Eosinophilic bronchitis - BHR

 Bronchial hyperreactivity is absent in Eosinophilic bronchitis and is present in asthma

Reference: Murray and Nadel’s textbook of respiratory medicine, 7th edition 

Causes of palpitation

 1.Extrasystoles- Atrial, ventricular

2. Tachyarrhythmias- Atrial, ventricular

3. Endocrine -

Pheochromocytoma

Thyrotoxicosis

Hypoglycaemia

4. High output states- Anaemia, pyrexia,

Aortic regurgitation,

Patent ductus arteriosus

5. Drugs -Atropine, adrenaline,

aminophylline, thyroxine,

coffee, tea, alcohol

6. Psychogenic -Prolonged anxiety state

(Soldier’s heart, neuro￾circulatory asthenia,

Da Costa’s syndrome)

Referenca: Davidson

Mechanism of action of Paracetamol

 Acetaminophen increases the pain threshold by inhibiting two isoforms of cyclooxygenase, COX-1 and COX-2, which are involved in prostaglandin (PG) synthesis. Prostaglandins are responsible for eliciting pain sensations.13 Acetaminophen does not inhibit cyclooxygenase in peripheral tissues and, therefore, has no peripheral anti-inflammatory effects.

acetaminophen selectively blocks a variant type of the COX enzyme that is unique from the known variants COX-1 and COX-2.6 This enzyme has been referred to as COX-3.

Serum cortisol

 Glucocorticoid synthesis is under inhibitory feedback control by the hypothalamus and the pituitary. Hypothalamic release of corticotropin-releasing hormone (CRH) occurs in response to endogenous or exogenous stress. CRH stimulates the cleavage of the 241–amino acid polypeptide proopiomelanocortin (POMC) by pituitary-specific prohormone convertase 1 (PC1), yielding the 39–amino acid peptide ACTH. ACTH is released by the corticotrope cells of the anterior pituitary. The release of CRH, and subsequently ACTH, occurs in a pulsatile fashion that follows a circadian rhythm under the control of suprachiasmatic nucleus (SCN), with additionalregulation by a complex network of cell-specific clock genes. Reflecting the pattern of ACTH secretion, adrenal cortisol secretionexhibits a distinct circadian rhythm, starting to rise in the early morning hours prior to awakening, with peak levels in the morning and low levels in the evening .

Reference: Harrison -21 st edition

CRPS

 Complex regional pain syndrome (CRPS) describes an array of painful conditions that are characterised by a continuing (spontaneous and/ or evoked) limb pain that is seemingly disproportionate in time or degree to the usual course of any known trauma or other lesion. CRPS had been divided into three stages of progression based on the duration of symptoms. 

Stage I (Acute stage, 0-3 months): It is characterised primarily by pain/ sensory abnormalities (eg: hyperalgesia, allodynia), signs of vasomotor dysfunction and prominent edema.

Stage II (Dystrophic stage, 3-9 months): It is characterised by more marked pain/ sensory dysfunction, continues evidence of vasomotor dysfunction with development of significant motor/ trophic changes.

Stage III (Atrophic stage, 9-18 months): It is characterised by decreased pain/ sensory disturbance, continued vasomotor disturbance and markedly increased motor/ trophic changes.

Reference: Harrison’s principles of internal medicine, 21st edition

Amphoric breathing

 Amphoric breathing is a high pitched, metallic sound that occurs when there is a tension pneumothorax over a collapsed lung, usually with an open bronchopleural fistula. 

Reference: Fraser and Pare, Volume 1

Causes of non pitting pedal edema

 1)Myxedema

2) Lymphedema

3)Angioedema

4)Lipedema

Ref-hutchison 25 edition 

 

Causes of Unilateral pedal edema

 Causes of Unilateral pedal edema

1. Thrombophlebitis
2. Varicose veins
3. Primary venous valve failure
4. Chronic lymphangitis
5. Resection of regional lymph nodes
6. Filariasis
7. Genetic /primary lymphedema
8. Trauma
9. Compartment syndrome
10. Cellulitis
11. Complex Regional Pain Syndrome
12. Lymphatic obstruction by tumor or lymph nodes

Anion gap

 Anion gap =( Na+) + (K+)  -  (Hco3 -) + (Cl-)

Normal range-8 to 12 mmol/L

Ref-MD Vasudevan textbook of biochemistry 6th edition 

Vesicular breath sounds - Physiology

Normal breath sounds originate from the larynx. When the sound leaves the larynx it travels down the trachea and then divides when the airway divides. Some sound must be transmitted through the lung parenchyma but most travels down the airway. Eventually the sound travels along airways of different lengths and therefore becomes out of phase. Next it arrives in the respiratory bronchioles and alveoli and then gets transmitted through the chest wall to your stethoscope. The fat layer filters out much of the high frequency sound (above 4 kHz). The resulting sounds are much softer (because the sound has effectively been diluted throughout the whole of the lungs). There is no gap between inspiration and expiration (because all of the sound has become out of phase and therefore ‘filled in’ the gap). Finally, the first third of expiration is now the only part that is audible because the latter two-thirds are much quieter.

REFERENCE: Chamberlain’s, 13th edition, page no: 97