Month: November 2015

Definition:- Typhoid fever is an acute communicable disease caused by Salmonella typhi . The disease is marked by prolonged fever, toxic symptoms& constitutional disturbances.
The term “enteric fever” includes both typhoid & paratyphoid fevers.
Epidemiological factors:-
(1) Agent:- Salmonella typhi is responsible for 95% of cases. S. para A is responsible for about 5% of cases.
(2) Source of infection:- patients & carriers of typhoid fever
(3) Infective material:- Faeces and urine of infected persons.
(4) Age:-The diseases affects all age groups, but more commonly between 5 and 19 years.
(5) Immunity:- An attack of typhoid fever gives a fairly lasting immunity. Second attacks may also occur.
(6) Poor sanitation:- Lack of sanitation and safe water are involved in transmission.
(7) Unhygienic habits:- Open air defecation , urination, low standards of food hygiene, illiteracy & health ignorance are responsible for the endemicity of typhoid fever in India.
(8) Mode of transmission:- Faecal –oral & urine- oral routes.
(9) Incubation period:- 7 to 28 days.
Control of typhoid fever:-
Several control measures are common to all gastro-intestinal diseases. These are discussed in the section on “Control of Cholera”
The principles of control of typhoid fever are given below:-
(1)Patients
• Notification
• Isolation
• Treatment:-Fluroquinolone e.g.ofoxacin or ciprofloxacin, cefixime, azithromycinetc.
• Proper disposal of feaces urine.
• Disinfection of clothing , linen and fomites.
• Immunization of contents with typhoid fever
(2) Community
• Immunization with typhoid fever vaccine
• Provision of safe water & improvement of sanitation.
• Food sanitation:- protection of food from flies dust, preventing from carriers.
• Detection of typhoid carriers and treating them.
• Health education in matters of food & personal hygiene.
Anti typhoid vaccines:- The anti- typhoid vaccine currently manufactured in India is –
— monovalent & bivalent
— Heat killed
–Phenol-preserved vaccine

Description:-POLIOMYLITIS
Definition:-Poliomyelitis is a virus infection. It is primarily an infectious disease of the human alimentary tract, but may affect the brain, spinal cord & nerves resulting in paralysis.
Polio does not always cause paralysis.
Epidemiological factors:-
(1)Agents:- The causative agents is polio virus which has 3 serotypes designated as type1, type2& type 3. Type 1 is responsible for all major epidemics.
(2) Sources of infection:– Faeces mostly in young children
–Pharyngeal secretions
(3)Age:- The majority of cases contract polio between 1&2 years.
(4) Environmental conditions:– Overcrowding , poor sanitation,
rainy season, rural& urban areas.
(5) Mode of transmission:– Faecal-oral route by contaminated
Water,food or flies.
–Droplet infection from nasopharynx
(6)Incubation period:- 7-21 days (range 3-35 days)

Clinical Features:- 90% of cases are asymptomatic , about 8 % suffer from mild illness ,& 1-2 % are severely affected.
Other symptoms:-
• Fever
• Headache
• Diarrhea& vomiting
• Drowsiness
• Pain, weakness & stiffness of neck & back
• Paralysis of affected limb
Diagnosis Investigations:-
• Serological testing for polio viral antibiotics.
• X-ray
• Physical examination
Prevention:-
(1)Polio can be prevented by active immunization of all infects & children.
(2) The vaccine widely used is oral polio vaccine (OPV) which is a Sabin type of vaccine.
(3)It can also be administered soon after birth.
(4)Hot milk & hot fluids should not be given for at least half an hour after the administration.
(5)Recent studies indicate that breast feeding does not impede the effectiveness of OPV.
(6) Breast milk can be given whenever the child Hungary.
(7) A point of great importance is that polio vaccine should be stored at sub – zero temperature in a deep freeze to prevent inactivation.
Strategies for polio eradication in India:-
(1) Conduct pulse polio immunization days every year until poliomyelitis is eradicated.
(2)Sustain high levels of routine immunization coverage.
(3)Monitor OPV coverage at district level & below
Key Words:-
(1) Pulse polio
(2) Vaccine
(3)Paralysis
(4)sign & symptoms
(5)faecal route

