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

Aplasticanaemia and pancytopenia.

Aplastic anaemia is a reduction in all the formed elements of blood due to marrow hypoplasia.

Causes

- Primary or Idiopathic.
- Secondary to :

1    Drugs :

Antimetabolites and antimitotic agents.
Antiepileptics.
Phenylbutazone.
Chloramphenicol.

2    Industrial chemicals.

Benzene.
DDT and other insecticides.
TNT (used in explosives).

3    Ionising radiation

- Familial aplasia

Pancytopenia (or reduction in the formed elements of blood) can be caused  by other conditions also like:
-Subleukaemic acute leukaemia.
-Megaloblastic anaemia
-S.L.E.
-hypersplenism.
-Marrow infiltration by lymphomas  metastatic deposits, tuberculosis, myeloma etc

Features:
- Anaemia.
- Leucopenia upper respiratory infections.
- Thrombocytopenis :- petechiae and bruising.

Blood picture:

- Normocytic normochromic  anaemia with minimal anisopoikilocytosis in aplastic anaemia. Other causes of pancytopenia may show varying degrees of anisopoikilocytosis
- Neutropenia with hypergranulation and high alkaline phosphatase.
- Low platelet counts

Bone marrow:
- Hypoplastic (may have patches  of norm cellular or hyper cellular marrow) which may -> dry tap. .
- Increase in fat cells , fibroblasts , reticulum cells, lymphocytes and plasma cells
- Decrease in precursors of all three-Series.
- Underlying cause if any, of pancytopenia may be seen
 

A dermatofibroma is a benign tumor of the dermis, MC located on the lower extremity, where it has a nodular, pigmented appearance.
 - composed of benign histiocytes.

Bronchitis

Bronchitis is an obstructive pulmonary disease characterized by inflammation of the bronchi of the lungs

Signs and symptoms

persistent cough that produces sputum

shortness of breath (dyspnea) on exertion

hypercapnia

insufficient oxygenation of the blood hypoxemia leading to cynosis

Severe chronic bronchitis will commonly lead to cor pulmonale and heart failure.

Pathology

an increase in the number of goblet cells with mucus blocking the airway clusters of pigmented alveolar macrophages

the presence of inflammatory cells (e.g. neutrophils) scarring (fibrosis) of the walls of the bronchioles

Diagnosis

• decreased intensity of breath sounds (rhonchi) and extended expiration.
• a sputum culture has pathogenic microorganisms
• a chest x-ray that reveals hyperinflation and increased bronchovascular markings
• a pulmonary function test that shows an increase in the lung's residual volume and a decreased vital capacity

Pathophysiology

• The initiating event in developing bronchitis appears to be chronic irritation due to inhalation of certain chemicals
• earliest clinical feature of bronchitis is increased secretion of mucus by submucousal glands of the trachea and bronchi
• Damage caused by irritation of the airways leads to inflammation and infiltration of the lung tissue by neutrophils
• The neutrophils release substances that promote mucousal hypersecretion
• As bronchitis persists to become chronic bronchitis, a substantial increase in the number of goblet cells in the small airways is seen
• The role of infection in the pathogenesis of chronic bronchitis appears to be secondary.

Treatment

Quit smoking, Oxygen therapy, bronchodilator drugs

Prognosis

Pulmonary hypertension, cor pulmonale, and chronic respiratory failure are possible complications of chronic bronchitis

In severe chronic bronchitis is poor

Megaloblastic anaemia

Metabolism: B12(cyanocobalamin) is a coenzyme in DNA synthesis and for maintenance of nervous system. Daily requirement 2 micro grams. Absorption in terminal ileum in the presence gastric intrinsic factor. It is stored in liver mainly-

Folic acid (Pteroylglutamic acid) is needed for DNA synthesis.. Daily requirement 100 micro grams. Absorption in duodenum  and jejunum

Causes of deficiency .-

- Nutritional deficiency-
- Malabsorption syndrome.
- Pernicious anaemia (B12).
- Gastrectomy (B12).
- Fish tapeworm infestation (B12).
- Pregnancy and puerperium (Folic acid mainly).
- Myeloproliferative disorders (Folic acid).
- Malignancies (Folic acid).
- Drug induced (Folic-acid)

Features:

(i) Megaloblastic anaemia.
(ii) Glossitis.
(iii) Subacute combined degeneration (in B12deficiency).

