ACUTE RESPIRATORY DISTRESS SYNDROME

 

Introduction: Acute respiratory distress syndrome (ARDS) is a severe form of acute lung injury characterized by sudden and progressive pulmonary edema, increasing bilateral infiltrates, hypoxemia unresponsive to oxygen supplementation, and the absence of an elevated left atrial pressure. ARDS occurs when inflammatory triggers initiate the release of cellular and chemical mediators, causing injury to the alveolar capillary membrane in addition to other structural damage to the lungs. Inflammatory mediators  Factors associated with the development of ARDS include direct injury to the lungs such as during smoke inhalation, or indirect insult to the lungs such as in the case of shock. Shock  ARDS has been associated with a mortality rate ranging from 25% to 58%, with the major cause of death in ARDS being non-pulmonary multiple-system organ failure, often with sepsis.

Clinical Manifestations: Rapid onset of severe dyspnea, usually 12 to 48 hours after an initiating event. Intercostal retractions and crackles may be present. Arterial hypoxemia not responsive to oxygen supplementation. Lung injury then progresses to fibrosing alveolitis with persistent, severe hypoxemia. Increased alveolar dead space and decreased pulmonary compliance.

Assessment and Diagnostic Findings: Plasma brain natriuretic peptide (BNP) levels. Echocardiography. Pulmonary artery catheterization.

Medical Management: Identify and treat the underlying condition; provide aggressive, supportive care (intubation and mechanical ventilation; circulatory support, adequate fluid volume, and nutritional support). Use supplemental oxygen as the patient begins the initial spiral of hypoxemia. Monitor ABG values, pulse oximetry, and pulmonary function testing. As disease progresses, use positive end-expiratory pressure (PEEP). Treat hypovolemia carefully; avoid overload (inotropic or vasopressor agents may be required). There is no specific pharmacologic treatment for ARDS except supportive care.

RELATED;

1.  PNEUMONIA

2.  TUBERCULOSIS  

3.  PULMONARY EMBOLISM

4.  MEDICAL CONDITIONS

REFERENCES

ACQUIRE IMMUNODEFICIENCY SYNDROME (AIDS)

 

INTRODUCTION: Acquired immunodeficiency syndrome (AIDS) is defined as the most severe form of a continuum of illnesses associated with human immunodeficiency virus (HIV) infection. HIV belongs to a group of viruses known as retroviruses. These viruses carry their genetic material in the form of ribonucleic acid (RNA) rather than deoxyribonucleic acid (DNA). Retroviruses  Infection with HIV occurs when it enters the host CD4 (T) cell and causes this cell to replicate viral RNA and viral proteins, which in turn invade other CD4 cells. Invasion of human CD4 cells byHIV

CLINICAL STAGING: The stage of HIV disease is based on clinical history, physical examination, laboratory evidence of immune dysfunction, signs and symptoms, and infections and malignancies. The Centers for Disease Control and Prevention (CDC) standard case definition of AIDS categorizes HIV infection and AIDS in adults and adolescents on the basis of clinical conditions associated with HIV infection and CD4 T-cell counts. Four categories of infected states have been denoted:

1) Primary infection (acute/recent HIV infection, acute HIV syndrome: dramatic drops in CD4 T-cell counts, which are normally between 500 and 1,500 cells/mm3 ).

2) HIV asymptomatic (CDC Category A: more than 500 CD4 T lymphocytes/mm3 ),

3) HIV symptomatic (CDC Category B: 200 to 499 CD4 T lymphocytes/mm3 ).

4) AIDS (CDC Category C: fewer than 200 CD4 T lymphocytes/mm3 ).

RISK FACTORS: HIV is transmitted through bodily fluids by high-risk behaviors such as heterosexual intercourse with an HIV-infected partner, injection drug use, and male homosexual relations. People who received transfusions of blood or blood products contaminated with HIV, children born to mothers with HIV infection, breast-fed infants of HIV-infected mothers, and health care workers exposed to needle-stick injury associated with an infected patient are also at risk.

