PATHOLOGY...
DIAGRAMS ARE NECESSARY
SHORT NOTES
(5 MARKS)
1) DEFINE THROMBOSIS CLASSIFY AND WRITE DETAIL ABOUT ARTERIAL THROMBOSIS
Thrombosis (from Ancient Greek thrómbōsis "clotting”) is the formation of a blood clot inside a blood vessel, obstructing the flow of blood through the circulatory system. When a blood vessel (a vein or an artery) is injured, the body uses platelets (thrombocytes) and fibrin to form a blood clot to prevent blood loss. Even when a blood vessel is not injured, blood clots may form in the body under certain conditions. A clot, or a piece of the clot, that breaks free and begins to travel around the body is known as an embolus.[1][2]
Thrombosis may occur in veins (venous thrombosis) or in arteries (arterial thrombosis).
Arterial thrombosis is a blood clot that develops in an artery. It's dangerous as it can obstruct or stop the flow of blood to major organs, such as the heart or brain. If a blood clot narrows one or more of the arteries leading to the heart, muscle pain known as angina can occur
cassification;
venous thromboembolism (VTE) – a blood clot in a vein. DVT (deep vein thrombosis) – a blood clot in one of the deep veins in the body, usually in the leg. embolism – where the blood flow in an artery is blocked by a foreign body; this can be a blood clot or something else such as an air bubble.
2) DEFINE INFLAMMATION CLASSIFY AND WRITE A NOTE ON ACUTE INFLAMMATION
Inflammation is a process by which the body's white blood cells and substances they produce protect us from infection with foreign organisms, such as bacteria and viruses. ... In these diseases, called autoimmune diseases, the body's normally protective immune system causes damage to its own tissues.
ACUTE INFLAMMATION;
Inflammation refers to the initial physiological response to tissue damage, such as that caused by mechanical, thermal, electrical, irradiation, chemical, or infection.
It can be acute (lasting for a few days) or chronic (in response to an ongoing and unresolved insult). Inflammation can develop into permanent tissue damage or fibrosis.
Characteristic Features
Acute inflammation begins within seconds to minutes following injury to tissues. It is characterised by four key features (Latin terms in brackets):
Redness (rubor) – secondary to vasodilatation and increased blood flow
Heat (calor) – localised increase in temperature, also due to increased blood flow
Swelling (tumour) – results from increased vessel permeability, allowing fluid loss into the interstitial space
Pain (dolor) – caused by stimulation of the local nerve endings, from mechanical and chemical mediators
3) DEFINE EMBOLISM
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An embolism is the lodging of an embolus, a blockage-causing piece of material, inside a blood vessel.[1] The embolus may be a blood clot (thrombus), a fat globule (fat embolism), a bubble of air or other gas (gas embolism), or foreign material. An embolism can cause partial or total blockage of blood flow in the affected vessel.[2] Such a blockage (a vascular occlusion) may affect a part of the body distant from the origin of the embolus. An embolism in which the embolus is a piece of thrombus is called a thromboembolism.
An embolism is usually a pathological event, i.e., accompanying illness or injury. Sometimes it is created intentionally for a therapeutic reason, such as to stop bleeding or to kill a cancerous tumor by stopping its blood supply. Such therapy is called embolization.
TYPES;
Main types : pulmonary embolism (usually from a leg thombosis), arterial embolism (usually from a clot formed in the heart), and air embolism
AIR EMBOLISM;
A blockage of blood supply caused by air bubbles in a blood vessel or the heart.
Causes of an air embolism include trauma, surgery and decompression sickness, the latter of which affects deep-sea divers.
Breathing difficulty, chest pain and confusion are symptoms.
Treatments include hospital care, oxygen, removing air from the heart and a high-pressure chamber.
4) WRITE DIFFERENCES BETWEEN BENIGN AND MALIGNANT TUMORS
BENIGN TUMORS;
A tumor is an abnormal growth of cells that serves no purpose. A benign tumor is not a malignant tumor, which is cancer. It does not invade nearby tissue or spread to other parts of the body the way cancer can. In most cases, the outlook with benign tumors is very good. But benign tumors can be serious if they press on vital structures such as blood vessels or nerves. Therefore, sometimes they require treatment and other times they do not.
Malignant
Malignant tumors are cancerous. They develop when cells grow uncontrollably. If the cells continue to grow and spread, the disease can become life threatening.
Malignant tumors can grow quickly and spread to other parts of the body in a process called metastasis.
The cancer cells that move to other parts of the body are the same as the original ones, but they have the ability to invade other organs. If lung cancer spreads to the liver, for example, the cancer cells in the liver are still lung cancer cells.
Different types of malignant tumor originate in different types of cell.
Examples include:
Carcinoma: These tumors form from epithelial cells, which are present in the skin and the tissue that covers or lines the body’s organs. Carcinomas can occur in the stomach, prostate, pancreas, lung, liver, colon, or breast. They are a common type of malignant tumor.
Sarcoma: These tumors start in connective tissue, such as cartilage, bones, fat, and nerves. They originate in the cells outside the bone marrow. Most sarcomas are malignant.
5) DEFINE GANGRENE. CLASSIFY AND GIVE EXAMPLE FOR EACH
Dead tissue caused by an infection or lack of blood flow.
The death of tissue often occurs in the extremities or skin from loss of blood supply. The condition often affects toes, fingers and limbs, but can affect muscles and organs.
Symptoms include discoloured skin, severe pain followed by numbness and foul discharge.
Gangrene requires urgent care. Treatment includes antibiotics and removing dead tissue.
DRY GANGRENE;
Dry gangrene is a form of coagulative necrosis that develops in ischemic tissue, where the blood supply is inadequate to keep tissue viable. It is not a disease itself, but a symptom of other diseases.[10] The term dry is used only when referring to a limb or to the gut (in other locations, this same type of necrosis is called an infarction, such as myocardial infarction).[11] Dry gangrene is often due to peripheral artery disease, but can be due to acute limb ischemia. As a result, people with arteriosclerosis, high cholesterol, diabetes and smokers commonly have dry gangrene.
Examples are war zones and railway, machinery, and street accidents, if lacerated and bruised tissues are contaminated
Wet gangrene[edit]
Wet gangrene of the foot
Wet, or infected, gangrene is characterized by thriving bacteria and has a poor prognosis (compared to dry gangrene) due to sepsis resulting from the free communication between infected fluid and circulatory fluid. In wet gangrene, the tissue is infected by saprogenic microorganisms (Clostridium perfringens or Bacillus fusiformis, for example), which cause tissue to swell and emit a bad smell. Wet gangrene usually develops rapidly due to blockage of venous (mainly) or arterial blood flow.
for example), which cause tissue to swell and emit a bad smell. Wet gangrene usually develops rapidly due to blockage of venous (mainly) or arterial blood flow.
Gas gangrene[edit]
Main article: Gas gangrene
Gas gangrene is a bacterial infection that produces gas within tissues. It can be caused by Clostridium, most commonly alpha toxin-producing C. perfringens, or various nonclostridial species.[8][18] Infection spreads rapidly as the gases produced by the bacteria expand and infiltrate healthy tissue in the vicinity. Because of its ability to quickly spread to surrounding tissues, gas gangrene should be treated as a medical emergency.
example, Klebsiella pneumoniae in the context of diabetes).
6) DEFINE INFRACTION CLASSIFY AND GIVE EXAMPLES FOR EACH
Infarction is tissue death (necrosis) due to inadequate blood supply to the affected area. It may be caused by artery blockages, rupture, mechanical compression, or vasoconstriction.[1] The resulting lesion is referred to as an infarct[2][3] (from the Latin infarctus,
Classification;
White infarctions (anemic infarcts) affect solid organs such as the spleen, heart and kidneys wherein the solidity of the tissue substantially limits the amount of nutrients (blood/oxygen/glucose/fuel) that can flow into the area of ischaemic necrosis. Similar occlusion to blood flow and consequent necrosis can occur as a result of severe vasoconstriction as illustrated in severe Raynaud's phenomenon that can lead to irreversible gangrene.
Red infarctions (hemorrhagic infarcts) generally affect the lungs or other loose organs (testis, ovary, small intestines). The occlusion consists more of red blood cells and fibrin strands. Characteristics of red infarcts include:
occlusion of a vein
loose tissues that allow blood to collect in the infarcted zone
tissues with a dual circulatory system (lung, small intestines)
tissues previously congested from sluggish venous outflow
reperfusion (injury)[5] of previously ischemic tissue that is associated with reperfusion-related diseases,[6] such as myocardial infarction, stroke (cerebral infarction), shock-resuscitation, replantation surgery, frostbite, burns, and organ transplantation
Common Examples Of Infractions
Traffic violations (although sometimes these can rise to the level of misdemeanors and felonies)
Littering.
Boating violations.
Fishing without a license.
Building permit violations.
Operating a business without a proper license.
Jaywalking.
Drinking in public
7) WRITE DIFFERENCES BETWEEN REGENERATION AND REPAIR
refer book
8) WRITE DIFFERENCES BETWEEN LEPROMATOUS AND TUBERCULOID LEPROSY
Lepromatous leprosy is a form of leprosy characterized by pale macules in the skin.[1]:346
It results from the failure of Th1 cell activation which is necessary to eradicate the mycobacteria (Th1 response is required to activate macrophages that engulf and contain the disease). In lepromatous leprosy, TH2 response is turned on, and because of reciprocal inhibition (IL-4; IL-10), the cell-mediated response (TH1) is depressed. Lepromatous leprosy, in contrast to the tuberculoid form of leprosy, is characterized by the absence of epithelioid cells in the lesions. In this form of leprosy Mycobacterium leprae are found in lesion in large numbers. This is the most unfavorable clinical variant of leprosy.[2][3]
This debilitating form of leprosy begins to spread causing the eyebrows to disappear and spongy tumor like swellings appear on the face and body. The disease attacks the internal organs, bones, joints and marrow of the body resulting in physical degeneration
TUBERCULOID LEPROSY;
Tuberculoid leprosy is a milder, less severe form of leprosy. People with this type have only one or a few patches of flat, pale-colored skin (called paucibacillary leprosy). The affected area of skin may feel numb because of nerve damage underneath. Tuberculoid leprosy is less contagious than other forms.
9) PATHOGENESIS OF SYSTAMIC HYPERTENSION
Systemic hypertension can be regarded as a quantitative disorder of blood pressure regulation. No single cause of hypertension has been identified, and it is likely that different mechanisms may be dominant in different individuals. In patients with sustained hypertension, there is usually increased peripheral resistance and normal cardiac output. The hemodynamic pattern of hypertension appears to vary according to the subject's age. Factors that may increase peripheral resistance are a decrease in the number of arterioles, changes in the caliber of the arterioles and increase in blood viscosity. Possible components of increased vascular tone in hypertensive patients include elevation of levels of circulating catecholamines and angiotensin II, increased number/affinity of receptors, changes in membrane permeability and increased excitation-contraction coupling. The major hormonal component that mediates vasoconstriction is the renin-angiotensin-aldosterone system. Genetic, environmental and psychologic factors may also play a role in hypertension.
