Introduction
Transport of O2 in the blood
Oxygen movement in the lungs and tissues
O2 dissociation curve
Bohr effect
Applied
Transport of CO2
The haldane effect
Chloride Shift or Hamburger Phenomenon
Reverse Chloride Shift
6) transport of oxygen and carbon dioxdideAyub Abdi
lecture 6: transportaion of both gases need a hemoglobin and part of them are transported by plasma. if Hb is low the saturation of oxygen also low and leads a hypoxia, fatigue, dyspnea, etc. in other hand acidosis can occur.
Once the oxygen diffuses across the alveoli, it enters the bloodstream and is transported to the tissues where it is unloaded, and carbon dioxide diffuses out of the blood and into the alveoli to be expelled from the body. Although gas exchange is a continuous process, the oxygen and carbon dioxide are transported by different mechanisms.
What You’ll Learn to Do
Describe how oxygen is bound to hemoglobin and transported to body tissues
Explain how carbon dioxide is transported from body tissues to the lungs
Transport of cabon dioxide in the bloodmed_students0
At the end of this session, the student should be able to:
Describe the forms in which carbon dioxide is transported in the blood.
Describe the importance of the chloride shift in the transport of carbon dioxide by blood and the changes caused by this shift.
Describe carbon dioxide dissociation curves and how it is affected by oxygen binding to hemoglobin.
Discuss respiratory acidosis and alkalosis, and their compensatory role (revise).
Define respiratory exchange ratio and mention the significance of its estimation.
GUYTON & HALL Textbook of Medical Physiology, 12th edition, page: 502-504.
Introduction
Transport of O2 in the blood
Oxygen movement in the lungs and tissues
O2 dissociation curve
Bohr effect
Applied
Transport of CO2
The haldane effect
Chloride Shift or Hamburger Phenomenon
Reverse Chloride Shift
6) transport of oxygen and carbon dioxdideAyub Abdi
lecture 6: transportaion of both gases need a hemoglobin and part of them are transported by plasma. if Hb is low the saturation of oxygen also low and leads a hypoxia, fatigue, dyspnea, etc. in other hand acidosis can occur.
Once the oxygen diffuses across the alveoli, it enters the bloodstream and is transported to the tissues where it is unloaded, and carbon dioxide diffuses out of the blood and into the alveoli to be expelled from the body. Although gas exchange is a continuous process, the oxygen and carbon dioxide are transported by different mechanisms.
What You’ll Learn to Do
Describe how oxygen is bound to hemoglobin and transported to body tissues
Explain how carbon dioxide is transported from body tissues to the lungs
Transport of cabon dioxide in the bloodmed_students0
At the end of this session, the student should be able to:
Describe the forms in which carbon dioxide is transported in the blood.
Describe the importance of the chloride shift in the transport of carbon dioxide by blood and the changes caused by this shift.
Describe carbon dioxide dissociation curves and how it is affected by oxygen binding to hemoglobin.
Discuss respiratory acidosis and alkalosis, and their compensatory role (revise).
Define respiratory exchange ratio and mention the significance of its estimation.
GUYTON & HALL Textbook of Medical Physiology, 12th edition, page: 502-504.
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
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
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Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
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- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
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New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
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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ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
3. Ventilation of the lungs supplies O₂ to the alveolus
Diffusion of O₂ across the alveolus to the pulmonary
capillaries
O₂ carriage by blood ( Hb or dissolved in plasma)
Diffusion from capillary to miochondria
4. OXYGEN CASCADE
• Describe the sequential reduction in Po₂ from atmosphere to cellular
mitochondria (site of consumption)
6. Alveolar gas equation
PAO2 = PIO2 – PACO2 / R
= 150 – (40/0.8)
= 100mmHg
• PACO2 = Alveolar partial pressure of oxygen
• PIO2 = Inspired partial pressure of oxygen
• PACO2 = Alveolar partial pressure of carbon dioxide
• RQ = Respiratory quotient = CO2 produced/ O2consumed = 0.8
• Respiratory exchange ratio
7.
8. Arterial Blood PO₂
• Source of contribution
• Blood from bronchial and Thebesian vein drain directly into the
pulmonary vein, avoiding pulmonary capillaries
• V/Q mismatch – blood not fully oxygenated as it passes through poorly
ventilated areas of the lung eg, pulm pathology
9. • 3 factors my cause the Po₂ in the pulmonary vein < PAO2
1. V/Q mismatch
2. Shunt
3. Diffusion impairment
Increase Alveolar-arterial (A-a) gradient
12. DISSOLVED O₂
• Obeys Henry’s law : the amount dissolved gas is proportional to the
partial pressure, Pa
• At T of 37°C, plasma contains 0.003ml O₂/mmHgPo2
16. • Hemoglobin is a complex molecule with a molecular weight of 64,500
• The protein globin has a tetrameric structure contains four
polypeptide chains
• Each of it is attached to a heme (iron porphyrin)
• Center ferrous ion
• Each hb molecule can bind with four oxygen molecules
• The chain are of two types, alpha and beta
• Hemoglobin A (normal adult Hb): 2α 2β
17. • Differences in their amino acid sequences give rise to various type of
human hemoglobin
• Hemoglobin F (fetal): 2α 2γ
• Higher affinity to oxygen
18. • Hemoglobin S (sickle): has valine instead of glutamic acid in the beta
chains
• Deoxygenated form is poorly soluble and crystallizes within the red
cell
• Cell shape changes from biconcave to crescent or sickle shaped
with increased fragility and a tendency to thrombus formation
19. • Methemoglobin
• Ferrous ion (Fe2+) oxidised to ferric (Fe3+) form by various drugs including
nitrites, sulfonamides and acetanilid or congenital cause in which the enzyme
methemoglobin reductase is deficient within the red blood cell.
