulsus paradoxus. 

Ref- Hutchison's 24E

CARDINAL SYMPTOMS OF GASTROINTESTINAL SYSTEM

1. Dysphagia and odynophagia
2. Heartburn and reflux
3. Indigestion
4. Flatulence
5. Vomiting
6. Anorexia
7. Constipation
8. Diarrhoea
9. Alteration of bowel pattern
10. Abdominal pain
11. Abdominal distension
12. Weight loss
13. Haematemesis
14. Rectal bleeding
15. Melaena
16. Jaundice
17. Itching
18. Urinary symptoms

Ref- Hutchison's clinical methods 24E

What is pulsus paradoxus and what are its respiratory causes?

 Pulsus paradoxus is an exaggerated fall in systolic blood pressure during inspiration.

Normally during inspiration, systolic BP falls slightly (≤10 mmHg).

In pulsus paradoxus, the fall is >10 mmHg.

Despite the name, there is no true paradox. The “paradox” refers to the fact that:

Heart sounds may still be heard,

But the peripheral pulse becomes weak or disappears during inspiration.

Mechanism

During inspiration:

More venous blood enters the right ventricle.

In conditions with limited cardiac space/filling (e.g., tamponade), the RV expands at the expense of the LV.

LV filling decreases → stroke volume falls → systolic BP drops markedly.

Conditions causing pulsus paradoxus

Cardiac causes

Cardiac tamponade (classic)

Constrictive pericarditis (less common)

Severe heart failure

Respiratory causes

Severe asthma

Severe COPD exacerbation

Tension pneumothorax

Massive pulmonary embolism

Aggravating factors of cough

PDFCE 

Pollution, Pollen, Posture

Drugs, Diurnal, Dry air

Food

Cold weather, Common cold

Exercise

Normal cortisol levels, diurnal variation and it's significance in respiratory system

Serum cortisol levels

Normal levels

Morning -8am- 5-23 mcg/dL

Evening -4pm- 3-13 mcg/dl

Diurnal variation is maintained by suprachiasmatic nucleus of the hypothalamus.

Cortisol levels peak during early morning and gradually decline throughout the day reaching lowest point around midnight 

Effects on the respiratory system

Increased Inflammatory response when the levels of cortisol reach lowest at around midnight. 

Low cortisol levels at midnight lead to airway hyper responsiveness leading to morning dip in Peak expiratory flow rate.

During cortisol trough at around late night, eosinophil counts rise leading to influx of inflammatory cells into the airway mucosa, exacerbating conditions like Eosinophilic Bronchitis or severe asthma.

Cortisol is essential for surfactant production in fetus. It stimulates the maturation of Type II pneumocytes, which is why exogenous glucocorticoids are administered in cases of threatened preterm labor to prevent Respiratory Distress Syndrome (RDS).

Stridor vs wheeze

 Stridor – Definition

A harsh, high-pitched, monophonic sound produced by turbulent airflow through a narrowed upper airway (larynx or trachea), typically heard best over the neck.

 Wheeze – Definition

A continuous, musical, high-pitched sound caused by airflow through narrowed lower airways (bronchi/bronchioles), typically heard over the chest.

Stridor vs Wheeze – Key Differences

Anatomical site

Upper airway (larynx, trachea) -stridor 

Lower airway (bronchi, bronchioles) - wheeze 

Sound quality

Harsh, loud, non-musical -stridor

Musical, whistling - wheeze

Best heard over

Neck -stridor

Chest (lung fields) - wheeze

Mechanism

Extrathoracic airway narrowing -stridor

Intrathoracic airway narrowing - wheeze

Common causes

Croup, epiglottitis, foreign body (upper airway), laryngeal edema -stridor

Asthma, COPD, bronchiolitis - wheeze

Clinical significance

Often emergency (airway compromise) -stridor

Suggests airflow limitation, not always immediately life-threatening - wheeze

causes of bronchial breath sounds

Primary Causes

Pneumonia (consolidation from bacterial, viral, or fungal infection)

Lung abscess or cavitary lesions (e.g., necrotic tumor, tuberculosis cavity)

Bronchiectasis (dilated airways with chronic inflammation)

Pleural effusion (over compressed underlying lung)

