This document discusses carbon monoxide (CO) poisoning, its pathophysiology, effects on fetuses, and management. CO poisoning occurs when endogenous or exogenous CO levels in the air rise. It binds to hemoglobin, reducing oxygen delivery. Fetuses are particularly susceptible due to higher CO-hemoglobin levels and slower CO elimination. Acute exposure can cause death from anoxia, while chronic exposure increases CO-hemoglobin levels. Effects on fetuses depend on gestational age and can include neurological and skeletal abnormalities as well as growth restriction. Management involves removal from the source, high-flow oxygen therapy, and hyperbaric oxygen in severe cases or when the fetus is compromised.
Please find the power point on Carbonmonoxide poisioning and Its management. I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
Please find the power point on Carbonmonoxide poisioning and Its management. I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
why people immediately or fastly died when they exposed or swallowed cyanide beacause their respiration inhibited.why it is inhibited here is the explanation .....
Lead is a blue-gray, heavy, soft metallic element that occurs naturally in the earth’s crust. It is a malleable metal, so it can be easily worked - you can hammer it into protective sheets or make pipes and bend them easily. It is dense, and has good shielding protection against radiation, so it is used as ballast or to shield against penetrating forms of ionizing radiation. Metallic lead is tasteless and odorless, although some of the oxides and salts of lead taste sweet. (This sweet taste of lead salts is a source of problems for children!). Lead is insoluble in water, but some of the salts do dissolve, hence lead salts can be carried long distances in water supplies. Lead fumes will be easily formed when lead is heated. Although there is not a lot of lead in the earth’s crust – lead is ubiquitous, especially in modern industry.
why people immediately or fastly died when they exposed or swallowed cyanide beacause their respiration inhibited.why it is inhibited here is the explanation .....
Lead is a blue-gray, heavy, soft metallic element that occurs naturally in the earth’s crust. It is a malleable metal, so it can be easily worked - you can hammer it into protective sheets or make pipes and bend them easily. It is dense, and has good shielding protection against radiation, so it is used as ballast or to shield against penetrating forms of ionizing radiation. Metallic lead is tasteless and odorless, although some of the oxides and salts of lead taste sweet. (This sweet taste of lead salts is a source of problems for children!). Lead is insoluble in water, but some of the salts do dissolve, hence lead salts can be carried long distances in water supplies. Lead fumes will be easily formed when lead is heated. Although there is not a lot of lead in the earth’s crust – lead is ubiquitous, especially in modern industry.
Bronchopulmonary dysplasia is a pathologic process leading to signs and symptoms of chronic lung disease that originates in the neonatal period.
Presented by Dr. Tahir
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
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- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
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.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
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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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.
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
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.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
2. PATHO-PHYSIOLOGY
CO is endogenous by- product of heme degradation
Its normal level increases during pregnancy 20%_40%
About 30% to 40% of this increase due to increase of
RBC load, and 15% comes from the fetus .
Fetus CO-HB 20% more than the mother .
Cause of this increase related to increase progesterone level
which induce heme metabolism by hepatic enzyme .
3.
4. Exogenous CO comes from partial burn of carbon
CO poisoning comes from increase its level in the air in closed
space .
Factors affecting CO uptakes :
1)Partial pressure of CO/ O2
2)ventilator rate
3)Duration of exposure
Minutes ventilation increase during
pregnancy make mother and fetus in the
highest level of suitability .
5. BIOCHEMICAL ASPECT OF CO POISONING
In the lung CO binds more slowly to Hb than O2
but once it binds to Hb its becomes extremely slow to dissociate
There is two form of Hb:
1)De-oxy state ( T ) chain has high affinity to
O2
2)Oxy state (R) chain has high affinity to CO
At CO partial pressure of 0.16 mmHg 75%
of Hb combine with CO
Less than 0.1% of inspired air
6.
7. FETUS AND CO POISONING
Fetus has( Hb F) which has high affinity to O2
than (Hb A) of the mother .
(Hb F) shift O2_ Hb dissociation curve to the left (
decrease dissociation of O2 from Hb ).
CO level in the fetus is also higher and also makes
the curve shifts to the left.
8. Acute CO exposure: death due to anoxia before
COHb increases .
Chronic exposure: COHb increases +++
Critical level 60% not possible to measure in the fetus but you
evaluated in the mother
Elimination in mother need 2hr
Elimination in fetus needs 7Hr
9.
10. TERATOGENIC EFFECT OF CO POISONING
Depends on gestational age:
Embryonic stage : neurological skeletal effect
Cleft palate .
Fetal phase: anoxia encephalopathy, growth restriction .
3rd trimester: premature delivery, decrease immunity, Rt side
cardiomegaly, delay myelination .
11. CO NEUROTOXICITY
23% to 47% of patients with CO poisoning develop delayed
neurological injury (the most frequent CO morbidity) .
Patient develops within 6 days to 3 weeks despite appropriate
management:
Impairment concentration and, or learning,
dementia,
cogwheel rigidity,
amnesia,
depression
12. PATHOLOGY OF CO NEUROTOXICITY
NE and dopamine increase after CO poisoning .
Oxidative stress and inflammatory response leads to
demyelination of nerves decrease nerve conductivity.
CO increase NO level in the blood vessels lead to vasodilatation;
increase brain blood flow and
neutrophils; secrete inflammatory response cause perivasciular
cell injury .
In the brain tissue microglia attacks oligodendrocytes produce
demyelination effect
14. Skeletal muscle necrosis can happen due to ischemia
Rhabdomyelesis leads to acute renal failure
Can be prevented or managed by supportive care with good
hydration
15. MANAGEMENT OF CO POISONING
symptoms and signs are not specific mimic viral
infection and gastroenteritis .
Best way to diagnose is to consider it often in
D.D (differential diagnosis) .
One needs high degree of suspicious to discover
CO poisoning
16. First aid starts with removal from closed space to open .
Start with 15 L 100% hyperbaric( HBO) O2 with
non rebreathing mask
HBO reduces elimination time from 4hr on room air to
about 20 minutes .
17. Indication of HBO in pregnancy
COHb > 15-20%
Maternal neurological signs
Evidence of fetal compromise
100% O2 recommended 5 times period longer in
pregnant patient than slandered considering fetal
CO elimination delay
