Adrenal cortical disorders can cause hyperfunction or hypofunction of the adrenal cortex. Adrenal cortical hyperfunction includes Cushing syndrome, Conn syndrome (hyperaldosteronism), and adrenogenital syndrome. Cushing syndrome is caused by excessive glucocorticoids and results in adrenal cortical hyperplasia. Conn syndrome is characterized by autonomous overproduction of aldosterone and is commonly caused by an aldosterone-producing adrenal adenoma. Adrenal cortical hypofunction includes primary adrenocortical insufficiency (Addison's disease) and secondary adrenocortical insufficiency caused by decreased ACTH stimulation of the adrenals. Primary adrenocortical insufficiency is often auto
Hemolytic Anemia - Dr. Julius King Kwedhi - PediatricsDr. Julius Kwedhi
Definition:
Premature Destruction of Red Blood Cells, either intramuscularly or extravascularly, leading to a shortened red cell survival time.
Causes:
Premature Destruction of Red Blood Cells, either intramuscularly or extravascularly, leading to a shortened red cell survival time.
Simmonds disease is a chronic deficiency of function of the pituitary gland, a form of hypopituitarism, that leads to atrophy of many of the viscera, including the heart, liver, spleen, kidneys, thyroid, adrenals, and gonads. The disease results in emaciation and death if left untreated.
re-view of physiology of adrenal cortex. congenital adrenal hyperplasia. Disorder of adrenocortical insufficiency - primary and secondary adrenocortical insufficiency.pathology of primary insufficiency. hypoaldosteronism. ACTH stimulation test.
multi day ACTH stimulation test.
Hemolytic Anemia - Dr. Julius King Kwedhi - PediatricsDr. Julius Kwedhi
Definition:
Premature Destruction of Red Blood Cells, either intramuscularly or extravascularly, leading to a shortened red cell survival time.
Causes:
Premature Destruction of Red Blood Cells, either intramuscularly or extravascularly, leading to a shortened red cell survival time.
Simmonds disease is a chronic deficiency of function of the pituitary gland, a form of hypopituitarism, that leads to atrophy of many of the viscera, including the heart, liver, spleen, kidneys, thyroid, adrenals, and gonads. The disease results in emaciation and death if left untreated.
re-view of physiology of adrenal cortex. congenital adrenal hyperplasia. Disorder of adrenocortical insufficiency - primary and secondary adrenocortical insufficiency.pathology of primary insufficiency. hypoaldosteronism. ACTH stimulation test.
multi day ACTH stimulation test.
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The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
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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.
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Title: Sense of Smell
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 primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
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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
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2. Learning outcomes
Describe the clinico-pathological affects of adrenal cortical hyperfunction
Describe the clinico-pathological affects of adrenal cortical hypofunction
5. Adrenals in Cushing Syndrome
Exogenous: bilateral cortical atrophy due to
suppression of endogenous ACTH
Endogenous: adrenal cortical hyperplasia, which
may be;
Diffuse Type; (in 70%of cases)
Cortex diffusely thickened and yellow due to increase in the size and
number of lipid-rich cells in zonae fasciculata and reticularis
Nodular Type; Bilateral glands may weigh from 30- 50 gm and shows 0.5
to 2.0cm, yellow nodules scattered throughout hyperplastic cortex
6. Hyperaldosteronism
Primary or Secondary hyperaldosteronism:
Primary Hyperaldosteronism: autonomous
overproduction of aldosterone, with resultant
suppression of renin-angiotensin system and
decreased plasma renin activity, causes includes;
Aldosterone-producing unilateral adrenal