DESCRIPTION:-
INTRODUCTION- plague epidemic had been a cause of many deaths in the world. In Bhagwat Purana and Bible also, plague is described as an epidemic.
This is also called ‘black death’. The bacteria’s are responsible for the disease pasteurella pastis. This spreads through the bite of fleas which gets the infection from sick rates. Fleas are found on rates and rodents.
EPIDEMIOLOGICAL FACTORS –
• Bacteria are found on wild rodents like rates, carnivorous animals, and in other smaller animals.
• In India source of plague is wild rodents. But the fleas living on rates are the fleas living on rates are the main source of plague against the disease.
• Along with infected rates and fleas, pneumonic plague patients are also responsible for the spread of the disease.
• Plague is transmitted by direct contact with the tissues of infected animals.
• Disease spreads more in winter. During heavy rain the rat holes are destroyed and the chances of spreading of plague becomes less.
INCUBATION PERIOD- This depends upon the type of plague and may range from 1 to 7 days.
CLINICAL MENIFESTATION- Three types of plague are found in humans:
 Bubonic plague
 Pneumonic plague
 Septicaemic plague
The beginning of bubonic plague is sudden with fever, shivering and headache. Face and eyes turn red and person feels extremely tired. Pain and swelling develop in all the lymph glands especially in the thigh.
This plague does not spread from one person to another because infection is locked in buboes and they cannot get out.
DIAGNOSISTIC TESTS-
• Smear examination of secretion of glands, fluids and sputum.
• Blood culture.
• Serum examination
COMPLICATION-
Intensive bleeding, pneumonia, toxicity, death
MANAGEMENT-
 Controlling the disease through early diagnosis, notification and isolation is the primary necessity in the management.
 Streptomycin is given.
 Tetracycline is also given.
 Control of fleas.
 Use plague vaccines.
 Health education.
 Prevention.

DESCRPITION
DEFINITION
The inflammation of meninges (membranes surrounding the brain and spinal cord) which is caused by viral, bacterial or fungal organisms.
Classification
There are three classifications –
1. Aseptic – viral or causes or meningeal irritation from other causes such as brain abscess, encephalitis, leukaemia etc.
2. Septic — bacterial origin ex. Meningococcus, Neisseria meningitides, Staphylococcus, Influenza Bacillus.
3. Tuberculous – Tubercle Bacillus

Pathophysiology
The causative organisms enter the blood stream, cross the blood brain barrier, and trigger an inflammatory reaction in the meninges. Independent of the causative agents, inflammation of the subarachnoid and piamater occurs. Increased intra cranial pressure results. Meningeal infections generally originate in one of two ways: either through the blood stream from other infections or by direct extensions. In a few cases, the cause is iatrogenic or secondary to invasive procedures or devices.
Bacterial meningitis is the most significant form. The common bacterial pathogens are Neisseria meningitides, Streptococcus, Pneumoniae and Haemophylus Influenzae.
Clinical signs
Headache, Neck stiffness, Photophobia (intolerance to bright light), Irritability
Changes in level of consciousness, disorientation, memory impairment
Behavioural changes, coma
Positive Kernig’s sign
Vomiting bradycardia, increased ICP (intra cranial pressure)
Phonophobia (intolerance to loud noises)
Abnormal skin colour, cold extremities
Petechial rash
Morphology
• Grossly, pyogenic meningitis shows a thick layer of supportive exudates covers the leptomenings over the surface of the brain.
Diagnosis
• Culture of CSF
• Blood culture
• Urine specimen
• MRI
• CT-Scan

Management
1. Medical management
• Antimicrobial therapy- penicillin, ampicillin chloramphenicol
• Vancomycin, along with refampin is given for bacterial infection
• For dehydration or shock, fluid volume expenders are given
• Seizures are controlled by diazepam or phentoin
• Osmotic diuretics used to treat cerebral edema ex. Mannitol

2. Nursing management
• Management resolve around, prevention of dehydration, electrolytes imbalance and edema and fever.
• Body weight, serum electrolyte and urine volume are closely monitored.
• Arterial pressure is monitored to asses cardiac or respiratory failure and risk of shock
• Asses the patient neurologic status.
• Watch for cyanosis, cold extremities.
• Administer I.V. (intra venous) fluids and medications.
• Monitor vital signs and neurological status.
• Provide basic patients need care.
Complications
The complications of meningitis can be severe. The longer persistent in a human and child without treatment, the greater the risk of seizures permanent neurological damage including-
• Hearing loss
• Memory difficulty
• Learning disabilities
• Brain damage
• Gait problems
• Seizures
• Kidney failure

