BURNS

OBJECTIVES OF THE DICUSSION:  By the end of this presentation, the reader/medical student will be able to;

1.  List the groupings of burns

2.  Describe the types of injury that can be caused by wounds on the human body

3.  Explain the different appearances of structure visible with the different degree on burns

INTRODUCTION: Burns and wounds are some of the most common presenting complaints in health facilities in developing countries.  Burns of the skin may be caused by flames, hot water or steam, sunlight, electricity, or corrosive chemicals including the most commonly used inorganic acids. The severity of burns ranges from minor to fatal, and the classification of burns is based on the extent of damage.

FIRST-DEGREE BURN: Here, only the superficial epidermis is burned, and is painful but not blistered. Light colored skin will appear red due to localized vasodilation in the damaged area. Vasodilation is part of the inflammatory response that brings more blood to the injured site.

SECOND-DEGREE BURN: Here, deeper layers of the epidermis are affected. Another aspect of inflammation is that damaged cells release histamine, which makes capillaries more permeable. More plasma leaves these capillaries and becomes tissue fluid, which collects at the burn site, creating blisters. The burned skin is often very painful.

THIRD-DEGREE BURN: The entire epidermis is charred or burned away, and the burn may extend into the dermis or subcutaneous tissue. Often such a burn is not painful at first, if the receptors in the dermis have been destroyed. Extensive third-degree burns are potentially life-threatening because of the loss of the stratum corneum. Without this natural barrier, living tissue is exposed to the environment and is susceptible to infection and dehydration. Bacterial infection is a serious problem for burn patients; the pathogens may get into the blood (septicemia) and quickly spread throughout the body. Dehydration may also be fatal if medical intervention does not interrupt and correct the following sequence: Tissue fluid evaporates from the burned surface, and more plasma is pulled out of capillaries into the tissue spaces. As more plasma is lost, blood volume and blood pressure decrease. This is called circulatory shock; eventually the heart simply does not have enough bloodto pump, and heart failure is the cause of death.

To prevent these serious consequences, third-degree burns are covered with donor skin or artificial skin until skin grafts of the patient’s own skin can be put in place.

RELATED;

1. INFLAMMATION  

2. HISTAMINE  

3. SHOCK

4.  PATHOLOGY

REFERENCES

LONGITUDINAL STUDY DESIGNS

In longitudinal studies the study population is visited a number of times at regular intervals, usually over a long period, to collect the required information. These intervals are not fixed so their length may vary from study to study. Intervals might be as short as a week or longer than a year.  Irrespective of the size of the interval, the information gathered each time is identical.

RELATED;

1.  RETROSPECTIVE STUDY DESIGN

THE NEUROMASCULAR JUNCTION IMPULSE TRANSMITION

 

Introduction:  Skeletal muscle relaxation and paralysis can occur from interruption of function at several sites along the pathway from the central nervous system (CNS) to myelinated somatic nerves, unmyelinated motor nerve terminals, nicotinic acetylcholine receptors, the motor end plate, the muscle membrane, and the intracellular muscular contractile apparatus itself.  Blockade of end plate function can be accomplished by two basic mechanisms. Pharmacologic blockade of the physiologic agonist acetylcholine is characteristic of the antagonist neuromuscular blocking drugs (ie, nondepolarizing neuromuscular blocking drugs). These drugs prevent access of the transmitter to its receptor and thereby prevent depolarization. The prototype of this nondepolarizing subgroup is d-tubocurarine.   The second type of blockade can be produced by an excess of a depolarizing agonist, such as acetylcholine. This seemingly paradoxical effect of acetylcholine also occurs at the ganglionic nicotinic acetylcholine receptor. The prototypical depolarizing blocking drug is  succinylcholine.  A similar depolarizing block can be produced by acetylcholine itself when high local concentrations are achieved in the synaptic apparatus.

