The document discusses the renin-angiotensin-aldosterone system (RAAS) which regulates blood pressure and fluid balance. RAAS involves the hormones renin, angiotensin II, and aldosterone. Renin is released by the kidneys in response to low sodium levels, low blood pressure, or sympathetic stimulation. Renin converts angiotensinogen to angiotensin I, which is then converted to angiotensin II by the lungs. Angiotensin II causes vasoconstriction, sodium reabsorption by the kidneys, aldosterone release by the adrenals, and thirst stimulation. This increases blood pressure and volume.
Introduction
HORMONES OF ADRENAL CORTEX
MINERALOCORTICOIDS
Aldosterone
Life-saving Hormone
Actions of aldosterone
Aldosterone escape or escape phenomenon
Regulation of aldosterone secretion
Renin–angiotensin system
Applied
I am a medical student. I have one friend who is persuing his MBBS degree in Taishan Medical UNiversity. I got these notes from him.
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"Let the Knowledge be spread" Dr. Bikesh
Introduction
HORMONES OF ADRENAL CORTEX
MINERALOCORTICOIDS
Aldosterone
Life-saving Hormone
Actions of aldosterone
Aldosterone escape or escape phenomenon
Regulation of aldosterone secretion
Renin–angiotensin system
Applied
I am a medical student. I have one friend who is persuing his MBBS degree in Taishan Medical UNiversity. I got these notes from him.
These notes are by Dr. Bikesh, He is a famous lecturer of TMU.
These notes have helped me a lot and i also watch his lecture videos , which are great; highly simple and huge content.
I am uploading with Renal physiology. If you want some other topics i would upload for you.
"Let the Knowledge be spread" Dr. Bikesh
BLOOD PRESSURE
BY: SAIYED FALAKAARA
ASSISTANT PROFESSOR
DEPARTMENT OF PHARMACY
SUMANDEEP VIDYAPEETH
Definition
Arterial blood pressure can be defined as the lateral pressure exerted by moving the column of blood on the walls of the arteries.
Significance
To ensure the blood flow to various organs
Plays an important role in exchange of nutrients and gases across the capillaries
Required to form urine
Required for the formation of lymph
Normal values
Normal adult range can fluctuate within a wide range and still be normal
Systolic/diastolic
100/60 – 140/80
Unit - mmHg
Describes the secretion and functions of Antidiuretic hormone, abnormalities associated with ADH secretion, reasons of SIADH etc in details with figures.
3. Renal Block-Water and Electrolyte Balance-MBBS-2024.pptxRajendra Dev Bhatt
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4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
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. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
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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
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
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
3. ANTIDIURETIC HORMONE
OVERVIEW
‣ Antidiuretic hormone (ADH), also known as vasopressin, is
a small peptide hormone which regulates the body’s
retention of water
‣ It is one of only two hormones secreted by the posterior
pituitary gland
‣ Learning Goal
‣ To discuss the synthesis, storage, release and action of
ADH, and consider its clinical relevance
4. ANTIDIURETIC HORMONE
SYNTHESIS AND STORAGE
‣ The synthesis of ADH occurs in the supraoptic and
paraventricular nuclei in the hypothalamus
‣ It is then transported to the posterior pituitary gland via
the neurohypophysial capillaries
‣ In the posterior pituitary gland, its synthesis is completed
and it is stored here until it is ready to be secreted into the
circulation
5. ANTIDIURETIC HORMONE
RELEASE
‣ The release of ADH is controlled by several factors
‣ The two most influential factors are changes in plasma
osmotic pressure, and volume status
‣ Other factors that promote the release of ADH include
exercise, angiotensin II, and emotional states such as pain
‣ ADH release is inhibited by atrial natriuretic peptide (ANP),
which is released by stretched atria in response to increases
in blood pressure, as well as alcohol and certain medications
6. ANTIDIURETIC HORMONE
OSMOTIC PRESSURE