CLINICAL MANIFESTATIONS: Symptoms are widespread and may affect any organ system. Manifestations range from mild abnormalities in immune response without overt signs and symptoms to profound immunosuppression, life-threatening infection, malignancy, and the direct effect of HIV on body tissues.

Respiratory; Shortness of breath, dyspnea, cough, chest pain, and fever are associated with opportunistic infections, such as those caused by Pneumocystis jiroveci (Pneumocystis pneumonia [PCP], the most common infection), Mycobacterium avium-intracellulare, cytomegalovirus (CMV), and Legionella species. HIV-associated tuberculosis occurs early in the course of HIV infection, often preceding a diagnosis of AIDS.

Gastrointestinal; Loss of appetite, Nausea and vomiting, Oral and esophageal candidiasis (white patches, painful swallowing, retrosternal pain, and possibly oral lesions), Chronic diarrhea, possibly with devastating effects (eg, profound weight loss, fluid and electrolyte imbalances, perianal skin excoriation, weakness, and inability to perform activities of daily living).

Wasting Syndrome (Cachexia); Multifactorial protein-energymalnutrition (PEM)  Profound involuntary weight loss exceeding 10% of baseline body weight. Either chronic diarrhea (for more than 30 days) or chronic weakness and documented intermittent or constant fever with no concurrent illnes. Certain types of cancer occur often in people with AIDS and are considered AIDS-defining conditions: Kaposi’s sarcoma (KS) is the most common HIV-related malignancy and involves the endothelial layer of blood and lymphatic vessels (exhibits a variable and aggressive course, ranging from localized cutaneous lesions to disseminated disease involving multiple organ systems). B-cell lymphomas are the second most common malignancy; they tend to develop outside the lymph nodes, most commonly in the brain, bone marrow, and GI tract. These types of lymphomas are characteristically of a higher grade, indicating aggressive growth and resistance to treatment. Invasive cervical cancer. 

Neurologic; HIV-associated neurocognitive disorders consist of cognitive impairment that is often accompanied by motor dysfunction and behavioral change. HIV-related peripheral neuropathy is common across the trajectory of HIV infection and may occur in a variety of patterns, with distal sensory polyneuropathy (DSPN) or distal symmetrical polyneuropathy the most frequently occurring type. DSPN can lead to significant pain and decreased function.

HIV encephalopathy; (formerly referred to as AIDS dementia complex [ADC]) is a clinical syndrome that is characterized by a progressive decline in cognitive, behavioral, and motor functions. Symptoms include memory deficits, headache, difficulty concentrating, progressive confusion, psychomotor slowing, apathy, and ataxia, and in later stages global cognitive impairments, delayed verbal responses, a vacant stare, spastic paraparesis, hyperreflexia, psychosis, hallucinations, tremor, incontinence, seizures, mutism, and death.

Cryptococcus neoformans, a fungal infection (fever, headache, malaise, stiff neck, nausea, vomiting, mental status changes, and seizures).

RELATED;

1.  VIROLOGY

2.  INVASION OF HUMAN CD4 CELLS BY HIV

3.  KAPOSI'S SARCOMA

REFERENCES

ANATOMY AND PHYSIOLOGY OF THE HEART

 

