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
Fluid and electrolytes management in post op patientsDr.Sonal Dixit
sonal dixit , mbbs , ms obg
After surgery modification in normal physiology of fluid and electrolytes balance.
- ACUTE STRESS leads to increased sympathetic stimuli- tachycardia, vasoconstriction & stress.
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Sodium is necessary for the body to maintain fluid balance and is critical for normal body function. It also helps to regulate nerve function and muscle contraction.
Hyponatremia and Hyponatremia.
Biochemical changes in pregnancy, Physiological changes in pregnancy, maternal and fetal health assessment, assessment of complications in pregnancy, hormonal changes and physiological evaluations in pregnancy
overview of calcium physiology
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MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
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Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
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Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
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
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
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
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
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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
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
2. OUTLINE
• Introduction
• Brief pathophysiology of DI
• Diagnostic work-ups for DI
• Management of DI
• Conclusion
• References
2
3. INTRODUCTION
• Whereas:
• Diabetes mellitus (DM) is a group of metabolic
diseases characterized by hyperglycemia resulting
from defects in insulin secretion, insulin action, or both.
•
• Diabetes insipidus (DI) is a disorder of water balance
characterized by large amounts of dilute urine and
increased thirst, due to defects in antidiuretic hormone
(ADH) secretion or its responsiveness.
3
4. The neurohypophysis
• Both ADH and Oxytocin are
nanopeptides which circulates as
free (unbound) hormones in
plasma, at physiologic pH.
• Oxytoin: Uterine contraction &
milk letdown reflexes.
4
5. Physiological actions of ADH
• V1a - smooth muscle of blood vessels, VEGF
(platelets aggregation, coagulation factor release)
• V1b - Anterior pituitary (ACTH release) & islet cells
(insulin release) in response to stress.
• In the kidneys, a transmembrane G-protein coupled
receptor for ADH, called V2 receptor, is located in the
collecting ducts of the renal tubules.
5
6. • ADH action at
the collecting
duct of renal
tubules:
6
7. • Normally, ADH is released in response to hypovolemia,
or an increase in plasma osmolality.
• Disorders of ADH involves excess hormone, as in
syndrome of inappropriate ADH secretion (SIADH), or
deficient states as in diabetes insipidus (DI).
• DI can result from ADH deficiency, ADH resistance or
renal tubular disease
7
8. • Normal plasma osmolality ranges from 275 – 295,
expressed either as mosm/kg or mmol/kg
• Plasma osmolality can be measured using an
osmometer, or calculated using the formula:
• 2[Na] + 2[K] + [Urea(mmol/L)] + [Glucose(mmol/L)]
• Normal urine osmolality varies widely from 250 – 750
mmol/kg
8
9. DIABETES INSIPIDUS (DI)
• DI is defined as a polyuric state (>3 L/24 hr)
characterized by low urine osmolality (< 300
mOsm/kg), high-normal plasma sodium & high-normal
plasma osmolality due to inadequate ADH activity.
• It is a pathologic diagnosis.
• Majorly, DI can be cranial or nephrogenic.
• Other forms are: gestational DI & primary polydipsia.
9
10. Causes of DI 10
CENTRAL D.I
Congenital Accquired
Familial DI
Midline malformations of the brain,
Pituitary malformations
DIDMOAD (Wolfram) syndrome
Brain tumours: craniopharyngioma, optic glioma, pituitary
adenoma, metastatic tumours
Head injury/trauma
Pituitary gland infarction, from: septic shock, Sheehan syndr,
hypoxic injury.
Infiltrative diseases: sarcoidosis, histiocytosis, leukemias
Brain cysts and cerebral aneurysms
Drugs: Opiates, alcohol, phenytoin etc
NEPHROGENIC D.I
Mutation of AVPR2 gene
Mutation of AQP2 gene
Lithium toxicity
Pyelonephritis
Ureteric obstruction: kidney stones, strictures renal damage
11. • There could also be idiopathic cause of DI.
• The most common form is central DI after trauma or
surgery to the region of the pituitary and
hypothalamus, which could manifest either as transient
or permanent.
• NOTE other causes of polyuria: psychogenic (primary)
polydipsia, osmotic diuretics and diabetes mellitus.
11
12. • Neurogenic/central DI results from a lack of ADH;
occasionally it can present with decreased thirst as
regulation of thirst center and ADH production are in
close proximity in the hypothalamus.
• Nephrogenic DI results from lack of aquaporin
channels in the distal collecting duct (decreased
surface expression and transcription).
12
13. • The lack of ADH prevents water reabsorption and the
osmolarity of the blood increases.
• With increased osmolarity, the osmoreceptors in the
hypothalamus detect this change and stimulate thirst.
With increased thirst, the person now experiences a
polydipsia and polyuria cycle.
13
14. Clinical features of DI
• Thirst / polydipsia is a common
feature, in patients with an
intact nervous thirst
mechanism.