RELATED;

1.  THE MECHANISM OF IMPULSE PROPAGATION

2.  SYNAPSES

3.  THE NEUROTRANSMITTER SYSTEMS

4.  DIVISIONS OF THE NERVOUS SYSTEM

NON-PROBABILITY SAMPLING DESIGNS

 

INTRODUCTION:  These do not follow the theory of probability in the selection of elements from the sampling population. Non-probability sampling designs are used when the number of elements in a population is either unknown or cannot be individually identified. In such situations the selection of elements is dependent upon other considerations. Non-probability sampling designs are commonly used in both quantitative and qualitative research.  

CATEGORIES OF NON PROBABILITY SAMPLING DESIGNS:  Some of the categories in non probability sampling include; 

1.  Convenience sampling 

2.  Judgement sampling

3.  Quota sampling and

4.  Snowball sampling

RELATED;

1.  PROBLEM STATEMENT

2.  PROBABILITY SAMPLING DESIGNS

SOFTWARE DOWNLOAD LINKS AND VIDEO DEMONSTRATIONS

SOFTWARE DOWNLOAD LINKS AND VIDEO DEMONSTRATIONS:  Get links to download some of the most handy software in doing a couple of things and enjoy your windows PC with maximum workforce and minimum workload.  There are times when getting things done were hard and would require a technician but now, Google did it all you can get to know the way things can be done from your house.

When it comes to software and computer literacy, people have mixed reactions and for some it is complete phobia for them to get used and practice or even bather to learn a few basic tactics.  I used to be like that too but sometimes back I got notice that via Google docs, or even just visiting www.google.com and key in a few words about your problem, more than 10 sources of solutions can be generated.  I therefore started using Google as one of my parents.

On this page, we are going to look at the most basic software downloads we can use in everyday life when using a computer as a basic user, and the YouTube video demonstration on the way you can do such procedures.

1.  Full use of windows inbuilt tools

2.  Windows software downloads

3.  Download accelerators

4.  Android apps download

5.  Android PC connectivity

6.  Google earth setup

7.  Adobe reader 11 setup

8.  Foxit reader 95 setup

9.  Opera browser for windows

10.  Video demo on the bacterial cell wall

11.  Spike email setup for windows

12.  How to temporarily turn off windows defender

13.  Pharmacology albums-routes of drug administration

RELATED;

1.  Windows software downloads

2.  Android to PC connectivity

SYNAPSES

INTRODUCTION: There are two types of connections between electrically active cells, chemical synapses and electrical synapses. In a chemical synapse, a chemical signal namely, a neurotransmitter is released from one cell and it affects the other cell. In an electrical synapse, there is a direct connection between the two cells so that ions can pass directly from one cell to the next. If one cell is depolarized in an electrical synapse, the joined cell also depolarizes because the ions pass between the cells. Chemical synapses involve the transmission of chemical information from one cell to the next. An example of a chemical synapse is the neuromuscular junction (NMJ).

CHARACTERISTICS OF A SYNAPSE: In the nervous system, there are many more synapses that are essentially the same as the NMJ. All synapses have common characteristics, which can be summarized in this list:

1) Presynaptic element.

2) Neurotransmitter (packaged in vesicles)

3) Synaptic cleft

4) Receptor proteins

5) Postsynaptic element

6) Neurotransmitter elimination or re-uptake

For the NMJ, these characteristics are as follows: the presynaptic element is the motor neuron's axon terminals, the neurotransmitter is acetylcholine, the synaptic cleft is the space between the cells where the neurotransmitter diffuses, the receptor protein is the nicotinic acetylcholine receptor, the postsynaptic element is the sarcolemma of the muscle cell, and the neurotransmitter is eliminated by acetylcholinesterase. Other synapses are similar to this, and the specifics are different, but they all contain the same characteristics.