INTRODUCTION: Normal resting Heart Rate of an adult will be in the range of 60–100 bpm. Bradycardia is the condition in which resting rate drops below 60 bpm, and tachycardia is the condition in which the resting rate is above 100 bpm. Trained athletes typically have very low HRs. If the patient is not exhibiting other symptoms, such as weakness, fatigue, dizziness, fainting, chest discomfort, palpitations, or respiratory distress, bradycardia is not considered clinically significant.  However, if any of these symptoms are present, they may indicate that the heart is not providing sufficient oxygenated blood to the tissues. The term relative bradycardia may be used with a patient who has a HR in the normal range but is still suffering from these symptoms. Most patients remain asymptomatic as long as the HR remains above 50 bpm. Bradycardia may be caused by either inherent factors or causes external to the heart. While the condition may be inherited, typically it is acquired in older individuals. Inherent causes include abnormalities in either the SA or AV node. If the condition is serious, a pacemaker may be required. Other causes include ischemia to the heart muscle or diseases of the heart vessels or valves. External causes include metabolic disorders, Metabolic disorders pathologies of the endocrine system often involving the thyroid, electrolyte imbalances, neurological disorders including inappropriate autonomic responses, autoimmune pathologies, over-prescription of beta blocker drugs that reduce HR, recreational drug use, or even prolonged bed rest.

Treatment relies upon establishing the underlying cause of the disorder and may necessitate supplemental oxygen. Tachycardia is not normal in a resting patient but may be detected in pregnant women or individuals experiencing extreme stress. In the latter case, it would likely be triggered by stimulation from the limbic system or disorders of the autonomic nervous system. In some cases, tachycardia may involve only the atria. Some individuals may remain asymptomatic, but when present, symptoms may include dizziness, shortness of breath, lightheadedness, rapid pulse, heart palpations, chest pain, or fainting (syncope). While tachycardia is defined as a HR above 100 bpm, there is considerable variation among people. 

Further, the normal resting HRs of children are often above 100 bpm, but this is not considered to be tachycardia. Many causes of tachycardia may be benign, but the condition may also be correlated with fever, anemia, hypoxia, hyperthyroidism, hypersecretion of catecholamines, some cardiomyopathies, some disorders of the valves, and acute exposure to radiation. Elevated rates in an exercising or resting patient are normal and expected. Resting rate should always be taken after recovery from exercise.  Treatment depends upon the underlying cause but may include medications, implantable cardioverter defibrillators, ablation, or surgery.

RELATED;

1.  SHOCK  

2.  CHAMBERS AND CIRCULATION THROUGH THE HEART  

3.  CARDIAC CYCLE AND THE HEART SOUNDS

4.  ANATOMY AND PHYSIOLOGY

REFERENCES

HYPERTHYROIDISM (GRAVE’S DISEASE)

 

INTRODUCTION: Hyperthyroidism is the second most common endocrine disorder, and Graves’ disease is the most common type. It results from an excessive output of thyroid hormones due to abnormal stimulation of the thyroid gland by circulating immunoglobulins. The disorder affects women eight times more frequently than men and peaks between the second and fourth decades of life. It may appear after an emotional shock, stress, or infection, but the exact significance of these relationships is not understood. Other common causes include thyroiditis and excessive ingestion of thyroid hormone such as from the treatment of hypothyroidism.

CLINICAL MANIFESTATIONS: Hyperthyroidism presents a characteristic group of signs and symptoms collectively known as thyrotoxicosis. 

1) Nervousness characterised by emotionally being hyperexcitable, irritability, apprehensiveness; inability to sit quietly; palpitations; rapid pulse on rest and exertion. 

 2) Poor tolerance of heat; excessive perspiration; skin that is flushed, with a characteristic salmon color, and likely to be warm, soft, and moist. 

 3) Dry skin and diffuse pruritus. 

 4) Fine tremor of the hands. 

 5) Increased appetite and dietary intake, progressive loss of weight, abnormal muscle fatigability, weakness, amenorrhea, and changes in bowel function (constipation or diarrhea). 

6) Pulse ranges between 90 and 160 beats per minute; systolic (but not diastolic) blood pressure elevation (increased pulse pressure). 

7) Atrial fibrillation; cardiac decompensation in the form of congestive HF, especially in the elderly. 

 8) Osteoporosis and fracture. 

 9) Cardiac effects may include sinus tachycardia or dysrhythmias, increased pulse pressure, and palpitations; myocardial hypertrophy and HF may occur if the hyperthyroidism is severe and untreated.

