these slides contain a brief introduction of neurons and its classification as well as details of generation of action potential, resting potential and eletrotonic potential.
these slides contain a brief introduction of neurons and its classification as well as details of generation of action potential, resting potential and eletrotonic potential.
This presentation explains Physiology of blood, Variations in blood cells-Oral manifestations and Clinical importance, Blood groups and Transfusion of blood
metabolic effect of different hormones i.e insulin, glucagon, epinephrine and cortisol with their short introduction, structures, biosynthesis, mechanism of action and individual action on carbohydrate , lipid and protein metabolism.
Cardiac muscle (The Guyton and Hall Physiology)Maryam Fida
In the heart there is Atrial muscle and Ventricular muscle which are separated from each other by the fibrous AV Rings containing Valves.
ATRIAL MUSCLE: thin walled. There are two sheets, superficial and deep sheet. Superficial sheet is common over both atria. Deep sheet is separate for each atrium. Muscle fibers in the deep sheet are at right angle to the muscle fibers in the superficial sheet.
FUNCTIONS OF THE ATRIUM:
1. Receive venous blood from large veins. So atria act as reservoir.
2. Conduct the blood into the ventricles.
3. Atrial contraction is responsible for last 25 % of ventricular filling.
4. In the right atrium there is SA Node(Pace maker) and AV node.
5. In the wall of the atria, there are low pressure stretch receptors and these are involved in various reflexes like brain bridge reflex and left atrial reflex.
6. Atria also produce a hormone i.e. Atrial Natriuretic Hormone. Whenever NaCl increases in ECF, it causes release of ANH which causes natriuresis.
VENTRICULAR MUSCLE:
Much thicker than atrial muscle. Thickness of right ventricle wall is 3-4 mm and thickness of left ventricle is 8 – 12 mm.
1.Involuntary
2.Has cross striations
3.Each cardiac muscle fiber consists of a number of cardiac cells, united at ends in series. Where as in skeletal muscle each muscle fiber is individual cell.
4.Cardiac muscle cells are branching and interdigitate.
5.Single central nucleus in each cell.
6. Atrial muscle and ventricular muscle act as separate functional syncytium and impulses from atria are conducted to ventricles through the AV Node and AV Bundle.
7. Sarcoplasmic system is present. In skeletal muscle triad is at the junction of A and I bands. In cardiac muscle T Tubules are much large and thus in cardiac muscle if we take a section it may form a diad or a triad. And these diads and triads are present at the level of Z Disks.
8.Between adjacent cardiac cells there are side to side and end to end connections and these are the intercellular junctions. These junctions are Gap Junctions. Or intercalated discs
9.When one part of myocardium is excited the whole muscle is excited.
10.Whole myocardium obeys all or none law as a whole.
11.No spike potential but action potential with plateau.
12.Has got long refractory period.
Absolute refractory period in ventricular muscle is 250 – 300 milli sec.
In atrial muscle Absolute refractory period is 150 milli sec
Because of long refractory period cardiac muscle cannot be tetanized.
This presentation explains Physiology of blood, Variations in blood cells-Oral manifestations and Clinical importance, Blood groups and Transfusion of blood
metabolic effect of different hormones i.e insulin, glucagon, epinephrine and cortisol with their short introduction, structures, biosynthesis, mechanism of action and individual action on carbohydrate , lipid and protein metabolism.
Cardiac muscle (The Guyton and Hall Physiology)Maryam Fida
In the heart there is Atrial muscle and Ventricular muscle which are separated from each other by the fibrous AV Rings containing Valves.
ATRIAL MUSCLE: thin walled. There are two sheets, superficial and deep sheet. Superficial sheet is common over both atria. Deep sheet is separate for each atrium. Muscle fibers in the deep sheet are at right angle to the muscle fibers in the superficial sheet.