10) DISCUSS ETIOPATHOGENESIS OF ATHEROSCLEROSIS
Atherosclerosis is a chronic inflammatory disease. Atherosclerosis begins with fatty streak which is a accumulation of lipid laden foam cells in the intimal layer of the artery [4]. Lipid retention is the first step in the pathogenesis of atherosclerosis which is followed by chronic inflammation at susceptible sites in the walls of the major arteries lead to fatty streaks, which then progress to fibroatheromas which are fibrous in nature
Atherosclerosis is a leading cause of mortality and morbidity in the western world. It has been recognized for over a century, and the understanding of its pathogenesis has undergone many changes. Pathophysiological studies have unravelled the interactions of molecular and cellular elements involved in atherogenesis. The focus has shifted to the novel risk factors as well as characteristics and stability of atherosclerotic plaque; the genetic predisposition has further broadened the pathogenetic mechanisms. This review focuses on the molecular mechanisms involved in the evolution of the atherosclerotic plaque that may pave the way for selecting optimal therapies and preventing plaque complications. Atherosclerosis is no longer a disease attributed mainly to the high lipid content of the body. New insight into the disease pathology has shown it to be a disease of much greater ramifications. Endothelial damage and reactive oxygen species (and other free radicals) have predominantly emerged as factors in virtually all pathways leading to the development of atherosclerosis due to hyperlipidemia, diabetes, hypertension or smoking. Novel risk factors such as hyperhomocysteinemia, infections and systemic lupus erythematosus have emerged. Atherosclerosis has come to be regarded as a chronic inflammatory disease with an autoimmune component.
11) DISCUSS ETIOPATHOGENESIS OF POLLIOMYELITIS
The primary determinant of infection for any virus is its ability to enter a cell and produce additional infectious particles. The presence of CD155 is thought to define the animals and tissues that can be infected by poliovirus. CD155 is found (outside of laboratories) only on the cells of humans, higher primates, and Old World monkeys. Poliovirus is, however, strictly a human pathogen, and does not naturally infect any other species (although chimpanzees and Old World monkeys can be experimentally infected).[45]
The CD155 gene appears to have been subject to positive selection.[46] The protein has several domains of which domain D1 contains the polio virus binding site. Within this domain, 37 amino acids are responsible for binding the virus.
Poliovirus is an enterovirus. Infection occurs via the fecal–oral route, meaning that one ingests the virus and viral replication occurs in the alimentary tract.[47] Virus is shed in the feces of infected individuals. In 95% of cases only a primary, transient presence of viremia (virus in the bloodstream) occurs, and the poliovirus infection is asymptomatic. In about 5% of cases, the virus spreads and replicates in other sites such as brown fat, reticuloendothelial tissue, and muscle. The sustained viral replication causes secondary viremia and leads to the development of minor symptoms such as fever, headache, and sore throat.[48] Paralytic poliomyelitis occurs in less than 1% of poliovirus infections. Paralytic disease occurs when the virus enters the central nervous system (CNS) and replicates in motor neurons within the spinal cord, brain stem, or motor cortex, resulting in the selective destruction of motor neurons leading to temporary or permanent paralysis. This is a very rare event in babies, who still have anti-poliovirus antibodies acquired from their mothers.[49] In rare cases, paralytic poliomyelitis leads to respiratory arrest and death. In cases of paralytic disease, muscle pain and spasms are frequently observed prior to onset of weakness and paralysis. Paralysis typically persists from days to weeks prior to recovery.[50]
12) CLASSIFY OSTEOARTHRITIS AND WRITE DETAILS ABOUT RHEUMATOID ARTHRITIS
Osteoarthritis (OA) is a type of joint disease that results from breakdown of joint cartilage and underlying bone.[5] The most common symptoms are joint pain and stiffness.[1] Usually the symptoms progress slowly over years.[1] Initially they may only occur after exercise, but can become constant over time.[1] Other symptoms may include joint swelling, decreased range of motion, and, when the back is affected, weakness or numbness of the arms and legs.[1] The most commonly involved joints are the two near the ends of the fingers and the joint at the base of the thumbs; the knee and hip joints; and the joints of the neck and lower back.[1] Joints on one side of the body are often more affected than those on the other.[1] The symptoms can interfere with work and normal daily activities.[1] Unlike some other types of arthritis, only the joints, not internal organs, are affected.
Osteoarthritis can be classified by the joint affected:
Hand:
Wrist (wrist osteoarthritis)
Hip osteoarthritis
Knee osteoarthritis
RHEUMATOID ARTHRITIS;
Rheumatoid arthritis (RA) is a long-term autoimmune disorder that primarily affects joints.[1] It typically results in warm, swollen, and painful joints.[1] Pain and stiffness often worsen following rest.[1] Most commonly, the wrist and hands are involved, with the same joints typically involved on both sides of the body.[1] The disease may also affect other parts of the body.[1] This may result in a low red blood cell count, inflammation around the lungs, and inflammation around the heart.[1] Fever and low energy may also be present.[1] Often, symptoms come on gradually over weeks to months.[2]
While the cause of rheumatoid arthritis is not clear, it is believed to involve a combination of genetic and environmental factors.[1] The underlying mechanism involves the body's immune system attacking the joints.[1] This results in inflammation and thickening of the joint capsule.[1] It also affects the underlying bone and cartilage.[1] The diagnosis is made mostly on the basis of a person's signs and symptoms.[2] X-rays and laboratory testing may support a diagnosis or exclude other diseases with similar symptoms.[1] Other diseases that may present similarly include systemic lupus erythematosus, psoriatic arthritis, and fibromyalgia among others.[2]
13) DEFINE PNEUMONIA CLASSIFY AND LIST THE STAGES
Pneumonia is an inflammatory condition of the lung affecting primarily the small air sacs known as alveoli.[3][14] Symptoms typically include some combination of productive or dry cough, chest pain, fever and difficulty breathing.[1] The severity of the condition is variable.[1
Community-acquired[edit]
Main article: Community-acquired pneumonia
Community-acquired pneumonia (CAP) is infectious pneumonia in a person who has not recently been hospitalized. CAP is the most common type of pneumonia. The most common causes of CAP vary depending on a person's age, but they include Streptococcus pneumoniae, viruses, the atypical bacteria, and Haemophilus influenzae. Overall, Streptococcus pneumoniae is the most common cause of community-acquired pneumonia worldwide.
Pneumonia has four stages, namely consolidation, red hepatization, grey hepatization and resolution.
Consolidation
Occurs in the first 24 hours
Cellular exudates containing neutrophils, lymphocytes and fibrin replaces the alveolar air
Capillaries in the surrounding alveolar walls become congested
The infection spreads to the hilum and pleura fairly rapidly
Pleurisy occurs
Red Hepatization
Occurs in the 2-3 days after consolidation
At this point, the consistency of the lungs resembles that of the liver
The lungs become hyperaemic
Alveolar capillaries are engorged with blood
Fibrinous exudates fill the alveoli
This stage is "characterized by the presence of many erythrocytes, neutrophils, desquamated epithelial cells, and fibrin within the alveoli"[12][13]
Grey Hepatization
Occurs in the 2-3 days after Red Hepatization
This is an avascular stage
The lung appears "grey-brown to yellow because of fibrinopurulent exudates, disintegration of red cells, and hemosiderin"
The pressure of the exudates in the alveoli causes compression of the capillaries
Resolution
This stage is characterized by the "resorption and restoration of the pulmonary architecture"
A large number of macrophages enter the alveolar spaces
Phagocytosis of the bacteria-laden leucocytes occurs
"Consolidation tissue re-aerates and the fluid infiltrate causes sputum"
"Fibrinous inflammation may extend to and across the pleural space, causing a rub heard by auscultation, and it may lead to resolution or to organization and pleural adhesions"[12][13]
Risk Factors
The elderly, infants, young children and those with a weakened immune system are at a higher risk of acquiring Pneumonia. Other causes such as frequent exposure to asbestos and cigarette smoke have an increased risk of contracting community-acquired pneumonia than young and middle-aged adults. Some common risk factors are:
Flu
Cancer
Age >65years
Smoking
Heart disease
Immunosuppressive disorders and therapy
Debility or stroke
Coma
Problems with swallowing
Intravenous drug abuse
Signs and Symptoms
Signs and symptoms can vary and are also dependent on the cause and initially, symptoms are similar to that of a cold followed by[14]:
A high fever (pyrexia)
Chills
Productive cough
As the infection continues sputum may be discoloured and may become blood-stained as pneumonia progresses. The following may also occur:
Dyspnoea
Sharp chest pain
Worsening cough
Fever/chills
Tachycardia
Pleuritic chest pain
Headaches
Malaise
Muscle pains
Cyanosis due to poorly oxygenated blood
Loss of appetite
Rapid breathing
Wheezing or grunting during breathing
Intercostal muscle recession during breathing
Vomiting[15]
Diagnosis
There are several ways to diagnose pneumonia:
Physical examination
Auscultation- Bronchial breath sounds or fine cracks over the affected area
Pleural friction rub - an adventitious breath sound heard during auscultation. The sound is caused by the movement of inflamed and roughened pleural surfaces[16]
Chest X-rays often lag behind the clinical presentation.The X-ray will show decreased lung expansion and patchy opacity on the affected side with ill defined margins[17][9]
usually done to confirm the diagnosis
Sputum samples and blood tests
done to diagnose the type of pneumonia that is present
sputum test is done to determine whether it is a fungal or bacterial infection
blood test is done to examine the White Blood Cell count of the involved patient
this can be used to indicate the severity of pneumonia, as well as to determine whether it is a viral or bacterial infection.
bacterial infection would result in a blood count that has an increased amount of neutrophils
a blood count that has an increased amount of lymphocytes would indicate a viral infection.
Increased CRP
Complications
Pleural effusion - When fluid accumulates between the pleura and the chest wall due to the large amount of fluid already present in the lungs. As a result of the Pneumonia, a pleural effusion may develop which could lead to the collapse of the lungs if not treated appropriately[7]
Empyema - Pus may be present in the lungs due to the infection. Thus pockets of pus may develop in the cavity between the pleura and the chest wall, or in the lung itself which is otherwise known as empyema[7]
Lung abscess - A lung abscess develops when the infection has destroyed lung tissue and a cavity filled with pus is formed[7]
Bacteremia - This occurs when the infection is no longer contained within the lungs and moves into the bloodstream, thus the blood is infected[7]
Septicemia - When bacteremia occurs septicemia can follow, as this is an infection that is spread throughout the body. The infected blood is the best way for the infection to manifest in other parts of the body (Health-cares.net, 2005).