Assessment and Diagnostic Findings: Thyroid gland is enlarged; it is soft and may pulsate; a thrill may be felt and a bruit heard over thyroid arteries. Laboratory tests show a decrease in serum TSH, increased free T4, and an increase in radioactive iodine uptake.

Medical Management: Treatment is directed toward reducing thyroid hyperactivity to relieve symptoms and preventing complications. Three forms of treatment are available: 1) Radioactive iodine therapy for destructive effects on the thyroid gland. 2) Antithyroid medications. 3) Surgery with the removal of most of the thyroid gland.

RELATED;

1.  Metabolism and metabolic disorders  

2.  Addison's disease

3.  Pruritus

REFERENCES  

ARTEMISININ & ITS DERIVATIVES

INTRODUCTION: Artemisinin is a sesquiterpene lactone endoperoxide, the active component of an herbal medicine that has been used as an antipyretic in China for over 2000 years. Artemisinin is insoluble and can only be used orally. However, analogs have been synthesized to increase solubility and improve antimalarial efficacy. The most important of these analogs are artesunate which is water-soluble and is useful for oral, intravenous, intramuscular, and rectal administration. The other one is artemether which is lipid-soluble and useful for oral, intramuscular, and rectal administration, and dihydroartemisinin which is water-soluble and useful for oral administration.

CHEMISTRY & PHARMACOKINETICS: Artemisinin and its analogs are rapidly absorbed, with peak plasma levels occurring in 1–2 hours and half-lives of 1–3 hours after oral administration. Artemisinin, artesunate, and artemether are rapidly metabolized to the active metabolite dihydroartemisinin. Drug levels appear to decrease after a number of days of therapy.

Artemether-lumefantrine (Coartem, Lumartem, Combiat, Riamet): Co-formulated; first-line therapy in many countries; approved in the USA

Artesunate-amodiaquine (ASAQ, Arsucam, Coarsucam): Co-formulated; first-line therapy in many African countries

Artesunate-mefloquine: Co-formulated; first-line therapy in parts of Southeast Asia and South America.

Dihydroartemisinin-piperaquine (Artekin, Duocotecxin): Co-formulated; first-line therapy in some countries in Southeast Asia

Artesunate-sulfadoxine-pyrimethamine: First-line therapy in some countries, but efficacy lower than other regimens in most areas.

CLINICAL USES: Artemisinin-based combination therapy is now the standard for treatment of uncomplicated falciparum malaria in nearly all areas endemic for falciparum malaria. These regimens were developed because the short plasma half-lives of the artemisinins led to unacceptably high recrudescence rates after short-course therapy, which were reversed by inclusion of longer-acting drugs. Combination therapy also helps to protect against the selection of artemisinin resistance. However, with completion of dosing after 3 days, the artemisinin components are rapidly eliminated, and so selection of resistance to partner drugs is of concern. The WHO recommends five artemisinin-based combinations for the treatment of uncomplicated falciparum malaria. One of these, artesunate-sulfadoxine-pyrimethamine is not recommended in many areas owing to unacceptable levels of resistance to sulfadoxine-pyrimethamine, but it is the first-line therapy in some countries in Asia, South America, and North Africa. The other four recommended regimens are now all available as combination formulations, although manufacturing standards may vary. Artesunate-mefloquine is highly effective in Southeast Asia, where resistance to many antimalarials is common; it is the first-line therapy in some countries in Southeast Asia and South America. This regimen is less practical for other areas, particularly Africa, because of its relatively high cost and poor tolerability. Either artesunate-amodiaquine or artemether-lumefantrine is now the standard treatment for uncomplicated falciparum malaria in most countries in Africa and some additional endemic countries on other continents. Dihydroartemisinin-piperaquine is a newer regimen that has shown excellent efficacy; it is the first-line therapy for falciparum malaria in Vietnam. T he relative efficacy and safety of artemisinin-based combination therapies are now under active investigation. In general, the leading regimens are highly efficacious, safe, and well tolerated, and they are the new standard of care for the treatment of uncomplicated falciparum malaria. Artemisinins are also proving to have outstanding efficacy in the treatment of complicated falciparum malaria. Large randomized trials and meta-analyses have shown that intramuscular artemether has an efficacy equivalent to that of quinine and that intravenous artesunate is superior to intravenous quinine in terms of parasite clearance time and—most important—patient survival. Intravenous artesunate also has a superior side-effect profile compared with that of intravenous quinine or quinidine. Thus, intravenous artesunate will likely replace quinine as the standard of care for the treatment of severe falciparum malaria, although it is not yet widely available in most areas. Artesunate and artemether have also been effective in the treatment of severe malaria when administered rectally, offering a valuable treatment modality when parenteral therapy is not available.

