Peptic Ulcer

 Peptic ulcers are sores that develop in the lining of the stomach, lower esophagus, or small intestine. They’re usually formed as a result of inflammation as well as from erosion from stomach acids. Peptic ulcers are a fairly common health problem.

There are three types of peptic ulcers:

• gastric ulcers: ulcers that develop inside the stomach 
• esophageal ulcers: ulcers that develop inside the esophagus 
• duodenal ulcers: ulcers that develop in the upper section of the small intestines, called the duodenum

Predisposing Factors

• Helicobacter pylori (H. pylori), a type of bacteria that can cause a stomach infection and inflammation 
• Frequent use of aspirin and other antiinflammatory drugs (risk associated with this behavior increases in women and people over the age of 60) 
• Smoking 
• drinking too much alcohol 
• Radiation therapy 
• stomach cancer

Peptic ulcer It might be asymptomatic (No S & S) Other common signs of a peptic ulcer include:

• Changes in appetite 
• Nausea 
• Bloody or dark stools 
• unexplained weight loss
• Indigestion 
• Vomiting 
• Chest pain

Peptic Ulcer Complications 

• Perforation: A hole develops in the lining of the stomach or small intestine and causes an infection. A sign of a perforated ulcer is sudden, severe abdominal pain.
• Internal bleeding: Bleeding ulcers can result in significant blood loss and thus require hospitalization. Signs of a bleeding ulcer include lightheadedness, dizziness, and black stools.
• Scar tissue: This is thick tissue that develops after an injury. This tissue makes it difficult for food to pass through your digestive tract. Signs of scar tissue include vomiting and weight loss.

Peptic Ulcer Diagnosis

• Laboratory tests for H. pylori. 
• Endoscopy. 
• Upper gastrointestinal series.

Peptic Ulcer Management

• Antibiotic medications to kill H. pylori. 
• Medications that block acid production and promote healing. 
• Medications to reduce acid production. Acid blockers — also called histamine (H-2) blockers
• Antacids that neutralize stomach acid. 
• Medications that protect the lining of your stomach and small intestine.

Hypothyroidism & Hyperthyroidism

 Hypothyroidism Deficit secretion of thyroid hormones

Pathophysiology

• Primary hypothyroidism : the most cases : 
• Fails to produce enough TH that stimulate TSH is secreted by the pituitary gland
•  Secondary hypothyroidism : 

• low levels of TSH which fail to stimulate release of TH 
• Tertiary hypothyroidism :
•  inadequate release of TRH(thyrotropin-releasing hormone) secreted by hypothalamus  low level of hormones that slow metabolism

Etiology

Primary hypothyroidism : congenital ,inflammation or iodine deficiency, autoimmune disorder (Hashimoto’s thyroiditis) ,thyroid surgery, radiation therapy 

Secondary or tertiary : pituitary or hypothalamic lesion or postpartum pituitary necrosis or treatment of hyperthyroidism

Risk factor 

woman age 50 and over, man age 60 and over 

high cholesterol 

autoimmune disease such as , rheumatoid arthritis or lupus.

Signs and symptom

• Cardiovascular: Bradycardia , decreased cardiac output , cool skin , cold intolerance, fatigue
•  Neurologic: Lethargy , slowed movements , loss concentration , confusion, depression, muscles weakness, hoarse voice 
• Pulmonary : Dyspnea , hypoventilation 
• Integumentary : cool, dry skin, brittle , dry hair hair loss (eyebrow)
• Gastrointestinal : Decreased appetite , weight gain , constipation , increased serum lipid levels 
• Reproductive : Decreased libido , erectile dftitl

Complications

.1- Myxedema coma 

• Hypothermic , decreased respiration 
• Depressed mental function and lethargy • Blood glucose drops , cardiac output drops 
• Reduced perfusion of kidney , non pitting edema 
• Death from respiratory failure

2- Cretinism a decreased production of T4 and results in mental retardation

Diagnostic test

• Level of T3&T4 are low 
• Level of TSH low or high depend on cause 
• Serum cholesterol and triglycerides are elevated 
• Antibodies present in autoimmune disease 
• ↓Radioactive iodine uptake test

Therapeutic measure

• 1- thyroid replacement hormone (Levothyroxine ) 
• Doses are started low and are slowly increased to prevent symptoms of hyperthyroidism or cardiac complication 
• 2- Iodine Deficiency 
• Iodized Salt 
• Increase intake of seafood 
• SSKI- saturated solution of potassium iodide
•  3. Nutritional Therapy A low-calorie diet to promote weight loss or prevent weight gain 

Hyperthyroidism Excess secretion of thyroid hormones

Pathophysiology

• Primary hyperthyroidism problem within thyroid gland causes excess hormone release 
• Secondary hyperthyroidism Excess TSH from pituitary so overstimulation of thyroid gland
• Tertiary hyperthyroidism Excess TRH 
• High level of thyroid hormone increase the metabolic rate 

Etiology

• Graves disease :autoimmune disorder (hereditary ) 
• Thyroid nodules , inflammation or tumor , medication 
• Secondary Malfunctioning pituitary Malfunctioning hypothalamus Risk factor . iodine intake, cigarett common in the 30's and 40's women . excessive doses of thyroid hormone 

Signs and symptom

• Tachycardia , palpitation , increased cardiac out put , warm skin , heat intolerance, chest pain 
• Fatigue , restlessness , exophthalmose, hyperactive reflexes , tremor , insomnia , emotional instability 
• Dyspnea 
• Diaphoresis , warm , moist skin , fine soft hair, Hair loss, goiter
• Increased appetite ,weight loss , frequent stools , decreased serum lipid levels 
• Decreased libido , erectile dysfunctionamonorrhea