Meningitis - The infection may spread to the meninges that cover the brain and spinal cord, leading to meningitis[7]
Septic arthritis - When bacteremia has occurred septic arthritis is also a danger, as the bacteria manifests in the joints through which blood passes[7]
Endocarditis or pericarditis - As blood is also circulated through the heart muscles and the pericardium, the risk of developing an infection there is very high if bacteremia is present[7]
Medical Management
Treatment will vary depending on how bad the symptoms are, and what the cause of the infection is.
Bacterial Pneumonia can be treated with penicillin and/or anti-biotics
Viral Pneumonia cannot be treated with anti-biotics, as they have no effect. This type of pneumonia normally resolves over time.
Mycoplasma Pneumonia is usually treated with anti-biotics.
Doctors will also include the following when treating patients with pneumonia:
Analgesic administration
Cough suppressant medication
Fever-reducing medication (i.e.: Aspirin)
Oxygen therapy (when indicated)
Physiotherapy Management
Chest physiotherapy is an adjunct commonly used in the treatment of pneumonia, however there being little reliable evidence to suggest that physiotherapy has an effect on the rate of recovery of the patient.[18] However, respiratory techniques are still commonly used to aid airway clearance and improve the rate of breathing.
Modified postural drainage - this allows gravity to drain secretions from specific segments of the lungs
Shaking and vibes - to mobilize secretions
Coughing and huffing exercises - to expectorate secretions
Administer humidification - to mobilize secretions
Breathing exercises - Localized and Diaphragmatic
IPPB administration - to increase lung volumes
Mobilization of the patient - done to increase air entry, increase chest expansion, and to loosen secretions[19]
A state-of-art review suggests avoiding repeated airway clearance in infants and children with acute pulmonary disease. The treatment should be based on patient assessment and presentation of symptoms[20].
A retrospective study[21] shows that skeletal muscle index measured at Intensive Care Unit Admission is a predictor of Intensive Care Unit-Acquired Weakness in patients with sepsis.
Clinical Guidelines
Clinical Guidelines for Physiotherapy management of Community-Acquired Pneumonia[22]
For Patients admitted to hospital;
CPAP should be considered for patients with type 1 respiratory failure who remain hypoxaemic despite optimum medical therapy and oxygen. (Grade C)
NIV can be considered for selected patients with type II respiratory failure, especially those with underlying COPD. (Grade C)
Medical conditions permitting, patients should;
Sit out of bed for at least 20mins within the first 24hours
Increase mobility each subsequent day of hospitalisation (Grade B)
The regular use of PEP should be considered (Grade B)
Patients should NOT be treated with traditional airway clearance, +/- IPPB routinely. (Grade B_
Children and Pneumonia
Why Are Children Vulnerable?
Unlike healthy children with many natural defenses to protect them against the invasion of pathogens in the lungs, the unhealthy children with a compromised immune system has weak defenses.
Children who suffer from malnutrion, particularly inadequate zinc intake and lack of exclusive breastfeeding have a higher risk of developing pneumonia.
Other risk factors include:
Being born premature
Having asthma or genetic disorder such as sickle-cell disease
Having heart defects such as ventricular septal defect (VSD), atrial septal defect (ASD) or patent ductus arteriosus (PDA)[23]
Several environmental factors such as overcrowding homes and exposure to parental smoke increases a child's susceptibility to pneumonia and its complications.[24]
Signs and Symptoms in Children
In children, the signs and symptoms are similar to that of adults.
Sometimes a child's only sign may be rapid breathing and often when pneumonia exists in the lower part of the lungs, no breathing problems may be present but rather fever, abdominal pain or vomiting.
If pneumonia is caused by bacteria, the infected child becomes sick relative quickly and is prone to developing a high fever and rapid breathing.
If pneumonia is caused by viruses, symptoms may appear gradually and less severe than bacterial pneumonia.[25]
Parents should be aware of the following signs and symptoms:
Nostril flaring
Sternal retraction
Increased breath rate
> 60 breaths/min for newborns up to 2 months
> 50 breaths/min for 2 months to 12 months
> 40 breaths/min for a child older than 1 year of age[26]
Prevention
Vaccines are usually administered to prevent infection by viruses and bacteria.
Kids usually receive routine immunisation against Haemophilus Influenzae and Pertussis at the age of 2 months of age.
Some vaccines are also administered against pneumococcus organism, a common cause of pneumonia[25]
Transmission of pneumonia - Infection may occur in different ways may it be through contaminated air droplets, blood-borne infection or from coming into contact with contaminated substances during delivery. Either way, it is believed that babies already have the bacterial pathogens causing pneumonia in their nose and/ or throat and are inhaled into the lungs.
Related articles
Hospital Acquired Pneumonia - PhysiopediaDefinition/Description “Pneumonia is an infection of the lung tissue. It is defined as "inflammation of the lung caused by bacteria, in which the air sacs (alveoli) become filled with inflammatory cells and the lungs become solid". When a person has pneumonia the air sacs in their lungs become filled with microorganisms, fluid and inflammatory cells and their lungs are not able to work properly. Diagnosis of pneumonia is based on symptoms and signs of an acute lower respiratory tract infection, and can be confirmed by a chest X-ray showing new shadowing that is not due to any other cause (such as pulmonary oedema or infarction)." [1] (NICE clinical guidelines 2014) "Hospital-acquired pneumonia is defined as pneumonia that occurs 48 hours or more after hospital admission and is not incubating at hospital admission. Early-onset (occurring within 4 days of admission) hospital-acquired pneumonia is usually caused by the same bacteria and viruses as community-acquired pneumonia and has a good prognosis. Late-onset (starting 5 days or more after admission) hospital-acquired pneumonia has a worse prognosis and is usually caused by micro-organisms that are acquired from the hospital environment. MRSA, Pseudomonas aeruginosa and other non-pseudomonal Gram-negative bacteria are the most common causes."[2] (NICE Guidelines. Published: 15 July 2014) Epidemiology “At any time 1.5% of hospital inpatients in England have a hospital-acquired respiratory infection, more than half of which are hospital-acquired pneumonia and are not associated with intubation. Hospital-acquired pneumonia is estimated to increase hospital stay by about 8 days and has a reported mortality rate that ranges from 30–70%. Variations in clinical management and outcome occur across the UK.”[1] HAP and VAP together are the second most common cause of hospital-acquired infection and have been associated with a higher mortality than any other nosocomial infection.[3] HAP is the second most common nosocomial infection with a crude overall rate of 6.1 per 1000 discharges[4] Ventilator-acquired pneumonia (VAP) has been studied more comprehensively than HAP. A clear reason for this is VAP is responsible for 86% of the HAP reported[5]. The incidence rate of HAP is between 3 and 10 per 1000 hospital admissions[6][7]. Mortality rates from VAP are between 24 and 50% but it is reported to jump to 76% if it is caused my multi drug resistant pathogens that are often linked to later stage pneumonia (> 5days in hospital)[5]. Although it is difficult to determine the exact cause of death in critically ill patients, which will cause discrepancies in any date, Accurate antibiotics taken at the right time has shows to lower mortality rate for HAP. The chance of infection is estimated to be 3%/day during the first 5 days of ventilation, followed by 2%/day up to day 10 of ventilation and there- after 1%/day.[8] Aetiology The most common cause is an accumulation of bacteria, most ordinarily gram-negative bacilli and staphlycoccus aureus, which inhabit the oropharynx and upper airways in seriously ill and ventilated patients[9]. A less common cause is seeding of the lung due to bacteremia; a bacterium that originates in the patients’ blood supply and can transferred to the lungs during gas exchange. Finally inhalation of bacterially contaminated aerosols which transport airborne particles containing Legionella sp, Aspergillus sp, or influenza virus, although this is a relatively unfamiliar form of contracting hospitalized pneumonia[9]. Endotracheal intubation with mechanical ventilation poses the greatest overall risk[10]. Ventilation Associated Pneumonia is a subcategory of hospitalized and contributes more than 85% of all cases, with pneumonia occurring in up to 27% of ventilated patients[10]. Endotracheal intubation related bacteria embed themselves deep into the endotracheal tube cuff enabling them to avoid the body' nature immune response while also providing a biofilm of protection from antibiotics[9]. In non-intubated patients, risk factors include previous antibiotic treatment, high gastric pH, resulting from cardiac, pulmonary, hepatic, or renal deficiencies[9]. Major risk factors for postoperative pneumonia are patients older than 70, abdominal or thoracic surgery, and cardiorespiratory functional depletion[9]. Many patients at risk for HAP and VAP have underlying medical conditions that put them at higher risk for acquiring antibiotic-resistant organisms (AROs).[3] Investigations HAP or VAP should be suspected in all patients, whether ventilated or not, if two or more of the following clinical features are present: temperature greater than 38°C or less than 36°C; leukopenia or leukocytosis; purulent tracheal secretions and decreased partial pressure of oxygen in arterial blood (PaO2).[3] General investigations are not necessary for the majority of patients who are managed in the community. Pulse oximeters allow for simple assessment of oxygenation. When a patient is admitted to hospital: FBC with differential white cell count: Total white blood cells: All the white cell types are given as a percentage, and as an absolute number per liter. A high WBC is often an indicator of infection[11]. CRP (to aid diagnosis and as a baseline measure). The C-reactive protein (CRP) test is a diagnostic tool that identifies regions of inflammation[12]. CRP is a protein manufactured in the liver before dispersal into the blood which occurs a few hours after any form of tissue injury, an acute manifestation of infection, or inflammation caused by another source[12]. The CRP test can be used in adjunction with signs, symptoms and other tests in order to fully evaluate patients with HAP[12]. Blood cultures: Blood culture is a microbiological culture of blood. It is employed to detect infections that are spreading through the bloodstream (such as bacteremia, septicemia amongst others). Pneumococcal and legionella urinary antigen tests: Urine tests are administered and designed to locate the presence of both Streptococcus pneumoniae and Legionella species[13]. Two major pathogens in HAP, which also play a key role in community acquired Pneumonia. The tests are usually in conjunction with both sputum examination and blood testing due to their high specificity[13]. CXR: HAP may deliver signs of abnormal opacity in specific areas of the lungs, or even clear consolidation due to inflammation causing abnormal positioning of structures, such as the trachea and mediastinum[14]. Sputum examination and culture. Sputum Examination is a diagnostic tool used to identify bacteria and fungi located in the pulmonary facet[15]. Samples are often obtained through expectorating or in some cases an induced saline can produce the required volumes from lab testing. HAP normally produces sputum in a thick and purulent form, which is common in more cases of infection[15]. Blood gases: Blood gases will demonstrate how well both the respiratory and the renal systems are functioning[16]. In terms of HAP ABG’s can be used to gain insight into the patient’s oxygen saturation levels as well as demonstrate incidences of both acidosis and alkalosis, both of which can occur due to poor ventilation[16]. Aspiration of pleural fluid (for biochemistry and culture). Chest aspiration is a diagnostic tool used to investigate the cause of pleural fluid or to improve respiration rates that have dropped due to accumulated fluid[17]. Samples of the pleural fluid are sent for analysis which includes cytology for malignant cells and bacteriology for identification of foreign bacteria[17]. Clinical Manifestations A patient that develops new or extra pulmonary infiltrates and a fever are signs of HAP. In order to differentiate HAP and other pathologies diagnosis should be based on a radiographic x-ray. To diagnose HAP radiological opacity with alveolar condensation must be present.