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Pathophysiology of Chronic Obstructive Pulmonary Disease (COPD)

In this article, we will discuss the Pathophysiology of Chronic Obstructive Pulmonary (COPD). So, let’s get started.

Pathophysiology

Airflow obstruction (both large and small airways), hyperinflation due to air-trapping resulting in large voluminous lungs and inadequate gas exchange leading to hypoxemia and hypercapnia which are the most frequently encountered changes that constitute the clinical picture of COPD. A persistent reduction in the expiratory flow rate is the hallmark of COPD. An increase in residual volume, ratio of residual volume to total lung capacity, uneven ventilation, and ventilation-perfusion mismatch occur in COPD. Changes in the large airways (bronchitis) produce cough and sputum while changes in the small airways and alveoli are responsible for hypoxemia and hypercapnia. In most cases both bronchitis and emphysema are present but their relative contribution to obstruction varies from person to person.

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Causes of Asphyxia

In this article, we will discuss various Causes of Asphyxia. So, let’s get started

Asphyxia refers to an airway obstruction leading to less or non-delivery of atmospheric oxygen to the lungs resulting in carbon-di-oxide retention. Asphyxia can be caused due to mechanical or non-mechanical obstructions.

Causes

Mechanical causes

Covering of face (e.g. plastic bag)

Gag or pad smothering (closing of the external respiratory orifice by hand or by other means)

Gagging

Food or foreign body obstruction (choking)

Throttling (compression of the neck manually)

Hanging or strangulation

Drowning

Traumatic asphyxia

Non-mechanical causes

Diseases such as Diptheria, infectious mononucleosis, H.influenzae

Rupture of aortic aneurysm in air passages

Hemoptysis in pulmonary tuberculosis

Erosion of bronchus by a tubercular gland

Laryngeal edema because of steam inhalation, ingestion of irritant substances, drug allergies, and poisons

Retropharyngeal edema

Laryngeal or bronchial outgrowths

Non-penetrating injury to the front of the neck

Stages of Osteosarcoma

In this article, we will discuss the various Stages of Osteosarcoma. So, let’s get started.

Firstly, we will grade the tumor (cancer) in terms of histopathology (cancerous cells).

GX: The tumor grade cannot be identified

G1: The cancer cells are well differentiated (low-grade)

G2: The cancer cells are moderately differentiated (high-grade)

G3: The cancer cells are poorly differentiated (high-grade)

Stages

Stage IA: The tumor is low grade or cannot be graded and the size is 8 cm or smaller. It has not spread to any lymph node or other parts of the body.

Stage IB: The tumor is low grade or cannot be graded and the size of the tumor is larger than 8 cm or there are more than 1 separate tumors in the primary bone site. It has not spread to any lymph node or other parts of the body.

Stage IIA: The tumor is high-grade and the size is 8 cm or smaller. It has not spread to any lymph node or to other parts of the body.

Stage IIB: The tumor is high-grade and the size is larger than 8 cm. It has not spread to any lymph node or to other parts of the body.

Stage III: There are multiple high-grade tumors in the primary bone site, but has not spread to any lymph nodes or to other parts of the body.

Stage IVA: The tumor is of any size or grade and has spread to the lung(s).

Stage IVB: The tumor is of any size or grade and has spread to the lymph nodes or the tumor is of any size or grade and has spread to another bone or organ besides the lung.

(There are no stage grouping for primary bone cancer in the spine or pelvis)

Original and primary source: AJCC Cancer Staging Manual, Eighth Edition (2017), published by Springer International Publishing

Causes of Type II Respiratory Failure

In this article, we will discuss various Causes of Type II Respiratory Failure. So, let’s get started.

Causes

Respiratory causes

Severe acute asthma

Pulmonary embolism

Inhaled foreign body

Laryngeal edema

Multiple fractured ribs, flail chest

Chronic bronchitis (COPD)

Terminally ill patients

Progressive respiratory disease

Kyphoscoliosis (severe chest deformity)

Obesity hypoventilation syndrome (Pickwickian syndrome)

Sleep-apnea syndrome

Respiratory muscles paralysis

Sputum retention syndrome

Extrarespiratory causes

Drug (narcotics) overdose

Brainstem infarction

GB syndrome

Metabolic alkalosis

Infections

Myasthenia gravis

Eaton-Lambert syndrome

Myxoedema

Heart failure

Source: Emergency Medicine by SN Chugh and Ashima Chugh

Classification of Myocardial Infarction (MI)

In this article, we will discuss the Classification of Myocardial Infarction (MI). So, let’s get started.

Classification

Type 1 – Spontaneous MI – It is related to ischemia due to a primary coronary event such as plaque rupture, ulceration, fissuring, erosion or dissection resulting in coronary thrombosis

Type 2 – Supply/Demand mismatch – MI secondary to ischemia due to either increased oxygen demand or decreased oxygen supply e.g. coronary artery spasm, coronary embolism, anemia, arrhythmia, hypertension or hypotension.

Type 3 – Suspected MI-related death – Sudden unexpected cardiac death often with symptoms suggestive of myocardial infarction.

Type 4a – PCI related MI (percutaneous coronary intervention) – Rise in cardiac biomarkers accompanied by symptoms along with electrographic, angiographic or imaging evidence of ischemia after PCI (MI associated with PCI).

Type 4b – Stent thrombosis – Confirmed stent thrombosis in the context of ischemia and dynamic cardiac biomarkers changes (MI associated with stent thrombosis).

Type 5 – CABG related MI (coronary artery bypass graft) – Rise in cardiac biomarkers accompanied by electrographic, angiographic or imaging evidence of ischemia after CABG (MI associated with CABG).

 

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