• … while dehydration,
hypernatremia and weight loss
and shock can occur in
helpless patients.
14
15. DIAGNOSTIC WORK-UP FOR DI
• If the clinical presentation suggests DI, laboratory tests
must be performed to confirm the diagnosis, as
follows:
• A 24-hour urine collection for determination of urine volume
• Serum electrolyte concentrations, including calcium and
glucose levels
• Urinary specific gravity
• Simultaneous plasma and urinary osmolality
• Plasma ADH level
15
16. • Additional studies that may be indicated include the
following:
• Water deprivation (Miller-Moses) test to ensure
adequate dehydration and maximal stimulation of ADH
for diagnosis;
• Hypertonic saline infusion test;
• Pituitary studies, including magnetic resonance
imaging (MRI) and measurement of circulating pituitary
hormones other than ADH.
16
18. WATER DEPRIVATION TEST
• It is a dynamic, semiquantitative test tailored to ensure
adequate dehydration and maximal stimulation of ADH
for diagnosis, and is typically performed in patients with
chronic forms of DI.
• Water deprivation followed by the administration of 2 µg
i.m, of DDAVP; a synthetic analog of vasopressin may
help to differentiate central from nephrogenic DI.
• However, the result of this test must be interpreted with
caution, because patients with partial nephrogenic DI or
primary polydipsia may show similar response to that
seen in central DI.
18
19. • In healthy individuals, water deprivation
leads to a urinary osmolality that is 2-4
times greater than plasma osmolality.
• Additionally, in normal, healthy
subjects, administration of exogenous
ADH produces an increase of less than
10% in urinary osmolality.
• The duration of this test ranges from 4-
8 hours, as the time required to
achieve maximal urinary concentration
varies widely.
19
20. • Procedure:
• Patient should be in bed and closely observed.
• Patient not allowed food or water after 20.00 hr, on the night
before the test.
• Urinary osmolality and body weight are measured hourly.
• 08.00h: The bladder is emptied, blood and urine sample are
collected and their osmolalities are measured. If the plasma
osmolality is low-normal or low, water depletion is unlikely
and polyuria is probably due to an appropriate response to
a high intake.
20
21. • If the plasma osmolality is high-normal or high and the
urinary osmolality is more than 750 mmol/kg, the test
should be stopped.
• 09.00h… blood and urine are again collected and the
plasma and urinary osmolalities are measured hourly.
• If the urinary osmolality is more than 750 mmol/kg,
neither significant tubular disease nor DI is likely and
the test should be stopped.
21
22. • If the urinary osmolality is less than 750 mmol/kg and
plasma osmolality is normal, fluid restriction should be
continued and the estimations repeated at hourly
intervals. The test should be stopped as soon as the
urinary osmolality exceeds 750 mmol/kg.
• Failure of concentration of three (3) consecutive urine
specimens indicates either tubular disease or DI, from
which DDAVP should be administered henceforth.
22
23. • Remember:
• Urine osmolality below 300 mOsm/kg combined with
serum osmolality above 300 mOsm/kg (or with
hypernatremia) is diagnostic for diabetes insipidus.
• If urine osmolality is above 600 mOsm/kg and serum
osmolality is below 270 mOsm/kg, DI is unlikely.
23
Interpretation of the water deprivation test
25. • In central and nephrogenic DI, urinary osmolality will be
less than 300 mOsm/kg after water deprivation. After the
administration of ADH, the osmolality will rise to more than
750 mOsm/kg in central DI but will not rise at all in
nephrogenic DI.
• In primary polydipsia, urinary osmolality will be above 750
mOsm/kg after water deprivation. A urinary osmolality that
is 300-750 mOsm/kg after water deprivation and remains
below 750 mOsm/kg after administration of ADH may be
seen in partial central DI, partial nephrogenic DI, and
primary polydipsia.
25
26. • Water deprivation test results may be misleading in
patient with chronic primary polydipsia, who may
experience partial washout of the medullary interstitial
gradient and downregulation of ADH release. This
would resemble nephrogenic DI, with an inability to
concentrate urine.
• The combination of a plasma ADH assay with water
deprivation test, can lead to greater accuracy in
differentiating the different forms of DI from each other,
and from primary polydipsia.
26
28. HYPERTONIC SALINE INFUSION TEST
• Principles: the infusion of 5% hypertonic saline, by
raising plasma osmolality, would normally cause
maximal ADH secretion.
• The test overall lasts for about 3 hours and can be
initiated at 08:00 am. Medications that have diuretic or
anti-diuretic effects need to discontinued 24 hours prior
to testing.
• Results: patients with cranial DI have little or no rise in
ADH, but ADH is markedly released in nephrogenic DI.
28
29. • Procedures:
• The patient fasts from midnight till morning
• The patient lies in a supine position.