FUNCTIONS OF THE ATRIUM:
1. Receive venous blood from large veins. So atria act as reservoir.
2. Conduct the blood into the ventricles.
3. Atrial contraction is responsible for last 25 % of ventricular filling.
4. In the right atrium there is SA Node(Pace maker) and AV node.
5. In the wall of the atria, there are low pressure stretch receptors and these are involved in various reflexes like brain bridge reflex and left atrial reflex.
6. Atria also produce a hormone i.e. Atrial Natriuretic Hormone. Whenever NaCl increases in ECF, it causes release of ANH which causes natriuresis.
VENTRICULAR MUSCLE:
Much thicker than atrial muscle. Thickness of right ventricle wall is 3-4 mm and thickness of left ventricle is 8 – 12 mm.
1.Involuntary
2.Has cross striations
3.Each cardiac muscle fiber consists of a number of cardiac cells, united at ends in series. Where as in skeletal muscle each muscle fiber is individual cell.
4.Cardiac muscle cells are branching and interdigitate.
5.Single central nucleus in each cell.
6. Atrial muscle and ventricular muscle act as separate functional syncytium and impulses from atria are conducted to ventricles through the AV Node and AV Bundle.
7. Sarcoplasmic system is present. In skeletal muscle triad is at the junction of A and I bands. In cardiac muscle T Tubules are much large and thus in cardiac muscle if we take a section it may form a diad or a triad. And these diads and triads are present at the level of Z Disks.
8.Between adjacent cardiac cells there are side to side and end to end connections and these are the intercellular junctions. These junctions are Gap Junctions. Or intercalated discs
9.When one part of myocardium is excited the whole muscle is excited.
10.Whole myocardium obeys all or none law as a whole.
11.No spike potential but action potential with plateau.
12.Has got long refractory period.
Absolute refractory period in ventricular muscle is 250 – 300 milli sec.
In atrial muscle Absolute refractory period is 150 milli sec
Because of long refractory period cardiac muscle cannot be tetanized.
The muscle are biological motors which convert chemical energy into force and mechanical work.
This biological machinery is composed of proteins – which is actomyosin and the fuel is ATP.
With the use of muscles we are able to act on our environment.
It includes the basic anatomy physiology of skeletal muscles, the thorough working of the muscles, at superficial level to molecular level, the energy input, smooth muscle-cardiac-skeletal muscles differences, smooth muscle anatomy physiology.
Histology of the Digestive System II:
Stomach
Small intestine
Large intestine
Lecture presentation by Professor Tatiana Bororinkhina of First Moscow State Medical University
This presentation contains the basic information about nerve cells and action potential. This work is done for academic purpose only so if you are using give proper reference.
The nervous system is a complex collection of nerves and specialized cells known as neurons that transmit signals between different parts of the body. The presentation provides a simplified overview of the nervous system and its functions
Neuron communication belongs to subject ANIMAL PHYSIOLOGY in course of zoology.
nerve communication.
how neuron communicate?
RESTING MEMBRANE POTENTIAL
Measurement of Membrane Potential
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.
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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
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
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
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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.
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2. This Lecture is dedicated for all medical student
and for whom preparing for basic science exams
.Hope you will find it helpful.
3. What are the Excitable Tissue??
• cells and tissues in which excitation is accompanied by action
potential, distributed along the cellular membrane. This is a
property of the bodies of nerve cells and their processes—nerve
fibers, muscle fibers .
What is excitability?
• An ability of specialized cells to respond to certain stimuli by
producing electrical signals known as action potential at its
membrane .
Give examples of excitable tissues
• Nerve cells, muscle (cardiac/skeletal)
What are 2 basic properties of excitable cell membranes?
• 1. The membranes have an electrical excitability across the
membrane. (In response to depolarization of the membrane
above a certain threshold voltage) and may transmit an impulse
along the membrane
• 2. The membranes contain a variety of ion channels (pores) that
may be opened or closed, allowing specific ions to flow across.
What is Resting Membrane Potential (RMP)?
• Membrane potential difference (trans membrane voltage) that
exists when cell membranes of excitable tissues are not
producing an action potential (at rest)
4. Why does RMP occur?
• Because of build-up of negative charges inside the cells and
an equal build-up of positive charges outside the cells.