Complications

1. Thyrotoxic crisis (thyroid storm) is severe hyperthyroidism 

• Death in as little as 2 hrs if untreated (high fever , tachycardia 130 , hypertension , dehydration , restlessness and coma 

2.Hypothyroidism long term disease as result of treatment

Diagnostic test

• Level of T3&T4are high 
• Level of TSH low in primary hyperthyroidism or high on cause of pituitary 
• ↑Radioactive iodine uptake test 
• Palpation of thyroid gland 
• TSI(thyroid stimulating immunoglobulin) is present in Graves disease

Therapeutic measure

• 1- anti-thyroid drug •Propylthiouracil (PTU) And methimazole (Tapazole) continue for 12-18 months 2- beta-blocker Propranol (indral) 
• 3- Radioactive iodine 
• 4- Surgery (thyroidectomy) 
• 5-. Nutritional Therapy 

• High-calorie, high-protein diet, carbohydrates 
• Frequent meals 

Angina

 Angina pectoris, or angina, as it is commonly referred to, and coronary artery disease or arteriosclerosis are closely related. Angina occurs in people who have some form of blockage in the coronary arteries. In other words, it occurs in people with coronary heart disease. Angina pectoris: a heart condition marked by paroxysms of chest pain due to reduced oxygen to the heart. It occurs when the Oxygen Supply to the Myocardium is insufficient for its needs.

Types f Angina

• Stable angina
• Unstable angina 
• Variant angina (prinzmetal's angina )
• Microvascular angina

Stable angina  :

Stable angina is Predictable Occurs on exercise, emotion or eating. Caused by increase demand of the heart and by a fixed narrowing of coronary vessels. Coronary obstruction is ‘fixed’ Blood flow fails to increase during increased demand despite the local factors mediated ‘vasodilation’ and so ischeamic pain is felt. 

Unstable angina :  

This is characterized by Pain that occurs with less exertion , cumulating pain at rest. The pathology is similar to that involved in Myocardial Infraction, namely platelet-fibrin thrombus associated with a ruptured plaque, but without complete occulation of the vessels. The risk of infraction is large, and the main aim of therapy is to reduce this

Variant angina (prinzmetal's angina )

Uncommon Occurs at rest generally during sleep Caused by Large Coronary Artery Spasm Usually with abnormally reactive and hypertrophied segments in the Coronary Artery. Drugs aimed at preventing & relieving Coronary Spasm.

Microvascular Angina :

Microvascular Angina or Angina Syndrome X is characterized by angina-like chest pain, but the cause is different. The cause of Microvascular Angina is unknown, but it appears to be the result of spasm in the tiny blood vessels of the heart, arms, and legs. Since microvascular angina is not characterized by arterial blockages, it is harder to recognize and diagnose, but its prognosis is excellent

Major risk factors

• Age (≥ 55 years for men, ≥ 65 for women) 
• Cigarette smoking 
• Diabitis Mellitus 
• Dyslipidemia 
• Family history of premature cardiovascular disease (men <55 years, female <65 years old)
• Hypertension (HTN) 
• Kidney disease (microalbuminuria or GFR<60 mL/min) 
• Obesity (BMT ≥ 30 kg/m2) 
•  Physical inactivity 
• Prolonged psychosocial stress

Conditions that exacerbate or provoke angina 

• Medications 
• Vasodilators 
• Excessive thyroid replacement 
• Vasoconstrictors 
• Polycythemia which thickens the blood causing it to slow its flow through the heart muscle 
• Hypothermia 
• Hypovolaemia 
• Hypervolaemia
• Profound /deep anemia 
• Uncontrolled HTN 
• Hyperthyrodism 
• Hypoxemia 
• Tachyarrhythmia 
• Bradyarrhythmia Valvular heart disease 
• Hypertrophic cardiomyopathy

Medical Management of angina

• Nitroglycerin. 
• Beta blockers 
• Calcium channel blockers 
•  ACE inhibitors

Surgical Management of angina

• Coronary artery bypass graft (CABG)

Congestive Heart Failure

 Heart failure is a condition in which the heart can’t pump enough blood throughout the body. Heart failure does not mean that the heart has stopped or is about to stop working. It means that the heart is not able to pump blood the way that it should. The heart can ’t fill with enough blood or pump with enough force, or both.

Pathophysiology

Systolic HF decreases the amount of blood ejected from the ventricle, which stimulates the sympathetic nervous system to release epinephrine and norepinephrine. The purpose of this initial response is to support the failing myocardium. The sympathetic stimulation and the decrease in renal perfusion by the failing heart cause the release of renin by the kidney

Renin promotes the formation of angiotensin I. 

Angiotensin-converting enzyme (ACE) in the lumen of blood vessels converts angiotensin I to angiotensin II, a vasoconstrictor that also causes the release of aldosterone.

Aldosterone promotes sodium and fluid retention and stimulates the thirst center. Aldosterone causes additional detrimental effects to the myocardium and exacerbates myocardial fibrosis. All of this alteration causes increasing preload and afterload which increase workload on the heart

Diastolic HF develops because of continued increased workload on the heart, which responds by increasing the number and size of myocardial cells. These responses cause resistance to ventricular filling, which increases ventricular filling pressures despite a normal or reduced blood volume. Less blood in the ventricles causes decreased CO. The low CO and high ventricular filling pressures cause the same neurohormonal responses as described for systolic HF.

