Diabetes insipidus is an uncommon disorder that causes an imbalance of fluids in the body. This imbalance makes you very thirsty even if you've had something to drink. It also leads you to produce large amounts of urine
Diabetes insipidus is an uncommon disorder that causes an imbalance of fluids in the body. This imbalance makes you very thirsty even if you've had something to drink. It also leads you to produce large amounts of urine
Discussion #1
Diabetes Insipidus
Antidiuretic Hormone (ADH) is synthesized in the hypothalamus and secreted by the posterior pituitary. Its role plays part in the body’s osmotic balance, blood pressure regulation, and kidney function. ADH affects the ability of the kidney to reabsorb water and in addition induces expression of water transport proteins in the late distal tubule and collecting duct to increase water reabsorption (Cuzzo & Lappin, 2018). Diabetes Insipidus occurs with a decreased or absent ADH causing symptoms such as polyuria and polydipsia. Three types of diabetes insipidus include: neurogenic, nephrogenic, and polydipsic (McCance & Huether, 2014).
Neurogenic DI is the most commen and caused by insufficient amounts of ADH. Damage to the pituitary gland or hypothalamus from surgery, a tumor, a head injury or an illness can cause neurogenic diabetes insipidus by affecting the usual production, storage, and release of ADH (McCance & Huether, 2014).
Nephrogenic DI is often idiopathic. It occurs when there's a defect in the kidney tubules. The defect may be due to an inherited disorder or a chronic kidney disorder (McCance & Huether, 2014).
Polydipsic DI can cause production of large amounts of diluted urine. The underlying cause is drinking an excessive amount of fluids that is caused by damage to the thirst-regulating mechanism in the hypothalamus. The condition has also been linked to mental illness (McCance & Huether, 2014).
“DI must be distinguished from other polyuric states, including diabetes mellitus. The basic criteria for the diagnosis of DI include polyuria, polydipsia, low urine specific gravity (<1.010), low urine osmolality (<200 mOsm/kg), hypernatremia, high serum osmolality (300 mOsm or more depending on adequate water intake), and continued diuresis despite a serum sodium level of 145 mEq/L or greater” (McCance & Huether, p. 720).
Treatment for neurogenic diabetes insipidus includes increasing water intake or desmopressin (DDAVP).This medication replaces the missing anti-diuretic hormone and decreases urination. Treatment for nephrogenic diabetes insipidus includes stopping initial cause if medication induced or treatment with thiazide diuretics. Treatment for polydipsic diabetes insipidus includes decreasing fluid intake (McCance & Huether, 2014).
A red flag symptom requiring urgent treatment of diabetes insipidus would include passing large amounts of dilute urine. This can cause severe electrolyte disturbances and intravascular depletion leading to shock (McCance & Huether, 2014).
Discussion #2
Diabetes insipidus (DI) is a rare condition that occurs when your kidneys are not able to conserve water. DI is not related to diabetes mellitus, which is often referred to simply as diabetes. That means you can have DI without having diabetes. In fact, the condition can occur in anyone.
DI results in extreme thirst and frequent urination of dilute and odorless urine. There are several types of DI, and they can often .
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
Discussion #1
Diabetes Insipidus
Antidiuretic Hormone (ADH) is synthesized in the hypothalamus and secreted by the posterior pituitary. Its role plays part in the body’s osmotic balance, blood pressure regulation, and kidney function. ADH affects the ability of the kidney to reabsorb water and in addition induces expression of water transport proteins in the late distal tubule and collecting duct to increase water reabsorption (Cuzzo & Lappin, 2018). Diabetes Insipidus occurs with a decreased or absent ADH causing symptoms such as polyuria and polydipsia. Three types of diabetes insipidus include: neurogenic, nephrogenic, and polydipsic (McCance & Huether, 2014).
Neurogenic DI is the most commen and caused by insufficient amounts of ADH. Damage to the pituitary gland or hypothalamus from surgery, a tumor, a head injury or an illness can cause neurogenic diabetes insipidus by affecting the usual production, storage, and release of ADH (McCance & Huether, 2014).
Nephrogenic DI is often idiopathic. It occurs when there's a defect in the kidney tubules. The defect may be due to an inherited disorder or a chronic kidney disorder (McCance & Huether, 2014).
Polydipsic DI can cause production of large amounts of diluted urine. The underlying cause is drinking an excessive amount of fluids that is caused by damage to the thirst-regulating mechanism in the hypothalamus. The condition has also been linked to mental illness (McCance & Huether, 2014).
“DI must be distinguished from other polyuric states, including diabetes mellitus. The basic criteria for the diagnosis of DI include polyuria, polydipsia, low urine specific gravity (<1.010), low urine osmolality (<200 mOsm/kg), hypernatremia, high serum osmolality (300 mOsm or more depending on adequate water intake), and continued diuresis despite a serum sodium level of 145 mEq/L or greater” (McCance & Huether, p. 720).
Treatment for neurogenic diabetes insipidus includes increasing water intake or desmopressin (DDAVP).This medication replaces the missing anti-diuretic hormone and decreases urination. Treatment for nephrogenic diabetes insipidus includes stopping initial cause if medication induced or treatment with thiazide diuretics. Treatment for polydipsic diabetes insipidus includes decreasing fluid intake (McCance & Huether, 2014).
A red flag symptom requiring urgent treatment of diabetes insipidus would include passing large amounts of dilute urine. This can cause severe electrolyte disturbances and intravascular depletion leading to shock (McCance & Huether, 2014).
