BRIEF DESCRIPTION ABOUT ADDISONS DISEASE FOR DENTAL AND MEDICAL STUDENTS AND FOR GRADUATES AND FOR UNDERGRADUATES WHO FIND IT DIFFICULT TO UNDERSTAND FROM THE MEDICAL PUBLICATONS ABOUT THIS DISEASE AND ITS DIAGNOSIS AND ALSO DIFFERENTIAL DIAGNOSIS.
Hyperaldosteronism is a disorder in which the adrenal gland releases too much of the hormone aldosterone into the blood. Hyperaldosteronism can be primary or secondary.
A Condition that occurs from exposure to cortisol levels for a long time.the most common cause is the use of steroid drugs,but it can also occur from over production of cortisol by the sdrenal glands.
The adrenal cortex produces three major classes of steroids:
glucocorticoids,
(2) mineralocorticoids, and
(3) adrenal androgens.
Consequently, normal adrenal function is important for
-modulating intermediary metabolism and immune responses through glucocorticoids;
blood pressure, vascular volume, and electrolytes through mineralocorticoids;
secondary sexual characteristics (in females) through androgens.
The adrenal axis plays an important role in the stress response by rapidly increasing cortisol levels.
Adrenal disorders include hyperfunction (Cushing's syndrome) and hypofunction (adrenal insufficiency) as well as a variety of genetic abnormalities of steroidogenesis.
Hyperaldosteronism is a disorder in which the adrenal gland releases too much of the hormone aldosterone into the blood. Hyperaldosteronism can be primary or secondary.
A Condition that occurs from exposure to cortisol levels for a long time.the most common cause is the use of steroid drugs,but it can also occur from over production of cortisol by the sdrenal glands.
The adrenal cortex produces three major classes of steroids:
glucocorticoids,
(2) mineralocorticoids, and
(3) adrenal androgens.
Consequently, normal adrenal function is important for
-modulating intermediary metabolism and immune responses through glucocorticoids;
blood pressure, vascular volume, and electrolytes through mineralocorticoids;
secondary sexual characteristics (in females) through androgens.
The adrenal axis plays an important role in the stress response by rapidly increasing cortisol levels.
Adrenal disorders include hyperfunction (Cushing's syndrome) and hypofunction (adrenal insufficiency) as well as a variety of genetic abnormalities of steroidogenesis.
This is my PowerPoint that was presented at pioneer Pacific College. It took alot of work with my failing memory but I did It! I want to get the word out about Cushing's and my journey with this awful disease. The first picture is me now.
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
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Each examining system can be described using four elements;
- looking/inspection
- feeling/palpation
- tapping/percussion
- listening/auscultation
- assessment of function
This lecture talk about the disturbance of adrenal gland hormones and how it affect health. it also discuss in brief how to manage such condition in your dental clinic
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
ABDOMINAL TRAUMA in pediatrics part one.drhasanrajab
Abdominal trauma in pediatrics refers to injuries or damage to the abdominal organs in children. It can occur due to various causes such as falls, motor vehicle accidents, sports-related injuries, and physical abuse. Children are more vulnerable to abdominal trauma due to their unique anatomical and physiological characteristics. Signs and symptoms include abdominal pain, tenderness, distension, vomiting, and signs of shock. Diagnosis involves physical examination, imaging studies, and laboratory tests. Management depends on the severity and may involve conservative treatment or surgical intervention. Prevention is crucial in reducing the incidence of abdominal trauma in children.
Adv. biopharm. APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMSAkankshaAshtankar
MIP 201T & MPH 202T
ADVANCED BIOPHARMACEUTICS & PHARMACOKINETICS : UNIT 5
APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMS By - AKANKSHA ASHTANKAR
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
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2. ADDISON’S DISEASE
Addison’s disease is also called adrenal insufficiency
Addison’s disease is a hormonal disorder resulting from
a severe or total deficiency of the hormones made in the
adrenal cortex.
Clinically the disease is characterized by bronzing of the skin
and a pigmentation of the mucous membrane.