NEUROTRANSMITTER RELEASE: When an action potential reaches the axon terminals, voltage-gated Ca²⁺ channels in the membrane of the synaptic end bulb open. The concentration of Ca²⁺ increases inside the end bulb, and the Ca²⁺ ion associates with proteins in the outer surface of neurotransmitter vesicles. The Ca²⁺ facilitates the merging of the vesicle with the presynaptic membrane so that the neurotransmitter is released through exocytosis into the small gap between the cells, known as the synaptic cleft. Once in the synaptic cleft, the neurotransmitter diffuses the short distance to the postsynaptic membrane and can interact with neurotransmitter receptors. Receptors are specific for the neurotransmitter, and the two fit together like a key and lock. One neurotransmitter binds to its receptor and will not bind to receptors for other neurotransmitters, making the binding a specific chemical event.

RELATED;

1.  NEUROTRANSMITTER SYSTEMS  

2.  DIVISIONS OF THE NERVOUS SYTEM

3.  DOPAMINE

REFERENCES

FEVER AND IT'S EFFECTS ON THE HUMAN BODY

OBJECTIVES OF THE DISCUSSION: By the end of this discussion, the reader/medical student will be able to;

1.  Describe the term fever/pyrexia

2.  Identify the different causes of fever

3.  Outline the means by which fever can be prevented

INTRODUCTION: A fever is an abnormally high body temperature and may accompany infectious diseases, extensive physical trauma, cancer, or damage to the Central Nervous System. The substances that may cause a fever are called pyrogens. Pyrogens include bacteria, foreign proteins, and chemicals released during inflammation. Bacteria: Proteins: Inflammation  

These inflammatory chemicals are called endogenous pyrogens. It is believed that pyrogens chemically affect the hypothalamus and raise the setting of the hypothalamic thermostat. The hypothalamus will then stimulate responses by the body to raise body temperature to this higher setting.

PURPOSE OF FEVER: White blood cells increase their activity at moderately elevated temperatures, and the metabolism of some pathogens is inhibited. Thus, a fever may be beneficial in that it may shorten the duration of an infection by accelerating the destruction of the pathogen.

CONSEQUENCES OF HIGH FEVERS: High fevers, may have serious consequences. A fever increases the metabolic rate, which increases heat production, which in turn raises body temperature even more. This is a positive feedback mechanism that will continue until an external event such as, administration of an NSAID or death of the pathogens acts as a brake.

When the body temperature rises above 41°C, the hypothalamus begins to lose its ability to regulate temperature. The proteins of cells, especially the enzymes, are also damaged by such high temperatures. Enzymes become denatured, that is, lose their shape and do not catalyze the reactions necessary within cells. As a result, cells begin to die. This is most serious in the brain, because neurons cannot be replaced, and cellular death is the cause of brain damage that may follow a prolonged high fever.

CONTROL OF FEVERS: To help lower a high fever, the body may be cooled by sponging it with cool water. The excessive body heat will cause this external water to evaporate, thus reducing temperature. A very high fever requires medical attention.

RELATED;

1.  THE INFLAMMATORY PROCESS

2.  INFLAMMATORY CONDITIONS AND THE HUMAN BODY

3.  ANTIPYRETICS

REFERENCES

SYMPTOMATIC MANAGEMENT OF ILLINESSES

SYMPTOMATIC MANAGEMENT OF ILLINESSES:  Like we have seen in the previous discussions, almost 100% of all medical interventions require use of drugs to address the patients chief complaints.  It is surprising to say however that, some illnesses do not have radical cures and to bring relief for the patient, the health work must look at the patient's presenting signs and symptoms and decide on the Nursing or medical intervention to take.  In our discussion here, were going to look at some of the most common symptoms that are managed in patients besides the medications administered and Surgical or Nursing decisions made.

RELATED;

1.  PHARMACOLOGY AND DRUG USE

DISORDERS OF FOOD DIGETION AND METABOLISM

DISORDERS OF FOOD DIGESTION AND METABOLISM:  Every human being must rely on food and fluids to stay healthy and alive.  Our demand and daily requirement to eat starts way back with the recognition and demand by the central nervous system, and therefore the immediate to find what to eat.

