Respiratory Viral Diseases

Respiratory viral infections cause acute local and systemic illnesses. The common cold, influenza, pharyngitis, laryngitis (including croup), and tracheobronchitis are common.

An acute, usually afebrile, viral infection of the respiratory tract, with inflammation in any or all airways, including the nose, paranasal sinuses, throat, larynx, and sometimes the trachea and bronchi.

Etiology and Epidemiology

Picornaviruses, especially rhinoviruses and certain echoviruses and coxsackieviruses, cause the common cold. About 30 to 50% of all colds are caused by one of the > 100 serotypes of rhinoviruses.

Symptoms and Signs

Clinical symptoms and signs are nonspecific.

After an incubation period of 24 to 72 h, onset is abrupt, with a burning sensation in the nose or throat, followed by sneezing, rhinorrhea, and malaise.

Characteristically, fever is not present, particularly with a rhinovirus or coronavirus. Pharyngitis usually develops early; laryngitis and tracheobronchitis vary by person and causative agent. Nasal secretions are watery and profuse during the first days, but become more mucoid and purulent.

Cough is usually mild but often lasts into the 2nd wk.

Acute leukaemia
Lympheblastic is commoner in children and myeloblastic in adults .

Features:
- Anaemia.
- Fever and infections especially oral and respiratory.
- Haemorrhagic tendencies.
- Bone pains and tenderness (sternal).
- Lymphnode enlargement especially in lymphocytic.
- Gum hypertrophy especially in monocytic.

Blood picture:

- Anaemia and thrombocytopenia.
- Leucocyte count usually 20,-50,000/cu.mm. It may be less in subleukaemic leukaemia (even leucopenic levels may be seen).
- Blast cells form 30-90% of cells. Smudge cells and basket cells are seen .The type of balst cell may be recognised  by the associated more mature forms or by special cytochemical stains
- Blasts may be few in peripheral blood in the aleukamic stage

 Bone Marrow

- May be a dry tap , necessitating a trephine biopsy 
- Hypercellular with 70-90% blasts
- Reduction in megakaryocytes and erythroid cells
 

Other lung diseases

1.Sarcoidosis

1. Sarcoidosis

a. More common in African-Americans.

b. Associated with the presence of noncaseating granulomas.

Sarcoidosis is an immune system disorder characterised by non-necrotising granulomas (small inflammatory nodules). Virtually any organ can be affected, however, granulomas most often appear in the lungs or the lymph nodes.

Signs and symptoms

• Sarcoidosis is a systemic disease that can affect any organ. Common symptoms are vague, such as fatigue unchanged by sleep, lack of energy, aches and pains, dry eyes, blurry vision, shortness of breath, a dry hacking cough or skin lesions. The cutaneous symptoms are protean, and range from rashes and noduli (small bumps) to erythema nodosum or lupus pernio
• Renal, liver, heart or brain involvement may cause further symptoms and altered functioning. Manifestations in the eye include uveitis and retinal inflammation
• Sarcoidosis affecting the brain or nerves is known as neurosarcoidosis.
• Hypercalcemia (high calcium levels) and its symptoms may be the result of excessive vitamin D production
• Sarcoidosis most often manifests as a restrictive disease of the lungs, causing a decrease in lung volume and decreased compliance (the ability to stretch). The vital capacity (full breath in, to full breath out) is decreased, and most of this air can be blown out in the first second. This means the FEV1/FVC ratio is increased from the normal of about 80%, to 90%.

Treatment

Corticosteroids, most commonly prednisone

2. Cystic fibrosis

a. Transmission: caused by a genetic mutation (nucleotide deletion) on chromosome 7, resulting in abnormal chloride channels.

b. The most common hereditary disease in Caucasians.

c. Genetic transmission: autosomal recessive.

d. Affects all exocrine glands. Organs affected include lungs, pancreas, salivary glands, and intestines. Thick secretions or mucous plugs are

seen to obstruct the pulmonary airways and intestinal tracts.

e. Is ultimately fatal.

f. Diagnostic test: sweat test—sweat contains increased amounts of chloride.

3. Atelectasis

a. Characterized by collapse of the alveoli.

b. May be caused by a deficiency of surfactant and/or hypoventilation of alveoli.

Causes of disease

The causes of disease Diseases can be caused by either environmental factors, genetic factors or a combination of the two.

A. Environmental factors

Environmental causes of disease are many and are classified into:

 1. Physical agents

 2. Chemicals

 3. Nutritional deficiencies & excesses

 4. Infections & infestations

 5. Immunological factors

 6. Psychogenic factors

 1. Physical agents

These include trauma, radiation, extremes of temperature, and electric power. These agents

apply excess physical energy, in any form, to the body.

2. Chemicals

With the use of an ever-increasing number of chemical agents such as drugs,

3. Nutritional deficiencies and excesses

Nutritional deficiencies may arise as a result of poor supply, interference with absorption, inefficient transport within the body, or defective utilization. It may take the form of deficiency.

4. Infections and infestations

Viruses, bacteria, fungi, protozoa, and metazoa all cause diseases. They may do so by causing cell destruction directly as in virus infections (for example poliomyelitis) or protozoal infections (for example malaria).

5. Immunological factors

A. Hypersensitivity reaction

This is exaggerated immune response to an antigen. For example, bronchial asthma can occur due to exaggerated immune response to the harmless pollen.

B. Immunodeficiency

This is due to deficiency of a component of the immune system which leads to increased susceptibility to different diseases. An example is AIDS.

C. Autoimmunity

This is an abnormal (exaggerated) immune reaction against the self antigens of the host. Therefore, autoimmunity is a hypersensitivity reaction against the self antigens. 4

6. Psychogenic factors

The mental stresses imposed by conditions of life, particularly in technologically advanced

communities, are probably contributory factors in some groups of diseases.