Both oral and skin pigmentation are thought to be result from
melanocytes stimulating hormonal activity.
3. Addison’s disease is an un common condition
estimated to occur in 1 in 100000 of the population.
PREPARED BY
AIJIN.A.MOHAN
4. ETIOLOGY
TUBERCULOSIS-It was a leading cause of addison’s
disease until the antibiotics were introduced that
successfully treated T.B.
Autoimmune disorders-Here the body’s immune
system makes antibiotics which cells of the adrenal
cortex and slowly destroys them.
Adrenocortical destruction-Bilateral adrenocortical
destruction after T.B or fungal infection and an
idiopathic atrophy are the most frequent causes .
PREPARED BY
AIJIN.A.MOHAN
5. Others- Occasionally , bilateral tumor metastasis
leukemic infiltration and amyloidosis of the
adrenal cortex have been found to be responsible
,other less common causes include cancer ,
chronic infection , Cytomegalovirus , surgical
removal of adrenal glands.
Whatever may be the cause the loss of adrenal
cortex results in deficiency in both glucocoticoids
and mineralocorticoids
PREPARED BY
AIJIN.A.MOHAN
6. PATHOGENESIS
ACTH and MSH are similar in structure and ACTH is
believed to have some degree of melanocyte stimulating
activity.
Normally pituitary gland produces ACTH which causes
adrenal cortex to produce glucocorticoids which inturn
secreted into the circulation .When glucocorticoids reach
a certain concentration in the blood they cause the
anterior pituitary to cease the production of the ACTH . In
Addison’s disease however the defective cortex is unable
to produce much glucocorticoid , so this feedback
mechanism is not activated and the pituitary continues to
produce ACTH .As a result increased production of
melanin changes the colour of skin in a smoky tan or
chestnut brown..
8. Clinical features
Signs and symptoms - Fatigue , weakness , weight
loss , abdominal pain , vomiting and mood
disturbances (maniac,deppressive) . These
symptoms worsen overtime due to the slowly
progressive loss of cortisol and aldosterone
production.
Skin signs :
HYPER PIGMENTATION- It is most evident in areas
exposed to light, but also affects the body folds, the
sites of pressure and friction and in the areas of palm
and soles.
It is also prominent on the gums , buccal mucosa
,nipple , armpits , genitals
9. Women may have loss of androgen stimulated hair
such as pubic and under arm hair.
PIGMENTATION : Pigmentation usually appears
early and is one of the most prominent signs of the
disease.
The more usual being deep tanning of the skin and
mucous membrane with heavier deposits of melanin
over pressure points such as cheek . The increased
melanocytic activity is expressed by the development
of distinct brownish macule on the oral mucosa and
the skin.
COLOUR OF PIGMENTATION : Bluish black to pale
brown or deep chocolate spreading over buccal
mucosa from the angle of mouth or developing on the
gingiva tongue and lips.
14. DIAGNOSIS`
Test’s measuring cortisol and aldosterone blood
and urine levels must be performed to make a
definite diagnosis.
The diagnosis of addison’s disease is
based on the clinical sign as well as on
characteristic changes in the blood
sodium and chloride levels.
PREPARED BY
AIJIN.A.MOHAN
15. DIFFERENTIAL DIAGNOSIS
Hyper pituitarism- It can be distinguished by the
use of urine test levels of 17-ketosteroid in the urine
are decreased in the former but elevated in the latter
condition . A history of silver ingestion identifies
argyra.
Peutz-jeghers syndrome , Albrights syndrome
and Recklinhausens disease- The macular type of
discolouration that occasionally develop in place of
more generalized tanning might be mistaken for
peutz jegher’s syndrome , albrights syndrome or von
recklinghausens disease. PREPARED BY
AIJIN.A.MOHAN
19. MANAGEMENT
It is done by adequate corticosteroid
maintenance therapy provided by an
average daily dose of 25-40 mg
cortisone.
PREPARED BY
AIJIN.A.MOHAN