ADVERSE EFFECTS & CAUTIONS: Artemisinins are generally very well tolerated. The most commonly reported adverse effects are nausea, vomiting, diarrhea, and dizziness, and these may often be due to underlying malaria rather than the medications. Rare serious toxicities include neutropenia, anemia, hemolysis, elevated liver enzymes, and allergic reactions. Irreversible neurotoxicity has been seen in animals, but only after doses much higher than those used to treat malaria. Artemisinins have been embryotoxic in animal studies, but rates of congenital abnormalities, stillbirths, and abortions were not elevated, compared with those of controls, in women who received artemisinins during pregnancy. Based on this information and the significant risk of malaria during pregnancy, the WHO recommends artemisininbased combination therapies for the treatment of uncomplicated falciparum malaria during the second and third trimesters of pregnancy, intravenous artesunate or quinine for the treatment of severe malaria during the first trimester, and intravenous artesunate for treatment of severe malaria during the second and third trimesters.

RELATED;

1.  PENICILLINS  

2.  AZITHROMYCIN

3.  PHARMACOLOGY AND THERAPEUTICS

REFERENCES

METFORMIN

 

ACTIONS AND USES: Metformin is a preferred oral antidiabetic drug for managing type 2 DM because of its effectiveness and safety. It is used alone or in combination with other antidiabetic medications or insulin. It is approved for use in children age 10 or above. It is available as regular-release tablets, solution, and sustained-release forms. Metformin reduces fasting and postprandial glucose levels by decreasing the hepatic production of glucose by the process of gluconeogenesis and reducing insulin resistance. It does not promote insulin release from the pancreas. A major advantage of the drug is that it does not cause hypoglycemia. The drug's actions do not depend on stimulating insulin release, so it is able to lower glucose levels in patients who no longer secrete insulin. In addition to lowering blood glucose levels, it lowers triglyceride and total and low-density lipoprotein (LDL) cholesterol levels, and it promotes weight loss. Metformin reduces insulin resistance, which in turn lowers insulin and androgen levels, thus restoring normal menstrual cycles and ovulation.

ADMINISTRATION ALERTS: Sustained-release tablets must be swallowed whole and not crushed or chewed. Fasting blood glucose levels should be obtained every 3 months, and the dose adjusted accordingly. Discontinue the medication immediately if signs of acidosis are present. Pregnancy category B.

PHARMACOKINETICS: Onset Peak Duration Less than 1 h 1–3 h (regular release); 4–8 h (extended release) 12 h (regular release); 24 h (extended release)

ADVERSE EFFECTS: The most common adverse effects are GI related and include nausea, vomiting, abdominal discomfort, metallic taste, diarrhea, and anorexia. It may also cause headache, dizziness, agitation, and fatigue. Unlike the sulfonylureas, metformin rarely causes hypoglycemia or weight gain.

Warning: Lactic acidosis is a rare, though potentially fatal, adverse effect. The risk for lactic acidosis is increased in patients with renal insufficiency or any condition that puts them at risk for increased lactic acid production, such as liver disease, severe infection, excessive alcohol intake, shock, or hypoxemia.