‣ Osmoreceptors in the hypothalamus regulate the amount
of ADH released in response to changes in the osmotic
pressure of plasma
‣ They are located in the organum vasculosum of the lamina
terminalis (OVLT) and the subfornical organ, which are two
of the sensory circumventricular organs of the brain
‣ Both organs lack a blood-brain barrier, allowing them to
directly detect the osmolarity of the blood
7. ANTIDIURETIC HORMONE
OSMOTIC PRESSURE
‣ Osmotic pressure is dependent on the plasma osmolality
‣ Plasma osmolality is in turn affected by the total body plasma volume
‣ Following a fall in plasma volume there is an increase in the plasma
sodium (Na+) concentration, and therefore the osmolarity is increased
‣ Subsequently water exits cells, and moves down its concentration
gradient into the plasma
‣ This stimulates the osmoreceptors cells to contract, which results in
afferent signals being sent from the hypothalamus to the posterior
pituitary gland to increase the release of ADH
8. ANTIDIURETIC HORMONE
OSMOTIC PRESSURE
‣ Alternatively, if there is an increase in the total body
volume then the osmolality of the plasma will reduce
‣ In this situation, water will move down its concentration
gradient from the plasma, into osmoreceptor cells, causing
them to expand
‣ As a result, afferent signals are sent from the
hypothalamus to the posterior pituitary gland
to decrease the release of ADH
9. ANTIDIURETIC HORMONE
VOLUME STATUS
‣ ADH secretion also occurs during states of hypovolemia
‣ Baroreceptors in the left atrium, carotid artery and aortic arch
detect changes in arterial blood volume
‣ If blood pressure reduces, baroreceptors relay this to the vagus
nerve, which sends afferent signals that directly stimulates the
release of ADH from the posterior pituitary
‣ Conversely, in a hypervolemic state, the release of ADH will be
reduced
10. ANTIDIURETIC HORMONE
ACTION
‣ The main action of ADH in the kidney is to regulate the volume and osmolarity of
the urine
‣ Specifically, it acts in the distal convoluted tubule (DCT) and collecting ducts (CD)
‣ During states of increased plasma osmolality, ADH secretion is increased
‣ ADH acts through a G-protein coupled receptor to increase the transcription and
insertion of Aquaporin–2 channels to the apical membrane of the DCT and CD
cells
‣ Consequently, the permeability of the DCT and CD cells to water increases
‣ This allows water to move down its concentration gradient, out of the nephron
and back into the blood stream, thus normalizing plasma osmolality and
increasing total blood volume
11. ANTIDIURETIC HORMONE
ACTION
‣ In response to decreased plasma osmolarity, ADH release is reduced
‣ This reduces the number of Aquaporin-2 channels being inserted into the
apical membrane of the DCT and CD cells
‣ In turn, there is a subsequent reduction in the amount of water
reabsorbed from the nephron back in the blood stream
‣ In high concentrations, ADH can also act on the blood vessels to
increase peripheral vascular resistance, the result of which is increased
blood pressure
‣ This mechanism is useful in restoring blood pressure during hypovolemic
shock
17. ANTIDIURETIC HORMONE
REVIEW QUESTIONS
‣ Where is ADH stored and released into the circulation?
‣ Hypothalamus
‣ Posterior pituitary gland
‣ Juxtaglomerular apparatus
‣ Macula densa
18. ANTIDIURETIC HORMONE
REVIEW QUESTIONS
‣ Where is ADH stored and released into the circulation?
‣ Hypothalamus
‣ Posterior pituitary gland
‣ Juxtaglomerular apparatus
‣ Macula densa
‣ ADH is synthesized in the hypothalamus, but stored and
released by the posterior pituitary gland.
19. ANTIDIURETIC HORMONE
REVIEW QUESTIONS
‣ Where are osmoreceptors located in the brain?
‣ Subfornical terminalis
‣ Subfornical vasculosum of the lamina terminalis
‣ Organum vasculosum of the lamina temporalis
‣ Organum vasculosum of the lamina terminalis
20. ANTIDIURETIC HORMONE
REVIEW QUESTIONS
‣ Where are osmoreceptors located in the brain?
‣ Subfornical terminalis
‣ Subfornical vasculosum of the lamina terminalis
‣ Organum vasculosum of the lamina temporalis
‣ Organum vasculosum of the lamina terminalis
25. ANTIDIURETIC HORMONE
REVIEW QUESTIONS
‣ How will an increase of ADH impact sodium
concentration?
