COUGH (Health Tips)

 Noisy expulsion of air from lungs, at once is known as cough.

Causes

Acute (3 weeks)

• Upper respiratory viral or bacterial infection such as common cold and acute bronchitis.
• Other causes acute asthma, pneumonia, pulmonary embolism and pulmonary adema.

 Chronic

• Chronic bronchitis (smoker’s cough)
• Postnasal drip, gastroesophageal reflux disease
• Chronic bronchial asthma
• Tuberculosis
• Interstitial lung disease
• Bronchogenic carcinoma
• ACE inhibitors

 Treatment

Eliminate irritant exposure such as tobacco smoke, occupational agents and discontinue ACE inhibitors and beta-blockers.

Treatment of the cause

·         Common cold: antihistamine and decongestant combination.

·         Asthma: bronchodilators and corticosteroids.

·         Postnasal drip: intranasal steroid spray such as Nasacort AQ.

Symptomatic treatment

Dry cough

Syp: Actified DM

Syp: Pholcodine

Syp: Davenol

Syp: Tixylix

Syp: Sancos

Syp: Benatuss

Syp: Hydryllin DM

Productive cough: (Expectorants)

Syp: Hydryllin

Syp: Benadryl

Syp: Reltus

Syp: Histamol-D  

 Examination of sputum

 Quantity

• Scanty: Bronchitis, early stage of pneumonia, asthma.
• Moderate amount: Chronic bronchitis, tuberculosis.
• Large amount: Bronchiectasis, chronic bronchitis, and lung abscess.

 Appearance

• Watery: Pulmonary congestion, pulmonary edema.
• Mucoid: Acute & chronic bronchitis, asthma.
• Mucopurulent: All infections of lungs & bronchi.
• Purulent: Bronchiectasis, lung abscess, pulmonary tuberculosis.

 Color

• Blockish: due to inhalation of carbon.
• Rusty (khaki): due to altered blood mixed with sputum in lobar pneumonia.
• Reddish: indicates hemoptysis.
• Frothy pink: in pulmonary edema.
• Sticky brown to red: in Klebsiella infection.

 COUGH  (Health Tips)

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SHORTNESS OF BREATH (DYSPNEA)

Shortness of breath is an unpleasant subjective awareness of the sensation of breathing. Patient usually feels discomfort either from increased ventilatory drive or reduced ventilatory capacity.

Increased ventilatory drive causing increased respiratory rate occurs in:

• Fever
• Exercise
• Acidemia: ketoacidosis, lactic acidosis, uremia
• Hypoxia: asthma, COPD, cyanotic heart diseases.
• Hypercarbia: COPD

Reduced ventilatory capacity occurs in:

• Reduced lung volume in pneumonia, pulmonary edema and interstitial lung disease
• Pleural pain
• Increased resistance to airflow in asthma, COPD, laryngeal obstruction.

PATIENT EVALUATION

History

• Ask about cardiac and respiratory risk factors such as:
• Diabetes, hypertension, smoking for heart disease
• Asthma, COPD and tuberculosis for respiratory disease
• Renal disease for uremia
• Medication for lactic acidosis
• History of previous similar episodes and their diagnosis
• Associated features such as palpitation, syncope, chest pain, nausea, vomiting and sweating are cardiac manifestations while cough, chest pain related to breathing, sputum are features of respiratory disease and low urine output and anemia indicate renal disease.
• In acute, dyspnea, rule out cardiac failure, heart block, MI, angina, pulmonary embolism, pneumothorax and laryngeal edema.
• Chronic dyspnea is progressive i-e patient’s working capacity gradually decrease. Chronic episodic dyspnea occurs in asthma, heart failure, acute or chronic bronchitis and recurrent pulmonary embolism. Chronic constant dyspnea occurs in COPD, pulmonary fibrosis and pulmonary hypertension.

Examination

Quick and relevant examination related to cardiac disease such as pulse showing tachycardia, bradycardia, irregular pulse, displaced apex beat, murmurs and basal crepts.

Respiratory examination such as rapid respiratory rate, abnormal percussion note, wheeze, crepts or pleural rub.

Investigations

ECG, chest X-ray, ABGs, RBS, urea and creatinine are usually enough for diagnosis.

Shortness of breath
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HEPATITIS C

• Hepatitis C virus (HCV) is a RNA virus
• Mode of transmission: Blood and blood products, IV drug abuse, sexual contact (low risk), vertical transmission from infected mother to child, transmission via breast feeding has not been documented.
• Hepatitis C virus (HCV) caused 90% of post-transfusion hepatitis before serological tests that allowed the screening of blood donors. Intravenous drug abusers are at high risk of HCV infection.
• Incubation period averages 6-7 weeks.
• More than 85% of cases lead to chronic hepatitis. Cirrhosis develops in 20-30% within 5-30 years and about 15% develop hepatocellular carcinoma. Male patients and people acquiring infection over 40 years have more rapid development fibrosis.
• Hepatitis C may be a pathogenic factor in glomerulonephritis, autoimmune thyroiditis, idiopathic pulmonary fibrosis and probably lymphoma.