MEDICAL MICROBIOLOGY

THE MICRO ORGANISMS THAT CAUSE DISEASES:  Imagine life with very tinny living organisms capable of causing disease and not visible to a naked eye.  The things we use in life from clothes, utensils, our own bodies are living with millions of bacteria, virus and other microbes that can cause some of the most deadly diseases.  Looking at the human skin alone, every square inch of it is a home to more than 100 species of microbe some of which are deadly when they are introduced into the circulation.  In our discussions here, we shall be looking at the various microbes that cause diseases in humans and the diseases they cause.  We shall be looking at the virulence factor for such microbes and although there is a section for drug, here we shall briefly look at the possible antimicrobial therapy for such microbes.

i)  Normal flora of the human body:  When you look at the human skin, you may think it is free from microbes but you will surprised to find, every square inch of it is a home to more than 100 different species of bacteria.  It is not actually skin alone but also, mucous membranes, mouth, the vaginal canal and the rectum.

ii)  Virulence factors of microbes

iii)  Pathogenicity of microorgnisms

iv)  Dynamics of infectious diseases

BACTERIOLOGY

i)  The bacterial cell wall

1.  Brucella

2.  Pseudomonas aeruginosa

3.  Helicobacter pyroli

4.  Haemophilus influenzae

5.  Treponema pallidum

VIROLOGY

1.  Filoviruses

PATHOPHYSIOLOGY OF HYPERTENTION

PATHOPHYSIOLOGY OF HYPERTENTION:  In hypertension, the force exerted on the walls of blood vessels is higher than the expected value and the higher it goes, forces the rapture of the tinniest blood vessels we know as blood capillaries.  Remember these vital extremes of cardiovascular system are the areas where blood and body tissues exchange materials like glucose, oxygen and minerals.  The rapture of this microvasculature will lead to blood spilling over any associated organs and the resultant medical conditions will be depending on the organ associated.  If that happens in the brain tissue, that is where we are going to come up with conditions like hemorrhagic stroke also known as cerebral vascular accident linked in the related section below.

RELATED;

1.  STROKE

2.  PATHOPHYSIOLOGY OF CONGESTIVE HEART FAILURE

3.  PATHOPHYSIOLOGY OF PEPTIC ULCER DISEASE

4.  BLOOD PRESSURE AND HYPERTENSION

ZOLPIDEM

INTRODUCTION:  Favorable clinical features of zolpidem and the other newer hypnotics include rapid onset of activity and modest day-after psychomotor depression with few amnestic effects.  Zolpidem, one of the most frequently prescribed hypnotic drugs, is available in a biphasic release formulation that provides sustained drug levels for sleep maintenance.

ACTIONS AND USES:  Although it is a nonbenzodiazepine, zolpidem acts in a similar fashion to facilitate GABA-mediated CNS depression in the limbic, thalamic, and hypothalamic regions. It preserves stages III and IV of sleep and has only minor effects on REM sleep. The only indication for zolpidem is for short-term insomnia management (7 to 10 days).

ADMINISTRATION ALERTS:  Because of rapid onset, 7–27 minutes, give immediately before bedtime, care must be taken not to operate anything after taking the drug.

Pregnancy category B.

ADVERSE EFFECTS:  Adverse effects include daytime sedation, confusion, amnesia, dizziness, depression, nausea, and vomiting. 

Contraindications: Lactating women should not take this drug. 

INTERACTIONS:  Drug–Drug: Drug interactions with zolpidem include an increase in sedation when used concurrently with other CNS depressants, including alcohol. Phenothiazines augment CNS depression.  

Treatment of Overdose: Generalized symptomatic and supportive measures should be applied with immediate gastric lavage where appropriate. IV fluids should be administered as needed. Use of flumazenil as a benzodiazepine receptor antagonist may be helpful. 

