NEET MDS Lessons
General Pathology
Nephrosclerosis
Disease of the renal arteries.
Clinical manifestations:
(1) Benign (arterial) nephrosclerosis → Caused by the formation of atherosclerotic plaques in the renal artery. Results in narrowing of the arterioles.
(2) Malignant nephrosclerosis → Caused by malignant hypertension. Common signs of malignant hypertension include severe hypertension, retinal hemorrhages, and hypertrophy of the left ventricle. Results in inflammatory changes in the vascular walls, which may lead to rupture of the glomerular capillaries.
SHOCK
Definition. It is a clinical state of acute inadequacy of perfusion to tissues due to fall in effective circulating blood volume.
This inadequacy can be caused by :
- Increased vascular capacity
- Decreased blood volume
- Altered distribution of available blood
- Defective pumping system
Causes:
(1) Hypovolemic
- Massive hamorrhage (external or internal).
- Loss of plasma as in bums.
- Dehydration due to severe vomiting, diarrhea diabetic coma.
- Generalized capillary permeability as in anaphylaxis.
(2) Cardiogenic
- Myocardial infarction.
- Pulmonary embolism.
- Cardiac tamponade
(3) Peripheral pooling:
- Endotoxic shock.
- Disseminated intravascular coagulation (DIC).
(4) Neurogenic:
- Syncope.
- Contributory factor in trauma, bums etc.
Metabolic changes in shock
- Hyperglycaemia due to glycogenolysis.
- Increased blood lactate and pyruvate due to anaerobic glycolysis. This results in metabolic acidosis.
- Protein catabolism and increased blood urea.
- Interference with enzyme systems.
Organs involved in shock
(1) Kidneys:
- Renal tubular necrosis.
- Cortical necrosis.
(2) Lungs:
- Oedema, congestion and haemorrhage.
- Microthrombi.
(3) G.I.T. :
- Mucosal oedema.
- Ulceration and haemorrhage
(4) Degeneration and focal necrosis in:
- Heart.
- Liver.
- Adrenals
(5) Anoxic encephalopathy
Acanthosis nigricans is a pigmented skin lesion commonly present in the axilla which is a phenotypic marker for an insulin-receptor abnormality as well as a marker for adenocarcinoma, most commonly of gastric origin.
FUNGAL INFECTION
Aspergillosis
Opportunistic infections caused by Aspergillus sp and inhaled as mold conidia, leading to hyphal growth and invasion of blood vessels, hemorrhagic necrosis, infarction, and potential dissemination to other sites in susceptible patients.
Symptoms and Signs: Noninvasive or, rarely, minimally locally invasive colonization of preexisting cavitary pulmonary lesions also may occur in the form of fungus ball (aspergilloma) formation or chronic progressive aspergillosis.
Primary superficial invasive aspergillosis is uncommon but may occur in burns, beneath occlusive dressings, after corneal trauma (keratitis), or in the sinuses, nose, or ear canal.
Invasive pulmonary aspergillosis usually extends rapidly, causing progressive, ultimately fatal respiratory failure unless treated promptly and aggressively. A. fumigatus is the most common causative species.
Extrapulmonary disseminated aspergillosis may involve the liver, kidneys, brain, or other tissues and is usually fatal. Primary invasive aspergillosis may also begin as an invasive sinusitis, usually caused by A. flavus, presenting as fever with rhinitis and headache
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.
Hepatitis C virus.
It is most often mild and anicteric but occasionally severe with fulminant hepatic failure. It is caused an RNA virus, which may be transmitted parenterally (a cause of post-transfusion hepatitis); the route of transmission undetermined in 40%-50% of cases
a. 90% of blood transfusion-related hepatitis is caused by hepatitis C.
b. 50% progress to chronic disease.
c. Increased risk for hepatocellular carcinoma.
d. Incubation period: ranges from 2 to 26 weeks, but averages 8 weeks.
- Antibody is detected by enzyme-linked immunosorbent,assay (ELISA). The incubation period is between 2 and weeks with peak onset of illness 6-8 weeks after infection
- Most patients progress to chronic liver disease, specifically chronic persistent hepatitis or chronic active hepatitis
- Cirrhosis is common in patients with chronic active hepatitis and occurs in 20%-25% of infected patients. HCV is also associated with hepatocellular carcinoma.
e. Treatment and prevention: α-interferon is used to treat chronic hepatitis C. There is currently no vaccine available.
Neutrophilia
Causes
-Pyogenic infections.
-Haemorrhage and trauma.
-Malignancies.
-Infarction.
-Myelo proliferative disorders.