• The greater the difference in charges across the membrane,
the larger the membrane potential (voltage)
What is the RMP of nerve cells?
• -90mV (the potential inside the nerve fiber cells is 90 mV
more negative than the potential of the outside)
What is the RMP of skeletal muscle fibers?
• -80 to -90mV
What is the RMP of non-excitable tissue?
• +20mV out, -20mV in
“A cell that exhibits a membrane potential is said to be polarized”
2 main factors contribute to RMP. They are?
• 1. Distribution of ions across the membrane
• 2. Permeability of the membrane to Na⁺ and K⁺
5. What is the distribution of ions in extra and intracellular
fluid?
• Extracellular: rich in Na⁺ and Cl⁻ ions
• Intracellular: mainly K⁺ & organic phosphates + proteins
Explain about the permeability of the membrane to Na⁺ and K⁺
• Plasma membrane permeability to K⁺ is 50-100 times greater than its
permeability to Na⁺
The ion concentrations do not normally change very quickly (with the
exception of calcium). However, the membrane permeabilities can change in
a fraction of a milisecond, as a result of?
• Activation of ligand-gated or voltage-gated ion channels
The change in membrane potential can be large or small, depending on
how many ion channels are activated and what type they are. This type of
changes of the membrane potential are referred to as graded potentials
Explain a bit on graded potentials
• - affect locally
• - Non-propagated potential
• - In contrast to action potentials, AP have a constant amplitude and time
course, and propagated along the neighboring cell membranes.
2 types of voltage-gated ion channels are involved in these 2 phases.
What are they?
• 1. Na⁺ channels
• 2. K⁺ channels
6. Voltage-gated Na⁺ channels have 2 separate gates. What are
they?
• 1. Activation gates: close in resting membrane, open at
threshold
• 2. Inactivation gates: open in resting membrane, also open at
threshold
Following stimulation of excitable cells, a graded potential
causes membrane to depolarize to a critical level that is called
threshold .
Explain depolarization phase
• Rapid opening of Na+voltage-gated channels leads to Na+
inflow. this leads to loss of membrane polarization. (MP =
+30mV). An action potential rises to a constant and maximum
strength each time
Explain threshold depolarization
• Also stimulate slower opening of voltage gated K+ channels.
That its opening coincides with voltage-gated Na+ channels
closing.
What is the effect of K⁺ outflow?
• K+ outflow causes the resting membrane potential to be
restored = repolarization phase (MP = -70mV)
7. While the voltage-gated K⁺ channels are open, a large enough
outflow of K⁺ may lead to ????
After-hyperpolarization
What is hyperpolarization?
• Polarization more negative than the resting level (about -90mV)
• As the voltage-gated K⁺ channels close, what happens?
• RMP returns to the resting level (-70mV)
What is the refractory period?
• The period when excitable cells cannot generate another action potential
There are two types of refractory periods. What are they?
1. Absolute refractory period
2. Relative refractory period
What is the absolute refractory period?
Refers to the time period during which a 2nd action potential cannot be
initiated, even with a very strong stimulus. It coincides with Na⁺ channels
activation and inactivation. Inactivated Na⁺ channels cannot reopen, they must
first return to resting state.
What is relative refractory period?
• Refers to the time period during which a 2nd action potential can be
initiated, but only with a larger than threshold stimulus (supra threshold). It
coincides with the period when the voltage gated K⁺ channels are still open
after inactivated Na⁺ channels have returned to their resting state
Explain propagation (conduction) of action potentials
• As Na⁺ flows in, depolarization increases to threshold depolarization. This
open voltage-gated Na⁺ channels in adjacent patches of cell membrane
8. What is relative refractory period?
• Refers to the time period during which a 2nd action potential
can be initiated, but only with a larger than threshold stimulus
(supra threshold). It coincides with the period when the voltage
gated K⁺ channels are still open after inactivated Na⁺ channels
have returned to their resting state
Explain propagation (conduction) of action potentials
• As Na⁺ flows in, depolarization increases to threshold
depolarization. This open voltage-gated Na⁺ channels in adjacent
patches of cell membrane
What is the All-or-None principle?