[18] The time of onset of HAP is a large determinate of the type of bacteria causing the infection: Early-onset HAP occurring in the first 4 days of hospitalization) is often caused by community-acquired pathogens such as: Haemophilus influenzae, Streptococcus pneumoniae, or methicillin-susceptible S aureus (MSSA). In this context, pathogens with strong intrinsic or acquired antimicrobial resistances are rarely causative. Late-onset HAP developing ≥ 5 days after hospitalization is often caused by aerobic Gram-negative bacilli such as: P aeruginosa, Enterobacteriaceae, or Acinetobacter) or Methicillin-resistant Staphylococcus aureus (MRSA) Late-onset pneumonia is due to P aeruginosa, Acinetobacter, or MRSA in 30 to 71% of cases. Physiotherapy and Other Management Other health professionals will be treating your patient. What is their input?When addressing HAP, respiratory physiotherapy interventions should be individually tailored around the patient’s symptoms, observing aspects such as degree of pain, mobility capabilities and an array of complex factors[19]. Therefore techniques may include positional manipulations (addressing V/A matching and attempting to uses gravity to potentially enable drainage), manual hyperinflation, percussion, shaking, vibrations, suctioning (if huffing or cough promoting techniques are proving ineffective in regards to sputum extraction), breathing exercises including thoracic expansion and relaxing tidal volumes, while also engaging sputum reduction through active cycle and autogenic drainage techniques) as well as mobilization[19]. The later of course demonstrating great importance not only in terms of improving the patients’ respiratory distress, but also in reducing overall hospitalization. Published substantial evidence very much supports the role of physiotherapy in the respiratory managing HAF, demonstrating both short-term and longer term benefits[19]. However, its essential to promote physiotherapy treatment as part of a multi-disciplinary approach as aspects including pharmaceutical interventions play an integral part in controlling bacterial diseases, promoting lung function and reducing problematic symptoms[20]. Prevention Three European societies, (European Respiratory Society (ERS), European, Society of Clinical Microbiology and Infectious Diseases (ESCMID) and European Society of Intensive Care Medicine (ESICM), in 2008 produced a report to further the clinical guidelines of HAP and VAP. Within these guidelines they outline several measures that can have proven to reduce the likelihood of HAP. Generally recommended general measures: Alcohol-based hand disinfection Use of microbiologic surveillance Monitoring and early removal of invasive devices Programs to reduce antimicrobial prescriptions Generally recommended specific measures Avoidance of endotracheal intubation Avoidance of reintubation Preference of noninvasive ventilation (NIV) Preference of orotracheal intubation and orogastric tubes Maintenance of the ET cuff pressure at approximately 20 cmH2O Avoidance of flushing the condensate into the lower airway or to in-line medication nebulizers Patient positioning (semirecumbent position)[21] Additional measures which might be helpful in distinct settings and populations: Continuous aspiration of subglottic secretions Endotracheal tubes coated with antiseptics or silver Preference of heat-moisture exchangers (HMEs) over heater humidifiers (HH) Oral decontamination Selective decontamination of the digestive tract (SDD)[21] The VAP Guidelines Committee and the Canadian Critical Care Trials group in 2008 recommended several approaches to encourage a reduction in incidences[22]: The orotracheal route of intubation should be used when intubation is necessary There should be no scheduled ventilator circuit changes but new circuits for each patient, and changes if the circuits become soiled or damaged Changes of heat and moisture exchangers with each patient, also every 5-7 days and as clinically indicated Closed endotracheal suctioning system, and that the system is changed for each patient and as clinically indicated. The use of subglottic secretion drainage in patients expected to be mechanically ventilated for > 72hrs Bed head to be elevated to 45°. If this angle is not possible then as much elevation as possible is recommended The use of oral antiseptic chlorhexidine The use of oral antiseptic povidone-iodione should be considered with patients with severe head injury Rotating beds should be considered Resources NHS website http://www.nhs.uk/conditions/pneumonia/Pages/Introduction.aspx Patient website http://www.patient.co.uk/health/pneumonia-leafletBronchitis - PhysiopediaCondition Bronchitis can be defined as an inflammation of the bronchi. It is also noted to be an infection of the lower respiratory tract which, in general, will follow an upper respiratory tract infection. Acute bronchitis is caused either by a viral or bacterial infection. It is characterized by coughing, the production of excessive amounts of mucopurulent sputum and narrowing of the bronchi due to spasmodic contractions. The respiratory passages also become inflamed and irritated. This illness is commonly one of a viral nature and is usually self-limiting. It may progress to pneumonia if unaddressed or if treatment is not effective. Episodes of this disease mainly occur in middle and adult life, however, both adults and children can acquire bronchitis. It is more common in males than females and is also more common amongst smokers than non-smokers. Symptoms are noted to be similar for both age groups. Bronchitis is usually a progressive disease and could possibly lead to respiratory failure if not treated effectively. Pertussis, commonly known as whooping cough, can also be seen to mimic acute bronchitis and is often under-diagnosed, leading to the need for differential diagnosis. Infants usually get bronchiolitis, which involves the smaller airways and causes symptoms similar to asthma. In general, an infant will lead a relatively protected life. It is therefore noted that respiratory infections will usually only become common once the child starts school. These infections may also be seen to be recurrent through the early school-going years as the body's defence mechanisms are still developing as the child grows. Pathology Acute bronchitis is generally caused by a viral infection. In patients younger than 1 year, the respiratory syncytial virus, parainfluenza virus and the coronavirus are noted to be the most common causes. In patients between 1 and 10 years, the parainfluenza virus, enterovirus, respiratory syncytial virus and rhinovirus dominate the causes of acute bronchitis. In patients older than 10 years, the influenza virus, respiratory syncytial virus and adenovirus are the most common causes. Acute bronchitis was first described in the 1800’s as the inflammation of the bronchial mucous membranes. Subsequently this inflammation has been noted to be the end result of a complex series of events. These events include an infectious or non-infectious trigger. This leads to the injury of the bronchial epithelium resulting in an inflammatory response with hyper-responsiveness of the airways and mucous production. Bronchial wall repair takes a few weeks to occur. The patient will still suffer from a cough during these weeks. Half of the patients suffering from acute bronchitis will continue to cough for longer than 2 weeks and in a quarter of patients the cough will last for more than a month. Chronic bronchitis in children can be as result of two things: Excessive inflammation or continuous exposure to allergens or irrtants. This will result in a bronchospasm and cough. Later the airway will become inflamed with oedema and there will be mucous production(due to overactivity of mucous secreting glands. This mucous production can build up, covering the bronchial walls and in turn results in an obstruction being formed in the bronchioles. Therefore it can be said that chronic bronchitis in children is most probably diagnosed as asthma. General pathology: Hypertrophy of the mucous glands in the bronchial wall. Increased number of goblet cells. Recurrent infection, especially in childhood could lead to chronic inflammatory changes, fibrosis, distortion and even ulceration. The small airways are often affected which is partly due to a loss of elastic support from the surrounding alveoli. Risk Factors Exposure to second-hand smoke Contact with someone already infected with bronchitis A viral upper respiratory tract infection Asthma Enlarged tonsils and or adenoids Sputum retention Unexplained weight loss Cor pulmonale Ventilatory failure Weakened immune system Repeated exposure to lung irritants Causes Acute bronchitis is caused by viral and bacterial infections. This form of the disease may last up to several days, or even weeks. Viruses, which include the influenza A and B, adenovirus, rhinovirus and the respiratory synctial virus Acute exacerbations of chronic lung disease may be caused by bacteria, which include Streptococcus, Haemophilus, Moraxella catarrhalis and Mycoplasma pneumonia Atypical pathogens such as Mycoplasma pneumonia, Chlamydia pneumonia and Chlamydia psittaci Bacteria such as Streptococcus pneumonia and Moraxella Contributory or Predisposing Factors Bronchiectasis Cystic Fibrosis Congestive heart failure Some children may be more prone to the contraction of acute bronchitis than others and these include children with respiratory illnesses such as asthma and children exposed to high levels of airborne pollutants. Signs and Symptoms The signs and symptoms of this disorder will depend on the severity of the disease as well as considering which stage the disease has been diagnosed. This just means that some symptoms may be present in some cases and may be absent in others. General Symptoms Coughing which will be dry, hacking and painful in the initial stages. Coughing later becomes productive with purulent sputum. Sputum may also contain blood Coughing may last for more than two weeks Continued forceful coughing may cause chest and abdominal muscle pain Coughing can be severe enough at times to injure the chest wall or even cause the child to pass out Wheezing Coarse crackles may be heard on auscultation. Difficulty in breathing due to narrowing of the bronchi. General physical signs Barrel chest (increased anteroposterior diameter) Diaphragm appears lower and flatter Paradoxical inward movement of the lower ribs and visible interspaces during inspiration Sternum appears elevated The liver may become palpable as it is displaced downwards due to overinflation. The breath sounds have a longer expiratory phase and there may be decreases air entry. Other added sounds that may be heard on auscultation include rhonchi and crackles. Symptoms for Viral Acute Bronchitis: Non-productive cough Purulent sputum Symptoms will be aggravated by cold/dry/dusty air Symptoms for Bacterial Acute Bronchitis: Productive cough Pyrexia Pain behind the sternum, which will be aggravated by coughing Runny Nose Chills Slight fever Back and muscle pain Sore throat Prevalence/Incidence A study done by the School of Public Health and Family Medicine at the University of Cape Town (UCT), revealed that out of the sample population 2,3% of males and 2,8% of females had bronchitis. It was also found that the strongest predictor of this disease was a history of tuberculosis. Other predictors include smoking, occupational exposure, and other domestic exposure e.g exposed to smokey fuel and being underweight. The incidence rate of acute bronchitis in the United States of America (USA), according to www.wrongdiagnosis.com is approximately 1 in 21 or 4.60%, this is extrapolated out to 23 new cases per minute. The following statistics about acute bronchitis were posted on www.wrongdiagnosis.com and are all from the Hospital Episode Statistics, England Health Department and were all for the year 2002-2003. It was found that 0.017% of hospital consultant episodes were for acute bronchitis. 