• Two intravenous cannulas are inserted, one for infusion and the
other for blood sampling.
• 5% saline is infused 0.04ml/kg per minute for 2hrs
• Blood samples are taken at baseline and 30 mins interval
• Plasma ADH is measured before & after the test along with urine
and plasma osmolality
• The patient must be closely monitored during the test.
Blood pressure and heart rate must be constantly
assessed, preferably on a monitor; and weight recorded.
29
30. • Other biochemical evaluation for DI could include a
morning plasma measurement of pituitary hormones
(growth hormone, prolactin, ACTH, TSH, FSH, and
LH).
• An MRI of the sella and suprasellar regions with
gadolinium may be obtained to evaluate for any
anatomical disruptions of the pituitary or hypothalamic
anatomy (macroadenomas, empty sella, infiltrative
diseases etc).
30
31. Management of DI
• Most patients with DI can drink enough fluid to replace their urine
losses. When oral intake is inadequate and hypernatremia is
present, provide fluid replacement as follows:
• Give dextrose and water or an intravenous fluid that is hypo-
osmolar with respect to the patient’s serum; do not administer
sterile water without dextrose IV.
• Administer fluids at a rate no greater than 500-750 mL/hr; aim at
reducing serum sodium by approximately 0.5 mmol/L (0.5
mEq/L) every hour
31
32. Pharmacologic therapeutic options include the following:
• Desmopressin (drug of choice for central DI)
• Synthetic vasopressin
• Thiazides
• Carbamazepine (rarely used; employed only when all
other measures prove unsatisfactory).
• Nonsteroidal anti-inflammatory drugs (NSAIDs), such as
indomethacin (may be used in nephrogenic DI, but only
when no better options exist).
32
33. CONCLUSION
• Making an accurate diagnosis of DI and ascertaining
its type and the underlying etiology poses a clinical
challenge, as there can be significant overlap in the
results among the various forms of polyuria-polydipsia
syndromes.
• However, specific testing protocols, such as the water
deprivation test in conjunction with DDAVP or the
hypertonic saline infusion test can assist with providing
a diagnosis with increased accuracy.
33
34. REFERENCES
Central Diabetes Insipidus. NORD (National
Organization for Rare Disorders). 2015. Archived from
the original on 21 February 2017.
Tietz Textbook of Clinical Chemistry and Molecular
Diagnostics; fifth Ed., by Karl Burtis et al.
Martin A. Crook; Clinical Chemistry and Metabolic
Medicine, 8th Edition.
Clinical Chemistry; Principles, Techniques &
Correlations, 7th Ed., by Bishop et al.
Harrison Principles of Internal Medicine, 18th Edition,
by Longo, Kasper, Fauci et al. McGraw-Hills Publishers,
2012.
34
Diabetes insipidus is unrelated to diabetes mellitus and the conditions have a distinct mechanism, though both can result in the production of large amounts of urine
The pituitary gland is a groundnut-sized oval structure, suspended from the the brain by a stalk (known as infundibulum). It sits within a small depression in the sphenoid bone, known as the sella turcica
Rathke's pouch is an evagination at the roof of the buccopharyngeal membrane (roof of the mouth). It gives rise to the anterior pituitary (adenohypophysis).
…adenylyl cyclase second messenger system
…translocate the aquaporin complex from intracellular pool in the cell body of the collecting duct to apical plasma memb & basolateral memb
…both are caused by deficiencies in AVP, but these deficiencies do not result from a defect in the neurohypophysis or kidneys.
Measurement of plasma copeptin at baseline and following arginine stimulation used as an effective means of differentiating DI from primary polydipsia. Result: a rise in copeptin concentrations from 2.1 pM and 3.6 pM, respectively, to a maximum of 2.5 pM and 7.9 pM, in pts with CDI & primary polydipsia respectively.
Incr plasma osm stim thirst, and if the pt is active & has free access to water: drinks excessive – polydipsia.
…such as occur with no access to water, with physically impaired, comatose/moribund pts. Here the loss of solute free water hyperNa, hyperOsm. Urine Osm remains low & polyuria contd. Dehydratn sets in, low BP & tachycardia
1-desamino-8-d-arginine vasopressin
The restriction of water for some hours shd stim ADH secretn from the post pituitary reabsorption of solute-free water from the collecting duct & passage of concentrated urine. Except in cases where response to ADH is impaired, or the countercurrent multiplication mech is impaired
Although widely regarded as the gold standard in literature for diagnosing DI, the water deprivation test does have its limitations
Hypertonic saline (3% saline, 513 mOsm/L) infusion is an alternative test that can be used in place of water deprivation test.
…diuretics, desmopressin, cortisol, NSAIDs
Medications that have diuretic or anti-diuretic effects (diuretics, SGLT-2 inhibitors, desmopressin, carbamazepine, chlorpropamide, glucocorticoids, non-steroidal anti-inflammatory drugs)