Gastroesophageal Reflux Disease (GERD)

The initial symptoms consist of chest pain on heartburn due to the mucosa injury that may worsen after the ingestion of food or drugs.

Ethiology

GERD arises from conditions that lead to successive expositions of acids on the esophagus mucosa. These conditions (hormones, nerve agents, food and others) include disturbs that increase the LES spontaneous relaxation frequency. That conditions that increase the stomach volume or pressure (increased production of acid and pyloric obstruction) also contribute to esophagitis. Coffee and tobacco cause relaxation of the cardia.

The hiatal hernia (proximal portion of the stomach that slides to the chest cavity) causes descent LES and consequently the reflux occurrence.

Pathology and Pathogenesis

The LES tonic contraction allows a effective barrier to the acid reflux of stomach. These barrier efficiency can be changed by LES tone loss, increased frequency of the transitory relaxation and increased stomach volume, that may become the reflux acid enough to cause pain and erosion. The recurrent reflux can cause mucosa injury and inflammation (esophagitis resulting from granulocytes and eosinophils infiltration with basal cell hyperplasia and blooding ulcers formation). The reflux predisposes the occurrence of more reflux due to the cicatrisation of the inflamed epithelium.  

On regular conditions, the LES transient relaxations are accompanied by the increased esophageal peristalsis. Thus, the individuals with defects on the excitatory pathways that promote peristalsis may be at increased risk of developing esophagic reflux.

Clinical Manifestations

The usual symptom is heartburn, aggravated by a supine position. It can be developed a stenosis (esophagus narrowing) in the distal portion of the esophagus. The progressive obstruction manifests itself in the form of dysphagia. Other reflux complications include bleeding or perforation and pneumonia due to the gastric aspiration into the lungs.

Smoking and alcohol, associated to recurrent reflux, result in changes on the esophagic epithelium (columnar to squamous), called as Barrett’s Esophagus (it mat lead to adenocarcinoma development)

Treatament

1. Decreased stomach pressure (drugs that promote gastric emptying; avoid eating a lot before going to bed)

2. Decreased gastric acidity (antacids)

3. Maintaining of cardia pressure (reduce alcohol, coffee and fat; eat little portions each time)

4. Protection of the esophagus mucosa.

Diarrhea

Diarrhea is characterized by the elimination of feces that present excessive volume and frequency, and are abnormally liquid – more than 3 stools for day. The subjective evaluation of the feces by the patient is influenced by his bowel habits. The diarrhea can be acute (up to 3 to 4 week with infectious cause) or chronic (more than 4 weeks).

The diarrhea can be classified as osmotic, secretory or oily.

The osmotic diarrhea is caused by the poor nutrients absorption or by the poor absorption of electrolytes that retain the water in the lumen. The secretory diarrhea occurs when the secretory cells maintain a high rate of liquid transportation of the GI tract to the lumen. The oily diarrhea (by poor absorption) occurs when the ability to digest or absorb a certain nutrient is deficient.

Ethiology

The flow in the GI tract involves the massive discharge of liquid in the lumen and its absorption, causing the a dynamic balanced state. Changes in these characteristics (excessive osmotic charge, increased discharge or decreased liquid absorption) can origin diarrhea.

Causes:

Osmotic diarrhea –low absorbable solutes ingest (fructose, magnesium salts, phosphate and citrate anion); poor absorption of carbohydrates (flatulence by the sugar digestion made by bacteria).

 Secretory diarrhea – the substances that stimulate the electrolyte discharge by the bowel mucosa by the increased AMPc or GMPc (enterotoxins or production of VIP by the pancreas tumours).

Inflamatory diarrhea – organic injury of the bowel (colon) where occurs a decrease of water absorption and a production of exudate rich in proteins and sometimes pus (diarrhea with mucus, blood and pus of bacterial cause or non-infectious).  

Motor (mobility) – increased peristalsis by prokinetic agents, decreasing the available time for the absorption of any nutrient or liquid.

Pathology and Pathogenesis

The infectious agents are the most important cause of diarrhea because they cause severe diseases that sometimes are fatal. Diarrhea  caused by infectious agents symptoms are caused by toxins that changes the bowel discharge and the absorption.   

Clinical Manifestations

Depending of its cause, intensity and chronicity, the most common signs consists of dehydration (severe diahrrea mostly in children), height loss and specific vitamin deficiency syndrome (glossitis, stomatitis). It may also be hypokalemia and metabolic acidosis (bicarbonate loss).

Inflammatory Bowel Disease - Crohn’s and Colitis

The non-inflamatory bowel disease is differentiated from the infectious for exclusion because it is characterized by recurrent episodes of diarrhea with mucus and leukocytes.

Ethiology

There are two forms of inflammatory bowel disease: Crohn’s Disease (it is transmural and granulomatous) and Ulcerative Colitis (superficial and confined to the colon mucosa).