Discussion #2
Diabetes insipidus (DI) is a rare condition that occurs when your kidneys are not able to conserve water. DI is not related to diabetes mellitus, which is often referred to simply as diabetes. That means you can have DI without having diabetes. In fact, the condition can occur in anyone.
DI results in extreme thirst and frequent urination of dilute and odorless urine. There are several types of DI, and they can often .
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
3. LEARNING OUTCOMES
By the end of this presentation one will be able to:
define Diabetes insipidus (DI)
explain in detail the pathophysiology of DI
discuss the clinical manifestations of DI
explain clinical, laboratory and imaging diagnosis of DI
discuss the treatment for DI
explain the complications due to DI.
4. NORMAL REGULATION OF BODY
WATER
• Normally, low blood volume and high serum osmolarity
stimulates the hypothalamus to produce ADH which goes to
the posterior pituitary gland and is then released into the
blood stream. ADH reaches the nephrons of the kidney via
the bloodstream. Here, it acts on a specific part of the
nephron known as the collecting duct. In the collecting duct
are Aquaporin II channels which reabsorb water. ADH
stimulates production of more AQ2 channels, causing more
water reabsorption.
6. DIABETES INSIPIDUS
The disorder caused by hyposecretion or inadequate action of
Antidiuretic Hormone (ADH) or Vasopressin.
NB: ADH regulate the amount of body fluids(water).
In Diabetes Insipidus, there is decreased action of ADH, causing decrease
in aquaporin-II channels in collecting tubule and decreased water
reabsorption.
There are two main types of DI
1. Central Diabetes Insipidus
7. cont.
Cranial/ central DI is a common type of DI which
occurs when the body does not produce enough
ADH.
Nephrogenic DI: this is a type of DI where ADH is
produced at the right levels but kidneys do not
respond to the hormone (kidneys are resistant to the
ADH).
Other types of DI: gestational DI and dipsogenic DI
8. CAUSES OF DI
Central DI CAUSED BY:
• A brain tumor that damages hypothalamus
or pituitary gland.
• severe head injury that damages the
hypothalamus or pituitary.
9. cont.
• complications that occur during brain or pituitary
surgery.
• cancers that spread from another part of the body
to the brain.
• brain damage caused by a hypoxia, which can occur
during stroke or drowning.
10. cont.
Nephrogenic DI:
• Mutation of the aquaporin receptors.
• chronic kidney diseases such as
glomerulonephritis may also alter the response
of the kidney to ADH.
12. CLINICAL MANIFESTATION
• polyuria
the decreased action of ADH, leads to decreased collecting
tubule water reabsorption, leading to more urine production,
thereby resulting into frequent urination.
• polydipsia
Without ADH, the kidneys do not reabsorb water properly
leading to excessive water loss in large amounts of urine which
results in thirst increasing due to the body trying to balance the
water loss.
13. Cont.
• postural Hypotension
low level of ADH causes the failure of water
reabsorption. urine volume will increase
leading to dehydration and fall in blood
pressure.
14. • enuresis
decrease action of ADH, often intense with the
need to drink large amount of water, excessive
urine production, with the need to urinate
frequently(polyurea) often every hour,
throughout a day and night,thereby leading to
new onset of bedwetting.
15. Cont:
• hypovolemia
When there is low or no ADH released ,there
is no reabsorption which results in excessive
loss of water leading to dehydration.
16. cont.
• weight loss
low level of ADH leads to polydipsia which interferes with nutritional
intake
• Dehydration
Loss of water in Urine due to inadequate action of
ADH.
• Electrolytes imbalance
Low ADH result into failure of water reabsorption
leading to high electrolyte level in the body.
17. DIAGNOSIS
CLINICAL:
• Water deprivation test- involves not any liquid for several
hours to see how body respond .
LABORATORY
• Urinalysis: is the analysis of urine content
• decreased urine osmolality
19. cont.
IMAGING
• MRI scan: a scan that uses a strong magnetic
field and radio waves to produce images of the
brain.
• CT scan: a procedure that uses a computer
linked to an x-ray machine to make a series of
detailed pictures of brain.
20. TREATMENT
• Underlay cause management e.g. if DI is caused by
certain kidney diseases, the treatment must firstly
target the kidney disease.
• ADH replacement (desmopressin intake)
• symptoms management e.g. management of
hypotension, hypovolemia, weight loss.
• rehydration IV fluids (hypotonic)
21. COMPLICATIONS
• Chronic Dehydration:
A severe lack of water in the body caused by
Diabetes Insipidus due to failure of water
reabsorption.
Dehydration in DI can lead to:
- dizziness or lightheadedness
- headache
- dry mouth and lips
- sunken features (particularly the eyes)
- confusion and irritability
22. COMPLICATIONS
• Electrolytes imbalance
a condition of high minerals or electrolytes
concentration in the body fluids due to loss amount
of water they were contained in.
Which can in turn leads to
- Weakness
- Vomiting
- Loss of appetite
- muscles cramps
- Confusion
23. REFERENCES
Mayo clinic (2023) Diabetes Insipidus [online]. Available at:
https://www.mayoclinic.org/diseases-conditions/diabetes-
insipidus/symptoms-causes/syc-20351269 (Accessed 26 February 2023.
NHS (2023) Diabetes Insipidus [online]. Available at:
https://www.nhs.uk/conditions/diabetes-insipidus/ (Accessed 26 February
2023).
Sqadia (2023) Diabetes Insipidus [online].Available at:
https://www.sqadia.com/programs/diabetes-insipidus (Accessed 27 February
2023).
Gylyls, B. B, & Wedding, M, A. (2017) Medical Terminology System', "A Body
System Approach", F. A Davis Company, Philadelphia.