RELATED;

1. DIABETES MELLITUS

2. INSULIN

3.  PATHOPHYSIOLOGY OF DIABETES

4.  PHARMACOLOGY AND THERAPEUTICS

HEMORRHAGIC (RH) DISEASE OF THE NEW BORN

 

Introduction: Rh disease of the newborn may also be called erythroblastosis fetalis and is the result of an Rh incompatibility between mother and fetus. During a normal pregnancy, maternal blood and fetal blood do not mix in the placenta. However, during delivery of the placenta, some fetal blood may enter maternal circulation. If the woman is Rh negative and her baby is Rh positive, this exposes the woman to Rh-positive Red blood cells (RBCs). Red blood cell: Blood transfusion protocols  

THE RESPONSES OF MATERNAL AUTOTRANSFUSION:  In response, her immune system will now produce anti-Rh antibodies following this first delivery. In a subsequent pregnancy, these maternal antibodies will cross the placenta and enter fetalcirculation. If this next fetus is also Rh positive, the maternal antibodies will cause destruction (hemolysis) of the fetal RBCs. In severe cases this may result in the death of the fetus. 

In less severe cases, the baby will be born anemic and jaundiced from the loss of RBCs.  Such an infant may require a gradual exchange transfusion to remove the blood with the maternal antibodies and replace it with Rh-negative blood. The baby will continue to produce its own Rh-positive RBCs, which will not be destroyed once the maternal antibodies have been removed. Much better than treatment, however, is prevention. 

PREVENTION:  If an Rh-negative woman delivers an Rh positive baby, she should be given RhoGAM within 72 hours after delivery. RhoGAM is an anti-Rh antibody that will destroy any fetal RBCs that have entered the mother’s circulation before her immune system can respond and produce antibodies. The RhoGAM antibodies themselves break down within a few months. The woman’s next pregnancy will be like the first, as if she had never been exposed to Rh-positive RBCs.

RELATED;

1. IMMUNITY  

2. IMMUNOGLOBULINS  

3.  DRUG CATEGORY IN RELATION TO PREGNANCY

4. THE HUMAN RED BLOOD CELLS

5.  FETAL CIRCULATION

6.  JAUNDICE

TUBERCULOSIS

 

INTRODUCTION: Tuberculosis (TB), an infectious disease primarily affecting the lung parenchyma, is most often caused by Mycobacterium tuberculosis. It may spread to almost any part of the body, including the meninges, kidney, bones, and lymph nodes. The initial infection usually occurs 2 to 10 weeks after exposure. The patient may then develop active disease because of a compromised or inadequate immune system response. Immunity  The active process may be prolonged and characterized by long remissions when the disease is arrested, only to be followed by periods of renewed activity. TB is a worldwide public health problem that is closely associated with poverty, malnutrition, overcrowding, substandard housing, and inadequate health care. Mulnutrition

TRANSMISSION OF TUBERCULOSIS: TB is transmitted when a person with active pulmonary disease expels the organisms. A susceptible person inhales the droplets and becomes infected. Bacteria are transmitted to the alveoli and multiply. An inflammatory reaction results in exudate in the alveoli and bronchopneumonia, granulomas, and fibrous tissue. Bronchopneumonia  Onset is usually insidious.

RISK FACTORS: Close contact with someone who has active TB. Immunocompromised status such as the elderly, cancer patients, use of corticosteroid therapy, and HIV. Injection drug use and alcoholism. People lacking adequate health care such as, homeless or impoverished, minorities, children, and young adults. Preexisting medical conditions, including diabetes, chronic renal failure, silicosis, and malnourishment. Immigrants from countries with a high incidence of TB. Institutionalization for example, long-term care facilities, prisons. Living in overcrowded, substandard housing. Occupation such as, health care workers, particularly those performing high-risk activities.