Angiotensin II 

constricts the walls of arterioles closing down capillary beds; 

stimulates the proximal tubules in the kidney to reabsorb sodium ions; 

stimulates the adrenal cortex to release aldosterone. Aldosterone causes the kidneys to reclaim still more sodium and thus water. 

 increases the strength of the heartbeat; 

 stimulates the pituitary to release the vasopressin.

Classification of HF

• Class I: no limitation in any activities (ADLs); there are no symptoms (fatigue, dyspnea or chest pain) from ordinary activities. 
• Class II: slight, mild limitation of activity (ADLs); the patient is comfortable at rest but increased physical activities will cause symptoms. 
• Class III: marked limitation of any activity; the patient is comfortable only at rest.
•  Class IV: symptoms of cardiac insufficiency occur at rest.

Causes of HF

narrowed arteries that supply blood to the heart muscle — coronary artery disease. 

• past heart attack, or myocardial infarction, with scar tissue that interferes with the heart muscle's normal work. 
• high blood pressure. 
• heart valve disease due to past rheumatic fever or other causes. 
•  primary disease of the heart muscle itself, called cardiomyopathy. 
•  heart defects present at birth — congenital heart defects. 
• infection of the heart valves and/or heart muscle itself — endocarditis and/or myocarditis

Signs and sysmptoms

Generally 

• Pale, cyanotic skin (with decreased perfusion to extremities) 
• Dependent edema (with increased venous pressure) 
• Deceased activity tolerance 

Cardiovascular 

• Apical impulse, enlarged and left lateral displacement (with cardiac enlargement)
• Third heart sound (S3) 
• Murmurs (with valvular dysfunction) Tachycardia 
• Increased jugular venous distention (JVD)

Cerebrovascular 

• Lightheadness, Dizziness, Confusion 

Gastrointestinal 

• Nausea and anorexia & abdominal pain. 
• Enlarged liver, Ascites, 

Renal 

• Decreased urinary frequency during the day 
• Nocturia 

Respiratory 

• Dyspnea on exertion, Orthopnea 
• Paroxysmal nocturnal dyspnea 
• Bilateral crackles that do not clear with cough

Right side HF

Right-sided heart failure causes the blood entering the heart from the body to back up in the veins causing swelling of the legs, feet , and stomach.

Left side HF

Left-sided heart failure causes fluid to back up and accumulate in the lungs. This leads to the patient symptoms of shortness of breath, inability to sleep and waking up in the middle of the night gasping for breath, inability to exercise without shortness of breath, inability to catch your breath while at rest, and for severe cases coughing and gurgling with frothy sputum

Medical management

The basic objectives in treating patients with HF are the following:

Eliminate or reduce any etiologic contributory factors, especially those that may be reversible, such as atrial fibrillation or excessive alcohol ingestion. 

 Reduce the workload on the heart by reducing afterload and preload.

ex:

• Angiotensin-Converting Enzyme Inhibitors. 
• Angiotensin II Receptor Blockers (ARBs). 
• Beta-Blockers.
• Diuretics
• Digitalis
• Vasodilators

Asthma

 Asthma is Chronic inflammatory disorder associated with airway hyper responsiveness leading to recurrent episodes (attacks)

Often reversible airflow limitation

Prevalence increasing in many countries, especially in children

Pathophysiology of asthma

Allergy is the strongest predisposing factor for asthma. 

Chronic exposure to airway irritants or allergens also increases the risk for developing asthma. 

Airway irritants (eg, air pollutants, cold, heat, weather changes, strong odors or perfumes, smoke), 

Exercise, stress or emotional upsets, medications and viral respiratory tract infections. 

Cells that play a key role in the inflammation of asthma are mast cells, neutrophils, eosinophils, and lymphocytes. 

Mast cells, when activated, release several chemicals mediators. These chemicals, which include histamine, bradykinin, prostaglandins, and leukotrienes , perpetuate the inflammatory response, 

causing increased blood flow, vasoconstriction, fluid leak from the vasculature, attraction of white blood cells to the area, and broncho constriction

Clinical Manifestations

• Cough • Chest tightness 
• Wheezing (first on expiration and then possibly during inspiration as well. ) 
• Dyspnea • Expiration prolonged 1-3 or 1-4, due to bronchospasm, edema, and mucus 
• Feeling of suffocation- upright or slightly bent forward using accessory muscles 
• Behaviors of hypoxemia- restlessness, anxiety, ↑HR & BP and cyanosis.

Assessment and Diagnosis

History and patterns of symptoms 

Measurements of Pulmonary function tests 

CXR • ABGs and pulse oximetry 

Allergy testing (skin, IgE) 

sputum and blood tests 

complications of Asthma 

• ftigue or exhaustion
• poor  sleep
• being less productive at work or while studying
• an inability to exercise and be physically active
• reduced lung function
• poor mental health

Medical management 

Medications to Treat Asthma: Inhalers and Spacers

• Inhalers, which are devices that let you breathe in medicine, are the main treatment.
• Spacers can reduce potential for adverse effects from medication.

Quick-Relief Medications

• Rapid-acting inhaled β2 -agonists 
• Short-acting oral β2agonists 
• Systemic corticosteroids 
• Anticholinergics [Atrovent) 
• Theophylline

Long-Acting Control Medications.

• Inhaled corticosteroids 
•  Leukotriene modifiers 
• Long-acting inhaled β2 -agonists in combination with inhaled gluco-corticosteroids 
•  Systemic corticosteroids 
• Theophylline 
•  Cromones 
•  Anti-IgE

Diagnostic Tests

Pulmonary function tests (PFT) 

Pulmonary function tests (PFTs) are routinely used in patients with chronic respiratory disorders. They are performed to assess respiratory function and to determine the extent of dysfunction.

