Symptoms of Novel Coronavirus infection

In this article, we will discuss various Symptoms of the Novel Coronavirus infection. So, let’s get started.

Coronaviruses are enveloped non-segmented positive-sense RNA viruses belonging to the family Coronaviridae and the order Nidovirales. Although most human coronavirus infections are mild, the epidemics of the two beta coronaviruses, severe acute respiratory syndrome coronavirus (SARS-CoV) and the Middle East respiratory syndrome coronavirus (MERS-CoV) have caused more than 10000 cumulative cases in the past two decades, with mortality rates of 10% for SARS-CoV and 37% for MERS-CoV. In December 2019, a series of pneumonia cases of unknown cause emerged in Wuhan, Hubel, China, with clinical presentation greatly resembling pneumonia. Deep sequencing analysis from lower respiratory tract samples indicated a novel coronavirus, which was named 2019 novel coronavirus (2019-nCoV). The following are the symptoms of coronavirus infection (2019-nCoV). Majority cases are being reported from China, Thailand, Japan, South Korea, and the USA.


Common symptoms



Shortness of Breath



Less common symptoms include:

Sputum production





According to CDC symptoms of 2019-nCov may appear in 2 days or as long as 14 days after exposure.


Classification of Myocardial Infarction (MI)

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


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).


Tension Pneumothorax

In this article, we will discuss about Tension Pneumothorax. So, let’s gets started

Tension Pneumothorax

In tension pneumothorax, the mean pleural pressure is positive which means that air in the pleural cavity is under tension which causes compression collapse of the lung. It develops due to persistent air leak (air entry) inside the pleural cavity by the communication which opens during inspiration and closes during expiration preventing the air to escape. In this way, with each successive breath, the intrapleural pressure increases which eventually causes the mediastinum to shift to the opposite side and increased intrapleural pressure also puts pressure on the surrounding blood vessels.

There is decreased venous return to the heart and along with decreased cardiac output causing hypotension (cardiac tamponade) and cyanosis.

Clinical Features

Dyspnea, cough and acute exacerbation of pneumothorax symptoms

Trachea and mediastinum shifts to the opposite side

Decreased or absent breath sounds, there may be amphoric breathing present at a localized place.

Hyperinflated chest with decreased or absent chest wall movement of the involved side

Tachypnea, tachycardia, hypotension, cyanosis, and paradoxical pulse.



Clinical features of Pneumothorax

In this article, we will discuss about the Clinical features of Pneumothorax. So, let’s get started.

Clinical features

Chest pain ( Pain is sharp, pleuritic, and is localized to the same side of pneumothorax)


Fullness of intercoastal spaces

Decreased chest wall movement

Hyper-resonant percussion note

Decreased breath sounds, vocal fremitus, and vocal resonance in closed and tension pneumothorax. s

Increased vocal fremitus, vocal resonance, presence of whispering pectoriloquy (on development of large bronchopleural fistula), and amphoric bronchial breathing.

Accumulation of fluid or pus in the pleural cavity in case ocharacterized by f an associated infection (open pneumothorax or pneumothorax due to tuberculosis) along with physical signs of horizontal shifting level of dullness and succussion splash, and additionally there is signs of toxemia

Recurrent spontaneous pneumothorax occurs with emphysema due to the rupture of bullae occurring on the same side.



Signs and Symptoms of Pleural Effusion

In this article, we will discuss about the various Signs and Symptoms of Pleural Effusion . So, let’s get started.

Sign and Symptoms

Chest pain often referred to the left shoulder or upper abdomen because of diaphragmatic irritation.


Dry cough

Shortness of breath

Difficulty in inspiration



Persistent hiccups

Lower extremity edema

Paroxysmal nocturnal dyspnea

Rotator Cuff Tendinopathy

It refers to the pain and weakness of rotator cuff musculature Rotator cuff comprises of four main muscles viz. Subscapularis, Supraspinatus, Infraspinatus, Teres Minor responsible for abduction and rotation movement of shoulder



Commonly affects athletes involved in sporting activities like Cricket, Swimming, Throwers etc and it can be age related problem affecting old aged patients their is an incidence of 11.2 cases per 1000 patients per year


Their is a difference between tendinitis and tendinopathy. Tendinitis is an inflammation of tendons whereas tendinopathy is deterioration of tendons. Rotator Cuff tendinopathy is clinically presented with

Pain, Weakness, Loss of strength to bear load aur lift weight on shoulders along with tenderness around shoulder joint painfull overhead movement localised swelling may also be present





For Physical examination two clinical tests are performed namely

Empty can test and Hawkins test

Other tests include Modified Belly press test, Palpation, ROM testing the latter two are not so significant In order to see how the tests are performed visit

Other diagnostic tools include ultrasound, radiographs, radionucleotide isotope scan, magnetic resonance imaging (MRI), computed axial tomography (CT), electromyography

Ultrasound reveal partial tear of tendon fibres partial thickened tears and thickened subacromial bursa MRI also reveals rotator cuff tears



Biceps tendinopathy

Frozen Shoulder

Cervical Disc Disease

Cervical Spondylosis


For measuring extent of rotator cuff tendinopathy VAS score, SPADI (Shoulder pain and disability index) have be adopted extensively by physiotherapist


Physiotherapy is the gold standard treatment for rotator cuff tendinopathy along with Medical Management in majority cases and rarely require surgical intervention if Conservative treatment doesn’t work Medical Management includes NSAIDS, Shoulder immobilisation etc Surgery involves Arthroscopic intervention Physiotherapy treatment includes step wise procedure firstly Stretching, ROM exercises and then Muscle Strengthening exercises for pain management Ultrasound, TENS etc Modalities can be applied Kinesiotaping have shown better result in patients with Rotator Cuff Tendinopathy. Other techniques include

Isometric exercises

Kinetic Chain exercises

Correcting scapulohumeral rhythm

Corrective Posture

Pilates technique

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Clinical Features and Pathogenesis of Cardiogenic Shock

In this article, we will discuss the Clinical Features and Pathogenesis of Cardiogenic Shock. So, let’s get started.