CLINICAL MANIFESTATIONS: Low-grade fever, cough, night sweats, fatigue, and weight loss. Nonproductive cough, which may progress to mucopurulent sputum with hemoptysis.

ASSESSMENT AND DIAGNOSTIC METHODS: TB skin test (Mantoux test); Chest x-ray; Acid-fast bacillus smear; Sputum culture.

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: First-line medications: isoniazid or INH, rifampin, pyrazinamide, and ethambutol, daily for 8 weeks and continuing for up to 4 to 7 months.

Second-line medications: capreomycin, ethionamide, para-aminosalicylate sodium, and cycloserine. Vitamin B (pyridoxine) usually administered with INH to prevent peripheral neuritis.

RELATED;

1.  PNEUMONIA  

2.  PULMONARY EMBOLISM 

3.  MEDICAL CONDITIONS

REFERENCES

ULBUM OF ANATOMY AND PHYSIOLOGY: LOCATION OF ORGANS

ULBUM OF ANATOMY AND PHYSIOLOGY:  LOCATION OF ORGANS

1.  THE LIVER

2.  THE HEART

RELATED;

1.  ALBUM OF BIOCHEMISTRY

DOPAMINE

 

Introduction: Dopamine plays several important roles in the brain and body. A member of the catecholamine and phenethylamine families, its name comes from the fact that it is an amine made by removing a carboxyl group from LDOPA. Dopamine is synthesized in the brain and kidneys. It is also made in plants, though its function in plants is not clear. Conversion of dopamine to norepinephrine requires vitamin C.  Dopamine is a neurotransmitter, being released by one nerve cell and then traveling across a synapse to signal an adjacent nerve cell. Generation of a nerve impulse  

Dopamine plays a major role in the brain’s reward-mediated behavior. Rewards, such as food or social interaction, increase dopamine levels in the brain, as do addictive drugs. Other brain dopamine pathways are involved in motor control and in managing the release of various hormones.

Chemical messenger: Outside the nervous system, dopamine is a local chemical messenger. In blood vessels, it inhibits norepinephrine release and causes vasodilation. In the kidneys, it increases sodium excretion and urine output. It reduces gastrointestinal motility and protects intestinal mucosa in the digestive system and in the immune system, it reduces lymphocyte activity. The effect dopamine has on the pancreas is to reduce insulin production. With the exception of the blood vessels, dopamine is synthesized locally and exerts its effects near the cells that release it.

RELATED;

1.  THE NEUROTRANSMITTER SYSTEMS

2.  THE NEUROMASCULAR JUNCTION IMPULSE TRANSMISSION

METABOLISM AND METABOLIC DISORDERS

 

INTRODUCTION: Thousands of chemical reactions are taking place inside a cell in an organized, well co-ordinated, and purposeful manner; all these reactions are collectively known as Metabolism. The metabolism serves the following purposes:

Purpose 1: Chemical energy is obtained from the degradation of energy rich nutrients including but not limited to carbohydrates and amino acids.  Some of the most common carbohydrates include; Starch, Glucose among others.  

Purpose 2: Food materials are converted into the building block precursors of cellular macromolecules. These building blocks are later made into macromolecules, such as proteins, nucleic acids, polysaccharides, and many others. Biomolecules required for specialized functions of the cell are synthesized.

Purpose 3: Metabolic pathways are taking place with the help of sequential enzyme systems. These pathways are regulated at three levels: 

(i) Regulation through the action of allosteric enzymes, which increase or decrease the activity under the influence of effector molecules. 

(ii) Hormonal regulation. Hormones are chemical messengers secreted by different endocrine glands. 

(iii) Regulation at the DNA level; the concentration of the enzyme is changed by regulation at the level of synthesis of the enzyme.

TYPES OF METABOLIC PATHWAYS:  

Catabolic (degradation) pathways: These are pathways, where energy rich complex macromolecules are degraded into smaller molecules. Energy released during this process is trapped as chemical energy, usually as ATP.