52% of hospital consultant episode were for men. The mean stay in hospital was 4.3 days and the mean age of hospitalised patients diagnosed with acute bronchitis was 40 years. The following results are shown as extrapolations of the research done in the USA and therefore the results are based on these methods. Chronic Bronchitis in Southern Africa (Extrapolated Statistics) ( Extrapolated Prevalence --- Population Estimated Used) Angola -- 488,384 --- 10,978,5522 Botswana -- 72,921 --- 1,639,2312 South Africa -- 1,977,303 --- 44,448,4702 Swaziland -- 52,014 --- 1,169,2412 Zambia -- 490,481 --- 11,025,6902 Zimbabwe -- 163,343 --- 1,2671,8602 Diagnosis Just like any respiratory disorder, the diagnosis will start with the history of the patient, including all details pertaining to the disorder (exposure to irritants, including being exposed to second-hand smoke). Upon physical examination, decreased breath sounds, wheezing, rhonchi and prolonged expiration will be evident. Various tests can be used to diagnose bronchitis in patients who present with prolonged coughing and shortness of breath. Chest X-ray This test is used to rule out pneumonia. In bronchitis, the x-ray will show no evidence of lung infiltrates or consolidation. Sputum Culture This allows the doctor to check for signs of inflammation or a bacterial infection Blood Tests These tests include arterial blood gasses to test for levels of oxygen, carbon dioxide and acidity of the blood. Pulse Oximetry This test will determine the amount of oxygen in the blood. An arterial blood gas test is more exact, but will be more painful and traumatic for the child. Pulmonary lung functions Pulmonary function tests are also known as lung function tests. These tests measure the amount of air ones' lungs can hold, the way your lungs function(moving oxygen into the lungs and carbon dioxide out of the lungs) and how quickly you can move air in and out of your lungs. The other advantages of these tests are that it can diagnose lung diseases, measure how severe the lung disease is and also evaluate how effective the treatments that have been administered are noted to be. Medical Management The physical examination of patients presenting with symptoms of acute bronchitis should focus on the vital signs. These should include the presence or absence of pyrexia and tachypnea, and pulmonary signs such as wheezing, rhonchi, and prolonged expiration. Evidence of consolidation must be absent, or a diagnosis of pneumonia can be made. In general, the patient needs to rest, may need the use of antipyretics, should have adequate hydration, and should avoid smoke where possible. Some of the main objectives of treatment for this disorder will be to keep the bronchioles open and functioning, to facilitate the removal of secretions, to prevent disability and to improve one's quality of life as much as possible. It is extremely important to correctly manage cases of bronchitis. In the case of an emergency, a child suffering from acute bronchitis or the exacerbation of chronic bronchitis should be adequately oxygenated as this would be the primary medical intervention at the time, and most important. Antibiotics can be used to treat acute bronchitis caused by a bacterial infection. They are ineffective in the treatment of acute bronchitis caused by a virus however. The treatment for the viral form is commonly symptomatic, and can include analgesics for a sore throat, antipyretic medication for fever, and cough suppressants where deemed necessary and effective. A humidifier may also be used in order to increase the humidity of the air and ease dryness of the respiratory passages, which can cause excessive coughing due to irritation. In rare cases, the patient may be hospitalized if they experience breathing difficulty that doesn't respond to treatment. This usually occurs because of a complication of bronchitis, not bronchitis itself. Pharmaceuticals Aspirin, Paracetamol, Ibuprofen or Acetaminophen These are used for the treatment of pain and fever and can be used to ease headaches caused by excessive coughing. Pertussives Pertussive therapy is used in order to induce coughing as an aid for expectoration. Antitussives Antitussives are used to control coughing, especially in cases if the cough is creating significant discomfort. The selection of an antitussive medication is dependent upon the cause of the cough. An antihistamine would be made use of to treat a cough caused by allergic rhinitis. A decongestant or an antihistamine would be utilized to treat a cough caused by a postnasal drip. And a bronchodilator when a cough results from the exacerbation of asthma. Non-specific antitussives are made use of to just suppress an unproductive, ineffective cough while not hampering the resolution of the infection. Bronchodilators These prevent excessive coughing which would lead to pain and fatigue. Antibiotics Used in the treatment of acute bronchitis caused by a bacterial infection.In paediatrics ,antibiotics will only be used for bronchitis related to bacteria.Physicians will prescribe Amoxicillin to children younger than 8 years old. Expectorants These may be beneficial in removal of sputum by mobilizing and aiding expectoration, preventing atelectasis and bronchospasm. Steroid Therapy This form of medical managemnet may be considered if conservative measures fail. Immunizations An important aspect of child care and is an important defence mechanism against viral agents of disease and illness. Physiotherapy Management According to Shepherd (1995)[1], bronchitis is one of the main respiratory disorders during which a child will be referred for physiotherapy treatment. Postural Drainage This can be exercised at an angle of 45º in prone and in side lying. This must first be cleared with the institution as necessary, as well as considering possible contra-indications such as a head injury. Manual Techniques Percussions, shaking and vibrations can be used to mobilize secretions and aid expectoration. Once again, precautions and contra-indications are to be observed. Breathing Exercises Active Cycle of Breathing Techniques(ACBT) could be used in order to mobilize secretions. Teaching relaxed breathing techniques as well as diaphragmatic breathing to aid oxygenation and prevent respiratory distress. Full thoracic expansion must be emphasized which will aid oxygenation. The patient should be encouraged to aid the mobilization of secretions through coughing and deep breathing during the day. The patient, and family, should be advised that the patient needs to rest and avoid bronchial irritants where possible. This, however, does not exempt the patient from partaking in physiotherapeutic activities. Education Teaching the importance of nose blowing into a tissue and not swallowing the secretions as well as discarding the tissue safely after blowing their nose is important,s as this will prevent the spread of infection. The patient and family/caregiver should be advised that a dry cough may persist after the bronchitis has resolved due to irritation of the respiratory passages. A humidifier at the bedside may be useful in combating the negative after-effects as it will saturate the air that is breathed in. Treatment Schedule and Home Advice Treatment should be carried out 3 to 4 times a day depending on the severity of the condition. If an upper respiratory tract infection is contracted again, treatment should be started as soon as possible to prevent it from developing into bronchitis or further severe complications. The patient and/or family should be able to recognize early signs and symptoms of acute bronchitis and report them immediately. [2] [3] [4] Prognosis If an underlying lung disorder is not present, symptoms of acute bronchitis will usually subside within 7 to 10 days. A dry, hacking cough may however be present for several months after this allotted time. Acute bronchitis usually heals completely, therefore leading to an excellent prognosis. Bronchitis commonly begins with a dry cough, which can wake the patient up at night. This will progress to a cough, which is productive in nature, and may accompany symptoms such as pyrexia, malaise and a headache. These symptoms will only last for a few days, but the productive cough will last for several weeks. If any of the symptoms associated with this disorder should remain untreated or uncontrolled it could lead to secondary complications such as pneumonia. This would thus lead to a poorer prognosis. Prevention In paediatric bronchitis as well as other medical conditions, prevention is always better than cure. Hands should be washed regularly to avoid the spreading of any viruses and other infections. A hand should be placed over the mouth during coughing, and the washing ones' hands after a cough will aid in the removal of any viruses or germs on the hands. If this is not observed, it may lead to the spread of infection. If and where possible, exposure to air pollution should be reduced. Smoking near children should be prevented as secondary smoke can damage the bronchial tree and makes it easier for viruses to cause an infection. If the child is easily susceptible to contracting infections, contact with people who are already suffering from bronchitis should be avoided. Antimicrobial therapy should be administered at the first sign of purulent sputum. Children suffering from bronchitis should always have a balanced diet and healthy eating plan in order to keep their immune system in an optimal condition. This allows it to fight off infection and prevent the development of acute bronchitis, disrupting daily life along with general well-being.Today is World Pneumonia Day – Physiospot – Physiotherapy and Physical Therapy in the SpotlightToday is “World Pneumonia Day” which was first hosted in 2009 when over 100 organisations joined to form the Global Coalition against Child Pneumonia. It’s marked every year on 12 November with the aim of: Raising awareness about pneumonia, the world’s leading killer of children under the age of five; Promoting interventions to protect against, prevent and treat pneumonia; and Generating action to combat pneumonia. Pneumonia is one of the most solvable problems in global health and yet a child dies from the infection every 20 seconds. Together, as physiotherapists, we can ensure the fight against pneumonia is won. Pneumonia is “a severe form of acute lower respiratory infection that specifically affects the lungs”. The lungs consist of bronchi, which divide into bronchioles that end in alveoli. The small blood vessels in the lungs are responsible for gaseous exchange (oxygen moving into the lungs and carbon dioxide moving out of the lungs). During a Pneumonia infection, the alveoli of one or both lungs fill up with pus or fluid. This increases the labor of breathing, and thus gaseous exchange cannot occur as it normally would. Learn More About Pneumonia Why are children vulnerable? Unlike healthy children with many natural defenses to protect them against the invasion of pathogens in the lungs, the unhealthy children with a compromised immune system has weak defenses. Children who suffer from malnutrion, particularly inadequate zinc intake and lack of exclusive breastfeeding have a higher risk of developing pneumonia. Other risk factors include: Being born premature Having asthma or genetic disorder such as sickle-cell disease Having heart defects such as ventricular septal defect (VSD), atrial septal defect (ASD) or patent ductus arteriosus (PDA) Several environmental factors such as overcrowding homes and exposure to parental smoke increases a child’s susceptibility to pneumonia and its complications. Through the use of simple physiotherapy treatments such as manual techniques, active cycle of breathing, IPPD breathing and exercises perhaps we could reduce this mortality rate even just a little bit. To do this we much enable those in developing countries, where antibiotic and healthcare accessibility is poor, to gain the knowledge of how to manage the condition. It is our duty, those with understanding and knowledge of this condition, to do so.Bronchopulmonary Dysplasia - PhysiopediaCondition/Definition Bronchopulmonary Dysplasia on X-ray Bronchopulmonary dysplasia (BPD) is a chronic lung condition that is caused by tissue damage to the lungs.[1] It usually occurs in immature infants who have had severe lung disease at birth, such as respiratory distress syndrome, and have needed to receive mechanical ventilation and supplemental oxygen as treatment for more than a few weeks after birth. The delicate tissues of the lungs can become injured when the alveoli (air sacs) are hyper inflated (over-stretched) by the ventilation or by high oxygen levels. As a result, the lungs become inflamed and additional fluid accumulates within the lungs.[2] BPD is marked by inflammation, exudates, scarring, fibrosis, and emphysema, and most commonly presents itself in pre-term infants to 21 days post natal.[3] Pathophysiology The pathophysiology of BPD is multifactorial and is not yet fully understood. It is believed that a variety of toxic factors contribute to the formation of BPD by injuring the small airways, eventually resulting in a reduction of the alveolar surface area. This affects gaseous exchange which further compromises blood oxygenation.[4] Stages of BPD BPD is believed to be a disease of scarring and repair. Even though the exact pathophysiology is still unclear, 4 stages in the development of BPD have been identified. In stage 1 (1-3 days), the pathologic appearances of BPD are identical to those of respiratory distress syndrome where there is not enough surfactant in the lungs. Surfactant helps to lower surface tension in the airways and this helps keep the lung alveoli open. It involves the presence of hyaline membranes, atelectasis, vascular hyperemia, and lymphatic dilatation.