Clinical features

In acute hepatitis C clinical illness is often mild, usually asymptomatic with about 10% of patients have mild, flue-like illness and a rise in serum aminotransferases. Most of the patients are diagnosed years later with complications of chronic liver disease.

Diagnosis

Diagnosis of hepatitis C is frequently by exclusion with negative markers for hepatitis A and hepatitis B. HVC RNA (PCR) is positive 1-2 weeks after infection. Anti-HCV antibodies in serum take 6 weeks to develop.

Treatment

Alpha interferon for 6-24 weeks in acute hepatitis decreases risk of chronic hepatitis. 

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HEPATITIS B ( Health tips)

 1. Mode of spread:

• Intravenous route: Transfusion of infected blood or blood products. Contaminated needles used by drug addicts, tattooists or acupuncturists.
• Sexual intercourse with infected person because virus is present in salvia, semen and vaginal secretions.
• From infected mother to child at the time of delivery.

2. High risk persons are IV drug abusers, patients and staff and hemodialysis centers,    homosexuals physicians, dentists, nurses and persons working in pathological laboratory and blood bank.

3. The risk of fulminant hepatitis is in 1-2% of persons with acute disease.

4. Can lead to chronic hepatitis, carrier state or hepatocellular carcinoma.

5. Perinatally infected infants generally have no clinical signs or symptoms, and infection produces typical illness in only 5-15% of children aged 1-5 years.

6. Incubation period: 1-6 months.

HEPATITIS B VIRUS (HBV)

Hepatitis B virus is a DNA virus also called Dane partcle; it consist of an inner core and an outer surface capsule.

The inner core is formed of core protein (hepatitis B core antigen-HBcAg). Core protein contains DNA and DNA polymerase. The capsule protein is referred to as hepatitis B surface antigen (HBsAg). Hepatitis B virus also contains e antigen (BHeAg).

VIRAL MARKERS

The hepatitis B virus proteins act as antigens to which infected person can make antibodies. These antigens an their antibodies are important in identifying hepatitis B virus infection; these are called viral markers.

1. Hepatitis B surface antigen (HBsAg).

• It is located in the capsular material of virus and is the first viral marker detectable after infection with hepatitis B.
• It appear in the blood in late incubation period before the elevation of aminotransferases and development of clinical features hepatitis.
• If becomes undetectable usually after 1-2 month after the onset of jaundice and rarely persists beyond 6 months. In chronic hepatitis it remains detectable beyond 6 months.

5. Antibodies to hepatitis B surface antigen (anti-HBs)

• Anti-HBs usually appear after clearance of surface antigen and persist for many years or perhaps permanently. Occasionally appearance of anti-HBs is delayed for several weeks of disappears of surface antigen (i.e. no antigen and no antibody detectable); this is called window period. During this period patient is infectious, therefore negative surface antigen does not rule out infection. If doubt is there, perform anti-HBc 1gM to confirm the infection.
• Presence of these antibodies indicates previous infection or vaccination.
• Disappearance of HBsAg and appearance of anti-HBs indicate recovery from HBV infection.

3. Hepatitis B core antibodies (anti-HBc)

• Hepatitis B core antigen (HBcAg) is located in the central part of the virus but it does not appear in the blood.
• Anti-HBc is the first antibody to appear, it appears shortly after HBsAg is detected. 1 gM type of Anti-HBc is a definitive evidence of acute infection and is predominant in first 6 months. 1 gG type of anti-HBc appear during acute hepatitis and is predominant beyond 6 months and persist indefinitely, whether the patient recovers (in which anti-HBsAg is also present) or develop chronic hepatitis (in which HBsAg is also present).

4. Hepatitis B 2 antigen (HBcAg).

• HBeAg appears during incubation period shortly after detection of HBsAg. It indicates viral replication and infectivity.
• Persistence of HBeAg in serum beyond 3 months suggests and increased likelihood of chronic hepatitis-B and presence of HBeAg during chronic hepatitis B is associated with ongoing viral replication, infectivity and inflammatory liver injury.
• Disappearance of HBeAg is followed by the appearance of anti-HBe indicating diminished viral replication and decreased infectivity.
• Some rare mutant forms of virus cannot synthesize the “e” antigen (pre-core mutant) and PCR for HBV DNA is required to confirm viral replication. Majority of hepatitis B virus is “wild type” that synthesizes ‘e’ antigen (HBeAg).
• HBsAg-positive serum containing HBeAg is more likely to be highly infectious. For example mothers with HBsAg and HBeAg transmit hepatitis B infection to their offspring in more than 90% while mothers with HBsAg with anti-HBe rarely infect their offspring.

5. Hepatitis B virus DNA (PCR for hepatitis B)

The presence of hepatitis B virus DNA in serum is a more sensitive marker of viral replication and infectivity. It can be detected by polymerase chain reaction (PCR) method.

Significance of viral markers in hepatitis B

• HBeAg: present in acute or chronic infection.
• HBeAg: rises early and fall rapidly in acute hepatitis, persistence indicates development of chronic hepatitis and increased sensitivity.
• HBV DNA (PCR): implies viral replication.
• Anti-HBe: indicates previous exposure and immunity to HBV.
• Anti-HBe: indicates diminished viral replication and low infectivity.
• Anti-HBc:

IgM: high titer in acute and low titer in chronic infection.

