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General Pathology

Clinical & biologic death

Clinical death

Clinical death is the reversible transmission between life and biologic death. Clinical death is defined as the period of respiratory, circulatory and brain arrest during which initiation of resuscitation can lead to recovery.

Signs indicating clinical death are

• The patient is without pulse or blood pressure and is completely unresponsive to the most painful stimulus.

• The pupils are widely dilated

• Some reflex reactions to external stimulation are preserved. For example, during intubations, respiration may be restored in response to stimulation of the receptors of the superior laryngeal nerve, the nucleus of which is located in the medulla oblongata near the respiratory center.

• Recovery can occur with resuscitation. 

Biological Death

Biological death (sure sign of death), which sets in after clinical death, is an irreversible state

of cellular destruction. It manifests with irreversible cessation of circulatory and respiratory

functions, or irreversible cessation of all functions of the entire brain, including brain stem.

Infectious Mononucleosis

It is an Epstein Barr virus infection in children and young adults.

Features

-Constitutional symptoms.
-Sore throat.
-Lymphnode enlargement.
-Skin rashes
-Jaundice.
-Rarely pneumonia, meningitis and encephalitis.

Blood Picture

- Total count of I0,000. 20,000 /cu.mm.
- Lymphocytosis (50-90%) with atypical forms. They are larger with more cytoplasm which may be vacuolated or basophilic. Nucleus may be indented. with nucleoli (Downy type I to III).
- Platelets may be reduced.
- Paul Bunell test (for heterophil antibody against sheep RBC) is positive
 

Alzheimer’s disease
a. The most common cause of dementia in older people.
b. Characterized by degeneration of neurons in the cerebral cortex.
c. Histologic findings include amyloid plaques and neurofibrillary tangles.
d. Clinically, the disease takes years to develop and results in the loss of cognition, memory, and the ability to ommunicate. Motor problems, contractures, and paralysis are some of the symptoms at the terminal stage.

Asthma

Asthma is

(1) An obstructive lung disease characterized by narrowing of the airways.

Inflammation of the airways is a major component of asthma.

(2) Common symptoms are dyspnea, wheezing on expiration, and coughing.

(3) Two types:

(a) Extrinsic (allergic, atopic) asthma

(i) An atopic allergy caused by a type I immediate hypersensitivity immune reaction to an allergen.

(ii) Seen in children, adults.

(b) Intrinsic (nonallergic) asthma

(i) Not caused by an allergic reaction.

(ii) Mostly seen in adults.

The disorder is a chronic inflammatory condition in which the airways develop increased responsiveness to various stimuli, characterized by bronchial hyper-responsiveness, inflammation, increased mucus production, and intermittent airway obstruction.

Signs and symptoms

  • The clinical hallmarks of an attack are shortness of breath (dyspnea) and wheezing
  • A cough—sometimes producing clear sputum—may also be present
  • The onset is often sudden; there is a "sense of constriction" in the chest, breathing becomes difficult, and wheezing occurs
  • Signs of an asthmatic episode are wheezing, rapid breathing (tachypnea), prolonged expiration, a rapid heart rate (tachycardia), rhonchous lung sounds (audible through a stethoscope), and over-inflation of the chest.
  • During very severe attacks asthma sufferer can turn blue due to lack of oxygen , can experience chest pain or even loss of consciousness, may lead to respiratory arrest and death

 

Pathophysiology

Bronchoconstriction : asthma is the result of an abnormal immune response in the bronchial airways. The airways of asthmatics are "hypersensitive" to certain triggers, also known as stimuli, these stimuli include allergens, medications , air pollution, early child hood infection, exercise, emotional stress

Bronchial inflammation asthma resulting from an immune response to inhaled allergens—are the best understood of the causal factors. In both asthmatics and non-asthmatics, inhaled allergens that find their way to the inner airways are ingested by a type of cell known as antigen presenting cells These activate an humoral immune response. The humoral immune system produces antibodies against the inhaled allergen. Later, when an asthmatic inhales the same allergen, these antibodies "recognize" it and activate a humoral response. Inflammation results: chemicals are produced that cause the airways to constrict and release more mucus, and the cell-mediated arm of the immune system is activated. The inflammatory response is responsible for the clinical manifestations of an asthma attack

Symptomatic Treatment

Episodes of wheeze and shortness of breath generally respond to inhaled  bronchodilators which work by relaxing the smooth muscle in the walls of the bronchi., More severe episodes may need short courses of inhaled, oral, or intravenous steroids which suppress  inflammation and reduce the swelling of the lining of the airway.

Bronchodilators (usually inhaled)

Short-acting selective  beta2-adrenoceptor agonists(salbutamol, terbutaline)

less selective adrenergic agonists, such as inhaled epinephrine and ephedrine tablets

Antimuscarinics

Systemic steroids

Oxygen to alleviate the hypoxia that is the result of extreme asthma attacks.

If chronic acid indigestion ( GERD) is part of the attack, it is necessary to treat it as well or it will restart the inflammatory process

Preventive Treatment

most effective preventive medication are

Inhaled  corticosteroids

Long-acting beta2-adrenoceptor agonists

Leukotriene modifiers

Mast cell stabilizers

Methylxanthines (theophylline and aminophylline),

Antihistamines, often used to treat allergic symptoms

Osteogenesis Imperfecta (OI) (Brittle bone diseases) 

It is a group of hereditary disorders caused by gene mutations that eventuate in defective synthesis of and thus premature degradation of type I collagen. The fundamental abnormality in all forms of OI is too little bone, resulting in extreme susceptibility to fractures. The bones show marked cortical thinning and attenuation of trabeculae. 

Extraskeletal manifestations also occur because type I collagen is a major component of extracellular matrix in other parts of the body. The classic finding of blue sclerae  is attributable to decreased scleral collagen content; this causes a relative transparency that allows the underlying choroid to be seen. Hearing loss can be related to conduction defects in the middle and inner ear bones, and small misshapen teeth are a result of dentin deficiency 

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