Pathology and Pathogenesis

Microorganisms, dietary factors, genetic factors and deficient immune answers contribute for Crohn’s Disease that is characterized by and uncontrolled inflammation. The ulcerative colitis can be originated by infections, allergies and dietary components, immune answers to bacteria and psychosocial factors.

The common characteristic of inflammatory bowel diseases consists in the mucosal ulceration and the GI tract inflammation.

Clinical Manifestations

A.    Crohn’s Disease

It can occur in any area of the GI tract in a discontinuous manner. It is characterized by ulceration and inflammation affecting the entire intestinal wall thickness. The disease complications consists are perforation, fistula formation, abscesses formation and small bowel obstruction.

The patients have symptoms outside the GI tract: skin, eyes and mucosa inflammatory disorders,  renal disorders (oxlate absorption associated to steatorrhea); thromboembolic and amyloidosis disease (disease in which amyloidosis, a rare protein that usually doesn’t exist in our body,  accumulates in several tissues). The patients may also present chronic diarrhea with periods of remission, height loss, anorexia, rectal bleeding and malabsorption of iron and B12 vitamin.

B.    Ulcerative Colitis

It is restricted to the colon and rectum mucosa. The obstruction, perforation and fistula formation aren’t complications because the colitis affects only the mucosa. There is a higher risk of developing carcinoma. It is characterized for acute and severe crises, and is more often in younger adults

It is manifested by feces with mucus and blood (severe anemia), diarrhea and peritonitis fistula.

Diverticular Disease

Constipation and lower abdominal pain with intermittent and unpredictable crampy. The patient with diverticulitis presents fever and peritoneal irritation (absent bower sons). The patient with diverticular bleeding presents bloody feces.

Ethiology

The diverticular disease results from a deformation acquired in the colon (sigmoid colon), when occurs the lining dilatation. It is more common in people older than 40 and in industrialized countries. Its prevalence it’s increased by a low-fiber diet with consequent increased constipation.

Pathology and Pathogenisis

A.    Diverticulosis

Individuals with genetic disease involving the connective tissue, as Ehlers-Danlos and Marfan Syndrome, are characterized by the disease appearance on a younger age. The decrease of fibers become harder the feces propulsion, causing vigorous muscular contraction of the colon wall, that can lead to abdominal pain that is the major symptom of the disease. The pain can last several hours or days, and during that period of time it may also occur constipation, diarrhea and flatulence.

B.    Diverticular bleeding

It is painless and arises because the colon intramural arteries are associated to the diverticular sac, leading to the occurrence of rupture and bleeding.

C.    Diverticulitis

It occurs when exists a inflamation on the diverticulum wall, in response to the irritation caused by fecal material. The patient presents abdominal pain, fever, intestinal necrosis and fistula formation.

Interstitial Lung Disease

Known ethiology: dust, drugs, poisons, radiation, infectious agents, secondary to pulmonary edema and chronic uraemia.

Unknown ethiology: Sarcoidosis, amyloidosis

Pathophysiology

Regardless the cause, after the initial pulmonary paremchyma injury it occurs a accumulation of inflammatory and immune cells, that origin an alveolitis that can progress for the pulmonary acid destruction, pulmonary fibrosis and the cystic cavity formation. These events can origin capillary evolvement, pulmonary hypertension and finally right cardiac insufficiency (cor pulmonale).

Clinical manifestations

Dyspnoea

Pain

Discomfort

Hemoptysis (diffuse alveolar bleeding)

Quick and superficial breathing (due to a major resistance for lack of elasticity)

por perda de elasticidade)

Increased dead space

Increased work by the respiratory muscles

Respiratory insuffciency: Increased oxygen

CO2 pressure increased or normal

Idiopathic Pulmonary Fibrosis

Disease characterized by the cells infiltration in interstitial respiratory tissues (interstitial pulmonary disease) with healing of lung parenchyma. This leads to an increase in elastic recoil of the lung and a decrease of compliace, that we known as characteristics of restrictive pulmonary diseases.

Clinical presentation

Also known as criptogenic fibrosing alveolitis, the pulmonary fribosis is an uncommon disease that includes dry and persistent cough with no fever or chest pain. With the progress of the disease the dyspnea proliferates and originates cyanosis. In more advanced stages it occurs pulmonary hypertension that leads to peripheral edema and right cardiac insufficiency.

Phatophysiology

The primary injury that leads to fibrosis remains unknown. Meanwhile it can be observed a series of cellular events that regulates the inflammatory process and the fibrotic answer.

These events are:

- Initial injury of the tissue;

- Damage and vascular activation and trombolises in several degrees;

- Injury and epithelium activation with loss on the barrier integrity and release of proinflammatory mediators;

- Increased adhesion of leukocytes;

- Continuous process of injury and healing characterized by changes in cellular populations, and increased production of matrix with increased deposits of collagen and elastin.

These events lead to a pattern of pulmonary injury that causes an increased of the elastic recoil and changes on  gas exchange and pulmonary and vascular abnormalities.  