Anabolic (biosynthesis) pathways: The cells synthesize complex molecules from simple precursors. This needs energy.  

Amphibolic pathways: These are seen at cross-roads of metabolism, where both anabolic and catabolic pathways are linked.

RELATED;

1.  STAGES OF METABOLISM

2.  STARCH

[REFERENCES]

IMMUNOGLOBULINS

IMMUNOGLOBULIN G (IgG):  IgG contains two heavy chains and two light chains; heavy chains being of gamma type. Due to its sedimentation coefficient, it is sometimes referred to as 7S lg.  IgG is the major antibody; it constitutes about 75-80% of total immunoglobulins in circulation.  It is the antibody seen in secondary immuno response.  It can pass from vascular compartment to interstitial space. It can cross-placental barrier, and protects the newborn child from infections. These maternal antibodies are seen in neonatal circulation up to 2-4 months of neonatal age.  Placental crossing of IgG also explains the Rh iso-immunization. This occurs when mother is Rh-negative, and fetus is Rh-positive, and when ABO system antigens are similar to both mother and fetus.

During parturition, fetal RBCs may enter into maternal circulation, leading to formation of anti-Rh antibodies.  During next pregnancy, these antibodies, being IgG in class, can enter into fetal circulation, causing fetal hemolysis, neonatal jaundice, and in severe cases, neonatal death or miscarriage. Passively injected anti-Rh antibody, when injected within 24 hrs of delivery of first child, will avert the isoimmunization and can protect future pregnancy.

IMMUNOGLOBULIN M (IgM):  IgM are macroglobulins or 19S immunoglobulins.  Five subunits, each having 4 peptide chains (total 10 heavy chains and 10 light chains) are joined together by a J-chain polypeptide. It can combine with 5 antigens simultaneously, and so IgM is very effective for agglutinating bacteria.  Being a large molecule, it cannot come out of vascular space.  IgM are the predominant class of antibodies in primary response.  Natural antibodies are IgM in nature. Thus, a person having blood group A antigen will have anti-B antibodies in his circulation (isohemagglutinins).  These are produced without any known antigenic stimulation, and hence called natural antibodies. These IgM antibodies cannot cross placenta, and therefore the fetus, even though it carries an incompatible antigen, is protected from natural antibodies of the mother.

IMMUNOGLOBULIN A (IgA):  IgA usually are dimers (total 4 heavy chains and 4 light chains). The J chain connects the dimers.  They are the secretory antibodies seen in seromucous secretions of gastrointestinal tract, nasopharyngeal tract, urogenital tract, tears, saliva, sweat, among others.  The dimers are stabilized against proteolytic enzymes by the secretory piece. The secretory piece is produced in liver, reaches to the intestinal mucosal cells, where it combines with IgA dimer to form the secretory IgA which is then released.

IMMUNOGLOBULIN E (IgE):  They are cytophilic antibodies. They mediate allergy, hypersensitivity and anaphylaxis.  They have the property to fix on mast cells and basophils. When certain antigens such as penicillin are injected a few times, IgE class antibodies are produced which anchor on mast cells. When the same chemical is injected next time, the antigens fix on such antibodies, causing mast cell degranulation, and release of histamine and slow reacting substance.  This leads to vasodilatation, hypotension and bronchiolar constriction. This is the basis of penicillin anaphylaxis, hay fever caused by fungus, asthma by pollen and urticaria by absorbed food elements.  The peak of this reaction will be at about 30 minutes; hence called immediate type hypersensitivity.  IgE level in serum is markedly increased in helminthic infections.

 

RELATED;

1.  HAY FEVER  

2. PASSIVE IMMUNISATION  

3. HAEMOLYTIC DISEASE OF THE NEW BORN

4.  SPECIFIC IMMUNITY

REFERENCES