Atelectasis or lung collapse (obstructive or compressive)

Secondary Causes

Pulmonary fibrosis (scarring stiffens parenchyma)

Pulmonary edema (fluid overload in alveoli)

Large tumors compressing airways

Sinusitis symptoms

 Major symptoms 

1.purulent anterior nasal discharge 

2.purulent or discolored posterior nasal discharge 

3.Nasal congestion or obstruction 

4.Facial congestion or fullness

5.Facial pain or pressure

6.Hyposmia or anosmia 

7.Fever

Minor symptoms 

1.Headache

2.Halitosis

3.Ear pain, pressure or fullness

4.Dental pain

5.Cough

6.Fever

7.Fatigue

Presence of atleast 2 major or 1 major and 2 minor criteria -diagnosis of Sinusitis is made.

Reference - IDSA 2012

Causes of dry cough with hemoptysis

 Causes of dry cough with hemoptysis 

Malignancy

Bronchiectasis sicca

Pulmonary embolism

Use of anticoagulants

Pulmonary vasculitis

Mitral stenosis

Dynamic auscultation in Respiratory System

 Dynamic auscultation is listening to breath sounds while the patient performs specific maneuvers (like deep breathing, coughing, forced expiration, or posture change) to reveal abnormal findings not heard during quiet breathing.

1. Forced expiratory auscultation

• Ask patient to blow out forcefully

         Example: Wheeze appears → Asthma, COPD

2. Post-tussive auscultation (after cough)

• Ask patient to cough, then listen again

         Example: Crackles disappear/change → secretions (Bronchiectasis)

Persistent crackles → Pneumonia

3. Deep inspiration auscultation

• Ask patient to take slow deep breaths

Example: Late inspiratory crackles → Pulmonary fibrosis

4.Mouth open vs closed breathing

• Compare breathing with mouth open vs closed

Example: Sound changes/stridor → upper airway obstruction

5.Postural (position) change auscultation

• Listen in sitting vs lying position

Example: Shifting findings → Pleural effusion

spurious and pseudo hemoptysis

Spurious hemoptysis

Spurious hemoptysis means there is real blood in the sputum, but it comes from the upper respiratory tract (above the larynx), such as from an upper‑airway infection, epistaxis, or gingival bleeding, rather than from the lungs or bronchi.

The blood is genuinely present under the microscope, but the source is not the lower respiratory tract (below the glottis).

Pseudo‑hemoptysis

Pseudo‑hemoptysis (or pseudohemoptysis) refers to blood‑like sputum that may look like blood but sometimes does not actually contain blood cells; for example, red pigment (prodigiosin) from Serratia marcescens infection can stain sputum red without true bleeding.

It can also include situations where blood is aspirated from the upper aerodigestive or gastrointestinal tract (e.g., hematemesis aspirated into the lungs) and then expectorated, so the bleeding source is extrapulmonary

kilip classification

Heart failure and predict mortality in patients with acute myocardial infarction (AMI), especially in the first 24–48 hours. 

Killip classes (I–IV)

Class I: No clinical evidence of heart failure.

Vital signs and physical exam are normal; no pulmonary rales, no S₃, no jugular venous distension. 

Class II: Mild to moderate left‑ventricular (LV) failure.

Rales/crackles in the lungs, S₃ gallop, elevated jugular venous pressure, or combination

Class III: Severe LV failure – acute pulmonary edema.

Frank pulmonary edema with marked dyspnea, frothy sputum, diffuse rales; oxygenation is impaired. 

Class IV: Cardiogenic shock.

Hypotension (systolic BP ≤90 mmHg), tachycardia, cold clammy skin, oliguria, and evidence of peripheral hypoperfusion; often with pulmonary edema. 

Higher the class , there increased risk or short term mortality 

Post TB sequelae

 -Airway-related

Bronchiectasis

Bronchial stenosis / stricture

Tracheobronchomalacia

-Parenchymal (lung tissue)

Fibrosis (fibro-cavitary disease)

Destroyed lung

Residual cavities

-Pleural

Pleural thickening

Fibrothorax

-Vascular

Pulmonary hypertension

Rasmussen aneurysm (pulmonary artery aneurysm in cavity wall)

-Infective / colonization

Aspergilloma (fungal ball)

Functional consequence

Chronic respiratory failure / COPD-like picture

Aggravating factors of cough

PDFCE 

Pollution, Pollen, Posture

Drugs, Diurnal, Dry air

Food

Cold weather, Common cold

Exercise

Tidal percussion on the left side

 Tidal percussion is a clinical percussion technique used to detect early splenomegaly by observing changes in percussion note during respiration.