Clinical Manifestations

Cough

Dyspnea and tachypnea: It is necessary a larger effort to pulmonary distension. A fast and superficial inspiration pattern decreases the ventilation effort.  

Respiratory rales: Reflect the sucessive opening of respiratory units due to fibrosis and loss of surfactant.

Cardiatic Examination: hypoxemia, pulmonary hypertension, increased jugular venous pressure, tricuspid regurgitation murmur.

Pulmonary function tests: Reduction of CPT, FEV1 and FVC. DLCO progressively reduces.

Arterial blood gas analysis: Hypoxemia due to the increased dead space.

Pulmonary Edema

The pulmonary edema is the accumulation of excess fluid in the extravascular space of the lungs. This accumulation can slowly occur in patients with renal insufficiency or abruptly on patients with heart insufficiency to myocardial infarction. The pulmonary edema presents itself usually as dyspnea. In severe cases the pulmonary edema may present also edema liquid on the phlegm, leading to acute respiratory insufficiency.

Etiology

Causes of pulmonary edema:

Transmural increased pulmonary capilary wedge pressure (increased hydrostatic pressure): Increased left atrial pressure, pulmonary venous hypertension, increased capillary blood volume, decreased interstitial pressure, reduced colloid osmotic pressure (hypoalbuminemia due to nephrotic syndrome and liver failure).

Permeability of increased pulmonary capillary endothelium: Circulatin toxins, infectious pneumonia, pulmonary edema due to the high altitude after pulmonary bypass.

Increased permeability of the alveolar epithelium: Inhaled toxins, aspiration of gastric contents, drowning or near drowning, decreased surfactant.

Decreased lymphatic drainage.

Phatophysiology

A problem in one or more of the following factors: The capillary or alveolar endothelial permeability and the colloid osmotic and hydrostatic pressure are related to almost every clinic presentations of pulmonary edema.

In clinical practice these four factors are grouped into two types of pulmonary edema:

 - Cardiogenic pulmonary edema related to edema resulting from increased hydrostatic or osmotic pressure.

 - Noncardiogenic pulmonary edema  related to edema resulting from changes in the endothelium and alveolar capillary permeability. This edema it’s often known as Adult Respiratory Distress Syndrome (ARDS). The alveolar liquid that accumulates as result of lost of integrity of alveolar epithelium allows that solutes and large molecules (as albumin) entering the alveolar spaces. These changes can result from the injury of the alveolar epithelium by inhaled toxins or by pulmonary infection or even by changes that occur after a primary injury of the endothelium by circulating toxins. The circulating factors may act directly on capillary endothelium or may affect it by immune mediators. For example in infections by Gram bacteria the bacterial endotoxins cause the adherence of neutrophils and macrophages to endothelial surfaces that also cause the release of prostaglandins, thromboxanes and leukotrienes as oxygen radicals that cause oxidative injury. Both neutrophils and macrophages can release proteolytic enzymes that cause more damage.

Clinical manifestations

There are two types of pulmonary edema that cause an increase of the extravascular liquid in the lung and both can lead to respiratory insufficiency.  

Dermocosmetics

The products of dermal and topic application may acquire different names depending on their physicochemical and therapeutic proprieties.

EXFOLIATING

Exfoliate your skin is very important and it is routine for many people. The exfoliating purpose is to eliminate the imperfections, remove dead epithelial cells and clear the sebaceous glands. With an exfoliant you can improve the global look of your skin (make you skin look healthy), and you can also prevent the bubbles. The acne treatment doesn’t usually demand an exfoliation, because it is applied only after the acne effects are attenuated.

The exfoliation, to be abrasive enough, has to contain granular substances with several sizes, incorporated into a cream or a gel.

The exfoliation shouldn’t be done everyday! Abrasive activity need to be substantial but not exaggerated.  Depending on the exfoliating effect of the cream or gel the use need to be ruled.

SERUM

The serums are active substances concentrates. When applied topically these active substances quickly penetrate  the skin and prepares it for the application of another cream. The purpose of the serum is different from the cream: the serum prepares the skin for the cream action; the serum doesn’t “care” about the treatment of the surface skin phenomena, because this is the “job” that creams do.

The serums don’t usually applied alone.

The serums aren’t used for acne treatment. Serums can be used for skin reconstruction because it helps regenerate the damaged tissues.

We can find in the market several types of serums that helps the elimination or improvement of wrinkles, spots or sagging. The serums prices are higher than the prices of creams, probably due to the higher concentration of active substances.

GEL MOUSSANT

The Gel Moussant is a gel that prepares the skin for the cream application. It leaves the skin more healthy and clean. It is used instead of exfoliating on the acne treatment. The gel is applied as soap: apply in a uniform and circular movement until friction forms foam. After that you have to wash with warm water, dry carefully and apply the treatment cream.

The ranges of cosmetics contains creams usually presents also gel moussant for the application for one after another that contains the same active substance.

MICELLAR WATER

It is used instead of the gel moussant and also as a makeup cleaner. It is applied with cotton on dry skin.