CARDINAL SYMPTOMS OF CVS:

 1) Chest pain

2) Brreathlessness

3) Palpitation 

4) Syncope

5) Edema

6) Fatigue

CAUSES OF PLEURITIC CHEST PAIN

CAUSES OF PLEURITIC CHEST PAIN

Pleuritic chest pain is a sharp, stabbing in the chest that worsens with respiratory movements such as deep breathing, coughing, sneezing, or laughing.

CAUSES:

1. Infectious Causes: These are among the most common reasons for pleuritic chest pain.

Viral Infections 

Bacterial Infections: Pneumonia, Tuberculosis

Fungal Infections: Though less common, fungal infections can also inflame the pleura, especially in individuals with weakened immune systems.

Parasitic Infections

2. Inflammatory and Autoimmune Conditions:

Pleuritis due to inflammation caused by conditions such as SLE, Rheumatoid arthritis, Sarcoidosis

Pleural Effusion

3. Cardiovascular Causes:

Pulmonary Embolism

Pericarditis

4. Neoplastic Causes (Cancers):

Lung Cancer invading or irritating the pleura.

I Mesothelioma

Pleural Metastatic Cancers

5. Traumatic Causes:

Rib Fractures or Chest Injury

Thoracic surgery or other procedures involving the chest can lead to temporary pleuritic pain.

ILD with family history - differential diagnosis

 Differential diagnosis of ILD with family history:

1. Idiopathic pulmonary fibrosis - most common form of familial ILD presenting as UIP pattern
2. Other idiopathic interstitial pneumonia - NSIP, cryptogenic organizing pneumonia
3. Connective tissue disorder associated ILD - rheumatoid arthritis, scleroderma associated ILD
4. Hypersensitivity pneumonitis - due to shared environmental exposure
5. Genetic mutations - Surfactant protein mutations (SFTPA2, SFTPC, ABCA3), telomeropathies (TERT, TERC), Hermansky pudlak syndrome, MUC5B polymorphism
6. Sarcoidosis

Health effects of dyes and chemicals used in Printing press

Process: Adhesive laminating 

Risk: Isocyanate prepolymers can cause an irritation of the airways and lungs leading to occupational asthma.

Process: Digital (ink-jet) printing

 Risk: Carbon present in black ink can cause lung irritation. Methyl ethyl ketone and propanol can cause abnormal heart rhythm and rate and can affect the liver and kidneys on long term exposure.

Process: UV lamps for photo processing, UV curing and high speed printing – ink misting 

Risk: Acrylates and methcrylates in  fumes can cause irritation of respiratory tracts with the potential for occupational asthma as well as severe headaches and nausea.

Health Effects Of Chemicals Used In Printing

Process: Etching, Engraving, Platemaking, Photographic Reproduction 

Risk: Nitric, sulphuric and hydrofluoric acids can cause skin burns, eye damage and blisters.

Process: Concentrated photographic developer or fixer solutions 

Risk: Acidic salt solutions and Hydroquinone can irritate eyes and even cause dermatitis

Process: UV and infra red curable inks, varnishes and lacquers 

Risk: Reactive acrylates or methacrylate’s can cause corrosion of the skin, eyes and mucous membranes.

Process: Lithographic platemaking, Gravure cylinder preparation and photoengraving. 

Risk: Ammonium, potassium and sodium dichromate’s are all very corrosive and can cause deep ulcers as well as a risk of cancer.

Process: Lithographic fount solution, blanket restorers, cleaning solvents, Gravure and flexographic Risk: Alcohol, Esters and Ketones can cause dermatitis, dizziness and other effects of the central nervous system.

Process: Flexographic, Dyeline Printing and Screen Inks Risk: Perchloroethylene, Ammonium hydroxide and Ketones can cause dizziness, drowsiness and other effects on the central nervous system via inhalation.

Process: Screen Cleaning chemicals 

Risk: Strong alkalis such as concentrated sodium or potassium hydroxide, Oxidisers and sodium hypochlorite solvents can cause corrosion of the skin, eyes and mucous membrane as well as dizziness and drowsiness

Progressive Pulmonary Fibrosis

 

Diagnostic Criteria for PPF:

To diagnose PPF, all three of the following must be present:

Underlying fibrosing ILD (non-IPF), with imaging or histology showing fibrosis.

