NEET MDS Lessons
General Pathology
Pulmonary embolism
A pulmonary embolism (thromboembolism) occurs when a blood clot, generally a venous thrombus, becomes dislodged from its site of formation and embolizes to the arterial blood supply of one of the lungs.
Clinical presentation
Signs of PE are sudden-onset dyspnea (shortness of breath, 73%), tachypnea (rapid breathing, 70%), chest pain of "pleuritic" nature (worsened by breathing, 66%), cough (37%), hemoptysis (coughing up blood, 13%), and in severe cases, cyanosis, tachycardia (rapid heart rate), hypotension, shock, loss of consciousness, and death. Although most cases have no clinical evidence of deep venous thrombosis in the legs, findings that indicate this may aid in the diagnosis.
Diagnosis
The gold standard for diagnosing pulmonary embolism (PE) is pulmonary angiography
An electrocardiogram may show signs of right heart strain or acute cor pulmonale in cases of large PEs
In massive PE, dysfunction of the right side of the heart can be seen on echocardiography, an indication that the pulmonary artery is severely obstructed and the heart is unable to match the pressure.
Treatment
Acutely, supportive treatments, such as oxygen or analgesia
In most cases, anticoagulant therapy is the mainstay of treatment. Heparin or low molecular weight heparins are administered initially, while warfarin therapy is given
Emphysema
Emphysema is a chronic lung disease. It is often caused by exposure to toxic chemicals or long-term exposure to tobacco smoke.
Signs and symptoms
loss of elasticity of the lung tissue
destruction of structures supporting the alveoli
destruction of capillaries feeding the alveoli
The result is that the small airways collapse during expiration, leading to an obstructive form of lung disease
Features are: shortness of breath on exertion
hyperventilation and an expanded chest.
As emphysema progresses, clubbing of the fingers may be observed, a feature of longstanding hypoxia.
Emphysema patients are sometimes referred to as "pink puffers". This is because emphysema sufferers may hyperventilate to maintain adequate blood oxygen levels. Hyperventilation explains why emphysema patients do not appear cyanotic as chronic bronchitis (another COPD disorder) sufferers often do; hence they are "pink" puffers (adequate oxygen levels in the blood) and not "blue" bloaters (cyanosis; inadequate oxygen in the blood).
Diagnosis
spirometry (lung function testing), including diffusion testing
X-rays, high resolution spiral chest CT-scan,
Bronchoscopy, blood tests, pulse oximetry and arterial blood gas sampling.
Pathophysiology :
Permanent destructive enlargement of the airspaces distal to the terminal bronchioles without obvious fibrosis
Oxygen is inhaled in normal breathing
When toxins such as smoke are breathed into the lungs, the particles are trapped by the hairs and cannot be exhaled, leading to a localised inflammatory response. Chemicals released during the inflammatory response (trypsin, elastase, etc.) are released and begin breaking down the walls of alveoli. This leads to fewer but larger alveoli, with a decreased surface area and a decreased ability to take up oxygen and loose carbon dioxide. The activity of another molecule called alpha 1-antitrypsin normally neutralizes the destructive action of one of these damaging molecules.
After a prolonged period, hyperventilation becomes inadequate to maintain high enough oxygen levels in the blood, and the body compensates by vasoconstricting appropriate vessels. This leads to pulmonary hypertension. This leads to enlargement and increased strain on the right side of the heart, which in turn leads to peripheral edema (swelling of the peripherals) as blood gets backed up in the systemic circulation, causing fluid to leave the circulatory system and accumulate in the tissues.
Emphysema occurs in a higher proportion in patient with decreased alpha 1-antitrypsin (A1AT) levels
Prognosis and treatment
Emphysema is an irreversible degenerative condition
Supportive treatmentis by supporting the breathing with anticholinergics, bronchodilators and (inhaled or oral) steroid medication, and supplemental oxygen as required
Lung volume reduction surgery (LVRS) can improve the quality of life for only selected patients.