PFTs generally are performed by a technician using a spirometer that has a volume-collecting device attached to a recorder that demonstrates volume and time simultaneously. 

lung volumes, ventilator function, mechanics of breathing and gas exchange. Observe for increased dyspnea or bronchospasm 

ARTERIAL BLOOD GAS STUDIES

Measurements of blood pH and of arterial oxygen and carbon dioxide tensions. 

Arterial blood gas studies aid in assessing the ability of the lungs to provide adequate oxygen and remove carbon dioxide. 

The arterial oxygen tension (PaO2) indicates the degree of oxygenation of the blood, and the arterial carbon dioxide tension (PaCO2) indicates the adequacy of alveolar ventilation.

Pulse oximetry

Pulse oximetry is a noninvasive method to monitor the oxygen saturation of hemoglobin (SaO2). 

A probe or sensor is attached to the fingertip , earlobe, or bridge of the nose. The sensor detects changes in oxygen saturation levels by monitoring light signals generated by the oximeter.

 Normal SaO2 values are 95% to 100%. Values less than 85% indicate that the tissues are not receiving enough oxygen, and the patient needs further evaluation.

SPUTUM STUDIES

Sputum is obtained for analysis to identify pathogenic organisms. 

Periodic sputum examinations may be necessary for patients receiving antibiotics, corticosteroids, and immunosuppressive medications for prolonged periods. 

In general, sputum cultures are used in diagnosis, for drug sensitivity testing, and to guide treatment. 

Bronchoscopy

Visualization (a thin flexible fiberoptic telescope) of the tracheo-bronchila tree via a scope advanced through the mouth or nose

As diagnostic bronchoscopy for :

• examine tissues or collect secretions, 
• determine the location and extent of the pathologic process and to obtain a tissue sample for diagnosis. 
• determine if a tumor can be resected surgically 
• diagnose bleeding sites.

As Therapeutic bronchoscopy to:

• Remove foreign bodies from the tracheobronchial tree,
• Remove secretions obstructing the tracheobronchial tree when the patient cannot clear them, 
• Destroy and excise lesions.

Thoracoscopy

Thoracoscopy is a diagnostic procedure in which the pleural cavity is examined with an endoscope. 

Small incisions are made into the pleural cavity in an intercostal space; the location of the incision depends on the clinic.

Thoracocentesis

A thin layer of pleural fluid normally remains in the pleural space. An accumulation of pleural fluid may occur with some disorders. 

A sample of this fluid can be obtained by thoracentesis (aspiration of pleural fluid for diagnostic or therapeutic purposes).

 Fluid obtained during thoracocentesis may be examined for abnormal cells, bacteria, and other substances to determine the cause of the pleural effusion.

BIOPSY

Biopsy, the excision of a small amount of tissue, may be performed to permit examination of cells from the pharynx, larynx, nasal passages, pleural and lung. 

Local, topical, or general anesthesia may be administered, depending on the site and the procedure.

Chronic obstructive pulmonary disease (COPD)

 COPD, or chronic obstructive pulmonary disease, is a progressive disease that makes it hard to breathe. "Progressive" means the disease gets worse over time.

It is a disease state characterized by airflow limitation that is not fully reversible.

COPD may include diseases that cause airflow obstruction (eg, emphysema, chronic bronchitis) or a combination of these disorders. 

Asthma was previously classified as types of chronic obstructive lung disease. 

asthma is now considered a separate disorder and is classified as an abnormal airway condition characterized primarily by reversible inflammation.

In COPD, less air flows in and out of the airways because of one or more of the following:

• The walls of the airways become thick and inflamed. 
• The airways and air sacs lose their elastic quality. 
• The walls between many of the air sacs are destroyed. 
• The airways make more mucus than usual, which tends to clog them.

1- Chronic Bronchitis

a disease of the airways, is defined as the presence of cough and sputum production for at least 3 months in each of 2 consecutive years. 

Characterized by Chronic inflammation

The most important cause is recurrent irritation of the bronchial mucosa by inhaled substances, as occurs in cigarette smokers. 

Bronchial walls thicken

• Bronchial Lumen narrows by increase in the size of the bronchial mucus glands
• Mucus plugs airway lead to obstruction

Plugs become areas for bacteria to grow and chronic infections which increases mucus secretions and eventually, areas of focal necrosis and fibrosis

Alveoli/bronchioles become damaged

2- Emphysema

Defined as destruction of the alveoli that deliver oxygen into the lung and remove the carbon dioxide.

Characterized by Chronic cough

Types of Emphysema

In the panlobular type

• There is destruction of the bronchiole, alveolar duct, and alveoli. All air spaces within the lobule are essentially enlarged. 
• The patient with this type of emphysema typically has a hyper inflated chest (barrel chest on physical examination), marked dyspnea on exertion, and weight loss.

In the centrilobular form,

• pathologic changes take place mainly in the center of the lobule, producing chronic hypoxemia, hypercapnia (increased CO2 in the arterial blood).

Pathophysiology of emphysema

• Affects alveolar membrane 
• Destruction of alveolar wall 
• Loss of elastic recoil 
• Over distended alveoli 
• → Impaired gas exchange 
• Hypoxemia 
• h CO2 →

Risk Factors of COPD

• Smoking irritates the mucus glands, causing an increased accumulation of mucus, which in turn produces more irritation, infection, and damage to the lung. 
• Smoking depresses the activity of the respiratory tract’s ciliary cleansing mechanism. 
• In addition, carbon monoxide (a byproduct of smoking) combines with hemoglobin to form carboxyhemoglobin that cannot carry oxygen efficiently. 
• Deficiency of alpha1 antitrypsin, an enzyme inhibitor that protects the lung parenchyma from injury. 