‣ Directly increase
‣ Decrease
‣ No change
‣ Indirectly increase
26. ANTIDIURETIC HORMONE
REVIEW QUESTIONS
‣ How will an increase of ADH impact sodium concentration?
‣ Directly increase
‣ Decrease
‣ No change
‣ Indirectly increase
‣ An increase of ADH will increase water reabsorption, and therefore
decrease sodium concentration. This can happen in dehydrated states,
but can also happen under normal conditions. This is then called
syndrome of inappropriate antidiuretic hormone secretion (SIADH).
28. THE RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM
OVERVIEW
‣ The Renin-Angiotensin-Aldosterone System (RAAS) is a hormone
system within the body that is essential for the regulation of blood
pressure and fluid balance
‣ The system is mainly comprised of the three hormones renin,
angiotensin II and aldosterone
‣ Primarily it is regulated by the rate of renal blood flow
‣ Learning Goal
‣ To describe the system, discuss how the system is regulated and
outline some clinically relevant points around it
30. THE RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM
RAAS - RENIN RELEASE
‣ The first stage of the RAAS is the release of the enzyme renin
‣ Renin released from granular cells of the renal juxtaglomerular
apparatus (JGA) in response to one of three factors:
‣ Reduced sodium delivery to the distal convoluted tubule detected
by macula densa cells
‣ Reduced perfusion pressure in the kidney detected by baroreceptors in
the afferent arteriole
‣ Sympathetic stimulation of the JGA via β1 adrenoreceptors
‣ The release of renin is inhibited by atrial natriuretic peptide (ANP), which is
released by stretched atria in response to increases in blood pressure
31. THE RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM
RAAS - PRODUCTION OF ANGIOTENSIN II
‣ Angiotensinogen is a precursor protein produced in the
liver and cleaved by renin to form angiotensin I
‣ Angiotensin I is then converted to angiotensin II
by angiotensin converting enzyme (ACE)
‣ This conversion occurs mainly in the lungs where ACE is
produced by vascular endothelial cells, although ACE is
also generated in smaller quantities within the renal
endothelium
32. THE RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM
RAAS - BINDING OF ANGIOTENSIN II
‣ Angiotensin II exerts its action by binding to various
receptors throughout the body
‣ It binds to one of two G-protein coupled receptors, the
AT1 and AT2 receptors
‣ Most actions occur via the AT1 receptor
‣ The following table outlines its effect at different points
34. THE RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM
EFFECTS OF ANGIOTENSIN II - CARDIOVASCULAR EFFECTS
‣ Angiotensin 2 acts on AT1 receptors found in the
endothelium of arterioles throughout the circulation to
achieve vasoconstriction
‣ This signalling occurs via a Gq protein, to activate
phospholipase C and subsequently increase intracellular
calcium
‣ The net effect of this is an increase in total peripheral
resistance and consequently, blood pressure
35. THE RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM
EFFECTS OF ANGIOTENSIN II - NEURAL EFFECTS
‣ Angiotensin II acts at the hypothalamus to stimulate the
sensation of thirst, resulting in an increase in fluid consumption
‣ This helps to raise the circulating volume and in turn, blood
pressure
‣ It also increases the secretion of ADH from the posterior
pituitary gland – resulting in the production of more
concentrated urine to reduce the loss of fluid from urination
‣ This allows the circulating volume to be better maintained until
more fluids can be consumed
36. THE RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM
EFFECTS OF ANGIOTENSIN II - NEURAL EFFECTS
‣ It also stimulates the sympathetic nervous system to increase
the release of noradrenaline (NA)
‣ This hormone is typically associated with the “fight or flight”
response in stressful situations and has a variety of actions
that are relevant to the RAAS:
‣ Increase in cardiac output
‣ Vasoconstriction of arterioles
‣ Release of renin
37. THE RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM
EFFECTS OF ANGIOTENSIN II - RENAL EFFECTS
‣ Angiotensin II acts on the kidneys to produce a variety of effects,
including afferent and efferent arteriole constriction and
increased Na+ reabsorption in the proximal convoluted tubule
‣ (These effects and their mechanisms are summarized in the table
on the next slide)
‣ Angiotensin II is also an important factor in tubuloglomerular
