In this article, we will discuss the Pathology of Acute Nephritic Syndrome. So, let’s get started.

Pathology

The hallmark of acute nephritic syndrome is glomerular inflammation (hypercellularity) and the classical pathologic correlation of the nephritic syndrome is proliferative glomerulonephritis. The proliferation of glomerular cells is due to infiltration of the glomerular tuft by neutrophils and monocytes with subsequent proliferation of endothelial and mesangial cells (endocapillary proliferation). In most severe form, nephritic syndrome is associated with acute inflammation of most of the glomeruli (more than 50%), e.g. acute diffuse proliferative glomerulonephritis. In less severe form, fewer than 50% of the glomeruli may be involved, i.e. focal proliferative glomerulonephritis. In its mildest form, cellular proliferation is just confined to the mesangium, i.e. mesangioproliferative glomerulonephritis.

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

Viral invasion and inflammation of the brain parenchyma is called viral encephalitis. It is an acute febrile illness with some evidence of meningeal involvement and signs and symptoms of diffuse and/or focal brain substance involvement. Some patients have involvement of meninges and brain parenchyma called meningoencephalitis. If the spinal cord is involved, then it is termed encephalomyelitis. It is far more serious than viral meningitis. Following are the various causes of viral encephalitis:

Causes

A. Immunocompetent individuals

  • Common
  • Arboviruses (Japanese, St. Louis, Western Equine, California, and WNV)
  • Herpes simplex virus HSV-I and HSV-II
  • Mumps
  • Less Common
  • Cytomegalovirus (CMV)
  • Epstein-Barr virus (EBV)
  • Human immunodeficiency virus (HIV)
  • Measles virus
  • Rare
  • Adenovirus
  • Influenza and Parainfluenza virus
  • Lymphocytic choriomeningitis virus (LCMV)
  • Rabies, rubella

B. Immunocompromised individuals, e.g. HSV, VZV, CMV, EBV, human herpes virus-6.

 

 

In this article, we will discuss some of the Common Causes of Coma. So, let’s get started.

Causes

A. Brainstem and Cerebellar lesions

  • Infarction, hemorrhage of brainstem and cerebellum
  • Tumor, trauma
B. Lesions of cerebral hemisphere with edema and brainstem compression
  • Infarction, hemorrhage
  • Encephalitis, meningitis, brain abscess
  • Tumor, trauma (subdural, extradural)
  • Hydrocephalus
  • Hypertensive encephalopathy
  • Status epilepticus
  • Cerebral malaria
C. Metabolic abnormalities
  • Diabetic and hypoglycemic coma
  • Hepatic failure, renal failure, cardiac failure, respiratory failure
  • Severe hyponatremia or hypokalemia
  • Hyper and hypocalcaemia
  • Hypoxia
  • Myxoedema coma, hypopituitarism
  • Adrenal crisis
  • Vitamin deficiencies (e.g. B1, nicotinic acid, B12)
D. Drugs and physical agents
  • Anaesthetic agents
  • Drug overdose or poisoning and alcohol ingestion
  • Hyper and hypothermia
E. Psychogenic/hysteria

In this article, we will discuss the Definition of Dengue Hemorrhagic Fever. So, let’s get started.

Definition

Dengue hemorrhagic fever is characterized by all manifestations of classical dengue fever, thrombocytopenia, vascular instability, and increased permeability resulting in leakage of intravascular fluid to interstitial space (hemoconcentration) and local hemorrhage (positive tourniquet test, spontaneous petechiae, and/or purpura) or frank hemorrhage (epistaxis, gum bleeding, bleeding into GI tract, i.e. melena or hematochezia) have been described. The hemorrhage is inconstant and is thought to be a combined effect of vascular damage and thrombocytopenia.

As the plasma leakage increases, patient may become restless, irritable, and develops hypotension and shock (cold extremities) called dengue shock syndrome (DSS). In severe cases, frank shock is present with low pulse pressure (<20 mmHg), cyanosis, hepatomegaly, pleural effusion, and ascites. In some cases, severe ecchymosis and GI bleeding may be seen.

In this article, we will discuss the Pathogenesis and Pathophysiology of Acute Syncope. So, let’s get started.

Pathogenesis and Pathophysiology

Syncope results from transient ischemia of the brain usually in upright stature, brought about by reduction in cardiac output or hypotension due to any underlying cause. Depending upon the pathophysiologic mechanisms, syncope may be naturally mediated syncope (vasovagal, neurocardiogenic), postural (orthostatic), and cardiac. The underlying mechanisms in syncope are:

I. Inadequate vasoconstrictive response, examples are vasodepressor, postural syncope.

II. Reduced venous return, i.e. cough, micturition, defecation syncope.

III. Reduced cardiac output, i.e. myocardial and pericardial diseases, obstructive valvular lesions, and arrhythmia.

IV. Altered state of blood, e.g. anemia, hypoxia, hypoxemia etc.