      IgG: indicates past exposure to hepatitis B.

      Patient may be recovered or developed chronic hepatitis.

Clinical application to viral markers.

·         Identify hepatitis B infection (HBsAg).

·         Identify either acute or chronic infection (anti-HBc antibodies).

·         Identify virus replication (HbeAg) that is required for treatment with interferon.

CLINICAL FEATURES

• Clinical features are similar to hepatitis A although the illness may be more sever; however infection may be asymptomatic.
• In addition, a serum sickness-like immunological syndrome may be seen in acute hepatitis during prodromal stage in up to 25% of cases. This consists of rashes (e.g. urticaria, maculopapular rash, Henoch-Schonlein purpura and polyarthritis affecting small joints.
• Fever is usually present.

Extrahepatic immune complex-mediated conditions such as polyarteritis nodosa, or glomerulonephritis are occasionally seen.

INVESTIGATIONS

Non-specific

LFTs, complete blood count, urine analysis, PT and blood sugar-as performed in  hepatitis A.

Specific

• HBsAg and anti-HBc 1gM should be performed. If HBsAg is positive, a full viral profile is then performed.
• In routine HBsAg is performed but it may be profile is then performed.
• In routine HBsAg is performed but it may be cleared rapidly or titer is very low, therefore anti-HBc IgM should also be performed simultaneously.
• HBV DNA (PCR) is the most sensitive test of viral replication.

COMPLICATIONS

1. Fulminant hepatic failure.
2. Post hepatitis syndrome: fatigue, fat intolerance and right upper quadrant pain.
3. Chronic hepatitis.
4. Cirrhosis.
5. Hepatocellular carcinoma.
6. Rare complications of viral hepatitis are as follows:
• Pancreatitis, myocarditis
• Atypical pneumonia
• Aplastic anemia
• Transverse myelitis
• Peripheral neuropathy 

HEPATITIS A (Health Tips)

1. This is the most common type of viral hepatitis, highly infectious and is caused by hepatitis A virus. This disease commonly affects children and young adults.
2. Spread of infection is mainly by the oro-fecal route and arises from the ingestion of contaminated water and food (e.g milk). Overcrowding and poor sanitation facilitate the spread. Infected person excretes virus in the feces for about 2 weeks before the onset of clinical illness and for up to 7 days after.
3. Hepatitis A is maximally infectious just before the onset of jaundice. Blood and stools are infectious during the incubation period (2-6 weeks) and during early illness.
4. Clinical illness is more severe in adults than in children.
5. No carrier state, complete recovery, does not lead to chronic hepatitis.
6. Mortality is low and fulminant hepatitis is uncommon except in cases where hepatitis A occurs in a patient with chronic hepatitis C.
7. incubation period 2-6 weeks.

 DIAGNOSIS

Antibody to hepatitis A (anti-HAV) appears early in the course of the illness. Detection of 1gM anti-HAV is and excellent test for diagnosis of acute hepatitis A. Peak titers of 1gM occur during the first week of clinical disease and usually disappear within 3-6 months. Titers of 1 gG peak after one month of the disease and may persist for years.

CLINICAL FEATURES

Pre-icteric or prodromal phase

This phase of constitutional symptoms precedes the onset of jaundice by 1-2 weeks. Onset may be abrupt or insidious.

• Initially there is flue-like illness such as malaise, easy fatigability, headache, arthralgia, myalgia and upper respiratory symptoms e.g. nasal discharge, cough and pharyngitis.
• Anorexia: Out of proportion to the degree of illness.
• Nausea, vomiting are frequent, diarrhea or constipation may occur.
• Mild fever (100-102-F) with chills is usually present.
• Abdominal pain: mild and constant pain in right upper quadrant or epigastrium due to stretching of capsule of enlarged liver.
• Dark-colored urine (due to bilirubinuria) may be noticed

 Icteric phase

After 1-2 weeks patient develops jaundice. This phase is called icteric phase. With the onset of jaundice there is often improvement of the prodromal symptoms. Features of this phase are:

• Jaundice occurs in most (70-85%) adults with acute HAV infection. Jaundice is less likely in children and is uncommon in infants. The degree of icterus also increases with age.
• Liver becomes enlarged and tender with pain in right hypochondrium due to stretching of liver capsule.
• Splenomegaly and cerical lymphadenopathy are present in 10-20% of patients particularly in children.
• Dark colored urine, pale stool due to intrahepatic cholestasis

.Convalescent phase

This recovery phase comes within 3-6 weeks of illness and is characterized by increasing sense of well being, return of appetite and disappearance of jaundice, abdominal pain and tenderness.

COURSE OF HEPATITIS A

The acute illness subsides over 2-3 weeks with complete clinical and laboratory recovery by 9 weeks. Less than 1% develop acute fulminant hepatic failure. Relapse may occur in hepatitis A but ultimate recovery is the rule.

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