feedback, which helps to maintain a stable glomerular filtration rate
‣ The local release of prostaglandins, which results in a preferential
vasodilation to the afferent arteriole in the glomerulus, is also vital to
this process
38. https://teachmephysiology.com/urinary-system/regulation/the-renin-angiotensin-aldosterone-system/
Target Action Mechanism
Renal artery and afferent
arteriole
Vasoconstriction
Voltage-gated calcium
channels open and allow an
influx of calcium ions
Efferent arteriole
Vasoconstriction (greater
than the afferent arteriole)
Activation of AT1 receptor
Mesangial cells
Contraction, leading to a
decreased filtration area
Activation of Gq receptors
and opening of voltage-gated
calcium channels
Proximal convoluted tubule Increased Na+ reabsorption
Increased Na+/H+ antiporter
activity and adjustment of the
Starling forces in peritubular
capillaries to increase
paracellular reabsorption
39. THE RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM
ALDOSTERONE
‣ Finally, angiotensin II acts on the adrenal cortex to stimulate the release
of aldosterone
‣ Aldosterone is a mineralocorticoid, a steroid hormone released from
the zona glomerulosa of the adrenal cortex
‣ Aldosterone acts on the principal cells of the collecting ducts in the
nephron
‣ It increases the expression of apical epithelial Na+ channels (ENaC) to
reabsorb urinary sodium
‣ Furthermore, the activity of the basolateral Na+/K+/ATPase is increased
40. THE RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM
ALDOSTERONE
‣ This causes the additional sodium reabsorbed through ENaC
to be pumped into the blood by the sodium/potassium pump
‣ In exchange, potassium is moved from the blood into the
principal cell of the nephron
‣ This potassium then exits the cell into the renal tubule to be
excreted into the urine
‣ As a result, increased levels of aldosterone cause reduced
levels of potassium in the blood
46. THE RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM
REVIEW QUESTIONS
‣ What is the prime regulator of the RAAS?
‣ Serum sodium
‣ Renal blood flow
‣ Serum potassium
‣ Levels of cortisol
‣ Reduced flow, reduced pressure and sympathetic
stimulation drive the RAAS
48. THE RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM
REVIEW QUESTIONS
‣ From where is renin released?
‣ Granular cells of renal juxtoglomerular apparatus
‣ Liver
‣ Adrenal glands
‣ Renal tubules
‣ Renin is released from the juxtaglomerular apparatus is
response to specific triggers
50. THE RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM
REVIEW QUESTIONS
‣ Where is ACE predominantly found?
‣ Kidneys
‣ Brain
‣ Skin
‣ Lungs
‣ ACE is predominantly produced by vascular endothelial
cells in the lungs
55. THE RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM
REVIEW QUESTIONS
‣ From which structure is ADH released in response to
angiotensin 2?
‣ Anterior pituitary
‣ Hypothalamus
‣ Adrenal glands
‣ Posterior pituitary
56. THE RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM
REVIEW QUESTIONS
‣ From which structure is ADH released in response to
angiotensin 2?
‣ Anterior pituitary
‣ Hypothalamus
‣ Adrenal glands
‣ Posterior pituitary
57. THE RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM
REVIEW QUESTIONS
‣ Aldosterone causes which of the following electrolyte
changes?
‣ Increased serum sodium, increased serum potassium
‣ Increased serum sodium, reduced serum potassium
‣ Decreased serum sodium, decreased serum potassium
‣ Decreased serum sodium, increased serum potassium
58. THE RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM
REVIEW QUESTIONS
‣ Aldosterone causes which of the following electrolyte changes?
‣ Increased serum sodium, increased serum potassium
‣ Increased serum sodium, reduced serum potassium
‣ Decreased serum sodium, decreased serum potassium
‣ Decreased serum sodium, increased serum potassium
‣ By stimulating the Na/K pump, it causes increased sodium re-
absorption and increased potassium excretion
59. References
These slide reflect a summary of the contents of
TeachMePhysiology.com and are to be used for
educational purposes only in compliance with the terms of
use policy.
Specific portions referenced in this summary are as follows:
‣ https://teachmephysiology.com/urinary-system/regulation/antidiuretic-hormone/
‣ https://teachmephysiology.com/urinary-system/regulation/the-renin-angiotensin-
aldosterone-system/
Additional sources are referenced on the slide containing
that specific content.