B. Genetic Factors

These are hereditary factors that are inherited genetically from parents.

Post viral (post hepatitic) cirrhosis (15-20%) 

Cause:- Viral hepatitis (mostly HBV or HCV) 
Acute hepatitis  → chronic hepatitis → cirrhosis.  

Pathology
Liver is shrunken.  Fatty change is absent (except with HCV). Cirrhosis is mixed.

M/E  :-
Hepatocytes-show degeneration, necrosis  as other types of cirrhosis. 
Fibrous septa   -They are thick and immature (more cellular and vascular).
- Irregular margins (piece meal necrosis).
- Heavy lymphocytic infiltrate.

Prognosis:- - More rapid course than alcoholic cirrhosis.Hepatocellular carcinoma is more liable to occur 
 

Nephrotic Syndrome
The patient will present with a triad of symptoms:
- Proteinuria, i.e. >3g/24hr-3.5g/24 hr
- Hypoalbuminaemia, i.e. <30g/L
- Oedema 
 >80% of cases are due to glomerulonephritis. In this syndrome, there is damage to podocytes 
 
 Clinical signs
- Pitting oedema, particularly in the limbs and around the eyes; may also cause genital oedema and ascites.
- Possible hypertension 

Causes
- Primary causes – these are diagnoses of exclusion that are only made if secondary causes cannot be found
    o Minimal change disease (MCD)
    o Focal segmental glomerulosclerosis
    o Membranous nephropathy
- Secondary causes – note that these fall into the same three categories as above:
    o Minimal change disease – Hep B, SLE, diabetes M, sarcoidosis, syphilis, malignancy
    o Focal segmental glomerulosclerosis –HIV, obesity, diabetes M, hypertensive nephrosclerosis
    o Minimal change disease –drugs, malignancy, particularly Hodgkin’s lymphoma  
    
 - Differential diagnoses include cardiac failure, i.e. increased JVP, pulmonary oedema and mild proteinuria, and liver disease, i.e. reduced serum albumin.
- The condition causes an increased susceptibility to infection – partly due to loss of immunoglobulin in the urine. Patients tend to be prone to streptococcus infection, as well as bacterial peritonitis and cellulitis.
- Nephrotic syndrome also increases the risk of thromboembolism and hyperlipidaemia.
- The former is due to an increase in the synthesis of clotting factors and to platelet abnormalities, and the latter is a result of increased synthesis of these by the liver to counteract reduced oncotic pressure.  

Investigations

- These are the same as those carried out in GN.
- Also, check for cholesterol as part of confirming the presence of hyperlipidemia.
- Renal biopsy – order this for all adults. In children, because the main cause is minimal change GN, steroids are the first-line treatment. Therefore, in children, biopsy is necessary only if pharmaceutical intervention fails to improve the situation.
- The hypercoagulant state seen in the nephrotic syndrome can be a risk factor for renal vein thrombosis. This can present as loin pain, haematuria, palpable kidney and sudden deterioration in kidney function. This should be investigated with Doppler USS, MRI or even renal angiography.
- Once diagnosed, give warfarin for 3 to 6 months.

Management

- Generally, this involves treatment of the underlying condition which is usually GN. Therefore, fluid management and salt intake restriction are priorities. The patient is usually given furosemide along with an ACE inhibitor and/or an angiotensin II receptor antagonist. Prophylactic heparin is given if the patient is immobile. Hyperlipidaemia can be treated with a statin. 

Nephritic Syndrome 

Acute and chronic
forms of the syndrome exist. The main difference between this and nephrotic syndrome is that in nephritic syndrome haematuria is present. There is also proteinuria, hypertension, uraemia, and possibly oliguria. The two standout features are hypertension and RBC casts. The urine will often appear ‘smoky’ in colour due to the presence of RBC casts. Very rarely, it may appear red 

Causes

1. Post-streptococcal
2. Primary:
- Membranous glomerulonephritis
- Rapidly progressive glomerulonephritis
- IgA nephropathy (Berger’s disease)
3. Secondary
- HSP
- Vasculitis

Clinical Features

- Abrupt onset of :
    o Glomerular haematuria (RBC casts or dysmorphic RBC)
    o Non-nephrotic range proteinuria (< 2 g in 24 hrs)
    o Oedema (periorbital, sacral )
    o Hypertension
    o Transient renal impairment (oliguria, uraemia)
- Urinary casts – these are cylindrical structures produced by the kidney and present in the urine in certain renal diseases. They form in the DCT and collecting duct, dislodging and passing in the urine where they are detected by microscopy. RBC casts are usually associated with nephritic syndrome. The presence of RBCs within a cast is always pathologic and strongly indicative of glomerular damage.
- The proteinuria present is often smaller than in nephrotic syndrome, thus a coexistent condition of nephrotic syndrome is not usually present.
- Encepelopathy may be present, particularly in children, due to electrolyte imbalances and hypertension. This type of presentation is indicative of glomerular damage, but requires renal biopsy to determine the exact problem. In this respect it is similar to nephrotic syndrome.
Overlapping of the two syndromes is possible as nephrotic syndrome may precede nephritic syndrome, although not vice-versa.

Mechanisms of the syndrome vary according to cause; both primary and secondary causes exist. Post-infectious GN is the classic illustration of nephritic syndrome, but the condition may be caused by other glomerulopathies and by systemic diseases such as connective tissue disorders 

Two clinical terms to remember:
- Nephritic syndrome; which comprises edema, proteinuria, hypoalbuminemia, hematuria (smoky urine), oligurua and hypertension.
- Nephrotic syndrome; which comprises of albuminuria, hypoalbuminemia, edema, hyperlipidemia, lipiduria.