Sysmptoms

• cough 
• sputum
•  dyspnea

Complications

• Hypoxemia may further increase pulmonary artery pressure. 
• Right-sided heart failure (cor pulmonale) is one of the complications of emphysema 
• Congestion, dependent edema, distended neck veins, or pain in the region of the liver suggests the development of cardiac failure. 

Diagnostic Findings

• Pulmonary function tests are used to help confirm the diagnosis of COPD, 
• Arterial blood gas 
• chest x-ray 
• alpha1 antitrypsin deficiency screening may be performed for patients under age 45 or for those with a strong family history of COPD. 

PHARMACOLOGIC THERAPY

Bronchodilators. To relieve bronchospasm To reduce airway obstruction To increase oxygen distribution throughout the lungs and improving lung ventilation

Corticosteroids. Inhaled and systemic corticosteroids (oral or intravenous) Examples of corticosteroids in the inhaled form are beclomethasone (Beclovent, Vanceril), budesonide (Pulmicort), flunisolide (AeroBid), fluticasone (Flovent), and triamcinolone (Azmacort). 

Influenza vaccine and the pneumococcal vaccine every 5 to 7 years as preventive measures.

Alpha1 antitrypsin augmentation therapy,

Antibiotic , mucolytic agents

OXYGEN THERAPY 

Oxygen therapy can be administered as long-term continuous therapy, during exercise, or to prevent acute dyspnea. Long term oxygen therapy has been shown to improve the patient’s quality of life and survival

Oxygen therapy can be administered as long-term continuous therapy, during exercise, or to prevent acute dyspnea. Long term oxygen therapy has been shown to improve the patient’s quality of life and survival

SURGICAL MANAGEMENT

Lung Volume Reduction Surgery.

• It involves the removal of a portion of the diseased lung parenchyma. 
• This allows the functional tissue to expand, resulting in improved elastic recoil of the lung and improved chest wall and diaphragmatic mechanics. 

Lung Transplantation

• Surgical treatment for the end-stage of emphysema. It has been shown to improve quality of life and functional capacity

Breathing Exercises

Diaphragmatic breathing

• To reduces the respiratory rate, 
• To increases alveolar ventilation, 
• To expel as much air as possible during expiration. 

Pursed lip breathing

• To slow expiration, 
• To prevent collapse of small airways. 
• To control the rate and depth of respiration. 

PULMONARY TUBERCULOSIS

 Tuberculosis (TB) is an infectious disease that primarily affects the lung parenchyma.

It also may be transmitted to other parts of the body, including the meninges, kidneys, bones, and lymph nodes (Extra pulmonary Tuberculosis).

The primary infectious agent, Mycobacterium tuberculosis, is an acid-fast aerobic rod that grows slowly and is sensitive to heat and ultraviolet light.

Different Categories of Tuberculosis

Latent TB Infection

Many of those who are infected with TB do not develop overt disease. They have no symptoms and their chest x-ray may be normal. 

The only manifestation of this encounter may be reaction to the tuberculin skin test (TST). 

The risk to be an active disease is increased by other illnesses such as HIV or medications which compromise the immune system.

Active TB Disease

Active TB is an illness in which the TB bacteria are rapidly multiplying and invading different organs of the body. 

A person with active pulmonary TB disease may spread TB to others by airborne transmission of infectious particles coughed into the air.

Miliary TB

Miliary TB is a rare form of active disease that occurs when TB bacteria find their way into the blood stream. 

In this form, the bacteria quickly spread all over the body in tiny nodules and affect multiple organs at once. This form of TB can be rapidly fatal.

Transmission and Risk Factors

• TB spreads from person to person by airborne transmission.
•  An infected person releases droplet nuclei through talking, coughing, sneezing, laughing, or singing. Larger droplets settle; smaller droplets remain suspended in the air and are inhaled by the susceptible person. 

Pathophysiology of TB

Inhalation of tubercle bacilli 

Reach the alveoli of the lungs 

Ingested by alveolar macrophages 

Accumulation of exudate in the alveoli, causing bronchopneumonia.( 2 to 10 weeks after exposure). 

A small number of the bacilli spread through the blood stream to the apex of the lung, the kidneys, the brain, the bones, and through the lymphatic channels to regional lymph nodes (Extra pulmonary TB).

new tissue masses of live and dead bacilli, are surrounded by macrophages( granulomas).

Granulomas are then transformed to a fibrous tissue mass.

Then becomes necrotic, forming a cheesy mass. 

This mass may become calcified and form a collagenous scar. 

At this point, the bacteria become dormant, and there is no further progression of active disease (Latent TB). • After initial exposure and infection or inadequate immune system response. 

Active disease also may occur with re infection and activation of dormant bacteria. 

In this case, the cheesy material is released into the bronchi

Assessment and Diagnostic Findings

• A complete history, 
• Physical examination, 
• Tuberculin skin test, 
• Chest x-ray, 
• Sputum culture are used to diagnose TB. 

MANTOUX TUBERCULIN SKIN TEST (TST)

The Mantoux tuberculin skin test, or TST, is performed by placing an intradermal injection of 0.1 ml of purified protein derivative (PPD) containing 5 tuberculin units (TU) into the intradermal layer of the inner aspect of the forearm. 

This should produce a wheal 6 mm to 10 mm in diameter. Institutional guidelines regarding universal precautions for infection control (e.g., use of gloves) should be followed . The reaction to the TST should be read 48 to 72 hours after the injection by a trained healthcare worker.

