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.ATS GUIDELINES OF TB DEFAULT AND RELAPSE (1) 1.WHY FASCIAL PUFFINESS OCCURS FIRST IN RENAL EDEMA (1) Acute (2) ACUTE EXACERBATION OF COPD CRITERIA (2) ACUTE EXACERBATION OF ILD CRITERIA (1) ACUTE EXACERBATION OF IPF criteria (1) AE COPD (1) Aggravating factors of cough (2) Air crescent sign and Monod sign (1) Alveolar arterial oxygen gradient (1) Aminophylline in asthma (1) Amphoric breathing (1) Anuria and oliguria definition (1) apical cap (1) Apical impulse (1) Assessment of respiratory muscle strength (1) Asthma PEF variablity (1) Att in hepatotoxicity (1) ATT weight band recent (1) Austin flint murmur and Graham steel murmur (1) BEQ (1) Berryliosis causes (1) BMI (1) Borg dyspnoea score (1) Breathlessness - Aggravating relieving factors (1) breathlessness-sherwood jones (1) Bronchial breath sounds (1) Bronchiectasis- Definition (1) BRONCHOPULMONARY SEGMENTS (1) CARDINAL SYMPTOMS OF GASTROINTESTINAL SYSTEM (1) Cardinal symptoms of Gastrointestinal system & Tree in bud opacities (1) Cardinal symptoms: aggravating and relieving facto (1) Cardinal symptoms: aggravating and relieving factors (1) Causes of chest pain aggrevated by cough (1) Causes of localised bulging of chest wall (1) Causes of orthopnea (1) Causes of palpitation (1) Causes of Trepopnea and platypnea (1) Causes of Unilateral pedal edema (1) Cavity (1) check post (1) Chest physiotherapy (1) Chromogranin A (1) Chronic (2) Classification (1) Clinical features of different stages of syphilis (1) Clubbing (1) clubbing -mechanism of (1) Clubbing Unilateral (1) CLUBBING-PATHOGENESIS PDGF (1) CNS - 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Wednesday, June 17, 2026

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


Wednesday, June 10, 2026

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.

Wednesday, June 3, 2026

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.