[4] In stage 2 (4-10 days), lung destruction resulting in ischeamic necrosis of airways occurs due to stretching of the terminal bronchioles. Immediate reparative changes in the lungs as well as bronchiolar obstruction are also seen in this stage. Hyaline membranes can persist into this stage and emphysematous coalescence of the alveoli is seen.[4] Stage 3 (11-20 days) involves progressive repair of the lung, with a decreased number of alveoli. There is compensatory hypertrophy of the remaining alveoli, and hypertrophy of bronchial-wall muscle and glands. Regenerating clear cells are seen, along with exudation of alveolar macrophages and histiocytes into airways. Airtrapping, pulmonary hyperinflation, tracheomegaly, tracheomalacia, interstitial edema, and ciliary dysfunction may also be present.[4] In stage 4 (>1 month), emphysematous alveoli are seen. Chronic lung damage eventually causes Pulmonary hypertension (caused by thickening of the inner-most lining of pulmonary arterioles), and results in cor pulmonale. Fibrosis, atelectasis, a cobblestone appearance due to uneven lung aeration, and pleural pseudofissures are often seen. Marked hypertrophy of peribronchiolar smooth muscle is present.[4] Causes and Risk Factors BPD occurs in severely ill infants who have received high levels of oxygen for long periods of time or who have been on a ventilator during treatment for respiratory distress syndrome. It is more common in infants born early (premature) whose lungs were not fully developed at birth.[1] The following risk factors have been identified: Premature birth. Respiratory Infection. Meconium aspiration. Congenital heart disease. It may also occur as a secondary problem for the neonate attached to a mechanical ventilator.[1][5] Signs and Symptoms The most noted signs in an infant with BPD.[1][5] The most Common signs of BPD are: Shortness of breath Cough Wheezing If BPD worsens, the infant will present with: Severely difficult breathing with grunting The chest and abdomen move in opposite directions with every breath Rib retractions: ribs are visible during each breath Nasal flaring: nostrils open wide during each breath Use of accessory muscles: neck muscles are prominent during each breath Rapid breathing rate Complications of BPD Pulmonary Edema Despite overcoming the most serious stages of BPD, some infants still suffer long term complications. The possibility of obtaining serious long-term complications however is minute. These complications include: They are often more susceptible to respiratory infections such as influenza and pneumonia. The infection is worse in children with BPD than in normal infants. Pulmonary oedema, an excess fluid build-up in the lungs, which decreases air entry into the lungs and infants cannot breathe which results in respiratory distress. Infants with a history of BPD may also develop a rare complication in their circulatory system known as pulmonary hypertension. This occurs when the blood vessels carrying blood from the heart to the lungs become narrowed, resulting in high blood pressure. Infants with BPD have stunted growth and have problems gaining weight. They also tend to lose more weight when they are sick. Premature infants with severe BPD also have a higher incidence of cerebral palsy. Diagnosis It is difficult to determine whether or not a baby has bronchopulmonary dysplasia (BPD) before he or she is about 14 to 30 days old. By this time the baby should be showing improvement in breathing problems, instead the condition seems to be getting worse and the baby requires more oxygen and assistance from a ventilator.[6] According to kidshealth.com when making a diagnosis the following factors should be taken into account: Prematurity Infection Mechanical Ventilator dependence for a prolonged period BPD is confirmed as a diagnosis if the infant requires additional oxygen and continues to shows signs of respiratory distress after 28 days of age. A number of tests are also conducted on newborns with breathing problems to make sure they diagnose their condition correctly. According to the National heart, lung and blood institute these tests include: Blood tests. Blood samples are checked to see whether the baby has enough oxygen in his or her blood. Chest x-rays. It shows larger areas of air and changes from inflammation or infection. It also shows areas of the lung that have collapsed and may help confirm that the lungs aren't developing normally. On a chest x – ray, the lung tissue appears spongy. Echocardiogram. The use of sound waves to create a moving picture of the heart. Echocardiogram is used to rule out congenital heart defects or pulmonary arterial hypertension as the cause of the breathing problems. Doctors grade BPD as mild, moderate, or severe, depending on how much supplemental oxygen the baby needs and how long he or she needs it.[6] Prevention There are a number of things a mother can do to prevent her baby from being born before their lungs have fully developed: During pregnancy, regular check ups with the doctor should be done. Dietary supplements are essential, along with good, healthy eating habits. Avoid smoking, consuming alcohol and taking illegal drugs. It is vital that the mother-to-be is controlling any chronic diseases (e.g. Diabetes, Hypertension etc.) with proper medication. Mothers-to-be must make sure that they attend to all cuts and bruises as soon as possible to prevent infections and other easily attainable communicable diseases. Medical Management Doctors begin treatment for respiratory distress at birth and before they even know whether the baby has BPD. According to the National Heart, Lung and Blood Institute, medical management of a child with RDS and possibly BPD includes:[6] Breathing Support The baby is usually put on a mechanical ventilator. The ventilator, which is connected to a breathing tube that runs through the baby's mouth or nose into the windpipe, can be set to help a baby breathe or to completely control a baby's breathing. It also is set to give the amount of oxygen the baby requires. With help breathing, the baby's lungs have a chance to develop.[6] Surfactant Replacement Therapy The baby is given surfactant to open his or her lungs until the lungs have developed enough to start making their own surfactant. Surfactant is given through a tube that is attached to the ventilator, which pushes the surfactant directly into the baby's lungs.[6] Medication Medication is usually prescribed to reduce swelling in the airways and improve the flow of air in and out of the lungs. These medications include: Bronchodilators – Bronchoconstriction and airway hyper reactivity. Diuretics - Pulmonary edema, and removal of extra fluid in the lungs. Steroids - To decrease airway inflammation. Vasodilators - Cor pulmonale. Antibiotics - Control infections Supportive Therapy Treatment in the NICU is designed to limit stress on the baby and meet his or her basic needs of warmth, nutrition, and protection. According to the National Heart, Lung and Blood Institute, such treatment usually includes:[6] Using a radiant warmer or incubator to keep your baby warm and reduce the chances of infection. Ongoing monitoring of blood pressure, heart rate, breathing, temperature and the amount of oxygen in the baby's blood. Monitoring fluid intake to make sure that fluid doesn't build up in the baby's lungs. Physiotherapy Management It must be noted that infants with Bronchopulmonary Dysplasia are cared for in the Neonatal Intensive Care Unit. The mainstay of physiotherapy treatment is to clear the chest of secretions. This can be done by: Vibrations and light percussions. Changing positions helps to mobilise secretions out of the small airways. Suctioning and mucolytics may be an option for tenacious sputum and when the child has difficulty coughing. [7] [8] Evidence There is limited evidence for the role of physiotherapy in the treatment of BPD. A study carried out by Gomez-Comesa et al, reported that physiotherapy treatment in the NICU was effective in improving BPD in prematurely born children with respiratory distress syndrome. Physiotherapy assisted in reducing the number of days that ventilation and hospitalization were required and favoured the prevention of future disabilities.[9]Pneumocystis Jirovecii Pneumonia - PhysiopediaIntroduction Pneumocystis Jirovecii Pneumonia (PJP) was previously called as Pneumocystis Carinii Pneumonia (PCP), it is one of the most common opportunistic fungal infection in immuno-compromised conditions such as haematological malignancy, congenital immunodeficiency, organ transplantation, immunosuppressive therapy, under medication and predominantly in HIV/AIDS. [1] Epidemiology PJP has a high incidence before the advent of prophylaxis treatment and highly active antiretroviral therapy (HAART). A study about the epidemiology of PJP showed that the incidence has significantly decreased both for the adult and pediatric population.[2] However, the same study showed that there is difference with the prevalence of PJP in industrialized countries, such as those in Europe and North America, and in developing countries , such as in Southeast Asia and Sub-Saharan Africa, wherein the former has a continuous decline while the latter is at a greater risk of incidence.[2] A recent nationwide study in Spain, conducted by Pereira-Diaz et al, reported that PJP is an emerging disease in patients without HIV infection of which risk factors include haematological neoplasms, chronic lung diseases and, non-hematological cancers with high mean mortality and hospitalization costs.[3] Etiology The pathogen responsible for PJP is Pneumocystis Jirovecii, an organism classified as a fungus. Pathophysiology PJP Pathophysiology Signs and Symptoms Subacute onset exertional dyspnea[4] Dry and non-productive cough[4] Fever or subfebrile temperatures[4] Chest pain Tachypnea Tachycardia Cyanosis Weight loss Diagnostic Procedures Diagnosis of PJP relies on combination of laboratory findings and diagnostic imaging together with physical examination and history-taking. Laboratory procedures and findings pertinent to PJP diagnosis include: Quantitative polymerase chain reaction (qPCR)- more accurate way to diagnose PJP[5] (1–3)-β-d-glucan (BG) -most reliable serologic biomarker for PJP diagnosis[6] Krebs von den Lungen-6 antigen (KL-6)- together with BG, is the most accurate serologic apptoach for PJP diagnosis[6] Lactate dehydrogenase (LDH)[6] S-adenosyl methionine (SAM)[6] Sputum induction Imaging studies used in the diagnosis of PJP include: Chest CT Scan- most pertinent finding is ground glass opacity (GGO) indicative of alveolar subtotal consolidation[7] Chest Radiography- nonspecific, can be normal, less common patterns have been reported, including lobar infiltrates, pulmonary nodules, and pneumatoceles and other cystic changes.[8] Differential Diagnosis Thorough evaluation that includes physical examination, laboratory findings and/or imaging studies are warranted in order to make a specific diagnosis of PJP and to differentiate it from other conditions with similar presentation, which include but not limited to: Bacterial pneumonia[8] Acute Respiratory Distress Syndrome[1] Viral pneumonia Pulmonary Tuberculosis[8] Pulmonary Embolism[1] Mycobacterium Avium Complex[1] Cytomegalovirus[8] Histoplasmosis Prognosis A meta-analysis conducted by Liu et al, stated that risk factors associated with increased mortality rate including old age, female sex, longer time from onset of symptoms to diagnosis, respiratory failure, solid tumors, high lactate dehydrogenase, low serum albumin, bacterial, and aspergillus co-infection, etc.[9] The findings of their study revealed that even in non-HVI patients, mortatlity rate for PJP infection is high.[9] A predictive model to evaluate mortality in HIV/AIDS patients with PCP was constructed by Wu L. et al, based on routine laboratory and clinical parameters, which may be a simple tool for physicians to assess the prognosis in HIV/AIDS patients with PCP in China. [10] This includes 7 predictors, including LDH >350U/L, HR>130 times/min, room air PaO2 <70mmHg, later admission to ICU, Anemia (HGB≤90g/L), CD4<50cells/ul, and development of a pneumothorax. [10] Pharmacological Management Trimethoprim/sulfamethoxazole (TMP-SMX)- first-line agent for the treatment of mild to severe PJP[8] Atovaquone- one of the oral treatment alternatives for mild and moderate PCP[8] Pentamidine isethionate- preferred alternative drug regimen to TMP-SMX[1][8] Clindamycin and Primaquine-good alternative choice for treatment of mild to moderate PJP[1] Caspofungin[1] Prophylaxis TMP-SMX- recommended prophylactic agent[8] Aerosolized pentamidine[8] Atovaquone[8] Dapsone[8] Physiotherapy Intervention Physiotherapy interventions for the treatment of PJP would be the same as treating Pneumonia. This includes: Modified postural drainage Shaking, vibrations and percussion Coughing and huffing exercises Segmental and Diaphragmatic breathing exercises Mobilization of the patient General body conditioning exercises See also Pulmonary Rehabilitation
References
Jump up↑ Martin, E.A. (Ed.). (2003). Oxford Concise Medical Dictionary, 6th Edition. Oxford, United Kingdom. Oxford University Press.