The reaction is read by measuring in millimeters the diameter of induration (palpable raised hardened area) across the forearm. If there is no induration, the result should be recorded as 0 mm. The area of erythema should not be measured, just the induration.

Interpretation of Results

The size of the induration determines the significance of the reaction. 

A reaction of 0 to 4 mm is considered not significant; 

a reaction of 5 mm or greater may be significant in individuals who are considered at risk. 

An induration of 10 mm or greater is usually considered significant in individuals who have normal or mildly impaired immunity. 

A significant reaction indicates that a patient has been exposed to M. tuberculosis recently or in the past or has been vaccinated with bacille Calmette-Guerin (BCG) vaccine. 

Medical Management

• Pulmonary TB is treated primarily with (antituberculosis agents) for 6 to 12 months. 
• A prolonged treatment duration is necessary to ensure eradication of the organisms and to prevent relapse.

PHARMACOLOGIC THERAPY

• In current TB therapy, five first-line medications are used: isoniazid (INH), rifampin, pyrazinamide, and either streptomycin or ethambutol. 
•  second-line medications. Capreomycin, ethionamide, paraaminosalicylate sodium, and cycloserine 
• Additional potentially effective medications include other aminoglycosides, quinolones, rifabutin, clofazimine, and combinations of medications.

Pneumonia

 Pneumonia Is an inflammatory process of the lung parenchyma that is commonly caused by infectious agents.

Causes of pneumonia

• Bacterial (the most common cause of pneumonia) 
• Viral pneumonia 
• Fungal pneumonia 
• Chemical pneumonia (ingestion of kerosene or inhalation of irritating substance) 
• Aspiration pneumonia (food, liquids, vomits from the mouth into your lungs)

Classification of pneumonia According to areas involved

Lobar pneumonia; if one or more lobe is involved 

Broncho-pneumonia; the pneumonic process has originated in one or more bronchi and extends to the surrounding lung tissue.

Bronchopneumonia is more common than lobar pneumonia

Types of pneumonia

• Community-acquired pneumonia (CAP), 
• Hospital acquired pneumonia (HAP), 
• Pneumonia in the immuno compromised host, 
• Aspiration pneumonia

Community-acquired pneumonia 

It occurs either in the community setting or within the first 48 hours of hospitalization. 

Pneumonia caused by Streptococcus pneumoniae (pneumococcus) and Haemophilus influenzae.

It is most prevalent during the winter and spring, when upper respiratory tract infections are most frequent.

Hospital-acquired pneumonia

It also known as nosocomial pneumonia, is defined as the onset of pneumonia symptoms more than 48 hours after admission to the hospital. 

HAP accounts for approximately 15% of hospital-acquired infections. 15% to 20% of intensive care patients. pneumonia that is associated with endotracheal intubation and mechanical ventilation.

The common organisms responsible for HAP include the pathogens Pseudomonas, Staphylococcus Aureus (MRSA), Escherichia coli.

Pneumonia in immunocompromised host

Immuno-compromised states occur with the use of :

    • corticosteroids, 

    • chemotherapy, 

    •use of broad-spectrum antimicrobial agents, 

    • AIDS, • genetic immune disorders 

    • (mechanical ventilation). 

Pneumonia in the compromised host may be caused by the organisms also observed in CAP or HAP (S. pneumoniae, S. aureus, H. influenzae, P. aeruginosa, M. tuberculosis).

 Aspiration pneumonia

It resulting from the entry of endogenous or exogenous substances into the lower airway

The most common form of aspiration pneumonia is bacterial infection from aspiration of bacteria that normally reside in the upper airways.

Other substances may be aspirated into the lung, such as gastric contents, chemical contents, or irritating gases. 

Complications

• Respiratory failure and Hypotension 
• Atelectasis may occur at any stage of acute pneumonia. 
• Pleural effusions occur in at least 40% of bacterial pneumonias. 
• An empyema occurs when thick, purulent fluid accumulates within the pleural space where the infection is located. 
• Super infection may occur with the administration of very large doses of antibiotics, such as penicillin, or with combinations of antibiotics.

Risk Factors 

    • Cigarette smoking 

    • Immuno-suppressed patients 

    • Prolonged immobility 

    • Depressed cough reflex (due to medications, or weak respiratory muscles); 

    • Abnormal swallowing mechanism 

    •  Placement of nasogastric, oro-gastric, or endotracheal tube

     • Antibiotic therapy - Alcohol intoxication 

    • General anesthetic, sedative. 

    • Advanced age 

    • Respiratory therapy with improperly cleaned equipment

Clinical Manifestations

    • Dyspnea, tachypnea, orthopnea 

    • Cough (productive but may be dry if the patient is dehydrated: requires hydration to loosen and                expectorate viscous sputum) 

    • Purulent sputum may be tinged with blood 

    • Cyanosis • Pyrexia, tachycardia, sweating 

    • Pain especially with lobar, over affected lobe 

    • Some patients exhibit an upper respiratory tract infection (nasal congestion, sore throat), 

    • poor Appetite

Diagnostic Findings

• physical examination, 
• chest x-ray studies,
• sputum studies and sputum culture. 
• Pulse oximetry or arterial blood gas analysis

Medical Management

• Antibiotic (erythromycin, azithromycin [Zithromax], or clarithromycin [Biaxin]), doxycycline (Vibramycin). 
• Antipyretics may be used to treat headache and fever; 
•  Mucolytic medications. 
• Warm, moist inhalations. 
• Antihistamines may provide benefit with reduced sneezing and rhinorrhea. 
• Nasal decongestants to relieve nasal congestion. 
• If hypoxemia develops, oxygen is administered. 