Site

Over Traube's space. Typically along the left mid-axillary line

Boundaries of Traube’s Space

Superior: Left 6th rib

Inferior: Left costal margin

Lateral: Left anterior axillary line

This area overlies the fundus of the stomach (normally tympanic due to air). In splenomegaly, this area becomes dull → basis of tidal percussion.

Technique 

Patient lies supine

Start percussion over Traube’s space (normally tympanic)

Ask patient to take a deep inspiration

Continue percussion during breathing

 - Interpretation

Normal:

Remains tympanic during inspiration

Positive tidal percussion:

Tympany → dullness on inspiration

Indicates splenic enlargement (spleen descends and occupies the space)

 Mechanism

During inspiration, the diaphragm descends

Enlarged spleen moves inferiorly & anteriorly

Replaces air-filled stomach → dull note

Ctd criteria from Murray and nadal

 Systemic Sclerosis (Scleroderma)

CRITERIA FOR DIAGNOSIS*

Major

Thickening of the skin of the hands

Minor

Sclerodactyly (i.e., the changes of the major criterion but limited to

the fingers)

Digital pitting scars or loss of substance from the finger pad:

depressed areas at tips of fingers or loss of digital pad tissue as a

result of ischemia

Bibasilar pulmonary fibrosis

LUNG MANIFESTATIONS

Interstitial pulmonary fibrosis

Organizing pneumonia

Isolated pulmonary vascular disease

Aspiration pneumonia (secondary to esophageal dysmotility)

Chest wall restriction

*The major or ≥ 2 minor criteria required for diagnosis.

Rheumatoid Arthritis

CRITERIA FOR DIAGNOSIS*

Morning stiffness (lasting at least 1 hr)

Arthritis (soft tissue swelling or fluid) of 3 or more joints (PIP, MCP, 

wrist, elbow, knee, ankle, MTP joints)

Arthritis of hand joints (swelling of at least 1 wrist, MCP, or PIP joint)

Symmetrical arthritis (i.e., simultaneous arthritis of the same joints on 

both sides of the body)

Rheumatoid nodules

Serum rheumatoid factor positivity (at a level such that < 5% of 

normal controls are positive)

Radiographic hand or wrist changes typical of rheumatoid arthritis

LUNG MANIFESTATIONS

Interstitial pulmonary fibrosis

Organizing pneumonia

Obliterative bronchiolitis

Follicular bronchiolitis

Bronchiectasis

Vasculitis

Nodules

Pleural disease

Lymphocytic interstitial pneumonia

Drug induced

*At least 4 criteria for a minimum of 6 weeks.

Systemic Lupus Erythematosus

CRITERIA FOR DIAGNOSIS*

Malar rash

Discoid rash

Photosensitivity skin rash

Oral or nasopharyngeal ulceration

Nonerosive arthritis involving ≥ 2 peripheral joints

Serositis (pleuritis or pericarditis)

Renal disorder (persistent proteinuria or cellular casts)

Neurologic disorder (unexplained seizures or psychosis)

Hematologic disorder (hemolytic anemia, leukopenia, lymphopenia, 

or thrombocytopenia)

Immunologic disorder (positive LE cell, anti-DNA antibody, anti-Sm 

antibody, false-positive syphilis serology)

Elevated antinuclear antibodies

LUNG MANIFESTATIONS

Acute lupus pneumonitis

Interstitial pulmonary fibrosis

Pulmonary vasculitis

Diffuse alveolar hemorrhage

Pulmonary hypertension

Shrinking lung syndrome

Antiphospholipid antibody syndrome

Organizing pneumonia

Pleural disease

*Minimum of 4 criteria required.