Jump up↑ Health24. (2008). Pneumonia. Retrieved February 13, 2009 from http://health24.com/medical/Head2Toe/777-778-782,13491.asp
↑ Jump up to:3.0 3.1 3.2 https://www.unicef.org/health/index_91917.html
↑ Jump up to:4.0 4.1 Koenig, S., & Truwit, J. (2006). Ventilator-associated pneumonia: Diagnosis, treatment and prevention. Clin Microbiol Rev. 2006 October; 19(4): 637–657. Retrieved April 12, 2009 from http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1592694
↑ Jump up to:5.0 5.1 5.2 Healthscout. (2009). Health Encyclopedia - Diseases and Conditions: Pneumonia. Retrieved April 8, 2009 from http://www.healthscout.com/ency/68/205/main.html
↑ Jump up to:6.0 6.1 Smith, B., & Ball, V. (1998). Cardiovascular/Respiratory Physiotherapy. Mosby International Limited: Italy
↑ Jump up to:7.00 7.01 7.02 7.03 7.04 7.05 7.06 7.07 7.08 7.09 7.10 Health-cares. (2005). What is pneumonia? Retrieved February 13, 2009 from http://respiratory-lung.health-cares.net/pneumonia.php
Jump up↑ Bartleby. The Lungs. Retrieved April 8, 2009 from http://education.yahoo.com/reference/gray/subjects/subject/240
↑ Jump up to:9.0 9.1 Torpy, J. (2007). Ventilator associated pneumonia. Retrieved April 12, 2009 from http://jama.ama-assn.org/cgi/content/full/297/14/1616
Jump up↑ https://www.who.int/news-room/fact-sheets/detail/pneumonia
Jump up↑ AFP. (2009). 1.6 million die of pneumonia annually: studies. Retrieved April 8, 2009 from http://www.google.com/hostednews/afp/article/ALeqM5j9-UqSxOOJLWxxBUz1lv9HR5YTgg
↑ Jump up to:12.0 12.1 12.2 12.3 Atkuri, L.V., & King, B.R. (2006). Pediatrics, Pneumonia. Retrieved April 10, 2009, from http://emedicine.medscape.com/article/803364-overview
↑ Jump up to:13.0 13.1 13.2 13.3 Steyl, T. (2007). Applied Physiotherapy 403 notes: Intensive Care Notes. University of the Western Cape.
Jump up↑ Ruuskanen, O., Lahti, E., Jennings, L. C., & Murdoch, D. R. (2011). Viral pneumonia. The Lancet, 377(9773), 1264–1275. doi:10.1016/s0140-6736(10)61459-6
Jump up↑ Schiffman, G., & Stoppler, M. (2009). Pneumonia. Medicine Net. Com. Retrieved April 12, 2009 from Causes, Symptoms, Signs and Treatment (Viral, Bacterial) on MedicineNet_com.mht
Jump up↑ Adderley N, Sharma S. Pleural Friction Rub. Accessed 16 March 2020
Jump up↑ Klein, J. (2008). Pneumonia. Retrieved February 13, 2009 from http://kidshealth.org/PageManager.jsp?dn=KidsHealth&lic=1&ps=107&cat_id=20043&article_set=23001
Jump up↑ Yang, M., Yan, Y., Yin, X., Wang, B. Y., Wu, T., Liu, G. J., & Dong, B. R. (2010). Chest physiotherapy for pneumonia in adults. Cochrane Database of Systematic Reviews. doi:10.1002/14651858.cd006338.pub2
Jump up↑ Madjoe, L., & Marais, M. (2007). Applied Physiotherapy 203 notes: Physiotherapy in Respiratory Care. University of the Western Cape.
Jump up↑ Morrow BM. Airway clearance therapy in acute paediatric respiratory illness: A state-of-the-art review. South African Journal of Physiotherapy. 2019 Jun 25;75(1):12.
Jump up↑ Mitobe Y, Morishita S, Ohashi K, Sakai S, Uchiyama M, Abeywickrama H, Yamada E, Kikuchi Y, Nitta M, Honda T, Endoh H. Skeletal Muscle Index at Intensive Care Unit Admission Is a Predictor of Intensive Care Unit-Acquired Weakness in Patients With Sepsis. Journal of Clinical Medicine Research. 2019 Dec;11(12):834.
Jump up↑ BTS Guidelines for the Physiotherapy Management of the Adult, Medical, Spontaneously Breathing Patient 2009
Jump up↑ PDR health. (2009). Pneumonia in children. Retrieved April 11, 2009 from http://www.pdrhealth.com/disease/mono.aspx
Jump up↑ Unicef (2006). Pneumonia: The Forgotten Killer of Children. Retrieved April 8, 2009, from http://www.childinfo.org/pneumonia.html
↑ Jump up to:25.0 25.1 Kids Health. (2009). Pneumonia. Retrieved April 11, 2009 from http://kidshealth.org/parent/infections/lung/pneumonia.html
Jump up↑ Drugs information online. (2009). Pneumonia in children care Guidelines information. Retrieved April 11, 2009 from http://www.drugs.com/cg/pneumonia-in-children.html
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14) BRONCHOPNEUMONIA
Bronchopneumonia is a subtype of pneumonia. It is the acute inflammation of the bronchi, accompanied by inflamed patches in the nearby lobules of the lungs.[1]
It is often contrasted with lobar pneumonia but in clinical practice the types are difficult to apply, as the patterns usually overlap.[2] Bronchopneumonia (lobular) often leads to lobar pneumonia as the infection progresses. The same organism may cause one type of pneumonia in one patient, and another in a different patient.
Causes[edit]
Bronchopneumonia is usually a bacterial pneumonia rather than being caused by viral disease.[4]
It is more commonly a hospital-acquired pneumonia than a community-acquired pneumonia, in contrast to lobar pneumonia.[5]
Bronchopneumonia is less likely than lobar pneumonia to be associated with Streptococcus pneumoniae.[6] Rather, the bronchopneumonia pattern has been associated mainly with the following: Staphylococcus aureus, Klebsiella, E. coli and Pseudomonas.[7]
Pathology
Bronchopneumonia may sometimes be diagnosed after death, during autopsy.
On gross pathology there are typically multiple foci of consolidation present in the basal lobes of the human lung, often bilateral. These lesions are 2–4 cm in diameter, grey-yellow, dry, often centered on a bronchiole, poorly delimited, and with the tendency to confluence, especially in children.
Light microscopy typically shows neutrophils in bronchi, bronchioles and adjacent alveolar spaces
15) CLASSIFY MUSCULAR DYSTROPHY
A group of genetic diseases that cause progressive weakness and loss of muscle mass.
In muscular dystrophies, abnormal genes (mutations) lead to muscle degeneration. Most forms begin in childhood.
Damaged muscles become progressively weaker. Most people who have the condition eventually need a wheelchair. Other symptoms include trouble breathing or swallowing.
Medication, therapy, breathing aids or surgery may help maintain function, but life span is often shortened.
Myotonic.
Duchenne.
Becker.
Limb-girdle.
Facioscapulohumeral.
Congenital.
Oculopharyngeal.
Distal.
16) LAB DIAGNOSIS OF TUBERCULOSIS
During the physical exam, your doctor will check your lymph nodes for swelling and use a stethoscope to listen carefully to the sounds your lungs make while you breathe.
The most commonly used diagnostic tool for tuberculosis is a simple skin test, though blood tests are becoming more commonplace. A small amount of a substance called PPD tuberculin is injected just below the skin of your inside forearm. You should feel only a slight needle prick.
Within 48 to 72 hours, a health care professional will check your arm for swelling at the injection site. A hard, raised red bump means you're likely to have TB infection. The size of the bump determines whether the test results are significant.
17) DISCUSS THE PROCESS OF THROUMBUS FORMATION
A thrombus, colloquially called a blood clot, is the final product of the blood coagulation step in hemostasis. There are two components to a thrombus: aggregated platelets and red blood cells that form a plug, and a mesh of cross-linked fibrin protein. The substance making up a thrombus is sometimes called cruor. A thrombus is a healthy response to injury intended to prevent bleeding, but can be harmful in thrombosis, when clots obstruct blood flow through healthy blood vessels.
Mural thrombi are thrombi that adhere to the wall of a blood vessel. They occur in large vessels such as the heart and aorta, and can restrict blood flow but usually do not block it entirely. They appear grey-red with alternating light and dark lines (known as lines of Zahn) which represent bands of entrapped white blood cells and red blood cells (darker).