Preventive Measure

• Promote coughing and expectoration of secretions. 
• Stop smoking. • Initiate special precautions against infection.
• Perform suctioning and chest physical therapy if indicated. 
• Promote frequent oral hygiene. 
• Observe the respiratory rate and depth during recovery from general anesthesia 
• Promote frequent turning, early ambulation and mobilization, 
• Healthy balanced diet. 
• Make sure that respiratory equipment is cleaned properly.

Rhinitis

 Rhinitis is an inflammation and irritation of the mucous membranes of the nose. It may be classified as allergic or non-allergic.

Rhinitis may be an acute or chronic condition.

The signs and symptoms of rhinitis include:

• Rhinorrhea (excessive nasal drainage, runny nose), 
• Nasal congestion, 
• Nasal discharge (purulent with bacterial rhinitis), 
• Nasal itchiness, and sneezing. 
• Headache may occur, particularly if sinusitis is also present.

The Allergic Appearance:

• in chronic nasal congestion Mouth breathing and a gaping mouth
• Nasal itching causes repeated wiggling of the nose (bunny nose), or wiping and pushing of the nose 

Complication

• Sinusitis which is inflammation or swelling of the tissue that lines the sinuses
• Eustachian tube dysfunction. Eustachian tubes connect the middle ears to the back of the throat
• Chronic ear infection, known as otitis media 
• Loss of smell or anosmia
• Asthma 
• Obstractive sleep apnea

Pathophysiology of Allergic Rhinitis

It occurs when the body’s immune system over-responds to specific, non-infectious particles such as plant pollens, dust mites, animal hair, industrial chemicals (including tobacco smoke).

During an allergic attack, antibodies, primarily immunoglobin E (IgE), attach to mast cells (cells that release histamine) in the lungs, skin, and mucous membranes.

Once IgE connects with the mast cells, a number of chemicals are released. One of the chemicals, histamine, opens the blood vessels and causes skin redness and swollen membranes.

Pathophysiology of Non-Allergic Rhinitis

The symptoms can be initiated by cigarette smoke, strong odors, alcoholic beverages and changes in temperature or humidity, or foods.

These agents do not act through immune mediated systems, but are an irritant to the nasal mucosa and cause hyper responsive reactions. They trigger both the Olfactory nerve and the Trigeminal nerve that senses burning and irritation by airborne. 

Other causes may include: 

• Blockages in the nose 
• a deviated septum 
• Infections 
• Drug-induced rhinitis is associated with use of antihypertensive agents and oral contraceptives and chronic use of nasal decongestants (Ephedrine), NSAIDs nonsteroidal antiinflammatory drugs such as aspirin and ibuprofen

Medical Therapy

• Medication therapy for allergic and non- allergic rhinitis focuses on symptom relief.
• Antihistamines are administered for sneezing, itching, and rhinorrhea. 
• Oral decongestant agents are used for nasal obstruction. 
• Intranasal corticosteroids may be used for severe congestion. 
• Ophthalmic agents are used to relieve irritation, itching, and redness of the eyes.  

Coronavirus

 Coronavirus is a type of virus that causes of varying severities, ranging from the common cold to more serious respiratory disease . A novel (new) coronavirus is anew strain of coronavirus that hasn't been identified before in humans

Human Coronavirus Types

Coronaviruses are named for the crown-like spikes on their surface. There are four main sub-groupings of coronaviruses, known as alpha, beta, gamma, and delta.

Human coronaviruses were first identified in the mid-1960s. The seven coronaviruses that can infect people are:(CDC February 2020).

Common human coronaviruses 

    • 229E (alpha coronavirus) 

    • NL63 (alpha coronavirus) 

    • OC43 (beta coronavirus) 

    • HKU1 (beta coronavirus)

Other human coronaviruses

    • MERS-CoV (the beta coronavirus that causes Middle East Respiratory Syndrome, or MERS) 

    • SARS-CoV (the beta coronavirus that causes severe acute respiratory syndrome, or SARS) 

    • SARS-CoV-2 (the novel coronavirus that causes coronavirus disease 2019, or COVID19)

Numbers of cases 

WHO in September 2020 reported that There have been 30,369,778 confirmed cases of COVID-19, including 948,795 deaths globally

coronavirus-disease-covid-19-how-is-it-transmitted

• spreads between people through direct, indirect (through contaminated objects or surfaces), or close contact with infected people via mouth and nose secretions. These include
•     saliva,
•     respiratory secretions or droplets through coughs, sneezes, speaks or sings  
• People who are in close contact (within 1 metre) with an infected person can catch COVID-19 when those infectious droplets get into their mouth, nose or eyes

How to Protect yourself and others from getting sick

•  Maintain at least 1 metre (3 feet) distance between yourself and others. 
•  Maintain at least 1 metre (3 feet) distance between yourself and others. 
• Avoid going to crowded places.
•  Governments should encourage the general public to wear a fabric mask if there is widespread community transmission, and especially where physical distancing cannot be maintained. 
• follow good respiratory hygiene (coughing and sneezing) 
• Avoid touching eyes, nose and mouth.
• Stay home and self-isolate even with minor symptoms such as cough, headache, mild fever, until you recover.
• If you need to leave your house, wear a mask to avoid infecting others.
• If you have a fever, cough and difficulty breathing, seek medical attention by telephone if possible and follow the directions.
• Keep up to date on the latest information from trusted sources.

Management 

There are currently over 169 COVID-19 vaccine candidates under development, with 26 of these in the human trial phase.