adenoma (Conn syndrome) (80%) in less than
1%, surgically curable form of hypertension
Primary adrenocortical nodular hyperplasia
(15%) in children/young adults, best managed
with medicine
7. Hyperaldosteronism
Secondary hyperaldosteronism
Aldosterone release as a consequence of any high renin state as in:
Renal ischemia due to decreased renal perfusion; e.g arteriolar
nephrosclerosis, renal artery stenosis
Arterial hypovolemia and edema; e.g congestive heart failure,
cirrhosis, nephrotic syndrome
Pregnancy; caused by estrogen-induced increases in plasma renin
substrate
8. Adrenocortical Insufficiency
Primary adrenocortical insufficiency
- Acute insufficiency (Adrenal crisis)
- Chronic insufficiency (Addison disease)
Secondary adrenocortical insufficiency
- Due to decreased stimulation of the adrenals resulting from a deficiency
of ACTH release from the pituitary gland
9. Primary Adrenocortical Insufficiency
Acute Adrenocortical Insufficiency, occurs in;
- Massive adrenal hemorrhage
- Sudden with drawls of long term corticosteroid therapy
- Stress in patient with underlying chronic adrenal insufficiency
Chronic Adrenocortical Insufficiency, causes Includes:
- Autoimmune adrenalitis
- Tuberculous adrenalitis
- Infarction
- Acquired immune deficiency syndrome (AIDS)
- Metastatic cancers
10. Primary Acute Adrenocortical Insufficiency
Massive adrenal hemorrhage:
It destroys adrenal cortex, can be seen in;
- Patients maintained on anticoagulants
- Postoperative patients who develop DIC
- Pregnancy
Waterhouse-Friderichsen syndrome
Classically associated with Neisseria
meningitidis septicemia, can be caused by
pseudomonas , pneumococci and haemophilus
influenza infection, probably due to endotoxin-
induced vascular injury with associated DIC
11. Primary Acute Adrenocortical Insufficiency
Sudden with drawal of long term corticosteroid therapy or failure
to increase its dosage in response to an acute stress;
May precipitate adrenal crisis, because of inability of the atrophic adrenals
to produce glucocorticoids
Stress in patient with chronic adrenal Insufficiency;
Such as infections, trauma, or surgical procedures may precipitate an acute
adrenal crisis, manifested by intractable vomiting, abdominal pain,
hypotension, coma, and vascular collapse
Death follows rapidly unless corticosteroids are replaced immediately
12. Primary Chronic Adrenocortical Insufficiency
Autoimmune Adrenalitis
(Addison disease) 60-70%
Autoimmune destruction of steroid producing
cells, caused by mutations in autoimmune
Regulator gene(AIRE)
Autoimmune Polyendocrinopathy
Syndrome (APS)
Coexist, Hashimoto thyroiditis, pernicious
anemia, type I DM, and idiopathic
hypoparathyroidism
Shrunken adrenals cortex
Shows scattered residual
cortical cells in a collapsed
network of connective tissue
infiltrated by lymphocytes
13. Secondary Adrenocortical Insufficiency
Secondary to disorder of hypothalamus or pituitary;
Metastatic cancer, infection, infarction or radiations that, reduces the output
of ACTH, this leads to hypoadrenalism without hyperpigmentation because
melanotropic hormone levels are low
Gross; adrenals reduced to a thin rim of uniform atrophic flat, yellow cortex
which surrounds an intact medulla
Microscopy; atrophy of cortical cells with loss of cytoplasmic lipid, in the
zonae fasciculata and reticularis
14. Pathogenesis of Hypoadrenalism
Clinical manifestation occurs when at least 90% of the adrenal cortex is
destroyed
Primary hypoadrenalism; due to primary adrenal disease;
- increased levels of ACTH precursor hormone stimulate melanocytes,
results in hyperpigmentation of skin and mucosal surfaces (not in
secondary adrenocortical insufficiency)
- decreased aldosterone activity, results in potassium retention and
sodium loss, with resultant hyperkalemia, hyponatremia, volume
depletion, and hypotension
Secondary hypoadrenalism; deficient cortisol and androgen output but
normal or near-normal aldosterone synthesis, occasionally hypoglycemia
as a result of glucocorticoid deficiency and impaired gluconeogenesis