RELATED;

1.  DRUGS USED IN INDUCTION OF SLEEP  2.  

PATHOPHYSIOLOGY OF CONGESTIVE HEART FAILURE

PATHOPHYSIOLOGY OF CONGESTIVE HEART FAILURE:  In congestive heart failure, the heart muscle fails to contract sufficiently to pump blood throughout the body.  This makes blood retained in the venous system and in the pulmonary circulation.  It therefore turns out that the blood that would return to the heart from the venous system is retained and the blood that would return from the lungs to the left heart side is not delivered to sufficiency.  The insufficient delivery of blood to the starving tissues does not only affect the body organs but also, the heart itself, making it not able to work more and more.  This make a compensatory mechanism of the heart muscle enlarging to generate enough energy which actually exaggerates the condition where the size of the heart becomes excessively more that the expected potential for contraction.  So in brief, there is congestion in delivery of blood versus an excessively enlarging heart with subsequent accumulation of fluids in tissues and the lungs and hence the term congestive cardiac failure.

RELATED;

1.  PATHOPHYSIOLOGY OF PEPTIC ULCER DISEASE

2.  HEART FAILURE

3.  PATHOPHYSIOLOGY OF HYPERTENSION

AMPHOTERICIN B

Amphotericin B is an antifungal antibiotics produced by Streptomyces nodosus.

PHARMACOKINETICS: Amphotericin B is an amphoteric polyene macrolide. It is nearly insoluble in water and is therefore prepared as a colloidal suspension of amphotericin B and sodium desoxycholate for intravenous injection. Several formulations have been developed in which amphotericin B is. Amphotericin B is poorly absorbed from the gastrointestinal tract. Oral amphotericin B is thus effective only on fungi within the lumen of the tract and cannot be used for treatment of systemic disease. The intravenous injection of 0.6 mg/kg/d of amphotericin B results in average blood levels of 0.3–1 mcg/mL; the drug is more than 90% bound by serum proteins. Although it is mostly metabolized, some amphotericin B is excreted slowly in the urine over a period of several days. The serum half-life is approximately 15 days. Hepatic impairment, renal impairment, and dialysis have little impact on drug concentrations, and therefore no dose adjustment is required. The drug is widely distributed in most tissues, but only 2–3% of the blood level is reached in cerebrospinal fluid, thus occasionally necessitating intrathecal therapy for certain types of fungal meningitis.

MECHANISMS OF ACTION: Amphotericin B is selective in its fungicidal effect because it exploits the difference in lipid composition of fungal and mammalian cell membranes. Ergosterol, a cell membrane sterol, is found in the cell membrane of fungi, whereas the predominant sterol of bacteria and human cells is cholesterol. Amphotericin B binds to ergosterol and alters the permeability of the cell by forming amphotericin B-associated pores in the cell membrane. So the cell will expand and finally rapture.

ADVERSE EFFECTS: The toxicity of amphotericin B can be divided into two broad categories: immediate reactions, related to the infusion of the drug, and those occurring more slowly.

A. INFUSION-RELATED TOXICITY: Infusion-related reactions are nearly universal and consist of fever, chills, muscle spasms, vomiting, headache, and hypotension.

They can be ameliorated by slowing the infusion rate or decreasing the daily dose. Premedication with antipyretics, antihistamines, meperidine, or corticosteroids can be helpful. When starting therapy, many clinicians administer a test dose of 1 mg intravenously to gauge the severity of the reaction. This can serve as a guide to an initial dosing regimen and premedication strategy.

B. CUMULATIVE TOXICITY: Renal damage is the most significant toxic reaction. Renal impairment occurs in nearly all patients treated with clinically significant doses of amphotericin. The degree of azotemia is variable and often stabilizes during therapy, but it can be serious enough to necessitate dialysis. A reversible component is associated with decreased renal perfusion and represents a form of prerenal renal failure. An irreversible component results from renal tubular injury and subsequent dysfunction. The irreversible form of amphotericin nephrotoxicity usually occurs in the setting of prolonged administration (> 4 g cumulative dose). Renal toxicity commonly manifests as renal tubular acidosis and severe potassium and magnesium wasting. There is some evidence that the prerenal component can be attenuated with sodium loading, and it is common practice to administer normal saline infusions with the daily doses of amphotericin B. Abnormalities of liver function tests are occasionally seen, as is a varying degree of anemia due to reduced erythropoietin production by damaged renal tubular cells.