Polymyositis with Dermatomyositis

CRITERIA FOR DIAGNOSIS

Symmetrical proximal muscle weakness

Muscle biopsy specimen showing myositis

Elevation of serum skeletal muscle enzymes

Characteristic electromyographic pattern of myositis

Typical rash of dermatomyositis

LUNG MANIFESTATIONS

Interstitial pulmonary fibrosis

Acute pneumonitis (with diffuse alveolar damage)

Organizing pneumonia

Aspiration pneumonia

Pulmonary vasculitis and alveolar hemorrhage

Respiratory muscle weakness

Behçet Syndrome

CRITERIA FOR DIAGNOSIS

Major (required)

Recurrent aphthous ulceration at least 3 times in a 12-mo period

Minor (2 of 4)

Recurrent genital ulceration

Ocular disease

Skin lesions (erythema nodosum, skin ulcers)

Positive pathergy test (a 2-mm erythematous papule or pustule at

the prick site 48 hr after the application of a sterile hypodermic

20- to 22-gauge needle that obliquely penetrated avascular

antecubital skin to a depth of 5 mm)

Cardinal symptoms of Gastrointestinal system & Tree in bud opacities

Cardinal symptoms of Gastrointestinal system

 Abdominal pain

Dysphagia 

Heartburn

Nausea and vomitting 

Alteration of bowel habits

GI bleeding 

Abdominal distension 

Jaundice

Loss of appetite and weight 

Mechanism of tree in bud opacities 

They occur due to infectious bronchiolitis leading to filling of terminal bronchioles with mucous, pus, or fluid

They indicate endobronchial spread of infection 

1)Cardinal symptoms of cns 2) Acceptble pH range in type 2 respiratory failure

 1) Cardinal symptoms of CNS disease:

Headache, vomiting, seizures, altered consciousness, focal neurological deficit (motor or sensory), visual disturbance, and gait or balance disturbance.

2) Acceptable pH range in Type 2 respiratory failure:

pH 7.25 – 7.35 (permissive hypercapnia range during management).

Massive hemoptysis

Massive hemoptysis - definition

      Massive hemoptysis is blood loss of 400 mL in 24 hours or 100–150 mL expectorated at one time.

Causes-

Bronchiectasis, 

Bronchogenic Carcinoma,

Eroding Tuberculous cavity,

Rasmussen's aneurysm,

mycetoma

Ref: Harrison's principles of internal medicine(20th edition)

TYPES OF FEVER

Types of fever 

Continuous (Sustained) Fever

Definition:

Fever in which the temperature remains above normal throughout the day and does not fluctuate more than 1°C in 24 hours.

2. Remittent Fever

Definition:

Fever in which the temperature fluctuates more than 1°C in 24 hours but never returns to normal

3. Intermittent Fever

Definition:

Fever in which the temperature elevation is present only for several hours of the day and returns to normal for the remaining hours.

4. Relapsing Fever

Definition:

Fever characterized by episodes of fever lasting several days separated by periods of normal temperature lasting several days.

Causes of Trepopnea and platypnea

Platypnea - Dyspnea in upright position 

Always associated with Orthodeoxia

Occurs in 

- Hepatopulmonary syndrome

- Pulmonary AV malformations

Trepopnea- Dyspnea in Lateral decubitus position 

- Unilateral severe pneumonia or pleural effusion 

Patient feels better on lying on normal side to improve V/Q matching 

Define small airways and % of small airways in lungs, Terminal vs Respiratory bronchioles

 Small airways are defined as airways with an internal diameter less than 2 mm and lacking cartilage, consisting mainly of the terminal bronchioles and respiratory bronchioles located distal to the segmental bronchi. Although individually small, they collectively contribute to about 98–99 % of the total cross-sectional airway area of the lungs, which is why they normally produce little airflow resistance and are called the “silent zone” of the lung. Terminal bronchioles represent the last part of the conducting zone, are lined by simple cuboidal epithelium with club (Clara) cells, contain smooth muscle, do not have alveoli in their walls, and therefore do not participate in gas exchange. In contrast, respiratory bronchioles are the first part of the respiratory zone, arise from terminal bronchioles, have scattered alveoli opening from their walls, and therefore participate in the beginning of gas exchange, eventually continuing as alveolar ducts and alveolar sacs.