Description:– It is commonly known as Angina; is chest pain often due to Ischemia of the heart muscle , due in general to obstruction or spasm of the coronary Arteries.
The term derives from the Latin Angina (infection of the throat) and the Latin pectus (Chest) and can therefore, be translated as “a strangling feeling in the chest”
There is a weak relationship between severity of pain and degree of oxygen deprivation in the heart muscle
Classification:- the angina pectoris has classified under 2 category that is-
1) Stable Angina
2) Unstable Angina

1) Stable Angina:- Also known as effort Angina, this refers to the more common understanding of angina related to Myocardial Ischemia. Typicl presentation of stable angina is that of chest discomfort and associated symptions precipitated by some activity (running, walking, etc) with minimal or non existent symptoms at rest or with administration of sublingual nitroglycerin. Symptoms typically abate several minutes following cessation of precipitating activities and recur when activity resumes. In this way, stable angina may be thought of as being similar to intermittent claudication symptoms.

2) Unstable Angina(UA):- It is define ass angina pectoris that changes or worsens .
It has at least one of these 3 features:
a) It occur at rest, usually lasting 3-5 min. is severe and of new onset(i.e., within the prior 4-6 weeks)
b) It occur with a crescendo pattern(i.e., distinctly more severe prolonged or frequent than before)
c) It may occur unpredictably at rest, which may be a serious indicator of an impending heart attack.
The pathophysiology of UA is the reduction of coronary flow due to transient platelet aggregation on apparently normal endothelium, coronary artery spasms or coronary thrombosis
Cause:-
1). Major risk factors; > Age(> 55 year for men, > 65 for women)
> Cigarette smoking
> Diabetes mellitus
> Family history of premature cardiovascular disease
> Hypertension
– kidney disease
2) Other medical problems;
Profound Anemia, uncontrolled Hypertension, Hyperthyroidism and hypoxemia

Signs and symptoms:- Angina pectoris can be quite painful, but many patients with angina complain of chest discomport rather than actual pain
The discompert is usually described as:-
A pressure, heaviness, tightness, squeezing, burning, or choking sensation
– In this case , the BP and pulse rate increases
– Myocardial ischemia
– Autonomic Symptoms like nausea
– , vomiting, and pallor
Major risk factors Angina pectoris:-
1) Smoking,
2) Diabetes,
3) High cholesterol,
4) High BP,
5) Sedentary lifestyle and
6) Family history of premature heart diseases

Treatment:-
 The most specific medicine to treat Angina is NITROGLYCERIN.
 Balloon Angioplasty
 Coronary bypass surgery
 Beta blocker (atenolol,propranolol)
 Calcium channel blockers (nifedipine,amlodipine)

Definition:-
It may be define as administration of blood &blood components by iv route. It is known as blood transfusion.
Pre transfusion assessment:-

1. Patients history:-
Collect the patients history about previous transfusionor as well as previous reaction to transfusion.
2. Physical assessment:-
A baseline vital sign are important before transfusion of the blood.
3. Preparation of the patient environment:-
a. Explain the procedure to the patient
b. Provide the food & fluid as patient need .
c. Assess or note the vital sign of the patient .
d. Provide comfortable position
e. Clear all the doubts of the patients well as family member regarding blood transfusion.
f. Maintain the proper lighting.
Selection of the donor:-
1. Donor should be free from the infectious disease.
2. Vital sign should be normal
3. He did not given blood from last 3 months
4. Hb level should be normal
5. Blood cross matching should be done
Selection of the receiver:-
1. Assess the blood group.
2. Note the vital sign
Procedure:-
1. Wash the hands
2. Confirm the transfusion had been prescribed
3. Check the patient for blood grouping verify that patient has sign a written consent form as per as agency policy.
4. Explain the procedure to the patient
5. Instruct the patient about sign & symptoms during transfusion such as nausea , vomiting etc.
6. Monitor vital sign use hand hygiene & wear gloves .
7. Set the blood bottles on iv poles
8. Fix the cannula in the vein
9. Connect the cannula from blood set
10. Monitor vital sign throughout the transfusion. If there is any changes in transfusion or allergic reaction then,
a. Stop the transfusion
b. Inform the dutry doctor
c. Keep ready loaded inj.dexomethasone & avil.
After the complete of transfusion remove the iv line or set 7 press the vein with cotton.
After blood transfusion record & report should be maintain by the nurse it incluse:-
a. Type of blood which is transfused
b. Amount of blood
c. Flow rate of the transfusion
d. Any reaction which occur during the procedure.
e. Name of the donor
f. Written consent for medicolegal purpose.