• A principle of action potential generation. The depolarization
process travels over the entire membrane but if it does not
generate sufficient voltage to stimulate the next area of the
membrane, the spread of depolarization stops.
9. Compare between different excitable tissues in terms of
resting membrane potential
• The initiation and conduction of nerve and muscle action
potentials are similar, but they have different RMP's.
Neuron = -70mV Skeletal and cardiac muscle fibers = -90mV
Compare between different excitable tissues in terms of
velocity of conduction
• Nerve action potentials are 18x faster than muscle
Compare between different excitable tissues in terms of
duration of AP
• Neuron = 0.5 - 2.0 msec
Skeletal muscle fibers = 1.0 - 5.0 msec
Cardiac & smooth muscle fibers = 10 - 300 msec
What helps spread the action potential deep with the skeletal
muscle fiber?
• Transverse tubules. The T tubule action potentials cause
release of calcium ions inside the muscle fiber
10. • Cardiac muscle tissues contract without neural
stimulation. This property is called Automaticity
• This uploaded video will explain the RMP.
Click play
11. Resting Membrane Potential
When a neuron is not sending a signal, it is "at rest." When a neuron is
at rest, the inside of the neuron is negative relative to the outside.
Although the concentrations of the different ions attempt to balance
out on both sides of the membrane, they cannot because the cell
membrane allows only some ions to pass through channels (ion
channels). At rest, potassium ions (K+) can cross through the membrane
easily. Also at rest, chloride ions (Cl-)and sodium ions (Na+) have a more
difficult time crossing. The negatively charged protein molecules (A-)
inside the neuron cannot cross the membrane. In addition to these
selective ion channels, there is a pump that uses energy to move three
sodium ions out of the neuron for every two potassium ions it puts in.
Finally, when all these forces balance out, and the difference in the
voltage between the inside and outside of the neuron is measured, you
have the resting potential. The resting membrane potential of a neuron
is about -70 mV (mV=millivolt) - this means that the inside of the
neuron is 70 mV less than the outside. At rest, there are relatively more
sodium ions outside the neuron and more potassium ions inside that
neuron.
12. Action Potential
The resting potential tells about what happens when a neuron is at
rest. An action potential occurs when a neuron sends information
down an axon, away from the cell body. Neuroscientists use other
words, such as a "spike" or an "impulse" for the action potential.
The action potential is an explosion of electrical activity that is
created by a depolarizing current. This means that some event (a
stimulus) causes the resting potential to move toward 0 mV. When
the depolarization reaches about -55 mV a neuron will fire an action
potential. This is the threshold. If the neuron does not reach this
critical threshold level, then no action potential will fire. Also, when
the threshold level is reached, an action potential of a fixed sized
will always fire...for any given neuron, the size of the action
potential is always the same. There are no big or small action
potentials in one nerve cell - all action potentials are the same size.
Therefore, the neuron either does not reach the threshold or a full
action potential is fired - this is the "ALL OR NONE" principle.
13. Action potentials are caused when different ions cross the neuron
membrane. A stimulus first causes sodium channels to open. Because
there are many more sodium ions on the outside, and the inside of the
neuron is negative relative to the outside, sodium ions rush into the
neuron. Remember, sodium has a positive charge, so the neuron
becomes more positive and becomes depolarized. It takes longer for
potassium channels to open. When they do open, potassium rushes out
of the cell, reversing the depolarization. Also at about this time, sodium
channels start to close. This causes the action potential to go back
toward -70 mV (a repolarization). The action potential actually goes past
-70 mV (a hyperpolarization) because the potassium channels stay open
a bit too long. Gradually, the ion concentrations go back to resting levels
and the cell returns to -70 mV.
And there you have it...the Action Potential