At home

• Staying physically active
• Healthy diet
• Healthy parenting
• Quitting tobacco
• Mental health 

Malaria

Malaria is an acute febrile illness caused by Plasmodium parasites, which are spread to people through the bites of infected female Anopheles mosquitoes

Malaria is one of the most common debilitating infections worldwide.

The WHO estimated that in 2015 there were 214 million new cases of malaria worldwide and more than 400,000 malaria related deaths, more than 90% occurring in Africa, and most of whom were children.

 Malaria is caused by

 five species of Plasmodium parasites that infect humans :

P. falciparum, P. vivax, P. ovale, P. malariae, P. knowlesi  

(a simian parasite that causes human malaria primarily in Malaysia), although two species account for the most cases and deaths.

Plasmodium falciparum is the most prevalent in Africa and accounts for most fatalities.

P. vivax is the primary cause of malaria outside of Africa it's Symptoms are severe flulike in nature and with less morbidity and mortality than observed with P.falciparum.

The signs and symptoms of Malaria

§  severe chills

§  high fever

§  sweating

§  headache

§  muscle pains

§  vomiting

§  Fatigue

§  severe anemia

§  Rapid breathing

§  Rapid heart rate

§  Cough

All forms of malaria are characterized by paroxysm (cyclic chills followed by fever).

 Cycles range from every 2 days for P. vivax to 36 hours for P. falciparum.

Complications of Malaria

Neurologic complications may result from infected red blood cells (RBCs)

adhering to endothelium in capillaries of the brain causing hypoxia and degradation of neural tissue.3 The most severely affected individuals may develop cardiovascular collapse, shock, coma, and death.

Pathophysiology of Malaria

The life cycle of Plasmodium requires two hosts:

Mosquito and human.

The parasite undergoes a sexual reproductive cycle in the salivary gland of the female Anopheles mosquito and is transmitted to humans during a blood meal.

The infectious form (sporozoite) enters the tissue and migrates to the bloodstream.

The sporozoite has the capacity to traverse through cells in the tissue, mediated by a variety of parasitic proteins that bind to specific substance on the cell surface and facilitate entry.

4 The parasite enters hepatocytes using sporozoite proteins that bind to sulfated molecules on endothelial cells and Kupffer cells.

Protection against malaria

 may occur by means of stage-specific immune responses against different phases of the life cycle:

Invasive stage, hepatic stage, pre-erythrocyte stage, erythrocyte stage, and sexual stages.

Phagocytic cells, like Kupffer cells, are the primary means of protection against the prehepatic invasive stage and hepatic stage. Traversal of phagocytic cells results in modulation of the cell's cytokine profile, causing decrease  regulation of proinflammatory cytokines and increase regulation of antiinflammatory cytokines blocked production of reactive oxygen species, and reduced expression of class I MHC to suppress antigen presentation.

The parasite in the blood avoids destruction by phagocytes in the spleen by expressing adhesion proteins that cause adherence and sequestration along the walls of

the small vessels.

Sequestration in the liver begins an asymptomatic stage during which several rounds of multiplication occur.

P. vivax and P. ovale can remain dormant in the liver for years, protected from the

immune system by intracellular residence. In the hepatocytes, the parasites transform to the merozoite form, thousands of which are released into the blood during hepatocyte rupture and infect erythrocytes.

The blood-borne phase and infection of erythrocytes begin the

symptomatic stage of the disease P. falciparum uses a  variety of parasite surface proteins (e.g., merozoite surface protein-1 [MSP-1]) for adhesion to erythrocyte membrane glycophorins and entrance into the cell.

Symptoms of malaria occur after an approximate 2-week period from the initial mosquito bite and are the result of asexual multiplication in the erythrocytes and cell lysis upon the release of daughter parasites that reinfect other erythrocytes. During this erythrocytic cycle, the merozoites mature into male and female gametocytes within the erythrocyte, which after another blood meal can establish another cycle of further sexual multiplication in the mosquito vector. The erythrocytic cycle will resolve, but many relapses will occur upon new cycles of merozoite release from infected hepatocytes

P. vivax seems to use the erythrocyte Duffy antigen for adhesion. Thus individuals who are negative for the Duffy blood group antigen are naturally resistant to P. vivax malaria.

During the erythrocytic cycle, the infected individual produces protective antibodies against antigens expressed on the surface of infected erythrocytes. Plasmodium expresses several families of antigens on the erythrocyte's surface and uses antigen variation through gene switching diversity to mitigate the effects of antibody. 

Other antigen-directed responses contribute to protection of the parasite. Antibodies against P. falciparum asparagine-rich protein enhance merozoite invasion of erythrocytes, which is further facilitated by the addition of complement. The PfEMP1 antigen also can protect the infected erythrocyte by epitope masking. The antigen contains Fc binding sites where IgM antibody, regardless of specificity, is bound by its Fc region, thus masking the PfEMP1 epitopes. Parasites also can bind complement regulator factor, factor H, which protects the parasite from damage by activated complement factors.

Malarial infection also may induce immune suppression by inhibiting macrophage and dendritic cell phagocytosis, as well as inducing apoptosis of antigen-presenting cells. Phagocytic cell function is diminished by a malarial pigment (hemozoin), which is taken up and reduces the ability to phagocytize merozoites or infected erythrocytes. Numbers of CD4 and CD8 T-cells are diminished by apoptosis combined with induction of immunosuppressive Treg cells. Malarial parasites have developed broad drug resistance including against chloroquine, the previous mainstay of the preventive and therapeutic arsenal of antimalarial drugs. Drug resistance appears to result from increased activity of drug transporters that eliminate the drugs from the parasitic microorganism.