Evidence of progression within the past year, based on at least one of the following:

1.Worsening respiratory symptoms, such as increasing dyspnea or cough.

2.Decline in lung function, especially:

Absolute decline in FVC ≥ 5% predicted

Decline in DLCO (diffusing capacity for carbon monoxide) ≥ 10% predicted

3.Progressive fibrosis on imaging, shown by:

Increased reticulation

New ground-glass opacities with traction bronchiectasis

Increased honeycombing

No alternative explanation (e.g., infection, heart failure, pulmonary embolism).

Aggravating factors for chief complaints

 AGGRAVATING FACTORS OF CARDINAL SYMPTOMS- MNEMONICS

COUGH:

PDFCE 

Pollution, Pollen, Posture

Drugs, Diurnal, Dry air

Food

Cold weather, Common cold

Exercise

SPUTUM

 "DRIVE DUST"

 

D – Dust exposure

R – Respiratory infections

I – Irritants (e.g., smoke, fumes)

V – Viral infections

E – Exercise or exertion

D – Dry air

U – Upper respiratory tract conditions (e.g., postnasal drip)

S – Smoking

T – Temperature changes (cold air or sudden temperature drops)

Breathlessness: 

 "BREATHE HARD"

 

B – Body position (e.g., lying flat in orthopnea)

R – Respiratory infections

E – Exercise or exertion

A – Anxiety or emotional stress

T – Temperature extremes (cold or heat)

H – Hypoxia or high altitude

E – Environmental triggers (allergens, pollutants)

H – Heart failure or fluid overload

A – Anemia

R – Reflux (gastroesophageal reflux disease)

D – Drugs (e.g., beta-blockers, 

WHEEZE:

“BREATHE WHEEZE”

B – Bronchial irritants (smoke, pollution)

R – Respiratory infections (viral or bacterial)

E – Exercise

A – Allergens (pollen, dust mites, animal dander)

T – Temperature changes (cold air)

H – Hormonal changes (pregnancy, menstruation)

E – Emotions (stress, anxiety)

W – Workplace irritants (occupational exposures)

H – Household triggers (perfumes, cleaning agents)

E – Environmental changes (high altitude)

E – Exposure to drugs (NSAIDs, beta-blockers)

Z – Zzz… sleep (nocturnal asthma triggers)

E – Eating (GERD-induced wheeze)

CHEST PAIN:

“CHEST PAINS”

C – Coughing or deep breathing (pleuritic pain)

H – Heat or cold exposure (vasospastic angina)

E – Emotion or stress (psychogenic pain, angina)

S – Swallowing (esophageal causes like GERD or spasm)

T – Trauma or movement (musculoskeletal pain, costochondritis)

P – Physical exertion (angina, cardiac ischemia)

A – Alcohol or large meals (GERD or esophageal spasm)

I – Infections (pleuritis, pericarditis, pneumonia)

N – Nighttime (GERD-related pain due to supine position)

S – Specific postures (pericarditis, GERD, musculoskeletal pain)

HEMOPTYSIS:

“COUGH BLOOD”

C – Coughing (increases airway pressure, ruptures small vessels)

O – Overexertion (exacerbates vascular stress)

U – Upper respiratory tract infections

G – GERD or vomiting (irritation of airways)

H – High altitude (pulmonary hypertension)

B – Bronchial infections (bronchitis, bronchiectasis)

L – Lung malignancy (coughing or irritation)

O – Operations (post-procedural bleeding, e.g., bronchoscopy)

O – Oral anticoagulants (worsen bleeding)

D – Deep breaths or physical strain (ruptures fragile capillaries)

Pathophysiology of early inspiratory crackles in OAD

Premature Airway Opening in Early Inspiration:

During the early phase of inspiration, as negative intrathoracic pressure builds, these collapsed small airways pop open. This sudden opening generates transient sounds—early inspiratory crackles.