Myocardial infarction (MI)—heart attack
A. Ischemia versus MI: Ischemia is a reversible mismatch between the supply and demand of oxygen. Infarction
is an irreversible mismatch that results in cell death caused by the lack of blood flow (oxygenation). For instance, chest pain caused by ischemia can be relieved by administering nitroglycerin (a vasodilator) to the patient. If the patient has an MI, the pain will not be relieved with nitroglycerin.
1. MIs most commonly occur when a coronary artery is occluded by a thrombus generated in an atherosclerotic artery.
2. Symptoms include:
a. Chest pain, shortness of breath.
b. Diaphoresis (sweating), clammy hands.
c. Nausea, vomiting.
3. Consequences:
a. Death (one third of patients).
b. Arrhythmias (most common immediate cause of death).
c. Congestive heart failure.
d. Myocardial rupture, which may result in death from cardiac tamponade.
e. Thrombus formation on infarcted tissue; may result in systemic embolism.
HYPERPLASIA
It is the increase in the size of an organ or tissue due to increase in the number of its constituent cells. This is seen in organs made up of labile and stable cells.
Causes
I. Increased demand:
- Bone marrow in hypoxia and haemolytic states.
- Thyroid gland in puberty
2. Persistant Trauma:
- Acanthosis of the epidermis in chronic inflammations and in warts.
- Hyperplasia of oral mucosa due tooth and denture trauma.
- Mucosa at the edges of a gastric ulcer.
3. Endocrine target organ:
- Pregnancy hyperplasia of breast.
- Prostatic hyperplasia.
4. Compensatory:
Hyperplasia of kidney when the other kidney has been removed.
5. Idiopathic:
Endocrine organs like thyroid, adrenals, pituitary etc. can undergo hyperplasia with no detectable stimulus. .
Enterococci
Most common are E. fecalis and E. fecium. Cause inflammation at site of colonization.
Serious resistance to antibiotics. E. fecium is now a vancomycin resistant enterococcus (VRE)
THE ADRENAL GLANDS
ADRENAL CORTEX
The adrenal cortex synthesizes three different types of steroids:
1. Glucocorticoids (principally cortisol), which are synthesized primarily in the zona fasciculata
2. Mineralocorticoids, the most important being aldosterone, which is generated in the zona glomerulosa; and
3. Sex steroids (estrogens and androgens), which are produced largely in the zona reticularis.
ADRENAL MEDULLA
The adrenal medulla is populated by cells derived from the neural crest (chromaffin cells) and their supporting (sustentacular) cells.
They secrete catecholamines in response to signals from preganglionic nerve fibers inthe sympathetic nervous system.
DEGENERATION
Definition: Reversible cell injury.
(1) Water accumulation in the form of
(i) Cloudy swelling.
(ii) Vacuolar degeneration.
.(ill) Hydropic degeneration.
This change is commonly seen in parenchymal cells e.g. kidneys.
Gross appearance: The organ is swollen, soft and pale.
Microscopic appearance: Cells show varying degrees of swelling. Cytoplasm may be granular, vacuolated, homogenously pale and ballooned out.
(2) Fatty change An excessive, demonstrable accumulation of fat is common in parenchymal cells of liver and heart
In the liver, it can be due to: .
(i) Excess fat entry into the liver as occurs in starvation and in steroid excess due to mobilization from stores.
(ii) Excess triglyceride formation
(iii) Reduced phosphorlyation of fat.
(iv) Decreased release as lipoprotein due to protein deficiency.
Causes
(i) Hypoxia as in severe anaemia and venous stasis
(ii) Protein malnutrition.
(iii) Hepatotoxins like CCl4.
(iv) Alcoholism
(v) Metabolic defects like Diabetes mellitus
(vi) Infections.
Gross appearance: The organ is enlarged, soft and greasy, with a pale yellowish colour. It may involve the organ uniformly or patchily ( thrush breast or tabby cat heart)
Microscopic appearance: The cells contain clear vacuoles (stainable by fat-sudan stains on frozen sections). These may be small and dispersed or large, displacing the nucleus peripherally. Several such cells may fuse to form fat cysts.
(3) Hyaline degeneration
In alcoholic liver damage, the cytoplasmic organelles are damaged and give the cytoplasm a deep eosinophilic staining-Mallory hyaline.