18) OSTEOMALCIA
Osteomalacia is a disease characterized by the softening of the bones caused by impaired bone metabolism primarily due to inadequate levels of available phosphate, calcium, and vitamin D, or because of resorption of calcium. The impairment of bone metabolism causes inadequate bone mineralization. Osteomalacia in children is known as rickets, and because of this, use of the term "osteomalacia" is often restricted to the milder, adult form of the disease. Signs and symptoms can include diffuse body pains, muscle weakness, and fragility of the bones. In addition to low systemic levels of circulating mineral ions necessary for bone and tooth mineralization, accumulation of mineralization-inhibiting proteins and peptides (such as osteopontin and ASARM peptides) occurs in the extracellular matrix of bones and teeth, likely contributing locally to cause matrix hypomineralization (osteomalacia).[1][2][3][4][5]
The most common cause of osteomalacia is a deficiency of vitamin D, which is normally derived from sunlight exposure and, to a lesser extent, from the diet.[6] The most specific screening test for vitamin D deficiency in otherwise healthy individuals is a serum 25(OH)D level.[7] Less common causes of osteomalacia can include hereditary deficiencies of vitamin D or phosphate (which would typically be identified in childhood) or malignancy.
Vitamin D and calcium supplements are measures that can be used to prevent and treat osteomalacia. Vitamin D should always be administered in conjunction with calcium supplementation (as the pair work together in the body) since most of the consequences of vitamin D deficiency are a result of impaired mineral ion homeostasis.[7]
19) POLYMYOSITIS
Polymyositis (PM) is a type of chronic inflammation of the muscles (inflammatory myopathy) related to dermatomyositis and inclusion body myositis. Its name means "inflammation of many muscles" (poly- + myos- + -itis). The inflammation of polymyositis is mainly found in the endomysial layer of skeletal muscle, where as dermatomyositis is characterized primarily by inflammation of the perimysial layer of skeletal muscles.[1]
Polymyositis and the associated inflammatory myopathies have an associated increased risk of cancer.[3] The features they found associated with an increased risk of cancer was older age, age greater than 45, male sex, difficulty swallowing, death of skin cells, cutaneous vasculitis, rapid onset of myositis (<4 weeks), elevated creatine kinase, higher erythrocyte sedimentation rate and higher C-reactive protein levels. Several factors were associated with lower-than-average risk, including the presence of interstitial lung disease, joint inflammation/joint pain, Raynaud's syndrome, or anti-Jo-1 antibody.[3] The malignancies that are associated are nasopharyngeal cancer, lung cancer, non-Hodgkin's lymphoma and bladder cancer, amongst others.[4]
Cardiac involvement manifests itself typically as heart failure, and is present in up to 77% of patients.[2] Interstitial lung disease is found in up to 65% of patients with polymyositis, as defined by HRCT or restrictive ventilatory defects compatible with interstitial lung disease.[5]
SHORT ANSWERS
(2 MARKS)
1) DEFINE NECROSIS
Necrosis (from Ancient Greek νέκρωσις, nékrōsis, "death") is a form of cell injury which results in the premature death of cells in living tissue by autolysis.[1] Necrosis is caused by factors external to the cell or tissue, such as infection, toxins, or trauma which result in the unregulated digestion of cell components. In contrast, apoptosis is a naturally occurring programmed and targeted cause of cellular death. While apoptosis often provides beneficial effects to the organism, necrosis is almost always detrimental and can be fatal.
2) TYPES OF CACIFICATION
Hypercalcaemia.
Milk-alkali syndrome (Burnett's)
Calcinosis (Calciphylaxis, Calcinosis cutis)
Calcification (Metastatic calcification, Dystrophic calcification)
Familial hypocalciuric hypercalcemia.
3) CLASSIFY CELL INJURY AND GIVE EXAMPLES
refer book
4) DEFINE EDEMA CLASSIFY
Edema, also known as fluid retention or swelling, is the buildup of fluid in the body's tissue.[1] Most commonly, the legs or arms are affected.[1] Symptoms may include skin which feels tight, the area may feel heavy, and affected joints may be hard to move.[1] Other symptoms depend on the underlying cause.[2]
CLASSIFICATION;
pitting edema
non pitting edema
5) DEFINE ATROPHY
Edema, also known as fluid retention or swelling, is the buildup of fluid in the body's tissue.[1] Most commonly, the legs or arms are affected.[1] Symptoms may include skin which feels tight, the area may feel heavy, and affected joints may be hard to move.[1] Other symptoms depend on the underlying cause.[2]
Examples of atrophying nerve diseases include Charcot-Marie-Tooth disease, poliomyelitis, amyotrophic lateral sclerosis
6) GIVE EXAMPLES FOR CONGESTIVE CARDIAC FAILURE
A chronic condition in which the heart doesn't pump blood as well as it should.
Heart failure can occur if the heart cannot pump (systolic) or fill (diastolic) adequately.
Symptoms include shortness of breath, fatigue, swollen legs and rapid heartbeat.
(NEEDS ADDITINOL REFRENCE)
7) CLASSIFY ISCHEMIC HEART DISEASE
Coronary artery disease (CAD), also known as coronary heart disease (CHD) or ischemic heart disease
Blood fats[edit]
High blood cholesterol (specifically, serum LDL concentrations). HDL (high density lipoprotein) has a protective effect over development of coronary artery disease.[38]
High blood triglycerides may play a role.[39]
High levels of lipoprotein(a),[40][41][42] a compound formed when LDL cholesterol combines with a protein known as apolipoprotein(a).
Dietary cholesterol does not appear to have a significant effect on blood cholesterol and thus recommendations about its consumption may not be needed.[43] Saturated fat is still a concern.[43]
Genetics[edit]
The heritability of coronary artery disease has been estimated between 40% and 60%.[44] Genome-wide association studies have identified over 160 genetic susceptibility loci for coronary artery disease
8) NAME THE VARIOUS TYPES OF COPD
There are 3 types of COPD:
Emphysema: Damage to air sacs in your lungs leaves you short of breath.
Chronic bronchitis: When you have coughing, shortness of breath, and mucus that lingers at least 3 months for 2 years in a row.
Refractory asthma: This type may also be called nonreversible.
9) WHAT IS MILIARY TUBERCULOSIS
Miliary tuberculosis is a form of tuberculosis that is characterized by a wide dissemination into the human body and by the tiny size of the lesions (1–5 mm). Its name comes from a distinctive pattern seen on a chest radiograph of many tiny spots distributed throughout the lung fields with the appearance similar to millet seeds—thus the term "miliary" tuberculosis. Miliary TB may infect any number of organs, including the lungs, liver, and spleen.[2] Miliary tuberculosis is present in about 2% of all reported cases of tuberculosis and accounts for up to 20% of all extra-pulmonary tuberculosis cases.
10) SEQUESTRUM
A sequestrum (plural: sequestra) is a piece of dead bone that has become separated during the process of necrosis from normal or sound bone.
It is a complication (sequela) of osteomyelitis. The pathological process is as follows:
infection in the bone leads to an increase in intramedullary pressure due to inflammatory exudates
the periosteum becomes stripped from the ostium, leading to vascular thrombosis
bone necrosis follows due to lack of blood supply
sequestra are formed
11) LEPRA CELLS
lep·ra cells
distinctive, large, mononuclear phagocytes (macrophages) with a foamlike cytoplasm, and also poorly staining saclike structures resulting from degeneration of such cells, observed characteristically in leprous inflammatory reactions; indistinct staining results from numerous, fairly closely packed leprosy bacilli, which are acid fast and resistant to staining by ordinary methods.
12) GRANULOMA
A granuloma is a structure formed during inflammation that is found in many diseases. It is a collection of immune cells known as macrophages.[1] Granulomas form when the immune system attempts to wall off substances it perceives as foreign but is unable to eliminate. Such substances include infectious organisms including bacteria and fungi, as well as other materials such as foreign objects, keratin and suture fragments.
13) GRANULATION TISSUE
Granulation tissue is new connective tissue and microscopic blood vessels that form on the surfaces of a wound during the healing process.[1] Granulation tissue typically grows from the base of a wound and is able to fill wounds of almost any size. Examples of granulation tissue can be seen in pyogenic granulomas and pulp polyps. Its histological appearance is characterized by proliferation of fibroblasts and new thin-walled, delicate capillaries (angiogenesis), infiltrated inflammatory cells in a loose extracellular matrix.
14) GIVE 2 EXAMPLES FOR BENIGN AND MALIGANT TUMORS
refer book
15) DEFINE NEOPALSIA
Neoplasia is new, uncontrolled growth of cells that is not under physiologic control. A "tumor" or "mass lesion" is simply a "growth" or "enlargement" which may not be neoplastic (such as a granuloma). The term "cancer" implies malignancy, but neoplasms can be subclassified as either benign or malignant.
16) WRITE 2 DIFFERENCE BETWEEN HYPERPLASIA AND HYPERTROPHY
refer book
17) DEFINE ATELECTASIS
Atelectasis is the collapse or closure of a lung resulting in reduced or absent gas exchange. It is usually unilateral, affecting part or all of one lung. It is a condition where the alveoli are deflated down to little or no volume, as distinct from pulmonary consolidation, in which they are filled with liquid
18) APOPTIOSIS
Apoptosis is a form of programmed cell death, or “cellular suicide.” It is different from necrosis, in which cells die due to injury. Apoptosis is an orderly process in which the cell's contents are packaged into small packets of membrane for “garbage collection” by immune cells.
19) OSTEOMYELITIS
Osteomyelitis is an infection in a bone. Infections can reach a bone by traveling through the bloodstream or spreading from nearby tissue. Infections can also begin in the bone itself if an injury exposes the bone to germ
20) GOUT
Gout is a form of inflammatory arthritis characterized by recurrent attacks of a red, tender, hot, and swollen joint.[4][5] Pain typically comes on rapidly, reaching maximal intensity in less than 12 hours.[8] The joint at the base of the big toe is affected in about half of cases.[10] It may also result in tophi, kidney stones, or kidney damage.[4]
Gout is due to persistently elevated levels of uric acid in the blood.[5][8] This occurs from a combination of diet, other health problems, and genetic factors.[4][5] At high levels, uric acid crystallizes and the crystals deposit in joints, tendons, and surrounding tissues, resulting in an attack of gout.[4] Gout occurs more commonly in those who regularly eat meat or seafood, drink beer, or are overweight.[4][6] Diagnosis of gout may be confirmed by the presence of crystals in the joint fluid or in a deposit outside the joint.[4] Blood uric acid levels may be normal during an attack.[4]
DIAGRAMS NESSARY...
13) 5 MARKS ( REFER BOOK)
PNEUMONIA and its stages needs additional reference...