Correlation with Disease Severity:

The presence of early inspiratory crackles often correlates with moderate to severe airway obstruction, especially in patients with chronic bronchitis or emphysema.

Neural control of respiration from Fishman

The respiratory control system, broadly speaking, comprises a controller, sensors, and a plan. This hierarchical structure, in which there is central processing of afferent input, is important for coordinating respiratory movements with behaviors such as eating, speaking, and moving. The controller is a neuronal network within the central nervous system (CNS), which is responsible for generating and modulating individual breaths and the overall breathing pattern. Often referred to as the respiratory central pattern generator (rCPG), the controller comprises reciprocally connected neuronal populations in the medulla and pons. Neural output from the rCPG drives the activity of various motor neuron pools. Motor neurons in the spinal cord (e.g., phrenic and intercostal) innervate the respiratory pump muscles, while brain stem motorneurons innervate upper airway muscles. The so-called “plant” is animportant component of breathing control and includes the CO2stores, which are made up of lung stores and circulating blood volume including hemoglobin. Closed loop feedback to the controller is supplied by chemoreceptors and mechanoreceptors. The consistent cycling of the ventilatory pattern is generated spontaneously from the spatial and functional architecture of the rCPG. Intrinsic membrane properties of rhythmically active neurons within the rCPG are capable of producing automatic periodicity.4 In addition, reciprocal (excitatory and inhibitory) synaptic connections between neuronal populations in the medulla and pons are believed to be critical for the automatic generation of the respiratory rhythm.

The neural respiratory cycle comprises three phases

Inspiration (I) involves ramp-like increases in inspiratory motor neuron firing, which drive phrenic nerve activity throughout this phase. The first phase of expiration (E1) is often called post-inspiration because inspiratory motor neurons are still active. Persistent inspira-
tory motor activity during E1, which declines throughout this phase, acts to slow the exit of air from the lungs. Finally, during the second phase of expiration (E2), expiratory muscles are typically electrically silent. During this phase of passive relaxation, gas is expelled as the
lungs and chest wall return to their equilibrium state (i.e., functional residual capacity). However, under conditions where respiratory drive is increased, expiratory muscles including the internal intercostal and abdominal muscles become active during E2. This notion is an
example of how the central controller, influenced by sensory feedback, modulates and alters the integrated motor response of the system.

SYSTEMIC SCLEROSIS - Diagnostic criteria

ACR/EULAR classification criteria for systemic sclerosis:

A total score of 9 or more is required for classification as systemic sclerosis.

1. Skin thickening of the fingers:

   - Proximal to the metacarpophalangeal joints (9 points).

2. Fingertip lesions:

   - Digital tip ulcers (2 points).

   - Fingertip pitting scars (3 points).

3. Telangiectasia (2 points).

4. Abnormal nailfold capillaries (2 points).

5. Pulmonary involvement:

   - Interstitial lung disease or pulmonary arterial hypertension (2 points).

6. Raynaud's phenomenon (3 points).

7. SSc-specific autoantibodies:

   - Anti-centromere, anti-topoisomerase I (Scl-70), or anti-RNA polymerase III (3 points).

SLE

SLE (American College of Rheumatology criteria )

1)Malar rash

2)Discoid rash

3)Photosensitivity skin rash

4)Oral or nasopharyngeal ulceration

5)Non erosive arthritis involving ≥ 2 peripheral joints

6)Serositis (pleuritis or pericarditis)

7)Renal disorder (persistent proteinuria or cellular casts)

8)Neurologic disorder (unexplained seizures or psychosis)

9)Hematologic disorder (hemolytic anemia, leukopenia, lymphopenia,or thrombocytopenia)

10)Immunologic disorder (positive LE cell, anti-DNA antibody, anti-Sm antibody, false-positive syphilis serology)

11)Elevated antinuclear antibodies

*Minimum of 4 criteria required

SJÖGREN SYNDROME

 sicca symptoms are mandatory

 supportive evidence including ocular signs (positive Schirmer test testing reduced tear formation, rose bengal score > 3 for staining of conjunction and cornea)

 typical histologic appearances salivary gland biopsy

antibodies to Ro (SS-A) or La (SS-B) or

 reduced salivary flow.