Blood picture :

- Macrocytic normochromic anaemia.
- Anisocytosis and poikilocytosis with Howell-Jolly bodies and  basophilic stippling.
- Occasional megalo blasts may be-seen.
- Neutropenia with hypersegmented neutrophills and macropolycytes.
- Thrombocytopenia.
- Increased MVC and MCH with normal or decreased MCHC.

Bone marrow:

- Megaloblasts are seen. They are larger with a more open stippled chromatin. The nuclear maturation lags behind. the cytoplasmic maturation. Maturation arrest is seen (more of early forms).
- Immature cells of granulocyte series are also larger.
 -Giant stab forms (giant metamyelocytes).
 

Cushing’s syndrome

The symptoms and signs of Cushing’s syndrome are associated with prolonged inappropriate elevation of free corticosteroid levels.

Clinical features

- Central obesity and moon face.
- Plethora and acne.
- Menstrual irregularity.
- Hirsutism and hair thinning.
- Hypertension.
- Diabetes.
- Osteoporosis—may cause collapse of vertebrae, rib fractures.
- Muscle wasting and weakness.
- Atrophy of skin and dermis—paper thin skin with bruising tendency, purple striae.

Aetiopathogenesis — patients with Cushing’s syndrome can be classified into two groups on the basis of whether the aetiology of the condition is ACTH dependent or independent. 

Classification of Cushing's syndrome

ACTH dependent- Iatrogenic (ACTH therapy) Pituitary hypersecretion of ACTH Ectopic ACTH syndrome (benign or malignant non-endocrine tumour)

Non-ACTH dependent - Iatrogenic, e.g. prednisolone Adrenal cortical adenoma , Adrenal cortical carcinoma

ACTH-dependent aetiology:

- Pituitary hypersecretion of ACTH (Cushing’s disease)—bilateral adrenal hyperplasia secondary to excessive secretion of ACTH by a corticotroph adenoma of the pituitary gland.
- Production of ectopic ACTH or corticotrophin- releasing hormone (CRH) by non-endocrine neoplasm, e.g. small cell lung cancer and some carcinoid tumours. In cases of malignant bronchial tumour, the patient rarely survives long enough to develop any physical features of Cushing’s syndrome.

Non-ACTH-dependent aetiology

Iatrogenic steroid therapy—most common cause of Cushing’s syndrome.
Adrenal cortical adenoma—well-circumscribed yellow tumour usually 2–5 cm in diameter.
Extremely common as an incidental finding in up to 30% of all post-mortem examinations. The yellow colour is due to stored lipid (mainly cholesterol) from which the hormones are synthesised. The vast majority have no clinical effects (i.e. they are non-functioning adenomas), with only a small percentage producing Cushing’s syndrome.

Adrenal cortical carcinoma—rare and almost always associated with the overproduction of hormones, usually glucocorticoids and sex steroids. 

Cushing’s syndrome mixed with androgenic effects which are particularly noticeable in women. Tumours are usually large and yellowish white in colour. Local invasion and metastatic spread are common.

Irrespective of the aetiology, the diagnosis is based on clinical features and the demonstration of a raised plasma cortisol level.
The aetiology of the disorder is elucidated through:
- Raised urinary cortisol in the first instance, but further testing is required.
- Low-dose dexamethasone suppression test (suppression of cortisol levels in Cushing’s disease due to suppression of pituitary ACTH secretion, but a lack of suppression suggests ACTH-independent Cushing’s syndrome).
- MRI and CT scan visualisation of pituitary and adrenal glands.
- Analysis of blood ACTH (high = pituitary adenoma or ectopic ACTH source; low = primary adrenal tumour due to feedback suppression).
- Treatment of the underlying cause is essential as untreated Cushing’s syndrome has a 50% 5-year mortality rate.

The therapeutic administration of glucocorticosteroids (e.g. prednisolone) is a common cause of the features of Cushing’s syndrome.