RELATED;

1.  fungi

2.  Candidiasis

3.  Opportunistic mycoses

REFERENCES

REFERENCES

1.  Rochelle, R., C., Othávio, P., B., Pedro, F., Flávio, A., Castro (2018).  Sampling procedures and calculation for sample size determination: criteria and methods adopted in theses and dissertations in Human Movement Sciences - a descriptive study.  Retrieved online https://doi.org/10.5007/1980-0037.2018v20n5p480 [12-oct-2020]

2.  Rensburg, V., R., Reuter, H. (2019).  An overview of analgesics: NSAIDs, paracetamol, and topical analgesics Part 1:  South African Family Practice, 61:sup1, S4-S10, retrieved online <DOI: 10.1080/20786190.2019.1610228> [23-December-2019]

3.  Amol, B., D, Jayprabha, R., Dhumane, Hrushikesh, V., Wagh, Rushikesh, B., S. (2019).  Asian Journal of Pharmaceutical Research and Development:  Open Access to Pharmaceutical and Medical Research. Retrieved online <15.12.2019 at http://ajprd.com> [March-17-2020]

4.  Jaycharan, C., Tamoghna, B. (2013).  How to calculate sample size for different study designs in medical research?  Indian Journal of medical research.  Retrieved online [December-20-2016]

5.  Laura, J., Hunter, Wood, M., D., Dargan, P., I. (2011).  The patterns of toxicity and management of acute nonsteroidal anti-inflammatory drug (NSAID) overdose:  Dove press journal.  Retrieved online <http://dx.doi.org/10.2147/OAEM.S22795> [June-3-2019]

6.  Centre for disease control and prevention [CDC] (2019).  Viral Hemorrhagic Fevers.  Fact sheet.  Retrieved online [27-March-2019]

7.  Amol, B., D, Jayprabha, R., Dhumane, Hrushikesh, V., Wagh, Rushikesh, B., S. (2019).  The Stages of Drug Discovery and Development Process;  Asian Journal of Pharmaceutical Research and Development: Retrieved online <15.12.2019 at http://ajprd.com> [March-10-2019]

8.  Cotran, R., S., Kumar, V., Collins, T. (2012).  Robins pathologic basis of diseases. J.B.Saunders Company Philadilphia, 6th edition

9.  Dey, N., C., Dey, T., K. (2014).  A Textbook of Pathology Calcatta, Messers Allied agency 10th edition 2014

10.  Gashaw, I., Ellinghaus, P., Sommer, A., Asadullah, K. (2012).  What makes a good drug target.  Drug Discovery Today, 17:S24-S30.

11.  Karara, A., H., Edeki, T., McLeod, J. (2010).  PhRMA survey on the conduct of first-in-human clinical trials under exploratory investigational new drug applications.  Journal of ClinicalPharmacology, 50:380– 391.

12.  Moffat, J., Vincent, F., Lee, J., Eder, J., Prunotto, M. (2017).  Opportunities and challenges in phenotypic drug discovery: an industry perspective.  Nature Reviews Drug Discovery, 16(8):531-543

13.  Patidar, A., K., Selvam, G., Jeyakandan, M., Mobiya, A., K., Bagherwal, A., Sanadya, G., Mehta, R. (2011). Lead Discovery and lead optimization: A useful strategy in molecular modification of lead compound in analog design. International journal of drug design and discovery. 2(2):458- 463.

14.  Winge, D., R. (2012). Principles of molecular biology.  32(14): 2647–2652 Retrieved onloine <doi: 10.1128/MCB.00573-12>  [12-12-2020]