Clinical Features and Pathogenesis

Irrespective of the cause of cardiogenic shock, it is characterized by a vicious circle of severe myocardial (systolic and diastolic) dysfunction. Systolic dysfunction results in fall in cardiac output, BP and thereby coronary perfusion pressure falls. Hypotension, oliguria, confusion or altered mental state, tachypnea, tachycardia and cold, clammy extremities are the manifestations of low output state or acute circulatory failure. Diastolic dysfunction on the other side of cycle causes a rise in CVP, left ventricular end-diastolic pressure, rise in PCWP, pulmonary congestion and edema, leading to hypoxia which further worsens the myocardial ischemia. Breathlessness, orthopnea, PND, cyanosis, cough, hemoptysis, hypoxia, perspiration and inspiratory crackles at the bases of the lungs, S3 and S4 gallops are features of acute pulmonary edema.

A systemic inflammatory response syndrome (SIRS) may accompany large infarction and shock. Inflammatory cytokines and excess nitric oxide may contribute to genesis of cardiogenic shock. Severe acidosis (lactic acidosis) reduces the efficacy of catecholamines and provoke arrhythmias. A Swan-Ganz catheter can be used to measure the pulmonary artery wedge pressure which is >18 mmHg.

Untreated or refractory shock leads to multiple organ dysfunction, e.g. heart, brain, lungs, kidney and liver.

Older patients mostly females, prior MI, diabetes and extensive anterior MI (EF<30%) are at increased risk of cardiogenic shock.

Difference between clinical features of Acute and Chronic Hepatic Encephalopathy

In this article, we will discuss the Difference between clinical features of Acute and Chronic Hepatic Encephalopathy. So, let’s get started.

  • Acute hepatic encephalopathy
  • Acute onset
  • Acute fulminant hepatitis is the common cause
  • No precipitating factors
  • Ascites and portal hypertension absent
  • Liver span is reduced
  • Prognosis is bad
  • Chronic hepatic encephalopathy
  • Slow chronic onset
  • Chronic hepatitis or cirrhosis is the commonest cause
  • It is precipitated by certain factors
  • Ascites and portal hypertension present
  • Liver span is normal or increased
  • Prognosis is better

Precipitating Factors and Differential Diagnosis of Myxoedema Coma

In this article, we will discuss the Precipitating Factors and Differential Diagnosis of Myxoedema Coma. So, let’s get started.

Precipitating Factors

The factors that push the patient of hypothyroidism into myxoedema coma are given below:

  • Infection, e.g. pneumonia
  • Exposure to cold
  • Hypoventilation
  • Hypoglycemia
  • Dilutional hyponatremia
  • Trauma
  • GI bleeding
  • Stroke (CVA)
  • CNS depressants, e.g. tranquillisers, sedatives and antidepressants
  • Cardiovascular disease (e.g. CHF), myocardial infarction
  • Respiratory disease (infection, COPD)

Hypoventilation leading to hypoxia and hypercapnia plays a major role in pathogenesis. Hypoglycemia and dilutional hyponatremia also contribute to the development of myxoedema coma.

Differential Diagnosis

The conditions which are associated with coma and hypothermia may mimic myxoedema coma. These include:

1. Brainstem infarction in older persons may lead to both coma and hypothermia

2. Hypothermia due to any cause and renal failure may itself induce physiological changes simulating myxoedema such as delayed relaxation of deep tendon reflexes. Coma is due to hypothermia and renal failure.

Difference between Vasogenic and Cytopathic Cerebral Edema

In this article, we will discuss the Difference between Vasogenic and Cytopathic Cerebral Edema. So, let’s get started.

  • Vasogenic Cerebral Edema
  • Produces focal signs and symptoms due to edema
  • Blood brain barrier remains open
  • Activated diffusion coefficient is increased
  • MRI shows increased interstitial fluid
  • Responds to steroids
  • It is associated with tumors, hemorrhage, abscess, meningitis, cerebral infarction
  • Cytopathic Cerebral Edema
  • The clinical signs are generalised, non-localising, i.e. convulsions, coma
  • Blood brain barrier is closed
  • Activated diffusion coefficient is reduced
  • MRI shows swollen cells
  • Does not respond to steroids
  • Seen in hemodialysis and ketoacidosis

Rapidly Progressive Glomerulonephritis

In this article, we will discuss Rapidly Progressive Glomerulonephritis (RPGN). So, let’s get started.

Rapidly Progressive Glomerulonephritis

It is a clinical correlate of nephritic syndrome but is of subacute onset characterized by development of renal failure over days to weeks, in association with a nephritic urinary sediments, subnephrotic proteinuria, oliguria, hypovolemia, edema and hypertension. The classic pathologic finding is severe extracapillary proliferation leading to crescents formation in more than 50% of glomeruli (crescentic glomerulonephritis). In practice, the clinical term rapidly progressive (proliferative) glomerulonephritis and the pathological term crescentic glomerulonephritis are interchangeably used.

The association of acute nephritic syndrome with hemoptysis (Goodpasture’s syndrome), antineutrophil cytoplasmic antibodies (ANCA) small vessel vasculitis, SLE or cryoglobulinemia is called pulmonary-renal syndrome.

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