21. P50
• The partial pressure of oxygen at which the oxygen carrying protein is 50%
saturated
• Normal p50 in adult hemoglobin is 26.6mmHg
• Lie at the steepest part of the curve, thus most sensitive point to detect the shift
of the curve
• Index of oxygen affinity
• P50 HbA = 26.6mmHg
• P50 HbF = 18mmHg
• P50 Myoglobin = 2.75mmHg
• The lower the P50 the higher the affinity towards O₂
22. Physiological significant
• Flat upper part acts as a buffer-
• PO2 can drop to 80mmHg, yet Hb remained highly saturated (96%) with
oxygen keeping the arterial [O2] high despite impairment in saturation in the
lungs
• Steep lower part allows large O2 unloading and maintain O2 diffusion
gradient (from capillary to cell) by only a small drop in PO2
23.
24. Bohr Effect
• The effect of CO2 and H+ (pH) toward the affinity of Hb for oxygen
• ↑CO2, H+ will cause ↓Hb affinity for O2, favour unloading, right
shifted ODC
25.
26.
27.
28.
29.
30.
31. Oxygen content
• 98% is carried bound to Hb in RBC, only 2% of O2 in arterial blood is
present as dissolved O2
• One gram of Hb can combine with 1.34 ml O2 when 100% saturated
• Functional Hb saturation= [HbO2] x ( [HbO2] + [DeoxyHb]
(1 gm pure Hb binds 1.39mls O2)
• Fractional saturation = ( [HbO2] x 100/total [Hb] )
where total [Hb] = [HbO2] + [DeoxyHb] + [metHb] + [COHb]
(Physiological value ~ 1.34 to 1.37 ml.O2/gmHb)
32. • Total O2 content of arterial blood
CaCO2 = [1.34x(Hb)xSaO2] + [PaCO2 x kO2]
• CaCO2=O2 content (mlO2/dl Blood)
• Hb= hemoglobin concentration (g/dl)
• SaO2= O2 saturation of Hb
• kO2= O2 solubility constant (0.003ml O2/mmHg/dl of blood)
• Normal blood contains 15 gm of Hb/dl of blood
• CaCO2= (1.34x15x1) + (0.003x100)
= 20.4 mls/dl blood
• Thus normal O2 content is about 20.4ml O2/ dl of blood
(if 100% saturated)
34. OXYGENT FLUX
• Amount of O₂ delivered to the peripheral tissues per minutes
• In healthy young adult, the tissues O₂ delivery is ~ 1000mls O₂/min
• Tissues extract 250mls O₂/min (body O₂ consumption)
• 750mls O₂ return to right heart
35. • Oxygen Flux equation
oxygen flux = chemical O2 delivery + Dissolved O2 delivery
= [CO x (Hb) x SaO2 x k] + [CO x PaO2 x 0.003]
= [50 x 15 x 0.99 x 1.34] + [50 x 100 x 0.003]
= 995 + 15
= approx 1000 mls O2/ min
k – Huffner’s number (1.34mlO2/gm.Hb)
CO in dl/min; Hb in gm/dl
36. CₐO₂ (O₂ content) X CO (cardiac output) = O₂ delivery ,DO₂ (Oxygen flux)
How to increase CₐO₂ and DO₂
• Increase circulating Hb
• Maintain high oxygen saturation
• Increase dissolved oxygen by increase partial pressure of oxygen
• Optimise HR and rhytm (sinus )
• Optimise SV (preload/contractality)
• Maintain perfusion pressure to ensure organ oxygen delivery (afterload)
37. • The amount of O₂ in the blood is determined by :
• Amount of dissolved O₂
• Amount of Hb in the blood
• Affinity of Hb to the O₂
43. Haldane Effect
• Refer to the effect of O2 on affinity of Hb to CO2
• Removal of O2 from Hb increases the affinity of Hb for CO2.
• Favour the loading of CO2 in the tissue level
• Arterial blood contains 48mls of CO2 at PCO2 of 40mmHg
• Mixed venous blood contains 52 mls of CO2 at PCO2 of 46mmHg
